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Title: Poisons: Their Effects and Detection - A Manual for the Use of Analytical Chemists and Experts
Author: Blyth, Alexander Wynter
Language: English
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Copyright Status: Not copyrighted in the United States. If you live elsewhere check the laws of your country before downloading this ebook. See comments about copyright issues at end of book.

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_Fourth Edition. At Press._


_With numerous Tables and Illustrations._

=General Contents.=

  History of Adulteration--Legislation, Past and Present--Apparatus
  useful to the Food Analyst--“Ash”--Sugar--Confectionery--Honey--
  Treacle--Jams and Preserved Fruits--Starches--Wheaten-Flour--Bread--
  Oats--Barley--Rye--Rice--Maize--Millet--Potato--Peas--Chinese Peas--
  Lentils--Beans--MILK--Cream--Butter--Cheese--Tea--Coffee--Cocoa and
  Wine--Vinegar--Lemon and Lime Juice--Mustard--Pepper--Sweet and Bitter
  Almond--Annatto--Olive Oil--Water. _Appendix_: Text of English and
  American Adulteration Acts.

    “Will be used by every Analyst.”--_Lancet._

    “STANDS UNRIVALLED for completeness of information. . . . A really
    ‘practical’ work for the guidance of practical men.”--_Sanitary

    “An ADMIRABLE DIGEST of the most recent state of knowledge. . . .
    Interesting even to lay-readers.”--_Chemical News._

_In Large 8vo, Handsome Cloth._ 21_s._



Professor of Medical Jurisprudence and Toxicology in Owens College,
Manchester; Examiner in Forensic Medicine in the University of London,
and in the Victoria University; Physician to the Salford Royal Hospital.

PART I.--Forensic Medicine. PART II.--Insanity in its Medico-legal
Bearings. PART III.--Toxicology.

    Medical Jurisprudence with which we are acquainted.”--_Dublin
    Medical Journal_.

    “A MOST USEFUL work of reference. . . . Of value to all those who,
    as medical men or lawyers, are engaged in cases where the testimony
    of medical experts forms a part of the evidence.”--_The Law





  M.R.C.S., F.I.C., F.C.S., &c.,


  With Tables and Illustrations.


  (_All Rights Reserved._)



The present edition, which appears on the same general plan as before,
will yet be found to have been in great part re-written, enlarged, and

Analytical methods which experience has shown to be faulty have been
omitted, and replaced by newer and more accurate processes.

The intimate connection which recent research has shown to exist between
the arrangement of the constituent parts of an organic molecule and
physiological action, has been considered at some length in a separate

The cadaveric alkaloids or ptomaines, bodies playing so great a part in
food-poisoning and in the manifestations of disease, are in this edition
treated of as fully as the limits of the book will allow.

The author, therefore, trusts that these various improvements,
modifications, and corrections will enable “POISONS” to maintain the
position which it has for so many years held in the esteem of
toxicologists and of the medical profession generally.

  _June, 1895_.




  Section                                                           Page

    1. The History of the _Poison-lehre_--The Origin of Arrow-Poison--
       Greek Myths,                                                    1
    2. Knowledge of the Egyptians relative to Poisons--Distillation of
       Peach-Water,                                                    2
    3. Roman and Greek Knowledge of Poison--Sanction of Suicide among
       the Ancients--The Classification of Poisons adopted by
       Dioscorides,                                                  2-4
    4. Poisoning among Eastern Nations--Slow Poisons,               4, 5
    5. Hebrew Knowledge of Poisons,                                    5
    6. The part which Poison has played in History--Statira--Locusta--
       Britannicus--The Rise of Anatomy--The Death of Alexander the
       Great--of Pope Alexander VI.--The Commission of Murder given by
       Charles le Mauvais--Royal Poisoners--Charles IX.--King John--A
       Female Poisoner boiled alive,                                 5-9
    7. The Seventeenth Century Italian Schools of Criminal Poisoning--
       The Council of Ten--John of Ragubo--The Professional Poisoner--
       J. B. Porta’s Treatise on _Natural Magic_--Toffana and the
       “_Acquetta di Napoli_”--Organic Arsenical Compounds--St. Croix
       and Madame de Brinvilliers--Extraordinary Precautions for the
       Preservation from Poison of the Infant Son of Henry VIII.,   9-13


    8. Phases through which the Art of Detecting Poisons has passed,  13
    9. Treatise of Barthélémy d’Anglais--Hon. Robert Boyle--Nicolas
       l’Emery’s _Cours de Chimie_--Mead’s _Mechanical Theory of
       Poisons_--Rise of Modern Chemistry--Scheele’s Discoveries, 13, 14
   10. History of Marsh’s Test,                                   14, 15
   11. Orfila and his _Traité de Toxicologie_--Orfila’s Method of
       Experiment,                                                    15
   12. The Discovery of the Alkaloids--Separation of Narcotine,
       Morphine, Strychnine, Delphinine, Coniine, Codeine, Atropine,
       Aconitine, and Hyoscyamine,                                15, 16
   13. Bibliography of the Chief Works on Toxicology of the Nineteenth
       Century,                                                    16-19



   14. The Legal Definition of Poison--English Law as to Poison,  20, 21
   15. German Law as to Poisoning--French Law as to Poisoning,    21, 22
   16. Scientific Definition of a Poison--The Author’s
       Definition,                                                22, 23


   17. Foderé’s, Orfila’s, Casper’s, Taylor’s, and Guy’s Definition of
       Poisons--Poisons arranged according to their Prominent
       Effects,                                                   23, 24
   18. Kobert’s Classification,                                   24, 25
   19. The Author’s Arrangement,                                   25-28


   20. Statistics of Poisoning in England and Wales during the Ten
       Years 1883-92--Various Tables,                              28-31
   21. German Statistics of Poisoning,                             31-33
   22. Criminal Poisoning in France,                              33, 34


   23. The Influence of Hydroxyl--The Replacement of Hydrogen by a
       Halogen--Bamberger’s Acylic and Aromatic Bases,            35, 36
   24. The Replacement of Hydrogen by Alkyls in Aromatic Bodies,   36-38
   25. The Influence of Carbonyl Groups,                              39
   26. Oscar Loew’s Theory as to the Action of Poisons,            39-41
   27. Michet’s Experiments on the relative Toxicity of Metals,   41, 42


   28. The Action of Poisons on Infusoria, Cephalopoda, Insects,   42-44
   29. Effect of Poisons on the Heart of Cold-blooded Animals,    44, 45
   30. The Effect of Poisons on the Iris,                         45, 46


   31. Concentration in a Vacuum--Drying the Substance--Solvents--
       Destruction of Organic Matter,                              46-50
   32. Autenrieth’s General Process--Distillation--Shaking up with
       Solvents--Isolation of Metals--Investigation of Sulphides
       Soluble in Ammonium Sulphide--of Sulphides Insoluble in Ammonium
       Sulphide--Search for Zinc and Chromium--Search for Lead, Silver,
       and Barium,                                                 50-53


   33. The Micro-Spectroscope--Oscar Brasch’s Researches of the Spectra
       of Colour Reactions--Wave Lengths,                          54-56

  _Examination of Blood or of Blood-Stains._

   34. Naked-eye Appearance of Blood-Stains--Dragendorff’s Process for
       Dissolving Blood,                                          56, 57
   35. Spectroscopic Appearances of Blood--Spectrum of Hydric Sulphide
       Blood--of Carbon Oxide Hæmoglobin--Methæmoglobin--of Acid
       Hæmatin--Tests for CO Blood--Piotrowski’s Experiments on CO
       Blood--Preparation of Hæmatin Crystals--The Guaiacum Test for
       Blood,                                                      57-62
   36. Distinction between the Blood of Animals and Men--The Alkalies
       in various Species of Blood,                               62, 63



   37. Properties of Carbon Monoxide,                                 64
   38. Symptoms--Acute Form--Chronic Form,                         64-66
   39. Poisonous Action on the Blood--Action on the Nervous
       System,                                                    66, 67
   40. _Post-mortem_ Appearances,                                     67
   41. Mass Poisonings by Carbon Monoxide--The Leeds Case--The
       Darlaston Cases,                                            67-70
   42. Detection of Carbon Monoxide--The Cuprous Chloride Method--
       Wanklyn’s Method--Hempel’s Method,                         70, 71


   43. Chlorine; its Properties--The Weldon Process of manufacturing
       “Bleaching Powder,”                                        71, 72
   44. Effects of Chlorine,                                           72
   45. _Post-mortem_ Appearances,                                     72
   46. Detection of Free Chlorine,                                    72


   47. Properties of Hydric Sulphide,                             72, 73
   48. Effects of breathing Hydric Sulphide--Action on the Blood--The
       Cleator Moor Case,                                         73, 74
   49. _Post-mortem_ Appearances,                                     74
   50. Detection,                                                     74




   51. Varieties and Strength of the Sulphuric Acids of Commerce--
       Properties of the Acid--Nordhausen Sulphuric Acid,         75, 76
   52. Properties of Sulphuric Anhydride,                             76
   53. Occurrence of Free Sulphuric Acid in Nature,                   76
   54. Statistics--Comparative Statistics of different Countries, 76, 77
   55. Accidental, Suicidal, and Criminal Poisoning--Sulphuric Acid in
       Clysters and Injections,                                   77, 78
   56. Fatal Dose,                                                78, 79
   57. Local Action of Sulphuric Acid--Effects on Mucous Membrane, on
       the Skin, on Blood,                                        79, 80
   58. Action of Sulphuric Acid on Earth, Grass, Wood, Paper, Carpet,
       Clothing, Iron--Caution necessary in judging of Spots--
       Illustrative Case,                                         80, 81
   59. Symptoms--(1) External Effects--(2) Internal Effects in the
       Gullet and Stomach--Intercostal Neuralgia,                  81-83
   60. Treatment of Acute Poisoning by the Mineral Acids,             83
   61. _Post-mortem_ Appearances--Rapid and Slow Poisoning--
       Illustrative Cases,                                         83-85
   62. Pathological Preparations in the different London Hospital
       Museums,                                                   85, 86
   63. Chronic Poisoning,                                             86

  _Detection and Estimation of Free Sulphuric Acid._

   64. General Method of Separating the Free Mineral Acids--The Quinine
       Process--The Old Process of Extraction by Alcohol--Hilger’s Test
       for Mineral Acid,                                          87, 88
   65. The Urine--Excretion of Sulphates in Health and Disease--The
       Characters of the Urine after taking Sulphuric Acid,        88-90
   66. The Blood in Sulphuric Acid Poisoning,                         90
   67. The Question of the Introduction of Sulphates by the Food--
       Largest possible Amount of Sulphates introduced by this Means--
       Sulphur of the Bile--Medicinal Sulphates,                  90, 91


   68. General Properties of Hydrochloric Acid--Discovery--Uses--
       Tests,                                                     91, 92
   69. Statistics,                                                92, 93
   70. Fatal Dose,                                                    93
   71. Amount of Free Acid in the Gastric Juice,                  93, 94
   72. Influence of Hydrochloric Acid on Vegetation--Present Law on the
       Subject of Acid Emanations from Works--The Resistant Powers of
       various Plants,                                                94
   73. Action on Cloth and Manufactured Articles,                     95
   74. Poisonous Effects of Hydrochloric Acid Gas--Eulenberg’s
       Experiments on Rabbits and Pigeons,                        95, 96
   75. Effects of the Liquid Acid--Absence of Corrosion of the Skin--
       Pathological Appearances--Illustrative Cases,              96, 97
   76. _Post-mortem_ Appearances--Preparations in the different London
       Museums,                                                   97, 98
   77. (1) Detection of Free Hydrochloric Acid--Günzburg’s Test--A.
       Villiers’s and M. Favolle’s Test--(2) Quantitative Estimation,
       Sjokvist’s Method--Braun’s Method,                         98-101
   78. Method of Investigating Hydrochloric Acid Stains on Cloth,
       &c.,                                                     101, 102


   79. Properties of Nitric Acid,                               102, 103
   80. Use in the Arts,                                              103
   81. Statistics,                                                   103
   82. Fatal Dose,                                                   104
   83. Action on Vegetation,                                         104
   84. Effects of Nitric Acid Vapour--Experiments of Eulenberg and O.
       Lassar--Fatal Effect on Man,                             104, 105
   85. Effects of Liquid Nitric Acid--Suicidal, Homicidal, and
       Accidental Deaths from the Acid,                         105, 106
   86. Local Action,                                                 106
   87. Symptoms--The Constant Development of Gas--Illustrative
       Cases,                                                   106, 107
   88. _Post-mortem_ Appearances--Preparations in various Anatomical
       Museums,                                                  107-109
   89. Detection and Estimation of Nitric Acid,                 109, 110


   90. Symptoms and Detection,                                       110


   91. Properties of Ammonia,                                        111
   92. Uses--Officinal and other Preparations,                  111, 112
   93. Statistics of Poisoning by Ammonia,                           112
   94. Poisoning by Ammonia Vapour,                                  112
   95. Symptoms--Illustrative Case,                             112, 113
   96. Chronic Effects of the Gas,                                   113
   97. Ammonia in Solution--Action on Plants,                        113
   98. Action on Human Beings and Animal Life--Local Action on Skin--
       Action on the Blood--Time of Death,                       113-115
   99. _Post-mortem_ Appearances,                                    115
  100. Separation of Ammonia--Tests,                            115, 116
  101. Estimation of Ammonia,                                        116


  102. Properties of Potassium Hydrate,                         116, 117
  103. Pharmaceutical Preparations,                                  117
  104. Carbonate of Potash,                                          117
  105. Bicarbonate of Potash,                                        117
  106. Caustic Soda--Sodium Hydrate,                            117, 118
  107. Carbonate of Soda,                                            118
  108. Bicarbonate of Soda,                                          118
  109. Statistics,                                                   118
  110. Effects on Animal and Vegetable Life,                    118, 119
  111. Local Effects,                                                119
  112. Symptoms,                                                     119
  113. _Post-mortem_ Appearances,                                119-121
  114. Chemical Analysis,                                            121
  115. Estimation of the Fixed Alkalies,                        121, 122


  116. Relative Toxicity of Sodium, Potassium, and Ammonium Salts,   122
  117. Sodium Salts,                                                 122
  118. Potassium Salts--Potassic Sulphate--Hydropotassic Tartrate--
       Statistics,                                                   122
  119. Action on the Frog’s Heart,                                   122
  120. Action on Warm-Blooded Animals,                          122, 123
  121. Elimination,                                                  123
  122. Nitrate of Potash,                                            123
  123. Statistics,                                                   123
  124. Uses in the Arts,                                             123
  125. Action of Nitrates of Sodium and Potassium--Sodic
       Nitrite,                                                 123, 124
  126. _Post-mortem_ Appearances from Poisoning by Potassic Nitrate, 124
  127. Potassic Chlorate,                                            124
  128. Uses,                                                         124
  129. Poisonous Properties,                                         124
  130. Experiments on Animals,                                  124, 125
  131. Effects on Man--Illustrative Cases of the Poisoning of Children
       by Potassic Chlorate,                                         125
  132. Effects on Adults--Least Fatal Dose,                          126
  133. Elimination,                                                  126
  134. Essential Action of Potassic Chlorate on the Blood and
       Tissues,                                                      126
  135. Detection and Estimation of Potassic Chlorate,           126, 127

  _Toxicological Detection of Alkali Salts._

  136. Natural occurrence of Potassium and Sodium Salts in the Blood
       and Tissues--Tests for Potassic and Sodic Salts--Tests for
       Potassic Nitrate--Tests for Chlorates--Ammonium Salts,   127, 128




  1.  _Petroleum._

  137. Petroleum,                                                    129
  138. Cymogene,                                                     129
  139. Rhigolene,                                                    129
  140. Gasolene,                                                     129
  141. Benzoline--Distinction between Petroleum-Naphtha, Shale-Naphtha,
       and Coal-Tar Naphtha,                                    129, 130
  142. Paraffin Oil,                                                 130
  143. Effects of Petroleum--Experiments on Rabbits, &c.,       130, 131
  144. Poisoning by Petroleum--Illustrative Cases,                   131
  145. Separation and Tests for Petroleum,                           131

  2. _Coal-Tar Naphtha--Benzene._

  146. Composition of Commercial Coal-Tar Naphtha,                   131
  147. Symptoms observed after Swallowing Coal-Tar Naphtha,          132
  148. Effects of the Vapour of Benzene,                             132

  _Detection and Separation of Benzene._

  149.  Separation of Benzene--(1) Purification; (2) Conversion into
        Nitro-Benzene; (3) Conversion into Aniline,             132, 133

  3. _Terpenes--Essential Oils--Oil of Turpentine._

  150. Properties of the Terpenes, Cedrenes, and Colophenes,         133

  4. _Oil of Turpentine--Spirits of Turpentine._

  151. Terebenthene--Distinction between French and English
       Turpentine,                                              133, 134
  152. Effects of the Administration of Turpentine,                  134


  153. Properties of Camphor,                                        135
  154. Pharmaceutical Preparations,                                  135
  155. Symptoms of Poisoning by Camphor,                             135
  156. _Post-mortem_ Appearances,                                    136
  157. Separation from the Contents of the Stomach,                  136


  1. _Ethylic Alcohol._

  158. Chemical Properties of Alcohol--Statistics of Poisoning by
       Alcohol,                                                      136
  159. Criminal or Accidental Alcoholic Poisoning,                   137
  160. Fatal Dose,                                                   137
  161. Symptoms of Acute Poisoning by Alcohol,                  137, 138
  162. _Post-mortem_ Appearances,                               138, 139
  163. Excretion of Alcohol,                                    139, 140
  164. Toxicological Detection,                                      140

  2. _Amylic Alcohol._

  165. Properties of Amylic Alcohol,                                 140
  166. Experiments as to the Effect on Animals of Amylic
       Alcohol,                                                 140, 141
  167. Detection and Estimation of Amylic Alcohol,                   141
  168. Amyl Nitrite--Properties--Symptoms--_Post-mortem_
       Appearances,                                                  141


  169. Properties of Ethylic Ether,                             141, 142
  170. Ether as a Poison,                                            142
  171. Fatal Dose,                                                   142
  172. Ether as an Anæsthetic,                                  142, 143
  173. Separation of Ether from Organic Fluids, &c.,                 143


  174. Discovery of Chloroform--Properties, Adulterations, and Methods
  for Detecting them,                                            143-145
  175. Methods of Manufacturing Chloroform,                     145, 146

  _Poisonous Effects of Chloroform._

  1. _As a Liquid._

  176. Statistics,                                                   146
  177. Local Action,                                                 146
  178. Action on Blood, Muscle, and Nerve-Tissue,                    146
  179. General Effects of Liquid Chloroform--Illustrative
       Cases,                                                   146, 147
  180. Fatal Dose,                                                   147
  181. Symptoms,                                                     148
  182. _Post-mortem_ Appearances,                               148

  2. _The Vapour of Chloroform._

  183. Statistics of Deaths through Chloroform--Anæsthesia,     148, 149
  184. Suicidal and Criminal Poisoning--Illustrative Cases,     149, 150
  185. Physiological Effects,                                        150
  186. Symptoms witnessed in Death from Chloroform Vapour,      150, 151
  187. Chronic Chloroform Poisoning--Mental Effects from Use of
       Chloroform,                                              151, 152
  188. _Post-mortem_ Appearances,                                    152
  189. The Detection and Estimation of Chloroform--Various
       Tests,                                                   152, 153
  190. Quantitative Estimation,                                      153


  191. Methyl Chloride--Methene Dichloride, &c.,                     154
  192. Pentane,                                                      154
  193. Aldehyde,                                                     154
  194. Paraldehyde,                                                  154


  195. Chloral Hydrate; its Composition and Properties,         154, 155
  196. Detection,                                                    155
  197. Quantitative Estimation of Chloral Hydrate,              155, 156
  198. Effects of Chloral Hydrate on Animals--Depression of Temperature
       --Influence on the Secretion of Milk, &c.,               156, 157
  199. Action upon the Blood,                                        157
  200. Effects on Man,                                          157, 158
  201. Fatal Dose,                                              158, 159
  202. Symptoms,                                                     159
  203. Action of Chloral upon the Brain,                             159
  204. Treatment of Acute Chloral Poisoning,                         160
  205. Chronic Poisoning by Chloral Hydrate,                    160, 161
  206. Manner in which Chloral is Decomposed in, and Excreted from, the
       Body,                                                    161, 162
  207. Separation from Organic Matters--Tests for Chloral,      162, 163


  208. Properties of Bisulphide of Carbon,                           163
  209. Poisoning by Bisulphide of Carbon,                            163
  210. Action on Animals,                                       163, 164
  211. Chronic Poisoning by Bisulphide of Carbon--Effects on the Brain,
       &c.,                                                     164, 165
  212. _Post-mortem_ Appearances,                                    165
  213. Separation and Detection of Carbon Bisulphide--Tests,         165
  214. Xanthogenic Acid,                                             165
  215. Potassic Xanthogenate,                                        165


  216. Properties and Sources of Carbolic Acid,                 165, 166
  217. Different Forms of Carbolic Acid--Calvert’s Carbolic Acid Powder
       --Carbolic Acid Soaps,                                   166, 167
  218. Uses of Carbolic Acid,                                        167
  219. Statistics Relative to Poisoning by Carbolic Acid,        167-169
  220. Fatal Dose,                                                   169
  221. Effects on Animals--Infusoria--Fish--Frogs,              169, 170
  222. Effects on Warm-Blooded Animals,                              170
  223. Symptoms Produced in Man--External Application--Action on the
       Skin--Effects of the Vapour--Use of Carbolic Acid Lotions--
       Injections, &c.--Illustrative Cases,                      170-172
  224. Internal Administration--Illustrative Cases,                  173
  225. General Review of the Symptoms induced by Carbolic Acid, 173, 174
  226. Changes Produced in the Urine by Carbolic Acid,          174, 175
  227. The Action of Carbolic Acid considered Physiologically,  175, 176
  228. Forms under which Carbolic Acid is Excreted,                  176
  229. _Post-mortem_ Appearances,                               176, 177

  _Tests for Carbolic Acid._

  230. (1) The Pine-Wood Test--(2) Ammonia and Hypochlorite Test--(3)
       Ferric Chloride--(4) Bromine,                            177, 178
  231. Quantitative Estimation of Carbolic Acid,                178, 179
  232. Properties of Cresol, and Tests for Distinguishing Cresol and
       Carbolic Acid,                                                179
  233. Properties of Creasote--Tests,                           179, 180
  234. Separation of Carbolic Acid from Organic Fluids or
       Tissues,                                                 180, 181
  235. Examination of the Urine for Phenol or Cresol,                181
  236. Assay of Disinfectants, Carbolic Acid Powders--E. Waller’s
       Process--Koppeschaar’s Volumetric Method--Colorimetric Method of
       Estimation,                                               181-183
  237. Carbolic Acid Powders,                                        183
  238. Carbolic Acid Soaps,                                          183


  239. Properties and Varieties,                                183, 184
  240. Effects of Poisoning by Nitro-Benzene,                        184
  241. Illustrative Cases of Poisoning by Nitro-Benzene Vapour, 184, 185
  242. Effects Produced by taking Liquid Nitro-Benzene,         185, 186
  243. Fatal Dose,                                              186, 187
  244. Pathological Appearances,                                     187
  245. The Essential Action of Nitro-Benzene,                   187, 188
  246. Detection and Separation from the Animal Tissues,             188


  247. Properties of Ortho-, Meta-, and Para-Dinitro-Benzol,         189
  248. Effects of Dinitro-Benzol,                               189, 190
  249. The Blood in Nitro-Benzol Poisoning,                          191
  250. Detection of Dinitro-Benzol,                                  192


  251. Properties of Hydrocyanic Acid,                               192
  252. Medicinal Preparations of Prussic Acid--Various Strengths of the
       Commercial Acid,                                         192, 193
  253. Poisoning by Prussic Acid--Uses in the Arts--Distribution in the
       Vegetable Kingdom,                                        193-195
  254. Composition and Varieties of Amygdalin,                       195
  255. Statistics of Poisoning by Prussic Acid,                  195-197
  256. Accidental and Criminal Poisoning,                       197, 198
  257. Fatal Dose,                                                   198
  258. Action of Hydric and Potassic Cyanides on Living
       Organisms,                                               198, 199
  259. Symptoms observed in Animals,                            199, 200
  260. Length of Interval between taking the Poison and Death in
       Animals,                                                 200, 201
  261. Symptoms in Man,                                         201, 202
  262. Possible Acts after taking the Poison--Nunneley’s
       Experiments,                                             202, 203
  263. Chronic Poisoning by Hydric Cyanide,                          203
  264. _Post-mortem_ Appearances,                               203, 204
  265. Tests for Hydrocyanic Acid and Cyanide of Potassium--Schönbein’s
       Test--Kobert’s Test,                                      204-206
  266. Separation of Hydric Cyanide or Potassic Cyanide from Organic
       Matters--N. Sokoloff’s Experiments,                       206-208
  267. How long after Death can Hydric or Potassic Cyanide be
       Detected?                                                208, 209
  268. Estimation of Hydrocyanic Acid or Potassic Cyanide,           209
  269. Case of Poisoning by Bitter Almonds,                     209, 210

  _Poisonous Cyanides other than Hydric and Potassic Cyanides._

  270. General Action of the Alkaline Cyanides--Experiments with
       Ammonic Cyanide Vapour,                                       210
  271. The Poisonous Action of several Metallic and Double Cyanides--
       The Effects of Mercuric and Silver Cyanides; of Potassic and
       Hydric Sulphocyanides; of Cyanogen Chloride; of Methyl Cyanide,
       and of Cyanuric Acid,                                    210, 211


  272. Properties of Phosphorus--Solubility--Effects of Heat on
       Phosphorus,                                              212, 213
  273. Phosphuretted Hydrogen--Phosphine,                            213
  274. The Medicinal Preparations of Phosphorus,                     213
  275. Matches and Vermin Paste,                                 213-215
  276. Statistics of Phosphorus Poisoning,                      215, 216
  277. Fatal Dose,                                                   216
  278. Effects of Phosphorus,                                        217
  279. Different Forms of Phosphorus Poisoning,                 217, 218
  280. Common Form,                                             218, 219
  281. Hæmorrhagic Form,                                             219
  282. Nervous Form,                                                 219
  283. Sequelæ,                                                 219, 220
  284. Period at which the First Symptoms commence,                  220
  285. Period of Death,                                              220
  286. Effects of Phosphorus Vapour--Experiments on Rabbits,    220, 221
  287. Effects of Chronic Phosphorus Poisoning,                 221, 222
  288. Changes in the Urinary Secretion,                             222
  289. Changes in the Blood,                                    222, 223
  290. Antidote--Treatment by Turpentine,                            223
  291. Poisonous Effects of Phosphine,                          223, 224
  292. Coefficient of Solubility of Phosphine in Blood compared with
       Pure Water,                                                   224
  293. _Post-mortem_ Appearances--Effects on the Liver,          224-228
  294. Pathological Changes in the Kidneys, Lungs, and Nervous
       System,                                                       228
  295. Diagnostic Differences between Acute Yellow Atrophy of the Liver
       and Fatty Liver produced by Phosphorus,                  228, 229
  296. Detection of Phosphorus--Mitscherlich’s Process--The Production
       of Phosphine--Tests Dependent on the Combustion of Phosphine,
  297. The Spectrum of Phosphine--Lipowitz’s Sulphur Test--Scherer’s
       Test,                                                    232, 233
  298. Chemical Examination of the Urine,                       233, 234
  299. Quantitative Estimation of Phosphorus,                        234
  300. How long can Phosphorus be recognised after Death?       234, 235




  301. General Tests for Alkaloids,                                  236
  302. Group-Reagents,                                          236, 237
  303. Phosphomolybdic, Silico-Tungstic, and Phospho-Tungstic Acids as
       Alkaloidal Reagents,                                      237-239
  304. Schulze’s Reagent,                                            239
  305. Dragendorff’s Reagent,                                        239
  306. Colour Tests,                                                 239
  307. Stas’s Process,                                               239

  _Methods of Separation._

  308. Selmi’s Process for Separating Alkaloids,                240, 241
  309. Dragendorff’s Process,                                    241-254
  310. Shorter Process for Separating some of the Alkaloids,    254, 255
  311. Scheibler’s Process for Alkaloids,                            255
  312. Grandval and Lajoux’s Method,                            255, 256
  313. Identification of the Alkaloids,                              256
  314. Sublimation of the Alkaloids,                             256-261
  315. Melting-point,                                                261
  316. Identification by Organic Analysis,                      261, 262
  317. Quantitative Estimation of the Alkaloids--Mayer’s Reagent--
       Compound of the Alkaloids with Chlorides of Gold and Platinum,


  1. _The Alkaloids of Hemlock_ (_Conium_).

  318. Botanical Description of Hemlock,                             264
  319. Properties of Coniine--Tests,                             264-266
  320. Other Coniine Bases,                                          266
  321. Pharmaceutical Preparations of Hemlock,                  266, 267
  322. Statistics of Coniine Poisoning,                              267
  323. Effects of Coniine on Animals,                           267, 268
  324. Effects of Coniine on Man,                                    268
  325. Physiological Action of Coniine,                              268
  326. _Post-mortem_ Appearances--Fatal Dose,                   268, 269
  327. Separation of Coniine from Organic Matters or Tissues,        269

  2. _Tobacco--Nicotine._

  328. General Composition of Tobacco,                          269, 270
  329. Quantitative Estimation of Nicotine in Tobacco,          270, 271
  330. Nicotine; its Properties and Tests,                       271-273
  331. Effects of Nicotine on Animals,                          273, 274
  332. Effects of Nicotine on Man,                              274, 275
  333. Some Instances of Poisoning by Tobacco and Tobacco Juice, 275-277
  334. Physiological Action of Nicotine,                        277, 278
  335. Fatal Dose,                                                   278
  336. _Post-mortem_ Appearances,                                    278
  337. Separation of Nicotine from Organic Matters, &c.,        278, 279

  3. _Piturie._

  338. Properties of Piturie,                                        279

  4. _Sparteine._

  339. Properties of Sparteine,                                 279, 280

  5. _Aniline._

  340. Properties of Aniline,                                        280
  341. Symptoms and Effects,                                    280, 281
  342. Fatal Dose,                                                   281
  343. Detection of Aniline,                                         281


  344. General Composition of Opium,                            281, 282
  345. Action of Solvents on Opium,                             282, 283
  346. The Methods of Teschemacher and Smith, of Dott and others for
       the Assay of Opium,                                      283, 284
  347. Medicinal and other Preparations of Opium,                284-288
  348. Statistics of Opiate Poisoning,                          288, 289
  349. Poisoning of Children by Opium,                               289
  350. Doses of Opium and Morphine--Fatal Dose,                 289, 290
  351. General Method for the Detection of Opium,               290, 291
  352. Morphine; its Properties,                                291, 292
  353. Morphine Salts; their Solubility,                        292, 293
  354. Constitution of Morphine,                                293, 294
  355. Tests for Morphine and its Compounds--Production of Morphine
       Hydriodide--Iodic Acid Test and other Reactions--Transformation
       of Morphine into Codeine,                                 294-296
  356. Symptoms of Opium and Morphine Poisoning--Action on Animals,
  357. Physiological Action,                                    298, 299
  358. Physiological Action of Morphine Derivatives,                 299
  359. Action on Man--(_a_) The Sudden Form; (_b_) the Convulsive Form;
       (_c_) a Remittent Form of Opium Poisoning--Illustrative Cases,
  360. Diagnosis of Opium Poisoning,                            303, 304
  361. Opium-Eating,                                             304-306
  362. Treatment of Opium or Morphine Poisoning,                     306
  363. _Post-mortem_ Appearances,                               306, 307
  364. Separation of Morphine from Animal Tissues and Fluids,        307
  365. Extraction of Morphine,                                  308, 309
  366. Narcotine; its Properties and Tests,                     309, 310
  367. Effects of Narcotine,                                         310
  368. Codeine--Properties of Codeine,                          310, 311
  369. Effects of Codeine on Animals--Claude Bernard’s Experiments,  311
  370. Narceine--Properties of Narceine--Tests,                 312, 313
  371. Effects of Narceine,                                     313, 314
  372. Papaverine--Properties of Papaverine--Tests,                  314
  373. Effects of Papaverine,                                        314
  374. Thebaine; its Properties,                                314, 315
  375. Thebaine; its Effects,                                        315
  376. Cryptopine,                                              315, 316
  377. Rhœadine,                                                     316
  378. Pseudomorphine,                                               316
  379. Opianine,                                                     316
  380. Apomorphine,                                             316, 317
  381. Reactions of some of the Rarer Opium Alkaloids,               317
  382. Tritopine,                                                    317
  383. Meconin (Opianyl),                                            317
  384. Meconic Acid--Effects of Meconic Acid--Tests,            318, 319


  1. _Nux Vomica Group--Strychnine--Brucine--Igasurine._

  385. Nux Vomica--Characteristics of the Entire and of the Powdered
       Seed,                                                         319
  386. Chemical Composition of Nux Vomica,                           319
  387. Strychnine--Microscopical Appearances--Properties--Medicinal
       Preparations--Strychnine Salts,                           319-322
  388. Pharmaceutical and other Preparations of Nux Vomica, with
       Suggestions for their Valuation--Vermin-Killers,          322-324
  389. Statistics,                                               324-325
  390. Fatal Dose--Falck’s Experiments on Animals as to the Least Fatal
       Dose--Least Fatal Dose for Man,                           325-328
  391. Action on Animals--Frogs,                                328, 329
  392. Effects on Man--Symptoms--Distinction between “Disease Tetanus”
       and “Strychnos Tetanus,”                                  329-331
  393. Diagnosis of Strychnine Poisoning,                       331, 332
  394. Physiological Action--Richet’s Experiments--The Rise of
       Temperature--Effect on the Blood-Pressure,               332, 333
  395. _Post-mortem_ Appearances,                                    333
  396. Treatment,                                                    333
  397. Separation of Strychnine from Organic Matters--Separation from
       the Urine, Blood, and Tissues,                            334-337
  398. Identification of the Alkaloid--Colour Tests--Physiological
       Tests,                                                    337-339
  399. Hypaphorine,                                                  339
  400. Quantitative Estimation of Strychnine,                   339, 340
  401. Brucine; its Properties,                                 340, 341
  402. Physiological Action of Brucine--Experiments of Falck,   341, 342
  403. Tests for Brucine,                                       342, 343
  404. Igasurine,                                                    344
  405. Strychnic Acid,                                               344

  2. _The Quebracho Group of Alkaloids._

  406. The Alkaloids of Quebracho--Aspidospermine--Quebrachine,      344

  3.  _Pereirine._

  407.  Pereirine,                                              344, 345

  4.  _Gelsemine._

  408.  Properties of Gelsemine,                                     345
  409.  Fatal Dose of Gelsemine,                                     345
  410.  Effects on Animals--Physiological Action,                    345
  411.  Effects of Gelsemine on Man,                                 346
  412.  Extraction from Organic Matters, or the Tissues of the Body, 347

  5. _Cocaine._

  413.  Cocaine; its Properties,                                 47, 348
  414.  Cocaine Hydrochlorate,                                       348
  415.  Pharmaceutical Preparations,                                 348
  416.  Separation of Cocaine and Tests,                        348, 349
  417.  Symptoms,                                                    349
  418.  _Post-mortem_ Appearances,                              349, 350
  419.  Fatal Dose,                                                  350

  6. _Corydaline._

  420.  Properties of Corydaline,                                    350


  421.  Varieties of Aconite--Description of the Flower, and of the
        Seeds,                                                  350, 351
  422.  Pharmaceutical Preparations of Aconite,                      351
  423.  The Aconite Alkaloids,                                       351
  424.  Aconitine,                                              351, 352
  425.  Tests for Aconitine,                                         352
  426.  Benzoyl-Aconine Properties--Recognition of Benzoic Acid,
                                                                353, 354
  427.  Pyraconitine,                                                354
  428.  Pyraconine,                                                  354
  429.  Aconine,                                                     355
  430.  Commercial Aconitine--English and German Samples of Aconitine--
        Lethal Dose of the Alkaloid and of the Pharmaceutical
        Preparations,                                            355-358
  431.  Effects of Aconitine on Animal Life--Insects, Fish, Reptiles,
        Birds, Mammals,                                          358-360
  432.  Statistics,                                                  361
  433.  Effects on Man,                                              361
  434.  Poisoning by the Root (_Reg. v. M’Conkey_),             361, 362
  435.  Poisoning by the Alkaloid Aconitine--Three Cases of
        Poisoning,                                              363, 364
  436.  Lamson’s Case,                                          364, 365
  437.  Symptoms of Poisoning by the Tincture, &c.,             365, 366
  438.  Physiological Action,                                        366
  439.  _Post-mortem_ Appearances,                              366, 367
  440.  Separation of Aconitine from the Contents of the Stomach or the
        Organs,                                                 367, 368


  1. _Atropine._

  441.  The _Atropa belladonna_; its Alkaloidal Content,        368, 369
  442.  The _Datura stramonium_--Distinction between Datura and
        Capsicum Seeds,                                         369, 370
  443.  Pharmaceutical Preparations--(a) Belladonna; (b)
        Stramonium,                                             370, 371
  444.  Properties of Atropine,                                 371, 372
  445.  Tests for Atropine, Chemical and Physiological,          372-374
  446.  Statistics of Atropine Poisoning,                            375
  447.  Accidental and Criminal Poisoning by Atropine--Use of
        _Dhatoora_ by the Hindoos,                              375, 376
  448.  Fatal Dose of Atropine,                                 376, 377
  449.  Action on Animals,                                           377
  450.  Action on Man,                                           377-380
  451.  Physiological Action of Atropine,                            380
  452.  Diagnosis of Atropine Poisoning,                             380
  453.  _Post-mortem_ Appearances,                                   380
  454.  Treatment of Cases of Poisoning by Atropine,            380, 381
  455.  Separation of Atropine from Organic Matters, &c.,            381

  2. _Hyoscyamine._

  456.  Distribution of Hyoscyamine--Properties,                 381-383
  457.  Pharmaceutical and other Preparations of Henbane,       383, 384
  458.  Dose and Effects,                                            384
  459.  Separation of Hyoscyamine from Organic Matters,              385

  3.  _Hyoscine._

  460.  Hyoscine,                                                    385

  4.  _Solanine._

  461.  Distribution of Solanine,                               385, 386
  462.  Properties of Solanine,                                      386
  463.  Solanidine,                                             386, 387
  464.  Poisoning from Solanine,                                     387
  465.  Separation from Animal Tissues,                              387

  5.  _Cytisine._

  466.  The _Cytisus laburnum_,                                      387
  467.  Reactions of Cytisine,                                       388
  468.  Effects on Animals,                                          389
  469.  Effects on Man--Illustrative Cases,                     389, 390


  470.  The Alkaloids found in the _Veratrum Viride_ and _Veratrum
        Album_--Yield per Kilogram,                              390-392
  471.  Veratrine--Cevadine,                                         392
  472.  Jervine,                                                     393
  473.  Pseudo-jervine,                                              393
  474.  Protoveratridine,                                            393
  475.  Rubi-jervine,                                                394
  476.  Veratralbine,                                                394
  477.  Veratroidine,                                                394
  478.  Commercial Veratrine,                                   394, 395
  479.  Pharmaceutical Preparations,                                 395
  480.  Fatal Dose,                                                  395
  481.  Effects on Animals--Physiological Action,               395, 396
  482.  Effects on Man--Illustrative Cases,                          396
  483.  Symptoms of Acute and Chronic Poisoning,                396, 397
  484.  _Post-mortem_ Signs,                                         397
  485.  Separation of the Veratrum Alkaloids from Organic Matters,   397


  486.  The Active Principle of the Calabar Bean,               397, 398
  487.  Physostigmine or Eserine--Properties,                   398, 399
  488.  Tests,                                                       399
  489.  Pharmaceutical Preparations,                            399, 400
  490.  Effects on Animals--On Man--The Liverpool Cases of Poisoning,
  491.  Physiological Action,                                        401
  492.  _Post-mortem_ Appearances,                                   401
  493.  Separation of Physostigmine,                            401, 402
  494.  Fatal Dose of Physostigmine,                                 402


  495.  Alkaloids from the Jaborandi,                                402
  496.  Pilocarpine,                                            402, 403
  497.  Tests,                                                       403
  498.  Effects of Pilocarpine,                                 403, 404


  499.  Properties of Taxine,                                        404
  500.  Poisoning by the Common Yew,                                 404
  501.  Effects on Animals--Physiological Action,                    404
  502.  Effects on Man,                                         404, 405
  503.  _Post-mortem_ Appearances,                                   405


  504.  Commercial Curarine--Properties,                         405-407
  505.  Physiological Effects,                                       407
  506.  Separation of Curarine,                                 407, 408


  507.  Contents of Colchicine in Colchicum Seeds,              408, 409
  508.  Colchicine--Method of Extraction--Properties,                409
  509.  Tests,                                                  409, 410
  510.  Pharmaceutical Preparations,                                 410
  511.  Fatal Dose,                                             410, 411
  512.  Effects of Colchicine on Animals,                            411
  513.  Effects of Colchicum on Man--Illustrative Cases,        411, 412
  514.  Symptoms Produced by Colchicum--_Post-mortem_ Appearances,
                                                                412, 413
  515.  Separation of Colchicine from Organic Matters,               413


  516.  Description of the _Amanita Muscaria_--Use of it by the Natives
        of Kamschatka,                                          413, 414
  517.  Cases of Poisoning by the Fungus itself,                414, 415
  518.  Muscarine--Its Properties and Effects,                  415, 416
  519.  Antagonistic Action of Atropine and Muscarine,               416
  520.  Detection of Muscarine,                                 416, 417
  521.  The _Agaricus Phalloides_--_Phallin_,                        417
  522.  _Post-mortem_ Appearances,                              417, 418
  523.  The _Agaricus Pantherinus_--The _Agaricus Ruber_--Ruberine
        --Agarythrine,                                               418
  524.  The _Boletus Satanus_, or _Luridus_,                         418
  525.  Occasional Effects of the Common Morelle,                    418

  Division II.--GLUCOSIDES


  526.  Description of the _Digitalis Purpurea_, or Foxglove,        419
  527.  Active Principles of the Foxglove--The Digitalins,           419
  528.  Digitalein,                                                  420
  529.  Digitonin--Digitogenin,                                      420
  530.  Digitalin,                                                   420
  531.  Digitaletin,                                                 420
  532.  Digitoxin--Toxiresin,                                   420, 421
  533.  Digitaleretin--Paradigitaletin,                              421
  534.  Other Active Principles in Digitalis; such as Digitin,
        Digitalacrin, Digitalein, &c.,                          421, 422
  535.  Reactions of the Digitalins,                                 422
  536.  Pharmaceutical Preparations of Digitalin,                    422
  537.  Fatal Dose,                                              422-424
  538.  Statistics of Poisoning by Digitalis,                        424
  539.  Effects on Man--Illustrative Cases,                      424-427
  540.  Physiological Action of the Digitalins,                      427
  541.  Local Action of the Digitalins,                         427, 428
  542.  Action on the Heart and Circulation,                    428, 429
  543.  Action of the Digitalins on the Muco-Intestinal Tract and other
        Organs,                                                      429
  544.  Action of Digitalin on the Common Blow-Fly,                  429
  545.  Action of the Digitalins on the Frog’s Heart,           429, 430
  546.  _Post-mortem_ Appearances,                                   430
  547.  Separation of the Digitalins from Animal Tissues, &c.--Tests,
        Chemical and Physiological,                                  431


  1. _Crystallisable Glucosides._

  548.  Antiarin--Chemical Properties,                               432
  549.  Effects of Antiarin,                                         432
  550.  Separation of Antiarin,                                      432
  551.  The Active Principles of the Hellebores--Helleborin--
        Helleborein--Helleboretin,                                   433
  552.  Symptoms of Poisoning by Hellebore,                          433
  553.  Euonymin,                                                    433
  554.  Thevetin,                                                    434

  2. _Substances partly Crystallisable, but which are not Glucosides._

  555.  Strophantin,                                                 434
  556.  Apocynin,                                                    434

  3. _Non-Crystallisable Glucosides almost Insoluble in Water._

  557.  Scillain, or Scillitin--Adonidin,                            434
  558.  Oleandrin,                                                   435
  559.  Neriin, or Oleander Digitalin,                               435
  560.  Symptoms of Poisoning by Oleander,                      435, 436
  561.  The Madagascar Ordeal Poison,                                436

  4. _Substances which, with other Toxic Effects, behave like the

  562.  Erythrophlein,                                               436


  563.  The Varieties of Saponins,                              436, 437
  564.  Properties of Saponin,                                       437
  565. Effects of Saponin,                                      437, 438
  566. Action on Man,                                                438
  567. Separation of Saponin,                                   438, 439
  568. Identification of Saponin,                                    439



  569. Properties of Santonin,                                  439, 440
  570. Poisoning by Santonin,                                        440
  571. Fatal Dose,                                                   440
  572. Effects on Animals,                                           440
  573. Effects on Man--Yellow Vision,                           440, 441
  574. _Post-mortem_ Appearances,                                    441
  575. Separation from the Contents of the Stomach,             441, 442


  576. Cases of Poisoning by the Mezereon,                           442



  577. Description of the Ergot Fungus,                         442, 443
  578. Chemical Constituents of Ergot--Ergotinine--_Ecboline_--
       _Scleromucin_--Sclerotic Acid--Sclererythrin--Scleroidin--
       Sclerocrystallin--Sphacelic Acid--Cornutin,               443-445
  579. Detection of Ergot in Flour,                                  445
  580. Pharmaceutical Preparations,                                  445
  581. Dose,                                                         446
  582. Ergotism--Historical Notice of Various Outbreaks,        446, 447
  583. Convulsive Form of Ergotism,                                  447
  584. Gangrenous Form of Ergotism--The Wattisham Cases,        447, 448
  585. Symptoms of Acute Poisoning by Ergot,                         448
  586. Physiological Action, as shown by Experiments on Animals, 448-450
  587. Separation of the Active Principles of Ergot,                 450


  588. Enumeration of the Active Principles contained in the
       _Menispermum Cocculus_,                                       451
  589. Picrotoxin; its Chemical Reactions and Properties,       451, 452
  590. Fatal Dose,                                                   452
  591. Effects on Animals,                                      452, 453
  592. Effects on Man,                                               453
  593. Physiological Action,                                         453
  594. Separation from Organic Matters,                         453, 454


  595. Dr. Langaard’s Researches,                                    454


  596. Properties of Picric Acid,                                    454
  597. Effects of Picric Acid,                                  454, 455
  598. Tests,                                                        455


  599. Description of the _Cicuta Virosa_,                           456
  600. Effects on Animals,                                           456
  601. Effects on Man,                                          456, 457
  602. Separation of Cicutoxin from the Body,                        457


  603. Dr. Harley’s Experiments,                                     457


  604. The Water Hemlock--Description of the Plant--Cases of
       Poisoning,                                               457, 458
  605. Effects of the Water Hemlock, as shown by the Plymouth Cases, 458
  606. _Post-mortem_ Appearances,                                    459


  607. Effects and Properties of Savin Oil,                          459
  608. _Post-mortem_ Appearances,                                    460
  609. Separation and Identification,                                460


  610. Chemical Properties of Croton Oil,                            461
  611. Dose--Effects--Illustrative Cases,                            461
  612. _Post-mortem_ Appearances,                                    461
  613. Chemical Analysis,                                            462


  614. The Toxalbumin of Castor Oil Seeds,                           462
  615. Toxalbumin of Abrus,                                     462, 463


  616. Ictrogen,                                                     463


  617. Cotton Seeds as a Poison,                                     464


  618. Poisonous Qualities of Vetchlings,                       464, 465


  619. Arum Maculatum,                                               465
  620. The Black Bryony,                                             465
  621. The Locust Tree,                                              465
  622. Male Fern                                                465, 466




  623. Poisonous Properties of the Skin of the _Salamandra Maculosa_
       --Salamandrine, &c.,                                          467
  624. Poison from the Toad,                                         468


  625. Various Species of Scorpions--Effects of the Scorpion Poison, 468


  626. Poisonous Fish--Illustrative Cases,                       468-470


  627. The Bite of the Tarantula--The Bite of the _Latrodectus
       Malmignatus_,                                                 470
  628. Effects of the Bite of the Katipo,                            471
  629. Ants, &c.,                                                    471
  630. The Poison of Wasps, Bees, and Hornets,                       471
  631. Cantharides,                                                  471
  632. Cantharidin,                                             471, 472
  633. Pharmaceutical Preparations of Cantharides,                   472
  634. Fatal Dose,                                                   472
  635. Effects on Animals--Radecki’s Experiments--Effects on Man--
       Heinrich’s Auto-Experiments,                             472, 473
  636. General Symptoms Produced by Cantharides,                473, 474
  637. _Post-mortem_ Appearances,                                    474
  638. Tests for Cantharidin--Distribution in the Body--Dragendorff’s
       Process,                                                  475-477


  639. Classes of Poisonous Snakes,                                  477
  640. The Poison of the Cobra,                                      478
  641. Fatal Dose of Cobra Poison,                                   479
  642. Effects on Animals,                                           479
  643. Effects on Man,                                          479, 480
  644. Antidotes and Treatment--Halford’s Treatment by Ammonia--
       Permanganate of Potash,                                  480, 481
  645. Detection of the Cobra Venom,                                 482
  646. Effects of the Bite of the _Duboia Russellii_, or Russell’s
       Viper,                                                        483
  647. The Poison of the Common Viper--The Venom of Naja Haje
       (Cleopatra’s Asp),                                       483, 484


  648. Definition of a Ptomaine,                                     485

  _Isolation of Ptomaines._

  649. Gautier’s Process,                                            485
  650. Brieger’s Process,                                        485-487
  651. Benzoyl Chloride Method,                                 487, 488
  652. The Amines,                                               488-490
  653. Methylamine,                                                  491
  654. Dimethylamine,                                                491
  655. Trimethylamine,                                               491
  656. Ethylamine,                                                   491
  657. Diethylamine,                                                 491
  658. Triethylamine,                                                491
  659. Propylamine,                                                  491
  660. Isoamylamine,                                                 492


  661. Rate of Formation of Diamines,                                492
  662. Ethylidenediamine,                                            492
  663. Neuridine,                                               493, 494
  664. Cadaverine,                                               494-496
  665. Putrescine,                                                   496
  666. Metaphenylenediamine,                                         497
  667. Paraphenylenediamine,                                         497
  668. Hexamethylenediamine,                                         497
  669. Diethylenediamine,                                       497, 498
  670. Mydaleine,                                                    498
  671. Guanidine,                                               498, 499
  672. Methylguanidine,                                         499, 500
  673. Saprine,                                                      500
  674. The Choline Group,                                       500, 501
  675. Neurine,                                                      501
  676. Betaine,                                                 501, 502
  677. Peptotoxine,                                                  502
  678. Pyridine-like Alkaloid from the Cuttle-fish,             502, 503
  679. Poisons connected with Tetanus--Tetanine,                     503
  680. Tetanotoxine,                                            503, 504
  681. Mydatoxine,                                                   504
  682. Mytilotoxine,                                                 505
  683. Tyrotoxicon,                                             504, 505
  684. Toxines connected with Hog Cholera,                      505, 506
  685. Other Ptomaines,                                              506


  686. The Welbeck--The Oldham--The Bishop Stortford--The
       Wolverhampton--The Carlisle, and other Mass Poisonings by
       changed Food--Statistics of Deaths from Unwholesome Food, 506-508
  687. German Sausage Poisoning,                                     509


  688. Distribution of Oxalic Acid in the Animal and Vegetable
       Kingdoms,                                                     510
  689. Properties and Reactions of Oxalic Acid,                 510, 511
  690. Oxalate of Lime; its Properties,                         511, 512
  691. Use of Oxalic Acid in the Arts,                               512
  692. Properties of Hydropotassic Oxalate (Binoxalate of Potash),   512
  693. Statistics of Oxalic Acid Poisoning,                          512
  694. Fatal Dose of Oxalic Acid,                                    513
  695. Effects of Oxalic Acid and Oxalates on Animals,               513
  696. Researches of Kobert and Küssner on the Effects of Sodic
       Oxalate,                                                 513, 514
  697. Effects of Vaporised Oxalic Acid,                        514, 515
  698. Effects of Oxalic Acid and Hydropotassic Oxalate on Man--
       Illustrative Cases,                                      515, 516
  699. Physiological Action,                                    516, 517
  700. Pathological Changes produced by Oxalic Acid and the Oxalates,
                                                                517, 518
  701. Preparations in Museums Illustrative of the Effects of Oxalic
       Acid,                                                         518
  702. Pathological Changes produced by the Acid Oxalate of Potash,
                                                                518, 519
  703. Separation of Oxalic Acid from Organic Substances, the Tissues
       of the Body, &c.,                                         519-521
  704. Oxalate of Lime in the Urine,                                 521
  705. Estimation of Oxalic Acid,                               521, 522

  _Certain Oxalic Bases--Oxalmethyline--Oxalpropyline._

  706. The Experiments of Schulz and Mayer on Oxalmethyline,
       Chloroxalmethyline, and Oxalpropyline,                   522, 523




  1. _Arsenic._

  707. Metallic Arsenic; its Chemical and Physical Properties,       524
  708. Arsenious Anhydride--Arsenious Acid; its Properties and
       Solubility,                                              524, 525
  709. Arseniuretted Hydrogen (Arsine),                          525-527
  710. Arseniuretted Hydrogen in the Arts, &c,                       527
  711. The Effects of Arseniuretted Hydrogen on Man--Illustrative
       Cases,                                                   527, 528
  712. The Sulphides of Arsenic,                                528, 529
  713. Orpiment, or Arsenic Trisulphide,                             529
  714. Haloid Arsenical Compounds--Chloride of Arsenic--Iodide of
       Arsenic,                                                      529
  715. Arsenic in the Arts,                                     529, 530
  716. Pharmaceutical Preparations of Arsenic--Veterinary Arsenical
       Medicines--Rat and Fly Poisons--Quack Nostrums--Pigments--
       External Application of Arsenic for Sheep--Arsenical Soaps--
       Arsenical Compounds used in Pyrotechny,                   530-534
  717. Statistics of Poisoning by Arsenic,                           534
  718. Law Relative to the Sale of Arsenic,                          535
  719. Dose of Arsenic,                                              535
  720. Effects of Arsenious Acid on Plants,                     535, 536
  721. Effects of Arsenic upon Life--Animalcules--Annelids--Birds--
       Mammals,                                                  536-538
  722. Effects of Arsenious Acid on Man--Arsenic Eaters,        538, 539
  723. Manner of Introduction of Arsenic,                            539
  724. Cases of Poisoning by the External Application of Arsenic,
  725. Arsenic in Wall-Papers,                                  541, 542
  726. Forms of Arsenical Poisoning--Acute Form,                     542
  727. Subacute Form--Case of the Duc de Praslin,                    543
  728. Nervous Form--Brodie’s Experiments on Rabbits--A “Mass”
       Poisoning reported by Dr. Coqueret,                      544, 545
  729. Absence of Symptoms,                                     545, 546
  730. Slow Poisoning,                                               546
  731. The Maybrick Case,                                        546-548
  732. Post-mortem Appearances met with in Animals after Arsenical
       Poisoning--The Researches of Hugo,                       548, 549
  733. Post-mortem Appearances in Man--Illustrative Pathological
  Preparations in Various Museums,                               549-551
  734. Pathological Changes induced in the Gullet and Stomach--Fatty
       Degeneration of the Liver and Kidneys--Glossitis--Retardation of
       Putrefaction,                                            551, 552
  735. Physiological Action of Arsenic,                         552, 553
  736. Elimination of Arsenic--Question of Accumulation of Arsenic,  553
  737. Antidotes and Treatment,                                 553, 554
  738. Detection of Arsenic--Identification of Arsenious Acid in
       Substance--Test of Berzelius--Identification of Arsenites and
       Arseniates--Detection of Arsenious Acid in Solution--
       Distinguishing Marks between the Sulphides of Tin, Cadmium,
       Antimony, and Arsenic--Marsh’s Original Test for Arsenic--
       Blondlot’s Modification of Marsh’s Test--Distinguishing Marks
       between Arsenical and Antimonial Mirrors--Reinsch’s Tests,
  739. Arsenic in Glycerin,                                          560
  740. Arsenic in Organic Matters--Orfila’s Method of Destroying
       Organic Matter--Extraction with Hydrochloric Acid--Modifications
       in the Treatment of Oils--Resinous Matters--Experiments on the
       Distribution of Arsenic by Scolosuboff, Ludwig, and Chittenden--
       The Question of Contamination of a Corpse by Arsenical Earth,
  741. Imbibition of Arsenic after Death--Mason’s Case,          563-565
  742. Analysis of Wall-Paper for Arsenic,                      565, 566
  743. Estimation of Arsenic--Galvanic Process of Bloxam--Colorimetric
       Methods,                                                  566-568
  744. Destruction of the Organic Matter by Nitric Acid, and Subsequent
       Reduction of the Arsenic Acid to Arseniuretted Hydrogen, and
       Final Estimation as Metallic Arsenic,                     568-571
  745. Arsine developed from an Alkaline Solution,                   571
  746. Precipitation as Tersulphide--Methods of Dealing with the
       Sulphides obtained--(_a_) Solution in Ammonia and Estimation by
       Iodine--(_b_) Drying the Purified Precipitate at a High
       Temperature, and then directly weighing--(_c_) Oxidation of the
       Sulphide and Precipitation as Ammonia Magnesian Arseniate, or
       Magnesia Pyro Arseniate--(_d_) Conversion of the Trisulphide of
       Arsenic into the Arseno-Molybdate of Ammonia--Conversion of the
       Sulphide into Metallic Arsenic,                           571-575
  747. Conversion of Arsenic into Arsenious Chloride,           575, 576

  2. _Antimony._

  748. Properties of Metallic Antimony,                              577
  749. Antimonious Sulphides,                                   577, 578
  750. Tartarated Antimony--Tartar Emetic,                      578, 579
  751. Metantimonic Acid,                                            579
  752. Pharmaceutical, Veterinary, and Quack Preparations of Antimony--
       (1)Pharmaceutical Preparations--(2) Patent and Quack Pills--(3)
       Antimonial Medicines, chiefly Veterinary,                 579-582
  753. Alloys,                                                       582
  754. Pigments,                                                     582
  755. Dose,                                                         582
  756. Effects of Tartar Emetic on Animals--Influence on Temperature--
       Dr. Nevin’s Researches on Rabbits,                       582, 583
  757. Effects of Tartar Emetic on Man--Illustrative Cases,     583, 584
  758. Chronic Antimonial Poisoning,                                 585
  759. _Post-mortem_ Appearances--Preparations in Museums--Pathological
       Appearances in Rabbits, according to Nevin,              585, 586
  760. Elimination of Antimony,                                      586
  761. Antidotes for Tartar Emetic,                                  586
  762. Effects of Chloride or Butter of Antimony,                    587
  763. Detection of Antimony in Organic Matters,                 587-589
  764. Quantitative Estimation of Antimony,                     589, 590

  3. _Cadmium._

  765. Properties of the Metal Cadmium,                              590
  766. Cadmium Oxide,                                                590
  767. Cadmium Sulphide,                                             590
  768. Medicinal Preparations of Cadmium--Cadmium Iodide--Cadmium
       Sulphate,                                                     590
  769. Cadmium in the Arts,                                          590
  770. Fatal Dose of Cadmium,                                        590
  771. Separation and Detection of Cadmium,                     590, 591



  1. _Lead._

  772. Lead and its Oxides--Litharge--Minium, or Red Lead,      591, 592
  773. Sulphide of Lead,                                             592
  774. Sulphate of Lead,                                             592
  775. Acetate of Lead,                                              592
  776. Chloride of Lead--Carbonate of Lead,                     592, 593
  777. Preparations of Lead used in Medicine, the Arts, &c.--(1)
       Pharmaceutical--(2) Quack Nostrums--(3) Preparations used in the
       Arts--Pigments--Hair Dyes--Alloys,                       593, 594
  778. Statistics of Lead-Poisoning,                                 594
  779. Lead as a Poison--Means by which Lead may be taken into the
       System,                                                  595, 596
  780. Effects of Lead Compounds on Animals,                    596, 597
  781. Effects of Lead Compounds on Man--Acute Poisoning--Mass
       Poisoning by Lead--Case of Acute Poisoning by the Carbonate of
       Lead,                                                     597-599
  782. Chronic Poisoning by Lead,                               599, 600
  783. Effects of Lead on the Nervous System--Lead as a Factor of
       Insanity                                                 600, 601
  784. Amaurosis Caused by Lead-Poisoning--Influence on the Sexual
       Functions--Caries--Epilepsy,                              601-603
  785. Uric Acid in the Blood after Lead-Poisoning,                  603
  786. Influence of Lead on Pregnant Women and on Fœtal Life--The
       Keighley Case of Poisoning by Water Contaminated by Lead--Case
       of _Reg._ v. _L. J. Taylor_,                              603-605
  787. _Post-mortem_ Appearances,                                    605
  788. Physiological Action of Lead,                            605, 606
  789. Elimination of Lead,                                          606
  790. Fatal Dose,                                              606, 607
  791. Antidotes and Treatment,                                      607
  792. Localisation of Lead,                                    607, 608
  793. Detection and Estimation of Lead,                        608, 609
  794. Detection of Lead in Tartaric Acid, in Lemonade and Aërated
       Waters,                                                  609, 610

  2. _Copper._

  795. Properties of Copper,                                         610
  796. Cupric Oxide,                                                 610
  797. Cupric Sulphide,                                              610
  798. Solubility of Copper in Water and Various Fluids--Experiments of
       Carnelley, W. Thompson, and Lehmann,                      610-612
  799. Copper as a Normal Constituent of Animal, Vegetable, and other
       Matters--Dupré’s Experiments--Bergeron and L. L’Hôte’s
       Researches,                                               612-614
  800. The “Coppering” of Vegetables--Copper in Green Peas--
       Phyllocyanic Acid,                                       614, 615
  801. Preparations of Copper used in Medicine and the Arts--(1)
       Medicinal Preparations--(2) Copper in the Arts,          615, 616
  802. Dose--Medicinal Dose of Copper,                          616, 617
  803. Effects of Soluble Copper Salts on Animals,               617-619
  804. Toxic Dose of Copper Salts,                                   619
  805. Cases of Acute Poisoning,                                619, 620
  806. Effects of Subacetate, Subchloride, and Carbonate of Copper,  620
  807. _Post-mortem_ Appearances seen in Acute Poisoning by Copper,
                                                                620, 621
  808. Chronic Poisoning by Copper,                             621, 622
  809. Detection and Estimation of Copper--General Method--Special
       Method for Copper in Solution in Water and other Liquids--
       Detection of Copper in Animal Matters,                    622-624
  810. Volumetric Processes for the Estimation of Copper,            624

  3. _Bismuth._

  811. Bismuth as a Metal,                                           624
  812. Teroxide of Bismuth,                                          624
  813. The Sulphide of Bismuth,                                      624
  814. Preparations of Bismuth used in Medicine and the Arts--(1)
       Pharmaceutical Preparations--(2) Bismuth in the Arts,    624, 625
  815. Medicinal Doses of Bismuth,                                   625
  816. Toxic Effects of Sub-nitrate of Bismuth,                 625, 626
  817. Extraction and Detection of Bismuth in Animal Matter,    626, 627
  818. Estimation of Bismuth--Volumetric Processes,             627, 628

  4. _Silver._

  819. Properties of Metallic Silver,                           628, 629
  820. Chloride of Silver,                                           629
  821. Sulphide of Silver,                                           629
  822. Preparations of Silver used in Medicine and the Arts--(1)
       Medicinal Preparations--(2) Silver in the Arts,          629, 630
  823. Medicinal Dose of Silver Compounds,                           630
  824. Effects of Nitrate of Silver on Animals--Chronic Poisoning,
                                                                630, 631
  825. Toxic Effects of Silver Nitrate on Man--(1) Acute--(2) Chronic
       Poisoning,                                               631, 632
  826. _Post-mortem_ Appearances,                                    632
  827. Detection and Estimation of Silver,                      632, 633

  5. _Mercury._

  828. The Metal Mercury--Mercurous Chloride, or Calomel,       633, 634
  829. Sulphide of Mercury,                                          634
  830. Medicinal Preparations of Mercury,                        634-638
  831. Mercury in the Arts--The Sulphocyanide of Mercury--Acid Solution
       of Nitrate of Mercury,                                        639
  832. The more common Patent and Quack Medicines containing Mercury,
                                                                639, 640
  833. Mercury in Veterinary Medicine,                               640
  834. Medicinal and Fatal Dose,                                640, 641
  835. Poisoning by Mercury--Statistics,                             641
  836. Effects of Mercurial Vapour and of the Non-Corrosive Compounds
       of Mercury--(_a_) On Vegetable Life--(_b_) On Animal Life,
                                                                641, 642
  837. Effects on Man,                                          642, 643
  838. Absorption of Mercury by the Skin,                            643
  839. Symptoms of Poisoning by Mercury Vapour,                 643, 644
  840. Mercurial Tremor,                                        644, 645
  841. Mercuric Methide--Effects of, as Illustrated by two Cases,
                                                                645, 646
  842. Effects of the Corrosive Salts of Mercury,               646, 647
  843. Death from the External Use of Corrosive Sublimate,           647
  844. Effects of the Nitrates of Mercury,                           647
  845. Case of _Reg._ v. _E. Smith_,                                 648
  846. Mercuric Cyanide,                                             648
  847. White Precipitate,                                            648
  848. Treatment of Acute and Chronic Poisoning,                     648
  849. _Post-mortem_ Appearances--Pathological Preparations in Various
  Anatomical Museums,                                            648-650
  850. Pathological Appearances from the Effects of Nitrate of Mercury,
  851. Elimination of Mercury,                                  650, 651
  852. Tests for Mercury,                                       651, 652
  853. The Detection of Mercury in Organic Substances and Fluids,
  854. Estimation of Mercury--The Dry Method,                        654
  855. Volumetric Processes for the Estimation of Mercury,      654, 655



  1. _Zinc._

  856. Properties of Metallic Zinc,                             655, 656
  857. Carbonate of Zinc,                                            656
  858. Oxide of Zinc,                                                656
  859. Sulphide of Zinc--Sulphate of Zinc,                           656
  860. Preparation and Uses of Chloride of Zinc,                656, 657
  861. Zinc in the Arts--Zinc Chromate--Zinc Pigments--Action of Fluids
       on Zinc Vessels,                                         657, 658
  862. Effects of Zinc, as shown by Experiments on Animals,          658
  863. Effects of Zinc Compounds on Man--Zinc Oxide,            658, 659
  864. Sulphate of Zinc,                                             659
  865. Zinc Chloride,                                           659, 660
  866. _Post-mortem_ Appearances--Illustrated by Specimens in
       Pathological Museums,                                    660, 661
  867. Detection of Zinc in Organic Liquids or Solids,          661, 662
  868. Identification of Zinc Sulphide,                              662

  2. _Nickel--Cobalt._

  869. Experiments of Anderson Stuart on the Toxic Action of Nickel and
       Cobalt,                                                  662, 663
  870. Symptoms witnessed in various Classes of Animals after taking
       Doses of Nickel or Cobalt,                               663, 664
  871. Effects on the Circulation and Nervous System,                664
  872. Action on Striped Muscle,                                     664
  873. Separation of Nickel or Cobalt from the Organic Matters or
       Tissues,                                                 664, 665
  874. Estimation of Cobalt or Nickel,                               665



  1. _Iron._

  875. Poisonous and Non-Poisonous Salts of Iron,                    665
  876. Ferric Chloride--Pharmaceutical Preparations of Ferric Chloride,
  877. Effects of Ferric Chloride on Animals,                        666
  878. Effects on Man--Criminal Case at Martinique,             666, 667
  879. Elimination of Ferric Chloride,                          667, 668
  880. _Post-mortem_ Appearances,                                    668
  881. Ferrous Sulphate,                                        668, 669
  882. Search for Iron Salts in the Contents of the Stomach,    669, 670

  2. _Chromium._

  883. Neutral Chromate of Potash,                                   670
  884. Potassic Bichromate,                                          670
  885. Neutral Lead Chromate,                                   670, 671
  886. Use in the Arts,                                              671
  887. Effects of some of the Chromium Compounds on Animal Life,     671
  888. Effects of some of the Chromium Compounds on Man--Bichromate
       Disease,                                                 671, 672
  889. Acute Poisoning by the Chromates--Illustrative Cases,    672, 673
  890. Lethal Effects of Chromate of Lead,                           673
  891. _Post-mortem_ Appearances,                                    674
  892. Detection of the Chromates and Separation of the Salts of
       Chromium from the Contents of the Stomach,               674, 675

  3. _Thallium._

  893. Discovery of Thallium--Its Properties,                   675, 676
  894. Effects of Thallium Salts,                                    676
  895. Separation of Thallium from Organic Fluids or Tissues,        676

  4. _Aluminium._

  896. Aluminium and its Salts,                                 676, 677
  897. Action of Alum Salts--Siem’s Researches--Alum Baking-Powders,
                                                                677, 678
  898. _Post-mortem_ Appearances,                                    678
  899. Detection of Alumina,                                    678, 679

  5. _Uranium._

  900. Poisonous Properties of Uranium Salts,                        679
  901. Detection and Estimation of Uranium,                          679



  902. Salts of Barium in Use in the Arts,                      679, 680
  903. Chloride of Barium,                                           680
  904. Baric Carbonate,                                              680
  905. Sulphate of Barium,                                           680
  906. Effects of the Soluble Salts of Barium on Animals,            681
  907. Effects of the Salts of Barium on Man--Fatal Dose,       681, 682
  908. Symptoms,                                                682, 683
  909. Distribution of Barium in the Body,                           683
  910. _Post-mortem_ Appearances,                               683, 684
  911. Separation of Barium Salts from Organic Solids or Fluids, and
       their Identification,                                         684



  912.  Instruments, Emetics, and Antidotes Proper for Furnishing an
        Antidote Bag,                                           685, 686
  913.  Poisons Arranged Alphabetically--Details of Treatment,   687-700


  914.  The “Antidote Cupboard,” and How to Furnish it,              701


  Williams’ Apparatus for Investigating Action of Poisons on the Frog’s
  Heart,                                                              44
  Ether Recovery Apparatus,                                           47
  Micro-spectroscope,                                                 48
  Diagram showing Absorption Bands Produced from Colour Reactions,    55
  Hæmatin Crystals,                                                   61
  Tube for Treatment of Liquids by Ethereal Solvents,                156
  Diagram of Visual Field in Dinitro-benzol Poisoning,               190
  Blondlot’s Apparatus for Production of Phosphine,                  231
  Apparatus for Sublimation,                                         258
  Brucine Hydriodide,                                                342
  Bocklisch’s Flask for Distillation in a Vacuum,                    486
  Berzelius’ Tube for Reduction of Arsenic,                          554
  Bent Tube for Assay of Mercury,                                    654

  Folding-Chart (Deaths from Intemperance and Liver Disease), to face
                                                                 p.  136



I.--The Old Poison-Lore.

§ 1. It is significant that the root “_tox_” of the modern word
_toxicology_ can be traced back to a very ancient word meaning “bow” or
“arrow,” or, in its broadest sense, some “tool” used for slaying: hence
it is no far-fetched supposition that the first poison-knowledge was
that of the septic poisons. Perchance the savage found that weapons
soiled with the blood of former victims made wounds fatal; from this
observation the next step naturally would be that of experiment--the
arrow or spear would be steeped in all manner of offensive pastes, and
smeared with the vegetable juices of those plants which were deemed
noxious; and as the effects were mysterious, they would be ascribed to
the supernatural powers, and covered with a veil of superstition.

The history of the _poison-lehre_, like all history, begins in the
region of the myths: there was a dark saga prevailing in Greece, that in
the far north existed a land ruled by sorcerers--all children of the
sun--and named Aeëtes, Perses, Hecate, Medea, and Circe. Later on, the
enchanted land was localised at Colchis, and Aeëtes and Perses were said
to be brothers. Hecate was the daughter of Perses; she was married to
Aeëtes, and their daughters were Medea and Circe. Hecate was the
discoverer of poisonous herbs, and learned in remedies both evil and
good. Her knowledge passed to Medea, who narcotised the dragon, the
guardian of the golden fleece, and incited Jason to great undertakings.

In the expedition of the Argonauts, the poets loved to describe Hecate’s
garden, with its lofty walls. Thrice-folding doors of ebony barred the
entrance, which was guarded by terrible forms: only the initiated few,
only they who bore the leavened rod of expiation, and the concealed
conciliatory offering of the Medea, could enter into the sanctuary.
Towering above all was the temple of the dread Hecate, whose priestesses
offered to the gods ghastly sacrifices.

§ 2. The oldest Egyptian king, Menes, and Attalus Phylometer, the last
king of Pergamus, were both famous for their knowledge of plants.
Attalus Phylometer was acquainted with hyoscyamus, aconite, conium,
veratrum, and others; he experimented on the preparation of poisons, and
occupied himself in compounding medicines. Mithradetes Eupator stood yet
higher: the receipt for the famous _theriaca_, prepared in later years
at an enormous price, and composed of fifty-four different ingredients,
is ascribed to him. The wonderful skill shown by the Egyptians in
embalming and technical works is sufficient to render it fairly certain
that their chemical knowledge was considerable; and the frequent
operations of one caste upon the dead must have laid the foundations of
a pathological and anatomical culture, of which only traces remain.

The Egyptians knew prussic acid as extracted in a dilute state from
certain plants, among the chief of which was certainly the peach; on a
papyrus preserved at the Louvre, M. Duteil read, “Pronounce not the name
of I. A. O. under the penalty of the peach!” in which dark threat,
without doubt, lurks the meaning that those who revealed the religious
mysteries of the priests were put to death by waters distilled from the
peach. That the priests actually distilled the peach-leaves has been
doubted by those who consider the art of distillation a modern
invention; but this process was well known to adepts of the third and
fourth centuries, and there is no inherent improbability in the
supposition that the Egyptians practised it.

§ 3. From the Egyptians the knowledge of the deadly drink appears to
have passed to the Romans. At the trial of Antipater,[1] Verus brought a
potion derived from Egypt, which had been intended to destroy Herod;
this was essayed on a criminal, he died at once. In the reign of
Tiberius, a Roman knight, accused of high treason, swallowed a poison,
and fell dead at the feet of the senators: in both cases the rapidity of
action appears to point to prussic acid.

[1] Jos. Ant., B. xvii. c. 5.

The use of poison by the Greeks, as a means of capital punishment,
without doubt favoured suicide by the same means; the easy, painless
death of the state prisoner would be often preferred to the sword by one
tired of life. The ancients looked indeed upon suicide, in certain
instances, as something noble, and it was occasionally formally
sanctioned. Thus, Valerius Maximus tells us that he saw a woman of
quality, in the island of Ceos, who, having lived happily for ninety
years, obtained leave to take a poisonous draught, lest, by living
longer, she should happen to have a change in her good fortune; and,
curiously enough, this sanctioning of self-destruction seems to have
been copied in Europe. Mead relates that the people of Marseilles of old
had a poison, kept by the public authorities, in which cicuta was an
ingredient: a dose was allowed to any one who could show why he should
desire death. Whatever use or abuse might be made of a few violent
poisons, Greek and Roman knowledge of poisons, their effects and methods
of detection, was stationary, primitive, and incomplete.

_Nicander of Colophon_ (204-138 B.C.) wrote two treatises, the most
ancient works on this subject extant, the one describing the effects of
snake venom; the other, the properties of opium, henbane, certain fungi,
colchicum, aconite, and conium. He divided poisons into those which kill
quickly, and those which act slowly. As antidotes, those medicines are
recommended which excite vomiting--_e.g._, lukewarm oil, warm water,
mallow, linseed tea, &c.

_Apollodorus_ lived at the commencement of the third century B.C.: he
wrote a work on poisonous animals, and one on deleterious medicines;
these works of Apollodorus were the sources from which Pliny,
Heraclitus, and several of the later writers derived most of their
knowledge of poisons.

_Dioscorides_ (40-90 A.D.) well detailed the effects of cantharides,
sulphate of copper, mercury, lead, and arsenic. By arsenic he would
appear sometimes to mean the sulphides, sometimes the white oxide.
Dioscorides divided poisons, according to their origin, into three
classes, viz.:--

1. =Animal Poisons.=--Under this head were classed cantharides and
allied beetles, toads, salamanders, poisonous snakes, a particular
variety of honey, and the blood of the ox, probably the latter in a
putrid state. He also speaks of the “_sea-hare_.” The sea-hare was
considered by the ancients very poisonous, and Domitian is said to have
murdered Titus with it. It is supposed by naturalists to have been one
of the genus _Aplysia_, among the _gasteropods_. Both Pliny and
Dioscorides depict the animal as something very formidable: it was not
to be looked at, far less touched. The aplysiæ exhale a very nauseous
and fœtid odour when they are approached: the best known of the species
resembles, when in a state of repose, a mass of unformed flesh; when in
motion, it is like a common slug; its colour is reddish-brown; it has
four horns on its head; and the eyes, which are very small, are situated
between the two hinder ones. This aplysia has an ink reservoir, like the
sepia, and ejects it in order to escape from its enemies; it inhabits
the muddy bottom of the water, and lives on small crabs, mollusca, &c.

2. =Poisons from Plants.=--Dioscorides enumerates opium, black and white
hyoscyamus (especially recognising the activity of the seeds),
mandragora, which was probably a mixture of various solanaceæ, conium
(used to poison the condemned by the people of Athens and the dwellers
of ancient Massilia), elaterin, and the juices of a species of euphorbia
and apocyneæ. He also makes a special mention of aconite, the name of
which is derived from _Akon_, a small city in Heraclea. The Greeks were
well aware of the deadly nature of aconite, and gave to it a mythical
origin, from the foam of the dog Cerberus. Colchicum was also known to
Dioscorides: its first use was ascribed to Medea. Veratrum album and
nigrum were famous medicines of the Romans, and a constituent of their
“_rat and mice powders_;” they were also used as insecticides. According
to Pliny, the Gauls dipped their arrows in a preparation of veratrum.[2]
Daphne mezereon, called by the Romans also smilax and taxus, appears to
have been used by Cativolcus, the king of the Eburones, for the purpose
of suicide, or possibly by “taxus” the yew-tree is meant.[3]

[2] Pliny, xxv. 5.

[3] _De Bello Gallico_, vi. 31.

The poisonous properties of certain fungi were also known. Nicander
calls the venomous mushrooms the “evil fermentation of the earth,” and
prescribes the identical antidotes which we would perhaps give at the
present time--viz., vinegar and alkaline carbonates.

3. =Mineral Poisons.=--Arsenic has been already alluded to. The ancients
used it as a caustic and depilatory. Copper was known as sulphate and
oxide; mercury only as cinnabar: lead oxides were used, and milk and
olive-oil prescribed as an antidote for their poisonous properties. The
_poison-lehre_ for many ages was considered as something forbidden.
Galen, in his treatise “On Antidotes,” remarks that the only authors who
dared to treat of poisons were Orpheus, Theologus, Morus, Mendesius the
younger, Heliodorus of Athens, Aratus, and a few others; but none of
these treatises have come down to us. From the close similarity of the
amount of information in the treatises of Nicander, Dioscorides, Pliny,
Galen, and Paulus Ægineta, it is probable that all were derived from a
common source.

§ 4. If we turn our attention to early Asiatic history, a very cursory
glance at the sacred writings of the East will prove how soon the art of
poisoning, especially in India, was used for the purpose of suicide,
revenge, or robbery.

The ancient practice of the Hindoo widow--self-immolation on the burning
pile of her husband--is ascribed to the necessity which the Brahmins
were under of putting a stop to the crime of domestic poisoning. Every
little conjugal quarrel was liable to be settled by this form of secret
assassination, but such a law, as might be expected, checked the

Poison was not used to remove human beings alone, for there has been
from time immemorial in India much cattle-poisoning. In the Institutes
of Menu, it is ordained that when cattle die the herdsman shall carry to
his master their ears, their hides, their tails, the skin below their
navels, their tendons, and the liquor oozing from their foreheads.
Without doubt these regulations were directed against cattle-poisoners.

The poisons known to the Asiatics were arsenic, aconite, opium, and
various solanaceous plants. There has been a myth floating through the
ages that a poison exists which will slay a long time after its
introduction. All modern authors have treated the matter as an
exaggerated legend, but, for my own part, I see no reason why it should
not, in reality, be founded on fact. There is little doubt that the
Asiatic poisoners were well acquainted with the infectious qualities of
certain fevers and malignant diseases. Now, these very malignant
diseases answer precisely to the description of a poison which has no
immediate effects. Plant small-pox in the body of a man, and for a whole
fortnight he walks about, well and hearty. Clothe a person with a
garment soaked in typhus, and the same thing occurs--for many days there
will be no sign of failure. Again, the gipsies, speaking a tongue which
is essentially a deformed _prakrit_, and therefore Indian in origin,
have long possessed a knowledge of the properties of the curious “_mucor
phycomyces_.” This was considered an alga by Agaron, but Berkeley
referred it to the fungi. The gipsies are said to have administered the
spores of this fungi in warm water. In this way they rapidly attach
themselves to the mucous membrane of the throat, all the symptoms of a
phthisis follow, and death takes place in from two to three weeks. Mr
Berkeley informed me that he has seen specimens growing on broth which
had been rejected from the stomach, and that it develops in enormous
quantities on oil-casks and walls impregnated with grease. The filaments
are long, from 12 to 18 inches, and it is capable of very rapid

There is also a modern poison, which, in certain doses, dooms the
unfortunate individual to a terrible malady, simulating, to a
considerable extent, natural disease,--that is phosphorus. This poison
was, however, unknown until some time in the eleventh century, when
Alchid Becher, blindly experimenting on the distillation of urine and
carbon, obtained his “_escarboucle_,” and passed away without knowing
the importance of his discovery, which, like so many others, had to be
rediscovered at a later period.

§ 5. The Hebrews were acquainted with certain poisons, the exact nature
of which is not quite clear. The words “_rosch_” and “_chema_” seem to
be used occasionally as a generic term for poison, and sometimes to mean
a specific thing; “_rosch_,” especially, is used to signify some
poisonous parasitic plant. They knew yellow arsenic under the name of
“_sam_,” aconite under the name of “_boschka_,” and possibly “_son_”
means _ergot_.[4] In the later period of their history, when they were
dispersed through various nations, they would naturally acquire the
knowledge of those nations, without losing their own.

[4] R. J. Wunderbar, _Biblisch-talmudische Medicin_. Leipzig, 1850-60.

§ 6. The part that poison has played in history is considerable. The
pharmaceutical knowledge of the ancients is more graphically and
terribly shown in the deaths of Socrates, Demosthenes, Hannibal, and
Cleopatra, than in the pages of the older writers on poisons.

In the reign of Artaxerxes II. (Memnon), (B.C. 405-359), Phrysa poisoned
the queen Statira by cutting food with a knife poisoned on one side
only. Although this has been treated as an idle tale, yet two poisons,
aconite and arsenic, were at least well known; either of these could
have been in the way mentioned introduced in sufficient quantity into
food to destroy life.

In the early part of the Christian era professional poisoners arose, and
for a long time exercised their trade with impunity. Poisoning was so
much in use as a political engine that Agrippina (A.D. 26) refused to
eat of some apples offered to her at table by her father-in-law,

It was at this time that the infamous Locusta flourished. She is said to
have supplied, with suitable directions, the poison by which Agrippina
got rid of Claudius; and the same woman was the principal agent in the
preparation of the poison that was administered to Britannicus, by order
of his brother Nero. The details of this interesting case have been
recorded with some minuteness.

It was the custom of the Romans to drink hot water, a draught nauseous
enough to us, but, from fashion or habit, considered by them a luxury;
and, as no two men’s tastes are alike, great skill was shown by the
slaves in bringing the water to exactly that degree of heat which their
respective masters found agreeable.[5]

[5] Tacitus, lib. xii., xiii. Mentioned also by Juvenal and Suetonius.

The children of the Imperial house, with others of the great Roman
families, sat at the banquets at a smaller side table, while their
parents reclined at the larger. A slave brings hot water to Britannicus;
it is too hot; Britannicus refuses it. The slave adds cold water; and it
is this cold water that is supposed to have been poisoned; in any case,
Britannicus had no sooner drunk of it than he lost voice and
respiration. Agrippina, his mother, was struck with terror, as well as
Octavia, his sister. Nero, the author of the crime, looks coldly on,
saying that such fits often happened to him in infancy without evil
result; and after a few moments’ silence the banquet goes on as before.
If this were not sudden death from heart or brain disease, the poison
must have been either a cyanide or prussic acid.

In those times no autopsy was possible: although the Alexandrian school,
some 300 years before Christ, had dissected both the living and the
dead, the work of Herophilus and Erasistratus had not been pursued, and
the great Roman and Greek writers knew only the rudiments of human
anatomy, while, as to pathological changes and their true
interpretation, their knowledge may be said to have been absolutely
_nil_. It was not, indeed, until the fifteenth century that the Popes,
silencing ancient scruples, authorised dissections; and it was not until
the sixteenth century that Vesalius, the first worthy of being
considered a great anatomist, arose. In default of pathological
knowledge, the ancients attached great importance to mere outward marks
and discolorations. They noted with special attention spots and
lividity, and supposed that poisons singled out the heart for some quite
peculiar action, altering its substance in such a manner that it
resisted the action of the funeral pyre, and remained unconsumed. It
may, then, fairly be presumed that many people must have died from
poison without suspicion, and still more from the sudden effects of
latent disease, ascribed wrongfully to poison. For example, the death of
Alexander was generally at that time ascribed to poison; but Littré has
fairly proved that the great emperor, debilitated by his drinking
habits, caught a malarious fever in the marshes around Babylon, and died
after eleven days’ illness. If, added to sudden death, the body, from
any cause, entered into rapid putrefaction, such signs were considered
by the people absolutely conclusive of poisoning: this belief, indeed,
prevailed up to the middle of the seventeenth century, and lingers still
among the uneducated at the present day. Thus, when Britannicus died, an
extraordinary lividity spread over the face of the corpse, which they
attempted to conceal by painting the face. When Pope Alexander VI. died,
probably enough from poison, his body (according to Guicciardini) became
a frightful spectacle--it was livid, bloated, and deformed; the gorged
tongue entirely filled the mouth; from the nose flowed putrid pus, and
the stench was horrible in the extreme.

All these effects of decomposition, we know, are apt to arise in coarse,
obese bodies, and accompany both natural and unnatural deaths; indeed,
if we look strictly at the matter, putting on one side the preservative
effects of certain metallic poisons, it may be laid down that generally
the corpses of those dying from poison are _less_ apt to decompose
rapidly than those dying from disease--this for the simple reason that a
majority of diseases cause changes in the fluids and tissues, which
render putrefactive changes more active, while, as a rule, those who
take poison are suddenly killed, with their fluids and tissues fairly

When the Duke of Burgundy desired to raise a report that John, Dauphin
of France, was poisoned (1457), he described the imaginary event as

“One evening our most redoubtable lord and nephew fell so grievously
sick that he died forthwith. His lips, tongue, and face were swollen;
his eyes started out of his head. It was a horrible sight to see--for so
look people that are poisoned.”

The favourite powder of the professional poisoner, arsenic, was known to
crowned heads in the fourteenth century; and there has come down to us a
curious document, drawn out by Charles le Mauvais, King of Navarre. It
is a commission of murder, given to a certain Woudreton, to poison
Charles VI., the Duke of Valois, brother of the king, and his uncles,
the Dukes of Berry, Burgundy, and Bourbon:--

“Go thou to Paris; thou canst do great service if thou wilt: do what I
tell thee; I will reward thee well. Thou shalt do thus: There is a thing
which is called sublimed arsenic; if a man eat a bit the size of a pea
he will never survive. Thou wilt find it in Pampeluna, Bordeaux,
Bayonne, and in all the good towns through which thou wilt pass, at the
apothecaries’ shops. Take it and powder it; and when thou shalt be in
the house of the king, of the Count de Valois, his brother, the Dukes of
Berry, Burgundy, and Bourbon, draw near, and betake thyself to the
kitchen, to the larder, to the cellar, or any other place where thy
point can be best gained, and put the powder in the soups, meats, or
wines, provided that thou canst do it secretly. Otherwise, do it not.”
Woudreton was detected, and executed in 1384.[6]

[6] _Trésor de Chartes._ Charles de Navarre. P. Mortonval, vol. ii. p.

A chapter might be written entitled “royal poisoners.” King Charles IX.
even figures as an experimentalist.[7] An unfortunate cook has stolen
two silver spoons, and, since there was a question whether “_Bezoar_”
was an antidote or not, the king administers to the cook a lethal dose
of corrosive sublimate, and follows it up with the antidote; but the man
dies in seven hours, although Paré also gives him oil. Truly a grim

[7] _Œuvres de Paré_, 2nd ed., liv. xx. _Des Vennes_, chap. xliv. p.

The subtle method of removing troublesome subjects has been more often
practised on the Continent than in England, yet the English throne in
olden time is not quite free from this stain.[8] The use of poison is
wholly opposed to the Anglo-Saxon method of thought. To what anger the
people were wrought on detecting poisoners, is seen in the fact that, in
1542, a young woman was boiled alive in Smithfield for poisoning three

[8] For example, King John is believed to have poisoned Maud Fitzwalter
by “a poisoned egg.”

“In the reign of King John, the White Tower received one of the first
and fairest of a long line of female victims in that Maud Fitzwalter who
was known to the singers of her time as Maud the Fair. The father of
this beautiful girl was Robert, Lord Fitzwalter, of Castle Baynard, on
the Thames, one of John’s greatest barons. Yet the king, during a fit of
violence with the queen, fell madly in love with this young girl. As
neither the lady herself nor her powerful sire would listen to his
disgraceful suit, the king is said to have seized her by force at
Dunmow, and brought her to the Tower. Fitzwalter raised an outcry, on
which the king sent troops into Castle Baynard and his other houses; and
when the baron protested against these wrongs, his master banished him
from the realm. Fitzwalter fled to France with his wife and his other
children, leaving his daughter Maud in the Tower, where she suffered a
daily insult in the king’s unlawful suit. On her proud and scornful
answer to his passion being heard, John carried her up to the roof, and
locked her in the round turret, standing on the north-east angle of the
keep. Maud’s cage was the highest, chilliest den in the Tower; but
neither cold, nor solitude, nor hunger could break her strength. In the
rage of his disappointed love, the king sent one of his minions to her
room with a poisoned egg, of which the brave girl ate and died.”--_Her
Majesty’s Tower_, by Hepworth Dixon. Lond., 1869; i. p. 46.

[9] “This yeare, the 17th of March, was boyled in Smithfield one
Margaret Davie, a mayden, which had pouysoned 3 householdes that she
dwelled in. One being her mistress, which dyed of the same, and one
Darington and his wyfe, which she also dwelled with in Coleman Street,
which dyed of the same, and also one Tinleys, which dyed also of the
same.”--Wriotherley’s _Chronicle_, A.D. 1542.

§ 7. Two great criminal schools arose from the fifteenth to the
seventeenth centuries in Venice and Italy. The Venetian poisoners are of
earlier date than the Italian, and flourished chiefly in the fifteenth
century. Here we have the strange spectacle, not of the depravity of
individuals, but of the government of the State formally recognising
secret assassination by poison, and proposals to remove this or that
prince, duke, or emperor, as a routine part of their deliberations.
Still more curious and unique, the dark communings of “_the council of
ten_” were recorded in writing, and the number of those who voted for
and who voted against the proposed crime, the reason for the
assassination, and the sum to be paid, still exist in shameless black
and white. Those who desire to study this branch of secret history may
be referred to a small work by Carl Hoff, which gives a brief account of
what is known of the proceedings of the council. One example will here
suffice. On the 15th of December 1513 a Franciscan brother, John of
Ragubo, offered a selection of poisons, and declared himself ready to
remove any objectionable person out of the way. For the first successful
case he required a pension of 1500 ducats yearly, which was to be
increased on the execution of future services. The presidents, Girolando
Duoda and Pietro Guiarina, placed the matter before the “ten” on the 4th
of January 1514, and on a division (10 against 5) it was resolved to
accept so patriotic an offer, and to experiment first on the Emperor
Maximilian. The bond laid before the “ten” contained a regular
tariff--for the great Sultan 500 ducats, for the King of Spain 150
ducats, but the journey and other expenses were in each case to be
defrayed; the Duke of Milan was rated at 60, the Marquis of Mantua at
50, the Pope could be removed at 100 ducats. The curious offer thus
concludes:--“The farther the journey, the more eminent the man, the more
it is necessary to reward the toil and hardships undertaken, and the
heavier must be the payment.” The council appear to have quietly
arranged thus to take away the lives of many public men, but their
efforts were only in a few cases successful. When the deed was done, it
was registered by a single marginal note, “_factum_.”

What drugs the Venetian poisoners used is uncertain. The Italians
became notorious in the sixteenth and seventeenth centuries for their
knowledge of poisons, partly from the deeds of Toffana and others, and
partly from the works of J. Baptista Porta, who wrote a very
comprehensive treatise, under the title of _Natural Magic_,[10] and
managed to slide into the text, in the sections on cooking (_De Re
Coquinaria_, lib. xiv.), a mass of knowledge as to the preparation of
poisons. There are prescriptions that little accord with the title,
unless indeed the trades of cook and poisoner were the same. He gives a
method of drugging wine with belladonna root, for the purpose of making
the loaded guest loathe drink; he also gives a list of solanaceous
plants, and makes special mention of nux vomica, aconite, veratrum, and
mezereon. Again, in the section (_De Ancupio_, lib. xv.) he gives a
recipe for a very strong poison which he calls “_venenum lupinum_;” it
is to be made of the powdered leaves of _Aconitum lycoctonum_, _Taxus
baccata_, powdered glass, caustic lime, sulphide of arsenic, and bitter
almonds, the whole to be mixed with honey, and made into pills the size
of a hazel-nut.

[10] J. Bapt. Porta, born 1537, died 1615. _Neapolitani Magiæ
Naturalis._ Neapoli, 1589.

In the section _De Medicis Experimentis_ he gives a process to poison a
sleeping person: the recipe is curious, and would certainly not have the
intended effect. A mixture of hemlock juice, bruised datura, stramonium,
belladonna, and opium is placed in a leaden box with a perfectly fitting
cover, and fermented for several days; it is then opened under the nose
of the sleeper. Possibly Porta had experimented on small animals, and
had found that such matters, when fermented, exhaled enough carbonic
acid gas to kill them, and imagined, therefore, that the same thing
would happen if applied to the human subject. However this may be, the
account which Porta gives of the effects of the solanaceous plants, and
the general tone of the work, amply prove that he was no theorist, but
had studied practically the actions of poisons.

The iniquitous Toffana (or Tophana) made solutions of arsenious acid of
varying strength, and sold these solutions in phials under the name of
“_Acquetta di Napoli_” for many years. She is supposed to have poisoned
more than 600 persons, among whom were two Popes--viz., Pius III. and
Clement XIV. The composition of the Naples water was long a profound
secret, but is said to have been known by the reigning Pope and by the
Emperor Charles VI. The latter told the secret to Dr Garelli, his
physician, who, again, imparted the knowledge to the famous Friedrich
Hoffman in a letter still extant. Toffana was brought to justice in
1709, but, availing herself of the immunity afforded by convents,
escaped punishment, and continued to sell her wares for twenty years
afterwards. When Kepfer[11] was in Italy he found her in a prison at
Naples, and many people visited her, as a sort of lion (1730). With the
_Acqua Toffana_, the “_Acquetta di Perugia_” played at the same time its
part. It is said to have been prepared by killing a hog, disjointing the
same, strewing the pieces with white arsenic, which was well rubbed in,
and then collecting the juice which dropped from the meat; this juice
was considered far more poisonous than an ordinary solution of arsenic.
The researches of Selmi on compounds containing arsenic, produced when
animal bodies decompose in arsenical fluids, lend reason and support to
this view; and probably the juice would not only be very poisonous, but
act in a different manner, and exhibit symptoms different from those of
ordinary arsenical poisoning. Toffana had disciples; she taught the art
to Hieronyma Spara, who formed an association of young married women
during the popedom of Alexander VII.; these were detected on their own

[11] Kepfer’s _Travels_. Lond., 1758.

[12] Le Bret’s _Magazin zu Gebrauche der Staat u. Kirchen-Geschichte_,
Theil 4. Frankfort and Leipzig, 1774.

Contemporaneously with Toffana, another Italian, Keli, devoted himself
to similar crimes. This man had expended much as an adept searching for
the philosopher’s stone, and sought to indemnify himself by entering
upon what must have been a profitable business. He it was who instructed
M. de St. Croix in the properties of arsenic; and St. Croix, in his
turn, imparted the secret to his paramour, Madame de Brinvilliers. This
woman appears to have been as cold-blooded as Toffana; she is said to
have experimented on the patients at the Hôtel Dieu, in order to
ascertain the strength of her powders, and to have invented “les poudres
de succession.” She poisoned her father, brothers, sister, and others of
her family; but a terrible fate overtook both her and St. Croix. The
latter was suffocated by some poisonous matters he was preparing, and
Madame de Brinvilliers’ practices having become known, she was obliged
to take refuge in a convent. Here she was courted by a police officer
disguised as an abbé, lured out of the convent, and, in this way brought
to justice, was beheaded[13] and burnt near Nôtre Dame, in the middle
of the reign of Louis XIV.[14]

[13] The Marchioness was imprisoned in the Conciergerie and tortured.
Victor Hugo, describing the rack in that prison, says, “The Marchioness
de Brinvilliers was stretched upon it stark naked, fastened down, so to
speak, quartered by four chains attached to the four limbs, and there
suffered the frightful extraordinary torture by water,” which caused her
to ask “How are you going to contrive to put that great barrel of water
in this little body?”--_Things seen by Victor Hugo_, vol. i.

The water torture was this:--a huge funnel-like vessel was fitted on to
the neck, the edge of the funnel coming up to the eyes; on now pouring
water into the funnel so that the fluid rises above the nose and mouth,
the poor wretch is bound to swallow the fluid or die of suffocation; if
indeed the sufferer resolve to be choked, in the first few moments of
unconsciousness the fluid is swallowed automatically, and air again
admitted to the lungs; it is therefore obvious that in this way
prodigious quantities of fluid might be taken.

[14] For the court of poisoners (_chambre ardente_) and the histories of
St. Croix, De Brinvilliers, the priest Le Sage, the women La Voisin, and
La Vigoureux, the reader may be referred to Voltaire’s _Siècle de Louis
XIV._, Madame de Sévigné’s _Lettres_, Martinière’s _Hist. de la Règne de
Louis XIV._, Strutzel, _De Venenis_, &c.

The numerous attempts of the Italian and Venetian poisoners on the lives
of monarchs and eminent persons cast for a long time a cloud over regal
domestic peace. Bullets and daggers were not feared, but in their place
the dish of meat, the savoury pasty, and the red wine were regarded as
possible carriers of death. No better example of this dread can be found
than, at so late a period as the reign of Henry VII.,[15] the
extraordinary precautions thought necessary for preserving the infant
Prince of Wales.

[15] Henry VIII., at one time of his life, was (or pretended to be)
apprehensive of being poisoned; it was, indeed, a common belief of his
court that Anne Boleyn attempted to dose him. “The king, in an interview
with young Prince Henry, burst into tears, saying that he and his sister
(meaning the Princess Mary) might thank God for having escaped from the
hands of that accursed and venomous harlot, who had intended to poison
them.”--_A Chronicle of England during the Reign of the Tudors_, by W.
J. Hamilton. Introduction, p. xxi.

“No person, of whatsoever rank, except the regular attendants in the
nursery, should approach the cradle, except with an order from the
king’s hand. The food supplied to the child was to be largely
‘_assayed_,’ and his clothes were to be washed by his own servants, and
no other hand might touch them. The material was to be submitted to all
tests. The chamberlain and vice-chamberlain must be present, morning and
evening, when the prince was washed and dressed, and nothing of any kind
bought for the use of the nursery might be introduced until it was
washed and perfumed. No person, not even the domestics of the palace,
might have access to the prince’s rooms except those who were specially
appointed to them, nor might any member of the household approach
London, for fear of their catching and conveying infection.”[16]

[16] Froude’s _History of England_, vol. iii. p. 262.

However brief and imperfect the foregoing historical sketch of the part
that poison has played may be, it is useful in showing the absolute
necessity of a toxicological science--a science embracing many branches
of knowledge. If it is impossible now for Toffanas, Locustas, and other
specimens of a depraved humanity to carry on their crimes without
detection; if poison is the very last form of death feared by eminent
political persons; it is not so much owing to a different state of
society, as to the more exact scientific knowledge which is applied
during life to the discrimination of symptoms, distinguishing between
those resulting from disease and those due to injurious substances, and
after death to a highly developed pathology, which has learned, by
multiplied observations, all the normal and abnormal signs in tissues
and organs; and, finally, to an ever-advancing chemistry, which is able
in many instances to separate and detect the hurtful and noxious thing,
although hid for months deep in the ground.

II.--Growth and Development of the Modern Methods of Chemically
Detecting Poisons.

§ 8. The history of the detection of poisons has gone through several
phases. The first phase has already been incidentally touched
upon--_i.e._, detection by antecedent and surrounding circumstances,
aided sometimes by experiments on animals. If the death was sudden, if
the post-mortem decomposition was rapid, poison was indicated: sometimes
a portion of the food last eaten, or the suspected thing, would be given
to an animal; if the animal also died, such accumulation of proof would
render the matter beyond doubt. The modern toxicologists are more
sceptical, for even the last test is not of itself satisfactory. It is
now known that meat may become filled with bacilli and produce rapid
death, and yet no poison, as such, has been added.

In the next phase, the doctors were permitted to dissect, and to
familiarise themselves with pathological appearances. This was a great
step gained: the apoplexies, heart diseases, perforations of the
stomach, and fatal internal hæmorrhages could no longer be ascribed to
poison. If popular clamour made a false accusation, there was more
chance of a correct judgment. It was not until the end of the eighteenth
and the beginning of the present century, however, that chemistry was
far enough advanced to test for the more common mineral poisons; the
modern phase was then entered on, and toxicology took a new departure.

§ 9. From the treatise of Barthélémy d’Anglais[17] in the thirteenth
century (in which he noticed the poisonous properties of quicksilver
vapour), up to the end of the fifteenth century, there are numerous
treatises upon poison, most of which are mere learned compilations, and
scarcely repay perusal. In the sixteenth century, there are a few works,
such, for example, as Porta, which partook of the general advancement of
science, and left behind the stereotyped doctrine of the old classical

[17] _De Rerum Proprietaribus._

[18] In the sixteenth century it was not considered proper to write upon
poisons. Jerome Cardan declared a poisoner worse than a brigand, “and
that is why I have refused not only to teach or experiment on such
things, but even to know them.”--_J. Cardan: De Subtilitate_. Basel,

In the seventeenth century the Honourable Robert Boyle made some shrewd
observations, bearing on toxicology, in his work on “The usefulness of
Natural Philosophy,” &c.: Oxford, 1664. Nicolas L’Emery also wrote a
_Cours de Chimie_,--quite an epitome of the chemical science of the

[19] _Cours de Chimie, contenant la manière de faire les opérations qui
sont en usage dans la Médecine._ Paris, 1675.

In the eighteenth century still further advances were made. Richard Mead
published his ingenious _Mechanical Theory of Poisons_. Great chemists
arose--Stahl, Marggraf, Brandt, Bergmann, Scheele, Berthollet,
Priestley, and lastly, Lavoisier--and chemistry, as a science, was born.
Of the chemists quoted, Scheele, in relation to toxicology, stands
chief. It was Scheele who discovered prussic acid,[20] without, however,
noting its poisonous properties; the same chemist separated oxalic acid
from sorrel,[21] and made the important discovery that arsenic united
with hydrogen, forming a fœtid gas, and, moreover, that this gas could
be decomposed by heat.[22] From this observation, a delicate test for
arsenic was afterwards elaborated, which for the first time rendered the
most tasteless and easily administered poison in the whole world at once
the easiest of detection. The further history of what is now called
“Marsh’s Test” is as follows:--

[20] _Opuscula Chemica_, vol. ii. pp. 148-174.

[21] _De Terra Rhubarbi et Acido Acetosellæ._ _Nova Acta Acad. Veg.
Sued. Anni_, 1784. _Opuscula Chemica_, vol. ii. pp. 187-195.

Bergmann first described oxalic acid as obtained by the oxidation of
saccharine bodies; but Scheele recognised its identity with the acid
contained in sorrel.

[22] _Mémoires de Scheele_, t. i., 1775.

§ 10. Proust[23] observed that a very fœtid hydrogen gas was disengaged
when arsenical tin was dissolved in hydrochloric acid, and that arsenic
was deposited from the inflamed gas on cold surfaces which the flame
touched. Trommsdorff next announced, in 1803, that when arsenical zinc
was introduced into an ordinary flask with water and sulphuric acid, an
arsenical hydrogen was disengaged; and if the tube was sufficiently
long, arsenic was deposited on its walls.[24] Stromeyer, Gay-Lussac,
Thénard, Gehlen, and Davy later studied this gas, and Serullas in 1821
proposed this reaction as a toxicological test. Lastly, in 1836, Marsh
published his Memoir.[25] He elaborated a special apparatus of great
simplicity, developed hydrogen by means of zinc and sulphuric acid,
inflamed the issuing gas, and obtained any arsenic present as a metal,
which could be afterwards converted into arsenious acid, &c.

[23] Proust, _Annales de Chimie_, t. xxviii., 1798.

[24] _Nicholson’s Journal_, vol. vi.

[25] “Description of a New Process of Separating Small Quantities of
Arsenic from Substances with which it is mixed.” _Ed. New. Phil.
Journal_, 1836.

This brief history of the so-called “Marsh’s Test” amply shows that
Marsh was not the discoverer of the test. Like many other useful
processes, it seems to have been evolved by a combination of many minds.
It may, however, be truly said that Marsh was the first who perfected
the test and brought it prominently forward.

§ 11. Matthieu Joseph Bonaventura Orfila must be considered the father
of modern toxicology. His great work, _Traité de Toxicologie_, was first
published in 1814, and went through many editions. Orfila’s chief merit
was the discovery that poisons were absorbed and accumulated in certain
tissues--a discovery which bore immediate fruit, and greatly extended
the means of seeking poisons. Before the time of Orfila, a chemist not
finding anything in the stomach would not have troubled to examine the
liver, the kidney, the brain, or the blood. The immense number of
experiments which Orfila undertook is simply marvellous. Some are of
little value, and teach nothing accurately as to the action of
poisons--as, for example, many of those in which he tied the gullet in
order to prevent vomiting, for such are experiments under entirely
unnatural conditions; but there are still a large number which form the
very basis of our pathological knowledge.

Orfila’s method of experiment was usually to take weighed or measured
quantities of poison, to administer them to animals, and then after
death--first carefully noting the changes in the tissues and organs--to
attempt to recover by chemical means the poison administered. In this
way he detected and recovered nearly all the organic and inorganic
poisons then known; and most of his processes are, with modifications
and improvements, in use at the present time.[26]

[26] Orfila’s chief works are as follows:--

_Traité de Toxicologie._ 2 vols. 8vo. Paris, 1814.

_Leçons de Chimie, appliquées à la Méd. Pratique._ 16mo. Brussels, 1836.

_Mémoire sur la Nicotine et la Conicine._ Paris, 1851.

_Leçons de la Méd. Légale._ 8vo. Paris, 1821.

_Traité des Exhumations Juridiques, et Considérations sur les Changemens
Physiques que les Cadavres éprouvent en se pourrissant._ 2 tom. Paris,

§ 12. The discovery of the alkaloids at the commencement of this century
certainly gave the poisoner new weapons; yet the same processes
(slightly modified) which separated the alkaloids from plants also
served to separate them from the human body. In 1803 Derosne discovered
narcotine and morphine, but he neither recognised the difference between
these two substances, nor their basic properties. Sertürner from 1805
devoted himself to the study of opium, and made a series of discoveries.
Robiquet, in 1807, recognised the basic characters of narcotine. In 1818
Pelletier and Caventou separated strychnine; in 1819 brucine; and in the
same year delphinine was discovered simultaneously by Brande, Lassaigne,
and Feneuille. Coniine was recognised by Giesecke in 1827, and in the
following year, 1828, nicotine was separated by Reimann and Posselt. In
1832 Robiquet discovered codeine; and in 1833 atropine, aconitine, and
hyoscyamine were distinguished by Geiger and Hesse. Since then, every
year has been marked by the separation of some new alkaloid, from either
animal or vegetable substances. So many workers in different countries
now began to study and improve toxicology, that it would exceed the
limits and be foreign to the scope of this treatise to give even a brief
_résumé_ of their labours. It may, notwithstanding, be useful to append
a short bibliography of the chief works on toxicology of the present


    ANGLADA, JOS.--“Traité de Toxicologie Générale, &c.” Montpellier et
    Paris, 1835.

    AUTENRIETH.--“Kurze Anleitung zur Auffindung der Gifte.” Freiburg,

    BANDLIN, O.--“Die Gifte.” Basel, 1869-1873.

    BAUMERT, G.--“Lehrbuch der gerichtl. Chemie.” Braunschweig, 1889-92.

    BAYARD, HENRI.--“Manuel Pratique de Médecine Légale.” Paris, 1843.

    BELLINI, RANIERI.--“Manuel de Tossicologia.” Pisa, 1878.

    BERLIN, N. J.--“Nachricht, die gewöhnlichen Gifte chemisch zu
    entdecken.” Stockholm, 1845.

    BERNARD, C.--“Leçons sur les Effets des Substances Toxiques et
    Médicamenteuses.” Paris, 1857.

    BERTRAND, C. A. R. A.--“Manuel Médico-Légale des Poisons introduits
    dans l’Estomac, et les Moyens Thérapeutiques qui leur conviennent:
    suivi d’un Plan d’Organisation Médico-Judiciaire, et d’un Tableau de
    la Classification Générale des Empoisonnemens.” Paris, 1818.

    BINZ, C.--“Intoxicationen” in Gerhardt’s “Handbuch der
    Kinderkrankheiten.” iii. Heft. Tübingen, 1878.

    BLYTH, A. WYNTER.--“A Manual of Practical Chemistry: The Analysis of
    Foods and the Detection of Poisons.” London, 1879.

    BOCKER, FRIEDER. WILHELM.--“Die Vergiftungen in forensischer u.
    klinischer Beziehung.” Iserlohn, 1857.

    BÖHM, R., NAUNYN, B., und VON BOECK, H.--“Handbuch der
    Intoxicationen.” (Bd. 15 of the German edition of Ziemssen’s

    BRANDT, PHÖBUS, und RATZEBURG.--“Deutschlands Giftgewächse.” Berlin,
    1834-38 (2 vols. with 56 coloured plates).

    BRIAND, J., et CHAUDE, ERN.--“Manuel Complet de Médecine Légale.”
    (The latest edition, 1879.) The chemical portion is by J. Bouis.

    BUCHNER, E.--“Lehrbuch der gerichtlichen Medicin für Aerzte u.
    Juristen.” 3rd ed. München, 1872.

    CASPER, J. L.--“Handbuch der gerichtlichen Medicin.” 7th ed. Berlin,

    CHEVALLIER, A.--“Traité de Toxicologie et de Chimie Judiciaire.”
    Paris, 1868.

    CHIAJE, STEF.--“Enchiridis di Tossicologia teorico-pratica.” 3rd ed.
    Napoli, 1858.

    CHRISTISON, ROBERT.--“A Treatise on Poisons.” Edinburgh, 1830. (A
    third edition appeared in 1836.)

    CORNEVIN, C.--“Des Plantes Vénéneuses.” Paris, 1887.

    DEVERGIE, ALPHONSE.--“Médecine Légale, Théorique, et Pratique.” 3rd
    ed. Paris, 1852.

    DRAGENDORFF, JEAN GEORGES.--“Die gerichtlich-chemische Ermittelung
    von Giften in Nahrungsmitteln, Luftgemischen, Speiseresten,
    Körpertheilen.” &c. St. Petersburg, 1868. 3rd ed. Göttingen, 1888.

    ---- “Untersuchungen aus dem Pharmaceutischen Institute in Dorpat.
    Beiträge zur gerichtlichen Chemie einzelner organischer Gifte.”
    Erstes Heft. St. Petersburg, 1871.

    ---- “Jahresbericht über die Fortschritte der Pharmacognosie,
    Pharmacie, und Toxicologie.” Herausgegeben von Dr. Dragendorff.

    DUFLOS, A.--“Handbuch der angewandten gerichtlich-chemischen Analyse
    der chemischen Gifte, ihre Erkennung in reinem Zustande u. in
    Gemengen betreffend.” Breslau u. Leipzig, 1873.

    EULENBERG, DR. HERMANN.--“Handbuch der Gewerbe-Hygiene.” Berlin,

    FALCK, C. PH.--“Die Klinischwichtigen Intoxicationen.” (Handbuch der
    spec. Pathologie u. Therapie red. von R. Virchow, Bd. 2.) Erlangen,

    FALCK, FERD. AUG.--“Lehrbuch der praktischen Toxicologie.”
    Stuttgart, 1880.

    FLANDIN, C.--“Traité des Poisons, ou Toxicologie appliquée à la
    Médecine Légale, à la Physiologie, et à la Thérapeutique.” Paris,
    1847, 1853.

    FRÖHNER, EUG.--“Lehrbuch der Toxicologie für Thierärzte.” Stuttgart,

    GALTIER, C. P.--“Traité de Toxicologie Médico-Légale et de la
    Falsification des Aliments,” &c. Paris, 1845.

    ---- “Traité de Toxicologie Médicale, Chimique et Légale,” &c.
    Paris, 1855. A later edition of the same work.

    GREENE, WILL. H.--“A Practical Handbook of Medical Chemistry,
    applied to Clinical Research and the Detection of Poisons.”
    Philadelphia, 1880.

    GUÉRIN, G.--“Traité Pratique d’Analyse Chimique et de Recherches
    Toxicologiques.” Paris, 1893.

    GUY, W. A., and FERRIER, DAVID.--“Principles of Forensic Medicine.”
    London, 1874.

    HARNACK, ERICH.--“Lehrbuch der Arzneimittellehre,” &c. Hamburg,

    HASSELT, VAN, A. W. M.--“Handbuch der Giftlehre für Chemiker,
    Aerzte, Apotheker, u. Richtspersonen.” (A German translation of the
    original Dutch edition, edited by J. B. Henkel. Braunschweig, 1862.
    Supplemental vol. by N. Husemann, Berlin, 1867.)

    HELWIG, A.--“Das Mikroskop in der Toxicologie.” 64 photographs, roy.
    8vo, Mainz, 1865.

    HEMMING, W. D.--“Aids to Forensic Medicine and Toxicology.” London,

    HERMANN, L.--“Lehrbuch der experimentellen Toxicologie.” 8vo.
    Berlin, 1874.

    HOFFMANN, E. R.--“Lehrbuch der gerichtlichen Medicin.” 5th ed. Wien,

    HUSEMANN and A. HILGER.--“Die Pflanzenstoffe in chemischer,
    pharmakologischer, u. toxicologischer Hinsicht.” 2nd ed. Berlin,

    HUSEMANN, TH., and HUSEMANN, A.--“Handbuch der Toxicologie.” Berlin,
    1862. (Suppl. Berlin, 1867.)

    KOBERT, RUD.--“Lehrbuch der Intoxicationen.” Stuttgart, 1893.

    KOEHLER, R.--“Handbuch der speciellen Therapie, einschliesslich der
    Behandlung der Vergiftungen.” 3rd ed. 2 vols. roy. 8vo. Tübingen,

    LESSER, ADOLF.--“Atlas der gerichtlichen Medicin.” Berlin, 1883.

    LOEW, OSCAR.--“Ein natürliches System der Gift-Wirkungen.” München,

    LUDWIG, E.--“Medicinische Chemie in Anwendung auf gerichtliche

    MAHON, A.--“Médecine Légale et Police Médicale.” Paris, 1807.

    MARX, K. F. H.--“Die Lehre von den Giften.” Göttingen, 1827-29.

    MASCHKA, J.--“Handbuch der gerichtlichen Medicin.” Tübingen,
    1881-82. This work is under the editorship of Dr. Maschka, and
    contains separate articles on medico-legal and toxicological
    questions by various eminent toxicologists, somewhat after the
    manner of Ziemssen’s Cyclopædia.

    MENDE, LUD. JUL. CASP.--“Ausführliches Handbuch der gerichtlichen
    Medicin.” 1819-32.

    MOHR, FRIED.--“Chemische Toxicologie.” Braunschweig, 1874.

    MONTGARNY, H. DE.--“Essai de Toxicologie, et spécialement avec la
    Jurisprudence Médicale.” Paris, 1878.

    MONTMAHON, E. S. DE.--“Manuel Médico-Légale des Poisons,” &c. Paris,

    MUTEL, D. PH.--“Des Poisons, considérés sous le rapport de la
    Médecine Pratique,” &c. Montpellier et Paris, 1835.

    NACQUET, A.--“Legal Chemistry: A guide to the detection of Poisons,
    Examination of Stains, &c., as applied to Chemical Jurisprudence.”
    New York, 1876.

    A translation from the French; see “Foods, their Composition and
    Analysis,” page 43.

    NICOLAI, JOH. ANT. HEINR.--“Handbuch der gerichtlichen Medicin.”
    Berlin, 1841.

    The chemical portion is by F. R. Simon.

    OGSTON, F.--“Lectures on Medical Jurisprudence.” London, 1878.

    ORFILA, MATTHIEU JOS. BONAVENTURA.--“Traité des Poisons, ou
    Toxicologie Générale.” Paris, 1st ed., 1814; 5th ed., 1852.

    ORFILA et LESUEUR.--“Traité de Médecine légale.” Paris, 1821; 4th
    ed., Paris, 1848.

    OTTO, F. G.--“Anleitung zur Ausmittelung der Gifte.” Braunschweig,
    1856; 5th ed., 1875. 6th ed. by Robert Otto, Braunschweig, 1884.

    PRAAG VAN, LEONIDES, u. OPWYRDA, R. J.--“Leerboek voor practische
    giftleer.” In Zwei Theilen. Utrecht, 1871.

    RABUTEAU, A.--“Élémens de Toxicologie et de Médecine Légale,
    appliquées à l’Empoisonnement.” Paris, 1873. 2nd ed. by Ed.
    Bourgoing. Paris, 1888.

    REESE, JOHN J.--“Manual of Toxicology, including the consideration
    of the Nature, Properties, Effects, and Means of Detection of
    Poisons, more especially in their Medico-legal relations.”
    Philadelphia, 1874.

    REMER, W. H. G.--“Lehrbuch der polizeilich-gerichtlichen Chemie.”
    Bd. 1 u. 2. 3. Auflage, Helmstadt, 1824.

    SCHNEIDER, F. C.--“Die gerichtliche Chemie für Gerichtsärzte u.
    Juristen.” Wien, 1852.

    SCHNEIDER, P. J.--“Ueber die Gifte in medicinisch-gerichtlicher u.
    gerichtlich-polizeilicher Rücksicht.” 2nd ed., 1821.

    SELMI, F.--“Studi di Tossicologia Chimica.” Bologna, 1871.

    SOBERNHEIM, JOS. FR. u. SIMON, J. F.--“Handbuch der praktischen
    Toxicologie,” &c. Berlin, 1838.

    SONNENSCHEIN, L.--“Handbuch der gerichtlichen Medicin.” Berlin,
    1860. A new edition by Dr. A. Classen. Berlin, 1881.

    TARDIEU, A.--“Étude Médico-Légale et Clinique sur l’Empoisonnement,
    avec la Collaboration de M. T. Roussin pour la partie de l’expertise
    relative à la Recherche Chimique des Poisons.” Paris, 1867.

    TAYLOR, ALFRED SWAINE.--“On Poisons in relation to Medical
    Jurisprudence and Medicine.” 3rd ed. 1875. Manual, 1879.

    ---- “Principles and Practice of Medical Jurisprudence.” 3 vols.
    London, 1873.

    WERBER, ANT.--“Lehrbuch der praktischen Toxicologie.” Erlangen,

    WOOD, HORATIO C.--“Therapeutics, Materia Medica, and Toxicology.”
    Philadelphia, 1874.

    WOODMANN, W. BATHURST, and TIDY, CH.--“A Handy-Book of Forensic
    Medicine and Toxicology.” London, 1877.

    WORMLEY, THEODORE G.--“Micro-Chemistry of Poisons, including their
    Physiological, Pathological, and Legal Relations.” New York, 1857.

    WURTZ, A.--“Traité Elémentaire de Chimie Médicale, comprenant
    quelques notions de Toxicologie,” &c. 2nd ed. Paris, 1875.


I.--Definition of Poison.

§ 14. The term “_Poison_” may be considered first in its legal, as
distinct from its scientific, aspect.

_The legal definition_ of “poison” is to be gathered from the various
statute-books of civilised nations.

The English law enacts that: “Whoever shall administer, or cause to be
administered to, or taken by any person, any poison or other destructive
thing, with intent to commit murder, shall be guilty of felony.”

Further, by the Criminal Consolidation Act, 1861: “Whosoever shall, by
any other means other than those specified in any of the preceding
sections of this Act, attempt to commit murder, shall be guilty of

It is therefore evident that, by implication, the English law defines a
poison to be a destructive thing administered to, or taken by, a person,
and it must necessarily include, not only poisons which act on account
of their inherent chemical and other properties after absorption into
the blood, but mechanical irritants, and also specifically-tainted
fluids. Should, for example, a person give to another milk, or other
fluid, knowing, at the same time, that such fluid is contaminated by the
specific poison of scarlet fever, typhoid, or any serious malady capable
of being thus conveyed, I believe that such an offence could be brought
under the first of the sections quoted. In fine, the words “_destructive
thing_” are widely applicable, and may be extended to any substance,
gaseous, liquid, or solid, living or dead, which, if capable at all of
being taken within the body, may injure or destroy life. According to
this view, the legal idea of “poison” would include such matters as
boiling water, molten lead, specifically-infected fluids, the flesh of
animals dying of diseases which may be communicable to man, powdered
glass, diamond dust, &c. Evidence must, however, be given of guilty

The words, “administered to or taken by,” imply obviously that the
framers of the older statute considered the mouth as the only portal of
entrance for criminal poisoning, but the present law effectually guards
against any attempt to commit murder, no matter by what means. There is
thus ample provision for all the strange ways by which poison has been
introduced into the system, whether it be by the ear, nose, brain,
rectum, vagina, or any other conceivable way, so that, to borrow the
words of Mr. Greaves (_Notes on Criminal Law Consolidation_), “the
malicious may rest satisfied that every attempt to murder which their
perverted ingenuity may devise, or their fiendish malignity suggest,
will fall within some clause of this Act, and may be visited with penal
servitude for life.”

Since poison is often exhibited, not for the purpose of taking life, but
from various motives, and to accomplish various ends--as, for example,
to narcotise the robber’s victim (this especially in the East), to quiet
children, to create love in the opposite sex (love philters), to detect
the secret sipper by suitably preparing the wine, to expel the
inconvenient fruit of illicit affection, to cure inebriety by polluting
the drunkard’s drink with antimony, and, finally, to satisfy an aimless
spirit of mere wantonness and wickedness, the English law enacts “that
whosoever shall unlawfully or maliciously administer to, or cause to be
taken by, any other person, any poison or other destructive or noxious
thing, so as thereby to endanger the life of such person, or so as
thereby to inflict upon such person any grievous bodily harm, shall be
guilty of felony.”

There is also a special provision, framed, evidently, with reference to
volatile and stupefying poisons, such as chloroform, tetrachloride of
carbon, &c.:--

“Whoever shall unlawfully apply, or administer to, or cause to be taken
by any person, any chloroform, laudanum, or other stupefying or
overpowering drug, matter, or thing, with intent, in any such case,
thereby to enable himself or any other person to commit, or with intent,
&c., to assist any other person in committing, any indictable offence,
shall be guilty of felony.”

§ 15. The German statute, as with successive amendments it now stands,
enacts as follows:[27]--

[27] “Wer vorsätzlich einem Andern, um dessen Gesundheit zu beschädigen,
Gift oder andere Stoffe beibringt, welche die Gesundheit zu zerstören
geeignet sind, wird mit Zuchthaus von zwei bis zu zehn Jahren bestraft.

“Ist durch die Handlung eine schwere Körperverletzung verursacht worden,
so ist auf Zuchthaus nicht unter fünf Jahren, und wenn durch die
Handlung der Tod verursacht worden, auf Zuchthaus nicht unter zehn
Jahren oder auf lebenslängliches Zuchthaus zu erkennen.

“Ist die vorsätzliche rechtswidrige Handlung des Gift--&c.,--Beibringens
auf das ‘Tödten’ gerichtet, soll also durch dieselbe gewollter Weise der
Tod eines Anderen herbeigeführt werden, so kommt in betracht: Wer
vorsätzlich einen Menschen tödtet, wird, wenn er die Tödtung mit
Ueberlegung ausgeführt hat, wegen Mordes mit dem Tode bestraft.”

“Whoever wilfully administers (_beibringt_) to a person, for the purpose
of injuring health, poison, or any other substance having the property
of injuring health, will be punished by from two to ten years’

“If by such act a serious bodily injury is caused, the imprisonment is
not to be less than five years; if death is the result, the imprisonment
is to be not under ten years or for life.

“If the death is wilfully caused by poison, it comes under the general
law: ‘Whoever wilfully kills a man, and if the killing is premeditated,
is on account of murder punishable with death.’”

The French law runs thus (Art. 301, _Penal Code_):--“Every attempt on
the life of a person, by the effect of substances which may cause death,
more or less suddenly, in whatever manner these substances may have been
employed or administered, and whatever may have been the results, is
called poisoning.”[28]

[28] “Est qualifié _empoisonnement_--tout attentat à la vie d’une
personne par l’effet de substances qui peuvent donner la mort plus ou
moins promptement, de quelque manière que ces substances aient été
employées ou administrées, et quelles qu’en aient été les suites.”--Art.
301, _Penal Code_.

There is also a penalty provided against any one who “shall have
occasioned the illness or incapacity for personal work of another, by
the voluntary administration, in any manner whatever, of substances
which, without being of a nature to cause death, are injurious to

[29] “Celui qui aura occasionné à autrui une maladie ou incapacité de
travail personnel en lui administrant volontairement, de quelque manière
que ce soit, des substances qui, sans être de nature à donner la mort,
sont nuisibles à la santé.”--Art. 317, _Penal Code_.

§ 16. =Scientific Definition of a Poison.=--A true scientific definition
of a poison must exclude all those substances which act
mechanically,--the physical influences of heat, light, and electricity;
and parasitic diseases, whether caused by the growth of fungus, or the
invasion of an organism by animal parasites, as, for example,
“trichinosis,” which are not, so far as we know, associated with any
poisonous product excreted by the parasite;--on the other hand, it is
now recognised that pathogenic micro-organisms develop poisons, and the
symptoms of all true infections are but the effects of “toxines.” The
definition of poison, in a scientific sense, should be broad enough to
comprehend not only the human race, but the dual world of life, both
animal and vegetable.

Husemann and Kobert are almost the only writers on poisons who have
attempted, with more or less success, to define poison by a
generalisation, keeping in view the exclusion of the matters enumerated.
Husemann says--“We define poisons as such inorganic, or organic
substances as are in part capable of artificial preparation, in part
existing, ready-formed, in the animal or vegetable kingdom, which,
without being able to reproduce themselves, through the chemical nature
of their molecules under certain conditions, change in the healthy
organism the form and general relationship of the organic parts, and,
through annihilation of organs, or destruction of their functions,
injure health, or, under certain conditions, destroy life.” Kobert
says:--“Poisons are organic or inorganic unorganised substances
originating in the organism itself, or introduced into the organism,
either artificially prepared, or ready formed in nature, which through
their chemical properties, under certain conditions, so influence the
organs of living beings, that the health of these beings is seriously
influenced temporarily or permanently.”

In the first edition of this work I made an attempt to define a poison
thus:--_A substance of definite chemical composition, whether mineral or
organic, may be called a poison, if it is capable of being taken into
any living organism, and causes, by its own inherent chemical nature,
impairment or destruction of function_. I prefer this definition to
Kobert’s, and believe that it fairly agrees with what we know of

II.--Classification of Poisons.

§ 17. At some future time, with a more intimate knowledge of the way in
which each poison acts upon the various forms of animal and vegetable
life, it may be possible to give a truly scientific and philosophical
classification of poisons--one based neither upon symptoms, upon local
effects, nor upon chemical structure, but upon a collation and
comparison of all the properties of a poison, whether chemical,
physical, or physiological. No perfect systematic arrangement is at
present attainable: we are either compelled to omit all classification,
or else to arrange poisons with a view to practical utility merely.

From the latter point of view, an arrangement simply according to the
most prominent symptoms is a good one, and, without doubt, an assistance
to the medical man summoned in haste to a case of real or suspected
poisoning. Indeed, under such circumstances, a scheme somewhat similar
to the following, probably occurs to every one versed in toxicology:--


There are but few poisons which destroy life in a few minutes. Omitting
the strong mineral acids, carbon monoxide, carbon dioxide, with the
irrespirable gases,--_Prussic acid_, _the cyanides_, _oxalic acid_, and
occasionally _strychnine_, are the chief poisons coming under this head.

B. IRRITANT POISONS (symptoms mainly pain, vomiting, and purging).

_Arsenic_, _antimony_, _phosphorus_, _cantharides_, _savin_, _ergot_,
_digitalis_, _colchicum_, _zinc_, _mercury_, _lead_, _copper_, _silver_,
_iron_, _baryta_, _chrome_, _yew_, _laburnum_, _and putrid animal

C. IRRITANT AND NARCOTIC POISONS (symptoms those of an irritant nature,
with the addition of more or less pronounced cerebral indications).

To this class more especially belong _oxalic acid_ and _the oxalates_,
with several poisons belonging to the purely narcotic class, but which
produce occasionally irritant effects.


1. NARCOTICS (chief symptom insensibility, which may be preceded by more
or less cerebral excitement): _Opium_, _Chloral_, _Chloroform_.

2. DELIRIANTS (delirium for the most part a prominent symptom):
_Belladonna_, _hyoscyamus_, _stramonium_, _with others of the
Solanaceæ_, to which may be added--_poisonous fungi_, _Indian hemp_,
_lolium temulentum_, _œnanthe crocata_, and _camphor_.

3. CONVULSIVES.--Almost every poison has been known to produce
convulsive effects, but the only true convulsive poisons are the
_alkaloids of the strychnos class_.

4. COMPLEX NERVOUS PHENOMENA: _Aconite_, _digitalis_, _hemlock_,
_calabar bean_, _tobacco_, _lobelia inflata_, and _curara_.

       *       *       *       *       *

§ 18. KOBERT’S CLASSIFICATION.--The latest authority on
poisons--Kobert--has classified poisons according to the following


    A. Those which specially irritate the part to which they are

    1. _Acids._

    2. _Caustic alkalies._

    3. _Caustic salts_, especially those of the heavy metals.

    4. Locally irritating organic substances which neither can be
    classified as corrosive acids nor alkalies, nor as corrosive salts;
    such are:--_cantharidine_, _phrynine_, and others in the animal
    kingdom, _croton oil_ and _savin_ in the vegetable kingdom. Locally
    irritating colours, such as the _aniline dyes_.

    5. Gases and vapours which cause local irritation when breathed,
    such as _ammonia_, _chlorine_, _iodine_, _bromine_, and _sulphur

    B. Those which have but little effect locally, but change
    anatomically other parts of the body; such as _lead_, _phosphorus_,
    and others.


    1. Blood poisons interfering with the circulation in a purely
    physical manner, such as _peroxide of hydrogen_, _ricine_, _abrine_.

    2. Poisons which have the property of dissolving the red blood
    corpuscle, such as the _saponins_.

    3. Poisons which, with or without primary solution of the red blood
    corpuscles, produce in the blood methæmoglobin; such as _potassic
    chlorate_, _hydrazine_, _nitrobenzene_, _aniline_, _picric acid_,
    _carbon disulphide_.

    4. Poisons having a peculiar action on the colouring matter of the
    blood, or on its decomposition products, such as _hydric sulphide_,
    _hydric cyanide_, and the _cyanides_ and _carbon monoxide_.


    1. Poisons affecting the cerebro-spinal system; such as
    _chloroform_, _ether_, _nitrous oxide_, _alcohol_, _chloral_,
    _cocaine_, _atropine_, _morphine_, _nicotine_, _coniine_,
    _aconitine_, _strychnine_, _curarine_, and others.

    2. Heart Poisons; such as, _digitalis_, _helleborin_, _muscarine_.


    1. Poisonous albumin.

    2. Poisons developed in food.

    3. Auto-poisoning, _e.g._ uræmia, glycosuria, oxaluria.

    4. The more important products of tissue change; such as, _fatty
    acids_, _oxyacids_, _amido-fatty acids_, _amines_, _diamines_, and

       *       *       *       *       *

§ 19. I have preferred an arrangement which, as far as possible, follows
the order in which a chemical expert would search for an unknown
poison--hence an arrangement partly chemical and partly symptomatic.
First the chief gases which figure in the mortality statistics are
treated, and then follow in order other poisons.

A chemist, given a liquid to examine, would naturally test first its
reaction, and, if strongly alkaline or strongly acid, would at once
direct his attention to the mineral acids or to the alkalies. In other
cases, he would proceed to separate volatile matters from those that
were fixed, lest substances such as prussic acid, chloroform, alcohol,
and phosphorus be dissipated or destroyed by his subsequent operations.

Distillation over, the alkaloids, glucosides, and their allies would
next be naturally sought, since they can be extracted by alcoholic and
ethereal solvents in such a manner as in no way to interfere with an
_after_-search for metals.

The metals are last in the list, because by suitable treatment, after
all organic substances are destroyed, either by actual fire or powerful
chemical agencies, even the volatile metals may be recovered. The metals
are arranged very nearly in the same order as that in which they would
be separated from a solution--viz., according to their behaviour to
hydric and ammoniac sulphides.

There are a few poisons, of course, such as the oxalates of the
alkalies, which might be overlooked, unless sought for specially; but it
is hoped that this is no valid objection to the arrangement suggested,
which, in greater detail, is as follows:--


  1. Carbon monoxide.
  2. Chlorine.
  3. Hydric sulphide.


  1. Sulphuric acid.
  2. Hydrochloric acid.
  3. Nitric acid.
  4. Potash.
  5. Soda.
  6. Ammonia.
  7. Neutral sodium, potassium, and ammonium salts.

In nearly all cases of death from any of the above, the analyst, from
the symptoms observed during life, from the surrounding circumstances,
and from the pathological appearances and evident chemical reactions of
the fluids submitted, is put at once on the right track, and has no
difficulty in obtaining decided results.


  1. Hydrocarbons.
  2. Camphor.
  3. Alcohols.
  4. Amyl-nitrite.
  5. Chloroform and other anæsthetics.
  6. Carbon disulphide.
  7. Carbolic acid.
  8. Nitro-benzene.
  9. Prussic acid.
  10. Phosphorus.

The volatile alkaloids, which may also be readily distilled by strongly
alkalising the fluid, because they admit of a rather different mode of
treatment, are not included in this class.



   1. Liquid volatile alkaloids, alkaloids of hemlock, nicotine,
      piturie, sparteine, aniline.
   2. The opium group of alkaloids.
   3. The strychnine or tetanic group of alkaloids--strychnine, brucine,
   4. The aconite group of alkaloids.
   5. The mydriatic group of alkaloids--atropine, hyoscyamine, solanin,
   6. The alkaloids of the veratrines.
   7. Physostigmine.
   8. Pilocarpine.
   9. Taxine.
  10. Curarine.
  11. Colchicin.
  12. Muscarine and the active principles of certain fungi.

There would, perhaps, have been an advantage in arranging several of the
individual members somewhat differently--_e.g._, a group might be made
of poisons which, like pilocarpine and muscarine, are antagonistic to
atropine; and another group suggests itself, the physiological action of
which is the opposite of the strychnos class; solanin (although classed
as a mydriatic, and put near to atropine) has much of the nature of a
glucoside, and the same may be said of colchicin; so that, if the
classification were made solely on chemical grounds, solanin would have
followed colchicin, and thus have marked the transition from the
alkaloids to the glucosides.


  1. The digitalis group.
  2. Other poisonous glucosides acting on the heart.
  3. Saponin.

The glucosides, when fairly pure, are easily recognised; they are
destitute of nitrogen, neutral in reaction, and split up into sugar and
other compounds when submitted to the action of saponifying agents, such
as boiling with dilute mineral acids.


  1. Santonin.
  2. Mezereon.

It is probable that this class will in a few years be extended, for
several other organic anitrogenous poisons exist, which, when better
known, will most likely prove to be anhydrides.


Ergot, picrotoxin, the poison of _Illicium religiosum_, cicutoxin,
_Æthusa cynapium_, _Œnanthe crocata_, croton oil, savin oil, the
toxalbumins of castor oil and _Abrus_.

The above division groups together various miscellaneous toxic
principles, none of which can at present be satisfactorily classified.



  1. Poisonous amphibia.
  2. Poison of the scorpion.
  3. Poisonous fish.
  4. Poisonous insects--spiders, wasps, bees, beetles, &c.
  5. Snake poison.


  1. Ptomaines.
  2. Poisoning by putrid or changed foods--sausage poisoning.




    Arsenic, antimony, cadmium.


    Lead, copper, bismuth, silver, mercury.


    Zinc, nickel, cobalt.


    Iron, chromium, thallium, aluminium.




§ 20. The number of deaths from poison (whether accidental, suicidal, or
homicidal), as compared with other forms of violent, as well as natural
deaths, possesses no small interest; and this is more especially true
when the statistics are studied in a comparative manner, and town be
compared with town, country with country.

The greater the development of commercial industries (especially those
necessitating the use or manufacture of powerful chemical agencies), the
more likely are accidents from poisons to occur. It may also be stated,
further, that the higher the mental development of a nation, the more
likely are its homicides to be caused by subtle poison--its suicides by
the euthanasia of chloral, morphine, or hemlock.

Other influences causing local diversity in the kind and frequency of
poisoning, are those of race, of religion, of age and sex, and the
mental stress concomitant with sudden political and social changes.

In the ten years from 1883-1892, there appear to have died from poison,
in England and Wales, 6616 persons, as shown in the following tables:--


  |                            |Accident |         |         |         |
  |                            |   or    |         |         |         |
  |                            | Negli-  |Suicide. | Murder. | Total.  |
  |                            | gence.  |    |    |    |    |    |    |
  |                            | M. | F. | M. | F. | M. | F. | M. | F. |
  |                            |    |    |    |    |    |    |    |    |
  |           METALS.          |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Arsenic,                    |  37|  14|  37|  20|   1|   1|  75|  35|
  |Antimony,                   |   3| ...|   1|   2| ...| ...|   4|   2|
  |Copper,                     |   4|   1|   2|   1| ...| ...|   6|   2|
  |Lead,                       | 831| 209|   1|   2| ...| ...| 832| 211|
  |Silver Nitrate,             |   1| ...| ...| ...| ...| ...|   1| ...|
  |Zinc Chloride (or Sulphate),|   7| ...|   4| ...| ...| ...|  11| ...|
  |Mercury,                    |  22|  11|  16|   8|   2|   1|  40|  20|
  |Chromic Acid,               |   1| ...| ...| ...| ...| ...|   1| ...|
  |Iron Perchloride,           | ...| ...| ...|   1| ...| ...| ...|   1|
  |                            |    |    |    |    |    |    |    |    |
  |     ALKALINE EARTHS.       |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Lime,                       |   2| ...| ...|   1| ...| ...|   2|   1|
  |Barium Chloride,            |   1| ...| ...| ...| ...| ...|   1| ...|
  |                            |    |    |    |    |    |    |    |    |
  |  THE ALKALIES AND THEIR    |    |    |    |    |    |    |    |    |
  |          SALTS.            |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Ammonia,                    |  39|  25|  18|  16| ...| ...|  57|  41|
  |Caustic Soda,               |   3|   4| ...|   1| ...| ...|   3|   5|
  |   „    Potash,             |   8|  10|   1| ...| ...| ...|   9|  10|
  |Potassic Chlorate,          |   1| ...| ...| ...| ...| ...|   1| ...|
  |   „     Bichromate,        |   2|   2|   7|   3| ...| ...|   9|   5|
  |   „     Bromide,           |   1| ...| ...| ...| ...| ...|   1| ...|
  |   „     Binoxalate         |    |    |    |    |    |    |    |    |
  |         (Sorrel),          |   1|   3|   1|   4| ...| ...|   2|   7|
  |                            |    |    |    |    |    |    |    |    |
  |          ACIDS.            |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Sulphuric Acid,             |  30|   9|  29|  24|   1| ...|  60|  33|
  |Nitric     „                |  18|   7|  18|   9| ...| ...|  36|  16|
  |Hydrochloric Acid,          |  48|  18|  83|  55| ...| ...| 131|  73|
  |Oxalic         „            |  17|   6| 114|  86| ...| ...| 131|  92|
  |Tartaric       „            | ...|   1| ...| ...| ...| ...| ...|   1|
  |Acetic         „            |   4|   3| ...|   2| ...| ...|   4|   5|
  |Carbolic       „            | 169| 101| 219| 271| ...|   1| 388| 373|
  |Hydrofluoric   „            | ...| ...| ...|   1| ...| ...| ...|   1|
  |Phosphorus (including       |    |    |    |    |    |    |    |    |
  |Lucifer matches),           |  24|  47|  28|  56| ...| ...|  52| 103|
  |Iodine,                     |   6|   7|   1|   1| ...| ...|   7|   8|
  |                            |    |    |    |    |    |    |    |    |
  |      VOLATILE LIQUIDS.     |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Paraffin (Petroleum),       |   9|   2|   1| ...| ...| ...|  10|   2|
  |Benzoline,                  |   3|   2| ...|   1| ...| ...|   3|   3|
  |Naphtha,                    |   1| ...| ...| ...| ...| ...|   1| ...|
  |Carbon Bisulphide,          | ...| ...|   1| ...| ...| ...|   1| ...|
  |Turpentine,                 |   5|   1| ...|   3| ...| ...|   5|   4|
  |Methylated Spirit,          | ...|   2|   1|   2| ...| ...|   1|   4|
  |Alcohol,                    |  81|  24|   1|   2| ...| ...|  82|  26|
  |Chloroform,                 |  57|  41|   9|   5|   1| ...|  67|  46|
  |Ether,                      |   5|   2| ...| ...| ...| ...|   5|   2|
  |Spt. Etheris Nitrosi,       |   1| ...| ...| ...| ...| ...|   1| ...|
  |Anæsthetic (kind not        |    |    |    |    |    |    |    |    |
  |stated),                    |   4|   3| ...| ...| ...| ...|   4|   3|
  |Oil of Juniper,             |   1| ...| ...| ...| ...| ...|   1| ...|
  |                            |    |    |    |    |    |    |    |    |
  |   OPIATES AND NARCOTICS.   |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Opium, Laudanum--Morphia,   | 503| 373| 330| 167|  4 |  2 | 837| 542|
  |Soothing Syrup, Paregoric,  |    |    |    |    |    |    |    |    |
  |&c.                         |  18|  22|   2|   3| ...| ...|  20|  25|
  |Chlorodyne,                 |  56|  30|   8|   8| ...| ...|  64|  38|
  |Chloral,                    |  89|  22|  14|   1|  1 | ...| 104|  23|
  |                            |    |    |    |    |    |    |    |    |
  |         CYANIDES.          |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Prussic Acid, and Oil of    |    |    |    |    |    |    |    |    |
  |    Almonds,                |  17|  11| 203|  19|  2 |  8 | 222|  38|
  |Potassium Cyanide,          |  19|  21| 100|  22|  3 |  1 | 122|  44|
  |                            |    |    |    |    |    |    |    |    |
  |        ALKALOIDS.          |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Strychnine and Nux Vomica,  |  22|  21|  65|  85|  4 |  4 |  91| 110|
  |Vermin-Killer,              |   2|   6|  49|  69|  1 | ...|  52|  75|
  |Atropine,                   |   2| ...|   1| ...| ...| ...|   3| ...|
  |Belladonna,                 |  36|  20|  11|   9| ...| ...|  47|  29|
  |Aconite,                    |  19|  21|   9|  10| ...| ...|  28|  31|
  |Ipecacuanha,                |   1|   1| ...| ...| ...| ...|   1|   1|
  |Cocaine,                    |   3| ...| ...| ...| ...| ...|   3| ...|
  |                            |    |    |    |    |    |    |    |    |
  |       MISCELLANEOUS.       |    |    |    |    |    |    |    |    |
  |                            |    |    |    |    |    |    |    |    |
  |Antipyrine,                 |   1| ...| ...| ...| ...| ...|   1| ...|
  |Cantharides,                |   1| ...| ...|   1| ...| ...|   1|   1|
  |Camphorated Oil,            |   1| ...| ...| ...| ...| ...|   1| ...|
  |Croton Oil,                 |   1| ...| ...| ...| ...| ...|   1| ...|
  |Cayenne Pepper,             |   1| ...| ...| ...| ...| ...|   1| ...|
  |Syrup of Rhubarb,           |   1| ...| ...| ...| ...| ...|   1| ...|
  |Colchicum,                  |   2| ...| ...| ...| ...| ...|   2| ...|
  |Hemlock,                    |   3|   1| ...| ...| ...| ...|   3|   1|
  |Water Hemlock,              |   5|   6| ...| ...| ...| ...|   5|   6|
  |Colocynth,                  | ...|   2| ...| ...| ...| ...| ...|   2|
  |Castor Oil Seeds,           |   1|   1| ...| ...| ...| ...|   1|   1|
  |Laburnum Seeds,             |   2|   1| ...| ...| ...| ...|   2|   1|
  |Thorn Apple,                |   1| ...| ...| ...| ...| ...|   1| ...|
  |Yew Leaves or Berries,      |   3|   2| ...| ...| ...| ...|   3|   2|
  |Crow-foot,                  | ...|   1| ...| ...| ...| ...| ...|   1|
  |Whin-flower,                |   1| ...| ...| ...| ...| ...|   1| ...|
  |Pennyroyal,                 | ...|   1| ...| ...| ...| ...| ...|   1|
  |Meadow Crow-foot,           | ...|   1| ...| ...| ...| ...| ...|   1|
  |Arum Seeds,                 | ...|   1| ...| ...| ...| ...| ...|   1|
  |Bitter Aloes,               | ...|   1| ...|   1| ...| ...| ...|   2|
  |Cocculus Indicus,           | ...| ...|   1| ...| ...| ...|   1| ...|
  |Horse Chestnut,             | ...|   1| ...| ...| ...| ...| ...|   1|
  |Creosote,                   |   1| ...| ...| ...| ...| ...|   1| ...|
  |Spirits of Tar (Oil of Tar),|   2|   1| ...| ...| ...| ...|   2|   1|
  |Nitro-Glycerine,            |   1| ...| ...| ...| ...| ...|   1| ...|
  |Camphor,                    | ...|   1| ...| ...| ...| ...| ...|   1|
  |Tobacco,                    |   4| ...|   1| ...| ...| ...|   5| ...|
  |Lobelia,                    |   1| ...| ...| ...| ...| ...|   1| ...|
  |Fungi,                      |  13|  10| ...| ...| ...| ...|  13|  10|
  |Poisonous Weeds,            |   2| ...| ...| ...| ...| ...|   2| ...|
  |Hellebores,                 | ...| ...|   1|   1| ...| ...|   1|   1|
  |Kind not stated,            | 216| 158| 256| 167|  3 |  1 | 475| 326|
  |                            +----+----+----+----+----+----+----+----+
  |                            |2498|1292|1644|1140|  23|  19|4165|2551|
  |                            |  \    / |  \    / |  \    / |  \    / |
  |                            |   3790  |   2784  |    42   |   6616  |

Although so large a number of substances destroy life by accident or
design, yet there are in the list only about 21 which kill about 2
persons or above each year: the 21 substances arranged in the order of
their fatality are as follows:--

                         Actual deaths in
                      ten years ending 1892.
  Caustic potash                19
  Poisonous fungi               23
  Aconite                       59
  Mercury                       60
  Belladonna                    76
  Sulphuric acid                93
  Ammonia                       98
  Chlorodyne                   102
  Alcohol                      108
  Arsenic                      110
  Chloroform                   113
  Vermin-killer                127
  Chloral                      127
  Phosphorus                   155
  Cyanide of potassium         166
  Strychnine                   201
  Nitric acid                  204
  Prussic acid                 260
  Carbolic acid                762
  Lead                        1043
  Opiates                     1324

In each decade there are changes in the position on the list. The most
significant difference between the statistics now given and the
statistics for the ten years ending 1880, published in the last edition
of this work, is that in the former decade carbolic acid occupied a
comparatively insignificant place; whereas in the ten years ending 1892,
deaths from carbolic acid poisoning are the most frequent form of fatal
poisoning save lead and opiates.

The following table gives some German statistics of poisoning:--

YEARS 1876, 1877, 1878.

[30] Viz., the Königl. Charité, Allg. Städtisches Krankenhaus,
Städtisches Baracken-Lazareth, Bethanien, St. Helwög’s-Lazarus,
Elisabethen-Krankenhaus, Augusta Hospital, and the Institut für

  |                                      | Males. |Females.| Total. |
  | Charcoal Vapour,                     |   77   |    78  |   155  |
  | Sulphuric Acid,                      |   24   |    54 }|        |
  | Hydrochloric Acid,                   |    4   |     4 }|    93  |
  | Nitric Acid, and Aqua Regia,         |    7   |   ... }|        |
  | Phosphorus,                          |   13   |    28  |    41  |
  | Cyanide of Potassium,                |   29   |     3 }|        |
  | Prussic Acid,                        |    5   |     1 }|    38  |
  | Oxalic Acid, and Oxalate of Potash,  |   11   |     8  |    19  |
  | Alcohol,                             |   12   |     2  |    14  |
  | Arsenic,                             |    7   |     5  |    12  |
  | Morphine,                            |    8   |     1 }|        |
  | Opium,                               |    2   |     1 }|    12  |
  | Potash or Soda Lye,                  |    2   |     6  |     8  |
  | Chloral,                             |    3   |     4  |     7  |
  | Chloroform,                          |    4   |     2  |     6  |
  | Sewer Gas,                           |    5   |   ...  |     5  |
  | Strychnine,                          |  ...   |     4  |     4  |
  | Atropine,                            |    1   |     2  |     3  |
  | Copper Sulphate,                     |    1   |     2  |     3  |
  | Nitrobenzol,                         |    2   |   ...  |     2  |
  | Carbolic Acid,                       |  ...   |     2  |     2  |
  | Chromic Acid,                        |    1   |     1  |     2  |
  | Burnt Alum,                          |  ...   |     1  |     1  |
  | Ammonium Sulphide,                   |    1   |   ...  |     1  |
  | Datura Stramonium,                   |  ...   |     1  |     1  |
  | Petroleum,                           |  ...   |     1  |     1  |
  | Benzine,                             |    1   |   ...  |     1  |
  | Ether,                               |    1   |   ...  |     1  |
  | Prussic Acid and Morphine,           |    1   |   ...  |     1  |
  | Prussic Acid and Chloral,            |    1   |   ...  |     1  |
  | Turpentine and Sal Ammoniac,         |  ...   |     1  |     1  |
  |                                      +--------+--------+--------+
  |                                      |  223   |   212  |   435  |

=Suicidal Poisoning.=--Poisons which kill more than one person
suicidally each year are only 19 in number, as follows:--

                            Deaths from suicide
                            during the ten years
                               ending 1892.

  Potassic bichromate              10
  Chloroform                       14
  Chloral                          15
  Chlorodyne                       16
  Aconite                          19
  Belladonna                       20
  Mercury                          24
  Nitric acid                      27
  Ammonia                          34
  Sulphuric acid                   53
  Arsenic                          77
  Phosphorus                       84
  Vermin-killer                   118
  Prussic acid                    122
  Hydrochloric acid               138
  Strychnine                      150
  Oxalic acid                     200
  Prussic acid                    222
  Opiates                         281
  Phenol                          290

In the ten years ending 1880, suicidal deaths from vermin-killers, from
prussic acid, from cyanide of potassium, and from opiates were all more
numerous than deaths from phenol, whereas at present phenol appears to
be the poison most likely to be chosen by a suicidal person.

Criminal Poisoning.

§ 22. Some useful statistics of criminal poisoning have been given by
Tardieu[31] for the 21 years 1851-1871, which may be summarised as

[31] _Étude Médico-Légale sur l’Empoisonnement_, Paris, 1875.

  Total accusations of Poisoning in the 21 years,            793

    Death,                                        280 }
    Illness,                                      346 }      872
    Negative,                                     246 }

    Men,                                          304 }      703
    Women,                                        399 }

    Arsenic,                                                 287
    Phosphorus,                                              267

         { Sulphate,                              120 }
  Copper { Acetate (Verdigris),                    39 }      159

        { Sulphuric Acid,                          36 }
  Acids { Hydrochloric Acid,                        8 }       47
        { Nitric Acid,                              3 }

  Cantharides,                                                30

  Nux Vomica,                                       5 }       12
  Strychnine,                                       7 }

          { Opium,                                  6 }
  Opiates { Laudanum,                               3 }       10
          { Sedative Water,                         1 }

  Salts of Mercury,                                            8

  Sulphate of Iron,                                            6

  Preparations of Antimony,                                    5

  Ammonia,                                                     4

  Cyanides     {Prussic Acid,                       2 }
               {Cyanide of Potassium,               2 }        4

  Hellebore,                                                   3

  Datura Stramonium,                                           3

  Powdered Glass,                                              3

  Digitalin,                                                   2

  Potash,                                                      2

  Sulphate of Zinc,                                            2

  Eau de Javelle (a solution of Hypochlorite of Potash),       1

  Tincture of Iodine,                                          1

  Croton Oil,                                                  1

  Nicotine,                                                    1

  Belladonna,                                                  1

  “Baume Fiovarenti,”                                          1

  Euphorbia,                                                   1

  Acetate of Lead,                                             1

  Carbonic Acid Gas,                                           1

  Laburnum Seeds,                                              1

  Colchicum,                                                   1

  Mushrooms,                                                   1

  Sulphuric Ether,                                             1
  Total,                                                     867

It hence may be concluded, according to these statistics of criminal
poisoning, that of 1000 attempts in France, either to injure or to
destroy human life by poison, the following is the most probable
selective order:--

  Arsenic,                                                      331
  Phosphorus,                                                   301
  Preparations of Copper,                                       183
  The Mineral Acids,                                             54
  Cantharides,                                                   35
  Strychnine,                                                    14
  Opiates,                                                       12
  Mercurial preparations,                                         9
  Antimonial preparations,                                        6
  Cyanides (that is, Prussic Acid and Potassic Cyanide),          5
  Preparations of Iron,                                           5

This list accounts for 955 poisonings, and the remaining 45 will be
distributed among the less used drugs and chemicals.

IV.--The Connection between Toxic Action and Chemical Composition.

§ 23. Considerable advance has been made of late years in the study of
the connection which exists between the chemical structure of the
molecule of organic substances and physiological effect. The results
obtained, though important, are as yet too fragmentary to justify any
great generalisation; the problem is a complicated one, and as Lauder
Brunton justly observes:--

“The physiological action of a drug does not depend entirely on its
chemical composition nor yet on its chemical structure, so far as that
can be indicated even by graphic formula, but upon conditions of
solubility, instability, and molecular relations, which we may hope to
discover in the future, but with which we are as yet imperfectly

[32] _Introduction to Modern Therapeutics_, Lond., 1892. 136.

The occurrence of hydroxyl, whether the substance belong to the simpler
chain carbon series or to the aromatic carbon compounds, appears to
usually endow the substance with more or less active and frequently
poisonous properties, as, for example, in the alcohols, and as in
hydroxylamine. It is also found that among the aromatic bodies the toxic
action is likely to increase with the number of hydroxyls: thus phenol
has one hydroxyl, resorcin two, and phloroglucin three; and the toxic
power is strictly in the same order, for, of the three, phenol is least
and phloroglucin most poisonous.

Replacing hydrogen by a halogen, especially by chlorine, in the fatty
acids mostly produces substances of narcotic properties, as, for
instance, monochloracetic acid. In the sulphur compounds, the entrance
of chlorine modifies the physiological action and intensifies toxicity:
thus ethyl sulphide (C₂H₅)₂S is a weak poison, monochlorethyl sulphide
C₂H₅C₂H₄ClS a strong poison, and dichlorethyl sulphide C₄H₈Cl₂S a very
strong poison: the vapour kills rabbits within a short time, and a trace
of the oil applied to the ear produces intense inflammation of both the
eyes and the ear.[33]

[33] V. Meyer, _Ber. d. Chem. Ges._, XX., 1725.

The weight of the molecule has an influence in the alcohols and acids of
the fatty series; for instance, ethyl, propyl, butyl, and amyl alcohols
show as they increase in carbon a regular increase in toxic power; the
narcotic actions of sodium propionate, butyrate, and valerianate also
increase with the rising carbon. Nitrogen in the triad condition in the
amines is far less poisonous than in the pentad condition.

Bamberger[34] distinguishes two classes of hydrogenised bases derived
from α and β naphthylamine, by the terms “acylic” and “aromatic.” The
acylic contains the four added hydrogens in the amidogen nucleus, the
aromatic in the other nucleus, thus

[34] _Ber._, xxii. 777-778.

      CH    CNH₂
      /\   /\
     /  \C/  \
  CH |   |   | CH
     |   |   |
  CH |   |   | CH
     \  /C\  /
      \/   \/
      CH    CH

  α Naphthylamine.

      CH    CH
      /\   /\
     /  \C/  \
  CH |   |   | CNH₂
     |   |   |
  CH |   |   | CH
     \  /C\  /
      \/   \/
      CH    CH

  β Naphthylamine.

      CH    CH₂
      /\   /\
     /  \C/  \
  CH |   |   | CNH₃
     |   |   |
  CH |   |   | CH₂
     \  /C\  /
      \/   \/
      CH    CH₂

  Acylic tetrahydro-α Naphthylamine.

       CH₂   CH
       /\   /\
      /  \C/  \
  CH₂ |   |   | CNH₂
      |   |   |
  CH₂ |   |   | CH
      \  /C\  /
       \/   \/
       CH₂   CH

  Aromatic tetrahydro-β Naphthylamine.

The acylic β tetrahydro-naphthylamine, the β
tetrahydroethylnaphthylamine, and the β tetrahydromethylnaphthylamine
all cause dilatation of the pupil and produce symptoms of excitation of
the cervical sympathetic nerve; the other members of the group are

§ 24. The result of replacing hydrogen by alkyls in aromatic bodies has
been studied by Schmiedeberg and others; replacing the hydrogen of the
amidogen by ethyl or methyl, usually results in a body having a more or
less pronounced narcotic action. The rule is that methyl is stronger
than ethyl, but it does not always hold good; ortho-amido-phenol is not
in itself poisonous, but when two hydrogens of the amidogen group are
replaced by two methyls thus--

   /  \
  |    |NH₂
  |    |
  |    |
   \  /

   /  \
  |    |N(CH₃)₂
  |    |
  |    |
   \  /

the resulting body has a weak narcotic action.

It would naturally be inferred that the replacement of the H in the
hydroxyl by a third methyl would increase this narcotic action, but this
is not so: on the other hand, if there are three ethyl groups in the
same situation a decidedly narcotic body is produced.

The influence of position of an alkyl in the aromatic bodies is well
shown in ortho-, para- and meta-derivatives. Thus the author proved some
years ago that with regard to disinfecting properties, ortho-cresol was
more powerful than meta-; meta-cresol more powerful than para-; so again
ortho-aceto-toluid is poisonous, causing acute nephritis;
meta-aceto-toluid has but feeble toxic actions but is useful as an
antipyretic; and para-aceto-toluid is inactive.

In the trioxybenzenes, in which there are three hydroxyls, the toxic
action is greater when the hydroxyls are consecutive, as in pyrogallol,
than when they are symmetrical, as in phloroglucin.

   /  \
  |    |OH
  |    |
  |    |OH
   \  /


     /  \
    |    |
    |    |
  HO|    |OH
     \  /


The introduction of methyl into the complicated molecule of an alkaloid
often gives curious results: thus methyl strychnine and methyl brucine
instead of producing tetanus have an action on voluntary muscle like

Benzoyl-ecgonine has no local anæsthetic action, but the introduction of
methyl into the molecule endows it with a power of deadening the
sensation of the skin locally; on the other hand, cocethyl produces no
effect of this kind.

Drs. Crum Brown and Fraser[35] have suggested that there is some
relation between toxicity and the saturated or non-saturated condition
of the molecule.

[35] _Journ. Anat. and Phys._, vol. ii. 224.

Hinsberg and Treupel have studied the physiological effect of
substituting various alkyls for the hydrogen of the hydroxyl group in

Para-aceto-amido-phenol when given to dogs in doses of 0.5 grm. for
every kilogr. of body weight causes slight narcotic symptoms, with
slight paralysis; there is cyanosis and in the blood much methæmoglobin.

In men doses of half a gramme (7·7 grains) act as an antipyretic,
relieve neuralgia and have weak narcotic effects.

The following is the result of substituting certain alkyls for H in the
HO group.

(1) =Methyl.=--The narcotic action is strengthened and the antipyretic
action unaffected. The methæmoglobin in the blood is somewhat less.

(2) =Ethyl.=--Action very similar, but much less methæmoglobin is

(3) =Propyl.=--Antipyretic action a little weaker. Methæmoglobin in the
blood smaller than in para-acetamido-phenol, but more than when the
methyl or ethyl compound is administered.

(4) =Amyl.=--Antipyretic action decreased.

The smallest amount of toxicity is in the ethyl substitution; while the
maximum antipyretic and antineuralgic action belongs to the methyl

Next substitution was tried in the Imid group. It was found that
substituting ethyl for H in the imid group annihilated the narcotic and
antipyretic properties. No methæmoglobin could be recognised in the

Lastly, simultaneous substitution of the H of the HO group by ethyl and
the substitution of an alkyl for the H in the NH group gave the
following results:--

=Methyl.=--In dogs the narcotic action was strengthened, the
methæmoglobin in the blood diminished. In men the narcotic action was
also more marked as well as the anti-neural action. The stomach and
kidneys were also stimulated.

=Ethyl.=--In dogs the narcotic action was much strengthened, while the
methæmoglobin was diminished. In men the antipyretic and anti-neural
actions were unaffected.

=Propyl.=--In dogs the narcotic action was feebler than with methyl or
ethyl, and in men there was diminished antipyretic action.

=Amyl.=--In dogs the narcotic action was much smaller.

From this latter series the conclusion is drawn that the maximum of
narcotic action is obtained by the introduction of methyl and the
maximum antipyretic action by the introduction of methyl or ethyl. The
ethyl substitution is, as before, the less toxic.[36]

[36] _Ueber die physiologische Wirkung des p-amido-phenol u. einiger
Derivate desselben._ O. Hinsberg u. G. Treupel, _Archiv f. Exp. Pathol.
u. Pharm._, B. 33, S. 216.

The effect of the entrance of an alkyl into the molecule of a substance
is not constant; sometimes the action of the poison is weakened,
sometimes strengthened. Thus, according to Stolnikow, dimethyl resorcin,
C₆H₄(OCH₃)₂, is more poisonous than resorcin C₆H₄(OH)₂. Anisol C₆H₅OCH₃,
according to Loew, is more poisonous to algæ, bacteria, and infusoria
than phenol C₆H₅OH. On the other hand, the replacement by methyl of an
atom of hydrogen in the aromatic oxyacids weakens their action; methyl
salicylic acid


is weaker than salicylic acid

  C₆H₄      .

Arsen-methyl chloride, As(CH₃)Cl₂, is strongly poisonous, but the
introduction of a second methyl As(CH₃)₂Cl makes a comparatively weak

§ 25. In some cases the increase of CO groups weakens the action of a
poison; thus, in allantoin there are three carbonyl (CO) groups; this
substance does not produce excitation of the spinal cord, but it
heightens muscular irritability and causes, like xanthin, muscular
rigidity; alloxantin, with a similar structure but containing six
carbonyl groups, does not possess this action.

   |  |   |
  CO  |   CO
   |  |   |
  NH--CO  NH₂


  NH--CO  CO--HN
   |  |   |   |
   |  | O |   |
   |  |/ \|   |
  CO--C---C   CO
   |  |   |   |
  NH--CO  CO--HN


§ 26. A theory of general application has been put forward and supported
with great ability by Oscar Loew[37] which explains the action of
poisons by presuming that living has a different composition to dead
albumin; the albumin of the chemist is a dead body of a definite
composition and has a stable character; living albumin, such as
circulates in the blood or forms the protoplasm of the tissues, is not
“stable” but “labile”; Loew says:--“If the old idea is accepted that
living albumin is chemically the same substance as that which is dead,
numerous toxic phenomena are inexplicable. It is impossible, for
instance, to explain how it is that diamide N₂H₄ and hydroxylamine NH₂OH
are toxic, even with great dilution, on all living animals; whilst
neither of those substances have the smallest action on dead plasma or
the ordinary dissolved passive albumin, there must therefore be present
in the albumin of the living plasma a grouping of atoms in a “_labile_”
condition (_Atomgruppirungen labiler Art_) which are capable of entering
into reactions; such, according to our present knowledge, can only be
the aldehyde and the ketone groups. The first mentioned groups are more
labile and react in far greater dilution than the latter groups.”

[37] _Ein natürliches System der Gift-Wirkungen_, München, 1893.

Loew considers that all substances which enter into combination with
aldehyde or ketone groups must be poisonous to life generally. For
instance, hydroxylamine, diamide and its derivatives, phenylhydrazine,
free ammonia, phenol, prussic acid, hydric sulphide, sulphur dioxide and
the acid sulphites all enter into combination with aldehyde.

So again the formation of imide groups in the aromatic ring increases
any poisonous properties the original substance possesses, because the
imide group easily enters into combination with aldehyde; thus
piperidine (CH₂)₅NH is more poisonous than pyridine (CH)₅N; coniine
NH(CH₂)₄CH-CH₂-CH₂CH₃, is more poisonous than collidine
N(CH)₄C-CH-(CH₃)₂; pyrrol (CH)₄NH than pyridine (CH)₅N; and amarin,[38]

       |  \
       |   CH-C₆H₅,
       |  /

than hydrobenzamide


[38] Th. Weyl (_Lehrbuch der organischen Chemie_) states (p. 385) that
amarin is not poisonous, but Baccheti (_Jahr. d. Chemie_, 1855) has
shown that 250 mgrms. of the acetate will kill a dog, 80 mgrms. a
guinea-pig; and that it is poisonous to fishes, birds, and frogs:
hydrobenzamide in the same doses has no effect.

If the theory is true, then substances with “labile” amido groups, on
the one hand, must increase in toxic activity if a second amido group is
introduced; and, on the other, their toxic qualities must be diminished
if the amido group is changed into an imido group by the substitution of
an atom of hydrogen for an alkyl.

Observation has shown that both of these requirements are satisfied;
phenylenediamine is more poisonous than aniline; toluylenediamine more
poisonous than toluidine. Again, if an atom of hydrogen in the amido
(NH₂) group in aniline be replaced by an alkyl, _e.g._ methyl or ethyl,
the resulting substance does not produce muscular spasm; but if the same
alkyl is substituted for an atom of hydrogen in the benzene nucleus the
convulsive action remains unaffected.

If an acidyl, as for example the radical of acetic acid, enter into the
amido group, then the toxic action is notably weakened; thus,
acetanilide is weaker than aniline, and acetylphenylhydrazine is weaker
than phenylhydrazine. If the hydrogen of the imido group be replaced by
an alkyl or an acid radical, and therefore tertiary bound nitrogen
restored, the poisonous action is also weakened.

In xanthin there are three imido groups; the hydrogen of two of these
groups is replaced by methyl in theobromin; and in caffein the three
hydrogens of the three imido groups are replaced by three methyls,

  |   ║
  CO  C--NH
  |   |   \
  |   |    CO
  |   |   /


  |      ║
  CO     C--N.CH₃
  |      |   \
  |      |    CO
  |      |   /


  |      ║
  CO     C--N.CH₃
  |      |   \
  |      |    CO
  |      |   /


and experiment has shown that theobromin is weaker than xanthin, and
caffein still weaker than theobromin.

Loew[39] makes the following generalisations:--

[39] _Ein natürliches System der Gift-Wirkungen_, München, 1893.

1. Entrance of the carboxyl or sulpho groups weakens toxic action.

2. Entrance of a chlorine atom exalts the toxic character of the
catalytic poisons (Loew’s catalytic poisons are alcohols, ether,
chloroform, chloral, carbon tetrachloride, methylal, carbon disulphide
and volatile hydrocarbons).

3. Entrance of hydroxyl groups in the catalytic poisons of the fatty
series weakens toxic character; on the other hand, it exalts the
toxicity of the substituting poisons. (Examples of Loew’s class of
“substituting” poisons are hydroxylamine, phenylhydrazine, hydric
cyanide, hydric sulphide, aldehyde, and the phenols.)

4. A substance increases in poisonous character through every influence
which increases its power of reaction with aldehyde or amido groups. If,
for example, an amido or imido group in the poison molecule be made more
“labile,” or if thrice linked nitrogen is converted into nitrogen
connected by two bands, whether through addition of water or
transposition (_umlagerung_) or if a second amido group enters, the
poisonous quality is increased. Presence of a negative group may modify
the action.

5. Entrance of a nitro group strengthens the poisonous character. If a
carboxyl or a sulpho group is present in the molecule, or if, in passing
through the animal body, negative groups combine with the poison
molecule, or carboxyl groups are formed in the said molecule; in such
cases the poisonous character of the nitro group may not be apparent.

6. Substances with double carbon linkings are more poisonous than the
corresponding saturated substances. Thus neurine with the double linking
of the carbon of CH₂ is more poisonous than choline; vinylamine than









§ 27. M. Ch. Michet[40] has investigated the comparative toxicity of the
metals by experiments on fish, using species of _Serranus_,
_Crenolabrus_, and _Julius_. The chloride of the metal was dissolved in
water and diluted until just that strength was attained in which the
fish would live 48 hours; this, when expressed in grammes per litre, he
called “_the limit of toxicity_.”

[40] “_De la Toxicité comparée des différents Métaux._” _Note de M. Ch.
Michet. Compt. Rend._, t. xciii., 1881, p. 649.

The following is the main result of the inquiry, by which it will be
seen that there was found no relation between “the limit of toxicity”
and the atomic weight.


    No. of                     Limit of
  Experiments.   Metal.        Toxicity.

      20.       Mercury,          ·00029
       7.       Copper,           ·0033
      20.       Zinc,             ·0084
      10.       Iron,             ·014
       7.       Cadmium,          ·017
       6.       Ammonium,         ·064
       7.       Potassium,        ·10
      10.       Nickel,           ·126
       9.       Cobalt,           ·126
      11.       Lithium,          ·3
      20.       Manganese         ·30
       6.       Barium,           ·78
       4.       Magnesium,       1·5
      20.       Strontium,       2·2
       5.       Calcium,         2·4
       6.       Sodium,         24·17

V.--Life-Tests; or the Identification of Poison by Experiments on

§ 28. A philosophical investigation of poisons demands a complete
methodical examination into their action on every life form, from the
lowest to the highest. Our knowledge is more definite with regard to the
action of poisons on man, dogs, cats, rabbits, and frogs than on any
other species. It may be convenient here to make a few general remarks
as to the action of poisons on infusoria, the cephalopoda, and insects.

=Infusoria.=--The infusoria are extremely sensitive to the poisonous
alkaloids and other chemical agents. Strong doses of the alkaloids cause
a contraction of the cell contents, and somewhat rapid disintegration of
the whole body; moderate doses at first quicken the movements, then the
body gets perceptibly larger, and finally, as in the first case, there
is disintegration of the animal substance.

Rossbach[41] gives the following intimations of the proportion of the
toxic principle necessary to cause death:--Strychnine 1 part dissolved
in 1500 of water; veratrine 1 in 8000; quinine 1 in 5000; atropine 1 in
1000; the mineral acids 1 in 400-600; salts 1 in 200-300.

[41] N. J. Rossbach, _Pharm. Zeitschr. für Russland_, xix. 628.

The extraordinary sensitiveness of the infusoria, and the small amount
of material used in such experiments, would be practically useful if
there were any decided difference in the symptoms produced by different
poisons. But no one could be at all certain of even the class to which
the poison belongs were he to watch, without a previous knowledge of
what had been added to the water, the motions of poisoned infusoria.
Hence the fact is more curious than useful.

=Cephalopoda.=--The action of a few poisons on the cephalopoda has been
investigated by M. E. Yung.[42] Curara placed on the skin had no effect,
but on the branchiæ led to general paralysis. If given in even fifteen
times a greater dose than necessary to kill a rabbit, it was not always
fatal. Strychnine, dissolved in sea-water, in the proportion of 1 to
30,000, causes most marked symptoms. The first sign is relaxation of the
chromataphore muscle and the closing of the chromataphores; the animal
pales, the respiratory movements become more powerful, and at the end of
a notable augmentation in their number, they fall rapidly from the
normal number of 25 to 5 a minute. Then tetanus commences after a time,
varying with the dose of the poison; the arm stiffens and extends in
fan-like form, the entire body is convulsed, the respiration is in
jerks, the animal empties his pouch, and at the end of a few minutes is
dead, in a state of great muscular rigidity. If at this moment it is
opened, the venous heart is found still beating. Nicotine and other
poisons were experimented with, and the cephalopoda were found to be
generally sensitive to the active alkaloids, and to exhibit more or less
marked symptoms.

[42] _Compt. Rend._, t. xci. p. 306.

=Insects.=--The author devoted considerable time, in the autumn of 1882,
to observations on the effect of certain alkaloids on the common
blow-fly, thinking it possible that the insect would exhibit a
sufficient series of symptoms of physiological phenomena to enable it to
be used by the toxicologist as a living reagent. If so, the cheapness
and ubiquity of the tiny life during a considerable portion of the year
would recommend it for the purpose. Provided two blow-flies are caught
and placed beneath glass shades--the one poisoned, the other not--it is
surprising what a variety of symptoms can, with a little practice, be
distinguished. Nevertheless, the absence of pupils, and the want of
respiratory and cardiac movements, are, in an experimental point of
view, defects for which no amount or variety of merely muscular symptoms
can compensate.

From the nature of the case, we can only distinguish in the poisoned fly
dulness or vivacity of movement, loss of power in walking on smooth
surfaces, irritation of the integument, disorderly movements of the
limbs, protrusion of the fleshy proboscis, and paralysis, whether of
legs or wings. My experiments were chiefly made by smearing the extracts
or neutral solutions of poisons on the head of the fly. In this way some
of it is invariably taken into the system, partly by direct absorption,
and partly by the insect’s efforts to free itself from the foreign
substance, in which it uses its legs and proboscis. For the symptoms
witnessed after the application of saponin, digitalin, and aconitine,
the reader is referred to the articles on those substances.

In poisoning by sausages, bad meat, curarine, and in obscure cases
generally, in the present state of science, experiments on living
animals are absolutely necessary. In this, and in this way only, in very
many instances, can the expert prove the presence of zymotic, or show
the absence of chemical poison.

The Vivisection Act, however, effectually precludes the use of
life-tests in England save in licensed institutions. Hence the “methods”
of applying life-tests described in former editions will be omitted.

    § 29. =Effect of poisons on the heart of Cold-blooded Animals.=--The
    Vivisection Act does not, however, interfere with the use of certain
    living tests, such, for instance, as the testing of the action of
    poisons upon the recently extirpated hearts of cold-blooded animals.

[Illustration: Williams’ Apparatus.]

    The heart of the frog, of the turtle, of the tortoise, and of the
    shark will beat regularly for a long time after removal from the
    body, if supplied with a regular stream of nutrient fluid. The
    fluids used for this purpose are the blood of the herbivora diluted
    with common salt solution, or a serum albumin solution, or a 2 per
    cent. solution of gum arabic in which red blood corpuscles are
    suspended. The simplest apparatus to use is that known as
    “Williams’.” Williams’ apparatus consists of two glass bulbs (see
    diagram), the one, P, containing nutrient fluid to which a known
    quantity of the poison has been added; the other, N, containing the
    same fluid but to which no poison has been added; these bulbs are
    connected by caoutchouc tubing to a three-way tube, T, and each
    piece of caoutchouc tubing has a pressure screw clip, V¹ and V; the
    three-way tube is connected with a wider tube containing a valve
    float, F, which gives free passage of fluid in one direction only,
    that is, in the direction of the arrow; this last wide tube is
    connected with a Y piece of tubing, which again is connected with
    the aorta of the heart under examination, the other leg of the Y
    tube is connected with another wide tube, X, having a float valve,
    F²: the float containing a drop of mercury and permitting (like the
    float valve F) passage in one direction only of fluid, it is obvious
    that if the clip communicating with N is opened and the clip
    communicating with P is closed, the normal fluid will circulate
    alone through the heart; if, on the other hand, the P clip is open
    and the N clip closed, the poisoned blood will alone feed the heart.
    It is also clear that by raising or depressing the bulbs, the
    circulating fluid can be delivered at any pressure, high or low.
    Should a bubble of air get into the tubes, it can be got rid of by
    removing the cork at S and bringing the fluid up to the level of the
    top of the aperture. The observation is made by first ascertaining
    the number and character of the beats when the normal fluid is
    circulating, and then afterwards when the normal is replaced by the
    poisoned fluid. A simpler but less accurate process is to pith two
    frogs, excise their respective hearts, and place the hearts in
    watch-glasses containing either serum or a solution of common salt
    (strength 0·75 per cent.); to the one heart is now added a solution
    of the poison under examination, and the difference in the behaviour
    and character of the beats noted.

    The phenomena to be specially looked for are the following:--

  1. The heart at the height of the poisoning is arrested in diastole.
  2. The heart at the height of the poisoning is arrested in systole.

    =Arrest in diastole.=--The arrest may be preceded by the
    contractions becoming weaker and weaker, or after the so-called
    heart peristalsis; or it may be preceded by a condition in which the
    auricle shows a different frequency to the ventricle.

    The final diastole may be the diastole of paralysis or the diastole
    of irritation.

    The diastole of irritation is produced by a stimulus of the
    inhibitory ganglia, and only occurs after poisoning by the muscarine
    group of poisons. This condition may be recognised by the fact that
    contraction may be excited by mechanical and electrical stimuli or
    by the application of atropine solution; the latter paralyses the
    inhibitory nervous centres, and therefore sets the mechanism going
    again. The diastole of paralysis is the most frequent form of death.
    It may readily be distinguished from the muscarine diastole; for, in
    muscarine diastole, the heart is full of blood and larger than
    normal; but in the paralytic form the heart is not fully extended,
    besides which, although, if normal blood replace that which is
    poisoned, the beats may be restored for a short time, the response
    is incomplete, and the end is the same; besides which, atropine does
    not restore the beats. The diastole of paralysis may depend on
    paralysis of the so-called excito-motor ganglia (as with iodal), or
    from paralysis of the muscular structure (as with copper).

    § 30. =The effect of poisons on the iris.=--Several poisons affect
    the pupil, causing either contraction or dilatation. The most
    suitable animal is the cat; the pupil of the cat readily showing
    either state.

    =Toxic myosis, or toxic contraction of the pupil.=--There are two
    forms of toxic myosis, one of which is central in its origin. In
    this form, should the poison be applied to the eye itself, no marked
    contraction follows; the poison must be swallowed or injected
    subcutaneously to produce an effect. The contraction remains until

    The contraction in such a case is considered to be due to a
    paralysis of the dilatation centre; it is a “_myosis paralytica
    centralis_;” the best example of this is the contraction of the
    pupil caused by morphine.

    In the second case the poison, whether applied direct to the eye or
    entering the circulation by subcutaneous injection, contracts the
    pupil; the contraction persists if the eye is extirpated, but in all
    cases the contraction may be changed into dilatation by the use of
    atropine. An example of this kind of myosis is the action of
    muscarine. It is dependent on the stimulation of the ends of the
    nerves which contract the pupil, especially the ends of the _nervus
    oculomotorius_ supplying the sphincter iridis; this form of myosis
    is called _myosis spastica periphera_. A variety of this form is the
    _myosis spastica muscularis_, depending on stimulation of the musc.
    sphincter iridis, seen in poisoning by physostigmine. This causes
    strong contraction of the pupil when locally applied; the
    contraction is not influenced by small local applications of
    atropine, but it may be changed to dilatation by high doses.
    Subcutaneous injection of small doses of physostigmine does not
    alter the pupil, but large poisonous doses contracts the pupil in a
    marked manner.

    =Toxic mydriasis, or toxic dilatation of the pupil.=--The following
    varieties are to be noticed:--

    1. Toxic doses taken by the mouth or given by subcutaneous injection
    give rise to strong dilatation; this vanishes before death, giving
    place to moderate contraction. This form is due to stimulation of
    the dilatation centre, later passing into paralysis. An example is
    found in the action of aconite.

    2. After subcutaneous or local application, a dilatation neutralised
    by physostigmine in moderate doses. This is characteristic of

    3. After subcutaneous injection, or if applied locally in very small
    doses, dilatation occurs persisting to death. Large doses of
    physostigmine neutralise the dilatation, but it is not influenced by
    muscarine or pilocarpine: this form is characteristic of atropine,
    and it has been called _mydriasis paralytica periphera_.

    The heart at the height of the poisoning stops in systole.

    =2. Arrest in systole.=--The systole preceding the arrest is far
    stronger than normal, the ventricle often contracting up into a
    little lump. Contraction of this kind is specially to be seen in
    poisoning by digitalis. In poisoning by digitalis the ventricle is
    arrested before the auricle; in muscarine poisoning the auricle
    stops before the ventricle. If the reservoir of Williams’ apparatus
    is raised so as to increase the pressure within the ventricle the
    beat may be restored for a time, to again cease.

    A frog’s heart under the influence of any poison may be finally
    divided into pieces so as to ascertain if any parts still contract;
    the significance of this is, that the particular ganglion supplying
    that portion of the heart has not been affected: the chief ganglia
    to be looked for are Remak’s, on the boundary of the sinus and
    auricle; Ludwig’s, on the auricle and the septum of the auricle;
    Bidder’s, on the atrioventricular border, especially in the valves;
    and Dogiel’s ganglion, between the muscular fibres. According to
    Dogiel, poisons acting like muscarine affect every portion of the
    heart, and atropine restores the contractile power of every portion.

VI.--General Method of Procedure in Searching for Poison.

§ 31. Mineral substances, or liquids containing only inorganic matters,
can cause no possible difficulty to any one who is practised in
analytical investigation; but the substances which exercise the skill of
the expert are organic fluids or solids.

The first thing to be done is to note accurately the manner in which the
samples have been packed, whether the seals have been tampered with,
whether the vessels or wrappers themselves are likely to have
contaminated the articles sent; and then to make a very careful
observation of the appearance, smell, colour, and reaction of the
matters, not forgetting to take the weight, if solid--the volume, if
liquid. All these are obvious precautions, requiring no particular

If the object of research is the stomach and its contents, the contents
should be carefully transferred to a tall conical glass; the organ cut
open, spread out on a sheet of glass, and examined minutely by a lens,
picking out any suspicious-looking substance for closer observation.
The mucous membrane should now be well cleansed by the aid of a
wash-bottle, and if there is any necessity for destroying the stomach,
it may be essential in important cases to have it photographed. The
washings having been added to the contents of the stomach, the sediment
is separated and submitted to inspection, for it must be remembered
that, irrespective of the discovery of poison, a knowledge of the nature
of the food last eaten by the deceased may be of extreme value.

If the death has really taken place from disease, and not from poison,
or if it has been caused by poison, and yet no definite hint of the
particular poison can be obtained either by the symptoms or by the
attendant circumstances, the analyst has the difficult task of
endeavouring to initiate a process of analysis which will be likely to
discover any poison in the animal, vegetable, or mineral kingdom. For
this purpose I have devised the following process, which differs from
those that have hitherto been published mainly in the prominence given
to operations in a high vacuum, and the utilisation of biological
experiment as a matter of routine. Taking one of the most difficult
cases that can occur--viz., one in which a small quantity only of an
organic solid or fluid is available--the best method of procedure is the


A small portion is reserved and examined microscopically, and, if
thought desirable, submitted to various “cultivation” experiments. The
greater portion is at once examined for volatile matters, and having
been placed in a strong flask, and, if neutral or alkaline, feebly
acidulated with tartaric acid, connected with a second or receiving
flask by glass tubing and caoutchouc corks. The caoutchouc cork of the
receiving flask has a double perforation, so as to be able, by a second
bit of angle tubing, to be connected with the mercury-pump described in
the author’s work on “Foods,” the figure of which is here repeated (see
the accompanying figure). With a good water-pump having a sufficient
length of fall-tube, a vacuum may be also obtained that for practical
purposes is as efficient as one caused by mercury; if the fall-tube
delivers outside the laboratory over a drain, no offensive odour is
experienced when dealing with putrid, stinking liquids. A vacuum having
been obtained, and the receiving-flask surrounded with ice, a distillate
for preliminary testing may be generally got without the action of any
external heat; but if this is too slow, the flask containing the
substances or liquid under examination may be gently heated by a
water-bath--water, volatile oils, a variety of volatile substances, such
as prussic acid, hydrochloric acid, phosphorus, &c., if present, will
distil over. It will be well to free in this way the substance, as much
as possible, from volatile matters and water. When no more will come
over, the distillate may be carefully examined by redistillation and the
various appropriate tests.

[Illustration: This figure is from “Foods.” B is a bell-jar, which can
be adapted by a cork to a condenser; R is made of iron; the rim of the
bell-jar is immersed in mercury, which the deep groove receives.]

The next step is to dry the sample thoroughly. This is best effected
also in a vacuum by the use of the same apparatus, only this time the
receiving-flask is to be half filled with strong sulphuric acid. By now
applying very gentle heat to the first flask, and cooling the sulphuric
acid receiver, even such substances as the liver in twenty-four hours
may be obtained dry enough to powder.

Having by these means obtained a nearly dry friable mass, it is reduced
to a coarse powder, and extracted with petroleum ether; the extraction
may be effected either in a special apparatus (as, for example, in a
large “Soxhlet”), or in a beaker placed in the “Ether recovery
apparatus” (see fig.), which is adapted to an upright condenser. The
petroleum extract is evaporated and leaves the fatty matter, possibly
contaminated by traces of any alkaloid which the substance may have
contained; for, although most alkaloids are insoluble in petroleum
ether, yet they are taken up in small quantities by oils and fats, and
are extracted with the fat by petroleum ether. It is hence necessary
always to examine the petroleum extract by shaking it up with water,
slightly acidulated with sulphuric acid, which will extract from the fat
any trace of alkaloid, and will permit the discovery of such alkaloids
by the ordinary “group reagents.”

The substance now being freed for the most part from water and from fat,
is digested in the cold with absolute alcohol for some hours; the
alcohol is filtered off, and allowed to evaporate spontaneously, or, if
speed is an object, it may be distilled _in vacuo_. The treatment is
next with hot alcohol of 90 per cent., and, after filtering, the dry
residue is exhausted with ether. The ether and alcohol, having been
driven off, leave extracts which may be dissolved in water and tested,
both chemically and biologically, for alkaloids, glucosides, and organic
acids. It must also be remembered that there are a few metallic
compounds (as, for example, corrosive sublimate) which are soluble in
alcohol and ethereal solvents, and must not be overlooked.

The residue, after being thus acted upon successively by petroleum, by
alcohol, and by ether, is both water-free and fat-free, and also devoid
of all organic poisonous bases and principles, and it only remains to
treat it for metals. For this purpose, it is placed in a retort, and
distilled once or twice to dryness with a known quantity of strong, pure
hydrochloric acid.

If arsenic, in the form of arsenious acid, were present, it would distil
over as a trichloride, and be detected in the distillate; by raising the
heat, the organic matter is carbonised, and most of it destroyed. The
distillate is saturated with hydric sulphide, and any precipitate
separated and examined. The residue in the retort will contain the fixed
metals, such as zinc, copper, lead, &c. It is treated with dilute
hydrochloric acid, filtered, the filtrate saturated with SH₂ and any
precipitate collected. The filtrate is now treated with sufficient sodic
acetate to replace the hydric chloride, again saturated with SH₂ and any
precipitate collected and tested for _zinc_, _nickel_, and _cobalt_. By
this treatment, viz.:--

  1. Distillation in a vacuum at a low temperature,
  2. Collecting the volatile products,
  3. Dehydrating the organic substances,
  4. Dissolving out from the dry mass fatty matters and alkaloids,
     glucosides, &c., by ethereal and alcoholic solvents,
  5. Destroying organic matter and searching for metals,

--a very fair and complete analysis may be made from a small amount of
material. The process is, however, somewhat faulty in reference to
phosphorus, and also to oxalic acid and the oxalates; these poisons, if
suspected, should be specially searched for in the manner to be more
particularly described in the sections treating of them. In most cases,
there is sufficient material to allow of division into three parts--one
for organic poisons generally, one for inorganic, and a third for
reserve in case of accident. When such is the case, although, for
organic principles, the process of vacuum distillation just described
still holds good, it will be very much the most convenient way not to
use that portion for metals, but to operate on the portion reserved for
the inorganic poisons as follows by destruction of the organic matter.

The destruction of organic matter through simple distillation by means
of pure hydrochloric acid is at least equal to that by sulphuric acid,
chlorate of potash, and the carbonisation methods. The object of the
chemist not being to dissolve every fragment of cellular tissue, muscle,
and tendon, but simply all mineral ingredients, the less organic matter
which goes into solution the better. That hydrochloric acid would fail
to dissolve sulphate of baryta and sulphate of lead, and that sulphide
of arsenic is also almost insoluble in the acid, is no objection to the
process recommended, for it is always open to the analyst to treat the
residue specially for these substances. The sulphides precipitated by
hydric sulphide from an acid solution are--arsenic, antimony, tin,
cadmium, lead, bismuth, mercury, copper, and silver. Those not
precipitated are--iron, manganese, zinc, nickel, and cobalt.

As a rule, one poison alone is present; so that if there should be a
sulphide, it will belong only exceptionally to more than one metal.

The colour of the precipitate from hydric sulphide is either yellowish
or black. The yellow and orange precipitates are sulphur, sulphides of
arsenic, antimony, tin, and cadmium. In pure solutions they may be
almost distinguished by their different hues, but in solutions
contaminated by a little organic matter the colours may not be
distinctive. The sulphide of arsenic is of a pale yellow colour; and if
the very improbable circumstance should happen that arsenic, antimony,
and cadmium occur in the same solution, the sulphide of arsenic may be
first separated by ammonia, and the sulphide of antimony by sulphide of
sodium, leaving cadmic sulphide insoluble in both processes.

The black precipitates are--lead, bismuth, mercury, copper, and silver.
The black sulphide is freed from arsenic, if present, by ammonia, and
digested with dilute nitric acid, which will dissolve all the sulphides,
save those of mercury and tin, so that if a complete solution is
obtained (sulphur flocks excepted), it is evident that both these
substances are absent. The presence of copper is betrayed by the blue
colour of the nitric acid solution, and through its special reactions;
lead, by the deep yellow precipitate which falls by the addition of
chromate of potash and acetate of soda to the solution; bismuth, through
a white precipitate on dilution with water. If the nitric acid leaves a
black insoluble residue, this is probably sulphide of mercury, and
should be treated with concentrated hydrochloric acid to separate flocks
of sulphur, evaporated to dryness, again dissolved, and tested for
mercury by iodide of potassium, copper foil, &c., as described in the
article on _Mercury_. Zinc, nickel, and cobalt are likewise tested for
in the filtrate as described in the respective articles on these metals.


    § 32. A general method of procedure has been published by W.

[43] _Kurze Anleitung zur Auffindung der Gifte_, Freiburg, 1892.

    He divides poisonous substances, for the purposes of separation and
    detection, into three classes:--

    I. Poisons capable of distillation from an acid aqueous solution.
   II. Organic substances which are not capable of distillation from
       acid solutions.
  III. Metallic poisons.

    Where possible, the fluid or solids submitted to the research are
    divided into four equal parts, one of the parts to be kept in
    reserve in case of accident or as a control; one of the remaining
    three parts to be distilled; a second to be investigated for organic
    substances; and a third for metals. After the extraction of organic
    substances from part No. II. the residue may be added to No. III.
    for the purpose of search after metals; and, if the total quantity
    is small, the whole of the process may be conducted without


    The substances are placed in a capacious flask, diluted if necessary
    with water to the consistence of a thin soup, and tartaric acid
    added to distinct acid reaction, and distilled.

    In this way phosphorus, prussic acid, carbolic acid, chloroform,
    chloral hydrate, nitrobenzol, aniline,[44] and alcohol may be
    separated and identified by the reactions given in the sections of
    this work describing those substances.

[44] Aniline is a weak base, so that, although a solution be acid, some
of the aniline distils over on heating.


    Part No. II. is mixed with double its volume of absolute alcohol,
    tartaric acid added to distinct acid reaction and placed in a flask
    connected with an inverted Liebig’s condenser; it is then warmed for
    15 to 20 minutes on the water-bath. After cooling, the mixture is
    filtered, the residue well washed with alcohol and evaporated to a
    thin syrup in a porcelain dish over the water-bath. The dish is then
    allowed to cool and digested with 100 c.c. of water; fat and
    resinous matters separate, the watery solution is filtered through
    Swedish paper previously moistened: if the fluid filtrate is clear
    it may be at once shaken up with ether, but if not clear, and
    especially if it is more or less slimy, it is evaporated again on
    the water-bath to the consistence of an extract: the extract treated
    with 60 to 80 c.c. of absolute alcohol (which precipitates mucus and
    dextrin-like substances), the alcohol evaporated off and the residue
    taken up with from 60 to 80 c.c. of distilled water; it is then
    shaken up with ether, as in Dragendorff’s process, and such
    substances as digitalin, picric acid, salicylic acid, antipyrin and
    others separated in this way and identified.

    After this treatment with ether, and the separation of the ether
    extract, the watery solution is strongly alkalised with caustic soda
    and shaken up again with ether, which dissolves almost every
    alkaloid save morphine and apomorphine; the ethereal extract is
    separated and any alkaloid left identified by suitable tests.

    The aqueous solution, now deprived of substances soluble in ether
    both from acid and from solutions made alkaline by soda, is now
    investigated for morphine and apomorphine; the apomorphine being
    separated by first acidifying a portion of the alkaline solution
    with hydrochloric acid, then alkalising with ammonia and shaking out
    with ether. The morphine is separated from the same solution by
    shaking out with warm chloroform.[45]

[45] Hot amyl alcohol would be better (see “Morphine”).


    The substances are placed in a porcelain dish and diluted with a
    sufficient quantity of water to form a thin soup and 20 to 30 c.c.
    of pure hydrochloric acid added; the dish is placed on the
    water-bath and 2 grms. of potassic chlorate added. The contents are
    stirred from time to time, and successive quantities of potassic
    chlorate are again added, until the contents are coloured yellow.
    The heating is continued, with, if necessary, the addition of more
    acid, until all smell of chlorine has ceased. If there is
    considerable excess of acid, this is to be evaporated away by
    diluting with a little water and continuing to heat on the
    water-bath. The dish with its contents is cooled, a little water
    added, and the fluid is then filtered.

    The metals remaining on the filter are:--

  Silver chloride,
  Lead sulphate,
  Barium sulphate;

    in the filtrate will be all the other metals.

    The filtrate is put in a flask and heated to from 60 to 80 degrees
    and submitted to a slow stream of hydric sulphide gas; when the
    fluid is saturated with the gas, the flask is securely corked and
    allowed to rest for twelve hours; at the end of that time the fluid
    is filtered and the filter washed with water saturated with hydric

    The still moist sulphides remaining on the filter are treated with
    yellow ammonium sulphide containing some free ammonia and washed
    with sulphide of ammonium water. Now remaining on the filter, if
    present at all, will be:--

  Mercury sulphide,
  Lead sulphide,
  Copper sulphide,
  Cadmium sulphide;

    in the filtrate may be:--

  Arsenic sulphide,
  Antimony sulphide,
  Tin sulphide,

    and there may also be a small portion of copper sulphide, because
    the latter is somewhat soluble in a considerable quantity of
    ammonium sulphide.

    The filtrate from the original hydric sulphide precipitate will
    contain, if present, the sulphides of zinc and chromium in solution.


    The ammonium sulphide solution is evaporated to dryness in a
    porcelain dish, strong nitric acid added and again dried. To this
    residue a little strong caustic soda solution is added, and then it
    is intimately mixed with three times its weight of a mixture
    composed of 2 of potassic nitrate to 1 of dry sodium hydrate. This
    is now cast, bit by bit, into a red-hot porcelain crucible. The
    whole is heated until it has melted into a colourless fluid.

    Presuming the original mass contained arsenic, antimony, and tin,
    the melt contains sodic arseniate, sodic pyro-antimonate, sodic
    stannate, and tin oxide; it may also contain a trace of copper

    The melt is cooled, dissolved in a little water, and sodium
    bicarbonate added so as to change any caustic soda remaining into
    carbonate, and to decompose the small amount of sodic stannate; the
    liquid is then filtered.

    The filtrate will contain the arsenic as sodic arseniate; while on
    the filter there will be pyro-antimonate of soda, tin oxide, and,
    possibly, a little copper oxide.

    The recognition of these substances now is not difficult (see the
    separate articles on _Antimony_, _Tin_, _Zinc_, _Arsenic_,


    If the precipitate is contaminated with organic matter, it is
    treated with hydrochloric acid and potassic chlorate in the manner
    already described, p. 51.

    Afterwards it is once more saturated with hydric sulphide, the
    precipitate is collected on a filter, well washed, and the sulphides
    treated with moderately concentrated nitric acid (1 vol. nitric
    acid, 2 vols. water). The sulphides are best treated with this
    solvent on the filter; all the sulphides mentioned, save mercury
    sulphide, dissolve and pass into the filtrate. This mercury sulphide
    may be dissolved by nitro-muriatic acid, the solution evaporated to
    dryness, the residue dissolved in water acidified with hydrochloric
    acid and tested for mercury (see “Mercury”).

    The filtrate containing, it may be, nitrates of lead, copper and
    cadmium is evaporated nearly to dryness and taken up in a very
    little water. The lead is separated as sulphate by the addition of
    dilute sulphuric acid.

    The filtered solution, freed from lead, is treated with ammonia to
    alkaline reaction; if copper be present, a blue colour is produced,
    and this may be confirmed by other tests (see “Copper”). To detect
    cadmium in the presence of copper, potassic cyanide is added to the
    blue liquid until complete decolorisation, and the liquid treated
    with SH₂; if cadmium be present, it is thrown down as a yellow
    sulphide, while potassic cupro-cyanide remains in solution.


    The filtrate from the hydric sulphide precipitate is divided into
    two parts; the one half is used in the search for zinc, the other
    half is used for chromium.

    =Search for Zinc.=--The liquid is alkalised with ammonia and then
    ammonium sulphide is added. There will always be a precipitate of a
    dark colour; the precipitate will contain earthy phosphates, iron
    and, in some cases, manganese. The liquid with the precipitate is
    treated with acetic acid to strong acid reaction and allowed to
    stand for several hours. The portion of the precipitate remaining
    undissolved is collected on a filter, washed, dried and heated to
    redness in a porcelain crucible. The residue thus heated is cooled
    and dissolved in a little dilute sulphuric acid. To the acid
    solution ammonia is added, and any precipitate formed is treated
    with acetic acid; should the precipitate not completely dissolve,
    phosphate of iron is present; this is filtered off, and if SH₂ be
    added to the filtrate, white zinc sulphide will come down (see

    =Search for Chromium.=--The second part of the SH₂ filtrate is
    evaporated to a thin extract, mixed with double its weight of sodic
    nitrate, dried and cast, little by little, into a red-hot porcelain
    crucible. When the whole is fully melted, the crucible is removed
    from the flame, cooled, and the mass dissolved in water and
    filtered. Any chromium present will now be in solution in the easily
    recognised form of potassic chromate (see “Chromium”).


    The residue is dried and intimately mixed with three times its
    weight of a mixture containing 2 parts of sodic nitrate and 1 part
    of sodium hydrate, This is added, little by little, into a red-hot
    porcelain crucible. The melted mass is cooled, dissolved in a little
    water, a current of CO₂ passed through the solution to convert any
    caustic soda into carbonate, and the solution boiled. The result
    will be an insoluble portion consisting of carbonates of lead and
    baryta, and of metallic silver. The mixture is filtered; the
    insoluble residue on the filter is warmed for some time with dilute
    nitric acid; the solution of nitrates of silver, lead and barium are
    concentrated on the water-bath nearly to dryness so as to get rid of
    any excess of acid, and the nitrates dissolved in water; then the
    silver is precipitated by hydrochloric acid, the lead by SH₂, and
    the barium by sulphuric acid.

VII.--The Spectroscope as an aid to the Identification of certain

§ 33. The spectra of many of the metals, of phosphine, of arsine and of
several other inorganic substances are characteristic and easily

It is, however, from the employment of the _micro-spectroscope_ that the
toxicologist is likely to get most assistance.


Oscar Brasch[46] has within the last few years studied spectroscopy in
relation to the alkaloids and organic poisons. Some of these, when mixed
with Froehde’s reagent, or with sulphuric acid, or with sulphuric acid
and potassic dichromate, or with nitric acid, give characteristic
colours, and the resulting solutions, when examined by a spectroscope,
for the most part show absorption bands; these bands may, occasionally,
assist materially in the identification of a poison. By far the best
apparatus is a micro-spectroscope of the Sorby and Browning type, to
which is added an apparatus for measuring the position on a scale of the
lines and bands. Seibert and Kraft of Wetzlar make an excellent
instrument, in which a small bright triangle is projected on the
spectrum; this can be moved by a screw, so that the apex may be brought
exactly in the centre of any line or band, and its position read on an
outside scale. The first thing to be done with such an instrument is to
determine the position on the scale of the chief Fraunhofer lines or of
the more characteristic lines of the alkalies and alkaline earths,[47]
the wave lengths of which are accurately known. If, now, the scale
divisions are set out as abscissæ, and the wave lengths in millionths of
a millimetre are made the ordinates of a diagram, and an equable curve
plotted out, as fully explained in the author’s work on “Foods,” it is
easy to convert the numbers on the scale into wave lengths, and so make
the readings applicable to any spectroscope. For the purpose of
graphical illustration the curve method is convenient, and is adopted in
the preceding diagrams, all taken from Oscar Brasch’s monograph. Where
the curve is highest there the absorption band is thickest; where the
curve is lowest there the band is weak. The fluid to be examined is
simply placed in a watch-glass, the watch-glass resting on the
microscope stand.

[46] _Ueber Verwendbarkeit der Spectroscopie zur Unterscheidung der
Farbenreactionen der Gifte im Interesse der forensischen Chemie_,
Dorpat, 1890.

[47] The alkalies and earths used for this purpose, with their wave
lengths, are as follows: KCl, a line in the red λ 770, in the violet λ
404. Lithium chloride, red line, 670·5; sodium chloride, yellow, 589;
strontium chloride, line in the blue, 461. It is also useful to measure
the green line of thallium chloride = 535.



   1. Strychnine, treated with sulphuric acid and potassic dichromate
   2. Brucine, treated with potassic nitrate and sulphuric acid (clear
   3. Quebrachine, treated with vanadium sulphate (dark blue).
   4. Quinine, Vogel’s reaction (red).
   5. Caffein, Murexid reaction (violet-red).
   6. Dephinoidin, Froehde’s reagent (cherry-red).
   7. Veratrine, treated with sulphuric acid (straw-yellow).
   8.     „        „             „           (cherry-red).
   9.     „        „             „           (carmine-red).
  10. Veratrine, Furfurol reaction (blue-violet).
  11. Sabadillin, treated with sulphuric acid (red).
  12. Veratroidine,     „          „          (brown-red).
  13. Jervine, Furfurol reaction (blue).
  14. Sabadine,   „        „     (blue).
  15. Sabadine, treated with sulphuric acid (cherry-red).
  16. Physostigmine,   „         „          (grass-green).
  17. Morphine, treated with Froehde’s reagent and sugar (dark-green).
  18. Narcotine, treated with a mixture of sulphuric acid and nitric
      acid (30 drops of sulphuric to 1 drop of nitric), (red).
  19. Codeine, treated with Froehde’s reagent and sugar (dark violet).
  20. Papaverine, treated with Froehde’s reagent (green-blue).
  21. Sanguinarin,      „         „              (violet-red).
  22. Chelidonin,       „      sulphate of vanadium (dark green).
  23. Solanin,          „      sulphuric acid and allowed to stand 4
                               hours (brown-red).
  24. Digitalin,        „      Erdmann’s reagent (red).
  25. Aniline,          „      sulphuric acid and potassic dichromate

The wave lengths corresponding to the numbers on the scale in the
diagram are as follows:--

  0        732
  1        656
  2        589·2
  3        549·8
  4        510·2
  5        480·0
  6        458
  7        438

Examination of Blood, or of Blood-Stains.

§ 34. Spots, supposed to be blood--whether on linen, walls, or
weapons--should, in any important case, be photographed before any
chemical or microscopical examination is undertaken. Blood-spots,
according to the nature of the material to which they are adherent, have
certain naked eye peculiarities--_e.g._, blood on fabrics, if dry, has
at first a clear carmine-red colour, and part of it soaks into the
tissue. If, however, the tissue has been worn some time, or was
originally soiled, either from perspiration, grease, or filth, the
colour may not be obvious or very distinguishable from other stains;
nevertheless, the stains always impart a certain stiffness, as from
starch, to the tissue. If the blood has fallen on such substances as
wood or metal, the spot is black, has a bright glistening surface, and,
if observed by a lens, exhibits radiating fissures and a sort of
pattern, which, according to some, is peculiar to each species; so that
a skilled observer might identify occasionally, from the pattern alone,
the animal whence the blood was derived. The blood is dry and brittle,
and can often be detached, or a splinter of it, as it were, obtained.
The edges of the splinter, if submitted to transmitted light, are
observed to be red. Blood upon iron is frequently very intimately
adherent; this is specially the case if the stain is upon rusty iron,
for hæmatin forms a compound with iron oxide. Blood may also have to be
recovered from water in which soiled articles have been washed, or from
walls, or from the soil, &c. In such cases the spot is scraped off from
walls, plaster, or masonry, with as little of the foreign matters as may
be. It is also possible to obtain the colouring-matter of blood from its
solution in water, and present it for farther examination in a
concentrated form, by the use of certain precipitating agents (see p.

In the following scheme for the examination of blood-stains, it is
presumed that only a few spots of blood, or, in any case, a small
quantity, is at the analyst’s disposal.

(1) The dried spot is submitted to the action of a cold saturated
solution of borax. This medium (recommended by Dragendorff)[48] does
certainly dissolve out of linen and cloth blood-colouring matter with
great facility. The best way to steep the spots in the solution is to
scrape the spot off the fabric, and to digest it in about a cubic
centimetre of the borax solution, which must not exceed 40°; the
coloured solution may be placed in a little glass cell, with parallel
walls, ·5 centimetre broad, and ·1 deep, and submitted to spectroscopic
examination, either by the ordinary spectroscope or by the
micro-spectroscope; if the latter is used, a very minute quantity can be
examined, even a single drop. In order to interpret the results of this
examination properly, it will be necessary to be intimately acquainted
with the spectroscopic appearances of both ancient and fresh blood.

[48] _Untersuchungen von Blutspuren_ in Maschka’s _Handbuch_, Bd. i.
Halfband 2.

§ 35. =Spectroscopic Appearances of Blood.=--If defibrinated blood[49]
be diluted with water until it contains about ·01 per cent. of
oxyhæmoglobin, and be examined by a spectroscope, the layer of liquid
being 1 centimetre thick, a single absorption band between the wave
lengths 583 and 575 is observed, and, under favourable circumstances,
there is also to be seen a very weak band from 550 to 532. With
solutions so dilute as this, there is no absorption at either the violet
or the red end of the spectrum. A solution containing ·09 per cent. of
oxyhæmoglobin shows very little absorption in the red end, but the
violet end is dark up to about the wave length 428. Two absorption bands
may now be distinctly seen. A solution containing ·37 per cent. of
oxyhæmoglobin shows absorption of the red end to about W.L. 720; the
violet is entirely, the blue partly, absorbed to about 453. The bands
are considerably broader, but the centre of the bands occupies the same
relative position. A solution containing as much as ·8 per cent. of
oxyhæmoglobin is very dark; the two bands have amalgamated, the red end
of the spectrum is absorbed nearly up to Fraunhofer’s line a; the green
is just visible between W.L. 498 and 518. Venous blood, or arterial
blood, which has been treated with reducing agents, such, for example,
as an alkaline sulphide, gives the spectrum of reduced hæmoglobin. If
the solution is equivalent to about ·2 per cent., a single broad band,
with the edges very little defined, is seen to occupy the space between
W.L. 595 and 538, the band being darkest about 550; both ends of the
spectrum are more absorbed than by a solution of oxyhæmoglobin of the
same strength. In the blood of persons or animals poisoned with hydric
sulphide--to the spectrum of reduced hæmoglobin, there is added a weak
absorption band in the red, with its centre nearly corresponding with
the Fraunhofer line C. Blood which has been exposed to carbon oxide has
a distinct spectrum, due, it would seem, to a special combination of
this gas with hæmoglobin; in other words, instead of oxygen, the oxygen
of oxyhæmoglobin has been displaced by carbon oxide, and crystals of
carbon oxide-hæmoglobin, isomorphous with those of oxyhæmoglobin, may be
obtained by suitable treatment. The spectrum of carbon oxide-hæmoglobin,
however, differs so little from that of normal blood, that it is only
comparison with the ordinary spectrum, or careful measurements, which
will enable any person, not very familiar with the different spectra of
blood, to detect it; with careful and painstaking observation the two
spectra are seen to be distinct. The difference between the carbon oxide
and the normal spectrum essentially consists in a slight moving of the
bands nearer to E. According to the measurements of Gamgee, the band α
of CO-hæmoglobin has its centre approximately at W.L. 572, and the band
β has for its centre W.L. from 534 to 538, according to concentration.
If a small quantity of an ammoniacal solution of ferrous tartrate or
citrate be added to blood containing carbon oxide, the bands do not
wholly fade, but persist more or less distinctly; whereas, if the same
solution is added to bright red normal blood, the two bands vanish
instantly and coalesce to form the spectrum of reduced hæmoglobin. When
either a solution of hæmoglobin or blood is exposed to the air for some
time, it loses its bright red colour, becomes brownish-red, and presents
an acid reaction. On examining the spectrum, the two bands have become
faint, or quite extinct; but there is a new band, the centre of which
(according to Gamgee) occupies W.L. 632, but (according to Preyer) 634.
In solutions of a certain strength, four bands may be seen, but in a
strong solution only one. This change in the spectrum is due to the
passing of the hæmoglobin into _methæmoglobin_, which may be considered
as an intermediate stage of decomposition, prior to the breaking up of
the hæmoglobin into hæmatin and proteids.

[49] In this brief notice of the spectroscopic appearances of the blood,
the measurements in wave lengths are, for the most part, after
Gamgee.--_Text-Book of Physiological Chemistry_, London, 1880.

A spectrum very similar to that of methæmoglobin is obtained by treating
ancient blood-stains with acetic acid--viz., the spectrum of _acid
hæmatin_, but the band is nearer to its centre, according to Gamgee,
corresponding to W.L. 640 (according to Preyer, 656·6). The portion of
the band is a little different in alkaline solution, the centre being
about 592. Hæmatin is one of the bodies into which hæmoglobin splits up
by the addition of such agents as strong acetic acid, or by the
decomposing influence of exposure; the view most generally accepted
being that the colouring-matter of the blood is hæmatin in combination
with one or more albuminoid bodies. The hæmatin obtained by treating
blood with acetic acid may be dissolved out by ether, and the ethereal
solution then exhibits a remarkable distinctive spectrum. Hence, in the
spectroscopic examination of blood, or solutions of blood, for
medico-legal purposes, if the blood is fresh, the spectrum likely to be
seen is either that of oxyhæmoglobin or hæmoglobin; but, if the
blood-stain is not recent, then the spectrum of either hæmatin or

The colouring-matter of cochineal, to which alum, potassic carbonate,
and tartrate have been added, gives a spectrum very similar to that of
blood (see “Foods,” p. 82); but this is only the case when the solution
is fresh. The colour is at once discharged by chlorine, while the colour
of blood, although changed in hue, remains. The colouring-matter of
certain red feathers, purpurin-sulphuric acid, and a few other reds,
have some similarity to either the hæmatin or the hæmoglobin spectrum,
but the bands do not strictly coincide; besides, no one would trust to a
single test, and none of the colouring-matters other than blood yield

The blood in CO poisoning has also other characteristics. It is of a
peculiar florid vermilion colour, a colour that is very persistent,
lasting for days and even weeks.

Normal blood mixed with 30 per cent. potash solution forms _greenish_
streaky clots, while blood charged with CO forms red streaky clots.

Normal blood diluted to 50 times its volume of water, and then treated
successively with yellow ammonium sulphide in the proportion of 2 to 25
c.c. of blood, followed by three drops of acetic acid, gives a grey
colour, while CO blood remains bright red. CO blood shaken with 4 times
its volume of lead acetate remains red, but normal blood becomes

[50] M. Rubner, _Arch. Hyg._, x. 397.

Solutions of platinum chloride or zinc chloride give a bright red colour
with CO blood; normal blood is coloured brown or very dark brown.

Phospho-molybdic acid or 5 per cent. phenol gives a carmine-coloured
precipitate with CO blood, but a reddish-brown precipitate with normal
blood (sensitive to 16 per cent.).

A mixture of 2 c.c. of dilute acetic acid and 15 c.c. of 20 per cent.
potassic ferrocyanide solution added to 10 c.c. of CO blood produces an
intense bright red; normal blood becomes dark brown.

Four parts of CO blood, diluted with 4 parts of water and shaken with 3
vols. of 1 per cent. tannin solution, become at first bright red with a
bluish tinge, and remain so persistently. Normal blood, on the other
hand, also strikes bright red at first, but with a yellowish tinge; at
the end of 1 hour it becomes brownish, and finally in 24 hours grey.
This is stated to be delicate enough to detect 0·0023 per cent. in air.

If blood be diluted with 40 times its volume of water, and 5 drops of
phenylhydrazin solution be added, CO blood strikes rose-red; normal
blood grey-violet.[51]

[51] A. Welzel, _Centr. med. Wiss._, xxvii. 732-734.

Gustave Piotrowski[52] has experimented on the length of time blood
retains CO. The blood of dogs poisoned by this agent was kept in flasks,
and then the gas pumped out by means of a mercury pump on the following

[52] _Compt. Rend. Soc. de Biol._, v. 433.

  Date.                Content of gas in CO.
  Jan.  12, 1892,          24·7 per cent.
    „   20,   „            23·5    „
    „   28,   „            22·2    „
  Feb.   8,   „            20·3    „
    „   16,   „            15·5    „
    „   26,   „            10·2    „
  March  3,   „             6·3    „
    „   14,   „             4·6    „
    „   22,   „             1·2    „

The same dog was buried on the 12th of January, and exhumed on March
28th, and the gas pumped out from some of the blood; this gas gave 11·7
per cent. of CO; hence it is clear that burial preserves CO blood from
change to a certain extent.

N. Gréhant[53] treated the poisoned blood of a dog with acetic acid, and
found it evolved 14·4 c.c. CO from 100 c.c. of blood.

[53] _Compt. Rend._, cvi. 289.

Stevenson, in one of the cases detailed at p. 67, found the blood in the
right auricle to contain 0·03 per cent. by weight of CO.

(2) =Preparation of Hæmatin Crystals=--(Teichmann’s crystals).--A
portion of the borax solution is diluted with 5 or 6 parts of water, and
one or more drops of a 5 or 6 per cent. solution of zinc acetate added,
so long as a brownish-coloured precipitate is thrown down. The
precipitate is filtered off by means of a miniature filter, and then
removed on to a watch-glass. The precipitate may now be dissolved in 1
or 2 c.c. of acetic acid, and examined by the spectroscope it will show
the spectrum of hæmatin. A minute crystal of sodic chloride being then
added to the acetic acid solution, it is allowed to evaporate to dryness
at the ordinary temperature, and crystals of hæmatin hydrochlorate
result. There are other methods of obtaining the crystals. When a drop
of fresh blood is simply boiled with glacial acetic acid, on
evaporation, prismatic crystals are obtained.

Hæmatin is insoluble in water, alcohol, chloroform, and in cold dilute
acetic and hydrochloric acids. It may, however, be dissolved in an
alcoholic solution of potassic carbonate, in solutions of the caustic
alkalies, and in boiling acetic and hydrochloric acids. Hoppe-Seyler
ascribes to the crystals the formula C₆₈H₇₀N₈Fe₂O₁₀2HCl. Thudichum
considers that the pure crystals contain no chlorine, and are therefore
those of hæmatin. It is the resistance of the hæmatin to decomposition
and to ordinary solvents that renders it possible to identify a certain
stain to be that of blood, after long periods of time. Dr. Tidy seems to
have been able to obtain blood reactions from a stain which was supposed
to be 100 years old. The crystals are of a dark-red colour, and present
themselves in three forms, of which that of the rhombic prism is the
most common (see fig.). But crystals like _b_, having six sides, also
occur, and also crystals similar to _c_.


If the spot under examination has been scraped off an iron implement the
hæmatin is not so easily extracted, but Dragendorff states that borax
solution at 50° dissolves it, and separates it from the iron. Felletar
has also extracted blood in combination with iron rust, by means of warm
solution of caustic potash, and, after neutralisation with acetic acid,
has precipitated the hæmin by means of tannin, and obtained from the
tannin precipitate, by means of acetic acid, Teichmann’s crystals. A
little of the rust may also be placed in a test tube, powdered ammonium
chloride added, also a little strong ammonia, and after a time filtered;
a small quantity of the filtrate is placed on a slide with a crystal of
sodium chloride and evaporated at a gentle heat, then glacial acetic
acid added and allowed to cool; in this way hæmin crystals have been
obtained from a crowbar fifty days after having been blood-stained.[54]

[54] _Brit. Med. Journ._, Feb. 17, 1894.

(3) =Guaiacum Test.=--This test depends upon the fact that a solution of
hæmoglobin develops a beautiful blue colour, if brought into contact
with fresh tincture of guaiacum and peroxide of hydrogen. The simplest
way to obtain this reaction is to moisten the suspected stain with
distilled water; after allowing sufficient time for the water to
dissolve out some of the blood constituents, moisten a bit of
filter-paper with the weak solution thus obtained; drop on to the moist
space a single drop of tincture of guaiacum which has been prepared by
digesting the inner portions of guaiacum resin in alcohol, and which has
been already tested on known blood, so as to ascertain that it is really
good and efficient for the purpose; and, lastly, a few drops of peroxide
of hydrogen. Dragendorff uses his borax solution, and, after a little
dilution with water, adds the tincture and then Heunefeld’s turpentine
solution, which is composed of equal parts of absolute alcohol,
chloroform, and French turpentine, to which one part of acetic acid has
been added. The chloroform separates, and, if blood was present, is of a
blue colour.

§ 36. To prove by chemical and physical methods that a certain stain is
that of blood, is often only one step in the inquiry, the next question
being whether the blood is that of man or of animals. The
blood-corpuscles of man are larger than those of any domestic animal
inhabiting Europe. The diameter of the average red blood-corpuscle is
about the 1/126 of a millimetre, or 7·9 µ.[55] The corpuscles of man and
of mammals, generally speaking, are round, those of birds and reptiles
oval, so that there can be no confusion between man and birds, fishes or
reptiles; if the corpuscles are circular in shape the blood will be that
of a mammal. By careful measurements, Dr. Richardson, of Pennsylvania,
affirms that it is quite possible to distinguish human blood from that
of all common animals. He maintains, and it is true, that, by using very
high magnifying powers and taking much trouble, an expert can
satisfactorily identify human blood, if he has some half-dozen drops of
blood from different animals--such as the sheep, goat, horse, dog, cat,
&c., all fresh at hand for comparison, and _if the human blood is
normal_. However, when we come to the blood of persons suffering from
disease, there are changes in the diameter and even the form of the
corpuscles which much complicate the matter; while, in blood-stains of
any age, the blood-corpuscles, even with the most artfully-contrived
solvent, are so distorted in shape that he would be a bold man who
should venture on any definite conclusion as to whether the blood was
certainly human, more especially if he had to give evidence in a
criminal case.

[55] 1/3200 of an inch; the Greek letter µ is the micro-millimetre, or
1000th of a millimetre, ·00003937 inch.

Neumann affirms that the pattern which the fibrin or coagulum of the
blood forms is peculiar to each animal, and Dr. Day, of Geelong, has
independently confirmed his researches: this very interesting
observation perhaps has not received the attention it merits.

When there is sufficient of the blood present to obtain a few milligrms.
of ash, there is a means of distinguishing human blood from that of
other common mammals, which has been neglected by authorities on the
subject, and which may be found of real value. Its principle depends
upon the relative amounts of potassium and sodium in the blood of man as
compared with that in the blood of domestic animals. In the blood of the
cow, sheep, fowl, pig, and horse, the sodium very much exceeds the
potassium in the ash; thus the proportion of sodium oxide to that of
potassium oxide in the blood of the sheep is as K₂O ·1 : Na₂O ·6; in
that of the cow, as 1 : 8; in that of the domestic fowl, as 1 : 16;
while the same substances in human blood are sometimes equal, and vary
from 1 : 1 to 1 : 4 as extremes, the mean numbers being as 1 : 2·2. The
potassium is greater in quantity in the blood-corpuscles than in the
blood serum; but, even in blood serum, the same marked differences
between the blood of man and that of many animals is apparent. Thus, the
proportion of potash to soda being as 1 : 10 in human blood, the
proportion in sheep’s blood is 1 to 15·7; in horse’s serum as 1 to 16·4;
and in the ox as 1 to 17. Since blood, when burnt, leaves from 6 to 7
per thousand of ash, it follows that a quantitative analysis of the
relative amounts of potassium and sodium can only be satisfactorily
effected when sufficient of the blood is at the analyst’s disposal to
give a weighable quantity of mineral matter. On the other hand, much
work requires to be done before this method of determining that the
blood is either human, or, at all events, not that of an herbivorous
animal, can be relied on. We know but little as to the effect of the
ingestion of sodium or potassium salts on either man or animals, and it
is possible--nay, probable--that a more or less entire substitution of
the one for the other may, on certain diets, take place. Bunge seems in
some experiments to have found no sodium in the blood of either the cat
or the dog.

The source from which the blood has emanated may, in a few cases, be
conjectured from the discovery, by microscopical examination, of hair or
of buccal, nasal, or vaginal epithelium, &c., mixed with the


I.--Carbon Monoxide.

§ 37. Carbon monoxide, CO, is a colourless, odourless gas of 0·96709 sp.
gravity. A litre weighs 1·25133 grm. It is practically insoluble in
water. It unites with many metals, forming gaseous or volatile
compounds, _e.g._, nickel carbon oxide, Ni(CO)₄, is a fluid volatilising
at 40°. These compounds have, so far as is known, the same effects as

Whenever carbon is burned with an insufficient supply of air, CO in a
certain quantity is produced. It is always present in ordinary domestic
products of combustion, and must be exhaled from the various chimneys of
a large city in considerable volumes. A “smoky” chimney or a defective
flue will therefore introduce carbon monoxide into living-rooms. The
vapour from burning coke or burning charcoal is rich in carbon monoxide.
It is always a constituent of coal gas, in England the carbon monoxide
in coal gas amounting to about 8 per cent. Poisoning by coal gas is
practically poisoning by carbon monoxide. Carbon monoxide is also the
chief constituent in water gas.

Carbon monoxide poisoning occurs far more frequently in France and
Germany than in England; in those countries the vapour evolved from
burning charcoal is a favourite method of suicide, on account of the
supposed painlessness of the death. It has also occasionally been used
as an instrument of murder. In this country carbon monoxide poisoning
mainly takes place accidentally as the effect of breathing coal gas;
possibly it is the secret and undetected cause of ill health where
chimneys “smoke”; and it may have something to do with the sore throats
and debility so often noticed when persons breathe for long periods air
contaminated by small leakages of coal gas.

The large gas-burners (geysers) emit in burning under certain conditions
much carbon monoxide. It has been proved by Gréhant[56] that a bunsen
burner “lit below” also evolves large quantities of the same poisonous

[56] _Compt. Rend. Soc. de Biol._, ix. 779-780.

§ 38. =Symptoms.=--Nearly all the experience with regard to the symptoms
produced by carbon monoxide is derived from breathing not the pure gas,
but the gas diluted by air, by hydrogen or by carburetted hydrogen, as
in coal gas, or mixed with large quantities of carbon dioxide. Two
assistants of Christison breathed the pure gas: the one took from two to
three inhalations; he immediately became giddy, shivered, had headache
and then became unconscious. The second took a bigger dose, for, after
emptying his lungs as much as possible, he took from three to four
inhalations; he fell back paralysed, became unconscious and remained
half-an-hour insensible and had the appearance of death, the pulse being
almost extinguished. He was treated with inhalations of oxygen, but he
remained for the rest of the day extremely ill; he had convulsive
muscular movements, stupor, headache, and quick irregular pulse; on this
passing away he still suffered from nausea, giddiness, alternate feeling
of heat and chilliness, with some fever, and in the night had a restless
kind of sleep. The chemist Chenot was accidentally poisoned by the pure
gas, and is stated to have fell as if struck by lightning after a single
inspiration, and remained for a quarter of an hour unconscious. Other
recorded cases have shown very similar symptoms.

The pulse is at the onset large, full and frequent; it afterwards
becomes small, slow and irregular. The temperature sinks from 1° to 3°
C. The respiration at first slow, later becomes rattling. As vomiting
occurs often when the sufferer is insensible, the vomited matters have
been drawn by inspiration into the trachea and even into the bronchi, so
that death takes place by suffocation.

The fatal coma may last even when the person has been removed from the
gas from hours to days. Coma for three, four and five days from carbon
monoxide has been frequently observed. The longest case on record is
that of a person who was comatose for eight days, and died on the
twelfth day after the fatal inhalation. Consciousness in this case
returned, but the patient again fell into stupor and died.

The slighter kinds of poisoning by carbon monoxide, as in the
Staffordshire case recorded by Dr. Reid, in which for a long time a much
diluted gas has been breathed, produce pronounced headache and a general
feeling of ill health and _malaise_, deepening, it may be, into a fatal
slumber, unless the person is removed from the deadly atmosphere. To the
headache generally succeeds nausea, a feeling of oppression in the
temples, a noise in the ears, feebleness, anxiety and a dazed condition
deepening into coma. It is probably true that charcoal vapour is
comparatively painless, for when larger amounts of the gas are breathed
the insensibility comes on rapidly and the faces of those who have
succumbed as a rule are placid. Vomiting, without being constant, is a
frequent symptom, and in fatal cases the fæces and urine are passed
involuntarily. There are occasional deviations from this picture;
tetanic strychnine-like convulsions have been noticed and a condition of
excitement in the non-fatal cases as if from alcohol; in still rarer
cases temporary mania has been produced.

In non-fatal but moderately severe cases of poisoning sequelæ follow,
which in some respects imitate the sequelæ seen on recovery from the
infectious fevers. A weakness of the understanding, incapacity for
rational and connected thought, and even insanity have been noticed.
There is a special liability to local inflammations, which may pass into
gangrene. Various paralyses have been observed. Eruptions of the skin,
such as herpes, pemphigus and others. Sugar in the urine is an almost
constant concomitant of carbon monoxide poisoning.

§ 39. The poisonous action of carbon monoxide is, without doubt, due to
the fact that it is readily absorbed by the blood, entering into a
definite chemical compound with the hæmoglobin; this combination is more
stable than the similar compound with oxygen gas, and is therefore slow
in elimination.

Hence the blood of an animal remaining in an atmosphere containing
carbon monoxide is continually getting poorer in oxygen, richer in
carbon monoxide. Gréhant has shown that if an animal breathes for one
hour a mixture of 0·5 carbon monoxide to 1000 oxygen, the blood contains
at the end of that time one-third less oxygen than normal, and contains
152 times more carbon monoxide than in the mixture. An atmosphere of 10
per cent. carbon monoxide changes the blood so quickly, that after from
10 to 25 seconds the blood contains 4 per cent. of carbon monoxide, and
after from 75 to 90 seconds 18·4 per cent. Breathing even for half an
hour an atmosphere containing from 0·07 to 0·12 per cent. carbon
monoxide renders a fourth part of the red corpuscles of the blood
incapable of uniting with oxygen.

The blood is, however, never saturated with carbon monoxide, for the
animal dies long before this takes place.

The characteristics of the blood and its spectroscopic appearances are
described at p. 58.

Besides the action on the blood there is an action on the nervous
system. Kobert,[57] in relation to this subject, says:--“That CO has a
direct action on the nervous system is shown in a marked manner when an
atmosphere of oxygen, with at least 20 per cent. carbon oxide, is
breathed; for in the first minute there is acute cramp or total
paralysis of the limbs, when the blood in no way attains the saturation
sufficiently great to account for such symptoms. Geppert has, through a
special research, shown that an animal suffocated by withdrawal of
oxygen, increases the number and depth of the respirations; but when the
animal is submitted to CO, in which case there is quite as much a
withdrawal of oxygen as in the former case, yet the animal is not in a
condition to strengthen its respiratory movements; Geppert hence rightly
concludes that CO must have a primary specific injurious action on the
nerve centres. I (Kobert) am inclined to go a step further, and, on the
ground of unpublished researches, to maintain that CO not only affects
injuriously the ganglion cells of the brain, but also the peripheral
nerves (_e.g._, the phrenic), as well as divers other tissues, as
muscles and glands, and that it causes so rapidly such a high degree of
degeneration as not to be explained through simple slow suffocation;
even gangrene may be caused.”

[57] _Lehrbuch der Intoxicationen_, 526.

It is this rapid degeneration which is the cause of the enormous
increase of the products of the decomposition of albumin, found
experimentally in animals.

§ 40. =Post-mortem Appearances.=--The face, neck, chest, abdomen are
frequently covered with patches of irregular form and of clear rose-red
or bluish-red colour; these patches are not noticed on the back, and
thus do not depend upon the gravitation of the blood to the lower or
most dependent part of the body; similar red patches have been noticed
in poisoning by prussic acid; the cause of this phenomenon is ascribed
to the paralysis of the small arteries of the skin, which, therefore,
become injected with the changed blood. The blood throughout is
generally fluid, and of a fine peculiar red colour, with a bluish tinge.
The face is mostly calm, pale, and there is seldom any foam about the
lips. Putrefaction is mostly remarkably retarded. There is nearly always
a congestion of some of the internal organs; sometimes, and indeed
usually, the membranes of the brain are strongly injected; sometimes the
congestion is mainly in the lungs, which may be œdematous with effusion;
and in a third class of cases the congestion is most marked in the
abdominal cavity.

The right heart is commonly filled with blood, and the left side
contains only a little blood.

Poisoning by a small dose of carbon monoxide may produce but few
striking changes, and then it is only by a careful examination of the
blood that evidence of the real nature of the case will be obtained.

§ 41. =Mass poisonings by Carbon Monoxide.=--An interesting series of
cases of poisoning by water gas occurred at Leeds in 1889, and have been
recorded by Dr. Thos. Stevenson.[58]

[58] _Guy’s Hospital Reports_, 1889.

Water gas is made by placing coke in a vertical cylinder and heating the
coke to a red heat. Through the red-hot coke, air is forced up from
below for ten minutes; then the air is shut off and steam passes from
above downwards for four minutes; the gas passes through a scrubber, and
then through a ferric oxide purifier to remove SH₂. It contains about 50
per cent. of hydrogen and 40 per cent. of carbon monoxide, that is,
about five times more carbon monoxide than coal gas.

On November 20, 1889, two men, R. French and H. Fenwick, both
intemperate men, occupied a cabin at the Leeds Forge Works; the cabin
was 540 c. feet in capacity, and was lighted by two burners, each
burning 5·5 c. feet of water gas per hour; the cabin was warmed by a
cooking stove, also burning water gas, the products of combustion
escaping into the cabin. Both men went into the cabin after breakfast
(8.30 A.M.). French was seen often going to and fro, and Fenwick was
seen outside at 10.30 A.M. At 11.30 the foreman accompanied French to
the cabin, and found Fenwick asleep, as he thought. At 12.30 P.M.
French’s son took the men their dinner, which was afterwards found
uneaten. At that time French also appeared to be asleep; he was shaken
by his son, upon which he nodded to his son to leave. The door of the
cabin appears to have been shut, and all through the morning the lights
kept burning; no smell was experienced. At 2.30 P.M. both the men were
discovered dead. It was subsequently found that the stove was unlighted,
and the water gas supply turned on.

What attracted most attention to this case was the strange incident at
the _post-mortem_ examination. The autopsies were begun two days after
the death, November 22, in a room of 39,000 c. feet capacity. There were
present Mr. T. Scattergood (senior), Mr. Arthur Scattergood (junior),
Mr. Hargreaves, three local surgeons, Messrs. Brown, Loe and Jessop, and
two assistants, Pugh and Spray. Arthur Scattergood first fainted, Mr.
Scattergood, senior, also had some peculiar sensations, viz., tingling
in the head and slight giddiness; then Mr. Pugh became faint and
staggered; and Mr. Loe, Mr. Brown, and Mr. Spray all complained.

These symptoms were not produced, as was at first thought, by some
volatile gas or vapour emanating from the bodies of the poisoned men,
but, as subsequently discovered, admitted of a very simple explanation;
eight burners in the room were turned partly on and not lighted, and
each of the eight burners poured water gas into the room.

In 1891 occurred some cases of poisoning[59] by CO which are probably
unique. The cases in question happened in January in a family at
Darlaston. The first sign of anything unusual having happened to the
family most affected was the fact that up to 9 A.M., Sunday morning,
January 18, none of the family had been seen about. The house was broken
into by the neighbours; and the father, mother, and three children were
found in bed apparently asleep, and all efforts to rouse them utterly
failed. The medical men summoned arrived about 10 A.M. and found the
father and mother in a state of complete unconsciousness, and two of the
children, aged 11 and 14 years, suffering from pain and sickness and
diarrhœa; the third child had by this time been removed to a
neighbouring cottage.

[59] “Notes on cases of poisoning by the inhalation of carbon monoxide,”
by Dr. George Reid, Medical Officer of Health, County of Stafford.
_Public Health_, vol. iii. 364.

Dr. Partridge, who was in attendance, remained with the patients three
hours, when he also began to suffer from headache; while others, who
remained in the house longer, suffered more severely and complained of
an indefinite feeling of exhaustion. These symptoms pointed to some
exciting cause associated with the surroundings of the cottage;
consequently, in the afternoon the two children were removed to another
cottage, and later on the father and mother also. All the patients, with
the exception of the mother, who was still four days afterwards
suffering from the effects of an acute attack, had completely recovered.
The opinion that the illness was owing to some local cause was
subsequently strengthened by the fact that two canaries and a cat had
died in the night in the kitchen of the cottage; the former in a cage
and the latter in a cupboard, the door of which was open. Also in the
same house on the opposite side of the road, the occupants of which had
for some time suffered from headache and depression, two birds were
found dead in their cage in the kitchen. It is important to notice that
all these animals died in the respective kitchens of the cottages, and,
therefore, on the ground floor, while the families occupied the first

The father stated that for a fortnight or three weeks previous to the
serious illness, he and the whole family had complained of severe
frontal headache and a feeling of general depression. This feeling was
continuous day and night in the case of the rest of the family, but in
his case, during the day, after leaving the house for his work, it
gradually passed off, to return again during the night. The headaches
were so intense that the whole family regularly applied vinegar rags to
their heads, on going to bed each night during this period, for about
three weeks. About two o’clock on Sunday morning the headaches became so
severe that the mother got out of bed and renewed the application of
vinegar and water all round, after which they all fell asleep, and, so
far as the father and mother were concerned, remained completely
unconscious until Monday morning.

A man who occupied the house opposite the house tenanted by the
last-mentioned family informed the narrator (Dr. Reid) that on Sunday
morning the family, consisting of four, were taken seriously ill with a
feeling of sickness and depression accompanied by headache; and he also
stated that for some time they had smelt what he termed a “fire stink”
issuing from the cellar.

The cottage in which the family lived that had suffered so severely was
situated about 20 or 30 yards from the shaft of a disused coal mine, and
was the end house of a row of cottages. It had a cellar opening into the
outer air, but this opening was usually covered over by means of a piece
of wood. The adjoining house to this, the occupants of which had for
some time suffered from headache, although to a less extent, had a
cellar with a similar opening, but supplied with an ill-fitting cover.
The house on the opposite side of the road, in which the two birds were
found dead, had a cellar opening both at the front and the back; but
both these openings, until a little before the occurrence detailed, had
been kept closed. The cellars in all cases communicated with the houses
by means of doors opening into the kitchens. According to the general
account of the occupants, the cellars had smelled of “fire stink,”
which, in their opinion, proceeded from the adjoining mine.

The shaft of the disused mine communicated with a mine in working order,
and, to encourage the ventilation in this mine, a furnace had for some
weeks been lit and suspended in the shaft. This furnace had set fire to
the coal in the disused mine and smoke had been issuing from the shaft
for four weeks previously. Two days previous to the inquiry the opening
of the shaft had been closed over with a view to extinguish the fire.

Dr. Reid considered, from the symptoms and all the circumstances of the
case, that the illness was due to carbon monoxide gas penetrating into
the cellars from the mine, and from thence to the living- and
sleeping-rooms. A sample of the air yielded 0·015 per cent. of carbon
monoxide, although the sample had been taken after the cellar windows
had been open for twenty-four hours.

§ 42. =Detection of Carbon Monoxide.=--It may often be necessary to
detect carbon monoxide in air and to estimate its amount. The detection
in air, if the carbon monoxide is in any quantity, is easy enough; but
traces of carbon monoxide are difficult. Where amounts of carbon
monoxide in air from half a per cent. upwards are reasonably presumed to
exist, the air is measured in a gas measuring apparatus and passed into
an absorption pipette charged with alkaline pyrogallic acid, and when
all the oxygen has been abstracted, then the residual nitrogen and gases
are submitted to an ammoniacal solution of cuprous chloride.

The solution of cuprous chloride is prepared by dissolving 10·3 grms. of
copper oxide in 150 c.c. of strong hydrochloric acid and filling the
flask with copper turnings; the copper reduces the cupric chloride to
cuprous chloride; the end of the reduction is known by the solution
becoming colourless. The colourless acid solution is poured into some
1500 c.c. of water, and the cuprous chloride settles to the bottom as a
precipitate. The supernatant fluid is poured off as completely as
possible and the precipitate washed into a quarter litre flask, with 100
to 150 c.c. of distilled water and ammonia led into the solution until
it becomes of a pale blue colour. The solution is made up to 200 c.c. so
as to contain about 7·3 grms. per cent. of cuprous chloride.

Such a solution is an absorbent of carbon monoxide; it also absorbs
ethylene and acetylene.

A solution of cuprous chloride which has absorbed CO gives it up on
being treated with potassic bichromate and acid. It has been proposed by
Wanklyn to deprive large quantities of air of oxygen, then to absorb any
carbon monoxide present with cuprous chloride, and, lastly, to free the
cuprous chloride from the last gas by treatment with acid bichromate, so
as to be able to study the properties of a small quantity of pure gas.

By far the most reliable method to detect small quantities of carbon
monoxide is, however, as proposed by Hempel, to absorb it in the lungs
of a living animal.

A mouse is placed between two funnels joined together at their mouths by
a band of thin rubber; one of the ends of the double funnel is connected
with an aspirator, and the air thus sucked through, say for half an hour
or more; the mouse is then killed by drowning, and a control mouse,
which has not been exposed to a CO atmosphere, is also drowned; the
bodies of both mice are cut in two in the region of the heart, and the
blood collected. Each sample of blood is diluted in the same proportion
and spectroscopically examined in the manner detailed at p. 58.

Winkler found that, when large volumes of gas were used (at least 10
litres), 0·05 per cent. of carbon monoxide could be readily detected.


§ 43. Chlorine is a yellow-green gas, which may, by cold and pressure,
be condensed into a liquid. Its specific gravity is, as compared with
hydrogen, 35·37; as compared with air, 2·45; a litre under standard
conditions weighs 3·167 grms. It is soluble in water.

The usual method of preparation is the addition of hydrochloric acid to
bleaching powder, which latter substance is hypochlorite of lime mixed
with calcic chloride and, it may be, a little caustic lime. Another
method is to treat manganese dioxide with hydrochloric acid or to act on
manganese dioxide and common salt with sulphuric acid.

Accidents are liable to occur with chlorine gas from its extensive use
as a disinfectant and also in its manufacture. In the “Weldon” process
of manufacturing bleaching powder, a thick layer of lime is placed on
the floor of special chambers; chlorine gas is passed into these
chambers for about four days; then the gas is turned off; the unabsorbed
gas is drawn off by an exhaust or absorbed by a lime distributor and the
doors opened. Two hours afterwards the men go in to pack the powder. The
packers, in order to be able to work in the chambers, wear a respirator
consisting of about thirty folds of damp flannel; this is tightly bound
round the mouth with the nostrils free and resting upon it. The men are
obliged to inhale the breath through the flannel and exhale through the
nostril, otherwise they would, in technical jargon, be “gassed.” Some
also wear goggles to protect their eyes. Notwithstanding these
precautions they suffer generally from chest complaints.

§ 44. =Effects.=--Free chlorine, in the proportion of 0·04 to 0·06 per
thousand, taken into the lungs is dangerous to life, since directly
chlorine attacks a moist mucous membrane, hydrochloric acid is formed.
The effects of chlorine can hardly be differentiated from hydrochloric
acid gas, and Lehmann found that 1·5 per thousand of this latter gas
affected animals, causing at once uneasiness, evidence of pain with
great dyspnœa, and later coma. The eyes and the mucous membrane of the
nose were attacked. Anatomical changes took place in the cornea, as
evidenced by a white opacity.

In cases that recovered, a purulent discharge came from the nostrils
with occasional necrosis of the mucous membrane. The symptoms in man are
similar; there is great tightness of the breath, irritation of the nose
and eyes, cough and, with small repeated doses, bronchitis with all its
attendant evils. Bleaching powder taken by the mouth is not so deadly.
Hertwig has given 1000 grms. to horses, 30 grms. to sheep and goats, and
15 grms. to dogs without producing death. The symptoms in these cases
were quickening of the pulse and respiration, increased peristaltic
action of the bowels and a stimulation of the kidney secretion. The
urine smelt of chlorine.

§ 45. =Post-mortem Appearances.=--Hyperæmia of the lungs, with
ecchymoses and pneumonic patches with increased secretion of the
bronchial tubes. In the mucous membrane of the stomach, ecchymoses. The
alkalescence of the blood is diminished and there may be external signs
of bleaching. Only exceptionally has any chlorine smell been perceived
in the internal organs.

§ 46. =Detection of Free Chlorine.=--The usual method of detection is to
prepare a solution of iodide of potassium and starch and to soak strips
of filter-paper in this solution. Such a strip, when moistened and
submitted to a chlorine atmosphere, is at once turned blue, because
chlorine displaces iodine from its combination with potassium.
Litmus-paper, indigo blue or other vegetable colours are at once

To estimate the amount of chlorine a known volume of the air is drawn
through a solution of potassium iodide, and the amount of iodine set
free, determined by titration with sodic hyposulphite, as detailed at p.

III.--Hydric Sulphide (Sulphuretted Hydrogen).

§ 47. Hydric sulphide, SH₂, is a colourless transparent gas of sp.
gravity 1·178. It burns with a blue flame, forming water and sulphur
dioxide, and is soluble in water; water absorbing about three volumes
at ordinary temperatures. It is decomposed by either chlorine gas or
sulphur dioxide.

It is a common gas as a constituent of the air of sewers or cesspools,
and emanates from moist slag or moist earth containing pyrites or
metallic sulphides; it also occurs whenever albuminous matter putrefies;
hence it is a common constituent of the emanations from corpses of
either man or animals. It has a peculiar and intense odour, generally
compared to that of rotten eggs; this is really not a good comparison,
for it is comparing the gas with itself, rotten eggs always producing
SH₂; it is often associated with ammonium sulphide.

§ 48. =Effects.=--Pure hydric sulphide is never met with out of the
chemist’s laboratory, in which it is a common reagent either as a gas or
in solution; so that the few cases of poisoning by the pure gas, or
rather the pure gas mixed with ordinary air, have been confined to

The greater number of cases have occurred accidentally to men working in
sewers, or cleaning out cesspools and the like. In small quantities it
is always present in the air of towns, as shown by the blackening of any
silver ornament not kept bright by frequent use.

It is distinctly a blood poison, the gas uniting with the alkali of the
blood, and the sulphide thus produced partly decomposing again in the
lung and breathed out as SH₂. Lehmann[60] has studied the effects on
animals; an atmosphere containing from 1 to 3 per thousand of SH₂ kills
rabbits and cats within ten minutes; the symptoms are mainly convulsions
and great dyspnœa. An atmosphere containing from 0·4 to 0·8 per thousand
produces a local irritating action on the mucous membranes of the
respiratory tract, and death follows from an inflammatory œdema of the
lung preceded by convulsions; there is also a paralysis of the nervous
centres. Lehmann has recorded the case of three men who breathed 0·2 per
thousand of SH₂: within from five to eight minutes there was intense
irritation of the eyes, nose, and throat, and after thirty minutes they
were unable to bear the atmosphere any longer. Air containing 0·5 per
thousand of SH₂ is, according to Lehmann, the utmost amount that can be
breathed; this amount causes in half an hour smarting of the eyes, nasal
catarrh, dyspnœa, cough, palpitation, shivering, great muscular
weakness, headache and faintness with cold sweats. 0·7 to 0·8 per
thousand is dangerous to human life, and from 1 to 1·5 per thousand
destroys life rapidly. The symptoms may occur some little time after the
withdrawal of the person from the poisonous atmosphere; for example,
Cahn records the case of a student who prepared SH₂ in a laboratory and
was exposed to the gas for two hours; he then went home to dinner and
the symptoms first commenced in more than an hour after the first
breathing of pure air. Taylor[61] records an unusual case of poisoning
in 1857 at Cleator Moor. Some cottages had been built upon iron slag,
the slag contained sulphides of calcium and iron; a heavy storm of rain
washed through the slag and considerable volumes of SH₂ with, no doubt,
other gases diffused during the night through the cottages and killed
three adults and three children.

[60] K. B. Lehmann, _Arch. f. Hygiene_, Bd. xiv., 1892, 135.

[61] _Principles and Practice of Medl. Jurisp._, vol. ii. 122.

§ 49. =Post-mortem Appearances.=--The so-called apoplectic form of SH₂
poisoning, in which the sufferer dies within a minute or two, shows no
special change. The most frequent change in slower poisoning is,
according to Lehmann, œdema of the lungs. A green colour of the face and
of the whole body is sometimes present, but not constant. A
spectroscopic examination of the blood may also not lead to any
conclusion, the more especially as the spectrum of sulphur methæmoglobin
may occur in any putrid blood. The pupils in some cases have been found
dilated; in others not so.

=Chronic poisoning.=--Chronic poisoning by SH₂ is of considerable
interest in a public health point of view. The symptoms appear to be
conjunctivitis, headache, dyspepsia and anæmia. A predisposition to
boils has also been noted.

§ 50. =Detection.=--Both ammonium and hydric sulphides blacken silver
and filter-paper moistened with acetate of lead solution. To test for
hydric sulphide in air a known quantity may be aspirated through a
little solution of lead acetate. To estimate the quantity a decinormal
solution of iodine in potassium iodide[62] solution is used, and its
exact strength determined by d.n. sodic hyposulphite solution[63]; the
hyposulphite is run in from a burette into a known volume, _e.g._, 50
c.c., of the d.n. iodine solution, until the yellow colour is almost
gone; then a drop or two of fresh starch solution is added and the
hyposulphite run in carefully, drop by drop, until the blue colour of
the starch disappears. If now a known volume of air is drawn through 50
c.c. of the d.n. iodine solution, the reaction I₂ + SH₂ = 2HI + S will
take place, and for every 127 parts of iodine which have been converted
into hydriodic acid 17 parts by weight of SH₂ will be necessary; hence
on titrating the 50 c.c. of d.n. iodine solution, through which air
containing SH₂ has been passed, less hyposulphite will be used than on
the previous occasion, each c.c. of the hyposulphite solution being
equal to 1·11 c.c. or to 1·7 mgrm. of SH₂.

[62] 12·7 grms. of iodine, 16·6 grms. of potassium iodide, dissolved in
a litre of water.

[63] 24·8 grms. of sodic hyposulphite, dissolved in a litre of water.



I.--Sulphuric Acid.

§ 51. Sulphuric acid (hydric sulphate, oil of vitriol, H₂SO₄) occurs in
commerce in varying degrees of strength or dilution; the strong
sulphuric acid of the manufacturer, containing 100 per cent. of real
acid (H₂SO₄), has a specific gravity of 1·850. The ordinary brown acid
of commerce, coloured by organic matter and holding in solution metallic
impurities, chiefly lead and arsenic, has a specific gravity of about
1·750; and contains 67·95 of anhydrous SO₃ = 85·42 of hydric sulphate.

There are also weaker acids used in commerce, particularly in
manufactories in which sulphuric acid is made, for special purposes
without rectification. The British Pharmacopœia sulphuric acid is
directed to be of 1·843 specific gravity, which corresponds to 78·6 per
cent. sulphuric anhydride, or 98·8 per cent. of hydric sulphate. The
dilute sulphuric acid of the pharmacopœia should have a specific gravity
of 1·094, and is usually said to correspond to 10·14 per cent. of
anhydrous sulphuric acid; but, if Ure’s Tables are correct, such equals
11·37 per cent.

The general characters of sulphuric acid are as follows:--When pure, it
is a colourless, or, when impure, a dark brown to black, oily liquid,
without odour at common temperatures, of an exceedingly acid taste,
charring most organic tissues rapidly, and, if mixed with water,
evolving much heat. If 4 parts of the strong acid are mixed with 1 part
of water at 0°, the mixture rises to a heat of 100°; a still greater
heat is evolved by mixing 75 parts of acid with 27 of water.

Sulphuric acid is powerfully hygroscopic--3 parts will, in an ordinary
atmosphere, increase to nearly 4 in twenty-four hours; in common with
all acids, it reddens litmus, yellows cochineal, and changes all
vegetable colours. There is another form of sulphuric acid, extensively
used in the arts, known under the name of “Nordhausen sulphuric acid,”
“fuming acid,” formula H₂S₂O₄. This acid is produced by the distillation
of dry ferrous sulphate, at a nearly white heat--either in earthenware
or in green glass retorts; the distillate is received in sulphuric acid.
As thus manufactured, it is a dark fuming liquid of 1·9 specific
gravity, and boiling at 53°. When artificially cooled down to 0°, the
acid gradually deposits crystals, which consist of a definite compound
of 2 atoms of anhydrous sulphuric acid and 1 atom of water. There is
some doubt as to the molecular composition of Nordhausen acid; it is
usually considered as hydric sulphate saturated with sulphur dioxide.
This acid is manufactured chiefly in Bohemia, and is used, on a large
scale, as a solvent for alizarine.

§ 52. =Sulphur Trioxide, or Sulphuric Anhydride= (SO₃), itself may be
met with in scientific laboratories, but is not in commerce. Sulphur
trioxide forms thin needle-shaped crystals, arranged in feathery groups.
Seen in mass, it is white, and has something the appearance of asbestos.
It fuses to a liquid at about 18°, boils at 35°, but, after this
operation has been performed, the substance assumes an allotropic
condition, and then remains solid up to 100°; above 100° it melts,
volatilises, and returns to its normal condition. Sulphuric anhydride
hisses when it is thrown into water, chemical combination taking place
and sulphuric acid being formed. Sulphur trioxide is excessively
corrosive and poisonous.

Besides the above forms of acid, there is an officinal preparation
called “Aromatic Sulphuric Acid,” made by digesting sulphuric acid,
rectified spirit, ginger, and cinnamon together. It contains 10·19 per
cent. of SO₃, alcohol, and principles extracted from cinnamon and

§ 53. Sulphuric acid, in the free state, may not unfrequently be found
in nature. The author has had under examination an effluent water from a
Devonshire mine, which contained more than one grain of free sulphuric
acid per gallon, and was accused, with justice, of destroying the fish
in a river. It also exists in large quantities in volcanic springs. In a
torrent flowing from the volcano of Parcé, in the Andes, Boussingault
calculated that 15,000 tons of sulphuric acid and 11,000 tons of
hydrochloric acid were yearly carried down. In the animal and vegetable
kingdom, sulphuric acid exists, as a rule, in combination with bases,
but there is an exception in the saliva of the _Dolium galea_, a
Sicilian mollusc.

§ 54. =Statistics.=--When something like 900,000 tons of sulphuric acid
are produced annually in England alone, and when it is considered that
sulphuric acid is used in the manufacture of most other acids, in the
alkali trade, in the manufacture of indigo, in the soap trade, in the
manufacture of artificial manure, and in a number of technical
processes, there is no cause for surprise that it should be the annual
cause of many deaths.

The number of deaths from sulphuric acid will vary, other things being
equal, in each country, according to the manufactures in that country
employing sulphuric acid. The number of cases of poisoning in England
and Wales for ten years is given in the following table:--


                     ACCIDENT OR NEGLIGENCE.

  Ages,      1-5   5-15   15-25   25-65    65 &     Total
  Males,      11     4       2      14       2        33
  Females,     4   ...       2       3     ...         9
  Totals,     15     4       4      17       2        42


  Ages,                   15-25   25-65             Total
  Males,                     4      25                29
  Females,                   5      19                24
  Totals                     9      44                53

During the ten years, no case of murder through sulphuric acid is on
record; hence the total deaths, as detailed in the tables, amount to 95,
or a little over 9 a year.

Falck,[64] in comparing different countries, considers the past
statistics to show that in France sulphuric acid has been the cause of
4·5 to 5·5 per cent. of the total deaths from poison, and in England 5·9
per cent. In England, France, and Denmark, taken together, 10·8, Prussia
10·6; while in certain cities, as Berlin and Vienna, the percentages are
much higher--Vienna showing 43·3 per cent., Berlin 90 per cent.

[64] _Lehrbuch der praktischen Toxicologie_, p. 54.

§ 55. =Accidental, Suicidal, and Criminal Poisoning.=--Deaths from
sulphuric acid are, for the most part, accidental, occasionally
suicidal, and, still more rarely, criminal. In 53 out of 113 cases
collected by Böhm, in which the cause of the poisoning could, with fair
accuracy, be ascertained, 45·3 per cent. were due to accident, 30·2 were
suicidal, and 24·5 per cent. were cases of criminal poisoning, the
victims being children.

The cause of the comparatively rare use of sulphuric acid by the
poisoner is obvious. First of all, the acid can never be mixed with food
without entirely changing its aspect; next, it is only in cases of
insensibility or paralysis that it could be administered to an adult,
unless given by force, or under very exceptional circumstances; and
lastly, the stains on the mouth and garments would at once betray, even
to uneducated persons, the presence of something wrong. As an agent of
murder, then, sulphuric acid is confined in its use to young children,
more especially to the newly born.

There is a remarkable case related by Haagan,[65] in which an adult man,
in full possession of his faculties, neither paralysed nor helpless, was
murdered by sulphuric acid. The wife of a day-labourer gave her husband
drops of sulphuric acid on sugar, instead of his medicine, and finally
finished the work by administering a spoonful of the acid. The spoon was
carried well to the back of the throat, so that the man took the acid at
a gulp. 11 grms. (171 grains) of sulphuric acid, partly in combination
with soda and potash, were separated from his stomach.

[65] Gross: _Die Strafrechtspflege in Deutschland_, 4, 1861, Heft I. S.

Accidental poisoning is most common among children. The oily,
syrupy-looking sulphuric acid, when pure, may be mistaken for glycerin
or for syrup; and the dark commercial acid might, by a careless person,
be confounded with porter or any dark-looking medicine.

Serious and fatal mistakes have not unfrequently arisen from the use of
injections. Deutsch[66] relates how a midwife, in error, administered to
mother and child a sulphuric acid clyster; but little of the fluid could
in either case have actually reached the rectum, for the mother
recovered in eight days, and in a little time the infant was also
restored to health. Sulphuric acid has caused death by injections into
the vagina. H. C. Lombard[67] observed a case of this kind, in which a
woman, aged thirty, injected half a litre of sulphuric acid into the
vagina, for the purpose of procuring abortion. The result was not
immediately fatal, but the subsequent inflammation and its results so
occluded the natural passage that the birth became impossible, and a
Cæsarean section extracted a dead child, the mother also dying.

[66] _Preuss. Med. Vereins-Zeitung_, 1848, No. 13.

[67] _Journ. de Chim. Méd._, tom. vii., 1831.

An army physician prescribed for a patient an emollient clyster. Since
it was late at night, and the apothecary in bed, he prepared it himself;
but not finding linseed oil, woke the apothecary, who took a bottle out
of one of the recesses and placed it on the table. The bottle contained
sulphuric acid; a soldier noticed a peculiar odour and effervescence
when the syringe was charged, but this was unheeded by the doctor. The
patient immediately after the operation suffered the most acute agony,
and died the following day; before his death, the bedclothes were found
corroded by the acid, and a portion of the bowel itself came away.[68]

[68] Maschka’s _Handbuch_, p. 86; _Journal de Chimie Médicale_, t. i.
No. 8, 405, 1835.

§56. =Fatal Dose.=--The amount necessary to kill an adult man is not
strictly known; fatality so much depends on the concentration of the
acid and the condition of the person, more especially whether the
stomach is full or empty, that it will be impossible ever to arrive at
an accurate estimate. Christison’s case, in which 3·8 grms. (60 grains)
of concentrated acid killed an adult, is the smallest lethal dose on
record. Supposing that the man weighed 68½ kilo. (150 lbs.), this would
be in the proportion of ·05 grm. per kilo. There is also the case of a
child of one year, recorded by Taylor, in which 20 drops caused death.
If, however, it were asked in a court of law what dose of concentrated
sulphuric acid would be dangerous, the proper answer would be: so small
a quantity as from 2 to 3 drops of the strong undiluted acid might cause
death, more especially if conveyed to the back of the throat; for if it
is improbable that on such a supposition death would be sudden, yet
there is a possibility of permanent injury to the gullet, with the
result of subsequent contraction, and the usual long and painful
malnutrition thereby induced. It may be laid down, therefore, that all
quantities, even the smallest, of the _strong undiluted acid_ come under
the head of hurtful, noxious, and injurious.

§ 57. =Local Action of Sulphuric Acid.=--The action of the acid on
living animal tissues has been studied of late by C. Ph. Falck and L.
Vietor.[69] Concentrated acid precipitates albumen, and then redissolves
it; fibrin swells and becomes gelatinous; but if the acid is weak
(_e.g._, 4 to 6 per cent.) it is scarcely changed. Muscular fibre is at
first coloured amber-yellow, swells to a jelly, and then dissolves to a
red-brown turbid fluid. When applied to the mucous membrane of the
stomach, the mucous tissue and the muscular layer beneath are coloured
white, swell, and become an oily mass.

[69] _Deutsche Klinik_, 1864, Mo. 1-32, and Vietor’s
_Inaugur.-Dissert._, Marburg, 1803.

When applied to a rabbit’s ear,[70] the parenchyma becomes at first pale
grey and semi-transparent at the back of the ear; opposite the drop of
acid appear spots like grease or fat drops, which soon coalesce. The
epidermis with the hair remains adherent; the blood-vessels are narrowed
in calibre, and the blood, first in the veins, and then in the arteries,
is coloured green and then black, and fully coagulates. If the drop,
with horizontal holding of the ear, is dried in, an inflammatory zone
surrounds the burnt spot in which the blood circulates; but there is
complete stasis in the part to which the acid has been applied. If the
point of the ear is dipped in the acid, the cauterised part rolls
inwards; after the lapse of eighteen hours the part is brown and
parchment-like, with scattered points of coagulated blood; then there is
a slight swelling in the healthy tissues, and a small zone of redness;
within fourteen days a bladder-like greenish-yellow scab is formed, the
burnt part itself remaining dry. The vessels from the surrounding zone
of redness gradually penetrate towards the cauterised spot, the fluid
in the bleb becomes absorbed, and the destroyed tissues fall off in the
form of a crust.

[70] Samuel, _Entzündung u. Brand, in Virchow’s Archiv f. Path. Anat._,
Bd. 51, Hft. 1 u. 2, S. 41, 1870.

The changes that sulphuric acid cause in blood are as follows: the
fibrin is at first coagulated and then dissolved, and the colouring
matter becomes of a black colour. These changes do not require the
strongest acid, being seen with an acid of 60 per cent.

§ 58. The action of the acid on various non-living matters is as
follows: poured on all vegetable earth, there is an effervescence,
arising from decomposition of carbonates; any grass or vegetation
growing on the spot is blackened and dies; an analysis of the layer of
earth, on which the acid is poured, shows an excess of sulphates as
compared with a similar layer adjacent; the earth will only have an acid
reaction, if there has been more than sufficient acid to neutralise all
alkalies and alkaline earths.

Wood almost immediately blackens, and the spot remains moist.

Spots on paper become quickly dark, and sometimes exhibit a play of
colours, such as reddish-brown; ultimately the spot becomes very black,
and holes may be formed; even when the acid is dilute, the course is
very similar, for the acid dries in, until it reaches a sufficient
degree of concentration to attack the tissue. I found small drops of
sulphuric acid on a brussels carpet, which had a red pattern on a dark
green ground with light green flowers, act as follows: the spots on the
red at the end of a few hours were of a dark maroon colour, the green
was darkened, and the light green browned; at the end of twenty-four
hours but little change had taken place, nor could any one have guessed
the cause of the spots without a close examination. Spots of the strong
acid on thin cotton fabrics rapidly blackened, and actual holes were
formed in the course of an hour; the main difference to the naked eye,
between the stains of the acid and those produced by a red-hot body, lay
in the moistness of the spots. Indeed, the great distinction, without
considering chemical evidence, between recent burns of clothing by
sulphuric acid and by heat, is that in the one case--that of the
acid--the hole or spot is very moist; in the other very dry. It is easy
to imagine that this distinction may be of importance in a legal

Spots of acid on clothing fall too often under the observation of all
those engaged in practical chemical work. However quickly a spot of acid
is wiped off, unless it is immediately neutralised by ammonia, it
ultimately makes a hole in the cloth; the spot, as a rule, whatever the
colour of the cloth, is of a blotting-paper red.

Sulphuric acid dropped on iron, attacks it, forming a sulphate, which
may be dissolved out by water. If the iron is exposed to the weather
the rain may wash away all traces of the acid, save the corrosion; but
it would be under those circumstances impossible to say whether the
corrosion was due to oxidation or a solvent.

To sum up briefly: the characters of sulphuric acid spots on organic
matters generally are black, brown, or red-coloured destructions of
tissue, moisture, acid-reaction (often after years), and lastly the
chemical evidence of sulphuric acid or sulphates in excess.

=Caution necessary in judging of Spots, &c.=--An important case, related
by Maschka, shows the necessity of great caution in interpreting
results, unless all the circumstances of a case be carefully collated. A
live coal fell on the bed of a weakly infant, five months old. The child
screamed, and woke the father, who was dozing by the fire; the man, in
terror, poured a large pot of water on the child and burning bed. The
child died the following day.

A _post-mortem_ examination showed a burn on the chest of the infant 2
inches in length. The tongue, pharynx, and gullet were all healthy; in
the stomach a patch of mucous membrane, about half an inch in extent,
was found to be brownish, friable, and very thin. A chemical examination
showed that the portion of the bed adjacent to the burnt place contained
free sulphuric acid. Here, then, was the following evidence: the sudden
death of a helpless infant, a carbonised bed-cover with free sulphuric
acid, and, lastly, an appearance in the stomach which, it might be said,
was not inconsistent with sulphuric acid poisoning. Yet a careful
sifting of the facts convinced the judges that no crime had been
committed, and that the child’s death was due to disease. Afterwards,
experiment showed that if a live coal fall on to any tissue, and be
drenched with water, free sulphuric acid is constantly found in the
neighbourhood of the burnt place.

§ 59. =Symptoms.=--The symptoms may be classed in two divisions,
viz.:--1. External effects of the acid. 2. Internal effects and symptoms
arising from its interior administration.

1. =External Effects.=--Of late years several instances have occurred in
which the acid has been used criminally to cause disfiguring burns of
the face. The offence has in all these cases been committed by women,
who, from motives of revengeful jealousy, have suddenly dashed a
quantity of the acid into the face of the object of their resentment. In
such cases, the phenomena observed are not widely different from those
attending scalds or burns from hot neutral fluids. There is destruction
of tissue, not necessarily deep, for the acid is almost immediately
wiped off; but if any should reach the eye, inflammation, so acute as to
lead to blindness, is the probable consequence. The skin is coloured at
first white, at a later period brown, and part of it may be, as it were,
dissolved. If the tract or skin touched by the acid is extensive, death
may result. The inflammatory processes in the skin are similar to those
noticed by Falck and Vietor in their experiments, already detailed (p.

=Internal Effects of Acids generally.=--It may not be out of place,
before speaking of the internal effects of sulphuric acid, to make a few
remarks upon the action of acids generally. This action differs
according to the kind of animal; at all events, there is a great
difference between the action of acids on the herb-eating animals and
the carnivora; the latter bear large doses of acids well, the former
ill. For instance, the rabbit, if given a dose of any acid not
sufficient to produce local effects but sufficient to affect its
functions, will soon become paralysed and lie in a state of stupor, as
if dead; the same dose per kilo. will not affect the dog. The reason for
this is that the blood of the dog is able to neutralise the acid by
ammonia, and that the blood of the rabbit is destitute of this property.
Man is, in this respect, nearer to the dog than to the plant-eaters.
Stadelmann has shown that a man is able to ingest large relative doses
of oxybutyric acid, to neutralise the acid by ammonia, and to excrete it
by means of the kidneys as ammonium butyrate.

Acids, however, if given in doses too great to be neutralised, alike
affect plant- and flesh-eaters; death follows in all cases before the
blood becomes acid. Salkowsky[71] has, indeed, shown that the effect of
lessening the alkalinity of the blood by giving a rabbit food from which
it can extract no alkali produces a similar effect to the actual dosing
with an acid.

[71] Virchow’s _Archiv_, Bd. 58, 1.

2. =Internal Effects of Sulphuric Acid.=--When sulphuric acid is taken
internally, the acute and immediate symptom is pain. This, however, is
not constant, since, in a few recorded cases, no complaint of pain has
been made; but these cases are exceptional; as a rule, there will be
immediate and great suffering. The tongue swells, the throat is also
swollen and inflamed, swallowing of saliva even may be impossible. If
the acid has been in contact with the epiglottis and vocal apparatus,
there may be spasmodic croup and even fatal spasm of the glottis.

The acid, in its passage down the gullet, attacks energetically the
mucous membrane and also the lining of the stomach; but the action does
not stop there, for Lesser found in eighteen out of twenty-six cases (69
per cent.) that the corrosive action extended as far as the duodenum.
There is excessive vomiting and retching; the matters vomited are acid,
bloody, and slimy; great pieces of mucous membrane may be in this way
expelled, and the whole of the lining membrane of the gullet may be
thrown up entire. The bowels are, as a rule, constipated, but
exceptionally there has been diarrhœa; the urine is sometimes retained;
it invariably contains an excess of sulphates and often albumen, with
hyaline casts of the uriniferous tubes. The pulse is small and frequent,
the breathing slow, the skin very cold and covered with sweat; the
countenance expresses great anxiety, and the extremities may be affected
with cramps or convulsions. Death may take place within from twenty-four
to thirty-six hours, and be either preceded by dyspnœa or by
convulsions; consciousness is, as a rule, maintained to the end.

There are also more rapid cases than the above; a large dose of
sulphuric acid taken on an empty stomach may absolutely dissolve it, and
pass into the peritoneum; in such a case there is really no difference
in the symptoms between sudden perforation of the stomach from disease,
a penetrating wound of the abdomen, and any other sudden fatal lesion of
the organs in the abdominal cavity (for in all these instances the
symptoms are those of pure collapse); the patient is ashen pale, with
pulse quick and weak, and body bathed in cold sweat, and he rapidly
dies, it may be without much complaint of local pain.

If the patient live longer than twenty-four hours, the symptoms are
mainly those of inflammation of the whole mucous tract, from the mouth
to the stomach; and from this inflammation the patient may die in a
variable period, of from three to eleven days, after taking the poison.
In one case the death occurred suddenly, without any immediately
preceding symptoms rendering imminent death probable. If this second
stage is passed, then the loss of substance in the gullet and in the
stomach almost invariably causes impairment of function, leading to a
slow and painful death. The common sequence is stricture of the gullet,
combined with feeble digestion, and in a few instances stricture of the
pylorus. A curious sequel has been recorded by Mannkopf, viz., obstinate
intercostal neuralgia; it has been observed on the fourth, seventh, and
twenty-second day.

§ 60. =Treatment of Acute Poisoning by the Mineral Acids.=--The
immediate indication is the dilution and neutralisation of the acid. For
this purpose, finely-divided chalk, magnesia, or sodic carbonate may be
used, dissolved or suspended in much water. The use of the stomach-pump
is inadvisable, for the mucous membrane of the gullet may be so corroded
by the acid that the passage of the tube down will do injury; unless the
neutralisation is _immediate_, but little good is effected; hence it
will often occur that the bystanders, if at all conversant with the
matter, will have to use the first thing which comes to hand, such as
the plaster of a wall, &c.; and lastly, if even these rough antidotes
are not to be had, the best treatment is enormous doses of water, which
will dilute the acid and promote vomiting. The treatment of the
after-effects belongs to the province of ordinary medicine, and is based
upon general principles.

§ 61. =Post-mortem Appearances.=[72]--The general pathological
appearances to be found in the stomach and internal organs differ
according as the death is rapid or slow; if the death takes place within
twenty-four hours, the effects are fairly uniform, the differences being
only in degree; while, on the other hand, in those cases which terminate
fatally from the more remote effects of the acid, there is some variety.
It may be well to select two actual cases as types, the one patient
dying from acute poisoning, the other surviving for a time, and then
dying from ulceration and contraction of the digestive tract.

[72] It has been observed that putrefaction in cases of death from
sulphuric acid is slow. Casper suggests this may be due to the
neutralisation of ammonia; more probably it is owing to the antiseptic
properties all mineral acids possess.

A hatter, early in the morning, swallowed a large mouthful of strong
sulphuric acid, a preparation which he used in his work--(whether the
draught was taken accidentally or suicidally was never known). He died
within two hours. The whole tongue was sphacelated, parts of the mucous
membrane being dissolved; the inner surface of the gullet, as well as
the whole throat, was of a grey-black colour; the mucous membrane of the
stomach was coal-black, and so softened that it gave way like
blotting-paper under the forceps, the contents escaping into the cavity
of the abdomen. The peritoneum was also blackened as if burnt; probably
there had been perforation of the stomach during life; the mucous
membrane of the duodenum was swollen, hardened, and looked as if it had
been boiled; while the blood was of a cherry-red colour, and of the
consistence of a thin syrup. The rest of the organs were healthy; a
chemical research on the fluid which had been collected from the
stomach, gullet, and duodenum showed that it contained 87·25 grains of
free sulphuric acid.[73]

[73] Casper, vol. ii. case 194.

This is, perhaps, the most extreme case of destruction on record; the
cause of the unusually violent action is referable to the acid acting on
an empty stomach. It is important to note that even with this extensive
destruction of the stomach, life was prolonged for two hours.

The case I have selected to serve as a type of a chronic but fatal
illness produced from poisoning by sulphuric acid is one related by
Oscar Wyss. A cook, thirty-four years of age, who had suffered many
ailments, drank, on the 6th of November 1867, by mistake, at eight
o’clock in the morning, two mouthfuls of a mixture of 1 part of
sulphuric acid and 4 of water. Pain in the stomach and neck, and
vomiting of black masses, were the immediate symptoms, and two hours
later he was admitted into the hospital in a state of collapse, with
cold extremities, cyanosis of the face, &c. Copious draughts of milk
were given, and the patient vomited much, the vomit still consisting of
black pultaceous matters, in which, on a microscopical examination,
could be readily detected columnar epithelium of the stomach and mucous
tissue elements. The urine was of specific gravity 1·033,
non-albuminous; on analysis it contained 3·388 grms. of combined
sulphuric acid.

On the second day there was some improvement in the symptoms; the urine
contained 1·276 grm. of combined sulphuric acid; on the third day 2·665
grms. of combined sulphuric acid; and on the tenth day the patient
vomited up a complete cast of the mucous membrane of the gullet. The
patient remained in the hospital, and became gradually weaker from
stricture of the gullet and impairment of the digestive powers, and
died, two months after taking the poison, on the 5th of January 1868.

The stomach was found small, contracted, with many adhesions to the
pancreas and liver; it was about 12 centimetres long (4·7 inches), and
from 2 to 2·5 centimetres (·7 to ·9 inch) broad, contracted to somewhat
the form of a cat’s intestine; there were several transverse rugæ; the
walls were thickened at the small curvature, measurements giving 5 mm.
(·19 inch) in the middle, and beyond about 2·75 mm. (·11 inch); in the
upper two-thirds the lumen was so contracted as scarcely to admit the
point of the little finger. The inner surface was covered with a layer
of pus, with no trace of mucous tissue, and was everywhere pale red,
uneven, and crossed by cicatricial bands. In two parts, at the greater
curvature, the mucous surface was strongly injected in a ring-like form,
and in the middle of the ring was a deep funnel-shaped ulcer; a part of
the rest of the stomach was strongly injected and scattered over with
numerous punctiform, small, transparent bladders. The gullet was
contracted at the upper part (just below the epiglottis) from 20 to 22
mm. (·78 to ·86 inch) in diameter; it then gradually widened to measure
about 12 mm. (·47 inch) at the diaphragm; in the neighbourhood of the
last contraction the tissue was scarred, injected, and ulcerated; there
were also small abscesses opening into this portion of the gullet.

E. Fraenkel and F. Reiche[74] have studied the effects of sulphuric acid
on the kidney. In rapid cases they find a wide-spread coagulation of the
epithelium in the convoluted and straight urinary canaliculi, with
destruction of the kidney parenchyma, but no inflammation.

[74] Virchow’s _Archiv_, Bd. 131, f. 130.

§ 62. The museums of the different London hospitals afford excellent
material for the study of the effects of sulphuric acid on the pharynx,
gullet, and stomach; and it may be a matter of convenience to students
if the more typical examples at these different museums be noticed in
detail, so that the preparations themselves may be referred to.

    _In St. Bartholomew’s Museum_, No. 1942, is an example of excessive
    destruction of the stomach by sulphuric acid. The stomach is much
    contracted, and has a large aperture with ragged edges; the mucous
    membrane is thickened, charred, and blackened.

    No. 1941, in the same museum, is the stomach of a person who died
    from a large dose of sulphuric acid. When recent, it is described as
    of a deep red colour, mottled with black; appearances which, from
    long soaking in spirit, are not true at the present time; but the
    rough, shaggy state of the mucous tissue can be traced; the gullet
    and the pylorus appear the least affected.

    _St. George’s Hospital_, ser. ix., 146, 11 and 43, e.--The pharynx
    and œsophagus of a man who was brought into the hospital in a state
    of collapse, after a large but unknown dose of sulphuric acid. The
    lips were much eroded, the mucous membrane of the stomach, pharynx,
    and œsophagus show an extraordinary shreddy condition; the lining
    membrane of the stomach is much charred, and the action has extended
    to the duodenum; the muscular coat is not affected.

    _Guy’s Hospital_, No. 1799.--A preparation showing the mucous
    membrane of the stomach entirely denuded. The organ looks like a
    piece of thin paper.

    No. 1799²⁰. The stomach of a woman who poisoned herself by drinking
    a wine-glassful of acid before breakfast. She lived eleven days. The
    main symptoms were vomiting and purging, but there was no complaint
    of pain. There is extensive destruction of mucous membrane along the
    lesser curvature and towards the pyloric extremity; a portion of the
    mucous membrane is floating as a slough.

    No. 1799²⁵ is the gullet and stomach of a man who took about 3
    drachms of the strong acid. He lived three days without much
    apparent suffering, and died unexpectedly. The lining membrane of
    the œsophagus has the longitudinal wrinkles or furrows so often,
    nay, almost constantly, met with in poisoning by the acids. The
    mucous tissue of the stomach is raised in cloudy ridges, and

    No. 1799³⁵ is a wonderfully entire cast of the gullet from a woman
    who swallowed an ounce of sulphuric acid, and is said, according to
    the catalogue, to have recovered.

    _University College._--In this museum will be found an exquisite
    preparation of the effects of sulphuric acid. The mucous membrane of
    the œsophagus is divided into small quadrilateral areas by
    longitudinal and transverse furrows; the stomach is very brown, and
    covered with shreddy and filamentous tissue; the brown colour is
    without doubt the remains of extravasated and charred blood.

    No. 6201 is a wax cast representing the stomach of a woman who died
    after taking a large dose of sulphuric acid. A yellow mass was found
    in the stomach; there are two perforations, and the mucous membrane
    is entirely destroyed.

§ 63. =Chronic Poisoning by Sulphuric Acid.=--Weiske[75] has
experimentally proved that lambs, given for six months small doses of
sulphuric acid, grow thin, and their bones, with the exception of the
bones of the head and the long bones, are poor in lime salts, the
muscles also are poor in the same constituents. Kobert[76] thinks that
drunkards on the continent addicted to “Schnaps,” commonly a liquid
acidified with sulphuric acid to give it a sharp taste, often show
typical chronic sulphuric acid poisoning.

[75] H. Weiske, _Journ. f. Landwirthsch._, 1887, 417.

[76] _Lehrbuch der Intoxicationen_, S. 210.

Detection and Estimation of Free Sulphuric Acid.

§ 64. The general method of separating the mineral acids is as follows:
the tissues, or matters, are soaked in distilled water for some time. If
no free acid is present, the liquid will not redden litmus-paper, or
give an acid reaction with any of the numerous tinctorial agents in use
by the chemist for the purposes of titration. After sufficient digestion
in water, the liquid extract is made up to some definite bulk and
allowed to subside. Filtration is unnecessary. A small fractional part
(say, for example, should the whole be 250 c.c., 1/100th or 2·5 c.c.) is
taken, and using as an indicator cochineal or phenolphthalein, the total
acidity is estimated by a decinormal solution of soda. By this
preliminary operation, some guide for the conduct of the future more
exact operations is obtained. Should the liquid be very acid, a small
quantity of the whole is to be now taken, but if the acidity is feeble,
a larger quantity is necessary, and sufficient quinine then added to fix
the acid--100 parts of sulphuric acid are saturated by 342 parts of
quinine monohydrate. Therefore, on the supposition that all the free
acid is sulphuric, it will be found sufficient to add 3·5 parts of
quinine for every 1 part of acid, estimated as sulphuric, found by the
preliminary rough titration; and as it is inconvenient to deal with
large quantities of alkaloid, a fractional portion of the liquid extract
(representing not more than 50 mgrms. of acid) should be taken, which
will require 175 mgrms. of quinine.

On addition of the quinine, the neutralised liquid is evaporated to
dryness, or to approaching dryness, and then exhausted by strong
alcohol. The alcoholic extract is, after filtration, dried up, and the
quinine sulphate, nitrate, or hydrochlorate, as the case may be,
filtered off and extracted by boiling water, and precipitated by
ammonia, the end result being quinine hydrate (which may be filtered off
and used again for similar purposes) and a sulphate, nitrate or chloride
of ammonia in solution. It therefore remains to determine the nature and
quantity of the acids now combined with ammonia. The solution is made up
to a known bulk, and portions tested for chlorides by nitrate of silver,
and for nitrates by the copper or the ferrous sulphate test. If
sulphuric acid is present, there will be a precipitate of barium
sulphate, which, on account of its density and insolubility in nitric or
hydrochloric acids, is very characteristic. For estimating the sulphuric
acid thus found, it will only be necessary to take a known bulk of the
same liquid, heat it to boiling after acidifying by hydrochloric acid,
and then add a sufficient quantity of baric chloride solution. Unless
this exact process is followed, the analyst is likely to get a liquid
which refuses to filter clear, but if the sulphate be precipitated from
a hot liquid, it usually settles rapidly to the bottom of the vessel,
and the supernatant fluid can be decanted clear; the precipitate is
washed by decantation, and ultimately collected on a filter, dried, and

The sulphate of baryta found, multiplied by ·3434, equals the sulphuric

The older process was to dissolve the free sulphuric acid out by
alcohol. As is well known, mineral sulphates are insoluble in, and are
precipitated by, alcohol, whereas sulphuric acid enters into solution.
The most valid objection, as a quantitative process, to the use of
alcohol, is the tendency which all mineral acids have to unite with
alcohol in organic combination, and thus, as it were, to disappear; and,
indeed, results are found, by experiment, to be below the truth when
alcohol is used. This objection does not hold good if either merely
qualitative evidence, or a fairly approximate quantation, is required.
In such a case, the vomited matters, the contents of the stomach, or a
watery extract of the tissues, are evaporated to a syrup, and then
extracted with strong alcohol and filtered; a little phenolphthalein
solution is added, and the acid alcohol exactly neutralised by an
alcoholic solution of clear decinormal or normal soda. According to the
acidity of the liquid, the amount used of the decinormal or normal soda
is noted, and then the whole evaporated to dryness, and finally heated
to gentle redness. The alkaline sulphate is next dissolved in very
dilute hydrochloric acid, and the solution precipitated by chloride of
barium in the usual way. The quantitative results, although low, would,
in the great majority of cases, answer the purpose sufficiently.

A test usually enumerated, Hilger’s test for mineral acid, may be
mentioned. A liquid, which contains a very minute quantity of mineral
acid, becomes of a blue colour (or, if 1 per cent. or above, of a green)
on the addition of a solution of methyl aniline violet; but this test,
although useful in examining vinegars (see “Foods,” p. 519), is not of
much value in toxicology, and the quinine method for this purpose meets
every conceivable case, both for qualitative and quantitative purposes.

§ 65. =The Urine.=--Although an excess of sulphates is found constantly
in the urine of persons who have taken large doses of sulphuric acid,
the latter has never been found in that liquid in a free state, so that
it will be useless to search for free acid. It is, therefore, only
necessary to add HCl to filter the fluid, and precipitate direct with an
excess of chloride of barium. It is better to operate in this manner
than to burn the urine to an ash, for in the latter case part of the
sulphates, in the presence of phosphates, are decomposed, and, on the
other hand, any organic sulphur combinations are liable to be estimated
as sulphates.

It may also be well to pass chlorine gas through the same urine which
has been treated with chloride of barium, and from which the sulphate
has been filtered off. The result of this treatment will be a second
precipitate of sulphate derived from sulphur, in a different form of
combination than that of sulphate.

The greatest amount of sulphuric acid as mineral and organic sulphate is
separated, according to Mannkopf[77] and Schultzen,[78] within five
hours after taking sulphuric acid; after three days the secretion, so
far as total sulphates is concerned, is normal.

[77] “Toxicologie der Schwefelsäure,” _Wiener med. Wochen._, 1862, 1863.

[78] _Archiv. f. Anatom. u. Physiol._, 1864.

The normal amount of sulphuric acid excreted daily, according to
Thudichum, is from 1·5 to 2·5 grms., and organic sulphur up to ·2 grm.
in the twenty-four hours, but very much more has been excreted by
healthy persons.

Lehmann made some observations on himself, and found that, on an animal
diet, he excreted no less than 10·399 grms. of sulphuric acid per day,
while on mixed food a little over 7 grms.; but, as Thudichum justly
observes, this great amount must be referred to individual peculiarity.
The amount of sulphates has a decided relation to diet. Animal food,
although not containing sulphates, yet, from the oxidation of the
sulphur-holding albumen, produces a urine rich in sulphate. Thus Vogel
found that a person, whose daily average was 2·02 grms., yielded 7·3 on
a meat diet. The internal use of sulphur, sulphides, and sulphates,
given in an ordinary medicinal way, is traceable in the urine,
increasing the sulphates. In chronic diseases the amount of sulphates is
decreased, in acute increased.

Finally, it would appear that the determination of sulphates in the
urine is not of much value, _save when the normal amount that the
individual secretes is primarily known_. On the other hand, a low amount
of sulphates in the urine of a person poisoned by sulphuric acid has not
been observed within three days of the taking of the poison, and one can
imagine cases in which such a low result might have forensic importance.

The presence of albumen in the urine has been considered by some a
constant result of sulphuric acid poisoning, but although when looked
for it is usually found, it cannot be considered constant. O.
Smoler,[79] in eighteen cases of various degrees of sulphuric acid
poisoning, found nothing abnormal in the urine. Wyss[80] found in the
later stages of a case indican and pus. E. Leyden and Ph. Munn[81]
always found blood in the urine, as well as albumen, with casts and
cellular elements. Mannkopf[82] found albuminuria in three cases out of
five; in two of the cases there were fibrinous casts; in two the albumen
disappeared at the end of the second or third day, but in one it
continued for more than twenty days. Bamberger[83] has observed an
increased albuminuria, with separation of the colouring matter of the
blood. In this case it was ascribed to the action of the acid on the

[79] _Archiv der Heilkunde red. v._ E. Wagner, 1869, Hft. 2, S. 181.

[80] _Wiener Medicinal-Halle_, 1861, Jahr. 6, No. 46.

[81] Virchow’s _Archiv f. path. Anat._, 1861. Bd. 22, Hft. 3 u. 4, S.

[82] _Wien. med. Wochenschrift_, 1862, Nro. 35; 1863, Nro. 5.

[83] _Wien. Med.-Halle_, 1864, Nro. 29, 30.

§ 66. =The Blood.=--In Casper’s case, No. 193, the vena cava of a child,
who died within an hour after swallowing a large dose of sulphuric acid,
was filled with a cherry-red, strongly acid-reacting blood. Again,
Casper’s case, No. 200, is that of a young woman, aged 19, who died from
a poisonous dose of sulphuric acid. At the autopsy, four days after
death, the following peculiarities of the blood were thus noted:--“The
blood had an acid reaction, was dark, and had (as is usual in these
cases) a syrupy consistence, while the blood-corpuscles were quite
unchanged. The blood was treated with an excess of absolute alcohol,
filtered, the filtrate concentrated on a water-bath, the residue
exhausted with absolute alcohol, &c. It yielded a small quantity of
sulphuric acid.”

Other similar cases might be noted, but it must not for a moment be
supposed that the mass of the blood contains any free sulphuric acid
during life. The acidity of the blood in the vena cava may be ascribed
to _post-mortem_ endosmosis, the acid passing through the walls of the
stomach into the large vessel.

§ 67. =Sulphates.=--If the acid swallowed should have been entirely
neutralised by antidotes, such as chalk, &c., it becomes of the first
importance to ascertain, as far as possible, by means of a microscopical
examination, the nature of the food remaining in the stomach, and then
to calculate the probable contents in sulphates of the food thus known
to be eaten. It will be found that, with ordinary food, and under
ordinary circumstances, only small percentages of combined sulphuric
acid can be present.

As an example, take the ordinary rations of the soldier, viz.:--12 oz.
of meat, 24 oz. of bread, 16 oz. of potatoes, 8 oz. of other vegetables;
with sugar, salt, tea, coffee, and water. Now, if the whole quantity of
these substances were eaten at a meal, they would not contain more than
from 8 to 10 grains (·5 to ·6 grm.) of anhydrous sulphuric acid, in the
form of sulphates.

So far as the contents of the stomach are concerned, we have only to do
with sulphates introduced in the food, but when once the food passes
further along the intestinal canal, circumstances are altered, for we
have sulphur-holding secretions, which, with ordinary chemical methods,
yield sulphuric acid. Thus, even in the newly-born infant, according to
the analyses of Zweifler, the mineral constituents of meconium are
especially sulphate of lime, with a smaller quantity of sulphate of
potash. The amount of bile which flows into the whole tract of the
intestinal canal is estimated at about half a litre in the twenty-four
hours; the amount of sulphur found in bile varies from ·89 to 3 per
cent., so that in 500 c.c. we might, by oxidising the sulphur, obtain
from 2·2 to 7·5 grms. of sulphuric anhydride.

It is therefore certain that large quantities of organic
sulphur-compounds may be found in the human intestinal canal, for with
individuals who suffer from constipation, the residues of the biliary
secretion accumulate for many days. Hence, if the analyst searches for
sulphates in excretal matters, all methods involving destruction of
organic substances, whether by fire or by fluid-oxidising agents, are
wrong in principle, and there is nothing left save to separate soluble
sulphates by dialysis, or to precipitate direct out of an aqueous

Again, sulphate of magnesia is a common medicine, and so is sodic
sulphate; a possible medicinal dose of magnesia sulphate might amount to
56·7 grms. (2 oz.), the more usual dose being half that quantity.
Lastly, among the insane there are found patients who will eat
plaster-of-Paris, earth, and similar matters, so that, in special cases,
a very large amount of combined sulphuric acid may be found in the
intestinal tract, without any relation to poisoning by the free acid;
but in such instances it must be rare, indeed, that surrounding
circumstances or pathological evidence will not give a clue to the real
state of affairs.

II.--Hydrochloric Acid.

§ 68. _General Properties._--Hydrochloric acid, otherwise called
_muriatic acid_, _spirit of salt_, is, in a strictly chemical sense, a
pure gas, composed of 97·26 per cent. of chlorine, and 2·74 per cent. of
hydrogen; but, in an ordinary sense, it is a liquid, being a solution of
the gas itself.

Hydrochloric acid is made on an enormous scale in the United Kingdom,
the production being estimated at about a million tons annually.

The toxicology of hydrochloric acid is modern, for we have no evidence
that anything was known of it prior to the middle of the seventeenth
century, when Glauber prepared it in solution, and, in 1772, Priestley,
by treating common salt with sulphuric acid, isolated the pure gas.

The common liquid hydrochloric acid of commerce has a specific gravity
of from 1·15 to 1·20, and contains usually less than 40 parts of
hydrochloric acid in the 100 parts. The strength of pure samples of
hydrochloric acid can be told by the specific gravity, and a very close
approximation, in default of tables, may be obtained by simply
multiplying the decimal figures of the specific gravity by 200. For
example, an acid of 1·20 gravity would by this rule contain 40 per cent.
of real acid, for ·20 × 200 = 40.

The commercial acid is nearly always a little yellow, from the presence
of iron derived from metallic retorts, and usually contains small
quantities of chloride of arsenic,[84] derived from the sulphuric acid;
but the colourless hydrochloric acid specially made for laboratory and
medicinal use is nearly always pure.

[84] Some samples of hydrochloric acid have been found to contain as
much as 4 per cent. of chloride of arsenic, but this is very unusual.
Glenard found as a mean 2·5 grammes, As₂O₃ per kilogramme.

The uses of the liquid acid are mainly in the production of chlorine, as
a solvent for metals, and for medicinal and chemical purposes. Its
properties are briefly as follows:--

It is a colourless or faintly-yellow acid liquid, the depth of colour
depending on its purity, and especially its freedom from iron. The
liquid is volatile, and can be separated from fixed matters and the less
volatile acids by distillation; it has a strong attraction for water,
and fumes when exposed to the air, from becoming saturated with aqueous
vapour. If exposed to the vapour of ammonia, extremely dense clouds
arise, due to the formation of the solid ammonium chloride. The acid,
boiled with a small quantity of manganese binoxide, evolves chlorine.
Dioxide of lead has a similar action; the chlorine may be detected by
its bleaching action on a piece of paper dipped in indigo blue; a little
zinc foil immersed in the acid disengages hydrogen. These two
tests--viz., the production of chlorine by the one, and the production
of hydrogen by the other--separate and reveal the constituent parts of
the acid. Hydrochloric acid, in common with chlorides, gives a dense
precipitate with silver nitrate. The precipitate is insoluble in nitric
acid, but soluble in ammonia; it melts without decomposition. Exposed to
the light, it becomes of a purple or blackish colour. Every 100 parts of
silver chloride are equal to 25·43 of hydrochloric acid, HCl, and to
63·5 parts of the liquid acid of specific gravity 1·20.

The properties of pure hydrochloric acid gas are as follows:--Specific
gravity 1·262, consisting of equal volumes of hydrogen and chlorine,
united without condensation. 100 cubic inches must therefore have a
weight of 39·36 grains. The gas was liquefied by Faraday by means of a
pressure of 40 atmospheres at 10°; it was colourless, and had a less
refractive index than water.

Water absorbs the gas with avidity, 100 volumes of water absorbing
48,000 volumes of the gas, and becoming 142 volumes. The solution has
all the properties of strong hydrochloric acid, specific gravity 1·21.
The dilute hydrochloric acid of the Pharmacopœia should have a specific
gravity of 1·052, and be equivalent to 10·58 per cent. of HCl.

§69. =Statistics of Poisoning by Hydrochloric Acid.=--The following
tables give the deaths, with age and sex distribution, due to
hydrochloric acid for ten years (1883-92):--

ENDING 1892.

                        ACCIDENT OR NEGLIGENCE.

  Ages,     Under   1-5   5-15   15-25   25-65   65 and    Total
              1                                  above
  Males,       1    16      2      ...     26       3        48
  Females,   ...     8    ...      ...      9       1        18
  Totals,      1    24      2      ...     35       4        66


  Ages,                   5-15   15-25   25-65   65 and    Total
  Males,                  ...       2      73       8        83
  Females,                  1       8      42      65       116
  Totals,                   1      10     115      73       199

In 1889 a solitary case of the murder of a child is on record from
hydrochloric acid; hence, with that addition, the total deaths from
hydrochloric acid amount to 266 in the ten years, or about 26 a year.

§ 70. =Fatal Dose.=--The dose which destroys life is not known with any
accuracy. In two cases, adults have been killed by 14 grms. (half an
ounce) of the commercial acid; but, on the other hand, recovery is
recorded when more than double this quantity has been taken. A girl,
fifteen years of age, died from drinking a teaspoonful of the acid.[85]

[85] _Brit. Med. Journ._, March, 1871.

§ 71. =Amount of Free Acid in the Gastric Juice.=--Hydrochloric acid
exists in the gastric juice. This was first ascertained by Prout[86] in
1824; he separated it by distillation. The observation was afterwards
confirmed by Gmelin,[87] Children,[88] and Braconnot.[89] On the other
hand, Lehmann[90] pointed out that, as the stomach secretion contained,
without doubt, lactic acid, the act of distillation, in the presence of
this lactic acid, would set free hydrochloric acid from any alkaline
chlorides. Blondlot and Cl. Bernard also showed that the gastric juice
possessed no acid which would dissolve oxalate of lime, or develop
hydrogen when treated with iron filings; hence there could not be free
hydrochloric acid which, even in a diluted state, would respond to both
these tests. Then followed the researches of C. Schmidt,[91] who showed
that the gastric secretion of men, of sheep, and of dogs contained more
hydrochloric acid than would satisfy the bases present; and he
propounded the view that the gastric juice does not contain absolutely
free hydrochloric acid, but that it is in loose combination with the

[86] _Philosophical Transactions_, 1824, p. 45.

[87] P. Tiedmann and L. Gmelin, _Die Verdauung nach Versuchen_,
Heidelberg u. Leipsic, 1826, i.

[88] _Annals of Philosophy_, July, 1824.

[89] _Ann. de Chim._ t. lix. p. 348.

[90] _Journal f. prakt. Chemie_, Bd. xl. 47.

[91] Bidder u. Schmidt, _Verdauungs-Säfte_, &c.

The amount of acid in the stomach varies from moment to moment, and
therefore it is not possible to say what the average acidity of gastric
juice is. It has been shown that in the total absence of _free_
hydrochloric acid digestion may take place, because hydrochloric acid
forms a compound with pepsin which acts as a solvent on the food. The
amount of physiologically active acid varies with the food taken. It is
smallest when carbohydrates are consumed, greatest with meat. The
maximum amount that Jaksch found in his researches, when meat was
ingested, was ·09 per cent. of hydrochloric acid. It is probable that
anything above 0·2 per cent. of hydrochloric acid is either abnormal or
owing to the recent ingestion of hydrochloric acid.

§ 72. =Influence of Hydrochloric Acid on Vegetation.=--Hydrochloric acid
fumes, if emitted from works on a large scale, injure vegetation much.
In former years, before any legal obligations were placed upon
manufacturers for the condensing of the volatile products, the nuisance
from this cause was great. In 1823, the duty on salt being repealed by
the Government, an extraordinary impetus was given to the manufacture of
hydrochloric acid, and since all the volatile products at that time
escaped through short chimneys into the air, a considerable area of land
round the works was rendered quite unfit for growing plants. The present
law on the subject is, that the maximum quantity of acid escaping shall
not exceed 2 grains per cubic foot of the air, smoke, or chimney gases;
and, according to the reports of the alkali inspectors, the condensation
by the improved appliances is well within the Act, and about as perfect
as can be devised.

It appears from the reports of the Belgian Commission in 1855, when
virtually no precautions were taken, that the gases are liable to injure
vegetation to the extent of 2000 metres (2187 yards) around any active
works; the more watery vapour the air contains, the quicker is the gas
precipitated and carried to the earth. If the action of the vapour is
considerable, the leaves of plants dry and wither; the chlorophyll
becomes modified, and no longer gives the normal spectrum, while a
thickening of the rind of trees has also been noticed. The cereals
suffer much; they increase in stalk, but produce little grain. The
leguminosæ become spotted, and have an air of dryness and want of
vigour; while the potato, among plants utilised for food, appears to
have the strongest resistance. Vines are very sensitive to the gas.
Among trees, the alder seems most sensitive; then come fruit-trees, and
last, the hardy forest-trees--the poplar, the ash, the lime, the elm,
the maple, the birch, and the oak.[92]

[92] Those who desire to study more closely the effect of acids
generally on vegetation may consult the various papers of the alkali
inspectors contained in the Local Government Reports. See also
Schubarth, _Die saueren Gase, welche Schwefelsäure- und Soda-Fabriken
verbreiten_. _Verhandlungen des Vereins zur Beförderung des
Gewerbefleisses in Preussen_, 1857, S. 135. Dingler’s _Journal_, Bd.
145, S. 374-427.

Christel, _Ueber die Einwirkung von Säuren-Dämpfen auf die Vegetation_.

_Arch. f. Pharmacie_, 1871, p. 252.

_Vierteljahrsschrift für gerichtliche Medicin_, 17 Bd. S. 404, 1872.

§73. =Action upon Cloth and Manufactured Articles.=--On black cloth the
acid produces a green stain, which is not moist and shows no corrosion.
On most matters the stain is more or less reddish; after a little time
no free acid may be detected, by simply moistening the spot; but if the
stain is cut out and boiled with water, there may be some evidence of
free acid. The absence of moisture and corrosion distinguishes the stain
from that produced by sulphuric acid.

§74. =Poisonous Effects of Hydrochloric Acid Gas.=--Eulenberg[93] has
studied the effects of the vapour of this acid on rabbits and pigeons.
One of these experiments may be cited in detail. Hydrochloric acid gas,
prepared by heating together common salt and sulphuric acid, was passed
into a glass shade supported on a plate, and a rabbit was placed in the
transparent chamber thus formed. On the entrance of the vapour, there
was immediate blinking of the eyes, rubbing of the paws against the
nostrils, and emission of white fumes with the expired breath, while the
respiration was irregular (40 to the minute). After the lapse of ten
minutes, the gas was again introduced, until the atmosphere was quite
thick; the symptoms were similar to those detailed above, but more
violent; and in fourteen minutes from the commencement, the rabbit sank
down on its right side (respirations 32). When twenty-two minutes had
elapsed, the gas was again allowed to enter. The rabbit now lay quiet,
with closed eyes and laboured respiration, and, finally, after
half-an-hour of intermittent exposure to the gas, the animal was

[93] _Gewerbe Hygiene_, Berlin, 1876, S. 51.

The cornea were opalescent, and the eyes filled with water; there was
frequent shaking of the head and working of the forepaws. After three
minutes’ exposure to the air, the respirations were found to be 128 per
minute; this quickened respiration lasted for an hour, then gave place
to a shorter and more superficial breathing. On the second day after the
experiment, the rabbit suffered from laboured respiration (28 to the
minute) and pain, and there was a rattling in the bronchial tubes. The
animal died on the third day, death being preceded by slow respiration
(12 to the minute).

The appearances twenty-four hours after death were as follows:--The eyes
were coated with a thick slime, and both cornea were opalescent; there
was strong rigidity of the body. The pia mater covering the brain was
everywhere hyperæmic, and at the hinder border of both hemispheres
appeared a small clot, surrounded by a thin layer of bloody fluid. The
_plex. venos spin._ was filled with coagulated blood, and there was also
a thin extravasation of blood covering the medulla and pons. The lungs
were mottled bright brown-red; the middle lobe of the right lung was
dark brown, solid, and sank in water; the lower lobe of the same lung
and the upper lobe of the left lung were nearly in a similar condition,
but the edges were of a bright red. The parenchyma in the darker places
on section did not crepitate. On the cut surface was a little dark,
fluid, weakly-acid blood; the tracheal mucous membrane was injected. The
heart was filled with thick coagulated blood; the liver was congested,
of a reddish-brown colour, and rich in dark, fluid blood: in the vena
cava inferior was coagulated blood. The kidneys were not hyperæmic; the
intestines were superficially congested.

I think there can be little doubt that the symptoms during life, and the
appearances after death, in this case are perfectly consistent with the
following view:--The vapour acts first as a direct irritant, and is
capable of exciting inflammation in the lung and bronchial tissues; but
besides this, there is a secondary effect, only occurring when the gas
is in sufficient quantity, and the action sufficiently prolonged--viz.,
a direct coagulation of the blood in certain points of the living
vessels of the lungs. The consequence of this is a more or less general
backward engorgement, the right side of the heart becomes distended with
blood, and the ultimate cause of death is partly mechanical. The
hyperæmia of the brain membranes, and even the hæmorrhages, are quite
consistent with this view, and occur in cases where the obstruction to
the circulation is of a coarser and more obvious character, and can
therefore be better appreciated.

§ 75. =Effects of the Liquid Acid.=--There is one distinction between
poisoning by hydrochloric and the other mineral acids--namely, the
absence of corrosion of the skin. Ad. Lesser[94] has established, by
direct experiment, that it is not possible to make any permanent mark on
the skin by the application even of the strongest commercial acid (40
per cent.). Hence, in any case of suspected poisoning by acid, should
there be stains on the lips and face as from an acid, the presumption
will be rather against hydrochloric. The symptoms themselves differ very
little from those produced by sulphuric acid. The pathological
appearances also are not essentially different, but hydrochloric is a
weaker acid, and the extensive disorganisation, solution, and
perforation of the viscera, noticed occasionally with sulphuric acid,
have never been found in hydrochloric acid poisoning. We may quote here
the following case:--

[94] Virchow’s _Archiv f. path. Anat._, Bd. 83, Hft. 2, S. 215, 1881.

A woman, under the influence of great and sudden grief--not unmixed with
passion--drew a bottle from her pocket, and emptied it very quickly. She
immediately uttered a cry, writhed, and vomited a yellow-green fluid.
The abdomen also became enlarged. Milk was given her, but she could not
swallow it, and death took place, in convulsions, two hours after the
drinking of the poison.

The _post-mortem_ appearances were briefly as follows:--Mouth and tongue
free from textural change: much gas in the abdomen, more especially in
the stomach; the membranes of the brain congested; the lungs filled with
blood. The stomach was strongly pressed forward, of a dark brown-red,
and exhibited many irregular blackish spots, varying from two lines to
half an inch in diameter (the spots were drier and harder than the rest
of the stomach); the mucous membrane, internally, was generally
blackened, and changed to a carbonised, shaggy, slimy mass, while the
organ was filled with a blackish homogeneous pulp, which had no odour.
The gullet was also blackened. A considerable quantity of hydrochloric
acid was separated from the stomach.[95]

[95] _Preuss. Med. Vereinszeit. u. Friederichs Blätter f. gerichtl.
Anthropologie_, 1858, Hft. 6, S. 70.

The termination in this instance was unusually rapid. In a case detailed
by Casper,[96] in which a boy drank an unknown quantity of acid, death
took place in seven hours. In Guy’s Hospital museum, the duodenum and
stomach are preserved of a patient who is said to have died in nine and
a half hours from half an ounce of the acid. The same quantity, in a
case related by Taylor, caused death in eighteen hours. From these and
other instances, it may be presumed that death from acute poisoning by
hydrochloric acid will probably take place within twenty-four hours.
From the secondary effects, of course, death may take place at a remote
period, _e.g._, in a case recorded by Dr. Duncan (_Lancet_, April 12,
1890), a man drank about 1 oz. of HCl accidentally, was admitted to
Charing Cross Hospital the same day, and treated with small quantities
of sodium carbonate, and fed by the rectum. On the eighth day he brought
up 34 oz. of blood; in a month he left apparently perfectly well, but
was admitted again in about six weeks, and died of contraction of the
stomach and stricture of the pylorus on the ninety-fourth day.

[96] Case 230.--_Gerichtliche Medicin_, 6th Ed., Berlin, 1876.

§76. =Post-mortem Appearances.=--The pathological appearances are very
similar to those found in the case already detailed; though the skin of
the face may not be eroded in any way by the acid, yet the more delicate
mucous membrane of the mouth, gullet, &c., appears mostly to be changed,
and is usually white or whitish-brown. There is, however, in the museum
of the Royal College of Surgeons the stomach and gullet (No. 2386c.) of
an infant thirteen months old; the infant drank a tea-cupful of strong
hydrochloric acid, and died nine hours after the dose. The pharynx and
the upper end of the gullet is quite normal, the corrosive action
commencing at the lower end, so that, although the acid was
concentrated, not the slightest effect was produced on the delicate
mucous membrane of the throat and upper part of the gullet. The lower
end of the gullet and the whole of the stomach were intensely congested;
the rugæ of the latter were ecchymosed and blackened by the action of
the acid. There were also small hæmorrhages in the lungs, which were
ascribed to the action of the acid on the blood. Perforation of the
stomach has not been noticed in hydrochloric acid poisoning.

In Guy’s Hospital museum (prep. 1799¹⁰), the stomach and duodenum of the
case mentioned exhibit the mucous membrane considerably injected, with
extravasations of blood, which, at the time when the preparation was
first arranged, were of various hues, but are now somewhat altered,
through long keeping in spirit. In St. George’s Hospital museum (ser. x.
43, d. 200) are preserved the stomach and part of the duodenum of a
person who died from hydrochloric acid. The case is detailed in the
_Medical Times and Gazette_ for 1853, vol. ii. p. 513. The whole inner
surface appears to be in a sloughing state, and the larynx and lung were
also inflamed.

A preparation, presented by Mr. Bowman to King’s College Hospital
museum, exhibits the effects of a very large dose of hydrochloric acid.
The gullet has a shrivelled and worm-eaten appearance; the stomach is
injected with black blood, and was filled with an acid, grumous

[97] A drawing of parts of the gullet and stomach is given in Guy and
Ferrier’s _Forensic Medicine_.

Looking at these and other museum preparations illustrating the effects
of sulphuric and hydrochloric acids, I was unable (in default of the
history of the cases) to distinguish between the two, by the naked eye
appearances, save in those cases in which the disorganisation was so
excessive as to render hydrochloric acid improbable. On the other hand,
the changes produced by nitric acid are so distinctive, that it is
impossible to mistake its action for that of any other acid. The nitric
acid pathological preparations may be picked out at a glance.

Detection and Estimation of Free Hydrochloric Acid.

§ 77. (1) =Detection.=--A large number of colouring reagents have been
proposed as tests for the presence of free mineral acid; among the best
is _methyl-aniline violet_ decolorised by a large amount of hydrochloric
acid; the violet turns to green with a moderate quantity, and to blue
with a small quantity.

=Tropæolin= (00), in the presence of free mineral acid, strikes a
ruby-red to a dark brown-red.

=Congo-red= is used in the form of paper dyed with the material; large
amounts of free hydrochloric acid strike blue-black, small quantities

=Günzburg’s test= is 2 parts phloroglucin and 1 part vanillin, dissolved
in 100 parts of alcohol. Fine red crystals are precipitated on the
addition of hydrochloric acid. To test the stomach contents for free
hydrochloric acid by means of this reagent, equal parts of the fluid and
the test are evaporated to dryness in the water-bath in a porcelain
dish. If free hydrochloric acid be present, the evaporated residue shows
a red colour; 1 mgrm. of acid can by this test be detected. The reaction
is not interfered with by organic acids, peptones, or albumin.

Jaksch speaks highly of _benzopurpurin_ as a test. Filter-paper is
soaked in a saturated aqueous solution of benzopurpurin 6 B (the variety
1 or 4 B is not so sensitive), and the filter-paper thus prepared
allowed to dry. On testing the contents of the stomach with the reagent,
if there is more than 4 parts per 1000 of hydrochloric acid the paper is
stained intensely blue-black; but if the colour is brown-black, this is
from butyric or lactic acids, or from a mixture of these acids with
hydrochloric acid. If the paper is washed with pure ether, and the
colour was due only to organic acids, the original hue of the paper is
restored; if the colour produced was due to a mixture of mineral and
organic acids, the brown-black colour is weakened; and, lastly, if due
to hydrochloric acid alone, the colour is not altered by washing with
ether. Acid salts have no action, nor is the test interfered with by
large amounts of albumins and peptones.

A. Villiers and M. Favolle[98] have published a sensitive test for
hydrochloric acid. The test consists of a saturated aqueous solution of
colourless aniline, 4 parts; glacial acetic acid, 1 part; 0·1 mgrm. of
hydrochloric acid strikes with this reagent a blue colour, 1 mgrm. a
black colour. The liquid under examination is brought by evaporation, or
by the addition of water, to 10 c.c. and placed in a flask; to this is
added 5 c.c. of a mixture of equal parts of sulphuric acid and water,
then 10 c.c. of a saturated solution of potassic permanganate, and
heated gently, conveying the gases into 3 to 5 c.c. of the reagent
contained in a test-tube immersed in water. If, however, bromine or
iodine (one or both) should be present, the process is modified as
follows:--The hydracids are precipitated by silver nitrate; the
precipitate is washed, transferred to a small flask, and treated with 10
c.c. of water and 1 c.c. of pure ammonia. With this strength of ammonia
the chloride of silver is dissolved easily, the iodide not at all, and
the bromide but slightly. The ammoniacal solution is filtered, boiled,
and treated with SH₂; the excess of SH₂ is expelled by boiling, the
liquid filtered, reduced to 10 c.c. by boiling or evaporation,
sulphuric acid and permanganate added as before, and the gases passed
into the aniline. The process is inapplicable to the detection of
chlorides or hydrochloric acid if cyanides are present, and it is more
adapted for traces of hydrochloric acid than for the quantities likely
to be met with in a toxicological inquiry.

[98] _Comptes Rend._, cxviii.

(2) =Quantitative estimation of Free Hydrochloric Acid.=--The contents
of the stomach are diluted to a known volume, say 250 or 500 c.c. A
fractional portion is taken, say 10 c.c., coloured with litmus or
phenol-phthalein, and a decinormal solution of soda added drop by drop
until the colour changes; this gives total acidity. Another 10 c.c. is
shaken with double its volume of ether three times, the fluid separated
from ether and titrated in the same way; this last titration will give
the acidity due to mineral acids and acid salts;[99] if the only mineral
acid present is hydrochloric acid the results will be near the truth if
reckoned as such, and this method, although not exact for physiological
research, is usually sufficient for the purpose of ascertaining the
amount of hydrochloric acid or other mineral acids in a case of
poisoning. It depends on the fact that ether extracts free organic
acids, such as butyric and lactic acids, but does not extract mineral

[99] To distinguish between acidity due to free acid and acid salts, or
to acidity due to the combined action of acid salts and free acids, the
method of Leo and Uffelmann is useful. A fractional portion of the
contents of the stomach is triturated with pure calcium carbonate; if
all the acidity is due to free acid, the fluid in a short time becomes
neutral to litmus; if, on the other hand, the acidity is due entirely to
acid salts, the fluid remains acid; or, if due to both acid and acid
salts, there is a proportionate diminution of acidity due to the
decomposition of the lime carbonate by the free acid. A quantitative
method has been devised upon these principles. See Leo, _Diagnostik der
Krankheiten der Verdauungsorgane_, Hirschwald, Berlin, 1890.

The free mineral acid, after extracting the organic acid by ether, can
also be saturated with cinchonine; this hydrochlorate of cinchonine is
extracted by chloroform, evaporated to dryness, and the residue
dissolved in water acidified by nitric acid and precipitated by silver
nitrate; the silver chloride produced is collected on a small filter,
washed, and the filter, with its contents, dried and ignited in a
porcelain crucible; the silver chloride, multiplied by 0·25426, equals

The best method of estimating free hydrochloric acid in the stomach is
that of Sjokvist as modified by v. Jaksch;[100] it has the disadvantage
of its accuracy being interfered with by phosphates; it also does not
distinguish between actual free HCl and the loosely bound HCl with
albuminous matters,--this in a toxicological case is of small
importance, because the quantities of HCl found are likely to be large.

[100] _Klinische Diagnostik_, Dr. Rudolph v. Jaksch, Wien u. Leipzig,
1892. _Clinical Diagnosis_. English Translation, by Dr. Cagney. Second
Edition. London: Charles Griffin & Co., Limited.

The method is based upon the fact that if carbonate of baryta be added
to the contents of the stomach, the organic acids will decompose the
barium carbonate, forming butyrate, acetate, lactate, &c., of barium;
and the mineral acids, such as hydrochloric acid, will combine, forming
salts of barium.

On ignition, chloride of barium will be unaffected, while the organic
salts of barium will be converted into carbonate of barium, practically
insoluble in carbonic acid free water.

The contents of the stomach are coloured with litmus, and barium
carbonate added until the fluid is no longer acid (as shown by the
disappearance of the red colour); then the contents are evaporated to
dryness in a platinum dish, and ignited at a dull red heat; complete
burning to an ash is not necessary. After cooling, the burnt mass is
repeatedly exhausted with boiling water and filtered; the chloride of
barium is precipitated from the filtrate by means of dilute sulphuric
acid; the barium sulphate filtered off, washed, dried, and, after
ignition, weighed; 233 parts of barium sulphate equal 73 parts of HCl.

A method somewhat quicker, but depending on the same principles, has
been suggested by Braun.[101] A fractional part, say 10 c.c., of the
fluid contents is coloured by litmus and titrated with decinormal soda.
To the same quantity is added 2 or 3 more c.c. of decinormal soda than
the quantity used in the first titration; this alkaline liquid is
evaporated to dryness and ultimately ignited. To the ash is now added
exactly the quantity of decinormal sulphuric acid as the decinormal soda
last used to make it alkaline--that is to say, if the total acidity was
equal to 3·6 d.n. soda, and 5·0 d.n. soda was added to the 10 c.c.
evaporated to dryness and burned, then 5·6 c.c. of d.n. sulphuric acid
is added to the ash. The solution is now warmed to get rid of carbon
dioxide, and, after addition of a little phenolphthalein, titrated with
d.n. soda solution until the change of colour shows saturation, the
number of c.c. used, multiplied by 0·00365, equals the HCl.

[101] _Op. cit._, S. 157.

§78. In investigating the stains from hydrochloric acid on fabrics, or
the leaves of plants, any free hydrochloric acid may be separated by
boiling with water, and then investigating the aqueous extract. Should,
however, the stain be old, all free acid may have disappeared, and yet
some of the chlorine remain in organic combination with the tissue, or
in combination with bases. Dr. Angus Smith has found weighed portions of
leaves, &c., which had been exposed to the action of hydrochloric acid
fumes, richer in chlorides than similar parts of the plants not thus

The most accurate method of investigation for the purpose of separating
chlorine from combination with organic matters is to cut out the
stained portions, weigh them, and burn them up in a combustion-tube,
the front portion of the tube being filled with caustic lime known to be
free from chlorides; a similar experiment must be made with the
unstained portions. In this way a considerable difference may often be
found; and it is not impossible, in some instances, to thus detect,
after the lapse of many years, that certain stains have been produced by
a chlorine-holding substance.

III.--Nitric Acid.

§ 79. =General Properties.=--Nitric acid--commonly known in England as
_aqua fortis_, chemically as _nitric acid_, _hydric nitrate_, or _nitric
monohydrate_--is a mono-hydrate of nitrogen pentoxide (N₂O₅), two
equivalents, or 126 parts, of nitric acid containing 108 of N₂O₅, and 18
of H₂O. Anhydrous nitric acid, or nitrogen pentoxide, can be obtained by
passing, with special precautions, dry chlorine over silver nitrate; the
products are free oxygen and nitrogen pentoxide, according to the
following equation:--

   Silver    Chlorine.    Silver      Nitrogen    Oxygen.
  Nitrate.               Chloride.   Pentoxide.
  Ag₂O,N₂O₅ +   2Cl     =   2AgCl   +   N₂O₅      +   O

By surrounding the receiver with a freezing mixture, the acid is
condensed in crystals, which dissolve in water, with emission of much
heat, forming nitric acid. Sometimes the crystals, though kept in sealed
tubes, decompose, and the tube, from the pressure of the liberated
gases, bursts with a dangerous explosion.

Pure nitric acid has a specific gravity of 1·52, and boils at 98°. Dr.
Ure examined the boiling point and other properties of nitric acid very
fully. An acid of 1·5 specific gravity boils at 98·8°; of specific
gravity 1·45, at 115·5°; specific gravity 1·40, at 118·8°; of specific
gravity 1·42, at 122·8°. The acid of specific gravity 1·42 is the
standard acid of the British Pharmacopœia. It can always be obtained by
distilling either strong or moderately weak nitric acid; for, on the one
hand, the acid on distillation gets weaker until the gravity of 1·42 is
reached, or, on the other, it becomes stronger.

There is little doubt that acid of 1·42 gravity is a definite hydrate,
consisting of 1 atom of dry acid and 4 atoms of water; it corresponds to
75 per cent.[102] of the liquid acid HNO₃. There are also at least two
other hydrates known--one an acid of 1·485 specific gravity,
corresponding to 1 atom of dry acid and 2 of water, and an acid of
specific gravity 1·334, corresponding to 1 atom of dry acid and 7 atoms
of water.

[102] The British Pharmacopœia states that the 1·42 acid equals 70 per
cent. of HNO₃; but this is not in accordance with Ure’s Tables, nor with
the facts.

In Germany the officinal acid is of 1·185 specific gravity,
corresponding to about 30 per cent. of HNO₃. The dilute nitric acid of
the Pharmacopœia is a colourless liquid, of specific gravity 1·101, and
should contain about 17·4 per cent. of acid. The acids used in various
industries are known respectively as _dyers’_ and _engravers’_ acid.
_Dyers’_ acid has a specific gravity of 1·33 to 1·34 (66° to 68° Twad.),
that is, strength from 56 to 58 per cent. of HNO₃. _Engravers’_ acid is
stronger; being of 1·40 specific gravity (80° Twad.); and contains 70
per cent. of HNO₃. Although the _pure_ acid of commerce is (and should
be) almost colourless, most commercial specimens are of hues from yellow
up to deep red. An acid saturated with red oxides of nitrogen is often
known as “fuming nitric acid.”

§ 80. =Use in the Arts.=--Nitric acid is employed very extensively in
the arts and manufactures. The dyer uses it as a solvent for tin in the
preparation of valuable mordants for calico and other fabrics; the
engraver uses it for etching copper. It is an indispensable agent in the
manufacture of gun-cotton, nitro-glycerin, picric acid, and sulphuric
acid; it is also used in the manufacture of tallow, in preparing the
felt for hats, and in the gilding trades. It is said to be utilised to
make yellowish or fawn-coloured spots on cigar leaves, so as to give
them the appearance of age and quality. It is also used as a medicine.

§ 81. =Statistics of Poisoning by Nitric Acid.=--In the ten years
1883-1892 no case of murder was ascribed to nitric acid, but it caused
accidentally 25 deaths, and was used in 27 cases of suicide.

The following tables give the age and sex distribution of these



  Ages,      1-5  5-15  15-25  25-65  65 and  Total
  Males,      6     2      1      9    ...      18
  Females,    3   ...    ...      4    ...       7
  Totals,     9     2      1     13    ...      25


  Ages,                 15-25  25-65  65 and  Total
  Males,                   3     14      1      18
  Females,                 1      8    ...       9
  Totals,                  4     22      1      27

§ 82. =Fatal Dose.=--The dose which causes death has not been
ascertained with any exactness. As in the case of sulphuric acid, we may
go so far as to say that it is possible for a few drops of the strong
acid to be fatal, for if brought into contact with the vocal apparatus,
fatal spasm of the glottis might be excited. The smallest dose on record
is 7·7 grms. (2 drachms), which killed a child aged 13.

§ 83. =Action of Nitric Acid on Vegetation.=--Nitric acid acts on plants
injuriously in a two-fold manner--viz., by direct corrosive action, and
also by decomposing the chlorides which all plants contain, thus setting
free chlorine, which decomposes and bleaches the chlorophyll. The action
is most intense on soft and delicate leaves, such as those of clover,
the cabbage, and all the cruciferæ. The tobacco plant is particularly
injured by nitric acid. Next to all herbaceous plants, trees, such as
the apple, pear, and fruit trees, generally suffer. The coniferæ,
whether from their impregnation with resin, or from some other cause,
possess a considerable resisting-power against nitric acid vapours, and
the same is true as regards the cereals; in the latter case, their
siliceous armour acts as a preserving agent.

§ 84. =Nitric Acid Vapour.=--The action of nitric acid in a state of
vapour, as evolved by warming potassic nitrate and sulphuric acid
together, has been studied by Eulenberg. A rabbit was placed under a
shade into which 63 grains of nitric acid in a state of vapour were
introduced. From the conditions of the experiment, some nitric peroxide
must also have been present. Irritation of the external mucous membranes
and embarrassment in breathing were observed. The animal in forty-five
minutes was removed, and suffered afterwards from a croupous bronchitis,
from which, however, it completely recovered in eleven days. A second
experiment with the same animal was followed by death. On inspection,
there was found strong injection of the cerebral membranes, with small
extravasations of blood; the lungs were excessively congested; the right
middle lobe especially was of a liver-brown colour, and empty of air: it
sank in water.

O. Lassar[103] has also made a series of researches on the influence of
nitric acid vapour, from which he concludes that the acid is not
absorbed by the blood, but acts only by its mechanical irritation, for
he could not trace, by means of an examination of the urine, any
evidence of such absorption.

[103] Hoppe-Seyler’s _Zeitschrift f. physiol. Chemie_, Bd. i. S.
165-173, 1877-78.

There are a few instances on record of the vapour having been fatal to
men; for example, the well-known case of Mr. Haywood, a chemist of
Sheffield, may be cited. In pouring a mixture of nitric and sulphuric
acids from a carboy of sixty pounds capacity, the vessel broke, and for
a few minutes he inhaled the mixed fumes. He died eleven hours after
the accident, although for the first three hours there were scarcely any
symptoms of an injurious effect having been produced. On inspection,
there was found intense congestion of the windpipe and bronchial tubes,
with effusion of blood in the latter. The lining membrane of the heart
and aorta was inflamed; unfortunately, the larynx was not examined.[104]

[104] _Lancet_, April 15, 1854, p. 430.

A very similar case happened in Edinburgh in 1863.[105] Two young men
were carrying a jar of nitric acid; the jar broke, and they attempted to
wipe up the acid from the floor. The one died ten hours after the
accident, the other in less than twenty-four hours. The symptoms were
mainly those of difficult breathing, and it is probable that death was
produced from suffocation. Dr. Taylor relates also, that having
accidentally inhaled the vapour in preparing gun-cotton, he suffered
from severe constriction of the throat, tightness in the chest, and
cough, for more than a week.[106]

[105] _Chemical News_, March 14, 1863, p. 132.

[106] _Principles and Practice of Medical Jurisprudence_, vol. i., 1873,
p. 218.

§ 85. =Effects of Liquid Nitric Acid.=--Poisoning by nitric acid, though
still rare, is naturally more frequent than formerly. At the beginning
of this century, Tartra[107] wrote a most excellent monograph on the
subject, and collated all the cases he could find, from the first
recorded instances related by Bembo[108] in Venetian history, down to
his own time. The number of deaths in those 400 years was but
fifty-five, while, in our century, at least fifty can be numbered. Most
of these (74 per cent.) are suicidal, a very few homicidal, the rest
accidental. In one of Tartra’s cases, some nitric acid was placed in the
wine of a drunken woman, with fatal effect. Osenbrüggen[109] relates the
case of a father murdering his six children by means of nitric acid; and
C. A. Büchner[110] that of a soldier who poured acid into the mouth of
his illegitimate infant. A curious case is one in which a man poisoned
his drunken wife by pouring the acid into her right ear; she died after
six weeks’ illness. All these instances prove again, if necessary, that
the acid is only likely to be used with murderous intent in the case of
young children, or of sleeping, drunken, or otherwise helpless people.

[107] Tartra, A. E., Dr., _Traité de l’Empoisonnement par l’Acide
Nitrique_, Paris, An. 10 (1802), pp. 300.

[108] _Bembo Cardinalis, Rerum Venetarium Historiæ_, lib. xii., lib. i.
p. 12, Paris Ed., 1551.

[109] _Allgem.-Deutsche Strafrechtszeitung, herausgeg. v. Frz. v.
Holtzendorff_, 5 Jahrg., 1865, Hft. 5, S. 273.

[110] Friederich’s _Blätter f. ger. Med._, 1866, Hft. 3, S. 187.

As an example of the way in which accidents are brought about by
heedlessness, may be cited the recent case of a woman who bought a small
quantity of aqua fortis for the purpose of allaying toothache by a
local application. She attempted to pour the acid direct from the bottle
into the cavity of the tooth; the acid went down her throat, and the
usual symptoms followed. She threw up a very perfect cast of the gullet
(preserved in University College museum), and rapidly died. Nitric acid
has been mistaken for various liquids, and has also been used by
injection as an abortive, in every respect having a toxicological
history similar to that of sulphuric acid.

§ 86. =Local Action.=--When strong nitric acid comes in contact with
organic matters, there is almost constantly a development of gas. The
tissue is first bleached, and then becomes of a more or less intense
yellow colour. Nitric acid spots on the skin are not removed by ammonia,
but become of an orange-red when moistened with potash and a solution of
cyanide of potassium. The yellow colour seems to show that picric acid
is one of the constant products of the reaction; sulphide of ammonium
forms a sort of soap with the epidermis thus attacked, and detaches it.

§ 87. =Symptoms.=--The symptoms and course of nitric acid poisoning
differ in a few details only from those of sulphuric acid. There is the
same instant pain and frequent vomiting, destruction of the mucous
membranes, and, in the less severe cases, after-contraction of the
gullet, &c.

One of the differences in the action of nitric and sulphuric acids is
the constant development of gas with the former. This, without doubt,
adds to the suffering. Tartra made several experiments on dead bodies,
and showed that very considerable distension of the intestinal canal, by
gaseous products, was the constant result; the tissues were corroded and
almost dissolved, being transformed, ultimately, into a sort of greasy
paste. The vomited matters are of a yellow colour, unless mixed with
blood, when they are of a dirty-brown hue, with shreds of yellow mucus,
and have the strong acid reaction and smell of nitric acid. The teeth
may be partially attacked from the solvent action of the acid on the
enamel. The fauces and tongue, at first blanched, soon acquire a
citron-yellow, or even a brown colour; the whole cavity may swell and
inflame, rendering the swallowing of liquids difficult, painful, and
sometimes impossible. The air passages may also become affected, and in
one case tracheotomy was performed for the relief of the breathing.[111]
The stomach rejects all remedies; there are symptoms of collapse; quick,
weak pulse, frequent shivering, obstinate constipation, and death (often
preceded by a kind of stupor) in from eighteen to twenty-four hours. The
intellectual faculties remain clear, save in a few rare instances.

[111] Arnott, _Med. Gaz._, vol. xii. p. 220.

C. A. Wunderlich has recorded an unusual case, in which the symptoms
were those of dysentery, and the large intestine was found acutely
inflamed, while the small one was little affected. The kidneys had the
same appearance as in Bright’s disease.[112] The smallest fatal dose
given by Taylor is from 2 drachms, which killed a child aged 13 years.
Should the dose of nitric acid be insufficient to kill at once, or, what
amounts to the same thing, should the acid be immediately diluted with
water, or in some way be neutralised, the patient, as in the case of
sulphuric acid, may yet die at a variable future time from stenosis of
the gullet, impaired digestion, &c. For example, in an interesting case
related by Tartra,[113] a woman, who had swallowed 42 grms. (1·5 oz.) of
nitric acid, feeling acute pain, took immediately a quantity of water,
and three hours afterwards was admitted into hospital, where she
received appropriate treatment. At the end of a month she left,
believing herself cured; but in a little while returned, and was
re-admitted, suffering from marasmus, extreme weakness, and constant
vomiting; ultimately she died. The _post-mortem_ examination revealed
extreme contraction of the intestinal canal throughout. The lumen would
hardly admit a penholder. The stomach was no larger than an ordinary
intestine, and adherent to adjacent organs; on its internal surface
there were spots, probably cicatrices; there were also changes in the
gullet, but not so marked. A somewhat similar case is related by the
same author in his thirteenth observation. In the Middlesex Hospital
there is preserved the stomach (No. 1363) of a man who died forty days
after swallowing 2 ozs. of nitric acid diluted in a tumbler of water.
The stomach is contracted, the mucous membrane of the lower part of the
gullet, the lesser curvature, and the pyloric end of the stomach is
extensively corroded, showing ulcerated patches commencing to cicatrize.

[112] _De Actionibus quibusdam Acidi Nitrici Caustico in Corpus Humanum
immissi. Programma Academ._, Lipsiæ, 1857, 4.

[113] _Op. cit._

§ 88. =Post-mortem Appearances.=--The pathological changes in the
tongue, gullet, and stomach can be readily studied from the preparations
in the different museums. The staining by the nitric acid appears
unchanged to the naked eye for many years; hence, most of the nitric
acid preparations are in an excellent state of preservation. A very good
example of the pathological changes is to be found in Nos. 1049 and
1050, University College museum.

    No. 1049 presents the tongue, pharynx, and larynx of a man who had
    swallowed a tea-cupful of nitric acid. The epithelium of the
    œsophagus is for the most part wanting, and hangs in shreds; the
    dorsum of the tongue, in front of the circumvallate papillæ, is
    excavated, and over its central part superficially ulcerated; in
    other places the tongue is encrusted with a thick, loose,
    fawn-coloured layer, formed probably of desquamated epithelium. The
    whole of the mucous surface is stained of a dirty yellow.

    No. 1050 is a preparation showing the tongue, gullet, and stomach of
    a person who died from the effects of nitric acid. The tongue in
    places is smooth and glazed; in others, slightly depressed and
    excavated. On the anterior wall and lower portion of the gullet two
    large sloughs exist.

    Although perforation of the stomach is not so common with nitric as
    with sulphuric acid, such an accident may occur, as shown in a
    preparation at Guy’s Hospital, in which there is a perforation at
    the cardiac end. All the mucous membrane has disappeared, and the
    inner surface is for the most part covered with flocculent shreds.
    Three ounces of nitric acid are said to have been swallowed, and the
    patient lived seventeen hours. There is the usual staining. There is
    also in the Middlesex Hospital (No. 1364) the œsophagus and stomach
    of a woman aged 30, who died six hours after swallowing 2 to 3 ozs.
    of strong nitric acid. The inner coats of the mucous membrane of the
    gullet and stomach are in part converted into opaque yellow and
    black eschars, and in part to a shreddy pulpy condition. At the most
    depending part of the stomach is a large ragged perforation, with
    pulpy margins, which allowed the contents of the stomach to escape
    into the peritoneal cavity.

    In St. Bartholomew’s museum, there is a very good specimen (No.
    1870) of the appearances in the gullet and stomach after poisoning
    by nitric acid. The case is detailed in _St. Bartholomew’s Hospital
    Reports_, vol. v. p. 247. A male died in fifteen hours after
    swallowing 1 oz. of nitric acid. The whole mucous membrane is
    wrinkled, or rather ploughed, into longitudinal furrows, the yellow
    discoloration stops abruptly, with an irregular border, at the
    commencement of the stomach, the epithelial and mucous coats of
    which are wanting--its surface being rough and of a brownish-red

    The following preparations are to be found in the museum of the
    London Hospital:--A. b. 1. and A. b. 8.--A. b. 1. shows the pharynx,
    œsophagus, larynx, and stomach of a young woman, who, after taking
    half an ounce of nitric acid, died in eight hours. The staining is
    very intense; as an unusual feature, it may be noted that the larynx
    is almost as yellow as the œsophagus. The abrasion or solution of
    the epithelium on the dorsum of the tongue has dissected out the
    circumvallate and fungiform papillæ, so that they project with
    unusual distinctness. The lining membrane of the gullet throughout
    is divided into minute squares by longitudinal and transverse
    furrows. The mucous membrane of the stomach appears wholly
    destroyed, and presents a woolly appearance.

    A. b. 8. shows a very perfect cast of the œsophagus. The case was
    that of a woman, aged 35, who swallowed half an ounce of nitric
    acid. The symptoms for the first four days were the usual pain in
    the throat and stomach, which might be expected; the bowels were
    freely open, and the stools dark and offensive. On the sixth day,
    there was constant vomiting with offensive breath; on the ninth, the
    appearance of the patient was critical, and she threw up the cast
    preserved. She died on the tenth day after the taking of the acid.
    The gullet, stomach, trachea, and larynx were found after death much

    The following preparations are in St. Thomas’ Hospital:--P. 5.--a
    stomach with gullet attached. The stomach is covered with
    yellowish-green patches of false membrane and deposit; the gullet
    has the usual longitudinal furrows so characteristic of corrosive

    P. 6. is also from a case of nitric acid poisoning. It shows the
    lining membrane of the stomach partly destroyed and shreddy, yet but
    little discoloured, the hue being a sort of delicate fawn.

    To these may be added a case described and figured by Lesser; to a
    baby, a few days old, an unknown quantity of fuming nitric acid was
    given; the child made a gurgling, choking sound, and died in a few
    minutes. The corpse, nine days after death, showed no signs of
    decomposition. The tongue and gums were yellow, the gullet less so,
    the stomach still less, and the small intestine had no yellow tint;
    the whole of the mouth, gullet, and stomach showed the corrosive
    action of the acid. The graduation of tint, Lesser remarks, is what
    is not seen when the yellow colour is due to poisoning by chromic
    acid or by strong solution of ferric perchloride; in such cases,
    wherever the liquid has gone, there is a yellowness.[114]

[114] A. Lesser, _Atlas der gerichtlichen Medicin_, Berlin, 1884, Tafel
i. fig. 2.

§ 89. =Detection and Estimation of Nitric Acid.=--The detection either
of free nitric acid or of its salts is not difficult. Free nitric acid,
after preliminary estimation of the total acidity by decinormal soda,
may be separated by the cinchonine process given at p. 100. On
precipitation by ammonia or soda solution, the nitrate of ammonia or
soda (and, it may be, other similarly combined acids) remain in
solution. If free nitric acid is present in small quantity only, it may
be necessary to evaporate the filtrate from the quinine nearly to
dryness, and to test the concentrated liquid for nitric acid. The
ordinary tests are as follows:--

(1.) Nitrates, treated with mercury or copper and strong sulphuric acid,
develop nitric oxide, recognised by red fumes, if mixed with air or

(2.) A nitrate dissolved in a small quantity of water, with the addition
of a crystal of ferrous sulphate (allowed to partially dissolve), and
then of strong sulphuric acid--poured through a funnel with a long tube
dipping to the bottom of the test-tube, so as to form a layer at the
bottom--strikes a brown colour at the junction of the liquid. When the
test is properly performed, there will be three layers--the uppermost
being the nitrate solution, the middle ferrous sulphate, and the lowest
sulphuric acid; the middle layer becomes of a smoky or black hue if a
nitrate is present. Organic matter interferes much with the reaction.

(3.) Nitrates in solution, treated in the cold with a zinc copper
couple, are decomposed first into nitrites, and then into ammonia. The
nitrites may be detected by a solution of metaphenyldiamine, which
strikes a red colour with an infinitesimal quantity. Hence, a solution
which gives no red colour with metaphenyldiamine, when submitted to the
action of a zinc copper couple, and tested from time to time, cannot
contain nitrites; therefore, no nitrates were originally present.

(4.) Nitrates, on being treated with strong sulphuric acid, and then a
solution of indigo carmine dropped in, decolorise the indigo; this is a
useful test--not conclusive in itself, but readily applied, and if the
cinchonine method of separation has been resorted to, with few sources
of error.

There is a process of separating nitric acid direct from any organic
tissue, which may sometimes be useful:--Place the substance in a strong,
wide-mouthed flask, closed by a caoutchouc cork, and in the flask put a
small, short test-tube, charged with a strong solution of ferrous
chloride in hydrochloric acid. The flask is connected to the mercury
pump (see fig. p. 47), and made perfectly vacuous by raising and
lowering the reservoir. When this is effected, the tube SS′P is adjusted
so as to deliver any gas evolved into a eudiometer, or other
gas-measuring apparatus. By a suitable movement of the flask, the acid
ferrous chloride is allowed to come in contact with the tissue, a gentle
heat applied to the flask, and gases are evolved. These may be carbon
dioxide, nitrogen, and nitric oxide. On the evolution of gas ceasing,
the carbon dioxide is absorbed by passing up under the mercury a little
caustic potash. When absorption is complete, the gas, consisting of
nitrogen and nitric oxide, may be measured. A bubble or two of oxygen is
now passed into the eudiometer; if nitric oxide is present, red fumes at
once develop. On absorbing the excess of oxygen and the nitric peroxide
by alkaline pyrogallate, and measuring the residual gas, it is easy to
calculate how much nitric oxide was originally present, according to the
principles laid down in “Foods,” p. 587.

It is also obvious that, by treating nitric oxide with oxygen, and
absorbing the nitric peroxide present by an alkaline liquid of known
strength and free from nitrates or ammonia, the resulting solution may
be dealt with by a zinc copper couple, and the ammonia developed by the
action of the couple directly estimated by titration by a decinormal
hydrochloric acid, if large in quantity, or by “_nesslerising_,” if
small in quantity. Crum’s method of estimating nitrates (“Foods,” p.
568) in the cases of minute stains on fabrics, &c., with a little
modification, may be occasionally applicable.

IV.--Acetic Acid.

    § 90. In the ten years ending 1893 nine deaths (four males and five
    females) occurred in England and Wales from drinking, by mistake or
    design, strong acetic acid.

    A few cases only have been recorded in medical literature although
    there have been many experiments on animals.

    The symptoms in the human subject consist of pain, vomiting, and

    In animals it causes colic, paralysis of the extremities, bloody
    urine, and œdema of the lungs. The lethal dose for plant-eating
    animals is about 0·49 gramme per kilo.

    There should be no difficulty in recognising acetic acid; the odour
    alone is, in most cases, strong and unmistakable. Traces are
    detected by distilling, neutralising the distillate by soda,
    evaporating to dryness, and treating the residue as follows:--A
    portion warmed with alcohol and sulphuric acid gives a smell of
    acetic ether. Another portion is heated in a small tube of hard
    glass with arsenious acid; if acetic acid is present, or an acetate,
    a smell of kakodyl is produced.


§ 91. Ammonia, (NH₃), is met with either as a vapour or gas, or as a
solution of the pure gas in water.

=Properties.=--Pure ammonia gas is colourless, with a strong,
irritating, pungent odour, forming white fumes of ammonic chloride, if
exposed to hydric chloride vapour, and turning red moist litmus-paper
strongly blue. By intense cold, or by a pressure of 6½ atmospheres at
the ordinary temperature, the gas is readily liquefied; the liquid
ammonia boils at 38°; its observed specific gravity is ·731; it freezes
at -57·1°. Ammonia is readily absorbed by water; at 0° water will take
up 1000 times its own volume, and at ordinary temperatures about 600
times its volume. Alcohol also absorbs about 10 per cent. Ammonia is a
strong base, and forms a number of salts. Ammonia is one of the constant
products of the putrefaction of nitrogenous substances; it exists in the
atmosphere in small proportions, and in everything that contains water.
Indeed, water is the only compound equal to it in its universality of
diffusion. The minute quantities of ammonia thus diffused throughout
nature are probably never in the free state, but combinations of ammonia
with hydric nitrate, carbon dioxide, &c.

§ 92. =Uses.=[115]--A solution of ammonia in water has many applications
in the arts and industries; it is used in medicine, and is an
indispensable laboratory reagent.

[115] Sir B. W. Richardson has shown that ammonia possesses powerful
antiseptic properties.--_Brit. Med. Journal_, 1862.

The officinal caustic preparations of ammonia are--_ammoniæ liquor
fortior_ (_strong solution of ammonia_), which should contain 32·5 per
cent. of ammonia, and have a specific gravity of ·891.

_Liquor ammoniæ_ (_solution of ammonia_), specific gravity ·959, and
containing 10 per cent. of ammonia. There is also a _liniment of
ammonia_, composed of olive oil, 3 parts, and ammonia, 1 part.

_Spiritus Ammoniæ Fœtidus_ (_fœtid spirit of ammonia_).--A solution of
assafœtida in rectified spirit and ammonia solution, 100 parts by
measure, contains 10 of strong solution of ammonia.

Strong solution of ammonia is an important ingredient in the
“_linimentum camphoræ composita_” (_compound liniment of camphor_), the
composition of which is as follows:--camphor, 2·5 parts; oil of
lavender, ·125; strong solution of ammonia, 5·0; and rectified spirit,
15 parts. Its content of strong solution of ammonia is then about 22·6
per cent. (equivalent to 7·3 of NH₃).[116]

[116] There is a common liniment for horses used in stables, and
popularly known as “white oil.” It contains 1 part of ammonia, and 4
parts of olive or rape oil; not unfrequently turpentine is added.
Another veterinary liniment, called “egg oil,” contains ammonia, oil of
origanum, turpentine, and the yelks of eggs.

_The carbonate of ammonia_ is also caustic; it is considered to be a
compound of acid carbonate of ammonium, NH₄HCO₃, with carbamate of
ammonium, NH₄NH₂CO₂. It is in the form of colourless, crystalline
masses; the odour is powerfully ammoniacal; it is strongly alkaline, and
the taste is acrid. It completely volatilises with heat, is soluble in
water, and somewhat soluble in spirit.

The officinal preparation is the “_spiritus ammoniæ aromaticus_,” or
aromatic spirit of ammonia. It is made by distilling in a particular way
ammonic carbonate, 4 ozs.; strong solution of ammonia, 8 ozs.; rectified
spirit, 120 ozs.; water, 60 ozs.; volatile oil of nutmeg, 4½ drms.; and
oil of lemon, 6½ drms. Aromatic spirit of ammonia is a solution in a
weak spirit of neutral carbonate, flavoured with oil of lemon and
nutmeg; the specific gravity should be 0·896.

_Smelling salts_ (_sal volatile_) are composed of carbonate of ammonia.

§ 93. =Statistics.=--Falck has found throughout literature notices of
thirty cases of poisoning by ammonia, or some of its preparations. In
two of these it was used as a poison for the purpose of murder, and in
eight with suicidal intent; the remainder were all accidental. The two
criminal cases were those of children, who both died. Six out of eight
of the suicidal, and twelve of the twenty accidental cases also
terminated fatally.

Ammonia was the cause of 64 deaths (39 male, 25 female) by accident and
of 34 (18 male, 16 female) by suicide, making a total of 98 during the
ten years 1883-1892 in England and Wales. At present it occupies the
seventh place among poisons as a cause of accident, the ninth as a means
of suicide.

§ 94. =Poisoning by Ammonia Vapour.=--Strong ammoniacal vapour is fatal
to both animal and vegetable life. There are, however, but few instances
of poisoning by ammonia vapour; these few cases have been, without
exception, the result of accident. Two cases of death are recorded, due
to an attempt to rouse epileptics from stupor, by an injudicious use of
strong ammonia applied to the nostrils. In another case, when
hydrocyanic acid had been taken, there was the same result. An instance
is also on record of poisonous effects from the breaking of a bottle of
ammonia, and the sudden evolution in this way of an enormous volume of
the caustic gas. Lastly, a man employed in the manufacture of ice, by
means of the liquefaction of ammonia (Carré’s process), breathed the
vapour, and had a narrow escape for his life.

§ 95. =Symptoms.=--The symptoms observed in the last case may well serve
as a type of what may be expected to occur after breathing ammonia
vapour. The man remained from five to ten minutes in the stream of gas;
he then experienced a feeling of anxiety, and a sense of constriction in
the epigastrium, burning in the throat, and giddiness. He vomited. The
pulse was small and frequent, the face pale, the mouth and throat
strongly reddened, with increased secretion. Auscultation and percussion
of the chest elicited nothing abnormal, although during the course of
four days he had from time to time symptoms of suffocation, which were
relieved by emetics. He recovered by the eighth day.[117]

[117] Schmidt’s _Jahrbuch_, 1872, i. S. 30.

In experiments on animals, very similar symptoms are produced. There is
increased secretion of the eyes, nose, and mouth, with redness. The cry
of cats becomes remarkably hoarse, and they generally vomit. Great
difficulty in breathing and tetanic convulsions are present. When the
animal is confined in a small closed chamber, death takes place in about
a quarter of an hour.

_On section_, the bronchial tubes, to the finest ramifications, are
found to be filled with a tenacious mucus, and the air passages, from
the glottis throughout, reddened. The lungs are emphysematous, but have
not always any special colour; the heart contains but little coagulated
blood; the blood has a dark-red colour.

§ 96. The chronic effects of the gas, as shown in workmen engaged in
manufactures in which the fumes of ammonia are frequent, appear to be an
inflammation of the eyes and an affection of the skin. The latter is
thought to be due to the ammonia uniting to form a soap with the oil of
the lubricating skin glands. Some observers have also noticed deafness,
and a peculiar colour of the skin of the nose and forehead, among those
who work in guano manufactories. Its usual action on the body appears to
be a diminution of the healthy oxidation changes, and a general lowering
of bodily strength, with evident anæmia.

§ 97. =Ammonia in Solution.--Action on Plants.=--Solutions of strong
ammonia, or solutions of the carbonate, act injuriously on vegetable
life, while the neutral salts of ammonia are, on the contrary, excellent
manures. A 30 per cent. solution of ammonic carbonate kills most plants
within an hour, and it is indifferent whether the whole plant is watered
with this solution, or whether it is applied only to the leaves. If,
after this watering of the plant with ammonic carbonate water, the
injurious salt is washed out as far as possible by distilled water, or
by a weakly acidulated fluid, then the plant may recover, after having
shed more or less of its leaves. These facts sufficiently explain the
injurious effects noticed when urine is applied direct to plants, for
urine in a very short time becomes essentially a solution of ammonic

§ 98. =Action on Human Beings and Animal Life.=--The violence of the
action of caustic solutions of ammonia almost entirely depends on the
state of concentration.

The local action of the strong solution appears to be mainly the
extraction of water and the saponifying of fat, making a soluble soap.
On delicate tissues it has, therefore, a destructive action; but S.
Samuel[118] has shown that ammonia, when applied to the unbroken
epidermis, does not have the same intense action as potash or soda, nor
does it coagulate albumen. Blood, whether exposed to ammonia gas, or
mixed with solution of ammonia, becomes immediately dark-red; then,
later, through destruction of the blood corpuscles, very dark, even
black; lastly, a dirty brown-red. The oxygen is expelled, the hæmoglobin
destroyed, and the blood corpuscles dissolved.

[118] Virchow’s _Archiv f. path. Anat._, Bd. 51, Hft. 1 u. 2, S. 41,
&c., 1870.

The albumen of the blood is changed to alkali-albuminate, and the blood
itself will not coagulate. A more or less fluid condition of the blood
has always been noticed in the bodies of those poisoned by ammonia.

Blood exposed to ammonia, when viewed by the spectroscope, shows the
spectra of alkaline hæmatin, a weak absorption-band, in the
neighbourhood of D; but if the blood has been acted on for some time by
ammonia, then all absorption-bands vanish. These spectra, however, are
not peculiar to ammonia, the action of caustic potash or soda being
similar. The muscles are excited by ammonia, the functions of the nerves
are destroyed.

When a solution of strong ammonia is swallowed, there are two main
effects--(1) the action of the ammonia itself on the tissues it comes
into contact with, and (2) the effects of the vapour on the
air-passages. There are, therefore, immediate irritation, redness, and
swelling of the tongue and pharynx, a burning pain reaching from the
mouth to the stomach, with vomiting, and, it may be, nervous
symptoms. The saliva is notably increased. In a case reported by
Fonssagrives,[119] no less than 3 litres were expelled in the
twenty-four hours. Often the glands under the jaw and the lymphatics of
the neck are swollen.

[119] _L’Union Médicale_, 1857, No. 13, p. 49, No. 22, p. 90.

Doses of from 5 to 30 grammes of the strong solution of ammonia may kill
as quickly as prussic acid. In a case recorded by Christison,[120] death
occurred in four minutes from a large dose, doubtless partly by
suffocation. As sudden a result is also recorded by Plenk: a man, bitten
by a rabid dog, took a mouthful of spirits of ammonia, and died in four

[120] Christison, 167.

If death does not occur rapidly, there may be other symptoms--dependent
not upon its merely local action, but upon its more remote effects.
These mainly consist in an excitation of the brain and spinal cord, and,
later, convulsive movements deepening into loss of consciousness. It has
been noticed that, with great relaxation of the muscular system, the
patients complain of every movement causing pain. With these general
symptoms added to the local injury, death may follow many days after the
swallowing of the fatal dose.

Death may also occur simply from the local injury done to the throat and
larynx, and the patient may linger some time. Thus, in a case quoted by
Taylor,[121] in which none of the poison appears actually to have been
swallowed, the man died nineteen days after taking the poison from
inflammation of the throat and larynx. As with the strong acids, so with
ammonia and the alkalies generally, death may also be caused many weeks
and even months afterwards from the effects of contraction of the
gullet, or from the impaired nutrition consequent upon the destruction,
more or less, of portions of the stomach or intestinal canal.

[121] _Principles of Jurisprudence_, i. p. 235.

§ 99. =Post-mortem Appearances.=--In recent cases there is an intense
redness of the intestinal canal, from the mouth to the stomach, and even
beyond, with here and there destruction of the mucous membrane, and even
perforation. A wax preparation in the museum of University College (No.
2378) shows the effects on the stomach produced by swallowing strong
ammonia; it is ashen-gray in colour, and most of the mucous membrane is,
as it were, dissolved away; the cardiac end is much congested.

The contents of the stomach are usually coloured with blood; the
bronchial tubes and glottis are almost constantly found inflamed--even a
croup-like (or diphtheritic) condition has been seen. Œdema of the
glottis should also be looked for: in one case this alone seems to have
accounted for death. The blood is of a clear-red colour, and fluid. A
smell of ammonia may be present.

If a sufficient time has elapsed for secondary effects to take place,
then there may be other appearances. Thus, in the case of a girl who,
falling into a fainting fit, was treated with a draught of undiluted
spirits of ammonia, and lived four weeks afterwards, the stomach
(preserved in St. George’s Hospital museum, 43 b, ser. ix.) is seen to
be much dilated and covered with cicatrices, and the pylorus is so
contracted as hardly to admit a small bougie. It has also been noticed
that there is generally a fatty degeneration of both the kidneys and

It need scarcely be observed that, in such cases, no free ammonia will
be found, and the question of the cause of death must necessarily be
wholly medical and pathological.

§ 100. =Separation of Ammonia.=--Ammonia is separated in all cases by
distillation, and if the organic or other liquid is already alkaline,
it is at once placed in a retort and distilled. If neutral or acid, a
little burnt magnesia may be added until the reaction is alkaline. It is
generally laid down that the contents of the stomach in a putrid
condition cannot be examined for ammonia, because ammonia is already
present as a product of decomposition; but even under these
circumstances it is possible to give an opinion whether ammonia _in
excess_ is present. For if, after carefully mixing the whole contents of
the stomach, and then drying a portion and reckoning from that weight
the total nitrogen (considering, for this purpose, the contents to
consist wholly of albumen, which yields about 16 per cent. of
nitrogen)--under these conditions, the contents of the stomach yield
more than 16 per cent. of nitrogen as ammonia reckoned on the dry
substance, it is tolerably certain that ammonia not derived from the
food or the tissues is present.

If, also, there is a sufficient evolution of ammonia to cause white
fumes, when a rod moistened with hydrochloric acid is brought near to
the liquid, this is an effect never noticed with a normal decomposition,
and renders the presence of extrinsic ammonia probable.

An alkaline-reacting distillate, which gives a brown colour with the
“nessler” reagent, and which, when carefully neutralised with sulphuric
acid, on evaporation to dryness by the careful heat of a water-bath,
leaves a crystalline mass that gives a copious precipitate with platinic
chloride, but is hardly at all soluble in absolute alcohol, can be no
other substance than ammonia.

§ 101. =Estimation.=--Ammonia is most quickly estimated by distilling,
receiving the distillate in decinormal acid, and then titrating back. It
may also be estimated as the double chloride of ammonium and platinum
(NH₄Cl)₂PtCl₄. The distillate is exactly neutralised by HCl, evaporated
to near dryness, and an alcoholic solution of platinic chloride added in
sufficient quantity to be always in slight excess, as shown by the
yellow colour of the supernatant fluid. The precipitate is collected,
washed with a little alcohol, dried, and weighed on a tared filter; 100
parts of the salt are equal to 7·6 of NH₃.

VI.--Caustic Potash and Soda.

§ 102. There is so little difference in the local effects produced by
potash and soda respectively, that it will be convenient to treat them

=Potash= (=potassa caustica=).--Hydrate of potassium (KHO), atomic
weight 56, specific gravity 2·1.

=Properties.=--Pure hydrate of potassium is a compact, white solid,
usually met with in the form of sticks. When heated to a temperature a
little under redness, it melts to a nearly colourless liquid; in this
state it is intensely corrosive. It rapidly absorbs moisture from the
air, and moist potash also absorbs with great avidity carbon dioxide; it
is powerfully alkaline, changing red litmus to blue. It is soluble in
half its weight of cold water, great heat being evolved during solution;
it forms two definite hydrates--one, KHO + H₂O; the other, KHO + 2H₂O.
It is sparingly soluble in ether, but is dissolved by alcohol,
wood-spirit, fusel oil, and glycerin.

§ 103. =Pharmaceutical Preparations.=--Potassium hydrate, as well as the
solution of potash, is officinal in all pharmacopœias. The _liquor
potassæ_, or solution of potash, of the British Pharmacopœia, is a
strongly alkaline, caustic liquid, of 1·058 specific gravity, and
containing 5·84 per cent. by weight of KHO. It should, theoretically,
not effervesce, when treated with an acid, but its affinity for CO₂ is
so great that all solutions of potash, which have been in any way
exposed to air, contain a little carbonate. Caustic sticks of potash and
lime used to be officinal in the British Pharmacopœia. Filho’s caustic
is still in commerce, and is made by melting together two parts of
potassium hydrate and one part of lime in an iron ladle or vessel; the
melted mass is now moulded by pouring it into leaden moulds. Vienna
paste is composed of equal weights of potash and lime made into a paste
with rectified spirit or glycerin.

§ 104. =Carbonate of Potash= (K₂CO₃ + 1½H₂O), when pure, is in the form
of small white crystalline grains, alkaline in taste and reaction, and
rapidly deliquescing when exposed to moist air; it gives all the
chemical reactions of potassium oxide, and carbon dioxide. Carbonate of
potash, under the name of _salt of tartar_, or potashes, is sold by
oilmen for cleansing purposes. They supply it either in a fairly pure
state, or as a darkish moist mass containing many impurities.

§ 105. =Bicarbonate of Potash= (KHCO₃) is in the form of large
transparent rhombic prisms, and is not deliquescent. The effervescing
solution of potash (_liquor potassæ effervescens_) consists of 30 grains
of KHCO₃ in a pint of water (3·45 grms. per litre), and as much CO₂ as
the water will take up under a pressure of seven atmospheres.

§ 106. =Caustic Soda--Sodium Hydrate= (NaHO).--This substance is a white
solid, very similar in appearance to potassium hydrate; it absorbs
moisture from the air, and afterwards carbon dioxide, becoming solid
again, for the carbonate is not deliquescent. In this respect, then,
there is a great difference between potash and soda, for the former is
deliquescent both as hydrate and carbonate; a stick of potash in a
semi-liquid state, by exposure to the air, continues liquid, although
saturated with carbon dioxide. Pure sodium hydrate has a specific
gravity of 2·0; it dissolves in water with evolution of heat, and the
solution gives all the reactions of sodium hydrate, and absorbs carbon
dioxide as readily as the corresponding solution of potash. The _liquor
sodæ_ of the B.P. should contain 4·1 per cent. of NaHO.

§ 107. =Sodæ Carbonas--Carbonate of Soda=--(Na₂CO₃10H₂O).--The pure
carbonate of soda for medicinal use is in colourless and transparent
rhombic octahedrons; when exposed to air, the crystals effloresce and
crumble. The _sodæ carbonas exsiccata_, or dried carbonate of soda, is
simply the ordinary carbonate, deprived of its water of crystallisation,
which amounts to 62·93 per cent.

§ 108. =Bicarbonate of Soda= (NaHCO₃) occurs in the form of minute
crystals, or, more commonly, as a white powder. The _liquor sodæ
effervescens_ of the B.P. is a solution of the bicarbonate, 30 grains of
the salt in 20 ozs. of water (3·45 grms. per litre), the water being
charged with as much carbonic acid as it will hold under a pressure of
seven atmospheres. _The bicarbonate of soda lozenges_ (_trochisci sodæ
bicarbonatis_) contain in each lozenge 5 grains (327 mgrms.) of the
bicarbonate. The carbonate of soda sold for household purposes is of two
kinds--the one, “seconds,” of a dirty white colour and somewhat impure;
the other, “best,” is a white mass of much greater purity. _Javelle
water_ (_Eau de Javelle_) is a solution of hypochlorite of soda; its
action is poisonous, more from the caustic alkali than from the
chlorine, and may, therefore, be here included.

§ 109. =Statistics.=--Poisoning by the fixed alkalies is not so frequent
as poisoning by ammonia. Falck has collected, from medical literature,
27 cases, 2 of which were the criminal administering of _Eau de
Javelle_, and 5 were suicidal; 22, or 81·5 per cent., died--in 1 of the
cases after twenty-four hours; in the others, life was prolonged for
days, weeks, or months--in 1 case for twenty-seven months. In the ten
years 1883-1892, in England and Wales, there were 27 deaths from
poisoning by the fixed alkalies; 2 were suicidal (1 from potash, the
other from soda); the remaining 25 were due to accident; of these, 7 (3
males and 4 females) were from caustic soda, and 18 (8 males and 10
females) from caustic potash.

§ 110. =Effects on Animal and Vegetable Life.=--The fixed alkalies
destroy all vegetable life, if applied in strong solution or in
substance, by dehydrating and dissolving the tissues. The effects on
animal tissues are, in part, due also to the affinity of the alkalies
for water. They extract water from the tissues with which they come in
contact, and also attack the albuminous constituents, forming
alkali-albuminate, which swells on the addition of water, and, in a
large quantity, even dissolves. Cartilaginous and horny tissues are also
acted upon, and strong alkalies will dissolve hair, silk, &c. The action
of the alkali is by no means restricted to the part first touched, but
has a remarkable faculty of spreading in all directions.

§ 111. =Local Effects.=--The effects of strong alkali applied to the
epidermis are similar to, but not identical with, those produced by
strong acids. S. Samuel[122] has studied this experimentally on the ear
of the rabbit; a drop of a strong solution of caustic alkali, placed on
the ear of a white rabbit, caused stasis in the arteries and veins, with
first a greenish, then a black colour of the blood; the epidermis was
bleached, the hair loosened, and there quickly followed a greenish
coloration on the back of the ear, opposite to the place of application.
Around the burned spot appeared a circle of anastomising vessels, a
blister rose, and a slough separated in a few days. The whole thickness
of the ear was coloured yellowish-green, and, later, the spot became of
a rusty brown.

[122] Virchow’s _Archiv. f. path. Anat._, Bd. 51, Hft. 1 u. 2, 1870.

§ 112. =Symptoms.=--The symptoms observed when a person has swallowed a
dangerous dose of caustic (fixed) alkali are very similar to those
noticed with ammonia, with the important exception that there is no
respiratory trouble, unless the liquid has come into contact with the
glottis; nor has there been hitherto remarked the rapid death which has
taken place in a few ammonia poisonings, the shortest time hitherto
recorded being three hours, as related by Taylor, in a case in which a
boy had swallowed 3 ozs. of a strong solution of carbonate of potash.

There is instant pain, extending from the mouth to the stomach, and a
persistent and unpleasant taste; if the individual is not a determined
suicide, and the poison (as is mostly the case) has been taken
accidentally, the liquid is immediately ejected as much as possible, and
water, or other liquid at hand, drunk freely. Shock may at once occur,
and the patient die from collapse; but this, even with frightful
destruction of tissue, appears to be rare. Vomiting supervenes; what is
ejected is strongly alkaline, and streaked with blood, and has a soapy,
frothy appearance. There may be diarrhœa, great tenderness of the
abdomen, and quick pulse and fever. With caustic potash, there may be
also noticed its toxic effects (apart from local action) on the heart;
the pulse, in that case, is slow and weak, and loss of consciousness and
convulsions are not uncommon. If the collapse and after-inflammation are
recovered from, then, as in the case of the mineral acids, there is all
the horrid sequence of symptoms pointing to contractions and strictures
of the gullet or pylorus, and the subsequent dyspepsia, difficulty of
swallowing, and not unfrequently actual starvation.

§ 113. =Post-mortem Appearances.=--In cases of recent poisoning, spots
on the cheeks, lips, clothing, &c., giving evidence of the contact of
the alkali, should be looked for; but this evidence, in the case of
persons who have lived a few days, may be wanting. The mucous membrane
of the mouth, throat, gullet, and stomach is generally more or less
white--here and there denuded, and will be found in various stages of
inflammation and erosion, according to the amount taken, and the
concentration of the alkali. Where there is erosion, the base of the
eroded parts is not brown-yellow, but, as a rule, pale red. The gullet
is most affected at its lower part, and it is this part which is mostly
subject to stricture. Thus Böhm[123] found that in 18 cases of
contraction of the gullet, collected by him, 10 of the 18 showed the
contraction at the lower third.

[123] _Centralblatt für die Med. Wiss._, 1874.

The changes which the stomach may present if the patient has lived some
time, are well illustrated by a preparation in St. George’s museum (43
a. 264, ser. ix.). It is the stomach of a woman, aged 44, who had
swallowed a concentrated solution of carbonate of potash. She vomited
immediately after taking it, and lived about two months, during the
latter part of which she had to be nourished by injections. She died
mainly from starvation. The gullet in its lower part is seen to be much
contracted, its lining membrane destroyed, and the muscular coats
exposed. The coats of the stomach are thickened, but what chiefly
arrests the attention is a dense cicatrix at the pylorus, with an
aperture so small as only to admit a probe.

The colour of the stomach is generally bright red, but in that of a
child, preserved in Guy’s Hospital museum (No. 1798²⁴), the mucous
membrane is obliterated, the rugæ destroyed, and a dark-brown stain is a
noticeable feature. The stomach is not, however, necessarily affected.
In a preparation in the same museum (No. 1798²⁰) the mucous membrane of
the stomach of a child who swallowed soap-lees is seen to be almost
healthy, but the gullet is much discoloured. The action on the blood is
to change it into a gelatinous mass; the blood corpuscles are destroyed,
and the whole colour becomes of a dirty blackish-red; the spectroscopic
appearances are identical with those already described (see p. 114).

The question as to the effects of chronic poisoning by the alkalies or
their carbonates may arise. Little or nothing is, however, known of the
action of considerable quantities of alkalies taken daily. In a case
related by Dr. Tunstall,[124] a man for eighteen years had taken daily 2
ozs. of bicarbonate of soda for the purpose of relieving indigestion. He
died suddenly, and the stomach was found extensively diseased; but since
the man, before taking the alkali, had complained of pain, &c., it is
hardly well, from this one case, to draw any conclusion.

[124] _Med. Times_, Nov. 30, 1850, p. 564.

It is important to observe that the contents of the stomach may be acid,
although the death has been produced by caustic alkali. A child, aged 4,
drank from a cup some 14 per cent. soda lye. He vomited frequently, and
died in fifteen hours. The stomach contained 80 c.c. of sour-smelling
turbid fluid, the reaction of which was acid. There were hæmorrhagic
patches in the stomach, and signs of catarrhal inflammation; there was
also a similarly inflamed condition of the duodenum.[125]

[125] Lesser, _Atlas d. gericht. Med._, Tafel ii.

§ 114. =Chemical Analysis.=--The tests for potassium or sodium are too
well known to need more than enumeration. The intense yellow flame
produced when a sodium salt is submitted to a Bunsen flame, and the
bright sodium-line at D when viewed by the spectroscope, is a delicate
test; while potassium gives a dull red band in the red, and a faint but
very distinct line in the violet. Potassium salts are precipitated by
tartaric acid, while sodium salts do not yield this precipitate;
potassium salts also give a precipitate with platinic chloride insoluble
in strong alcohol, while the compound salt with sodium is rapidly
dissolved by alcohol or water. This fact is utilised in the separation
and estimation of the two alkalies.

§ 115. =Estimation of the Fixed Alkalies.=--To detect a fixed alkali in
the contents of the stomach, a convenient process is to proceed by
dialysis, and after twenty-four hours, to concentrate the outer liquid
by boiling, and then, if it is not too much coloured, to titrate
directly with a decinormal sulphuric acid. After exact neutralisation,
the liquid is evaporated to dryness, carbonised, the alkaline salts
lixiviated out with water, the sulphuric acid exactly precipitated by
baric chloride, and then, after separation of the sulphate, the liquid
treated with milk of lime. The filtrate is treated with a current of CO₂
gas, boiled, and any precipitate filtered off; the final filtrate will
contain only alkalies. The liquid may now be evaporated to dryness with
either hydrochloric or sulphuric acids, and the total alkalies weighed
as sulphates or chlorides. Should it be desirable to know exactly the
proportion of potassium to sodium, it is best to convert the alkalies
into chlorides--dry gently, ignite, and weigh; then dissolve in the
least possible quantity of water, and precipitate by platinic chloride,
which should be added so as to be a little in excess, but not much. The
liquid thus treated is evaporated nearly to dryness, and then extracted
with alcohol of 80 per cent., which dissolves out any of the double
chloride of platinum and sodium. Finally, the precipitate is collected
on a tared filter and weighed, after drying at 100°. In this way the
analyst both distinguishes between the salts of sodium and potassium,
and estimates the relative quantities of each. It is hardly necessary to
observe that, if the double chloride is wholly soluble in water or
alcohol, sodium alone is present. This, however, will never occur in
operating on organic tissues and fluids, for both alkalies are
invariably present. A correction must be made when complex organic
fluids are in this way treated for alkalies which may be naturally in
the fluid. Here the analyst will be guided by his preliminary
titration, which gives the total free alkalinity. In cases where the
alkali has been neutralised by acids, of course no free alkali will be
found, but the corresponding salt.

VII.--Neutral Sodium, Potassium, and Ammonium Salts.

    § 116. The neutral salts of the alkalies are poisonous, if
    administered in sufficient doses, and the poisonous effect of the
    sulphate, chloride, bromide, iodide, tartrate, and citrate appears
    to depend on the specific action of the alkali metal, rather than on
    the acid, or halogen in combination. According to the researches of
    Dr. Ringer and Dr. Harrington Sainsbury,[126] with regard to the
    relative toxicity of the three, as shown by their effect on the
    heart of a frog--first, the potassium salts were found to exert the
    most poisonous action, next come the ammonium, and, lastly, the
    sodium salts. The highest estimate would be that sodium salts are
    only one-tenth as poisonous as those of ammonium or potassium; the
    lowest, that the sodium salts are one-fifth: although the
    experiments mainly throw light upon the action of the alkalies on
    one organ only, yet the indications obtained probably hold good for
    the organism as a whole, and are pretty well borne out by clinical

[126] _Lancet_, June 24, 1882.

    There appear to be four cases on record of poisoning by the above
    neutral salts; none of them belong to recent times, but lie between
    the years 1837-1856. Hence, the main knowledge which we possess of
    the poisonous action of the potassium salts is derived from
    experiments on animals.

    § 117. =Sodium Salts.=--Common salt in such enormous quantity as
    half a pound to a pound has destroyed human life, but these cases
    are so exceptional that the poisonous action of sodium salts is of
    scientific rather than practical interest.

    § 118. =Potassium Salts.=--Leaving for future consideration the
    nitrate and the chlorate of potassium, potassic sulphate and
    tartrate are substances which have destroyed human life.

    =Potassic Sulphate= (K₂SO₄) is in the form of colourless rhombic
    crystals, of bitter saline taste. It is soluble in 10 parts of

    =Hydropotassic Tartrate= (KHC₄H₄O₆), when pure, is in the form of
    rhombic crystals, tasting feebly acid. It is soluble in 210 parts of
    water at 17°.

    § 119. =Action on the Frog’s Heart.=--Both excitability and
    contractility are affected to a powerful degree. There is a
    remarkable slowing of the pulsations, irregularity, and, lastly,
    cessation of pulsation altogether.

    § 120. =Action on Warm-Blooded Animals.=--If a sufficient quantity
    of a solution of a potassic salt is injected into the blood-vessels
    of an animal, there is almost immediate death from arrest of the
    heart’s action. Smaller doses, subcutaneously applied, produce
    slowing of the pulse, dyspnœa, and convulsions, ending in death.
    Small doses produce a transitory diminution of the force of arterial
    pressure, which quickly passes, and the blood-pressure rises. There
    is at first, for a few seconds, increase in the number of
    pulsations, but later a remarkable slowing of the pulse. The rise in
    the blood-pressure occurs even after section of the spinal cord.
    Somewhat larger doses cause rapid lowering of the blood-pressure,
    and apparent cessation of the heart’s action; but if the thorax be
    then opened, the heart is seen to be contracting regularly, making
    some 120-160 rhythmic movements in the minute. If the respiration be
    now artificially maintained, and suitable pressure made on the walls
    of the chest, so as to empty the heart of blood, the blood-pressure
    quickly rises, and natural respiration may follow. An animal which
    lay thirty-six minutes apparently dead was in this way brought to
    life again (_Böhm_). The action of the salts of potassium on the
    blood is the same as that of sodium salts. The blood is coloured a
    brighter red, and the form of the corpuscles changed; they become
    shrivelled through loss of water. Voluntary muscle loses quickly its
    contractility when a solution of potash is injected into its
    vessels. Nerves also, when treated with a 1 per cent. solution of
    potassic chloride, become inexcitable.

    § 121. =Elimination.=--The potassium salts appear to leave the body
    through the kidneys, but are excreted much more slowly than the
    corresponding sodium salts. Thus, after injection of 4 grms. of
    potassic chloride--in the first sixteen hours ·748 grm. of KCl was
    excreted in the urine, and in the following twenty-four hours 2·677

    § 122. =Nitrate of Potash= (KNO₃).--Pure potassic nitrate
    crystallises in large anhydrous hexagonal prisms with dihedral
    summits; it does not absorb water, and does not deliquesce. Its
    fusing point is about 340°; when melted it forms a transparent
    liquid, and loses a little of its oxygen, but this is for the most
    part retained by the liquid given off when the salt solidifies. At a
    red-heat it evolves oxygen, and is reduced first to nitrite; if the
    heat is continued, potassic oxide remains. The specific gravity of
    the fused salt is 2·06. It is not very soluble in cold water, 100
    parts dissolving only 26 at 15·6°; but boiling water dissolves it
    freely, 100 parts dissolving 240 of the salt.

    A solution of nitrate of potash, when treated with a zinc couple
    (see “Foods,” p. 566), is decomposed, the nitrate being first
    reduced to nitrite, as shown by its striking a red colour with
    metaphenylene-diamine, and then the nitrite farther decomposing, and
    ammonia appearing in the liquid. If the solution is alkalised, and
    treated with aluminium foil, hydrogen is evolved, and the same
    effect produced. As with all nitrates, potassic nitrate, on being
    heated in a test-tube with a little water, some copper filings, and
    sulphuric acid, evolves red fumes of nitric peroxide.

    § 123. =Statistics.=--Potassic nitrate, under the popular name of
    “_nitre_,” is a very common domestic remedy, and is also largely
    used as a medicine for cattle. There appear to be twenty cases of
    potassic nitrate poisoning on record--of these, eight were caused by
    the salts having been accidentally mistaken for magnesic sulphate,
    sodic sulphate, or other purgative salt; two cases were due to a
    similar mistake for common salt. In one instance, the nitrate was
    used in strong solution as an enema, but most of the cases were due
    to the taking of too large an internal dose.

    § 124. =Uses in the Arts=, &c.--Both sodic and potassic nitrates are
    called “nitre” by the public indiscriminately. Sodic nitrate is
    imported in large quantities from the rainless districts of Peru as
    a manure. Potassic nitrate is much used in the manufacture of
    gunpowder, in the preservation of animal substances, in the
    manufacture of gun cotton, of sulphuric and nitric acids, &c. The
    maximum medicinal dose of potassium nitrate is usually stated to be
    30 grains (1·9 grm.).

    § 125. =Action of Nitrates of Sodium and Potassium.=--Both of these
    salts are poisonous. Potassic nitrate has been taken with fatal
    result by man; the poisonous nature of sodic nitrate is established
    by experiments on animals. The action of the nitrates of the
    alkalies is separated from that of the other neutral salts of
    potassium, &c., because in this case the toxic action of the
    combined nitric acid plays no insignificant part. Large doses, 3-5
    grms. (46·3-77·2 grains), of potassic nitrate cause considerable
    uneasiness in the stomach and bowels; the digestion is disturbed;
    there may be vomiting and diarrhœa, and there is generally present a
    desire to urinate frequently. Still larger doses, 15-30 grms.
    (231·5-463 grains), rapidly produce all the symptoms of acute
    gastro-enteritis--great pain, frequent vomiting (the ejected matters
    being often bloody), with irregularity and slowing of the pulse;
    weakness, cold sweats, painful cramps in single muscles (especially
    in the calves of the legs); and, later, convulsions, aphonia, quick
    collapse, and death.

    In the case of a pregnant woman, a handful of “nitre” taken in
    mistake for Glauber’s salts produced abortion after half-an-hour.
    The woman recovered. Sodic nitrate subcutaneously applied to frogs
    kills them, in doses of ·026 grm. (·4 grain), in about two hours;
    there are fibrillar twitchings of single groups of muscles and
    narcosis. The heart dies last, but after ceasing to beat may, by a
    stimulus, be made again to contract. Rabbits, poisoned similarly by
    sodic nitrate, exhibit also narcotic symptoms; they lose
    consciousness, lie upon their side, and respond only to the sharpest
    stimuli. The breathing, as well as the heart, is “slowed,” and death
    follows after a few spasmodic inspirations.

    =Sodic nitrite= was found by Barth to be a more powerful poison,
    less than 6 mgrms. (·1 grain) being sufficient to kill a rabbit of
    455·5 grms. (7028 grains) weight, when subcutaneously injected. The
    symptoms were very similar to those produced by the nitrate.

    § 126. The _post-mortem_ appearances from potassic nitrate are as
    follows:--An inflamed condition of the stomach, with the mucous
    membrane dark in colour, and readily tearing; the contents of the
    stomach are often mixed with blood. In a case related by Orfila,
    there was even a small perforation by a large dose of potassic
    nitrate, and a remarkable preservation of the body was noted.

    It is believed that the action of the nitrates is to be partly
    explained by a reduction to nitrites, circulating in the blood as
    such. To detect nitrites in the blood, the best method is to place
    the blood in a dialyser, the outer liquid being alcohol. The
    alcoholic solution may be evaporated to dryness, extracted with
    water, and then tested by metaphenylene-diamine.

    § 127. =Potassic Chlorate= (KClO₃).--Potassic chlorate is in the
    form of colourless, tabular crystals with four or six sides. About 6
    parts of the salt are dissolved by 100 of water at 15°, the
    solubility increasing with the temperature, so that at 100° nearly
    60 parts dissolve; if strong sulphuric acid be dropped on the
    crystals, peroxide of chlorine is evolved; when rubbed with sulphur
    in a mortar, potassic chlorate detonates. When the salt is heated
    strongly, it first melts, and then decomposes, yielding oxygen gas,
    and is transformed into the perchlorate. If the heat is continued,
    this also is decomposed, and the final result is potassic chloride.

    § 128. =Uses.=--Potassic chlorate is largely used as an oxidiser in
    calico printing, and in dyeing, especially in the preparation of
    aniline black. A considerable quantity is consumed in the
    manufacture of lucifer matches and fireworks; it is also a
    convenient source of oxygen. Detonators for exploding dynamite are
    mixtures of fulminate of mercury and potassic chlorate. It is
    employed as a medicine both as an application to inflamed mucous
    membranes, and for internal administration; about 2000 tons of the
    salt for these various purposes are manufactured yearly in the
    United Kingdom.

    § 129. =Poisonous Properties.=--The facility with which potassic
    chlorate parts with its oxygen by the aid of heat, led to its very
    extensive employment in medicine. No drug, indeed, has been given
    more recklessly, or on a less scientific basis. Wherever there were
    sloughing wounds, low fevers, and malignant sore throats, especially
    those of a diphtheritic character, the practitioner administered
    potassic chlorate in colossal doses. If the patient died, it was
    ascribed to the malignity of the disease--if he recovered, to the
    oxygen of the salt; and it is possible, from the light which of
    recent years has been thrown on the action of potassic chlorate,
    that its too reckless use has led to many unrecorded accidents.

    § 130. =Experiments on Animals.=--F. Marchand[127] has studied the
    effects of potassic chlorate on animals, and on blood. If either
    potassic chlorate or sodic chlorate is mixed with fresh blood, it
    shows after a little while peculiar changes; the clear red colour at
    first produced passes, within a few hours, into a dark red-brown,
    which gradually becomes pure brown. This change is produced by a 1
    per cent. solution, in from fifteen to sixteen hours; and a 4 per
    cent. solution at 15° destroys every trace of oxyhæmoglobin within
    four hours. Soon the blood takes a syrupy consistence, and, with a
    2-4 per cent. solution of the salt, passes into a jelly-like mass.
    The jelly has much permanence, and resists putrefactive changes for
    a long time.

[127] _Virchow’s Archiv. f. path. Anat._, Bd. 77, Hft. 3, S. 455, 1879.

    Marchand fed a dog of 17 kilos. in weight with 5 grms. of potassic
    chlorate for a week. As there were no apparent symptoms, the dose
    was doubled for two days; and as there was still no visible effect,
    lastly, 50 grms. of sodic chlorate were given in 5 doses. In the
    following night the dog died. The blood was found after death to be
    of a sepia-brown colour, and remained unaltered when exposed to the
    air. The organs were generally of an unnatural brown colour; the
    spleen was enormously enlarged; the kidneys were swollen, and of a
    dark chocolate brown--on section, almost black-brown, the colour
    being nearly equal, both in the substance and in the capsule. A
    microscopical examination of the kidney showed the canaliculi to be
    filled with brownish cylinders consisting of altered blood. A
    spectroscopic examination of the blood showed weak hæmoglobin bands,
    and a narrow band in the red. With farther dilution, the hæmoglobin
    bands vanished, but the band in the red remained. The diluted blood,
    when exposed to the light, still remained of a coffee-brown colour;
    and on shaking, a white-brown froth was produced on the surface.

    A second experiment in which a hound of from 7-8 kilos. in weight
    was given 3-5 grm. doses of potassic chlorate in sixteen hours, and
    killed by bleeding seven to eight hours after the last dose, showed
    very similar appearances. The kidneys were intensely congested, and
    the peculiar brown colour was noticeable.

    § 131. =Effects on Man.=--I find in literature thirty-nine cases
    recorded, in which poisonous symptoms were directly ascribed to the
    action of chlorate of potassium; twenty-eight of these terminated
    fatally. A quadruple instance of poisoning, recorded by Brouardel
    and L’Hôte,[128] illustrates many of the points relative to the time
    at which the symptoms may be expected to commence, and the general
    aspect of potassic chlorate poisoning. The “_supérieure_” of a
    religious institution was in the habit of giving, for charitable
    purposes, a potion containing 15 grms. (3·8 drms.) of potassic
    chlorate, dissolved in 360 c.c. (about 12½ ozs.) of a vegetable

[128] _Annales d’Hygiène publique_, 1881, p. 232.

    This potion was administered to four children--viz., David, aged 2½;
    Cousin, aged 3½; Salmont, 2½; and Guérin, 2½. David took the whole
    in two and a half hours, the symptoms commenced after the potion was
    finished, and the child died five and a half hours after taking the
    first dose; there were vomiting and diarrhœa. Cousin took the
    medicine in seven hours; the symptoms also commenced after the last
    spoonful, and the death took place eight and a half hours from the
    first spoonful. The symptoms were mainly those of great depression;
    the lips were blue, the pulse feeble, there was no vomiting, no
    diarrhœa. Salmont took the medicine in nine hours, and died in
    twelve. There was some diarrhœa, the stools were of a green colour.
    Guérin took the whole in two hours, the symptoms commenced in four
    hours; the lips were very pale, the gums blue. Death took place in
    four days.

    There was an autopsy in the case of David only. The stomach showed a
    large ecchymosis on its mucous membrane, as if it had been burnt by
    an acid; the spleen was gorged with blood, and its tissue friable;
    the kidneys do not seem to have been thoroughly examined, but are
    said to have been tumefied. Potassic chlorate was discovered by
    dialysis. In the cases of the children just detailed, the symptoms
    appear to be a mixture of the depressing action of the potassium,
    and irritant action of the chlorate.

    § 132. In adults, the main symptoms are those of nephritis, and the
    fatal dose for an adult is somewhere about an ounce (28·3 grms.),
    but half this quantity would probably be dangerous, especially if
    given to a person who had congestion or disease of the kidneys.

    Dr. Jacobi[129] gives the following cases.

[129] _Amer. Med. Times_, 1860.

    Dr. Fountain in 1858, experimenting on himself, took 29·2 grms. (8·7
    drms.) of potassic chlorate; he died on the seventh day from
    nephritis. A young lady swallowed 30 grms. (8·5 drms.), when using
    it as a gargle; she died in a few days from nephritis. A man, thirty
    years of age, died in four days after having taken 48 grms. (12·3
    drms.) of sodic chlorate in six hours. The _shortest time_ in which
    I can find the salt to have been fatal, is a case related by Dr.
    Manouvriez, in which a woman took 45 grms., and died in five hours.
    The _smallest dose_ which has proved fatal is one in which an infant
    three years old was killed by 3 grms. (46·3 grains).

    Jacobi considers that the maximum dose to be given in divided doses
    during the twenty-four hours, to infants under three, should be from
    1-1·5 grm. (15·4-23·1 grains), to children from three years old, up
    to 2 grms. (30·8 grains); and adults from 6-8 grms. (92·6-123·4

    § 133. =Elimination.=--Potassic chlorate is quickly absorbed by
    mucous membranes, and by the inflamed skin, and rapidly separated
    from the body by the action of the kidneys. Wöhler, as early as
    1824, recognised that it in great part passed out of the body
    unchanged, and, lately, Isambert, in conjunction with Hirne,[130]
    making quantitative estimations, recovered from the urine no less
    than 95 per cent. of the ingested salts. Otto Hehner has also made
    several auto-experiments, and taking 2½ drms., found that it could
    be detected in the urine an hour and a half afterwards. At that time
    17·23 per cent. of the salt had been excreted, and, by the end of
    eleven hours, 93·8 per cent. was recovered. It is then difficult to
    believe that the salt gives any oxygen to the tissues, for though it
    is true that in all the investigations a small percentage remains to
    be accounted for, and also that Binz,[131] making experiments by
    mixing solutions of potassic chlorate with moist organic substances,
    such as pus, yeast, fibrin, &c., has declared that, at a blood heat
    the chlorate is rapidly reduced, and is no longer recognisable as
    chlorate--yet it may be affirmed that potassic chlorate is recovered
    from the urine as completely as anything which is ever excreted by
    the body, and that deductions drawn from the changes undergone by
    the salt in solutions of fibrin, &c., have only an indirect bearing
    on the question.

[130] _Gaz. Méd. de Paris_, 1875, Nro. 17, 35, 41, 43.

[131] _Berlin klin. Wochenschr._, xi. 10, S. 119, 1874.

    § 134. The essential action of potassic chlorate seems to be that it
    causes a peculiar change in the blood, acting on the colouring
    matter and corpuscles; the latter lose their property as oxygen
    carriers; the hæmoglobin is in part destroyed; the corpuscles
    dissolved. The decomposed and altered blood-corpuscles are crowded
    into the kidneys, spleen, &c.; they block up the uriniferous
    canaliculi, and thus the organs present the curious colouring seen
    after death, and the kidneys become inflamed.

Detection and Estimation of Potassic Chlorate.

    § 135. Organic fluids are best submitted to dialysis; the dialysed
    fluid should then be concentrated and qualitative tests applied. One
    of the best tests for the presence of a chlorate is, without doubt,
    that recommended by Fresenius. The fluid to be tested is acidulated
    with a few drops of sulphuric acid; sulphate of indigo added
    sufficient to colour the solution blue, and finally a few drops of
    sulphurous acid. In presence of potassic or sodic chlorate, the blue
    colour immediately vanishes. This method is capable of detecting 1
    part in 128,000; provided the solution is not originally coloured,
    and but little organic matter is present.

    The urine can be examined direct, but if it contain albumen, the
    blue colour may disappear and yet chlorate be present; if too much
    sulphurous acid be also added, the test may give erroneous results.
    These are but trivial objections, however, for if the analyst
    obtains a response to the test, he will naturally confirm or
    disprove it by the following process:--

    The liquid under examination, organic or otherwise, is divided into
    two equal parts. In the one, all the chlorine present is
    precipitated as chloride by silver nitrate in the usual way, and the
    chloride of silver collected and weighed. In the other, the liquid
    is evaporated to dryness and well charred by a dull red heat, the
    ash dissolved in weak nitric acid, and the chlorides estimated as in
    the first case. If chlorates were present, there will be a
    difference between the two estimations, proportionate to the amount
    of chlorates which have been converted into chlorides by the
    carbonisation, and the first silver chloride subtracted from the
    second will give an argentic chloride which is to be referred to
    chlorate. In this way also the amount present may be quantitatively
    estimated, 100 parts of silver chloride equalling 85·4 of potassic

Toxicological Detection of Alkali Salts.

(See also _ante_, p. 121.)

    § 136. Sodium, in combination, especially with chlorine, and also
    with sulphuric, carbonic, and phosphoric acids, is found in the
    plasma of the blood, in the urinary secretion, in the pancreatic
    juice, in human bile, and in serous transudations, &c. Potassium, in
    combination, is especially found in the red blood-corpuscles, in the
    muscles, in the nervous tissues, and in milk. Ammonia, in
    combination with acids, is naturally found in the stomach, in the
    contents of the intestine; it is also a natural constituent of the
    blood in small traces, and in a corpse is copiously evolved from
    putrefactive changes.

    It hence follows, that mere qualitative tests for these elements in
    the tissues or fluids of the body are of not the slightest use, for
    they are always present during the life of the healthiest
    individual, and can be found after death in persons dying from any
    malady whatever. To establish the fact of a person having taken an
    unusual dose of any of the alkali salts, by simply chemical
    evidence, it must be proved that the alkalies are present in unusual
    quantities or in an abnormal state of combination.

    In cases of rapid death, caused by sodic or potassic salts, they
    will be found in such quantity in the contents of the stomach, or in
    matters vomited, that there will probably be no difficulty in coming
    to a direct conclusion; but if some time has elapsed, the analyst
    may not find a sufficient ground for giving a decided judgment, the
    excretion of the alkali salts being very rapid.

    In most cases, it will be well to proceed as follows:--The contents
    of the stomach are, if necessary, diluted with distilled water, and
    divided into three parts, one of which is submitted to dialysis, and
    then the dialysed liquid evaporated to a small bulk and examined
    qualitatively, in order to ascertain whether a large amount of the
    alkaline salts is present, and in what form. In this way, the
    presence or absence of nitrate of potassium or sodium may be proved,
    or the iodide, bromide, sulphate, and chlorate detected.

    To find, in this way, nitrate of potassium, a coarse test is
    preferable to the finer tests dependent upon conversion of the
    nitrate into nitrites or into ammonia, for these tests are so
    delicate, that nitrates may be detected in traces; whereas, in this
    examination, to find traces is of no value. Hence, the old-fashioned
    test of treating the concentrated liquid in a test-tube with copper
    filings and then with sulphuric acid, and looking for the red fumes,
    is best, and will act very well, even should, as is commonly the
    case, some organic matters have passed through the dialyser.

    Chlorates are indicated if the liquid is divided into two parts and
    tested in the manner recommended at p. 127. If present in any
    quantity, chlorates or nitrates may be indicated by the brilliant
    combustion of the organic matter when heated to redness, as also by
    the action of strong sulphuric acid on the solid substances--in the
    one case, yellow vapours of peroxide of chlorine being evolved--in
    the other, the red fumes already mentioned of nitric peroxide.

    With regard to a substance such as the hydro-potassic tartrate, its
    insolubility in water renders it not easy of detection by dialysis;
    but its very insolubility will aid the analyst, for the contents of
    the stomach may be treated with water, and thus all soluble salts of
    the alkalies extracted. On now microscopically examining the
    insoluble residue, crystals of bitartrate, if present, will be
    readily seen. They may be picked up on a clean platinum wire and
    heated to redness in a Bunsen flame, and spectroscopically examined.
    After heating, the melted mass will have an alkaline reaction, and
    give a precipitate with platinic chloride. All other organic salts
    of potassium are soluble, and a white crystal giving such reaction
    must be hydro-potassic tartrate.

    =Ammonium Salts.=--If the body is fresh, and yet the salts of
    ammonium present in large amount, it is safe to conclude that they
    have an external origin; but there might be some considerable
    difficulty in criminal poisoning by a neutral salt of ammonium, and
    search for it in a highly putrid corpse. Probably, in such an
    exceptional case, there would be other evidence. With regard to the
    quantitative separation and estimation of the fixed alkalies in the
    ash of organic substances, the reader is referred to the processes
    given in “Foods,” p. 99, _et seq._, and in the present work, p. 121.





    § 137. Petroleum is a general term for a mixture of hydrocarbons of
    the paraffin series, which are found naturally in certain parts of
    the world, and are in commerce under liquid and solid forms of
    various density. Crude petroleum is not imported into England, the
    original substance having previously undergone more or less
    rectification. The lighter and more volatile portions are known
    under the name of cymogene, rhigolene, gasolene, and naphtha.

    § 138. =Cymogene= has a specific gravity of ·590, and boils at 0°.
    It has been employed in refrigerating machines. It appears to
    consist chiefly of butane (C₄H₁₀).

    § 139. =Rhigolene= is now used in medicine in the form of spray to
    produce local anæsthesia. It boils at 18°, and has a density of

    § 140. =Gasolene= has a density of ·680-·688; it has received
    technical applications in the “naphthalising” of air and gas.

    § 141. =Benzoline= (=mineral naphtha=, =petroleum naphtha=,
    =petroleum spirit=, =petroleum ether=) is a mixture of the lighter
    series of hydro-carbons; the greater part consists of heptane, and
    there is also a considerable quantity of pentane (C₇H₁₆) present.
    The specific gravity varies from ·69 to ·74. It is very inflammable,
    and is used in sponge lamps, and also as a solvent for gutta-percha,
    naphthalene, paraffin, wax, and many other bodies. By the practical
    chemist it is much employed.

    The similarity of the terms _benzoline_ and _benzene_ has caused
    benzoline to be often confused with _benzol_ or _benzene_, the
    leading constituent of coal-tar naphtha (C₆H₆). Mr Allen[132] gives
    in the following table a summary of the chief points of distinction,
    both between petroleum naphtha, shale naphtha, and coal-tar naphtha.
    The table is founded upon the examination of particular samples, and
    commercial samples may present a few minor deviations.

[132] _Commercial Organic Analysis_, vol. ii. p. 31.


  | Petroleum Naphtha.  |   Shale Naphtha.     |  Coal-tar Naphtha.   |
  |Contains at least 75 |Contains at least 60  |Consists almost wholly|
  |per cent. of heptane,|to 70 per cent. of    |of benzene, C₆H₆, and  |
  |C₇H₁₆, and other      |heptylene, C₇H₁₄, and  |other homologous     |
  |hydrocarbons of the  |other hydrocarbons of |hydrocarbons, with a  |
  |marsh gas or paraffin|the olefin series; the|small percentage of   |
  |series; the remainder|remainder paraffins.  |light hydrocarbons in |
  |apparently olefins,  |No trace of benzene or|some samples.         |
  |C_{n}H_{2n}, with    |its homologues.       |                      |
  |distinct traces of   |                      |                      |
  |benzene and its      |                      |                      |
  |homologues.          |                      |                      |
  |                     |                      |                      |
  |Specific gravity at  |Specific gravity at   |Specific gravity ·876.|
  |15°, ·600.           |15°, ·718.            |                      |
  |                     |                      |                      |
  |Distils between 65°  |Distils between 65°   |Distils between 80°   |
  |and 100°.            |and 100°.             |and 120°.             |
  |                     |                      |                      |
  |Dissolves coal-tar   |Behaves similarly to  |Readily dissolves     |
  |pitch, but slightly; |petroleum naphtha with|pitch, forming a deep |
  |liquid, but little   |regard to the solution|brown solution.       |
  |coloured even after  |of pitch.             |                      |
  |prolonged contact.   |                      |                      |
  |                     |                      |                      |
  |On shaking three     |When treated with     |The liquids form a    |
  |measures of the      |fused carbolic acid   |homogeneous mixture   |
  |sample with one      |crystals, the liquids |when treated with     |
  |measure of fused     |mix perfectly.        |fused carbolic acid   |
  |crystals of absolute |                      |crystals.             |
  |carbolic acid, no    |                      |                      |
  |solution. Liquids not|                      |                      |
  |miscible.            |                      |                      |
  |                     |                      |                      |
  |Combines with 10 per |Combines with upwards |Combines slowly with  |
  |cent. of its weight  |of 90 per cent. of its|30-40 per cent. of its|
  |of bromine in the    |weight of bromine.    |weight of bromine.    |
  |cold.                |                      |                      |

    § 142. =Paraffin Oil= (or =kerosine, mineral oil, photogen=, &c.) is
    the chief product resulting from the distillation of American
    petroleum--the usual specific gravity is about ·802--it is a mixture
    of hydrocarbons of the paraffin series. It should be free from the
    more volatile constituents, and hence should not take fire when a
    flame is applied near the surface of the cold liquid.

    § 143. =Effects of Petroleum.=--Since we have here to deal with a
    commercial substance of such different degrees of purity, and
    various samples of which are composed of such various proportions of
    different hydrocarbons, its action can only be stated in very
    general terms. Eulenberg[133] has experimented with the lighter
    products obtained from the distillation of Canadian petroleum. This
    contained sulphur products, and was extremely poisonous, the vapour
    killing a rabbit in a short time, with previous insensibility and
    convulsions. The autopsy showed a thin extravasation of blood on the
    surface of each of the bulbi, much coagulated blood in the heart,
    congested lungs, and a bloody mucus covering the tracheal mucous
    membrane. An experiment made on a cat with the lighter petroleum
    (which had no excess of sulphur) in the state of vapour, showed that
    it was an anæsthetic, the anæsthesia being accompanied by
    convulsions, which towards the end were tetanic and violent. The
    evaporation of 1·5 grm. in a close chamber killed the animal in
    three hours. The lungs were found congested, but little else was
    remarkable. Much petroleum vapour is breathed in certain factories,
    especially those in which petroleum is refined.[134] From this cause
    there have been rather frequent toxic symptoms among the workmen.
    Eulenberg[135] describes the symptoms as follows:--A person, after
    breathing an overdose of the vapour, becomes very pale, the lips are
    livid, the respiration slow, the heart’s action weak and scarcely to
    be felt. If he does not immediately go into the open air away from
    the poisonous vapour, these symptoms may pass on to insensibility,
    convulsions, and death. It often occasions a condition of the
    voluntary muscles similar to that induced by drunkenness, and on
    recovery the patient is troubled by singing in the ears and noises
    in the head. The smell and taste of the poison may remain for a long

[133] _Gewerbe-Hygiene._

[134] The vapour most likely to rise at the ordinary temperature, and
mix with the atmosphere, is that of the lighter series, from cymogene to

[135] _Op. cit._

    § 144. Poisoning by taking light petroleum into the stomach is not
    common. In a case recorded by Taylor,[136] a woman, for the purpose
    of suicide, swallowed a pint of petroleum, There followed a slight
    pain in the stomach, and a little febrile disturbance, and a
    powerful smell of petroleum remained about the body for six days;
    but she completely recovered. In August 1870 a sea-captain drank a
    quantity of paraffin, that is, lighting petroleum, and died in a few
    hours in an unconscious state. A child, 2 years old, was brought to
    King’s College Hospital within ten minutes after taking a
    teaspoonful of paraffin. It was semi-comatose and pale, with
    contracted pupils; there was no vomiting or purging. Emetics of
    sulphate of zinc were administered, and the child recovered in
    twenty-four hours. In another case treated at the same hospital, a
    child had swallowed an unknown quantity of paraffin. It fell into a
    comatose state, which simulated tubercular meningitis, and lasted
    for nearly three weeks.[137] In a case recorded by Mr Robert
    Smith,[138] a child, 4 years of age, had swallowed an unknown
    quantity of paraffin. A few minutes afterwards, the symptoms
    commenced; they were those of suffocation, with a constant cough;
    there was no expectoration; the tongue, gums, and cheeks were
    blanched and swollen where the fluid touched them; recovery
    followed. A woman, aged 32, who had taken a quarter of a pint of
    paraffin, was found unconscious and very cold; the stomach-pump was
    used, and she recovered.[139] Hence it is tolerably certain, from
    the above instances, that should a case of petroleum poisoning
    occur, the expert will not have to deal with infinitesimal
    quantities; but while the odour of the oil will probably be
    distinctly perceptible, there will be also a sufficient amount
    obtained either from matters vomited, or the contents of the
    stomach, &c., so that no difficulty will be experienced in
    identifying it.

[136] _Poisons_, p. 656

[137] _Brit. Med. Journ._, Sept. 16, 1876, p. 365.

[138] _Brit. Med. Journ._, Oct. 14, 1876.

[139] _Pharm. Journ._, Feb. 12, 1875; also for other cases see _Brit.
Med. Journ._, Nov. 4, 1876; and Köhler’s _Physiol. Therap._, p. 437.

    § 145. In order to separate petroleum from any liquid, the
    substances under examination must be carefully distilled in the
    manner recommended under “_Ether_.” The lighter petroleums will
    distil by the aid of a water-bath; but the heavier require a
    stronger heat; redistillation of the distillate may be necessary.
    The odour of the liquid, its inflammable character, and its other
    properties, will be sufficient for identification.


    § 146. Coal-tar-naphtha in its crude state, is an extremely complex
    liquid, of a most disagreeable smell. Much benzene (C₆H₆) is present
    with higher homologues of the benzene series. Toluene (C₇H₈),
    naphthalene (C₁₀H₈), hydrocarbons of the paraffin series,
    especially hexane (C₆H₁₄), and hydrocarbons of the olefin series,
    especially pentylene, hexylene, and heptylene (C₅H₁₀, C₆H₁₂ and
    C₇H₁₄). Besides these, there are nitrogenised bases, such as
    aniline, picoline, and pyridine; phenols, especially carbolic acid;
    ammonia, ammonium sulphide, carbon disulphide, and probably other
    sulphur compounds; acetylene and aceto-nitrile. By distillation and
    fractional distillation are produced what are technically known
    ”_once run_” _naphtha_, _90 per cent. benzol_, _50 and 90 per cent.
    benzol_,[140] _30 per cent. benzol_, _solvent naphtha_, and residue
    known as “_last runnings_.”

[140] Or 50/90 benzol, this indicates that 50 per cent. distils over
below 100°; and 40, making in all 90, below 120°.

    § 147. Taylor[141] records a case in which a boy, aged 12, swallowed
    about 3 ozs. of naphtha, the kind usually sold for burning in lamps,
    and died with symptoms of narcotic poisoning. The child, after
    taking it, ran about in wild delirium, he then sank into a state of
    collapse, breathing stertorously, and the skin became cold and
    clammy. On vomiting being excited, he rejected about two
    tablespoonfuls of the naphtha, and recovered somewhat, but again
    fell into collapse with great muscular relaxation. The breathing was
    difficult; there were no convulsions; the eyes were fixed and
    glassy, the pupils contracted; there was frothing at the mouth. In
    spite of every effort to save him, he died in less than three hours
    after taking the poison. The body, examined three days after death,
    smelt strongly of naphtha, but the _post-mortem_ appearances were in
    no way peculiar, save that the stomach contained a pint of
    semi-fluid matter, from which a fluid, having the characteristics of
    impure benzene, was separated.

[141] _Op. cit._, p. 657.

    § 148. The effects of the vapour of benzene have been studied by
    Eulenberg in experiments on cats and rabbits, and there are also
    available observations on men[142] who have been accidentally
    exposed to its influence. From these sources of information, it is
    evident that the vapour of benzene has a distinctly narcotic effect,
    while influencing also in a marked degree the spinal cord. There
    are, as symptoms, noises in the head, convulsive trembling and
    twitchings of the muscles, with difficulty of breathing.

[142] Dr. Stone, _Med. Gaz._, 1848, vol. xii. p. 1077.


    § 149. Benzene is separated from liquids by distillation, and may be
    recognised by its odour, and by the properties described at p. 130.
    The best process of identification, perhaps, is to purify and
    convert it into nitro-benzene, and then into aniline, in the
    following manner:--

    1. =Purification.=--The liquid is agitated with a solution of
    caustic soda; this dissolves out of the benzene any bodies of an
    acid character, such as phenol, &c. The purified liquid should again
    be distilled, collecting that portion of the distillate which passes
    over between 65° and 100°; directly the thermometer attains nearly
    the 100°, the distillation should be stopped. The distillate, which
    contains all the benzene present, is next shaken with concentrated
    sulphuric acid in the cold; this will dissolve out all the
    hydrocarbons of the ethylene and acetylene series. On removing the
    layer of benzene from the acid, it must be again shaken up with
    dilute soda, so as to remove any trace of acid. The benzene is, by
    this rather complicated series of operations, obtained in a very
    fair state of purity, and may be converted into nitro-benzene, as

    2. =Conversion into Nitro-Benzene.=--The oily liquid is placed in a
    flask, and treated with four times its volume of fuming nitric acid.
    The flask must be furnished with an upright condenser; a vigorous
    action mostly takes place without the application of heat, but if
    this does not occur, the flask may be warmed for a few minutes.

    After the conversion is over, the liquid, while still warm, must be
    transferred into a burette furnished with a glass tap, or to a
    separating funnel, and all, except the top layer, run into cold
    water; if benzene was originally present, either oily drops of
    nitro-benzene will fall, or if the benzene was only in small
    quantity, a fine precipitate will gradually settle down to the
    bottom of the vessel, and a distinct bitter-almond smell be
    observed; but, if there be no benzene in the original liquid, and,
    consequently, no nitro-benzene formed, no such appearance will be

    3. =Conversion into Aniline.=--The nitro-benzene may itself be
    identified by collecting it on a wet filter, dissolving it off the
    filter by alcohol, acidifying the alcoholic solution by hydrochloric
    acid, and then boiling it for some time with metallic zinc. In this
    way aniline is formed by reduction. On neutralising and diluting the
    liquid, and cautiously adding a little clear solution of
    bleaching-powder, a blue or purple colour passing to brown is in a
    little time produced.


    § 150. The terpenes are hydrocarbons of the general formula
    C_{n}H_{2n-4}. The natural terpenes are divided into three

    1. =The true terpenes=, _formula_ (C₁₀H₁₆)--a large number of
    essential oils, such as those of turpentine, orange peel, nutmeg,
    caraway, anise, thyme, &c., are mainly composed of terpenes.

    2. =The cedrenes=, _formula_ (C₁₅H₂₄)--the essential oil of cloves,
    rosewood, cubebs, calamus, cascarilla, and patchouli belong to this

    3. =The colophene hydrocarbons=, _formula_ (C₂₀H₃₂), represented by

    Of all these, oil of turpentine alone has any toxicological
    significance; it is, however, true that all the essential oils, if
    taken in considerable doses, are poisonous, and cause, for the most
    part, vascular excitement and complex nervous phenomena, but their
    action has not been very completely studied. They may all be
    separated by distillation, but a more convenient process for
    recovering an essential oil from a liquid is to shake it up with
    petroleum ether, separating the petroleum and evaporating
    spontaneously; by this means the oil is left in a fair state of


    § 151. Various species of pine yield a crude turpentine, holding in
    solution more or less resin. The turpentine may be obtained from
    this exudation by distillation, and when the first portion of the
    distillate is treated with alkali, and then redistilled, the final
    product is known under the name of “rectified oil of turpentine,”
    and is sometimes called “camphene.” It mainly consists of
    terebenthene. Terebenthene obtained from French turpentine differs
    in some respects from that obtained from English or American
    turpentine. They are both mobile, colourless liquids, having the
    well-known odour of turpentine and highly refractive; but the French
    terebenthene turns a ray of polarised light to the left -40·3° for
    the sodium ray, and the English to the right +21·5°; the latter
    terebenthene is known scientifically as austra-terebenthene. This
    action on polarised light is retained in the various compounds and
    polymers of the two turpentine oils.

    The specific gravity of turpentine oil is ·864; its boiling point,
    when consisting of pure terebenthene, 156°, but impurities may raise
    it up to 160°; it is combustible and burns with a smoky flame. Oil
    of turpentine is very soluble in ether, petroleum ether, carbon
    disulphide, chloroform, benzene, fixed and essential oils, and by
    the use of these solvents it is conveniently separated from the
    contents of the stomach. It is insoluble in water, glycerin, and
    dilute alkaline and acid solutions; and very soluble in absolute
    alcohol, from which it may be precipitated by the addition of water.

    It is polymerised by the action of strong sulphuric acid, the
    polymer, of course, boiling at a higher temperature than the
    original oil. With water it forms a crystalline hydrate
    (C₁₀H₂₀O₂,H₂O). On passing nitrosyl chloride gas into the oil,
    either pure or diluted with chloroform or alcohol, the mixture being
    cooled by ice, a white crystalline body is deposited, of the formula
    C₁₀H₁₆(NOCl). By treating this compound with alcoholic potash, the
    substitution product (C₁₀H₁₆NO) is obtained. By treating turpentine
    with an equal bulk of warm water, and shaking it in a large bottle
    with air, camphoric acid and peroxide of hydrogen are formed. When
    turpentine oil is left in contact with concentrated hydrochloric
    acid, there is formed terebenthene dihydrochloride (C₁₀H₁₆2HCl),
    which forms rhombic plates, insoluble in water, and decomposable by
    boiling alcoholic potash, with formation of terpinol, (C₁₀H₁₇)₂O.
    The dihydrochloride gives a colour-reaction with ferric chloride.
    This is an excellent test--not, it is true, confined to oil of
    turpentine--but common to the dihydrochlorides of all the terpenes.
    A few drops of the oil are stirred in a porcelain capsule with a
    drop of hydrochloric acid, and one of ferric chloride solution; on
    gently heating, there is produced first a rose colour, then a
    violet-red, and lastly a blue.

    § 152. =Effects of the Administration of Turpentine.=--L. W.
    Liersch[143] exposed animals to the vapour of turpentine, and found
    that a cat and a rabbit died within half an hour. There was observed
    uneasiness, reeling, want of power in the limbs (more especially in
    the hinder extremities), convulsions partial, or general, difficulty
    of respiration; and the heart’s action was quickened. Death took
    place, in part, from asphyxia, and in part was attributable to a
    direct action on the nervous centres. The autopsy showed congestion
    of the lungs, ecchymoses of the kidney, and much blood in the liver
    and spleen. Small doses of turpentine-vapour cause (according to Sir
    B. W. Richardson)[144] giddiness, deficient appetite, and anæmia.
    From half an ounce to an ounce is frequently prescribed in the
    country as a remedy for tape-worm; in smaller quantities it is found
    to be a useful medicine in a great variety of ailments. The larger
    doses produce a kind of intoxication with giddiness, followed often
    by purging and strangury, not unfrequently blood and albumen (or
    both) is found in the urine. When in medical practice I have given
    the oil, and seen it given by others, in large doses for tape-worm
    to adults, in perhaps 40 cases, but in no one instance were the
    symptoms severe; the slight intoxication subsided quickly, and in a
    few hours the patients recovered completely. Nevertheless it has
    been known to destroy the lives of children, and cause most serious
    symptoms in adults. Two fatal cases are mentioned by Taylor; one was
    that of a child who died fifteen hours after taking half an ounce of
    the oil; in another an infant, five months old, died rapidly from a
    teaspoonful. The symptoms in these fatal cases were profound coma
    and slight convulsions; the pupils were contracted, and there was
    slow and irregular breathing. Turpentine is eliminated in a changed
    form by the kidneys, and imparts an odour of violet to the urine;
    but the nature of the odoriferous principle has not yet been

[143] Clarus in Schmidt’s _Jahrbücher_, Bd. cxvii., i. 1863; and
_Vierteljahrsschr. für ger. Med._, xxii., Oct. 1862.

[144] _Brit. and For. Med.-Chir. Review_, April 1863.


    § 153. A great many essential oils deposit, after exposure to air,
    camphors produced by oxidation of their terpenes. Ordinary camphor
    is imported in the rough state from China and Japan, and is prepared
    by distilling with water the wood of _Camphora officinarum_; it is
    resublimed in England. The formula of camphor is C₁₀H₁₆O; it has a
    density of ·986 to ·996; melts at 175°, and boils at 205°. It is
    readily sublimed, especially in a vacuum, and is indeed so volatile
    at all temperatures, that a lump of camphor exposed to the air
    wastes away. It is somewhat insoluble in water (about 1 part in
    1000), but this is enough to impart a distinct taste to the water;
    it is insoluble in chloroform, ether, acetone, acetic acid, carbon
    disulphide, and oils. It has a fragrant odour and a burning taste. A
    10 per cent. solution in alcohol turns a ray of polarised light to
    the right +42·8°. By distillation with zinc chloride, cymene and
    other products are produced. By prolonged treatment with nitric
    acid, camphor is oxidised to camphoric acid (C₁₀H₁₆O₄). Camphor
    unites with bromine to form a crystalline, unstable dibromide, which
    splits up on distillation into hydrobromic acid and monobrom-camphor
    (C₁₀H₁₅BrO). The latter is used in medicine; it crystallises in
    prisms fusible at 76°, and is readily soluble in alcohol.

    § 154. =Pharmaceutical Preparations.=--The preparations officinal in
    the British Pharmacopœia are _camphor water_--water saturated with
    camphor, containing about one part per thousand.

    =Camphor Liniment.=--A solution of camphor in olive oil, strength 25
    per cent.

    =Compound Camphor Liniment.=--Composed of camphor, oil of lavender,
    strong solution of ammonia and alcohol; strength in camphor about 11
    per cent.

    =Spirit of Camphor.=--A solution of camphor in spirit; strength, 10
    per cent.

    Camphor is also a constituent of the _compound tincture of camphor_;
    but in this case it may be considered only a flavouring agent. There
    is a homœopathic solution of camphor in spirit (Rubini’s Essence of
    Camphor). The solution is made by saturating alcohol with camphor;
    it is, therefore, very strong--about half the bulk consisting of
    camphor. Camphor is used in veterinary medicine, both externally and

    § 155. =Symptoms.=--Camphor acts energetically on the brain and
    nervous system, especially if it is given in strong alcoholic
    solution, and thus placed under conditions favouring absorption.
    Some years ago, Dr. G. Johnson[145] published a series of cases
    arising from the injudicious use of “homœopathic solution of
    camphor,” from 7 to 40 drops of Rubini’s homœopathic camphor taken
    for colds, sore throat, &c., having produced coma, foaming at the
    mouth, convulsions, and partial paralysis. All the patients
    recovered, but their condition was for a little time alarming.

[145] _Brit. Med. Journ._, Feb. 27, 1878, p. 272; see also _ibid._, Feb.

    The cases of fatal poisoning by camphor are very rare. A woman, aged
    46, pregnant four months, took 12 grms. (about 184 grains) in a
    glass of brandy for the purpose of procuring abortion. In a very
    short time the symptoms commenced; she had intolerable headache, the
    face was flushed, and there was a sensation of burning in the
    stomach. In eight hours after taking the dose, she had strangury and
    vomiting, and the pain in the epigastrium was intense. These
    symptoms continued with more or less severity until the third day,
    when she became much worse. Her face was pale and livid, the eyes
    hollow, the skin cold and insensible, pulse weak and thready,
    breathing laboured. There were violent cramps in the stomach and
    retention of urine for twenty-four hours, and then coma. The patient
    lingered on yet another three days, aborted, and died.[146]

[146] _Journ. de Chim. Méd._, May 1860.

    Dr. Schaaf[147] has recorded three cases of poisoning--one of which
    was fatal. A woman gave about half a teaspoonful of a camphor
    solution to each of her three children, the ages being respectively
    five and three years and fifteen months. The symptoms noted were
    pallor of the face, a burning pain in the throat, thirst, vomiting,
    purging, convulsions, and afterwards coma. The youngest child died
    in seven hours; the others recovered. The smallest dose known to
    have produced violent symptoms in an adult is 1·3 grm. (20 grains);
    the largest dose known to have been recovered from is 10·4 grms.
    (160 grains).[148]

[147] _Journ. de Chim. Méd._, 1850, p. 507.

[148] Taylor on _Poisons_, 3rd ed., 661.

    § 156. =Post-mortem Appearances.=--The bodies of animals or persons
    dying from poisoning by camphor, smell strongly of the substance.
    The mucous membrane of the stomach has been found inflamed, but
    there seem to be no characteristic lesions.

    § 157. =Separation of Camphor from the Contents of the
    Stomach.=--The identification of camphor would probably in no case
    present any difficulty. It may be readily dissolved out from organic
    fluids by chloroform. If dissolved in fixed oils, enough for the
    purposes of identification may be obtained by simple distillation.
    It is precipitated from its alcoholic solution by the addition of



§ 158. The chemical properties of ordinary alcohol are fully described,
with the appropriate tests, in “Foods,” pp. 369-384, and the reader is
also referred to the same volume for the composition and strength of the
various alcoholic drinks.

=Statistics.=--If we were to include in one list the deaths indirectly
due to chronic, as well as acute poisoning by alcohol, it would stand
first of all poisons in order of frequency, but the taking of doses so
large as to cause death in a few hours is rare. The deaths from alcohol
are included by the English registrar-general under two heads, viz.,
those returned as dying from _delirium tremens_, and those certified as
due directly to intemperance.

During the twenty-five years, from 1868 to 1892, 30,219 deaths have been
registered as due to intemperance, which gives an average of 1209 per
year. The rate per million has varied during the period from 29 to 71;
and the figures taken as a whole show that deaths from intemperance
appear to be increasing; the increase may be only apparent, not real,
for it is a significant circumstance that deaths registered under liver
diseases show a corresponding decrease; it is, therefore, not unlikely
that deaths which formerly would be ascribed to liver disease, are more
often now stated to be the effects of intemperance.

Deaths directly due to large doses of alcohol are not uncommon; during
the ten years ending 1892, 105 deaths (81 males and 24 females) were
ascribed under the head of “accident or negligence” directly to alcohol.




                _Intemperance_  --------------
                _Liver disease_ ..............
  _The Scale for Intemperance is as printed._
  _That for Liver diseases is 10 times larger._]

§ 159. =Criminal or Accidental Alcoholic Poisoning.=--Suicide by
alcohol, in the common acceptation of the term, is rare, and murder
still rarer, though not unknown. In the ten years ending 1892, only
three deaths from alcohol (1 male and 2 females) are recorded as
suicidal. Perhaps the most common cause of fatal acute poisoning by
alcohol is either a foolish wager, by which a man bets that he can drink
so many glasses of spirits without bad effect; or else the drugging of a
person already drunk by his companions in a sportive spirit.

§ 160. =Fatal Dose.=--It is difficult to say what would be likely to
prove a lethal dose of alcohol, for a great deal depends, without doubt,
on the dilution of the spirit, since the mere local action of strong
alcohol on the mucous membranes of the stomach, &c., is severe (one may
almost say corrosive), and would aid the more remote effects. In
Maschka’s case,[149] a boy of nine years and a girl of five, died from
about two and a half ounces of spirit of 67 per cent. strength, or 48·2
c.c. (1·7 oz.) of absolute alcohol.

[149] Recorded by Maschka (_Gutachten der Prager Facultät_, iv. 239; see
also Maschka’s _Handbuch der gericht. Medicin_, Band. ii. p. 384). The
following is a brief summary:--Franz. Z., nine years old, and Caroline
Z., eight years old, were poisoned by their stepfather with spirit of 67
per cent. strength taken in small quantities by each--at first by
persuasion, and the remainder administered by force. About one-eighth of
a pint is said to have been given to each child. Both vomited somewhat,
then lying down, stertorous breathing at once came on, and they quickly
died. The autopsy, three days after death, showed dilatation of the
pupils; _rigor mortis_ present in the boy, not in the girl; and the
membranes of the brain filled with dark fluid blood. The smell of
alcohol was perceptible on opening the chest; the mucous membrane of the
bronchial tubes and gullet was normal, both lungs œdematous, the fine
tubes gorged with a bloody frothy fluid, and the mucous membrane of the
whole intestinal canal was reddened. The stomach was not, unfortunately,
examined, being reserved for chemical analysis. The heart was healthy;
the pericardium contained some straw-coloured fluid. Chemical analysis
gave an entirely negative result, which must have been from insufficient
material having been submitted to the analyst, for I cannot see how the
vapours of alcohol could have been detected by the smell, and yet have
evaded chemical processes.

In a case related by Taylor, a child, seven years old, died from some
quantity of brandy, probably about 113·4 c.c. (4 ozs.), which would be
equal to at least 56·7 c.c. (2 ozs.) of absolute alcohol. From other
cases in which the quantity of absolute alcohol can be, with some
approximation to the truth, valued, it is evident that, for any child
below ten or twelve, quantities of from 28·3 to 56·6 c.c. (1-2 ozs.) of
absolute alcohol contained in brandy, gin, &c., would be a highly
dangerous and probably fatal dose; while the toxic dose for adults is
somewhere between 71·8-141·7 c.c. (2·5-5 ozs.).

§ 161. =Symptoms.=--In the cases of rapid poisoning by a large dose of
alcohol, which alone concern us, the preliminary, and too familiar
excitement of the drunkard, may be hardly observable; but the second
stage, that of depression, rapidly sets in; the unhappy victim sinks
down to the ground helpless, the face pale, the eyes injected and
staring, the pupils dilated, acting sluggishly to light, and the skin
remarkably cold. Fräntzel[150] found, in a case in which the patient
survived, a temperature of only 24·6° in the rectum, and in that of
another person who died, a temperature of 23·8°. The mucous membranes
are of a peculiar dusky blue; the pulse, which at first is quick, soon
becomes slow and small; the respiration is also slowed, intermittent,
and stertorous; there is complete loss of consciousness and motion; the
breath smells strongly of the alcoholic drink, and if the coma continues
there may be vomiting and involuntary passing of excreta. Death
ultimately occurs through paralysis of the respiratory centres.
Convulsions in adults are rare, in children frequent. Death has more
than once been immediately caused, not by the poison, but by accidents
dependent upon loss of consciousness. Thus food has been sucked into the
air-tubes, or the person has fallen, so that the face was buried in
water, ordure, or mud; here suffocation has been induced by mechanical

[150] _Temperaturerniedrigung durch Alcoholintoxication, Charité
Annalen_, i. 371.

A remarkable course not known with any other narcotic is that in which
the symptoms remit, the person wakes up, as it were, moves about and
does one or more rational acts, and then suddenly dies. In this case
also, the death is not directly due to alcohol, but indirectly--the
alcohol having developed œdema, pneumonia, or other affection of the
lungs, which causes the sudden termination when the first effect of the
poison has gone off. The time that may elapse from the commencement of
coma till death varies from a few minutes to days; death has occurred
after a quarter of an hour, half an hour, and an hour. It has also been
prolonged to three, four, and six days, during the whole of which the
coma has continued. The average period may, however, be put at from six
to ten hours.

§ 162. =Post-mortem Appearances.=--Cadaveric rigidity lasts tolerably
long. Casper has seen it still existing nine days after death, and
Seidel[151] seven days (in February). Putrefaction is retarded in those
cases in which a very large dose has been taken, but this is not a very
noticeable or constant characteristic. The pupils are mostly dilated.
The smell of alcohol should be watched for; sometimes it is only present
in cases where but a short time has elapsed between the taking of the
poison and death; putrefaction may also conceal it, but under favourable
circumstances, especially if the weather is cold, the alcoholic smell
may remain a long time. Alcohol may cause the most intense redness and
congestion of the stomach. The most inflamed stomach I ever saw, short
of inflammation by the corrosive poisons, was that of a sailor, who died
suddenly after a twenty-four hours’ drinking bout: all the organs of the
body were fairly healthy, the man had suffered from no disease; analysis
could detect no poison but alcohol; and the history of the case,
moreover, proved clearly that it was a pure case of alcoholic poisoning.

[151] Seidel, Maschka’s _Handbuch_, Bd. ii. p. 380.

In a case related by Taylor, in which a child drank 4 ozs. of brandy and
died, the mucous membrane of the stomach presented patches of intense
redness, and in several places was thickened and softened, some portions
being actually detached and hanging loose, and there were evident signs
of extravasations of blood. The effect may not be confined to the
stomach, but extend to the duodenum and even to the whole intestinal
canal. The blood is generally dark and fluid, and usually the contents
of the skull are markedly hyperæmic, the pia very full of blood, the
sinuses and plexus gorged; occasionally, the brain-substance shows signs
of unusual congestion; serum is often found in the ventricles. The great
veins of the neck, the lungs, and the right side of the heart, are very
often found full of blood, and the left side empty. Œdema of the lungs
also occurs with tolerable frequency. The great veins of the abdomen are
also filled with blood, and if the coma has been prolonged, the bladder
will be distended with urine. A rare phenomenon has also been
noticed--namely, the occurrence of blebs on the extremities, &c., just
as if the part affected had been burnt or scalded. Lastly, with the
changes directly due to the fatal dose may be included all those
degenerations met with in the chronic drinker, provided the case had a
history of previous intemperance.

§ 163. =Excretion of Alcohol.=--Alcohol, in the diluted form, is quickly
absorbed by the blood-vessels of the stomach, &c., and circulates in the
blood; but what becomes of it afterwards is by no means settled. I think
there can be little doubt that the lungs are the main channels through
which it is eliminated; with persons given up to habits of intemperance,
the breath has constantly a very peculiar ethereal odour, probably
dependent upon some highly volatile oxidised product of alcohol.

Alcohol is eliminated in small proportion only by the kidneys.
Thudichum, in an experiment[152] by which 4000 grms. of absolute alcohol
were consumed by thirty-three men, could only find in the collected
urine 10 grms. of alcohol. The numerous experiments by Dupré also
establish the same truth, that but a fraction of the total alcohol
absorbed is excreted by the kidneys. According to Lallemand, Perrin, and
Duroy the content of the brain in alcohol is more than that of the
other organs. I have found also that the brain after death has a
wonderful attraction for alcohol, and yields it up at a water-heat very
slowly and with difficulty. In one experiment, in which a finely-divided
portion of brain, which had been soaking in alcohol for many weeks, was
submitted to a steam heat of 100°, twenty-four hours’ consecutive
heating failed to expel every trace of spirit.

[152] See Thudichum’s _Pathology of the Urine_, London, 1877, in which
both his own and Dr. Dupré’s experiments are summarised.

It is probable that true alcoholates of the chemical constituents of the
brain are formed. In the case of vegetable colloidal bodies, such, for
example, as the pulp of cherries, a similar attraction has been
observed, the fruit condensing, as it were, the alcohol in its own
tissues, and the outer liquid being of less alcoholic strength than that
which can be expressed from the steeped cherries. Alcohol is also
excreted by the sweat, and minute fractions have been found in the

§ 164. =Toxicological Detection of Alcohol= (see “Foods,” pp.
406-419).--The living cells of the body produce minute quantities of
alcohol, as also some of the bacteria normally inhabiting the small
intestine produce small quantities of alcohol, and it is often found in
traces in putrefying fluids. Hence, mere qualitative proofs of the
presence of alcohol are insufficient on which to base an opinion as to
whether alcohol had been taken during life or not, and it will be
necessary to estimate the quantity accurately by some of the processes
detailed in “Foods,” p. 409, _et seq._ In those cases in which alcohol
is found in quantity in the stomach, there can, of course, be no
difficulty; in others, the whole of the alcohol may have been absorbed,
and chemical evidence, unless extremely definite, must be supplemented
by other facts.


    § 165. =Amylic Alcohol=--_Formula_, C₅H₁₁HO.--There is more than one
    amylic alcohol according to theory; eight isomers are possible, and
    seven are known. The amylic alcohols are identical in their chemical
    composition, but differ in certain physical properties, primary
    amylic alcohol boiling at 137°, and iso-amyl alcohol at 131·6°. The
    latter has a specific gravity of ·8148, and is the variety produced
    by fermentation and present in fusel oil.

    § 166. The experiments of Eulenberg[153] on rabbits, Cross[154] on
    pigeons, Rabuteau[155] on frogs, and Furst on rabbits, with those of
    Sir B. W. Richardson[156] on various animals, have shown it to be a
    powerful poison, more especially if breathed in a state of vapour.

[153] _Gewerbe Hygiene_, 1876, p. 440.

[154] _De l’Alcohol Amylique et Méthyl sur l’Organisme (Thèse)_,
Strasburg, 1863.

[155] “Ueber die Wirkung des Aethyl, Butyl u. Amyl Alcohols,” _L’Union_,
Nos. 90, 91, 1870. Schmidt’s _Jahrb._, Bd. 149, p. 263.

[156] _Trans. Brit. Association_, 1864, 1865, and 1866. Also, _Brit. and
Foreign Med. Chir. Rev._, Jan. 7, 1867, p. 247.

    Richardson, as the result of his investigations, considers that amyl
    alcohol when breathed sets up quite a peculiar class of symptoms
    which last for many hours, and are of such a character, that it
    might be thought impossible for the animal to recover, although they
    have not been known to prove fatal. There is muscular paralysis with
    paroxysms of tremulous convulsions; the spasms are excited by
    touching the animal, breathing upon it, or otherwise subjecting it
    to trifling excitation.

    § 167. Hitherto, neither the impure fusel oil, nor the purer
    chemical preparation, has had any toxicological importance. Should
    it be necessary at any time to recover small quantities from organic
    liquids, the easiest way is to shake the liquid up with chloroform,
    which readily dissolves amylic alcohol, and on evaporation leaves it
    in a state pure enough to be identified. Amyl alcohol is identified
    by the following tests:--(1) Its physical properties; (2) if warmed
    with twice its volume of strong sulphuric acid, a rose or red colour
    is produced; (3) heated with an acetate and strong sulphuric acid,
    _amyl acetate_, which has the odour of the jargonelle pear, is
    formed; (4) heated with sulphuric acid and potassic dichromate,
    valeric aldehyde is first produced, and then valeric acid is formed;
    the latter has a most peculiar and strong odour.

    § 168. =Amyl Nitrite, Iso-amyl Ester Nitrite= (C₅H₁₁NO₂).--Boiling
    point 97° to 99°, specific gravity ·877. Amyl nitrite is a limpid,
    and, generally, slightly yellow liquid; it has a peculiar and
    characteristic odour. On heating with alcoholic potash, the products
    are nitrite of potash and amylic alcohol; the amylic alcohol may be
    distilled off and identified. The presence of a nitrite in the
    alkaline solution is readily shown by the colour produced, by adding
    a few drops of a solution of meta-phenylenediamine.

    Sir B. W. Richardson and others have investigated the action of amyl
    nitrite, as well as that of the acetate and iodide; they all act in
    a similar manner, the nitrite being most potent. After absorption,
    the effects of amyl nitrite are especially seen on the heart and
    circulation: the heart acts violently, there is first dilatation of
    the capillaries, then this is followed by diminished action of the
    heart and contraction of the capillaries.

    According to Richardson, it suspends the animation of frogs. No
    other substance known will thus suspend a frog’s animation for so
    long a time without killing it. Under favourable circumstances, the
    animal will remain apparently dead for many days, and yet recover.
    Warm-blooded animals may be thrown by amyl nitrite into a cataleptic
    condition. It is not an anæsthetic, and by its use consciousness is
    not destroyed, unless a condition approaching death be first
    produced. When this occurs there is rarely recovery, the animal
    passes into actual death.

    =Post-Mortem Appearances.=--If administered quickly, the lungs and
    all the other organs are found blanched and free from blood, the
    right side of the heart gorged with blood, the left empty, the brain
    being free from congestion. If administered slowly, the brain is
    found congested, and there is blood both on the left and right sides
    of the heart.


§ 169. =Ether, Ethylic Ether, Ethyl Oxide,= (C₂H₅)₂O.--Ethylic ether is
a highly mobile liquid of peculiar penetrating odour and sweetish
pungent taste. It is perfectly colourless, and evaporates so rapidly,
that when applied in the form of spray to the skin, the latter becomes
frozen, and is thus deprived of sensibility.

Pure ether has a density of ·713, its boiling-point is 35°, but
commercial samples, which often contain water (1 part of water is
soluble in 35 of ether), may have a higher gravity, and also a higher
boiling-point. The readiest way to know whether an ether is anhydrous or
not, is to shake it up with a little carbon disulphide. If it is
hydrous, the mixture is milky. Methylated ether is largely used in
commerce; its disagreeable odour is due to contamination by methylated
compounds; otherwise the ether made from methylated spirit is ethylic
ether, for methylic ether is a gas which escapes during the process.
Hence the term “methylated” ether is misleading, for it contains no
methylic ether, but is essentially a somewhat impure ethylic ether.

§ 170. =Ether as a Poison.=--Ether has but little toxicological
importance. There are a few cases of death from its use as an
anæsthetic, and a few cases of suicide. Ether is used by some people as
a stimulant, but ether drinkers are uncommon. It causes an intoxication
very similar to that of alcohol, but of brief duration. In a case of
chronic ether-taking recorded by Martin,[157] in which a woman took
daily doses of ether for the purpose of allaying a gastric trouble, the
patient suffered from shivering or trembling of the hands and feet,
muscular weakness, cramp in the calves of the legs, pain in the breast
and back, intermittent headaches, palpitation, singing in the ears,
vomitings, and wakefulness; the ether being discontinued, the patient
recovered. In one of Orfila’s experiments, half an ounce of ether was
administered to a dog. The animal died insensible in three hours. The
mucous membrane of the stomach was found highly inflamed, the
inflammation extending somewhat into the duodenum; the rest of the canal
was healthy. The lungs were gorged with fluid blood.

[157] Virchow’s _Jahresber._, 1870.

§ 171. =Fatal Dose.=--The fatal dose of ether, when taken as a liquid,
is not known. 4 grms. (1·28 drms.) cause toxic symptoms, but the effect
soon passes. Buchanan has seen a brandy-drinker consume 25 grms. (7
drms.) and yet survive. It is probable that most adults would be killed
by a fluid ounce (28·4 c.c.).

§ 172. =Ether as an Anæsthetic.=--Ether is now much used as an
anæsthetic, and generally in conjunction with chloroform. Anæsthesia by
ether is said to compare favourably with that produced by chloroform. In
92,000 cases of operations performed under ether, the proportion dying
from the effects of the anæsthetic was only ·3 per 10,000 (Morgan),
while chloroform gives a higher number (see p. 149). The mortality in
America, again, from a mixture of chloroform and ether in 11,000 cases
is reckoned at 1·7 per 10,000; but this proportion is rather above some
of the calculations relative to the mortality from pure chloroform, so
that the question can hardly be considered settled. The symptoms of
ether narcosis are very similar to those produced by chloroform. The
chief point of difference appears to be its action on the heart. Ether,
when first breathed, stimulates the heart’s action, and the
after-depression that follows never reaches so high a grade as with
chloroform. Ether is said to kill by paralysing the respiration, and in
cases which end fatally the breathing is seen to stop suddenly:
convulsions have not been noticed. The _post-mortem_ appearances, as in
the case of chloroform, are not characteristic.

§ 173. =Separation of Ether from Organic Fluids, &c.=--Despite the low
boiling-point of ether, it is by no means easy to separate it from
organic substances _so as to recover the whole of the ether present_.
The best way is to place the matters in a flask connected with an
ordinary Liebig’s condenser, the tube of the latter at its farther end
fitting closely into the doubly perforated cork of a flask. Into the
second perforation is adapted an upright tube about 2 feet long, which
may be of small diameter, and must be surrounded by a freezing mixture
of ice and salt. The upper end of this tube is closed by a thistle-head
funnel with syphon, and in the bend of the syphon a little mercury
serves as a valve. Heat is now applied to the flask by means of a
water-bath, and continued for several hours; the liquid which has
distilled over is then treated with dry calcic chloride and redistilled
exactly in the same way. To this distillate again a similar process may
be used, substituting dry potassic carbonate for the calcic chloride. It
is only by operating on these principles that the expert can recover in
an approximate state of anhydrous purity such a volatile liquid. Having
thus obtained it pure, it may be identified (1) by its smell, (2) by its
boiling-point, (3) by its inflammability, and (4) by its reducing
chromic acid. The latter test may be applied to the vapour. An asbestos
fibre is soaked in a mixture of strong sulphuric acid and potassic
dichromate, and then placed in the tube connected with the flask--the
ethereal (or alcoholic) vapour passing over the fibre, immediately
reduces the chromic acid to chromic oxide, with the production of a
green colour.



§ 174. Chloroform appears to have been discovered independently by
Soubeiran and Liebig, about 1830. It was first employed in medicine by
Simpson, of Edinburgh, as an anæsthetic. Pure chloroform has a density
of 1·491 at 17°, and boils at 60·8°; but commercial samples have
gravities of from 1·47 to 1·491. It is a colourless liquid, strongly
refracting light; it cannot be ignited by itself, but, when mixed with
alcohol, burns with a smoky flame edged with green. Its odour is heavy,
but rather pleasant; the taste is sweet and burning.

Chloroform sinks in water, and is only slightly soluble in that fluid
(·44 in 100 c.c.), it is perfectly neutral in reaction, and very
volatile. When rubbed on the skin, it should completely evaporate,
leaving no odour. Pure absolute chloroform gives an opaline mixture if
mixed with from 1 to 5 volumes of alcohol, but with any quantity above 5
volumes the mixture is clear; it mixes in all proportions with ether.
Chloroform coagulates albumen, and is an excellent solvent for most
organic bases--camphor, caoutchouc, amber, opal, and all common resins.
It dissolves phosphorus and sulphur slightly--more freely iodine and
bromine. It floats on hydric sulphate, which only attacks it at a
boiling heat.

Chloroform is frequently impure from faulty manufacture or
decomposition. The impurities to be sought are alcohol, methylated
chloroform,[158] dichloride of ethylene (C₂H₄Cl₂), chloride of ethyl
(C₂H₅Cl), aldehyde, chlorine, hydrochloric, hypochlorous, and traces of
sulphuric acid: there have also been found chlorinated oils. One of the
best tests for contamination by alcohol, wood spirit, or ether, is that
known as Roussin’s; dinitrosulphide of iron[159] is added to chloroform.
If it contain any of these impurities, it acquires a dark colour, but if
pure, remains bright and colourless.

[158] Methylated chloroform is that which is prepared from methylated
spirit. It is liable to more impurities than that made from pure
alcohol, but, of course, its composition is the same, and it has
recently been manufactured from this source almost chemically pure.

[159] Made by slowly adding ferric sulphate to a boiling solution of
ammonic sulphide and potassic nitrite, as long as the precipitate
continues to redissolve, and then filtering the solution.

The presence of alcohol or ether, or both, may also be discovered by the
bichromate test, which is best applied as follows:--A few milligrammes
of potassic bichromate are placed at the bottom of a test-tube with four
or five drops of sulphuric acid, which liberates the chromic acid; next,
a very little water is added to dissolve the chromic acid; and lastly,
the chloroform. The whole is now shaken, and allowed to separate. If the
chloroform is pure, the mass is hardly tinged a greenish-yellow, and no
layer separates. If, however, there is anything like 5 per cent. of
alcohol or ether present, the deep green of chromium chloride appears,
and there is a distinct layer at the bottom of the tube.

Another way to detect alcohol in chloroform, and also to make an
approximate estimation of its quantity, is to place 20 c.c. of
chloroform in a burette, and then add 80 c.c. of water. On shaking
violently, pure chloroform will sink to the bottom in clear globules,
and the measurement will be as nearly as possible the original quantity;
but if anything like a percentage of alcohol be present, the chloroform
is seen to be diminished in quantity, and its surface is opalescent, the
diminution being caused by the water dissolving out the alcohol. The
addition of a few drops of potash solution destroys the meniscus, and
allows of a close reading of the volume. The supernatant water may be
utilised for the detection of other impurities, and tested for sulphuric
acid by baric chloride, for free chlorine and hypochlorous acid by
starch and potassic iodide, and for hydrochloric acid by silver
nitrate.[160] Fuchsine, proposed by Stœdeler, is also a delicate reagent
for the presence of alcohol in chloroform, the sample becoming red in
the presence of alcohol, and the tint being proportionate to the
quantity present. The most delicate test for alcohol is, however, the
iodoform test fully described in “Foods,” p. 375.[161] Dichloride of
ethylene is detected by shaking up the chloroform with dry potassic
carbonate, and then adding metallic potassium. This does not act on pure
chloroform, but only in presence of ethylene dichloride, when the
gaseous chlor-ethylene (C₂H₃Cl) is evolved. Ethyl-chloride is detected
by distilling the chloroform and collecting the first portions of the
distillate; it will have a distinct odour of ethyl-chloride should it be
present. Methyl compounds and empyreumatic oils are roughly detected by
allowing the chloroform to evaporate on a cloth. If present, the cloth,
when the chloroform has evaporated, will have a peculiar disagreeable
odour. Aldehyde is recognised by its reducing action on argentic
nitrate; the mineral acids by the reddening of litmus paper, and the
appropriate tests. Hypochlorous acid first reddens, and then bleaches,

[160] Neither an alcoholic nor an aqueous solution of silver nitrate
causes the slightest change in pure chloroform.

[161] An attempt has been made by Besnou to estimate the amount of
alcohol by the specific gravity. He found that a chloroform of 1·4945
gravity, mixed with 5 per cent. of alcohol, gave a specific gravity of
1·4772; 10 per cent., 1·4602; 20 per cent., 1·4262; and 25 per cent.,
1·4090. It would, therefore, seem that every percentage of alcohol
lowers the gravity by ·0034.

Dr. Dott, _Pharm. Journ._, 1894, p. 629, gives the following
tests:--Specific gravity, 1·490 to 1·495. On allowing ½ fluid drm. to
evaporate from a clean surface, no foreign odour is perceptible at any
stage of the evaporation. When 1 fluid drm. is agitated with an equal
volume of solution of silver nitrate, no precipitate or turbidity is
produced after standing for five minutes. On shaking up the chloroform
with half its volume of distilled water, the water should not redden
litmus-paper. When shaken with an equal volume of sulphuric acid, little
or no colour should be imparted to the acid.

§ 175. The ordinary method of manufacturing chloroform is by distilling
alcohol with chlorinated lime; but another mode is now much in
use--viz., the decomposition of chloral hydrate. By distilling it with a
weak alkali, this process yields such a pure chloroform, that, for
medicinal purposes, it should supersede every other.

Poisonous Effects of Chloroform.


§ 176. =Statistics.=--Falck finds recorded in medical literature 27
cases of poisoning by chloroform having been swallowed--of these 15 were
men, 9 were women, and 3 children. Eighteen of the cases were suicidal,
and 10 of the 18 died; the remainder took the liquid by mistake.

§ 177. =Local Action of Chloroform.=--When applied to the skin or mucous
membranes in such a way that the fluid cannot evaporate--as, for
example, by means of a cloth steeped in chloroform laid on the bare
skin, and covered over with some impervious material--there is a burning
sensation, which soon ceases, and leaves the part anæsthetised, while
the skin, at the same time, is reddened and sometimes even blistered.

§ 178. Chloroform added to blood, or passed through it in the state of
vapour, causes it to assume a peculiar brownish colour owing to
destruction of the red corpuscles and solution of the hæmoglobin in the
plasma. The change does not require the presence of atmospheric air, but
takes place equally in an atmosphere of hydrogen. It has been shown by
Schmiedeberg that the chloroform enters in some way into a state of
combination with the blood-corpuscles, for the entire quantity cannot be
recovered by distillation; whereas the plasma, similarly treated, yields
the entire quantity which has in the first place been added.
Schmiedeberg also asserts that the oxygen is in firmer combination with
the chloroformised blood than usual, as shown by its slow extraction by
stannous oxide. Muscle, exposed to chloroform liquid by arterial
injection, quickly loses excitability and becomes rigid. Nerves are
first stimulated, and then their function for the time is annihilated;
but on evaporation of the chloroform, the function is restored.

§ 179. =General Effects of the Liquid.=--However poisonous in a state of
vapour, chloroform cannot be considered an extremely active poison when
taken into the stomach as a liquid, for enormous quantities, relatively,
have been drunk without fatal effect. Thus, there is the case recorded
by Taylor, in which a man, who had swallowed 113·4 grms. (4 ozs.),
walked a considerable distance after taking the dose. He subsequently
fell into a state of coma, with dilated pupils, stertorous breathing,
and imperceptible pulse. These symptoms were followed by convulsions,
but the patient recovered in five days.

In a case related by Burkart,[162] a woman desired to kill herself with
chloroform, and procured for that purpose 50 grms. (a little less than
one ounce and a half); she drank some of it, but the burning taste and
the sense of heat in the mouth, throat, and stomach, prevented her from
taking the whole at once. After a few moments, the pain passing off, she
essayed to drink the remainder, and did swallow the greater portion of
it, but was again prevented by the suffering it caused. Finally, she
poured what remained on a cloth, and placing it over her face, soon sank
into a deep narcosis. She was found lying on the bed very pale, with
blue lips, and foaming a little at the mouth; the head was rigidly bent
backwards, the extremities were lax, the eyes were turned upwards and
inwards, the pupils dilated and inactive, the face and extremities were
cold, the body somewhat warmer, there was no pulse at the wrist, the
carotids beat feebly, the breathing was deep and rattling, and after
five or six inspirations ceased. By the aid of artificial respiration,
&c., she recovered in an hour.

[162] _Vierteljahrsschr. für ger. Med._, 1876.

A still larger dose has been recovered from in the case of a young man,
aged 23,[163] who had swallowed no less than 75 grms. (2·6 ozs.) of
chloroform, but yet, in a few hours, awoke from the stupor. He
complained of a burning pain in the stomach; on the following day he
suffered from vomiting, and on the third day symptoms of jaundice
appeared,--a feature which has been several times noticed as an effect
of chloroform.

[163] _Brit. Med. Journ._, 1879.

On the other hand, even small doses have been known to destroy life. In
a case related by Taylor, a boy, aged 4, swallowed 3·8 grms. (1 drm.) of
chloroform and died in three hours, notwithstanding that every effort
was used for his recovery.

§ 180. The smallest dose that has proved fatal _to an adult_ is 15 grms.
(a little over 4 drms.).

From twenty-two cases in which the quantity taken had been ascertained
with some degree of accuracy, Falck draws the following conclusions:--In
eight of the cases the dose was between 4 and 30 grms., and one death
resulted from 15 grms. As for the other fourteen persons, the doses
varied from 35 to 380 grms., and eight of these patients died--two after
40, two after 45, one after 60, 90, 120, and 180 grms. respectively.
Hence, under conditions favouring the action of the poison, 15 grms.
(4·3 drms.) may be fatal to an adult, while doses of 40 grms. (11·3
drms.) and upwards will almost certainly kill.

§ 181. =Symptoms.=--The symptoms can be well gathered from the cases
quoted. They commence shortly after the taking of the poison; and,
indeed, the local action of the liquid immediately causes first a
burning sensation, followed by numbness.

Often after a few minutes, precisely as when the vapour is administered,
a peculiar, excited condition supervenes, accompanied, it may be, by
delirium. The next stage is narcosis, and the patient lies with pale
face and livid lips, &c., as described at p. 147; the end of the scene
is often preceded by convulsions. Sometimes, however, consciousness
returns, and the irritation of the mucous membranes of the
gastro-intestinal canal is shown by bloody vomiting and bloody stools,
with considerable pain and general suffering. In this way, a person may
linger several days after the ingestion of the poison. In a case
observed by Pomeroy, the fatal malady was prolonged for eight days.
Among those who recover, a common _sequela_, as before mentioned, is

A third form of symptoms has been occasionally observed, viz.:--The
person awakes from the coma, the breathing and pulse become again
natural, and all danger seems to have passed, when suddenly, after a
longer or shorter time, without warning, a state of general depression
and collapse supervenes, and death occurs.

§ 182. =Post-mortem Appearances.=--The _post-mortem_ appearances from a
fatal dose of liquid chloroform mainly resolve themselves into redness
of the mucous membrane of the stomach, though occasionally, as in
Pomeroy’s case, there may be an ulceration. In a case recorded by
Hoffman,[164] a woman, aged 30, drank 35 to 40 grms. of chloroform and
died within the hour. Almost the whole of the chloroform taken was found
in the stomach, as a heavy fluid, coloured green, through the bile. The
epithelium of the pharynx, epiglottis, and gullet was of a dirty colour,
partly detached, whitened, softened, and easily stripped off. The mucous
membrane of the stomach was much altered in colour and consistence, and,
with the duodenum, was covered with a tenacious grey slime. There was no

[164] _Lehrbuch der ger. Medicin_, 2te Aufl.


§ 183. =Statistics.=--Accidents occur far more frequently in the use of
chloroform vapour for anæsthetic purposes than in the use of the liquid.

Most of the cases of death through chloroform vapour, are those caused
accidentally in surgical and medical practice. A smaller number are
suicidal, while for criminal purposes, its use is extremely infrequent.

The percentage of deaths caused by chloroform administered during
operations is unaccountably different in different years, times, and
places. The diversity of opinion on the subject is partly (though not
entirely) explicable, by the degrees of purity in the anæsthetic
administered, the different modes of administration, the varying lengths
of time of the anæsthesia, and the varying severity of the operations.

During the Crimean War, according to Baudens and Quesnoy, 30,000
operations were done under chloroform, but only one death occurred
attributable to the anæsthetic. Sansom[165] puts the average mortality
at ·75 per 10,000, Nussbaum at 1·3, Richardson at 2·8,[166] Morgan[167]
at 3·4. In the American war of secession, in 11,000 operations, there
were seven deaths--that is, 6·3 per 10,000, the highest number on a
large scale which appears to be on record. In the ten years 1883-1892,
103 deaths are attributed to chloroform in England and Wales, viz., 88
deaths (57 males, 31 females) from accidents (no doubt in its use as a
general anæsthetic), 14 (9 males, 5 females) from suicide, and a
solitary case of murder.

[165] _Chloroform: its Action, &c._, London, 1865.

[166] _Med. Times and Gazette_, 1870.

[167] _Med. Soc. of Virginia_, 1872.

§ 184. =Suicidal and Criminal Poisoning by Chloroform.=--Suicidal
poisoning by chloroform will generally be indicated by the surrounding
circumstances; and in no case hitherto reported has there been any
difficulty or obscurity as to whether the narcosis was self-induced or
not. An interesting case is related by Schauenstein,[168] in which a
physician resolved to commit suicide by chloroform, a commencing
amaurosis having preyed upon his mind, and his choice having been
determined by witnessing an accidental death by this agent. He
accordingly plugged his nostrils, fitted on to the face an appropriate
mask, and fastened it by strips of adhesive plaster. In such an
instance, there could be no doubt of the suicidal intent, and the
question of accident would be entirely out of the question.

[168] Maschka: _Handbuch der gerichtlich. Medicin_, p. 787, Tübingen,

A dentist in Potsdam,[169] in a state of great mental depression from
embarrassed circumstances, killed his wife, himself, and two children by
chloroform. Such crimes are fortunately very rare.

[169] Casper: _Handbuch der ger. Med._

There is a vulgar idea that it is possible, by holding a cloth saturated
with chloroform to the mouth of a sleeping person (or one, indeed,
perfectly awake), to produce _sudden_ insensibility; but such an
occurrence is against all experimental and clinical evidence. It is true
that a nervous person might, under such circumstances, faint and become
insensible by mere nervous shock; but a true sudden narcosis is

Dolbeau has made some interesting experiments in order to ascertain
whether, under any circumstances, a sleeping person might be
anæsthetised. The main result appears to answer the question in the
affirmative, at least with certain persons; but even with these, it can
only be done by using the greatest skill and care, first allowing the
sleeper to breathe very dilute chloroform vapour, and then gradually
exhibiting stronger doses, and taking the cloth or inhaler away on the
slightest symptom of approaching wakefulness. In 75 per cent. of the
cases, however, the individuals awoke almost immediately on being
exposed to the vapour. This cautious and scientific narcosis, then, is
not likely to be used by the criminal class, or, if used, to be

§ 185. =Physiological Effects.=--Chloroform is a protoplasmic poison.
According to Jumelle, plants can even be narcotised, ceasing to
assimilate and no longer being sensitive to the stimulus of light.
Isolated animal cells, like leucocytes, lose through chloroform vapour
their power of spontaneous movement, and many bacteria cease to multiply
if in contact with chloroform water. According to Binx, chloroform
narcosis in man is to be explained through its producing a weak
coagulation of the cerebral ganglion cells. As already mentioned,
chloroform has an affinity for the red blood-corpuscles. Chloroform
stimulates the peripheral ends of the nerves of sensation, so that it
causes irritation of the skin or mucous membranes when locally applied.
Flourens considers that chloroform first affects the cerebrum, then the
cerebellum, and finally the spinal cord; the action is at first
stimulating, afterwards paralysing. Most anæsthetics diminish equally
the excitability of the grey and the white nervous substance of the
brain, and this is the case with chloroform, ether, and morphine; but
apparently this is not the case with chloral hydrate, which only
diminishes the conductivity of the cortical substance of the brain, and
leaves the grey substance intact. Corresponding to the cerebral
paralysis, the blood pressure sinks, and the heart beats slower and
weaker.[170] The Hyderabad Commission made 735 researches on dogs and
monkeys, and found that in fatal narcosis, so far as these animals are
concerned, the respiration ceased before the heart, and this may be
considered the normal mode of death; but it is probably going too far to
say that it is the exclusive form of death in man, for there have been
published cases in which the heart failed first.

[170] Kobert’s _Lehrbuch der Intoxicationen_.

§ 186. =Symptoms.=--There is but little outward difference between man
and animals, in regard to the symptoms caused by breathing chloroform;
in the former we have the advantage that the sensations preceding
narcosis can be described by the individual.

The action of chloroform is usually divided into three more or less
distinct stages. In the _first_ there is a “drunken” condition, changes
in the sense of smell and taste, and it may be hallucinations of vision
and hearing; there are also often curious creeping sensations about the
skin, and sometimes excessive muscular action, causing violent
struggles. I have also seen epileptiform convulsions, and delirium is
almost always present. The face during this stage is generally flushed,
covered with perspiration, and the pupils contracted. The first stage
may last from one minute to several, and passes into the _second stage_,
or that of depression. Spontaneous movements cease, sensibility to all
external stimuli vanishes, the patient falls into a deep sleep, the
consciousness is entirely lost, and reflex movements are more and more
annihilated. The temperature is less than normal, the respirations are
slow, and the pulse is full and slow. The pupils in this stage are
usually dilated, all the muscles are relaxed, and the limbs can be bent
about in any direction. If now the inhalation of chloroform is
intermitted, the patient wakes within a period which is usually from
twenty to forty minutes, but may be several hours, after the last

The _third stage_ is that of paralysis; the pulse becomes irregular, the
respirations superficial, there is a cyanotic colouring of the lips and
skin, while the pupils become widely dilated. Death follows quickly
through paralysis of the respiratory centre, the respirations first
ceasing, then the pulse; in a few cases, the heart ceases first to beat.

According to Sansom’s facts,[171] in 100 cases of death by chloroform,
44·6 per cent. occurred before the full narcosis had been attained, that
is in the first stage, 34·7 during the second stage, and 20·6 shortly
after. So, also, Kappeler has recorded that in 101 cases of death from
chloroform, 47·7 per cent. occurred before the full effect, and 52·2
during the full effect. This confirms the dictum of Billroth, that in
all stages of anæsthesia by chloroform, death may occur. The _quantity_
of chloroform, which, when inhaled in a given time, will produce death,
is unknown; for all depends upon the greater or less admixture of air,
and probably on other conditions. It has been laid down, that the
inhalation of chloroform should be so managed as to insure that the air
breathed shall never contain more than 3·9 per cent. of chloroform.
Fifteen drops have caused death, but Taylor, on the other hand, records
a case of tetanus, treated at Guy’s Hospital, in which no less a
quantity than 700 grms. (22·5 ozs.) was inhaled in twenty-four hours.
Frequent breathing of chloroform in no way renders the individual safe
from fatal accident. A lady[172] having repeatedly taken chloroform, was
anæsthetised by the same agent merely for the purpose of having a tooth
extracted. About 6 grms. (1·5 drm.) were poured on a cloth, and after
nine to ten inspirations, dangerous symptoms began--rattling breathing
and convulsive movements--and, despite all remedies, she died.

[171] _Op. cit._

[172] _Edin. Med. Journ._, 1855.

§ 187. Chronic chloroform poisoning is not unknown. It leads to various
ailments, and seems to have been in one or two instances the cause of

Buchner records the case of an opium-eater, who afterwards took to
chloroform; he suffered from periodic mania. In a remarkable case
related by Meric, the patient, who had also first been a morphine-eater,
took 350 grms. of chloroform in five days by inhalation; as often as he
woke he would chloroform himself again to sleep. In this case, there was
also mental disturbance, and instances in which chloroform produced
marked mental aberration are recorded by Böhm[173] and by Vigla.[174]

[173] Ziemssen’s _Handbuch_, Bd. 15.

[174] _Med. Times_, 1855.

§ 188. =Post-mortem Appearances.=--The lesions found on section are
neither peculiar to, nor characteristic of, chloroform poisoning. It has
been noted that bubbles of gas are, from time to time, to be observed
after death in the blood of those poisoned by chloroform, but it is
doubtful whether the bubbles are not merely those to be found in any
other corpse--in 189 cases, only eighteen times were these gas-bubbles
observed,[175] so that, even if they are characteristic, the chances in
a given case that they will _not_ be seen are greater than the reverse.
The smell of chloroform may be present, but has been noticed very

[175] Schauenstein (_Op. cit._).

§ 189. =The detection and estimation of chloroform= from organic
substances is not difficult, its low boiling-point causing it to distil
readily. Accordingly (whatever may be the ultimate modifications, as
suggested by different experimenters), the first step is to bring the
substances, unless fluid, into a pulp with water, and submit this pulp
to distillation by the heat of a water-bath. If the liquid operated upon
possesses no particular odour, the chloroform may in this way be
recognised in the distillate, which, if necessary, may be redistilled in
the same manner, so as to concentrate the volatile matters in a small

There are four chief tests for the identification of chloroform:--

(1.) The final distillate is tested with a little aniline, and an
alcoholic solution of soda or potash lye; either immediately, or upon
gently warming the liquid, there is a peculiar and penetrating odour of
phenylcarbylamine, C₆H₅NC; it is produced by the following reaction:--

  CHCl₃ + 3KOH + C₆H₅NH₂ = C₆H₅NC + 3KCl + 3H₂O.

Chloral, trichloracetic acid, bromoform and iodoform also give the same
reaction; on the other hand, ethylidene chloride does not yield under
these circumstances any carbylamine (isonitrile).

(2.) Chloroform reduces Fehling’s alkaline copper solution, _when
applied to a distillate_, thus excluding a host of more fixed bodies
which have the same reaction; it is a very excellent test, and may be
made quantitative. The reaction is as follows:--

  CHCl₃ + 5KHO + 2CuO = Cu₂O + K₂CO₃ + 3KCl + 3H₂O;

thus, every 100 parts of cuprous oxide equals 83·75 of chloroform.

(3.) The fluid to be tested (which, if acid, should be neutralised), is
distilled in a slow current of hydrogen, and the vapour conducted
through a short bit of red-hot combustion-tube containing platinum
gauze. Under these circumstances, the chloroform is decomposed and
hydrochloric acid formed; hence, the issuing vapour has an acid reaction
to test-paper, and if led into a solution of silver nitrate, gives the
usual precipitate of argentic chloride. Every 100 parts of silver
chloride equal 27·758 of chloroform.

(4.) The fluid is mixed with a little thymol and potash; if chloroform
be present, a reddish-violet colour is developed, becoming more distinct
on the application of heat.[176]

[176] S. Vidali in _Deutsch-Amerikan. Apoth.-Zeitung_, vol. iij., Aug.
15, 1882.

§ 190. For the quantitative estimation of chloroform the method
recommended by Schmiedeberg[177] is, however, the best. A
combustion-tube of 24 to 26 cm. long, and 10 to 12 mm. in diameter, open
at both ends, is furnished at the one end with a plug of asbestos, while
the middle part, to within 5-6 cm. of the other end, is filled with
pieces of caustic lime, from the size of a lentil to that of half a pea.
The lime must be pure, and is made by heating a carbonate which has been
precipitated from calcic nitrate. The other end of the tube is closed by
a cork, carrying a silver tube, 16-18 cm. long, and 4 mm. thick. The end
containing the asbestos plug is fitted by a cork to a glass tube. The
combustion-tube thus prepared is placed in the ordinary
combustion-furnace; the flask containing the chloroform is adapted, and
the distillation slowly proceeded with. It is best to add a tube, bent
at right angles and going to the bottom of the flask, to draw air
continuously through the apparatus. During the whole process, the tube
containing the lime is kept at a red heat. The chloroform is decomposed,
and the chlorine combines with the lime. The resulting calcic chloride,
mixed with much unchanged lime, is, at the end of the operation, cooled,
dissolved in dilute nitric acid, and precipitated with silver nitrate.
Any silver chloride is collected and weighed and calculated into

[177] _Ueber die quantitative Bestimmung des Chloroforms im Blute._
Inaug. Dissert., Dorpat, 1866.

[178] S. Vidali has made the ingenious suggestion of developing hydrogen
in the usual way, by means of zinc and sulphuric acid, in the liquid
supposed to contain chloroform, to ignite the hydrogen, as in Marsh’s
test, when it issues from the tube, and then to hold in the flame a
clean copper wire. Since any chloroform is burnt up in the hydrogen
flame to hydrochloric acid, the chloride of copper immediately
volatilises and colours the flame green.

VI.--Other Anæsthetics.

    § 191. When chlorine acts upon marsh-gas, the hydrogen can be
    displaced atom by atom; and from the original methane (CH₄) can be
    successively obtained chloromethane or methyl chloride (CH₃Cl),
    dichloromethane, or methene dichloride, methylene dichloride
    (CH₂Cl₂), trichloromethane, or chloroform (CHCl₃), already
    described, and carbon tetrachloride (CCl₄). All these are, more or
    less, capable of producing anæsthesia; but none of them, save
    chloroform, are of any toxicological importance.

    Methene dichloride, recommended by Sir B. W. Richardson as an
    anæsthetic, has come somewhat into use. It is a colourless, very
    volatile liquid, of specific gravity 1·360, and boiling at 41°. It
    burns with a smoky flame, and dissolves iodine with a brown colour.

    § 192. =Pentane= (C₅H₁₂).--There are three isomers of pentane; that
    which is used as an anæsthetic is normal pentane,
    CH₃-CH₂-CH₂-CH₂-CH₃; its boiling-point is 37-38°. It is one of the
    constituents of petroleum ether.

    Under the name of “Pental” it is used in certain hospitals
    extensively, for instance, at the Kaiser Friederich’s Children’s
    Hospital, Berlin.[179] It is stated to have no action on the heart.

[179] _Zeit. f. Kinderheilk._, Bd. iii.-iv., 1893.

    One death[180] has been recorded from its use:--A lad, aged 14, was
    put under pental for the purpose of having two molars painlessly
    extracted. He was only a minute or two insensible, and 4-5 grms. of
    pental was the quantity stated to have been inhaled. The boy spat
    out after the operation, then suddenly fainted and died. The
    _post-mortem_ showed œdema of the lungs; the right side of the heart
    was empty. The organs of the body smelled strongly of pental.

[180] Dr. Bremme, _Vierteljahrsschr. f. gerichtliche Medicin_, Bd. v.,

    § 193. =Aldehyde= (Acetaldehyde), C₂H₄O =

  CH₃-C   ,

    a fluid obtained by the careful oxidation of alcohol (boiling-point,
    20·8°), is in large doses toxic; in smaller, it acts as a narcotic.

    =Metaldehyde= (C₂H₄O₂)₂, obtained by treating acetaldehyde at a low
    temperature with hydrochloric acid. It occurs in the form of prisms,
    which sublime at about 112°; it is also poisonous.

    § 194. =Paraldehyde= (C₆H₁₂O₃) is a colourless fluid, boiling at
    124°; specific gravity ·998 at 15°. By the action of cold it may be
    obtained in crystals, the melting point of which is 10·5°. It is
    soluble in eight parts of water at 13°; in warm water it is less
    soluble; hence, on warming a solution, it becomes turbid.
    Paraldehyde acts very similarly to chloral; it causes a deep sleep,
    and (judging by experiments on animals) produces no convulsive


§ 195. =Chloral Hydrate= (C₂H₃Cl₃O₂) is made by mixing equivalent
quantities of anhydrous chloral[181] and water. The purest chloral is in
the form of small, granular, sugar-like crystals. When less pure, the
crystals are larger. These melt into a clear fluid at from 48° to 49°,
and the melted mass solidifies again at 48·9°. Chloral boils at 97·5°;
it is not very soluble in cold chloroform, requiring four times its
weight. The only substance with which chloral hydrate may well be
confused is chloral alcoholate (C₄H₇Cl₃O₂), but chloral alcoholate melts
at a lower temperature (45°), and boils at a higher (113·5°); it is
easily soluble in cold chloroform, and inflames readily, whereas chloral
scarcely burns.

[181] Anhydrous chloral (C₂HCl₃O) is an oily liquid, of specific gravity
1·502 at 18°; it boils at 97·7°. It is obtained by the prolonged action
of chlorine on absolute alcohol.

Chloral hydrate completely volatilises, and can be distilled in a vacuum
without change. If, however, boiled in air, it undergoes slow
decomposition, the first portions of the distillate being overhydrated,
the last underhydrated; the boiling-point, therefore, undergoes a
continuous rise. The amount of hydration of a commercial sample is of
practical importance; if too much water is present, the chloral
deliquesces, especially in warm weather; if too little, it may become
acid, and in part insoluble from the formation of meta-chloral
(C₆H₃Cl₉O₃). Chloral hydrate, by the action of the volatile or fixed
alkalies, is decomposed, an alkaline formiate and chloroform resulting

  C₂HCl₃O,H₂O + NaHO = NaCHO₂ + H₂O + CHCl₃.

Trichlor-acetic acid is decomposed in a similar manner.

=Statistics.=--Chloral caused, during the ten years 1883-1892 in England
and Wales, 127 deaths--viz., 111 (89 males, 22 females) accidentally, 15
(14 males, 1 female) from suicide, and a case in which chloral was the
agent of murder.

§ 196. =Detection.=--It is, of course, obvious that after splitting up
chloral into chloroform, the latter can be detected by distillation and
applying the tests given at p. 152 and _seq._ Chloral hydrate is soluble
in one and a half times its weight of water; the solution should be
perfectly neutral to litmus. It is also soluble in ether, in alcohol,
and in carbon disulphide. It may be extracted from its solution by
shaking out with ether. There should be no cloudiness when a solution is
tested with silver nitrate in the cold; if, however, to a boiling
solution nitrate of silver and a little ammonia are added, there is a
mirror of reduced silver.

§ 197. The assay of chloral hydrate in solutions is best effected by
distilling the solution with slaked lime; the distillate is received in
water contained in a graduated tube kept at a low temperature. The
chloroform sinks to the bottom, and is directly read off; the number of
c.c. multiplied by 2·064 equals the weight of the chloral hydrate

Another method, accurate but only applicable to the fairly pure
substance, is to dissolve 1 to 2 grms. in water, remove any free acid by
baric carbonate, and then treat the liquid thus purified by a known
volume of standard soda. The soda is now titrated back, using litmus as
an indicator, each c.c. of normal alkali neutralised by the sample
corresponds to 0·1655 grm. of chloral hydrate. Small quantities of
chloral hydrate may be conveniently recovered from complex liquids by
shaking them up with ether, and removing the ethereal layer, in the tube
represented in the figure.[182] The ether must be allowed to evaporate
spontaneously; but there is in this way much loss of chloral. The best
method of estimating minute quantities is to alkalise the liquid, and
slowly distil the vapour through a red-hot combustion-tube charged with
pure lime, as in the process described at p. 153. A dilute solution of
chloral may also be treated with a zinc-copper couple, the nascent
hydrogen breaks the molecule up, and the resulting chloride may be
titrated, as in water analyses, by silver nitrate and potassic chromate.


[182] The figure is from “Foods”; the description may be here
repeated:--A is a tube of any dimensions most convenient to the analyst.
Ordinary burette size will perhaps be the most suitable for routine
work; the tube is furnished with a stopcock and is bent at B, the tube
at K having a very small but not quite capillary bore. The lower end is
attached to a length of pressure-tubing, and is connected with a small
reservoir of mercury, moving up and down by means of a pulley. To use
the apparatus: Fill the tube with mercury by opening the clamp at H, and
the stopcock at B, and raising the reservoir until the mercury, if
allowed, would flow out of the beak. Now, the beak is dipped into the
liquid to be extracted with the solvent, and by lowering the reservoir,
a strong vacuum is created, which draws the liquid into the tube; in the
same way the ether is made to follow. Should the liquid be so thick that
it is not possible to get it in by means of suction, the lower end of
the tube is disconnected, and the syrupy mass worked in through the wide
end. When the ether has been sucked into the apparatus, it is emptied of
mercury by lowering the reservoir, and then firmly clamped at H, and the
stopcock also closed. The tube may now be shaken, and then allowed to
stand for the liquids to separate. When there is a good line of
demarcation, by raising the reservoir after opening the clamp and
stopcock, the whole of the light solvent can be run out of the tube into
a flask or beaker, and recovered by distillation. For heavy solvents
(such as chloroform), which sink to the bottom, a simple burette, with a
fine exit tube is preferable; but for petroleum ether, ordinary ether,
&c., the apparatus figured is extremely useful.

§ 198. =Effects of Chloral Hydrate on Animals.=--Experiments on animals
have taught us all that is known of the physiological action of
chloral. It has been shown that the drug influences very considerably
the circulation, at first exciting the heart’s action, and then
paralysing the automatic centre. The heart, as in animals poisoned by
atropine, stops in diastole, and the blood-pressure sinks in proportion
to the progressive paralysis of the cardiac centre. At the same time,
the respiration is slowed and finally ceases, while the heart continues
to beat. The body temperature of the warm-blooded animals is very
remarkably depressed, according to Falck, even to 7·6°. Vomiting has
been rather frequently observed with dogs and cats, even when the drug
has been taken into the system by subcutaneous injection.

The secretion of milk, according to Röhrig, is also diminished. Reflex
actions through small doses are intensified; through large, much
diminished. ·025-·05 grm. (·4-·7 grain), injected subcutaneously into
frogs, causes a slowing of the respiration, a diminution of reflex
excitability, and lastly, its complete cessation; this condition lasts
several hours; at length the animal returns to its normal state. If the
dose is raised to ·1 grm. (1·5 grain) after the cessation of reflex
movements, the heart is paralysed--and a paralysis not due to any
central action of the vagus, but to a direct action on the cardiac
ganglia. Rabbits of the ordinary weight of 2 kilos. are fully narcotised
by the subcutaneous injection of 1 grm.; the sleep is very profound, and
lasts several hours; the animal wakes up spontaneously, and is
apparently none the worse. If 2 grms. are administered, the narcotic
effects, rapidly developed, are much prolonged. There is a remarkable
diminution of temperature, and the animal dies, the respiration ceasing
without convulsion or other sign. Moderate-sized dogs require 6 grms.
for a full narcosis, and the symptoms are similar; they also wake after
many hours, in apparent good health.[183]

[183] C. Ph. Falck has divided the symptoms into (1) Preliminary
hypnotic; (2) an adynamic state; and (3) a comatose condition.

§ 199. Liebreich considered that the action of chloral was due to its
being broken up by the alkali of the blood, and the system being thus
brought into a state precisely similar to its condition when
anæsthetised by chloroform vapour. This view has, however, been proved
to be erroneous. Chloral hydrate can, it is true, be decomposed in some
degree by the blood at 40°; but the action must be prolonged for several
hours. A 1 per cent. solution of alkali does not decompose chloral at a
blood-heat in the time within which chloral acts in the body; and since
narcotic effects are commonly observed when, in the fatty group,
hydrogen has been displaced by chlorine, it is more probable that
chloral hydrate is absorbed and circulates in the blood as such, and is
not broken up into chloroform and an alkaline formiate.

§ 200. =Effects of Chloral Hydrate on Man.=--Since the year 1869, in
which chloral was first introduced to medicine, it has been the cause
of a number of accidental and other cases of poisoning. I find, up to
the year 1884, recorded in medical literature, thirty-one cases of
poisoning by chloral hydrate. This number is a small proportion only of
the actual number dying from this cause. In nearly all the cases the
poison was taken by the mouth, but in one instance the patient died in
three hours, after having injected into the rectum 5·86 grms. of chloral
hydrate. There is also on record a case in which, for the purpose of
producing surgical anæsthesia, 6 grms. of chloral were injected into the
veins; the man died in as many minutes.[184]

[184] This dangerous practice was introduced by M. Ore. In a case of
traumatic tetanus, in which M. Ore injected into the veins 9 grms. of
chloral in 10 grms. of water, there was profound insensibility, lasting
eleven hours, during which time a painful operation on the thumb was
performed. The next day 10 grms. were injected, when the insensibility
lasted eight hours; and 9 grms. were injected on each of the two
following days. The man recovered. In another case, Ore anæsthetised
immediately a patient by plunging the subcutaneous needle of his syringe
into the radial vein, and injected 10 grms. of chloral hydrate with 30
of water. The patient became insensible before the whole quantity was
injected with “_une immobilité rappellant celle du cadavre_.” On
finishing the operation, the patient was roused immediately by the
application of an electric current, one pole on the left side of the
neck, the other on the epigastrium. _Journ. de Pharm. et de Chimie._, t.
19, p. 314.

§ 201. =Fatal Dose.=--It is impossible to state with any exactness the
precise quantity of chloral which may cause death. Children bear it
better, in proportion, than adults, while old persons (especially those
with weak hearts, and those inclined to apoplexy) are likely to be
strongly affected by very small doses. A dose of ·19 grm. (3 grains) has
been fatal to a child a year old in ten hours. On the other hand,
according to Bouchut’s observations on 10,000 children, he considers
that the full therapeutic effect of chloral can be obtained safely with
them in the following ratio:--

  Children of 1 to 3 years, dose  1 to 1·5 grm. (15·4 to 23·1 grains)
      „       3  „ 5   „     „    2  „ 3    „   (30·8  „ 46·3   „   )
      „       5  „ 7   „     „    3  „ 4    „   (46·3  „ 61·7   „   )

  These quantities being dissolved in 100 c.c. of water.

These doses are certainly too high, and it would be dangerous to take
them as a guide, since death has occurred in a child, aged 5, from a
dose of 3 grms. (46·3 grains). Medical men in England consider 20 grains
a very full dose for a child of four years old, and 50 for an adult,
while a case is recorded in which a dose of 1·9 grm. (30 grains) proved
fatal in thirty-five hours to a young lady aged 20. On the other hand,
we find a case[185] in which, to a patient suffering from epileptic
mania, a dose of 31·1 grms. (1·1 oz.) of chloral hydrate was
administered; she sank into a deep sleep in five minutes. Subcutaneous
injections of strychnine were applied, and after sleeping for
forty-eight hours, there was recovery. On the third day a vivid
scarlatinal rash appeared, followed by desquamation. The examples
quoted--the fatal dose of 1·9 grm., and recovery from 31 grms.--are the
two extremes for adults. From other cases, it appears tolerably plain
that most people would recover, especially with appropriate treatment,
from a single dose under 8 grms., but anything above that quantity taken
at one time would be very dangerous, and doses of 10 grms. and above,
almost always fatal. If, however, 8 grms. were taken in divided doses
during the twenty-four hours, it could (according to Sir B. W.
Richardson) be done with safety. The time from the taking of the poison
till death varies considerably, and is in part dependent on the dose.

[185] _Chicago Medical Review_, 1882.

In seven cases of lethal poisoning, three persons who took the small
doses of 1·25, 2·5, and 1·95 grms. respectively, lived from eight to ten
hours; two, taking 4 and 5 grms. respectively, died very shortly after
the administration of the chloral. In a sixth case, related by Brown, in
which 3·12 grms. had been taken, the patient lived an hour; and in
another, after a dose of 5 grms., recorded by Jolly, death took place
within a quarter of an hour.

§ 202. =Symptoms.=--With moderate doses there are practically no
symptoms, save a drowsiness coming on imperceptibly, and followed by
heavy sleep. With doses up to 2 grms. (30·8 grains), the hypnotic state
is perfectly under the command of the will, and if the person chooses to
walk about or engage in any occupation, he can ward off sleep; but with
those doses which lead to danger, the narcosis is completely
uncontrollable, the appearance of the sleeper is often strikingly like
that of a drunken person. There is great diminution of temperature
commencing in from five to twenty minutes after taking the
dose--occasionally sleep is preceded by a delirious state. During the
deep slumber the face is much flushed, and in a few cases the sleep
passes directly into death without any marked change. In others,
symptoms of collapse appear, and the patient sinks through exhaustion.

§ 203. With some persons doses, which, in themselves, are insufficient
to cause death, yet have a peculiar effect on the mental faculties. A
case of great medico-legal interest is described by the patient himself,
Dr. Manjot.[186] He took in three doses, hourly, 12 grms. of chloral
hydrate. After the first dose the pain, for which he had recourse to
chloral, vanished; but Manjot, although he had all the appearance of
being perfectly conscious, yet had not the slightest knowledge of what
he was doing or speaking. He took the other two doses, and sank into a
deep sleep which lasted twelve hours. He then awoke and answered
questions with difficulty, but could not move; he lay for the next
twelve hours in a half slumber, and the following night slept
soundly--to wake up recovered.

[186] _Gaz. des Hôp._, 1875.

§ 204. The treatment of acute chloral poisoning which has been most
successful is that by strychnine injections, and the application of
warmth to counteract the loss of temperature which is so constant a
phenomenon. As an illustration of the treatment by strychnine, an
interesting case recorded by Levinstein[187] may be quoted.

[187] _Vierteljahrsschr. f. ger. Med._, Bd. xx., 1874.

A man, thirty-five years old, took at one dose, for the purpose of
suicide, 24 grms. of chloral hydrate. In half an hour afterwards he was
found in a deep sleep, with flushed face, swollen veins, and a pulse 160
in the minute. After a further half hour, the congestion of the head was
still more striking; the temperature was 39·5°; the pulse hard and
bounding 92; the breathing laboured, at times intermittent.

Artificial respiration was at once commenced, but in spite of this, in
about another half hour, the face became deadly pale, the temperature
sank to 32·9°. The pupils contracted, and the pulse was scarcely to be
felt; 3 mgrms. (·04 grain) of strychnine were now injected
subcutaneously; this caused tetanic convulsions in the upper part of the
body and trismus. The heart’s action again became somewhat stronger, the
temperature rose to 33·3°, and the pupils dilated; but soon followed,
again, depression of the heart’s action, and the respiration could only
be kept going by faradisation. Two mgrms. (·03 grain) of strychnine were
once more injected, and the heart’s action improved. During the
succeeding six hours the respiration had to be assisted by faradisation.
The temperature gradually rose to 36·5°; ten hours after taking the dose
the patient lay in a deep sleep, breathing spontaneously and reacting to
external stimuli with a temperature of 38·5°. Eighteen hours from the
commencement, the respiration again became irregular, and the galvanic
current was anew applied. The last application aroused the sleeper, he
took some milk and again slept; after twenty-seven hours he could be
awakened by calling, &c., but had not full consciousness; he again took
some milk and sank to sleep. It was not until thirty-two hours had
elapsed from the ingestion of the poison that he awoke spontaneously;
there were no after effects.

§ 205. =Chronic Poisoning by Chloral Hydrate.=--An enormous number of
people habitually take chloral hydrate. The history of the habit is
usually that some physician has given them a chloral prescription for
neuralgia, for loss of sleep, or other cause, and finding that they can
conjure sleep, oblivion, and loss (it may be) of suffering whenever they
choose, they go on repeating it from day to day until it becomes a
necessity of their existence. A dangerous facility to chloral-drinking
is the existence of patent medicines, advertised as sleep-producers, and
containing chloral as the active ingredient. A lady, aged 35, died in
1876, at Exeter, from an overdose of “Hunter’s solution of chloral, or
sedative draught and sleep producer.” Its strength was stated at the
inquest to be 25 grains to the drachm (41·6 per cent.).[188]

[188] _Exeter and Plymouth Gazette_, Jan. 12, 1876.

The evil results of this chloral-drinking are especially to be looked
for in the mental faculties, and the alienists have had since 1869 a new
insanity-producing factor. In the asylums may usually be found several
cases of melancholia and mania referred rightly (or wrongly) to
chloral-drinking. Symptoms other than cerebral are chilliness of the
body, inclination to fainting, clonic convulsions, and a want of
co-ordination of the muscles of the lower extremities. In a case
recorded by Husband,[189] a lady, after twelve days’ treatment by
chloral hydrate, in doses of from 1 to 2 grms. (15·4 to 30·8 grains),
suffered from a scarlatina-like rash, which was followed by
desquamation. Among the insane, it has also been noticed that its use
has been followed by nettle-rash and petechiæ (Reimer and others).

[189] _Lancet_, 1871.

§ 206. =Excretion of Chloral.=--Chloral hydrate is separated in the
urine partly as urochloral acid (C₈H₁₁Cl₃O₇). Butylchloral is separated
as butyl urochloral acid (C₁₀H₁₅Cl₂O₇). Urochloral acid is crystalline,
soluble in water, in alcohol, and in ether, reduces copper from
Fehling’s solution, and rotates a ray of polarised light to the left.
Urochloral acid, on boiling with either dilute sulphuric or hydrochloric
acid, splits up into trichlorethyl alcohol and glycuronic acid--

  C₈H₁₁Cl₃O₇ + H₂O = C₂H₃Cl₃O + C₆H₁₀O₇.

Trichloralcohol is an oily fluid (boiling-point 150°-152°); it yields by
oxidation trichloracetic acid.

Urobutyl chloral acid gives on treatment with mineral acids
trichlorbutyl alcohol and glycuronic acid.

To separate urochloral acid from the urine the following process has
been found successful:--

The urine is evaporated to a syrup at the heat of the water-bath, and
then strongly acidulated with sulphuric acid and repeatedly shaken out
in a separating tube with a mixture of 3 vols. of ether and 1 vol. of
alcohol. The ether-alcohol is separated and distilled off, the acid
residue is neutralised with KHO, or potassic carbonate, and evaporated;
the dry mass is then taken up with 90 per cent. alcohol, the filtrate
precipitated with ether, and the precipitate washed with ether and
absolute alcohol.

Next the precipitate is boiled with absolute alcohol and filtered hot.
On cooling, the potassium salt of urochloral acid separates out in tufts
of silky needles. The crystals are dried over sulphuric acid and again
washed several times with absolute alcohol and ether to remove

To obtain the free acid, the potassium salt is dissolved in a little
water and acidulated with hydrochloric acid; the liquid is then shaken
out in a separating tube, with a mixture of 8 vols. of ether and 1 of
alcohol. The ether-alcohol is distilled off, the residue treated with
moist silver oxide until no farther separation of silver chloride
occurs, the silver chloride is separated by filtration, the soluble
silver salt decomposed by SH₂, and the filtrate carefully evaporated to
a syrup; after a few hours, the acid crystallises in stars of needles.

Urobutylchloral acid can be obtained in quite a similar way.[190]

[190] V. Mering u. Musculus, _Ber._, viii. 662; v. Mering, _ibid._, xv.
1019; E. Kulz, _Ber._, xv., 1538.

§ 207. =Separation of Chloral from Organic Matters.=--It will be most
convenient to place the organic fluid or pulped-up solid, mixed with
water, in a retort, to acidify with tartaric acid, and to distil.

Chloral hydrate distils over from a liquid acidified with tartaric acid;
to obtain the whole of the chloral requires distillation in a vacuum
almost to dryness.

The distillation will, unless there is also some partly decomposed
chloral, not smell of chloroform, and yet give chloroform reactions.

To identify it, to the distillate should be added a little burnt
magnesia, and the distillate thus treated boiled for half an hour in a
flask connected with an inverted condenser; in this way the chloral
hydrate is changed into chloroform and magnesium formate--

  2CCl₃CH(OH)₂ + MgO = 2CHCl₃ + (HCOO)₂Mg + H₂O.

The fluid may now be tested for formic acid: it will give a black
precipitate with solution of silver nitrate--

  (HCOO)₂Mg + 4AgNO₃ = 4Ag + Mg(NO₃)₂ + 2CO₂ + 2HNO₃.

It will give a white precipitate of calomel when treated with mercuric
chloride solution--

  (HCOO)₂Mg + 4HgCl₂ = 2Hg₂Cl₂ + MgCl₂ + 2HCl + 2CO₂.

Chloral (or chloroform), when boiled with resorcinol and the liquid made
strongly alkaline with NaHO, gives a red colour, which disappears on
acidifying and is restored by alkalies. If, on the other hand, there is
an excess of resorcinol and only a very small quantity of NaHO used, the
product shows a yellowish-green fluorescence; 1/10 of a milligramme of
chloral hydrate gives this reaction distinctly when boiled with 50
mgrms. of resorcinol and 5 drops of a normal solution of sodium

[191] C. Schwarz, _Pharm. Zeit._, xxxiii. 419.

Dr. Frank Ogston[192] has recommended sulphide of ammonium to be added
to any liquid as a test for chloral. The contents of the stomach are
filtered or submitted to dialysis, and the test applied direct. If
chloral is present, there is first an orange-yellow colour; on standing,
the fluid becomes more and more brown, then troubled, an amorphous
precipitate falls to the bottom, and a peculiar odour is developed. With
10 mgrms. of chloral in 1 c.c. of water, there is an evident
precipitate, and the odour can readily be perceived; with 1 mgrm.
dissolved in 1 c.c. of water, there is an orange-yellow colour, and also
the odour, but no precipitate; with ·1 mgrm. in 1 c.c. of water, there
is a weak, pale, straw-yellow colour, which can scarcely be called
characteristic. The only substance giving in neutral solutions the same
reactions is antimony; but, on the addition of a few drops of acid, the
antimony falls as an orange-yellow precipitate, while, if chloral alone
is present, there is a light white precipitate of sulphur.

[192] _Vierteljahrsschrift f. gerichtl. Medicin_, 1879, Bd. xxx. Hft. 1,
S. 268.

VIII.--Bisulphide of Carbon.

§ 208. Bisulphide of carbon--_carbon disulphide_, _carbon sulphide_
(CS₂)--is a colourless, volatile fluid, strongly refracting light.
Commercial samples have a most repulsive and penetrating odour, but
chemically pure carbon sulphide has a smell which is not disagreeable.
The boiling-point is 47°; the specific gravity at 0° is 1·293. It is
very inflammable, burning with a blue flame, and evolving sulphur
dioxide; is little soluble in water, but mixes easily with alcohol or
ether. Bisulphide of carbon, on account of its solvent powers for
sulphur, phosphorus, oils, resins, caoutchouc, gutta-percha, &c., is in
great request in certain industries. It is also utilised for
disinfecting purposes, the liquid being burnt in a lamp.

§ 209. =Poisoning by Carbon Bisulphide.=--In spite of the cheapness and
numerous applications of this liquid, poisoning is very rare. There
appears to be a case on record of attempted self-destruction by this
agent, in which a man took 2 ozs. (56·7 c.c.) of the liquid, but without
a fatal result. The symptoms in this case were pallor of the face, wide
pupils, frequent and weak pulse, lessened bodily temperature, and
spasmodic convulsions. Carbon disulphide was detected in the breath by
leading the expired air through an alcoholic solution of
triethyl-phosphin, with which it struck a red colour. It could also be
found in the urine in the same way. An intense burning in the throat,
giddiness, and headache lasted for several days.

§ 210. Experiments on animals have been frequent, and it is found to be
fatal to all forms of animal life. There is, indeed, no more convenient
agent for the destruction of various noxious insects, such as moths, the
weevils in biscuits, the common bug, &c., than bisulphide of carbon. It
has also been recommended for use in exterminating mice and rats.[193]
Different animals show various degrees of sensitiveness to the vapour;
frogs and cats being less affected by it than birds, rabbits, and
guinea-pigs. It is a blood poison; methæmoglobin is formed, and there is
disintegration of the red blood corpuscles. There is complete anæsthesia
of the whole body, and death occurs through paralysis of the respiratory
centre, but artificial respiration fails to restore life.

[193] Cloëz, _Compt. Rend._, t. 63, 85.

§ 211. =Chronic Poisoning.=--Of some importance is the chronic poisoning
by carbon disulphide, occasionally met with in manufactures
necessitating the daily use of large quantities for dissolving
caoutchouc, &c. When taken thus in the form of vapour daily for some
time, it gives rise to a complex series of symptoms which may be divided
into two principal stages--viz., a stage of excitement and one of
depression. In the first phase, there is more or less permanent
headache, with considerable indigestion, and its attendant loss of
appetite, nausea, &c. The sensitiveness of the skin is also heightened,
and there are curious sensations of creeping, &c. The mind at the same
time in some degree suffers, the temper becomes irritable, and singing
in the ears and noises in the head have been noticed. In one factory a
workman suffered from an acute mania, which subsided in two days upon
removing him from the noxious vapour (_Eulenberg_). The sleep is
disturbed by dreams, and, according to Delpech,[194] there is
considerable sexual excitement, but this statement has in no way been
confirmed. Pains in the limbs are a constant phenomenon, and the French
observers have noticed spasmodic contractions of certain groups of

[194] _Mémoire sur les Accidents que développe chez les ouvrières en
caoutchouc du sulfure de carb. en vapeur_, Paris, 1856.

The stage of depression begins with a more or less pronounced anæsthesia
of the skin. This is not confined to the outer skin, but also affects
the mucous membranes; patients complain that they feel as if the tongue
were covered with a cloth. The anæsthesia is very general. In a case
recorded by Bernhardt,[195] a girl, twenty-two years old, who had worked
six weeks in a caoutchouc factory, suffered from mental weakness and
digestive troubles; there was anæsthesia and algesis of the whole skin.
In these advanced cases the mental debility is very pronounced, and
there is also weakness of the muscular system. Paralysis of the lower
limbs has been noted, and in one instance a man had his right hand
paralysed for two months. It seems uncertain how long a person is likely
to suffer from the effects of the vapour after he is removed from its
influence. If the first stage of poisoning only is experienced, then
recovery is generally rapid; but if mental and muscular weakness and
anæsthesia of the skin have been developed, a year has been known to
elapse without any considerable improvement, and permanent injury to the
health may be feared.

[195] _Ber. klin. Wochenschrift_, No. 32, 1866.

§ 212. =Post-mortem Appearances.=--The pathological appearances found
after sudden death from disulphide of carbon are but little different to
those found after fatal chloroform breathing.

§ 213. =Detection and Separation of Carbon Disulphide.=--The extreme
volatility of the liquid renders it easy to separate it from organic
liquids by distillation with reduced pressure in a stream of CO₂. Carbon
disulphide is best identified by (1) Hofman’s test, viz., passing the
vapour into an ethereal solution of triethyl-phosphin, (C₂H₅)₃P. Carbon
disulphide forms with triethyl-phosphin a compound which crystallises in
red scales. The crystals melt at 95° C., and have the following
formula--P(C₂H₅)₃CS₂. This will detect 0·54 mgrm. Should the quantity of
bisulphide be small, no crystals may be obtained, but the liquid will
become of a red colour. (2) CS₂ gives, with an alcoholic solution of
potash, a precipitate of potassic xanthate, CS₂C₂H₅OK.

    § 214. =Xanthogenic acid or ethyloxide-sulphocarbonate= (CS₂C₂H₅OH)
    is prepared by decomposing potassic xanthogenate by diluted
    hydrochloric or sulphuric acid. It is a colourless fluid, having an
    unpleasant odour, and a weakly acid and rather bitter taste. It
    burns with a blue colour, and is easily decomposed at 24°, splitting
    up into ethylic alcohol and hydric sulphide. It is very poisonous,
    and has an anæsthetic action similar to bisulphide of carbon. Its
    properties are probably due to CS₂ being liberated within the body.

    § 215. =Potassic xanthogenate= (CS₂C₂H₅OK) and =potassic
    xanthamylate= (CS₂C₅H₁₁OK) (the latter being prepared by the
    substitution of amyl alcohol for ethyl alcohol), both on the
    application of a heat below that of the body, develop CS₂, and are
    poisonous, inducing symptoms very similar to those already detailed.

IX.--The Tar Acids--Phenol--Cresol.

§ 216. =Carbolic Acid. Syn. Phenol, Phenyl Alcohol, Phenylic Hydrate;
Phenic Acid; Coal-Tar Creasote.=--The formula for carbolic acid is
C₆H₅HO. The pure substance appears at the ordinary temperature as a
colourless solid, crystallising in long prisms; the fusibility of the
crystals is given variously by different authors: from my own
observation, the pure crystals melt at 40°-41°, any lower melting-point
being due to the presence of cresylic acid or other impurity; the
crystals again become solid about 15°. Melted carbolic acid forms a
colourless limpid fluid, sinking in water. It boils under the ordinary
pressure at 182°, and distils without decomposition; it is very readily
and completely distilled in a vacuum at about the temperature of 100°.
After the crystals have been exposed to the air, they absorb water, and
a hydrate is formed containing 16·07 per cent. of water. The hydrate
melts at 17°, any greater hydration prevents the crystallisation of the
acid; a carbolic acid, containing about 27 per cent. of water, and
probably corresponding to the formula C₆H₆O,2H₂O, is obtained by
gradually adding water to carbolic acid so long as it continues to be
dissolved. Such a hydrate dissolves in 11·1 times its measure of water,
and contains 8·56 per cent. of real carbolic acid. Carbolic acid does
not redden litmus, but produces a greasy stain on paper, disappearing on
exposure to the air; it has a peculiar smell, a burning numbing taste,
and in the fluid state it strongly refracts light. Heated to a high
temperature it takes fire, and burns with a sooty flame.

When an aqueous solution of carbolic acid is shaken up with ether,
benzene, carbon disulphide, or chloroform, it is fully dissolved by the
solvent, and is thus easily separated from most solutions in which it
exists in the free state. Petroleum ether, on the other hand, only
slightly dissolves it in the cold, more on warming. Carbolic acid mixes
in all proportions with glycerin, glacial or acetic acid, and alcohol.
It coagulates albumen, the precipitate being soluble in an excess of
albumen; it also dissolves iodine, without changing its properties. It
dissolves many resins, and also sulphur, but, on boiling, sulphuretted
hydrogen is disengaged. Indigo blue is soluble in hot carbolic acid, and
may be obtained in crystals on cooling. Carbolic acid is contained in
castoreum, a secretion derived from the beaver, but it has not yet been
detected in the vegetable kingdom. The source of carbolic acid is at
present coal-tar, from which it is obtained by a process of
distillation. There are, however, a variety of chemical actions in the
course of which carbolic acid is formed.

§ 217. The common disinfecting carbolic acid is a dark reddish liquid,
with a very strong odour; at present there is very little phenol in it;
it is mainly composed of meta- and para-cresol. It is officinal in
Germany, and there must contain at least 50 per cent. of the pure
carbolic acid. The pure crystallised carbolic acid is officinal in our
own and all the continental pharmacopœias. In the British Pharmacopœia,
a solution of carbolic acid in glycerin is officinal; the proportions
are 1 part of carbolic acid and 4 parts of glycerin, that is, strength
by measure = 20 per cent. The Pharmacopœia Germanica has a _liquor natri
carbolici_, made with 5 parts carbolic acid, 1 caustic soda, and 4 of
water; strength in carbolic acid = 50 per cent. There is also a strongly
alkaline crude sodic carbolate in use as a preservative of wood.

There are various disinfecting fluids containing amounts of carbolic
acid, from 10 per cent. upwards. Many of these are somewhat complex
mixtures, but, as a rule, any poisonous properties they possess are
mainly due to their content of phenol or cresol. A great variety of
disinfecting powders, under various names, are also in commerce,
deriving their activity from carbolic acid. Macdougall’s disinfecting
powder is made by adding a certain proportion of impure carbolic acid to
a calcic sulphite, which is prepared by passing sulphur dioxide over
ignited limestone.

=Calvert’s carbolic acid powder= is made by adding carbolic acid to the
siliceous residue obtained from the manufacture of aluminic sulphate
from shale. There are also various carbolates which, by heating or
decomposing with sulphuric acid, give off carbolic acid.

=Carbolic acid soaps= are also made on a large scale--the acid is free,
and some of the soaps contain as much as 10 per cent. In the inferior
carbolic acid soaps there is little or no carbolic acid, but cresylic
takes its place. Neither the soaps nor the powders have hitherto
attained any toxicological importance, but the alkaline carbolates are
very poisonous.

§ 218. =The chief uses= of carbolic acid are indicated by the foregoing
enumeration of the principal preparations used in medicine and commerce.
The bulk of the carbolic acid manufactured is for the purposes of
disinfection. It is also utilised in the preparation of certain
colouring matters or dyes, and during the last few years has had another
application in the manufacture of salicylic acid. In medicine it is
administered occasionally internally, while the antiseptic movement in
surgery, initiated by Lister, has given it great prominence in surgical

§ 219. =Statistics.=--The tar acids, _i.e._, pure carbolic acid and the
impure acids sold under the name of carbolic acid, but consisting (as
stated before) mainly of cresol, are, of all powerful poisons, the most
accessible, and the most recklessly distributed. We find them at the
bedside of the sick, in back-kitchens, in stables, in public and private
closets and urinals, and, indeed, in almost all places where there are
likely to be foul odours or decomposing matters. It is, therefore, no
wonder that poisoning by carbolic acid has, of late years, assumed large
proportions. The acid has become vulgarised, and quite as popularly
known, as the most common household drugs or chemicals.[196] This
familiarity is the growth of a very few years, since it was not
discovered until 1834, and does not seem to have been used by Lister
until about 1863. It was not known to the people generally until much
later. At present it occupies the third place in fatality of all
poisons in England. The following table shows that, in the past ten
years, carbolic acid has killed 741 people, either accidentally or
suicidally; there is also one case of murder by carbolic acid within the
same period, bringing the total up to 742:--

[196] Although this is so, yet much ignorance still prevails as to its
real nature. In a case reported in the _Pharm. Journ._, 1881, p. 334, a
woman, thirty years of age, drank two-thirds of an ounce of liquid
labelled “_Pure Carbolic Acid_” by mistake, and died in two hours. She
read the label, and a lodger also read it, but did not know what it

ENDING 1892.

                       ACCIDENT OR NEGLIGENCE.

  Ages,       0-1  1-5  5-15  15-25  25-65  65 and  Total
  Males,       2   39    13      5     83      8     150
  Females,     2   21     7     13     51      7     101
  Totals,      4   60    20     18    134     15     251


  Ages,                       15-25  25-65  65 and  Total
  Males,                        26    186      7     219
  Females,                      72    194      5     271
  Totals,                       98    380     12     490

Falck has collected, since the year 1868, no less than 87 cases of
poisoning from carbolic acid recorded in medical literature. In one of
the cases the individual died in nine hours from a large dose of
carbolate of soda; in a second, violent symptoms were induced by
breathing for three hours carbolic acid vapour; in the remaining 85, the
poisoning was caused by the liquid acid. Of these 85 persons, 7 had
taken the poison with suicidal intent, and of the 7, 5 died; 39 were
poisoned through the medicinal use of carbolic acid, 27 of the 39 by the
antiseptic treatment of wounds by carbolic acid dressings, and of these
8 terminated fatally; in 8 cases, symptoms of poisoning followed the
rubbing or painting of the acid on the skin for the cure of scabies,
favus, or psoriasis, and 6 of these patients died. In 4 cases, carbolic
acid enemata, administered for the purpose of dislodging ascarides, gave
rise to symptoms of poisoning, and in one instance death followed.

The substitution of carbolic acid for medicine happened as follows:--

  Taken instead of Tincture of Opium,              1
    „      „       Infusion of Senna,              3
    „      „       Mineral Water,                  2
    „      „       other Mixtures,                 3
    „   inwardly instead of applied outwardly,     3

Of these 12, 8 died.

Again, 10 persons took carbolic acid in mistake for various alcoholic
drinks, such as schnapps, brandy, rum, or beer, and 9 of the 10
succumbed; 17 persons drank carbolic acid simply “by mistake,” and of
these 13 died. Thus, of the whole 85 cases, no less than 51 ended
fatally--nearly 60 per cent.

It must be always borne in mind that, with regard to statistics
generally, the term “carbolic acid” is not used by coroners, juries, or
medical men, in a strictly chemical sense, the term being made to
include disinfecting fluids which are almost wholly composed of the
cresols, and contain scarcely any phenol. In this article, with regard
to symptoms and pathological appearances, it is only occasionally
possible to state whether the pure medicinal crystalline phenol or a
mixture of tar-acids was the cause of poisoning.

§ 220. =Fatal Dose.=--The minimum fatal dose for cats, dogs, and
rabbits, appears to be from ·4 to ·5 grm. per kilogram. Falck has put
the minimum lethal dose for man at 15 grms. (231·5 grains), which would
be about ·2 per kilo., basing his estimate on the following reasoning.
In 33 cases he had a fairly exact record of the amount of acid taken,
and out of the 33, he selects only those cases which are of use for the
decision of the question. Among adults, in 5 cases the dose was 30
grms., and all the 5 cases terminated by death, in times varying from
five minutes to an hour and a half. By other 5 adults a dose of 15 grms.
was taken; of the 5, 3 men and a woman died, in times varying from
forty-five minutes to thirty hours, while 1 woman recovered. Doses of
11·5, 10·8, and 9 grms. were taken by different men, and recovered from;
on the other hand, a suicide who took one and a half teaspoonful (about
6 grms.) of the concentrated acid, died in fifty minutes. Doses of ·3 to
3 grms. have caused symptoms of poisoning, but the patients recovered,
while higher doses than 15 grms. in 12 cases, with only one exception,
caused death. Hence, it may be considered tolerably well established,
that 15 grms. (231·5 grains) may be taken as representing the minimum
lethal dose.

The largest dose from which a person appears to have recovered is, I
believe, that given in a case recorded by Davidson, in which 150 grms.
of crude carbolic acid had been taken. It must, however, be remembered
that, as this was the impure acid, probably only half of it was really
carbolic acid. The German Pharmacopœia prescribes as a maximum dose ·05
grm (·7 grain) of the crystallised acid, and a daily maximum quantity
given in divided doses of ·15 grm. (2·3 grains).

§ 221. =Effects on Animals.=--Carbolic acid is poisonous to both animal
and vegetable life.

=Infusoria.=--One part of the acid in 10,000 parts of water rapidly
kills ciliated animalcules,--the movements become sluggish, the sarcode
substance darker, and the cilia in a little time cease moving.

=Fish.=--One part of the acid in 7000 of water kills dace, minnows,
roach, and gold fish. In this amount of dilution the effect is not
apparent immediately; but, at the end of a few hours, the movements of
the fish become sluggish, they frequently rise to the surface to
breathe, and at the end of twenty-four hours are found dead. Quantities
of carbolic acid, such as 1 part in 100,000 of water, appear to affect
the health of fish, and render them more liable to be attacked by the
fungus growth which is so destructive to fish-life in certain years.

=Frogs.=--If ·01 to ·02 grm. of carbolic acid be dissolved in a litre of
water in which a frog is placed, there is almost immediately signs of
uneasiness in the animal, showing that pain from local contact is
experienced; a sleepy condition follows, with exaltation of reflex
sensibility; convulsions succeed, generally, though not always; then
reflex sensibility is diminished, ultimately vanishes, and death occurs;
the muscles and nerves still respond to the electric current, and the
heart beats, but slowly and weakly, for a little after the respiration
has ceased.

§ 222. =Warm-blooded Animals.=--For a rabbit of the average weight of 2
kilos., ·15 grm. is an active dose, and ·3 a lethal dose (that is ·15
per kilo.). The sleepy condition of the frog is not noticed, and the
chief symptoms are clonic convulsions with dilatation of the pupils, the
convulsions passing into death, without a noticeable paralytic stage.
The symptoms observed in poisoned dogs are almost precisely similar, the
dose, according to body-weight, being the same. It has, however, been
noticed that with doses large enough to produce convulsions, a weak
condition has supervened, causing death in several days. There appears
to be no cumulative action, since equal toxic doses can be given to
animals for some time, and the last dose has no greater effect than the
first or intermediate ones. The pathological appearances met with in
animals poisoned by the minimum lethal doses referred to are not
characteristic; but there is a remarkable retardation of putrefaction.

§ 223. =Symptoms in Man, external application.=--A 5 per cent. solution
of carbolic acid, applied to the skin, causes a peculiar numbness,
followed, it may be, by irritation. Young subjects, and those with
sensitive skins, sometimes exhibit a pustular eruption, and concentrated
solutions cause more or less destruction of the skin. Lemaire[197]
describes the action of carbolic acid on the skin as causing a slight
inflammation, with desquamation of the epithelium, followed by a very
permanent brown stain, but this he alone has observed. Applied to the
mucous membrane, carbolic acid turns the epithelial covering white; the
epithelium, however, is soon thrown off, and the place rapidly heals;
there is the same numbing, aconite-like feeling before noticed. The
vapour of carbolic acid causes redness of the conjunctivæ, and
irritation of the air-passages. If the application is continued, the
mucous membrane swells, whitens, and pours out an abundant secretion.

[197] Lemaire, Jul., “_De l’Acide phénique_,” Paris, 1864.

Dr. Whitelock, of Greenock, has related two instances in which children
were treated with carbolic acid lotion (strength 2½ per cent.) as an
application to the scalp for ringworm; in both, symptoms of poisoning
occurred--in the one, the symptoms at once appeared; in the other they
were delayed some days. In order to satisfy his mind, the experiment was
repeated twice, and each time gastric and urinary troubles followed.

Nussbaum, of Munich, records a case[198] in which symptoms were induced
by the forcible injection of a solution of carbolic acid into the cavity
of an abscess.

[198] _Leitfaden zur antiseptischer Wundbehandlung_, 141.

Macphail[199] gives two cases of poisoning by carbolic acid from
external use. In the one, a large tumour had been removed from a woman
aged 30, and the wound covered with gauze steeped in a solution of
carbolic acid, in glycerin, strength 10 per cent.; subsequently, there
was high fever, with diminished sulphates in the urine, which smelt
strongly of carbolic acid, and was very dark. On substituting boracic
acid, none of these troubles were observed. The second case was that of
a servant suffering from axillary abscess; the wound was syringed out
with carbolic acid solution, of strength 2½ per cent., when effects were
produced similar to those in the first case. It was noted that in both
these cases the pulse was slowed. Scattered throughout surgical and
medical literature, there are many other cases recorded, though not all
so clear as those cited. Several cases are also on record in which
poisonous symptoms (and even death) have resulted from the application
of carbolic acid lotion as a remedy for scabies or itch.

[199] “Carbolic Acid Poisoning (Surgical),” by S. Rutherford Macphail,
M.B., _Ed. Med. Journal_, cccxiv., Aug. 1881, p. 134.

A surgeon prescribed for two joiners who suffered from scabies a lotion,
which was intended to contain 30 grms. of carbolic acid in 240 c.c. of
water; but the actual contents of the flasks were afterwards from
analysis estimated by Hoppe-Seyler to be 33·26 grms., and the quantity
used by each to be equal to 13·37 grms. (206 grains) of carbolic acid.
One of the men died; the survivor described his own symptoms as
follows:--He and his companion stood in front of the fire, and rubbed
the lotion in; he rubbed it into his legs, breast, and the front part of
his body; the other parts were mutually rubbed. Whilst rubbing his right
arm, and drying it before the fire, he felt a burning sensation, a
tightness and giddiness, and mentioned his sensations to his companion,
who laughed. This condition lasted from five to seven minutes, but he
did not remember whether his companion complained of anything, nor did
he know what became of him, nor how he himself came to be in bed. He was
found holding on to the joiner’s bench, looking with wide staring eyes,
like a drunken man, and was delirious for half an hour. The following
night he slept uneasily and complained of headache and burning of the
skin. The pulse was 68, the appearance of the urine, appetite, and sense
of taste were normal; the bowels confined. He soon recovered.

The other joiner seems to have died as suddenly as if he had taken
prussic acid. He called to his mother, “_Ich habe einen Rausch_,” and
died with pale livid face, after taking two deep, short inspirations.

The _post-mortem_ examination showed the sinuses filled with much fluid
blood, and the vessels of the pia mater congested. Frothy, dark, fluid
blood was found in the lungs, which were hyperæmic; the mucous tissues
of the epiglottis and air-tubes were reddened, and covered with a frothy
slime. Both ventricles--the venæ cavæ and the vessels of the spleen and
kidneys--were filled with dark fluid blood. The muscles were very red;
there was no special odour. Hoppe-Seyler recognised carbolic acid in the
blood and different organs of the body.[200]

[200] R. Köhler, _Würtem. Med. Corr. Bl._, xlii., No. 6, April 1872; H.
Abelin, _Schmidt’s Jahrbücher_, 1877, Bd. 173, S. 163.

In another case, a child died from the outward use of a 2 per cent.
solution of carbolic acid. It is described as follows:--An infant of
seven weeks old suffered from varicella, and one of the pustules became
the centre of an erysipelatous inflammation. To this place a 2 per cent.
solution of carbolic acid was applied by means of a compress steeped in
the acid; the following morning the temperature rose from 36·5° (97·7°
F.) to 37° (98·6° F.), and poisonous symptoms appeared. The urine was
coloured dark. There were sweats, vomitings, and contracted pupils,
spasmodic twitchings of the eyelids and eyes, with strabismus, slow
respiration, and, lastly, inability to swallow. Under the influence of
stimulating remedies the condition temporarily improved, but the child
died twenty-three and a half hours after the first application. An
examination showed that the vessels of the brain and the tissue of the
lungs were abnormally full of blood. The liver was softer than natural,
and exhibited a notable yellowishness in the centre of the acini.
Somewhat similar appearances were noticed in the kidneys, the
microscopic examination of which showed the _tubuli contorti_ enlarged
and filled with fatty globules. In several places the epithelium was
denuded, in other places swollen, and with the nuclei very visible.

In an American case,[201] death followed the application of carbolic
acid to a wound. A boy had been bitten by a dog, and to the wound, at
one o’clock in the afternoon, a lotion, consisting of nine parts of
carbolic acid and one of glycerin, was applied. At seven o’clock in the
evening the child was unconscious, and died at one o’clock the following

[201] _American Journal of Pharmacy_, vol. li., 4th Ser.; vol. ix.,
1879, p. 57.

§ 224. =Internal Administration.=--Carbolic acid may be taken into the
system, not alone by the mouth, but by the lungs, as in breathing
carbolic acid spray or carbolic acid vapour. It is also absorbed by the
skin when outwardly applied, or in the dressing or the spraying of
wounds with carbolic acid. Lastly, the ordinary poisonous effects have
been produced by absorption from the bowel, when administered as an
enema. When swallowed undiluted, and in a concentrated form, the
symptoms may be those of early collapse, and speedy death. Hence, the
course is very similar to that witnessed in poisoning by the mineral

If lethal, but not excessive doses of the diluted acid are taken, the
symptoms are--a burning in the mouth and throat, a peculiarly unpleasant
persistent taste, and vomiting. There is faintness with pallor of the
face, which is covered by a clammy sweat, and the patient soon becomes
unconscious, the pulse small and thready, and the pupils sluggish to
light. The respiration is profoundly affected; there is dyspnœa, and the
breathing becomes shallow. Death occurs from paralysis of the
respiratory apparatus, and the heart is observed to beat for a little
after the respiration has ceased. All these symptoms may occur from the
application of the acid to the skin or to mucous membranes, and have
been noticed when solutions of but moderate strength have been
used--e.g., there are cases in gynæcological practice in which the
mucous membrane (perhaps eroded) of the uterus has been irrigated with
carbolic acid injections. Thus, Küster[202] relates a case in which,
four days after confinement, the uterus was washed out with a 2 per
cent. solution of carbolic acid without evil result. Afterwards a 5 per
cent. solution was used, but it at once caused violent symptoms of
poisoning, the face became livid, clonic convulsions came on, and at
first loss of consciousness, which after an hour returned. The patient
died on the ninth day. There was intense diphtheria of the uterus and
vagina. Several other similar cases (although not attended with such
marked or fatal effects) are on record.[203]

[202] _Centralblatt. f. Gynäkologie_, ii. 14, 1878.

[203] A practitioner in Calcutta injected into the bowel of a boy, aged
5, an enema of diluted carbolic acid, which, according to his own
statement, was 1 part in 60, and the whole quantity represented 144
grains of the acid. The child became insensible a few minutes after the
operation, and died within four hours. There was no _post-mortem_
examination; the body smelt strongly of carbolic acid.--_Lancet_, May
19, 1883.

§ 225. The symptoms of carbolic acid poisoning admit of considerable
variation from those already described. The condition is occasionally
that of deep coma. The convulsions may be general, or may affect only
certain groups of muscles. Convulsive twitchings of the face alone, and
also muscular twitchings only of the legs, have been noticed. In all
cases, however, a marked change occurs in the urine. Subissi[204] has
noted the occurrence of abortion, both in the pig and the mare, as a
result of carbolic acid, but this effect has not hitherto been recorded
in the human subject.

[204] _L’Archivio della Veterinaria Ital._, xi., 1874.

It has been experimentally shown by Küster, that previous loss of blood,
or the presence of septic fever, renders animals more sensitive to
carbolic acid. It is also said that children are more sensitive than

The course of carbolic acid poisoning is very rapid. In 35 cases
collected by Falck, in which the period from the taking of the poison to
the moment of death was accurately noted, the course was as follows:--12
patients died within the first hour, and in the second hour 3; so that
within two hours 15 died. Between the third and the twelfth hour, 10
died; between the thirteenth and the twenty-fourth hour, 7 died; and
between the twenty-fifth and the sixtieth hour, only 3 died. Therefore,
slightly over 71 per cent. died within twelve hours, and 91·4 per cent.
within the twenty-four hours.

§ 226. =Changes in the Urine.=--The urine of patients who have absorbed
in any way carbolic acid is dark in colour, and may smell strongly of
the acid. It is now established--chiefly by the experiments and
observations of Baumann[205]--that carbolic acid, when introduced into
the body, is mainly eliminated in the form of phenyl-sulphuric acid,
C₆H₅HSO₄, or more strictly speaking as potassic phenyl-sulphate,
C₆H₅KSO₄, a substance which is not precipitated by chloride of barium
until it has been decomposed by boiling with a mineral acid. Cresol is
similarly excreted as cresol-sulphuric acid, C₆H₄CH₃HSO₄, ortho-, meta-,
or para-, according to the kind of cresol injected; a portion may also
appear as hydro-tolu-chinone-sulphuric acid. Hence it is that, with
doses of phenol or cresol continually increasing, the amount of
sulphates naturally in the urine (as estimated by simply acidifying with
hydrochloric acid, and precipitating in the cold with chloride of
barium) continually decreases, and may at last vanish, for all the
sulphuric acid present is united with the phenol. On the other hand, the
precipitate obtained by prolonged boiling of the strongly acidified
urine, after filtering off any BaSO₄ thrown down in the cold, is ever

[205] _Pflüger’s Archiv_, 13, 1876, 289.

Thus, a dog voided urine which contained in 100 c.c., ·262 grm. of
precipitable sulphuric acid, and ·006 of organically-combined sulphuric
acid; his back was now painted with carbolic acid, and the normal
proportions were reversed, the precipitable sulphuric acid became ·004
grm., while the organically-combined was ·190 in 100 c.c. In addition to
phenyl-sulphuric acid, it is now sufficiently established[206] that

  (    OH)
  (C₆H₄  )
  (    OH)

(paradihydroxyl phenol) and pyrocatechin

  (    OH)
  (C₆H₄  )
  (    OH)

(orthodihydroxyl phenol) are constant products of a portion of the
phenol. The hydroquinone appears in the urine, in the first place, as
the corresponding ether-sulphuric acid, which is colourless; but a
portion of it is set free, and this free hydroquinone (especially in
alkaline urine) is quickly oxidised to a brownish product, and hence the
peculiar colour of urine. Out of dark coloured carbolic acid urine the
hydroquinone and its products of decomposition can be obtained by
shaking with ether; on separation of the ether, an extract is obtained,
reducing alkaline silver solution, and developing quinone on warming
with ferric chloride.

[206] E. Baumann and C. Preuss, _Zeitschrift f. phys. Chemie_, iii. 156;
_Anleitung zur Harn-Analyse_, W. F. Löbisch, Leipzig, 1881, pp. 142,
160; Schmiedeberg, _Chem. Centrbl._ (3), 13, 598.

To separate pyro-catechin, 200 c.c. of urine may be evaporated to an
extract, the extract treated with strong alcohol, the alcoholic liquid
evaporated, and the extract then treated with ether. On separation and
evaporation of the ether, a yellowish mass is left, from which the
pyro-catechin may be extracted by washing with a small quantity of
water. This solution will reduce silver solution in the cold, or, if
treated with a few drops of ferric chloride solution, show a marked
green colour, changing on being alkalised by a solution of sodic
hydro-carbonate to violet, and then on being acidified by acetic acid,
changing back again to green. According to Thudichum,[207] the urine of
men and dogs, after the ingestion of carbolic acid, contains a blue

[207] _On the Pathology of the Urine_, Lond., 1877, p. 198.

§ 227. =The Action of Carbolic Acid considered
physiologically.=--Researches on animals have elucidated, in a great
measure, the mode in which carbolic acid acts, and the general sequence
of effects, but there is still much to be learnt.

E. Küster[208] has shown that the temperature of dogs, when doses of
carbolic acid in solution are injected subcutaneously, or into the
veins, is immediately, or very soon after the operation, raised. With
small and moderate doses, this effect is but slight--from half to a
whole degree--on the day after the injection the temperature sinks below
the normal point, and only slowly becomes again natural. With doses that
are just lethal, first a rise and then a rapid sinking of temperature
are observed; but with those excessive doses which speedily kill, the
temperature at once sinks without a preliminary rise. The action on the
heart is not very marked, but there is always a slowing of the cardiac
pulsations; according to Hoppe-Seyler the arteries are relaxed. The
respiration is much quickened; this acceleration is due to an
excitement of the vagus centre, since Salkowsky has shown that section
of the vagus produces a retardation of the respiratory wave. Direct
application of the acid to muscles or nerves quickly destroys their
excitability without a previous stage of excitement. The main cause of
the lethal action of carbolic acid--putting on one side those cases in
which it may kill by its local corrosive action--appears to be paralysis
of the respiratory nervous centres. The convulsions arise from the
spinal cord. On the cessation of the convulsions, the superficial nature
of the breathing assists other changes by preventing the due oxidation
of the blood.

[208] _Archiv f. klin. Chirurgie_, Bd. 23, S. 133, 1879.

§ 228. Carbolic acid is separated from the body in the forms already
mentioned, a small portion is also excreted by the skin. Salkowsky
considers that, with rabbits, he has also found oxalic acid in the urine
as an oxidation product. According to the researches of Binnendijk,[209]
the separation of carbolic acid by the urine commences very quickly
after its ingestion; and, under favourable circumstances, it may be
completely excreted within from twelve to sixteen hours. It must be
remembered that normally a small amount of phenol may be present in the
animal body, as the result of the digestion of albuminous substances or
of their putrefaction. The amount excreted by healthy men when feeding
on mixed diet, Engel,[210] by experiment, estimates to be in the
twenty-four hours 15 mgrms.

[209] _Journal de Pharmacie et de Chimie._

[210] _Annal. de Chimie et de Physique_, 5 Sér. T. 20, p. 230, 1880.

§ 229. =Post-mortem Appearances.=--No fact is better ascertained from
experiments on animals than the following:--That with lethal doses of
carbolic acid, administered by subcutaneous injection, or introduced by
the veins, no appearances may be found after death which can be called
at all characteristic. Further, in the cases in which death has occurred
from the outward application of the acid for the cure of scabies, &c.,
no lesion was ascertained after death which could--apart from the
history of the case and chemical evidence--with any confidence be
ascribed to a poison.

On the other hand, when somewhat large doses of the acid are taken by
the mouth, very coarse and appreciable changes are produced in the upper
portion of the alimentary tract. There may be brownish, wrinkled spots
on the cheek or lips; the mucous membrane of the mouth, throat, and
gullet is often white, and if the acid was concentrated, eroded. The
stomach is sometimes thickened, contracted, and blanched, a condition
well shown in a pathological preparation (ix. 206, 43 _f_) in St.
George’s Hospital. The mucous membrane, indeed, may be quite as much
destroyed as if a mineral acid had been taken. Thus, in Guy’s Hospital
museum (1799⁴⁰), there is preserved the stomach of a child who died
from taking accidentally carbolic acid. It looks like a piece of paper,
and is very white, with fawn-coloured spots; the rugæ are absent, and
the mucous membrane seems to have entirely vanished. Not unfrequently
the stomach exhibits white spots with roundish edges. The duodenum is
often affected, and the action is not always limited to the first part
of the intestine.

The respiratory passages are often inflamed, and the lungs infiltrated
and congested. As death takes place from an asphyxiated condition, the
veins of the head and brain, and the blood-vessels of the liver, kidney
and spleen, are gorged with blood, and the right side of the heart
distended, while the left is empty. On the other hand, a person may die
of sudden nervous shock from the ingestion of a large quantity of the
acid, and in such a case the _post-mortem_ appearances will not then
exhibit precisely the characters just detailed. Putrefaction is retarded
according to the dose, and there is often a smell of carbolic acid.[211]
If any urine is contained in the bladder, it will probably be dark, and
present the characters of carbolic urine, detailed at p. 174.

[211] In order to detect this odour, it is well to open the head first,
lest the putrefaction of the internal viscera be so great as to mask the

Tests for Carbolic Acid.

§ 230. 1. =The Pinewood Test.=--Certain pinewood gives a beautiful blue
colour when moistened first with carbolic acid, and afterwards with
hydrochloric acid, and exposed to the light. Some species of pine give a
blue colour with hydrochloric acid alone, and such must not be used;
others do not respond to the test for carbolic acid. Hence it is
necessary to try the chips of wood first, to see how they act, and with
this precaution the test is very serviceable, and, in cautious hands, no
error will be made.

2. =Ammonia and Hypochlorite Test.=--If to a solution containing even so
small a quantity as 1 part of carbolic acid in 5000 parts of water,
first, about a quarter of its volume of ammonia hydrate be added, and
then a small quantity of sodic hypochlorite solution, avoiding excess, a
blue colour appears, warming quickens the reaction: the blue is
permanent, but turns to red with acids. If there is a smaller quantity
than the above proportion of acid, the reaction may be still produced
feebly after standing for some time.

3. =Ferric Chloride.=--One part of phenol in 3000 parts of water can be
detected by adding a solution of ferric chloride; a fine violet colour
is produced. This is also a very good test, when applied to a
distillate; but if applied to a complex liquid, the disturbing action of
neutral salts and other substances may be too great to make the
reaction under those circumstances of service.

4. =Bromine.=--The most satisfactory test of all is treatment of the
liquid by bromine-water. A precipitate of tri-bromo-phenol (C₆H₃Br₃O) is
rapidly or slowly formed, according to the strength of the solution; in
detecting very minute quantities the precipitate must be given time to
form. According to Allen,[212] a solution containing but 1/60000 of
carbolic acid gave the reaction after standing twenty-four hours.

[212] _Commercial Organic Analysis_, vol. i. p. 306.

The properties of the precipitate are as follows:--It is crystalline,
and under the microscope is seen to consist of fine stars of needles;
its smell is peculiar; it is insoluble in water and acid liquids, but
soluble in alkalies, ether, and absolute alcohol; a very minute quantity
of water suffices to precipitate it from an alcoholic solution; it is
therefore essential to the success of the test that the watery liquid to
be examined is either neutral or acid in reaction.

§ 231. Tri-bromo-phenol may be used for the quantitative estimation of
carbolic acid, 100 parts of tri-bromo-phenol are equal to 29·8 of
carbolic acid; by the action of sodium amalgam, tri-bromo-phenol is
changed back into carbolic acid.

That bromine-water precipitates several volatile and fixed alkaloids
from their solutions is no objection to the bromine test, for it may be
applied to a distillation product, the bases having been previously
fixed by sulphuric acid. Besides, the properties of tri-bromo-phenol are
distinct enough, and therefore there is no valid objection to the test.
It is the best hitherto discovered. There are also other reactions, such
as that Millon’s reagent strikes a red--molybdic acid, in concentrated
sulphuric acid, a blue--and potassic dichromate, with sulphuric acid, a
brown colour--but to these there are objections. Again, we have the
_Euchlorine_ test, in which the procedure is as follows:--A test-tube is
taken, and concentrated hydrochloric acid is allowed to act therein upon
potassic chlorate. After the gas has been evolved for from 30 to 40
seconds, the liquid is diluted with 1½ volume of water, the gas removed
by blowing through a tube, and solution of strong ammonia poured in so
as to form a layer on the top; after blowing out the white fumes of
ammonium chloride, a few drops of the sample to be tested are added. In
the presence of carbolic acid, a rose-red, blood-red, or red-brown tint
is produced, according to the quantity present. Carbolic acid may be
confounded with _cresol_ or with _creasote_, but the distinction between
pure carbolic acid, pure cresol, and creasote is plain.

§ 232. =Cresol (Cresylic Acid, Methyl-phenol)=,

  C₆H₄     .

--There are three cresols--ortho-, meta-, and para-. Ordinary
commercial cresol is a mixture of the three, but contains but little
ortho-cresol; the more important properties of the pure cresols are set
out in the following table:--

  |        | Melting-point.  | Boiling-point. | Converted by fusion |
  |        |                 |                | with Potash into--  |
  |Ortho-, |   31-31·5° C.   |    188·0°      |   Salicylic Acid    |
  |        |                 |                | (Ortho-oxybenzoic   |
  |        |                 |                |      acid).         |
  |        |                 |                |                     |
  |Meta-,  |Fluid at ordinary|    201·0°      |  Meta-oxybenzoic    |
  |        |   temperature.  |                |      acid.          |
  |        |                 |                |                     |
  |Para-,  |     36°         |    198°        |Para-oxybenzoic acid.|

Pure ortho-, meta-, or para-cresol have been obtained by synthetical
methods; they cannot be said to be in ordinary commerce.

=Commercial cresol= is at ordinary temperatures a liquid, and cannot be
obtained in a crystalline state by freezing. Its boiling-point is from
198° to 203°; it is almost insoluble in strong ammonia, and, when 16
volumes are added, it then forms crystalline scales. On the other hand,
carbolic acid is soluble in an equal volume of ammonia, and is then
precipitated by the addition of 1½ volume of water. Cresol is insoluble
in small quantities of pure 6 per cent. soda solution; with a large
excess, it forms crystalline scales; while carbolic acid is freely
soluble in small or large quantities of alkaline solutions.

Cold petroleum spirit dissolves cresol, but no crystalline scales can be
separated out by a freezing mixture. Carbolic acid, on the contrary, is
but sparingly soluble in cold petroleum, and a solution of carbolic acid
in hot petroleum, when exposed to sudden cold produced by a freezing
mixture, separates out crystals from the upper layer of liquid. Cresol
is miscible with glycerin of specific gravity 1·258 in all proportions;
1 measure of glycerin mixed with 1 measure of cresol is completely
precipitated by 1 measure of water. Carbolic acid, under the same
circumstances, is not precipitated. The density of cresol is about
1·044. It forms with bromine a tri-bromo-cresol, but this is liquid at
ordinary temperatures, while tri-bromo-phenol is solid. On the other
hand, it resembles carbolic acid in its reactions with ferric chloride
and with nitric and sulphuric acid.

    § 233. =Creasote= or =Kreozote= is a term applied to the mixture of
    crude phenols obtained from the distillation of wood-tar. It
    consists of a mixture of substances of which the chief are guaiacol
    or oxycresol (C₇H₈O₂), boiling at 200°, and creasol (C₈H₁₀O₂),
    boiling at 217°; also in small quantities phlorol (C₈H₁₀O), methyl
    creasol (C₉H₁₂O₂), and other bodies. Morson’s English creasote is
    prepared from Stockholm tar, and boils at about 217°, consisting
    chiefly of creasol; it is not easy, by mere chemical tests, to
    distinguish creasote from cresylic acid. Creasote, in its reactions
    with sulphuric and nitric acid, bromine and gelatin, is similar to
    carbolic and cresylic acids, and its solubility in most solvents is
    also similar. It is, however, distinguished from the tar acids by
    its insolubility in Price’s glycerin, specific gravity 1·258,
    whether 1, 2, or 3 volumes of glycerin be employed. But the best
    test is its action on an ethereal solution of nitro-cellulose.
    Creasote mixes freely with the B.P. collodium, while cresylic acid
    or carbolic acid at once coagulates the latter. With complicated
    mixtures containing carbolic acid, cresol, and creasote, the only
    method of applying these tests with advantage is to submit the
    mixture to fractional distillation.

    Flückiger[213] tests for small quantities of carbolic acid in
    creasote, by mixing a watery solution of the sample with one-fourth
    of its volume of ammonia hydrate, wetting the inside of a porcelain
    dish with this solution, and then carefully blowing bromine fumes on
    to the surface. A fine blue colour appears if carbolic acid is
    present, but if the sample consists of creasote only, then it is
    dirty green or brown. Excess of bromine spoils the reaction.[214]

[213] _Arch. der Pharmacie_, cxiii. p. 30.

[214] Creasote is, without doubt, poisonous, though but little is known
of its action, and very few experiments are on record in which pure
creasote has been employed. Eulenberg has studied the symptoms in
rabbits, by submitting them to vaporised creasote--_i.e._, the vapour
from 20 drops of creasote diffused through a glass shade under which a
rabbit was confined. There was at once great uneasiness, with a watery
discharge from the eyes, and after seven minutes the rabbit fell on its
side, and was slightly convulsed. The cornea was troubled, and the eyes
prominent; a white slime flowed from the mouth and eyes. After fifteen
minutes there was narcosis, with lessened reflex action; the temperature
was almost normal. There was rattling breathing, and in half an hour the
animal died, the respiration ceasing, and fluid blood escaping from the
nose. Section after death showed the brain to be hyperæmic, the mucous
membranes of the air-passages to be covered with a thin layer of fluid
blood, and the lungs to be congested; the right side of the heart was
gorged with fluid blood.

The _post-mortem_ appearances and the symptoms generally are, therefore,
closely allied to those produced by carbolic acid. A dark colour of the
urine has also been noticed.

§ 234. =Carbolic Acid in Organic Fluids or in the Tissues of the
Body.=--If the routine process given at page 51, where the organic fluid
is distilled in a vacuum after acidifying with tartaric acid, is
employed, phenol or cresol, if present, will certainly be found in the
distillate. If, however, a special search be made for the acids, then
the fluid must be well acidified with sulphuric acid, and distilled in
the usual way. The distillation should be continued as long as possible,
and the distillate shaken up with ether in the apparatus figured at page
156. On separation and evaporation of the ether, the tar acids, if
present, will be left in a pure enough form to show its reactions. The
same process applies to the tissues, which, in a finely-divided state,
are boiled and distilled with dilute sulphuric acid, and the distillate
treated as just detailed.

Like most poisons, carbolic acid has a selective attraction for certain
organs, so that, unless all the organs are examined, it is by no means
indifferent which particular portion is selected for the inquiry.
Hoppe-Seyler applied carbolic acid to the abdomen and thighs of dogs,
and when the symptoms were at their height bled them to death, and
separately examined the parts. In one case, the blood yielded ·00369 per
cent.; the brain, ·0034 per cent.; the liver, ·00125; and the kidneys,
·00423 per cent. of their weight of carbolic acid. The liver then
contains only one-third of the quantity found in an equal weight of
blood, and, therefore, the acid has no selective affinity for that
organ. On the other hand, the nervous tissue, and especially the
kidneys, appear to concentrate it.

§ 235. =Examination of the Urine for Phenol or Cresol.=--It has been
previously stated (see p. 174) that the urine will not contain these as
such, but as compounds--viz., phenyl or cresyl sulphate of potassium. By
boiling with a mineral acid, these compounds may be broken up, and the
acids obtained, either by distillation or by extraction with ether. To
detect very minute quantities, a large quantity of the urine should be
evaporated down to a syrup, and treated with hydrochloric acid and
ether. On evaporating off the ether, the residue should be distilled
with dilute sulphuric acid, and this distillate then tested with
bromine-water, and the tri-bromo-phenol or cresol collected, identified,
and weighed.

Thudichum[215] has separated crystals of potassic phenyl-sulphate itself
from the urine of patients treated endermically by carbolic acid, as

[215] _Pathology of the Urine_, p. 193.

The urine was evaporated to a syrup, extracted with alcohol of 90 per
cent., treated with an alcoholic solution of oxalic acid as long as this
produced a precipitate, and then shaken with an equal volume of ether.
The mixture was next filtered, neutralised with potassic carbonate,
evaporated to a small bulk, and again taken up with alcohol. Some
oxalate and carbonate of potassium were separated, and, on evaporation
to a syrup, crystals of potassic phenyl-sulphate were obtained. They
gave to analysis 46·25 per cent. H₂SO₄, and 18·1 K--theory requiring
46·2 of H₂SO₄ and 18·4 of K. Alkaline phenyl-sulphates strike a deep
purple colour with ferric chloride. To estimate the amount of
phenyl-sulphate or cresol-sulphate in the urine, the normal sulphates
may be separated by the addition of chloride of barium in the cold,
first acidifying with hydrochloric acid. On boiling the liquid a second
crop of sulphate is obtained, due to the breaking up of the compound
sulphate, and from this second weight the amount of acid can be
obtained, _e.g._, in the case of phenol--C₆H₅HSO₄ : BaSO₄ :: 174 : 233.

    § 236. =Assay of Disinfectants, Carbolic Acid Powders, &c.=--For the
    assay of crude carbolic acid, Mr. Charles Lowe[216] uses the
    following process:--A thousand parts of the sample are distilled
    without any special condensing arrangement; water first comes over,
    and is then followed by an oily fluid. When a hundred parts of the
    latter, as measured in a graduated tube, have been collected, the
    receiver is changed. The volume of water is read off. If the oily
    liquid floats on the water, it contains light oil of tar; if it is
    heavier than the water, it is regarded as hydrated acid, containing
    50 per cent. of real carbolic acid. The next portion consists of
    anhydrous cresylic and carbolic acids, and 625 volumes are distilled
    over; the remainder in the retort consists wholly of cresylic acid
    and the higher homologues. The relative proportions of carbolic and
    cresylic acids are approximately determined by taking the
    solidifying point, which should be between 15·5° and 24°, and having
    ascertained this temperature, imitating it by making mixtures of
    known proportions of carbolic and cresylic acids.

[216] _Allen’s Commercial Organic Analysis_, vol. i. p. 311.

    E. Waller[217] has recommended the following process for the
    estimation of carbolic acid. It is based on the precipitation of the
    tar acids by bromine, and, of course, all phenols precipitated in
    this way will be returned as carbolic acid. The solutions necessary

[217] _Chem. News_, April 1, 1881, p. 152.

    1. A solution containing 10 grms. of pure carbolic acid to the
    litre; this serves as a standard solution.

    2. A solution of bromine in water.

    3. Solution of alum in dilute sulphuric acid. A litre of 10 per
    cent. sulphuric acid is shaken with alum crystals until saturated.

    The actual process is as follows:--10 grms. of the sample are
    weighed out and run into a litre flask, water added, and the mixture
    shaken. The flask being finally filled up to the neck, some of the
    solution is now filtered through a dry filter, and 10 c.c. of this
    filtrate is placed in a 6 or 8-ounce stoppered bottle, and 30 c.c.
    of the alum solution added. In a similar bottle 10 c.c. of the
    standard solution of carbolic acid are placed, and a similar
    quantity of alum solution is added, as in the first bottle. The
    bromine-water is now run into the bottle containing the standard
    solution of carbolic acid from a burette until there is no further
    precipitate; the bottle is stoppered and shaken after every
    addition. Towards the end of the reaction the precipitate forms but
    slowly, and when the carbolic acid is saturated, the slight excess
    of bromine-water gives the solution a pale yellow tint. The solution
    from the sample is treated in the same way, and from the amount of
    bromine-water used, the percentage of the sample is obtained by
    making the usual calculations. Thus, supposing that 5 c.c. of the
    standard required 15 c.c. of the bromine-water for precipitation,
    and 10 c.c. of the solution of the sample required 17 c.c., the
    calculation would be 15 × 2 : 17 = 100 : _x_ per cent. With most
    samples of crude carbolic acid, the precipitate does not readily
    separate. It is then best to add a little of the precipitate already
    obtained by testing the standard solution, which rapidly clears the

    =Koppeschaar’s volumetric method= is more exact, but also more
    elaborate, than the one just described. Caustic normal soda is
    treated with bromine until permanently yellow, and the excess of
    bromine is then driven off by boiling. The liquid now contains 5NaBr
    + NaBrO₃, and on adding this to a solution containing carbolic acid,
    and a sufficient quantity of hydrochloric acid to combine with the
    sodium, the following reactions occur:--

  (1.) 5NaBr + NaBrO₃ + 6HCl = 6NaCl + 6Br + 3H₂O;


  (2.) C₆H₆O + 6Br = C₆H₃Br₃O + 3HBr.

    Any excess of bromine liberated in the first reaction above that
    necessary for the second, will exist in the free state, and from the
    amount of bromine which remains free the quantity of carbolic acid
    can be calculated, always provided the strength of the bromine
    solution is first known. The volumetric part of the analysis,
    therefore, merely amounts to the determination of free bromine,
    which is best found by causing it to react on potassium iodide, and
    ascertaining the amount of free iodine by titration with a standard
    solution of sodium thiosulphate. In other words, titrate in this way
    the standard alkaline bromine solution, using as an indicator starch
    paste until the blue colour disappears. Another method of indicating
    the end of the reaction is by the use of strips of paper first
    soaked in starch solution, and dried, and then the same papers
    moistened with zinc iodide, and again dried; the least excess of
    bromine sets free iodine, and strikes a blue colour.

    =Colorimetric Method of Estimation.=--A very simple and ever-ready
    way of approximately estimating minute quantities of the phenols
    consists in shaking up 10 grms. of the sample with water, allowing
    any tar or insoluble impurities to subside. Ten c.c. of the clear
    fluid are then taken, and half a c.c. of a 5 per cent. solution of
    ferric chloride added. The colour produced is imitated by a standard
    solution of carbolic acid, and a similar amount of the reagent, on
    the usual principles of colorimetric analysis.

    § 237. =Carbolic Acid Powders.=--Siliceous carbolic acid powders are
    placed in a retort and distilled. Towards the end the heat may be
    raised to approaching redness. The distillate separates into two
    portions--the one aqueous, the other consisting of the acids--and
    the volume may be read off, if the distillate be received in a
    graduated receiver. Carbolic acid powders, having lime as a basis,
    may be distilled in the same way, after first decomposing with
    sulphuric acid. The estimation of the neutral tar oils in the
    distillate is easily performed by shaking the distillate with
    caustic soda solution, which dissolves completely the tar acids. The
    volume of the oils may be directly read off if the receiver is a
    graduated tube. Allen[218] has suggested the addition of a known
    volume of petroleum to the distillate, which dissolves the tar oils,
    and easily separates, and thus the volume may be more accurately
    determined, a correction being of course made by subtracting the
    volume of petroleum first added.

[218] _Op. cit._, i. p. 310.

    § 238. =Carbolic Acid Soap.=--A convenient quantity of soap is
    carefully weighed, and dissolved in a solution of caustic soda by
    means of heat. A saturated solution of salt is next added,
    sufficient to precipitate entirely the soap, which is filtered off;
    the filtrate is acidified with hydrochloric acid, and bromine water
    added. The precipitated tribromo-phenol is first melted by heat,
    then allowed to cool, and the mass removed from the liquid, dried,
    and weighed.


§ 239.--Nitro-benzene is the product resulting from the action of strong
nitric acid on benzene. Its chemical formula is C₆H₅NO₂. When pure, it
is of a pale yellow colour, of a density of 1·186, and boils at from
205° to 210°. It may be obtained in prismatic crystals by exposure to a
temperature of 3°. Its smell is exactly the same as that from the oil or
essence of bitter almonds; and it is from this circumstance, under the
name of “essence of mirbane,” much used in the preparation of perfumes
and flavouring agents.

In commerce there are three kinds of nitro-benzene--the purest, with the
characters given above; a heavier nitro-benzene, boiling at 210° to
220°; and a very heavy variety, boiling at 222° to 235° The last is
specially used for the preparation of aniline, or aniline blue.
Nitro-benzene has been used as an adulterant of bitter almond oil, but
the detection is easy (see “Foods,” p. 551). Nitro-benzene was first
discovered by Mitscherlich in 1834, and its poisonous properties were
first pointed out by Casper[219] in 1859. Its technical use in perfumes,
&c., dates from about 1848, and in the twenty-eight years intervening
between that date and 1876, Jübell[220] has collected 42 cases of
poisoning by this agent, 13 of which were fatal. One of these cases was
suicidal, the rest accidental.

[219] _Vierteljahrsschrift für ger. Med._, 1859, Bd. xvi. p. 1.

[220] _Die Vergiftungen mit Blausäure u. Nitro-benzol in forensischer
Beziehung_, Erlangen, 1876.

§ 240. =Effects of Poisoning by Nitro-benzene.=--Nitro-benzene is a very
powerful poison, whether taken in the form of vapour or as a liquid. The
action of the vapour on animals has been studied by Eulenberg[221] and
others. One experiment will serve as an illustration. Fifteen grms. of
nitro-benzene were evaporated on warm sand under a glass shade, into
which a cat was introduced. There was immediately observed in the animal
much salivation, and quickened and laboured breathing. After thirty
minutes’ exposure, on removing the shade to repeat the dose of 15 grms.,
the cat for the moment escaped. On being put back there was again
noticed the salivation and running at the eyes, with giddiness, and
repeated rising and falling. The animal at last, about one hour and
forty minutes after the first dose, succumbed with dyspnœa, and died
with progressive paralysis of the respiration. The membranes of the
brain were found gorged with blood, the lungs liver-coloured, the mucous
membrane of the trachea--to the finest sub-divisions of the
bronchia--reddened, inflamed, and clothed with a fine frothy mucus. The
left side of the heart was filled with thick black blood. The bladder
contained 8 grms. of clear urine, in which aniline was discovered. There
was a notable smell of bitter almonds.

[221] _Gewerbe Hygiene_, S. 607, Berlin, 1876.

§ 241. The effects of the vapour on man are somewhat different in their
details to those just described. In a remarkable case related by Dr.
Letheby, a man, aged 42, had spilt some nitro-benzene over his clothes.
He went about several hours breathing an atmosphere of nitro-benzene, he
then became drowsy, his expression was stupid, and his gait unsteady,
presenting all the appearances of intoxication. The stupor suddenly
deepened into coma, and the man died; the fatal course being altogether
about nine hours--viz., four hours before coma, and five hours of total

An interesting case of poisoning by the vapour is recorded by
Taylor.[222] A woman, aged 30, tasted a liquid used for flavouring
pastry, which was afterwards chemically identified as pure
nitro-benzene. She immediately spat it out, finding that it had an acrid
taste, and probably did not swallow more than a drop. In replacing the
bottle, however, she spilt about a tablespoonful, and allowed it to
remain for some minutes; it was a small room, and the vapour rapidly
pervaded it, and caused illness in herself as well as in a
fellow-servant. She had a strange feeling of numbness in the tongue, and
in three hours and a quarter after the accident was seen by a medical
man; she then presented all the appearances of prussic acid poisoning.
The eyes were bright and glassy, the features pale and ghastly, the lips
and nails purple, as if stained with blackberries, the skin clammy, and
the pulse feeble, but the mind was then clear. An emetic was
administered, but she suddenly became unconscious; the emetic acted, and
brought up a fluid with an odour of nitro-benzene. The stomach-pump was
also used, but the liquid obtained had scarcely any odour of
nitro-benzene. In about eleven hours consciousness returned, and in
about seventeen hours she partially recovered, but complained of flashes
of light and strange colours before her eyes. Recovery was not complete
for weeks. In this case the small quantity swallowed would probably of
itself have produced no symptoms, and the effects are to be mainly
ascribed to the breathing of the vapour.

[222] _Poisons_, Third Edition, p. 665.

§ 242. The liquid, when swallowed, acts almost precisely in the same way
as the vapour, and the symptoms resemble very much those produced by
prussic acid. The great distinction between prussic acid and
nitro-benzene poisoning is that, in the latter, there is an interval
between the taking of the poison and its effects. This is, indeed, one
of the strangest phenomena of nitro-benzene poisoning, for the person,
after taking it, may appear perfectly well for periods varying from a
quarter of an hour to two or three hours, or even longer, and then there
may be most alarming symptoms, followed by rapid death. Poisoning by
nitro-benzene satisfies the ideal of the dramatist, who requires, for
the purposes of his plot, poisons not acting at once, but with an
interval sufficiently prolonged to admit of lengthy rhapsodies and a
complicated _dénouement_. On drinking the poison there is a burning
taste in the mouth, shortly followed by a very striking blueness or
purple appearance of the lips, tongue, skin, nails, and even the
conjunctivæ. This curious colour of the skin has, in one or two
instances, been witnessed an hour before any feeling of illness
manifested itself; vomiting then comes on, the vomited matter smelling
of nitro-benzene. The skin is cold, there is great depression, and the
pulse is small and weak. The respiration is affected, the breathing
being slow and irregular, the breath smelling strongly of the liquid,
and the odour often persisting for days. A further stage is that of loss
of consciousness, and this comes on with all the suddenness of a fit of
apoplexy. The coma is also similar in appearance to apoplectic coma,
but there have frequently been seen trismus and convulsions of the
extremities. The pupils are dilated and do not react to light, and
reflex sensibility is sometimes completely extinguished. Cases vary a
little in their main features; in a few the blue skin and the deep sleep
are the only symptoms noted. Death, for the most part, occurs after a
period of from eight to twenty-four hours (occasionally as soon as four
or five hours) after taking the poison.

From the following remarkable train of symptoms in a dog, it is
probable, indeed, that nitro-benzene, taken by a human being, might
produce death, after a rather prolonged period of time, by its secondary
effects:--To a half-bred greyhound[223] were administered 15 grms. of
nitro-benzene, when shortly after there were noticed much salivation,
shivering, and muscular twitchings. The same dose was repeated at the
end of five, of seven, and of eight hours respectively, so that the dog
altogether took 60 grms., but with no other apparent symptom than the
profuse salivation. On the following day, the dog voided a tapeworm;
vomiting supervened; the heart’s action was quickened, and the breathing
difficult; convulsions followed, and the pupils were seen to be dilated.
For eight days the dog suffered from dyspnœa, quickened pulse, shivering
of the legs or of the whole body, tetanic spasms, bloody motions, great
thirst and debility. The temperature gradually sank under 25°, and the
animal finally died. The autopsy showed, as the most striking change,
the whole mucous membrane of the intestinal tract covered with a yellow
layer, which chemical analysis proved to be caused by picric acid, and
in the urine, liver, and lungs, aniline was discovered.

[223] Eulenberg, _Gewerbe Hygiene_, S. 607.

§ 243. =Fatal Dose.=--It is probable, from recorded cases, that 1 grm.
(15·4 grains) would be quite sufficient to kill an adult, and, under
favourable circumstances, less than that quantity. It would seem that
spirituous liquids especially hasten and intensify the action of
nitro-benzene, so that a drunken person, _cæteris paribus_, taking the
poison with spirits, would be more affected than taking it under other

In a case related by Stevenson,[224] in which so small a quantity as
1·74 grm. was taken in seven doses, spread over more than forty-eight
hours; there were yet extremely alarming symptoms, and the patient seems
to have had a narrow escape. On the other hand, a woman admitted into
the General Hospital, Vienna, took 100 grms. (about 3½ ozs.) and
recovered; on admission she was in a highly cyanotic condition, with
small pulse, superficial respiration, and dribbling of urine, which
contained nitro-benzol. Artificial respiration was practised, and
camphor injections were administered. Under this treatment consciousness
was restored, and the patient recovered. On the fourth day the urine
resembled that of a case of cystitis (_Lancet_, Jan. 16, 1894). The
quantity of nitro-benzene which would be fatal, if breathed, is not
known with any accuracy.

[224] This case is not uninteresting. Through a mistake in reading an
extremely illegible prescription, M. S. S., æt. 21, was supplied by a
druggist with the following mixture;--

  ℞. Benzole-Nit., ʒiij.
     Ol. Menth, pep., ʒss.
     Ol. Olivæ, ʒx.
     gutt. xxx., t. ds.

He took on sugar seven doses, each of 20 minims, equalling in all 23
min. (or by weight 27·1 grains, 1·74 grm.) of nitro-benzene--viz., three
doses on the first day, three on the second, and one on the morning of
the third day. The first two days he was observed to be looking pale and
ill, but went on with his work until the seventh dose, which he took on
the third day at 9 A.M. About 2 P.M. (or six hours after taking the
seventh dose), he fell down insensible, the body pale blue, and with all
the symptoms already described in the text, and usually seen in
nitro-benzene poisoning. With suitable treatment he recovered. The next
morning, from 8 ounces of urine some nitro-benzene was extracted by
shaking with chloroform.--Thos. Stevenson, M.D., in _Guy’s Hospital
Reports_, MS., vol. xxi., 1876.

§ 244. =Pathological Appearances.=--The more characteristic appearances
seem to be, a dark brown or even black colour of the blood, which
coagulates with difficulty (an appearance of the blood that has even
been noticed during life), venous hyperæmia of the brain and its
membranes, and general venous engorgement. In the stomach, when the
fluid has been swallowed, the mucous membrane is sometimes reddened
diffusely, and occasionally shows ecchymoses of a punctiform character.

§ 245. =The essential action of nitro-benzene= is of considerable
physiological interest. The blood is certainly in some way changed, and
gives the spectrum of acid hæmatin.[225] Filehne has found that the
blood loses, in a great degree, the power of carrying and imparting
oxygen to the tissues, and its content of carbon dioxide is also
increased. Thus, the normal amount of oxygen gas which the arterial
blood of a hound will give up is 17 per cent.; but in the case of a dog
which had been poisoned with nitro-benzene, it sank to 1 per cent.
During the dyspnœa from which the dog suffered, the carbon dioxide
exhaled was greater than the normal amount, and the arterial blood (the
natural content of which should have been 30 per cent. of this gas),
only gave up 9 per cent. Filehne seeks to explain the peculiar colour of
the skin by the condition of the blood, but the explanation is not
altogether satisfactory. Some part of the nitro-benzene, without doubt,
is reduced to aniline in the body--an assertion often made, and as often
contradicted--but it has been found in too many cases to admit of
question. It would also seem from the experiment on the dog (p. 186),
that a conversion into picric acid is not impossible. A yellow colour
of the skin and conjunctivæ, as if picric-acid-stained, has been noticed
in men suffering under slow poisoning by nitro-benzene.

[225] Filehne, W., “_Ueber die Gift-Wirkungen des Nitrobenzols_,” _Arch.
für exper. Pathol. u. Pharm._, ix. 329.

§ 246. =Detection and Separation of Nitro-Benzene from the Animal
Tissues.=--It is evident from the changes which nitro-benzene may
undergo that the expert, in any case of suspected nitro-benzene
poisoning, must specially look (1) for nitro-benzene, (2) for aniline,
and (3) for picric acid. The best general method for the separation of
nitro-benzene is to shake up the liquid (or finely-divided solid) with
light benzoline (petroleum ether), which readily dissolves
nitro-benzene. On evaporation of the petroleum ether, the nitro-benzene
is left, perhaps mixed with fatty matters. On treating with cold water,
the fats rise to the surface, and the nitro-benzene sinks to the bottom;
so that, by means of a separating funnel, the nitro-benzene may be
easily removed from animal fats. The oily drops, or fine precipitate
believed to be nitro-benzene, may be dissolved in spirit and reduced to
aniline by the use of nascent hydrogen, developed from iron filings by
hydrochloric acid, and the fluid tested with bleaching powder, or, the
aniline itself may be recovered by alkalising the fluid, and shaking up
with ether in the separation-tube (p. 156), the ether dissolves the
aniline, and leaves it, on spontaneous evaporation, as an oily yellowish
mass, which, on the addition of a few drops of sodic hypochlorite,
strikes a blue or violet-blue--with acids, a rose-red--and with bromine,
a flesh-red. It gives alkaloidal reactions with such general reagents as
platinum chloride, picric acid, &c. Aniline itself may be extracted from
the tissues and fluids of the body by petroleum ether, but in any
special search it will be better to treat the organs as in Stas’
process--that is, with strong alcohol, acidified with sulphuric acid.
After a suitable digestion in this menstruum, filter, and then, after
evaporating the alcohol, dissolve the alcoholic extract in water;
alkalise the aqueous solution, and extract the aniline by shaking it up
with light benzoline. On separating the benzoline, the aniline will be
left, and may be dissolved in feebly-acid water, and the tests before
enumerated tried.

Malpurgo[226] recommends the following test for nitro-benzene:--2 drops
of melted phenol, 3 drops of water, and a fragment of caustic potash are
boiled in a small porcelain dish, and to the boiling liquid the aqueous
solution to be tested is added. On prolonged boiling, if nitro-benzene
is present, a crimson ring is produced at the edges of the liquid; this
crimson colour, on the addition of a little bleaching powder, turns

[226] _Zeit. anal. Chem._, xxxii. 235.

Oil of bitter almonds may be distinguished from nitro-benzene by the
action of manganese dioxide and sulphuric acid; bitter almond oil
treated in this way loses its odour, nitro-benzene is unaltered. To
apply the test, the liquid must be heated on the water-bath for a little


§ 247. =Dinitro-benzol=, C₆H₄(NO₂)₂ (ortho-, meta-, para-).--The
ortho-compound is produced by the action of nitric acid on benzol, aided
by heat in the absence of strong sulphuric acid to fix water. Some of
the para-dinitro-benzol is at the same time produced. The meta-compound
is obtained by the action of fuming nitric acid on nitro-benzol at a
boiling temperature.

The physical properties of the three dinitro-benzols are briefly as

Ortho-d. is in the form of needles; m.p. 118°.

Meta-d. crystallises in plates; m.p. 90°.

Para-d. crystallises, like the ortho-compound, in needles, but the
melting-point is much higher, 171° to 172°.

Just as nitro-benzol by reduction yields aniline, so do the
nitro-benzols on reduction yield ortho-, meta-, or para-phenylene

Meta-phenylene diamine is an excellent test for nitrites; and, since the
commercial varieties of dinitro-benzol either consist mainly or in part
of meta-dinitro-benzol, the toxicological detection is fairly simple,
and is based upon the conversion of the dinitro-benzol into

Dinitro-benzol is at present largely employed in the manufacture of
explosives, such as roburite, sicherheit, and others. It has produced
much illness among the workpeople in the manufactures, and amongst
miners whose duty it has been to handle such explosives.

§ 248. =Effects of Dinitro-benzol.=--Huber[227] finds that if
dinitro-benzol is given to frogs by the mouth in doses of from 100 to
200 mgrms., death takes place in a few hours. Doses of from 2·5 to 5
mgrms. cause general dulness and ultimately complete paralysis, and
death in from one to six days.

[227] “_Beiträge zur Giftwirkung des Dinitrobenzols_,” A. Huber,
Virchow’s _Archiv_, 1891, Bd. 126, S. 240.

Rabbits are killed by doses of 400 mgrms., in time varying from
twenty-two hours to four days.

In a single experiment on a small dog, the weight of which was 5525
grms., the dog died in six hours after a dose of 600 mgrms.

It is therefore probable that a dose of 100 mgrms. per kilo would kill
most warm-blooded animals.

A transient exposure to dinitro-benzol vapours in man causes serious
symptoms; for instance, in one of Huber’s cases, a student of chemistry
had been engaged for one hour and a half only in preparing
dinitro-benzol, and soon afterwards his comrades remarked that his face
was of a deep blue colour. On admission to hospital, on the evening of
the same day, he complained of slight headache and sleeplessness; both
cheeks, the lips, the muscles of the ear, the mucous membrane of the
lips and cheeks, and even the tongue, were all of a more or less intense
blue-grey colour. The pulse was dicrotic, 124; T. 37·2°. The next
morning the pulse was slower, and by the third day the patient had

Excellent accounts of the effects of dinitro-benzol in roburite
factories have been published by Dr. Ross[228] and Professor White,[229]
of Wigan. Mr. Simeon Snell[230] has also published some most interesting
cases of illness, cases which have been as completely investigated as
possible. As an example of the symptoms produced, one of Mr. Snell’s
cases may be here quoted.

[228] _Medical Chronicle_, 1889, 89.

[229] _Practitioner_, 1889, ii. 15.

[230] _Brit. Med. Journ._, March 3, 1894.

[Illustration: Diagram of Visual Field.]

C. F. W., aged 38, consulted Mr. Snell for his defective sight on April
9, 1892. He had been a mixer at a factory for the manufacture of
explosives. He was jaundiced, the conjunctiva yellow, and the lips blue.
He was short of breath, and after the day’s work experienced aching of
the forearms and legs and tingling of the fingers. The urine was black
in colour, of sp. gr. 1024; it was examined spectroscopically by Mr.
MacMunn, who reported the black colour as due neither to indican, nor to
blood, nor bile, but to be caused by some pigment belonging to the
aromatic series. The patient’s sight had been failing since the previous
Christmas. Vision in the right eye was 6/24, left 6/36, both optic
papillæ were somewhat pale. In each eye there was a central scotoma for
red, and contraction of the field (see diagram). The man gradually gave
up the work, and ultimately seems to have recovered. It is, however,
interesting to note that, after having left the work for some weeks, he
went back for a single day to the “mixing,” and was taken very ill,
being insensible and delirious for five hours.

§ 249. =The Blood in Nitro-benzol Poisoning.=--The effect on the blood
has been specially studied by Huber.[231] The blood of rabbits poisoned
by dinitro-benzol is of a dark chocolate colour, and the microscope
shows destruction of the red corpuscles; the amount of destruction may
be gathered from the following:--the blood corpuscles of a rabbit before
the experiment numbered 5,588,000 per cubic centimetre; a day after the
experiment 4,856,000; a day later 1,004,000; on the third day the rabbit

[231] _Op. cit._

In one rabbit, although the corpuscles sank to 1,416,000, yet recovery
took place.

Dr. MacMunn[232] has examined specimens of blood from two of Mr. Snell’s
patients; he found a distinct departure from the normal; the red
corpuscles were smaller than usual, about 5 or 6 µ in diameter, and the
appearances were like those seen in pernicious anæmia. Huber, in some of
his experiments on animals, found a spectroscopic change in the blood,
viz., certain absorption bands, one in the red between C and D, and two
in the green between D and E; the action of reducing agents on this
dinitro-benzol blood, as viewed in a spectroscope provided with a scale
in which C = 48, D = 62, and E = 80·5, was as follows:--

[232] _Op. cit._

                                 In Red.        In Green.
                                  50-52        62-66  70-77
  After NH₄SO₄,                   53-55        62-66  70-77
    „   NH₃,                      54-58        60-65  70-77
    „   NH₄SO₄ + NH₃,             52-55        60-65  70-77

Taking the symptoms as a whole, there has been noted:--a blue colour of
the lips, not unfrequently extending over the whole face, and even the
conjunctivæ have been of a marked blue colour, giving the sufferer a
strange livid appearance. In other cases there have been jaundice, the
conjunctivæ and the skin generally being yellow, the lips blue.
Occasionally gastric symptoms are present. Sleeplessness is common, and
not unfrequently there is some want of muscular co-ordination, and the
man staggers as if drunk. In more than one case there has been noticed
sudden delirium. There is in chronic cases always more or less anæmia,
and the urine is remarkable in its colour, which ranges from a slightly
dark hue up to positive blackness. In a large proportion of cases there
is ophthalmic trouble, the characteristics of which (according to Mr.
Snell) are “failure of sight, often to a considerable degree, in a more
or less equal extent on the two sides; concentric attraction of visual
field with, in many cases, a central colour scotoma; enlargement of
retinal vessels, especially the veins; some blurring, never extensive,
of edges of disc, and a varying degree of pallor of its surface--the
condition of retinal vessels spoken of being observed in workers with
the dinitro-benzol, independently of complaints of defective sight.
Cessation of work leads to recovery.”

§ 250. =Detection of Dinitro-benzol.=--Dinitro-benzol may be detected in
urine, in blood, and in fluids generally, by the following
process:--Place tinfoil in the fluid, and add hydrochloric acid to
strong acidity, after allowing the hydrogen to be developed for at least
an hour, make the fluid alkaline by caustic soda, and extract with ether
in a separating tube; any metaphenylene-diamine will be contained in the
ether; remove the ether into a flask, and distil it off; dissolve the
residue in a little water.

Acidify a solution of sodium nitrite with dilute sulphuric acid; on
adding the solution, if it contains metaphenylene-diamine, a yellow to
red colour will be produced, from the formation of Bismarck brown

XII.--Hydrocyanic Acid.

§ 251. =Hydrocyanic Acid= (=hydric cyanide=)--specific gravity of liquid
0·7058 at 18° C., boiling-point 26·5° (80° F.), HCy = 27.--The anhydrous
acid is not an article of commerce, and is only met with in the
laboratory. It is a colourless, transparent liquid, and so extremely
volatile that, if a drop fall on a glass plate, a portion of it freezes.
It has a very peculiar peach-blossom odour, and is intensely poisonous.
It reddens litmus freely and transiently, dissolves red oxide of mercury
freely, forms a white precipitate of argentic cyanide when treated with
silver nitrate, and responds to the other tests described hereafter.

§ 252. =Medicinal Preparations of Prussic Acid.=--The B.P. acid is a
watery solution of prussic acid; its specific gravity should be 0·997,
and it should contain 2 per cent. of the anhydrous acid, 2 per cent. is
also the amount specified in the pharmacopœias of Switzerland and
Norway, and in that of Borussica (VI. ed.); the latter ordains, however,
a spirituous solution, and the Norwegian an addition of 1 per cent. of
concentrated sulphuric acid. The French prussic acid is ordered to be
prepared of a strength equalling 10 per cent.

The adulterations or impurities of prussic acid are hydrochloric,
sulphuric,[233] and formic acids. Traces of silver may be found in the
French acid, which is prepared from cyanide of silver. Tartaric acid is
also occasionally present. Hydrochloric acid is most readily detected by
neutralising with ammonia, and evaporating to dryness in a water-bath;
the ammonium cyanide decomposes and volatilises, leaving as a saline
residue chloride of ammonium. This may easily be identified by the
precipitate of chloride of silver, which its solution gives on testing
with silver nitrate, and the deep brown precipitate with Nessler
solution. Sulphuric acid is, of course, detected by chloride of barium;
formic acid by boiling a small quantity with a little mercuric oxide; if
present, the oxide will be reduced, and metallic mercury fall as a grey
precipitate. Silver, tartaric acid, and any other fixed impurities are
detected by evaporating the acid to dryness, and examining any residue
which may be left. It may be well to give the various strengths of the
acids of commerce in a tabular form:--

[233] A trace of sulphuric or hydrochloric acid should not be called an
_adulteration_, for it greatly assists the preservation, and therefore
makes the acid of greater therapeutic efficiency.

                                                            Per cent.

  British Pharmacopœia, Switzerland, and Bor. (vj),            2
  France,                                                     10
  Vauquelin’s Acid,                                            3·3
  Scheele’s    „                                          4 to 5[234]
  Riner’s      „                                              10
  Robiquet’s   „                                              50
  Schraeder’s  „                                               1·5
  Duflos’      „                                               9
  Pfaff’s      „                                              10
  Koller’s     „                                              25

[234] Strength very uncertain.

In English commerce, the analyst will scarcely meet with any acid
stronger than Scheele’s 5 per cent.

Impure oil of bitter almonds contains hydric cyanide in variable
quantity, from 5 per cent. up to 14 per cent. There is an officinal
preparation obtained by digesting cherry-laurel leaves in water, and
then distilling a certain portion over. This _Aqua Lauro-cerasi_ belongs
to the old school of pharmacy, and is of uncertain strength, but varies
from ·7 to 1 per cent. of HCN.

§ 253. =Poisoning by Prussic Acid.=--Irrespective of suicidal or
criminal poisoning, accidents from prussic acid may occur--

1. From the use of the cyanides in the arts.

2. From the somewhat extensive distribution of the acid, or rather of
prussic-acid producing substances in the vegetable kingdom.

1. =In the Arts.=--The galvanic silvering[235] and gilding of metals,
photography, the colouring of black silks, the manufacture of Berlin
blue, the dyeing of woollen cloth, and in a few other manufacturing
processes, the alkaline cyanides are used, and not unfrequently fumes of
prussic acid developed.

[235] The preparation used for the silvering of copper vessels is a
solution of cyanide of silver in potassic cyanide, to which is added
finely powdered chalk. Manipulations with this fluid easily develop
hydrocyanic acid fumes, which, in one case related by Martin (_Aerztl.
Intelligenzbl._, p. 135, 1872), were powerful enough to produce symptoms
of poisoning.

2. =In the Animal Kingdom.=--One of the myriapods (_Chilognathen_)
contains glands at the roots of the hairs, which secrete prussic acid;
when the insect is seized, the poisonous secretion is poured out from
the so-called _foramina repugnatoria_.

3. =In the Vegetable Kingdom.=--A few plants contain cyanides, and many
contain amygdalin, or bodies formed on the type of amygdalin. In the
presence of emulsin (or similar principles) and water, this breaks up
into prussic acid and other compounds--an interesting reaction usually
represented thus--

  C₂₀H₂₇NO₁₁ + 2H₂O = CNH + C₇H₆O + 2C₆H₁₂O₆.

1 equivalent of amygdalin--_i.e._, 457 parts--yielding 1 equivalent of
CNH or 27 parts; in other words, 100 parts of amygdalin yield
theoretically 5·909 parts of prussic acid,[236] so that, the amount of
either being known, the other can be calculated from it.

[236] According to Liebig and Wöhler, 17 grms. of amygdalin yield 1 of
prussic acid (_i.e._, 5·7 per cent.) and 8 of oil of bitter almonds.
Thirty-four parts of amygdalin, mixed with 66 of emulsin of almonds,
give a fluid equalling the strength of acid of most pharmacopœias, viz.,
2 per cent.

Greshoff[237] has discovered an amygdalin-like glucoside in the two
tropical trees _Pygeum parriflorum_ and _P. latifolium_. The same author
states that the leaves of _Gymnema latifolium_, one of the Asclepiads,
yields to distillation benzaldehyde hydrocyanide. Both _Lasia_ and
_Cyrtosperma_, plants belonging to the natural family of the Orontads,
contain in their flowers potassic cyanide. _Pangium edule_, according to
Greshoff, contains so much potassic cyanide that he was able to prepare
a considerable quantity of that salt from one sample of the plant. An
Indian plant (_Hydnocarpus inebrians_) also contains a cyanide, and has
been used for the purpose of destroying fish. Among the Tiliads,
Greshoff found that _Echinocarpus Sigun_ yielded hydrocyanic acid on
distillation. Even the common linseed contains a glucoside which breaks
up into sugar, prussic acid, and a ketone.

[237] M. Greshoff--_Erster Bericht über die Untersuchung von
Pflanzenstoffen Niederländisch-Indiens. Mittheilungen aus dem
chemisch-pharmakologischen Laboratorium des botan. Gartens des Staates_,
vii., Batavia, 1890, Niederländisch. Dr. Greshoff’s research indicates
that there are several other cyanide-yielding plants than those
mentioned in the text.

The following plants, with many others, all yield, by appropriate
treatment, more or less prussic acid:--Bitter almonds (_Amygdalus
communis_); the _Amygdalus persica_; the cherry laurel (_Prunus
laurocerasus_); the kernels of the plum (_Prunus domestica_); the bark,
leaves, flowers, and fruit of the wild service-tree (_Prunus padus_);
the kernels of the common cherry and the apple; the leaves of the
_Prunus capricida_; the bark of the _Pr. virginiana_; the flowers and
kernels of the _Pr. spinosa_; the leaves of the _Cerasus acida_; the
bark and almost all parts of the _Sorbus aucuparia_, _S. hybrida_, and
_S. torminalis_; the young twigs of the _Cratægus oxyacantha_; the
leaves and partly also the flowers of the shrubby _Spiræaceæ_, such as
_Spiræa aruncus_, _S. sorbifolia_, and _S. japonica_;[238] together with
the roots of the bitter and sweet _Cassava_.

[238] The bark and green parts of the _Prunus avium_, L., _Prunus
mahaleb_, L., and herbaceous _Spirææ_ yield no prussic acid.

In only a few of these, however, has the exact amount of either prussic
acid or amygdalin been determined; 1 grm. of bitter almond pulp is about
equal to 2½ mgrms. of anhydrous prussic acid. The kernels from the
stones of the cherry, according to Geiseler, yield 3 per cent. of
amygdalin; therefore, 1 grm. equals 1·7 mgrm. of HCN.

§ 254. The wild service-tree (_Prunus padus_) and the cherry-laurel
(_Prunus Laurocerasus_) contain, not amygdalin but a compound of
amygdalin with amygdalic acid; to this has been given the name of
laurocerasin. It was formerly known as amorphous amygdalin; its formula
is C₄₀H₅₅NO₂₄; 933 parts are equivalent to 27 of hydric cyanide--that
is, 100 parts equal to 2·89.

In the bark of the service-tree, Lehmann found ·7 per cent. of
laurocerasin (= ·02 HCN), and in the leaves of the cherry-laurel 1·38
per cent. (= 0·39 HCN).

Francis,[239] in a research on the prussic acid in cassava root, gives
as the mean in the sweet cassava ·0168 per cent., in the bitter ·0275
per cent., the maximum in each being respectively ·0238 per cent., and
·0442 per cent. The bitter-fresh cassava root has long been known as a
very dangerous poison; but the sweet has hitherto been considered
harmless, although it is evident that it also contains a considerable
quantity of prussic acid.

[239] “On Prussic Acid from Cassava,” _Analyst_, April 1877, p. 5.

The kernels of the peach contain about 2·85 per cent. amygdalin (= ·17
HCN); those of the plum ·96 per cent. (= ·056 HCN); and apple pips ·6
per cent. (= ·035 per cent. HCN).

It is of great practical value to know, even approximately, the quantity
of prussic acid contained in various fruits, since it has been adopted
as a defence in criminal cases that the deceased was poisoned by prussic
acid developed in substances eaten.

§ 255. =Statistics.=--Poisoning by the cyanides (prussic acid or
cyanide of potassium) occupies the third place among poisons in order
of frequency in this country, and accounts for about 40 deaths annually.

In the ten years ending 1892 there were recorded no less than 395 cases
of accidental, suicidal, or homicidal poisoning by prussic acid and
potassic cyanide. The further statistical details may be gathered from
the following tables:--



  Ages,       0-1  1-5  5-15  15-25  25-65  65 and  Total
  Males,      ...    1    1      1     12      1      16
  Females,      1    1  ...      2      7    ...      11
  Totals,       1    2    1      3     19      1      27


  Ages,            1-5  5-15  15-25  25-65  65 and  Total
  Males,             1    1      4      1    ...       7
  Females,           1  ...    ...      3    ...       4
  Totals,            2    1      4      4    ...      11

                   PRUSSIC ACID (SUICIDE).

  Ages,                       15-25  25-65  65 and  Total
  Males,                        23    156     23     202
  Females,                       5     13      1      19
  Totals,                       28    169     24     221

                  POTASSIUM CYANIDE (SUICIDE).

  Ages,                 5-15  15-25  25-65  65 and  Total
  Males,                  1      6     88      5     100
  Females,              ...      6     15      1      22
  Totals,                 1     12    103      6     122

To these figures must be added 10 cases of murder (2 males and 8
females) by prussic acid, and 4 cases of murder (3 males and 1 female)
by potassic cyanide.

In order to ascertain the proportion in which the various forms of
commercial cyanides cause death, and also the proportion of accidental,
suicidal, and criminal deaths from the same cause, Falck collated twelve
years of statistics from medical literature with the following result:--

In 51 cases of cyanide poisoning, 29 were caused by potassic cyanide, 9
by hydric cyanide, 5 by oil of bitter almonds, 3 by peach stones (these
3 were children, and are classed as “domestic,” that is, taking the
kernels as a food), 3 by bitter almonds (1 of the 3 suicidal and
followed by death, the other 2 “domestic”), 1 by tartaric acid and
potassic cyanide (a suicidal case, an apothecary), and 1 by
ferro-cyanide of potassium and tartaric acid. Of the 43 cases first
mentioned, 21 were suicidal, 7 criminal, 8 domestic, and 7 medicinal;
the 43 patients were 24 men, 14 children, and 5 women.

The cyanides are very rarely used for the purpose of murder: a poison
which has a strong smell and a perceptible taste, and which also kills
with a rapidity only equalled by deadly bullet or knife-wounds, betrays
its presence with too many circumstances of a tragic character to find
favour in the dark and secret schemes of those who desire to take life
by poison. In 793 poisoning cases of a criminal character in France, 4
only were by the cyanides.

Hydric and potassic cyanides were once the favourite means of
self-destruction employed by suicidal photographers, chemists,
scientific medical men, and others in positions where such means are
always at hand; but, of late years, the popular knowledge of poisons has
increased, and self-poisoning by the cyanides scarcely belongs to a
particular class. A fair proportion of the deaths are also due to
accident or unfortunate mistakes, and a still smaller number to the
immoderate or improper use of cyanide-containing vegetable products.

§ 256. =Accidental and Criminal Poisoning by Prussic Acid.=--The poison
is almost always taken by the mouth into the stomach, but occasionally
in other ways--such, for example, as in the case of the illustrious
chemist, Scheele, who died from inhalation of the vapour of the acid
which he himself discovered, owing to the breaking of a flask. There is
also the case related by Tardieu, in which cyanide of potassium was
introduced under the nails; and that mentioned by Carrière,[240] in
which a woman gave herself, with suicidal intent, an enema containing
cyanide of potassium. It has been shown by experiments, in which every
care was taken to render it impossible for the fumes to be inhaled, that
hydrocyanic acid applied to the eye of warm-blooded animals may destroy
life in a few minutes.[241]

[240] “_Empoisonnement par le cyanure de potassium,--guérison_,”
_Bullet. général de Thérap._, 1869, No. 30.

[241] N. Gréhant, _Compt. rend. Soc. Biol._ [9], xi. 64, 65.

With regard to errors in dispensing, the most tragic case on record is
that related by Arnold:[242]--A pharmaceutist had put in a mixture for a
child potassic cyanide instead of potassic chlorate, and the child died
after the first dose: the chemist, however, convinced that he had made
no mistake, to show the harmlessness of the preparation, drank some of
it, and there and then died; while Dr. Arnold himself, incautiously
tasting the draught, fell insensible, and was unconscious for six hours.

[242] Arnold, A. B., “Case of Poisoning by the Cyanide of Potassium,”
_Amer. Journ. of Med. Scien._, 1869.

§ 257. =Fatal Dose.=--Notwithstanding the great number of persons who in
every civilised country fall victims to the cyanides, it is yet somewhat
doubtful what is the minimum dose likely to kill an adult healthy man.
The explanation of this uncertainty is to be sought mainly in the
varying strength of commercial prussic acid, which varies from 1·5
(Schraeder’s) to 50 per cent. (Robiquet’s), and also in the varying
condition of the person taking the poison, more especially whether the
stomach be full or empty. In by far the greater number, the dose taken
has been much beyond that necessary to produce death, but this
observation is true of most poisonings.

The dictum of Taylor, that a quantity of commercial prussic acid,
equivalent to 1 English grain (65 mgrm.) of the anhydrous acid, would,
under ordinary circumstances, be sufficient to destroy adult life, has
been generally accepted by all toxicologists. The minimum lethal dose of
potassic cyanide is similarly put at 2·41 grains (·157 grm.). As to
bitter almonds, if it be considered that as a mean they contain 2·5 per
cent. of amygdalin, then it would take 45 grms., or about 80 almonds, to
produce a lethal dose for an adult; with children less--in fact, 4 to 6
bitter almonds are said to have produced poisoning in a child.

§ 258. =Action of Hydric and Potassic Cyanides on Living
Organisms.=--Both hydric cyanide and potassic cyanide are poisonous to
all living forms, vegetable or animal, with the exception of certain
fungi. The cold-blooded animals take a larger relative dose than the
warm-blooded, and the mammalia are somewhat more sensitive to the
poisonous action of the cyanides than birds; but all are destroyed in a
very similar manner, and without any essential difference of action. The
symptoms produced by hydric and potassic cyanide are identical, and, as
regards general symptoms, what is true as to the one is also true as to
the other. There is, however, one important difference in the action of
these two substances, if the mere local action is considered, for
potassic cyanide is very alkaline, possessing even caustic properties. I
have seen, _e.g._, the gastric mucous membrane of a woman, who had taken
an excessive dose of potassic cyanide on an empty stomach, so inflamed
and swollen, that its state was similar to that induced by a moderate
quantity of solution of potash. On the other hand, the acid properties
of hydric cyanide are very feeble, and its effect on mucous membranes or
the skin in no way resembles that of the mineral acids.

It attacks the animal system in two ways: the one, a profound
interference with the ordinary metabolic changes; the other, a paralysis
of the nervous centres. Schönbein discovered that it affected the blood
corpuscles in a peculiar way; normal blood decomposes with great ease
hydrogen peroxide into oxygen and water. If to normal venous blood a
little peroxide of hydrogen be added, the blood at once becomes bright
red; but if a trace of prussic acid be present, it is of a dark brown
colour. The blood corpuscles, therefore, lose their power of conveying
oxygen to all parts of the system, and the phenomena of asphyxia are
produced. Geppert[243] has proved that this is really the case by
showing, in a series of researches, that, under the action of hydric
cyanide, less oxygen is taken up, and less carbon dioxide formed than
normal, even if the percentage of oxygen in the atmosphere breathed is
artificially increased. The deficiency of oxygen is in part due to the
fact that substances like lactic acid, the products of incomplete
combustion, are formed instead of CO₂.

[243] Geppert, _Ueber das Wesen der CNH-Vergift; mit einer Tafel_,
Berlin, 1889; _Sep.-Abdr. aus Ztschr. f. klin. Med._, Bd. xv.

At the same time the protoplasm of the tissues is paralysed, and unable
to take up the loosely bound oxygen presented. This explains a striking
symptom which has been noticed by many observers, that is, if
hydrocyanic acid be injected into an animal, the venous blood becomes of
a bright red colour; in warm-blooded animals this bright colour is
transitory, but in cold-blooded animals, in which the oxidation process
is slower, the blood remains bright red.

§ 259. =Symptoms observed in Animals.=--The main differences between the
symptoms induced in cold-blooded and warm-blooded animals, by a fatal
dose of hydric cyanide, are as follows:--

The respiration in frogs is at first somewhat dyspnœic, then much
slowed, and at length it ceases. The heart, at first slowed, later
contracts irregularly, and at length gradually stops; but it may
continue to beat for several minutes after the respiration has ceased.
But all these progressive symptoms are without convulsion. Among
warm-blooded animals, on the contrary, convulsions are constant, and the
sequence of the symptoms appears to be--dyspnœa, slowing of the pulse,
giddiness, falling down, then convulsions with expulsion of the urine
and fæces; dilatation of the pupils, exophthalmus, and finally cessation
of the pulse and breathing. The convulsions also frequently pass into
general paralysis, with loss of reflex movements, weak, infrequent
breathing, irregular, quick, and very frequent pulse, and considerable
diminution of temperature.

The commencement of the symptoms in animals is extremely rapid, the
rapidity varying according to the dose and the concentration of the
acid. It was formerly thought that the death from a large dose of the
concentrated acid followed far more quickly than could be accounted for
by the blood carrying the poison to the nervous centres; but Blake was
among the first to point out that this doubt was not supported by facts
carefully observed, since there is always a sufficient interval between
the entry of the poison into the body and the first symptoms, to support
the theory that the poison is absorbed in the usual manner. Even when
Preyer injected a cubic centimetre of 60 per cent. acid into the jugular
vein of a rabbit, twenty-nine seconds elapsed before the symptoms
commenced. Besides, we have direct experiments showing that the
acid--when applied to wounds in limbs, the vessels of which are tied,
while the free nervous communication is left open--only acts when the
ligature is removed. Magendie describes, in his usual graphic manner,
how he killed a dog by injecting into the jugular vein prussic acid, and
“_the dog died instantly, as if struck by a cannon ball_,” but it is
probable that the interval of time was not accurately noted. A few
seconds pass very rapidly, and might be occupied even by slowly pressing
the piston of the syringe down, and in the absence of accurate
measurements, it is surprising how comparatively long intervals of time
are unconsciously shortened by the mind. In any case, this observation
by Magendie has not been confirmed by the accurate tests of the more
recent experimenters; and it is universally acknowledged that, although
with strong doses of hydric cyanide injected into the circulation--or,
in other words, introduced into the system--in the most favourable
conditions for its speediest action, death occurs with appalling
suddenness, yet that it takes a time sufficiently long to admit of
explanation in the manner suggested. This has forensic importance, which
will be again alluded to. Experiments on animals show that a large dose
of a dilute acid kills quite as quickly as an equivalent dose of a
stronger acid, and in some cases it even seems to act more rapidly. If
the death does not take place within a few minutes, life may be
prolonged for hours, and even, in rare cases, days, and yet the result
be death. Coullon poisoned a dog with prussic acid; it lived for
nineteen days, and then died; but this is quite an exceptional case, and
when the fatal issue is prolonged beyond an hour, the chance of recovery
is considerable.

§ 260. The length of time dogs poisoned by fatal doses survive,
generally varies from two to fifteen minutes. The symptoms are
convulsions, insensibility of the cornea, cessation of respiration, and,
finally, the heart stops--the heart continuing to beat several minutes
after the cessation of the respirations.[244] When the dose is short of
a fatal one, the symptoms are as follows:--Evident giddiness and
distress; the tongue is protruded, the breath is taken in short, hurried
gasps, there is salivation, and convulsions rapidly set in, preceded, it
may be, by a cry. The convulsions pass into paralysis and insensibility.
After remaining in this state some time, the animal again wakes up, as
it were, very often howls, and is again convulsed; finally, it sinks
into a deep sleep, and wakes up well.

[244] N. Gréhant, _Compt. rend._, t. 109, pp. 502, 503.

Preyer noticed a striking difference in the symptoms after section of
the vagus in animals, which varied according to whether the poison was
administered by the lungs, or subcutaneously. In the first case, if the
dose is small, the respirations are diminished in frequency; then this
is followed by normal breathing; if the dose is larger, there is an
increase in the frequency of the respirations. Lastly, if a very large
quantity is introduced into the lungs, death quickly follows, with
respirations diminished in frequency. On the other hand, when the poison
is injected subcutaneously, small doses have no influence on the
breathing; but with large doses, there is an increase in the frequency
of the respirations, which sink again below the normal standard.

§ 261. =Symptoms in Man.=--When a fatal but not excessive dose of either
potassic or hydric cyanide is taken, the sequence of symptoms is as
follows:--Salivation, with a feeling of constriction in the throat,
nausea, and occasionally vomiting. After a few minutes a peculiar
constricting pain in the chest is felt, and the breathing is distinctly
affected. Giddiness and confusion of sight rapidly set in, and the
person falls to the ground in convulsions similar to those of epilepsy.
The convulsions are either general, or attacking only certain groups of
muscles; there is often true trismus, and the jaws are so firmly closed
that nothing will part them. The respiration is peculiar, the
inspiration is short, the expiration prolonged,[245] and between the two
there is a long interval ever becoming more protracted as death is
imminent. The skin is pale, or blue, or greyish-blue; the eyes are
glassy and staring, with dilated pupils; the mouth is covered with foam,
and the breath smells of the poison; the pulse, at first quick and
small, sinks in a little while in frequency, and at length cannot be
felt. Involuntary evacuation of fæces, urine, and semen is often
observed, and occasionally there has been vomiting, and a portion of the
vomit has been aspirated into the air-passages. Finally, the convulsions
pass into paralysis, abolition of reflex sensibility, and gradual
ceasing of the respiration. With large doses these different stages may
occur, but the course is so rapid that they are merged the one into the
other, and are undistinguishable. The shortest time between the taking
of the acid and the commencement of the symptoms may be put at about ten
seconds. If, however, a large amount of the vapour is inhaled at once,
this period may be rather lessened. The interval of time is so short
that any witnesses generally unintentionally exaggerate, and aver that
the effects were witnessed _before_ the swallowing of the liquid--“As
the cup was at his lips”--“He had hardly drunk it,” &c. There is
probably a short interval of consciousness, then come giddiness, and, it
may be, a cry for assistance; and lastly, there is a falling down in
convulsions, and a speedy death. Convulsions are not always present, the
victim occasionally appears to sink lifeless at once. Thus, in a case
related by Hufeland, a man was seen to swallow a quantity of acid,
equivalent to 40 grains of the pure acid--that is, about forty times
more than sufficient to kill him. He staggered a few paces, and then
fell dead, without sound or convulsion.

[245] In a case quoted by Seidel (Maschka’s _Handbuch_, p. 321), a man,
36 years of age, four or five minutes after swallowing 150 mgrms.
anhydrous HCN in spirits, lay apparently lifeless, without pulse or
breathing. After a few minutes was noticed an extraordinary deep
expiration, by which the ribs were drawn in almost to the spine, and the
chest made quite hollow.

§ 262. The very short interval that may thus intervene between the
taking of a dose of prussic acid and loss of consciousness, may be
utilised by the sufferer in doing various acts, and thus this interval
becomes of immense medico-legal importance. The question is simply
this:--What can be done by a person in full possession of his faculties
in ten seconds? I have found from experiment that, after drinking a
liquid from a bottle, the bottle may be corked, the individual can get
into bed, and arrange the bedclothes in a suitable manner; he may also
throw the bottle away, or out of the window; and, indeed, with practice,
in that short time a number of rapid and complicated acts may be
performed. This is borne out both by experiments on animals and by
recorded cases.

In Mr. Nunneley’s numerous experiments on dogs, one of the animals,
after taking poison, “went down three or four steps of the stairs, saw
that the door at the bottom was closed, and came back again.” A second
went down, came up, and went again down the steps of a long winding
staircase, and a third retained sufficient vigour to jump over another
dog, and then leap across the top of a staircase.

In a remarkable case related by Dr. Guy,[246] in which a young man,
after drinking more wine than usual, was seized by a sudden impulse to
take prussic acid, and drank about 2 drachms, producing symptoms which,
had it not been for prompt treatment, would, in all probability, have
ended fatally--the interval is again noteworthy. After taking the poison
in bed, he rose, walked round the foot of a chest of drawers, standing
within a few yards of the bedside, placed the stopper firmly in the
bottle, and then walked back to bed with the intention of getting into
it; but here a giddiness seized him, and he sat down on the edge, and
became insensible.

[246] _Forensic Medicine_, 4th ed., p. 615.

A case related by Taylor is still stronger. A woman, after swallowing a
fatal dose of essence of almonds, went to a well in the yard, drew
water, and drank a considerable quantity. She then ascended two flights
of stairs and called her child, again descended a flight of stairs, fell
on her bed, and died within half an hour from the taking of the poison.

Nevertheless, these cases and similar ones are exceptional, and only
show what is possible, not what is usual, the rule being that after
fatal doses no voluntary act of significance--save, it may be, a cry
for assistance--is performed.[247]

[247] Dr. J. Autal, a Hungarian chemist, states that cobalt nitrate is
an efficacious antidote to poisoning by either HCN or KCN. The brief
interval between the taking of a fatal dose and death can, however, be
rarely utilised.--_Lancet_, Jan. 16, 1894.

§ 263. =Chronic poisoning by hydric cyanide= is said to occur among
photographers, gilders, and those who are engaged daily in the
preparation or handling of either hydric or potassic cyanides. The
symptoms are those of feeble poisoning, headache, giddiness, noises in
the ears, difficult respiration, pain over the heart, a feeling of
constriction in the throat, loss of appetite, nausea, obstinate
constipation, full pulse, with pallor and offensive breath.
Koritschoner[248] has made some observations on patients who were made
to breathe at intervals, during many weeks, prussic acid vapour, with
the idea that such a treatment would destroy the tubercle bacilli.
Twenty-five per cent. of those treated in this way suffered from redness
of the pharynx, salivation, headache, nausea, vomiting, slow pulse, and
even albuminuria.

[248] _Wiener klin. Woch._, 1891.

§ 264. =Post-mortem Appearances.=[249]--If we for the moment leave out
of consideration any changes which may be seen in the stomach after
doses of potassic cyanide, then it may be affirmed that the pathological
changes produced by hydric and potassic cyanides mainly coincide with
those produced by suffocation. The most striking appearance is the
presence of bright red spots; these bright red spots or patches are
confined to the surface of the body, the blood in the deeper parts being
of the ordinary venous hue, unless, indeed, an enormous dose has been
taken; in that case the whole mass of blood may be bright red; this
bright colour is due, according to Kobert, to the formation of
cyanmethæmoglobin. The lungs and right heart are full of blood, and
there is a backward engorgement produced by the pulmonic block. The
veins of the neck and the vessels of the head generally are full of
blood, and, in like manner, the liver and kidneys are congested. In the
mucous membrane of the bronchial tubes there is a bloody foam, the lungs
are gorged, and often œdematous in portions; ecchymoses are seen in the
pleura and other serous membranes; and everywhere, unless concealed by
putrefaction, or some strong-smelling ethereal oil, there is an odour of
hydric cyanide.

[249] Hydric cyanide has, according to C. Brame, a remarkable antiseptic
action, and if administered in sufficient quantity to animals, preserves
them after death for a month. He considers that there is some more or
less definite combination with the tissues.

Casper has rightly recommended the head to be opened and examined first,
so as to detect the odour, if present, in the brain. The abdominal and
chest cavities usually possess a putrefactive smell, but the brain is
longer conserved, so that, if this course be adopted, there is a greater
probability of detecting the odour.

The stomach in poisoning by hydric cyanide is not inflamed, but if
alcohol has been taken at the same time, or previously, there may be
more or less redness.

In poisoning by potassic cyanide, the appearances are mainly the same as
those just detailed, with, it may be, the addition of caustic local
action. I have, however, seen, in the case of a gentleman who drank
accidentally a considerable dose of potassic cyanide just after a full
meal, not the slightest trace of any redness, still less of corrosion.
Here the contents of the stomach protected the mucous membrane, or
possibly the larger amount of acid poured out during digestion
sufficiently neutralised the alkali. Potassic cyanide, in very strong
solution, may cause erosions of the lips, and the caustic effect may be
traced in the mouth, throat, gullet, to the stomach and duodenum; but
this is unusual, and the local effects are, as a rule, confined to the
stomach and duodenum. The mucous membrane is coloured blood-red, reacts
strongly alkaline,[250] is swollen, and it may be even ulcerated. The
upper layers of the epithelium are also often dyed with the
colouring-matter of the blood, which has been dissolved out by the
cyanide. This last change is a _post-mortem_ effect, and can be imitated
by digesting the mucous membrane of a healthy stomach in a solution of
cyanide. The intensity of these changes are, of course, entirely
dependent on the dose and emptiness of the stomach. If the dose is so
small as just to destroy life, there may be but little redness or
swelling of the stomach, although empty at the time of taking the
poison. In those cases in which there has been vomiting, and a part of
the vomit has been drawn into the air-passages, there may be also
inflammatory changes in the larynx. If essence of almonds has been
swallowed, the same slight inflammation may be seen which has been
observed with other essential oils, but no erosion, no strong alkaline
reaction, nor anything approaching the effects of the caustic cyanide.

[250] The following case came under my own observation:--A stout woman,
35 years of age, the wife of a French polisher, drank, in a fit of rage,
a solution of cyanide of potassium. It was estimated that about 15
grains of the solid substance were swallowed. She died within an hour.
The face was flushed, the body not decomposed; the mouth smelt strongly
of cyanide; the stomach had about an ounce of bloody fluid in it, and
was in a most intense state of congestion. There was commencing fatty
degeneration of the liver, the kidneys were flabby, and the capsule
adherent. The contents of the stomach showed cyanide of potassium, and
the blood was very fluid. The woman was known to be of intemperate

In poisoning by bitter almonds no inflammatory change in the mucous
membrane of the coats of the stomach would be anticipated, yet in one
recorded case there seems to have been an eroded and inflamed patch.

§ 265. =Tests for Hydrocyanic Acid and Cyanide of Potassium.=--(1.) The
addition of silver nitrate to a solution containing prussic acid, or a
soluble cyanide,[251] produces a precipitate of argentic cyanide. 100
parts of argentic cyanide are composed of 80·60 Ag and 19·4 CN,
equivalent to 20·1 HCN. It is a white anhydrous precipitate, soluble
either in ammonia or in a solution of cyanide of potassium. It is
soluble in hot dilute nitric acid, but separates on cooling. A particle
of silver cyanide, moistened with strong ammonia, develops needles;
silver chloride treated similarly, octahedral crystals. It is insoluble
in water. Upon ignition it is decomposed into CN and metallic silver,
mixed with a little paracyanide of silver.

[251] In the case of testing in this way for the alkaline cyanides, the
solution must contain a little free nitric acid.

A very neat process for the identification of cyanide of silver is the
following:--Place the perfectly dry cyanide in a closed or sealed tube,
containing a few crystals of iodine. On heating slightly, iodide of
cyanogen is sublimed in beautiful needles. These crystals again may be
dissolved in a dilute solution of potash, a little ferrous sulphate
added, and hydrochloric acid, and in this way Prussian blue produced. If
the quantity to be tested is small, the vapour of the acid may be
evolved in a very short test-tube, the mouth of which is closed by the
ordinary thin discs of microscopic glass, the under surface of which is
moistened with a solution of nitrate of silver; the resulting crystals
of silver cyanide are very characteristic, and readily identified by the

(2.) If, instead of silver nitrate, the disc be moistened with a
solution of sulphate of iron (to which has been added a little potash),
and exposed to the vapour a short time, and then some dilute
hydrochloric acid added, the moistened surface first becomes yellow,
then green, lastly, and permanently, blue. No other blue compound of
iron (with the exception of Prussian blue) is insoluble in dilute
hydrochloric acid.

(3.) A third, and perhaps the most delicate of all, is the so-called
sulphur test. A yellow sulphide of ammonium, containing free sulphur, is
prepared by saturating ammonia by SH₂, first suspending in the fluid a
little finely-precipitated sulphur (or an old, ill-preserved solution of
sulphide of ammonium may be used). Two watch-glasses are now taken; in
the one the fluid containing prussic acid is put, and the second
(previously moistened with the sulphide of ammonium described) is
inverted over it. The glasses are conveniently placed for a few minutes
in the water-oven; the upper one is then removed, the moist surface
evaporated to dryness in the water-bath, a little water added, and then
a small drop of solution of chloride of iron. If hydrocyanic acid is
present, the sulphocyanide of iron will be formed of a striking
blood-red colour.

(4.) The reaction usually called Schönbein’s, or Pagenstecher and
Schönbein’s[252] (but long known,[253] and used before the publication
of their paper), consists of guaiacum paper, moistened with a very
dilute solution of sulphate of copper (1 : 2000). This becomes blue if
exposed to the vapour of hydrocyanic acid. Unfortunately, the same
reaction is produced by ammonia, ozone, nitric acid, hypochlorous acid,
iodine, bromine, chromate of potash, and other oxidising agents, so that
its usefulness is greatly restricted.

[252] _Neues Repert. de Pharm._, 18, 356.

[253] This reaction (with tincture of guaiacum and copper) has been long
known. “I remember a pharmaceutist, who attended my father’s laboratory,
showing me this test in 1828 or 1829.”--Mohr’s _Toxicologie_, p. 92.

(5.) A very delicate test for prussic acid is as follows:--About
one-half centigrm. of ammonia, ferrous sulphate (or other pure ferrous
salt), and the same quantity of uranic nitrate, are dissolved in 50 c.c.
of water, and 1 c.c. of this test-liquid is placed in a porcelain dish.
On now adding a drop of a liquid containing the smallest quantity of
prussic acid, a grey-purple colour, or a distinct purple precipitate is

[254] M. Carey Lea, _Amer. Journ. of Science_ [3], ix. pp. 121-123; _J.
C. Society_, 1876, vol. i. p. 112.

(6.) A hot solution of potassic cyanide, mixed with picric acid, assumes
a blood-red colour, due to the formation of picro-cyanic acid. Free HCN
does not give this reaction, and therefore must first be neutralised by
an alkali.

(7.) =Schönbein’s Test.=--To a few drops of defibrinated ox-blood are
added a few drops of the carefully-neutralised distillate supposed to
contain prussic acid, and then a little neutral peroxide of hydrogen is
added. If the distillate contains no prussic acid, then the mixture
becomes of a bright pure red and froths strongly; if, on the other hand,
a trace of prussic acid be present, the liquid becomes brown and does
not froth, or only slightly does so.

(8.) =Kobert’s Test.=--A 1-4 per cent. solution of blood, to which a
trace of ferridcyanide of potassium is added, is prepared, and the
neutralised distillate added to this solution. If hydric cyanide be
present, then the liquid becomes of a bright red colour, and, examined
spectroscopically, instead of the spectrum of methæmoglobin, will be
seen the spectrum of cyanmethæmoglobin. Kobert proposes to examine the
blood of the poisoned, for the purpose of diagnosis, during life. A drop
of blood from a healthy person, and a drop of blood from the patient,
are examined side by side, according to the process just given.

§ 266. =Separation of Hydric Cyanide or Potassic Cyanide from Organic
Matters, such as the Contents of the Stomach, &c.=--It is very
necessary, before specially searching for hydric cyanide in the contents
of the stomach, to be able to say, by careful and methodical
examination, whether there are or are not any fragments of bitter
almonds, of apples, peaches, or other substance likely to produce hydric
cyanide. If potassic cyanide has been taken, simple distillation will
always reveal its presence, because it is found partly decomposed into
hydric cyanide by the action of the gastric acids. Nevertheless, an acid
should always be added, and if, as in the routine process given at p.
48, there is reasonable doubt for suspecting that there will be no
cyanide present, it will be best to add tartaric acid (for this organic
acid will in no way interfere with subsequent operations), and distil,
as recommended, in a vacuum. If, however, from the odour and from the
history of the case, it is pretty sure to be a case of poisoning by
hydric or potassic cyanide, then the substances, if fluid, are at once
placed in a retort or flask, and acidified with a suitable quantity of
sulphuric acid, or if the tissues or other solid matters are under
examination, they are finely divided, or pulped, and distilled, after
acidifying with sulphuric acid as before. It may be well here, as a
caution, to remark that the analyst must not commit the unpardonable
error of first producing a cyanide by reagents acting on animal matters,
and then detecting as a poison the cyanide thus manufactured. If, for
example, a healthy liver is carbonised by nitric acid, saturated with
potash, and then burnt up, cyanide of potassium is always one of the
products; and, indeed, the ashes of a great variety of nitrogenous
organic substances may contain cyanides--cyanides not pre-existing, but
manufactured by combination. By the action of nitric acid even on
sugar,[255] hydric cyanide is produced.

[255] _Chemical News_, 68, p. 75.

The old method of distillation was to distil by the gentle heat of a
water-bath, receiving the distillate in a little weak potash water, and
not prolonging the process beyond a few hours. The experiments of
Sokoloff, however, throw a grave doubt on the suitability of this simple
method for quantitative results.

N. Sokoloff[256] recommends the animal substances to be treated by water
strongly acidified with hydric sulphate, and then to be distilled in the
water-bath for from two to three days; or to be distilled for
twenty-four hours, by the aid of an oil-bath, at a high temperature. He
gives the following example of quantitative analysis by the old process
of merely distilling for a few hours, and by the new:--

[256] _Ber. d. deutsch. chem. Gesellsch._, Berlin, ix. p. 1023.

=Old Process.=--(1.) Body of a hound--age, 2 years; weight, 5180 grms.;
dose administered, 57 mgrms. HCN; death in fifteen minutes. After five
days there was found in the saliva 0·6 mgrm., stomach 3·2 mgrms., in the
rest of the intestines 2·6 mgrms., in the muscles 4·1--total, 10·5.

(2.) Weight of body, 4000 grms.; dose given, 38 mgrms.; death in eleven
minutes. After fifteen days, in the saliva 0·8, in the stomach 7·2, in
the rest of the intestines 2·2, in the muscles 3·2--total, 13·4.

=New Process.=--Weight of body, 5700 grams; dose, 57 mgrms.; death in
twenty-four minutes. After fifteen days, in the saliva 1·1 mgrm., in the
stomach 2·6, in the rest of the intestines 9·6, in the muscles 31·9, and
in the whole, 45·2 mgrms. Duration of process, thirteen hours.

From a second hound, weighing 6800 grms.; dose, 67 mgrms.; 25·1 mgrms.
were separated three days after death.

From a third hound, weighing 5920 grms.; dose, 98 mgrms.; after forty
days, by distillation on a sand-bath, there were separated 2·8 mgrms.
from the saliva, 4·8 from the stomach, 16·8 from the intestines, 23·6
from the muscles--total, 48 mgrms.

It would also appear that he has separated 51·2 mgrms. of anhydrous acid
from the corpse of a dog which had been poisoned by 57 mgrms. of acid,
and buried sixty days.[257]

[257] Without wishing to discredit the statements of M. Sokoloff, we may
point out that a loss of half-a-dozen mgrms. only appears rather

From another canine corpse, three days laid in an oven, and left for
twenty-seven days at the ordinary temperature, 5·1 mgrms. were recovered
out of a fatal dose of 38 mgrms.

The estimation was in each case performed by titrating the distillate
with argentic nitrate, the sulphur compounds having been previously got
rid of by saturating the distillate with KHO, and precipitating by lead

Venturoli[258] has, on the contrary, got good quantitative results
without distillation at all. A current of pure hydrogen gas is passed
through the liquid to be tested and the gas finally made to bubble
through silver nitrate. He states that the whole of the hydric cyanide
present is carried over in an hour. Metallic cyanides must be decomposed
by sulphuric acid or tartaric acid. Mercury cyanide must be decomposed
with SH₂, the solution acidified with tartaric acid, neutralised with
freshly precipitated calcic carbonate to fix any ferro- or
ferri-cyanides present, and hydrogen passed in and the issuing gases led
first through a solution of bismuth nitrate to remove SH₂ and then into
the silver solution.

[258] L’Orosi. xv. 85-88.

§ 267. =How long after Death can Hydric or Potassic Cyanides be
Detected?=--Sokoloff appears to have separated prussic acid from the
body of hounds at very long periods after death--in one case sixty days.
Dragendorff recognised potassic cyanide in the stomach of a hound after
it had been four weeks in his laboratory,[259] and in man eight days
after burial. Casper also, in his 211th case, states that more than 18
mgrms. of anhydrous prussic acid were obtained from a corpse eight days
after death.[260] Dr. E. Tillner[261] has recognised potassic cyanide in
a corpse four months after death. Lastly, Struve[262] put 300 grms. of
flesh, 400 of common water, and 2·378 of KCy in a flask, and then opened
the flask after 547 days. The detection was easy, and the estimation
agreed with the amount placed there at first. So that, even in very
advanced stages of putrefaction, and at periods after death extending
beyond many months, the detection of prussic acid cannot be pronounced

[259] Dragendorff, G., _Beitr. zur gericht. Chem._, p. 59.

[260] Casper’s _Pract. Handbuch der gerichtlichen Medicin_, p. 561.

[261] _Vierteljahr. f. gerichtl. Med._, Berlin, 1881, p. 193.

[262] _Zeitschrift f. anal. Chemie_, von Fresenius, 1873, xii. p. 4.

§ 268. =Estimation of Hydrocyanic Acid or Potassic Cyanide.=--In all
cases, the readiest method of estimating prussic acid (whether it be in
the distillate from organic substances or in aqueous solution) is to
saturate it with soda or potash, and titrate the alkaline cyanide thus
formed with nitrate of silver. The process is based on the fact that
there is first formed a soluble compound (KCy, AgCy), which the
slightest excess of silver breaks up, and the insoluble cyanide is at
once precipitated. If grains are used, 17 grains of nitrate of silver
are dissolved in water, the solution made up to exactly 1000 grain
measures, each grain measure equalling ·0054 grain of anhydrous
hydrocyanic acid. If grammes are employed, the strength of the nitrate
of silver solution should be 1·7 grm. to the litre, each c.c. then =
·0054 hydrocyanic acid, or ·01302 grm. of potassic cyanide.

Essential oil of bitter almonds may also be titrated in this way,
provided it is diluted with sufficient spirit to prevent turbidity from
separation of the essential oil. If hydrocyanic acid is determined
gravimetrically (which is sometimes convenient, when only a single
estimation is to be made), it is precipitated as cyanide of silver, the
characters of which have been already described.

    § 269. =Case of Poisoning by Bitter Almonds.=--Instances of
    poisoning by bitter almonds are very rare. The following interesting
    case is recorded by Maschka:--

    A maid-servant, 31 years of age, after a quarrel with her lover, ate
    a quantity of bitter almonds. In a few minutes she sighed,
    complained of being unwell and faint; she vomited twice, and, after
    about ten minutes more had elapsed, fell senseless and was
    convulsed. An hour afterwards, a physician found her insensible, the
    eyes rolled upwards, the thumb clenched within the shut fists, and
    the breathing rattling, the pulse very slow. She died within an
    hour-and-a-half from the first symptoms.

    The autopsy showed the organs generally healthy, but all, save the
    liver, exhaling a faint smell of bitter almonds. The right side of
    the heart was full of fluid dark blood, the left was empty. Both
    lungs were rich in blood, which smelt of prussic acid. The stomach
    was not inflamed--it held 250 grms. of a yellow fluid, containing
    white flocks smelling of bitter almond oil. In the most dependent
    portion of the stomach there was a swollen patch of mucous membrane,
    partially denuded of epithelium. The mucous membrane of the duodenum
    was also swollen and slightly red. The contents of the stomach were
    acid, and yielded, on distillation, hydride of benzole and hydric
    cyanide. Residues of the almonds themselves were also found, and
    the whole quantity taken by the woman from various data was
    calculated to be 1200 grains of bitter almonds, equal to 43 grains
    of amygdalin, or 2·5 grains of pure hydric cyanide.

Poisonous Cyanides other than Hydric and Potassic Cyanides.

    § 270. The action of both _sodic and ammonic cyanides_ is precisely
    similar to that of potassic cyanide. With regard to ammonic cyanide,
    there are several experiments by Eulenberg,[263] showing that its
    vapour is intensely poisonous.

[263] _Gewerbe Hygiene_, p. 385.

    A weak stream of ammonic cyanide vapour was passed into glass
    shades, under which pigeons were confined. After a minute, symptoms
    of distress commenced, then followed convulsions and speedy death.
    The _post-mortem_ signs were similar to those produced by prussic
    acid, and this substance was separated from the liver and lungs.

    § 271. With regard to the _double cyanides_, all those are poisonous
    from which hydric cyanide can be separated through dilute acids,
    while those which, like potassic ferro-cyanide, do not admit of this
    decomposition, may be often taken with impunity, and are only
    poisonous under certain conditions.

    Sonnenschein records the death of a colourist, after he had taken a
    dose of potassic ferro-cyanide and then one of tartaric acid; and
    Volz describes the death of a man, who took potassic ferro-cyanide
    and afterwards equal parts of nitric and hydrochloric acids. In this
    latter case, death took place within the hour, with all the symptoms
    of poisoning by hydric cyanide; so that it is not entirely true, as
    most text-books declare, that ferro-cyanide is in no degree
    poisonous. Carbon dioxide will decompose potassic ferro-cyanide at
    72°-74°, potass ferrous cyanide being precipitated--K₂Fe₂(CN)₆. A
    similar action takes place if ferro-cyanide is mixed with a solution
    of peptone and casein, and digested at blood heat[264] (from 37° to
    40° C.), so that it is believed that when ferro-cyanide is swallowed
    HCN is liberated, but the quantity is usually so small at any given
    moment that no injury is caused: but there are conditions in which
    it may kill speedily.[265]

[264] Autenrieth, _Arch. Pharm._, 231, 99-109.

[265] The presence of ferro-cyanide is easily detected. The liquid is,
if necessary, filtered and then acidified with hydrochloric acid and a
few drops of ferric chloride added; if the liquid contains
ferro-cyanide, there is immediate production of Prussian blue. It may
happen that potassic or sodic cyanide has been taken as well as
ferro-cyanide, and it will be necessary then to devise a process by
which only the prussic acid from the simple cyanide is distilled over.
According to Autenrieth, if sodium hydrocarbonate is added to the liquid
in sufficient quantity and the liquid distilled, the hydric cyanide that
comes over is derived wholly from the sodium or potassium cyanide.
Should mercury cyanide and ferro-cyanide be taken together, then this
process requires modification; bicarbonate of soda is added as before,
and then a few c.c. of water saturated with hydric sulphide; under these
circumstances, only the hydric cyanide derived from the mercury cyanide
distils over. If the bicarbonate of soda is omitted, the distillate
contains hydric cyanide derived from the ferro-cyanide.

    =Mercuric cyanide=, it has been often said, acts precisely like
    mercuric chloride (corrosive sublimate), and a poisonous action is
    attributed to it not traceable to cyanogen; but this is erroneous
    teaching. Bernard[266] declares that it is decomposed by the gastric
    juice, and hydric cyanide set free; while Pelikan puts it in the
    same series as ammonic and potassic cyanides. Lastly,
    Tolmatscheff,[267] by direct experiment, has found its action to
    resemble closely that of hydric cyanide.[268]

[266] _Substances Toxiques_, pp. 66-103.

[267] “_Einige Bemerkungen über die Wirkung von Cyanquecksilber_,” in
Hoppe-Seyler’s _Med. Chem. Untersuchungen_, 2 Heft, p. 279.

[268] Mercury cyanide may be detected in a liquid after acidifying with
tartaric acid, and adding a few c.c. of SH₂ water and then distilling.
S. Lopes suggests another process: the liquid is acidified with tartaric
acid, ammonium chloride added in excess, and the liquid is distilled. A
double chloride of ammonium and mercury is formed, and HCN distils over
with the steam.--_J. Pharm._, xxvii. 550-553.

    =Silver cyanide= acts, according to the experiments of Nunneley,
    also like hydric cyanide, but very much weaker.

    =Hydric sulphocyanide= in very large doses is poisonous.

    =Potassic sulphocyanide=, according to Dubreuil and Legros,[269] if
    subcutaneously injected, causes first local paralysis of the
    muscles, and later, convulsions.

[269] _Compt. rend._, t. 64, 1867, p. 561.

    =Cyanogen chloride= (CNCl) and also the compound (C₃N₃Cl₃)--the one
    a liquid, boiling at 15°, the other a solid, which may be obtained
    in crystals--are both poisonous, acting like hydric cyanide.

    =Methyl cyanide= is a liquid obtained by distillation of a mixture
    of calcic methyl sulphate and potassic cyanide. It boils at 77°, and
    is intensely poisonous. Eulenberg[270] has made with this substance
    several experiments on pigeons. An example of one will suffice:--A
    young pigeon was placed under a glass shade, into which methyl
    cyanide vapour, developed from calcic methyl sulphate and potassic
    cyanide, was admitted. The pigeon immediately became restless, and
    the fæces were expelled. In forty seconds it was slightly convulsed,
    and was removed after a few minutes’ exposure. The pupils were then
    observed not to be dilated, but the respiration had ceased; the legs
    were feebly twitching; the heart still beat, but irregularly; a
    turbid white fluid dropped out of the beak, and after six minutes
    life was extinct.

[270] _Gewerbe Hygiene_, p. 392.

    The pathological appearances were as follows:--In the beak much
    watery fluid; the membranes covering the brain weakly injected; the
    _plexus venosus spinalis_ strongly injected; in the region of the
    cervical vertebra a small extravasation between the dura mater and
    the bone; the right lung of a clear cherry-red colour, and the left
    lung partly of the same colour, the parenchyma presented the same
    hue as the surface; on section of the lungs a whitish froth exuded
    from the cut surface. In the cellular tissue of the trachea, there
    were extravasations 5 mm. in diameter; the mucous membrane of the
    air-passages was pale; the right ventricle and the left auricle of
    the heart were filled with coagulated and fluid dark red blood;
    liver and kidneys normal; the blood dark red and very fluid,
    becoming bright cherry-red on exposure to the air; blood corpuscles
    unchanged. Cyanogen was separated, and identified from the lungs and
    the liver.

    =Cyanuric acid= (C₃O₃N₃H₃), one of the decomposition products
    obtained from urea, is poisonous, the symptoms and pathological
    effects closely resembling those due to hydric cyanide. In
    experiments on animals, there has been no difficulty in detecting
    prussic acid in the lungs and liver after poisoning by cyanuric


§ 272. =Phosphorus.=--Atomic weight 31, specific gravity 1·77 to 1·840.
Phosphorus melts at from 44·4° to 44·5° to a pale yellow oily fluid. The
boiling-point is about 290°.

The phosphorus of commerce is usually preserved under water in the form
of waxy, semi-transparent sticks; if exposed to the air white fumes are
given off, luminous in the dark, with a peculiar onion-like odour. On
heating phosphorus it readily inflames, burning with a very white flame.

At 0° phosphorus is brittle; the same quality may be imparted to it by a
mere trace of sulphur. Phosphorus may be obtained in dodecahedral
crystals by slowly cooling large melted masses. It may also be obtained
crystalline by evaporating a solution in bisulphide of carbon or hot
naphtha in a current of carbon dioxide. It is usually stated to be
absolutely insoluble in water, but Julius Hartmann[271] contests this,
having found in some experiments that 100 grms. of water digested with
phosphorus for sixty-four hours at 38·5° dissolved ·000127 grm. He also
investigated the solvent action of bile, and found that 100 grms. of
bile under the same conditions, dissolved ·02424 grm., and that the
solubility of phosphorus rose both in water and bile when the
temperature was increased. Phosphorus is somewhat soluble in alcohol and
ether, and also, to some extent, in fatty and ethereal oils; but the
best solvent is carbon disulphide.

[271] _Zur acuten Phosphor-Vergiftung_, Dorpat, 1866.

The following is the order of solubility in certain menstrua, the
figures representing the number of parts by weight of the solvent
required to dissolve 1 part of phosphorus:--

  Carbon Disulphide,                      4
  Almond Oil,                           100
  Concentrated Acetic Acid,[272]        100
  Ether,                                250
  Alcohol, specific gravity ·822,       400
  Glycerin,                             588

[272] Phosphorus is very little soluble in cold acetic acid, and the
solubility given is only correct when the boiling acid acts for some
time on the phosphorus.

Phosphorus exists in, or can be converted into, several allotropic
modifications, of which the red or amorphous phosphorus is the most
important. This is effected by heating it for some time, in the absence
of air, from 230° to 235°. It is not poisonous.[273] Commercial red
phosphorus does, however, contain very small quantities of unchanged or
ordinary phosphorus--according to Fresenius, from ·6 per cent.
downwards; it also contains phosphorous acid, and about 4·6 per cent. of
other impurities, among which is graphite.[274]

[273] A hound took 200 grms. of red phosphorus in twelve days, and
remained healthy.--Sonnenschein.

[274] Schrotter, _Chem. News_, vol. xxxvi. p. 198.

§ 273. =Phosphuretted Hydrogen.=--=Phosphine= (PH₃), mol. weight 34,
specific gravity 1·178, percentage composition, phosphorus 91·43,
hydrogen 8·57 by weight. The absolutely pure gas is not spontaneously
inflammable, but that made by the ordinary process is so. It is a
colourless, highly poisonous gas, which does not support combustion, but
is itself combustible, burning to phosphoric acid (PH₃ + 2O₂ = PO₄H₃).
Extremely dangerous explosive mixtures may be made by combining
phosphine and air or oxygen. Phosphine, when quite dry, burns with a
white flame, but if mixed with aqueous vapour, it is green; hence a
hydrogen flame containing a mixture of PH₃ possesses a green colour.

If sulphur is heated in a stream of phosphine, hydric sulphide and
sulphur phosphide are the products. Oxides of the metals, heated with
phosphine, yield phosphides with formation of water. Iodine, warmed in
phosphine, gives white crystals of iodine phosphonium, and biniodide of
phosphorus, 5I + 4PH₃ = 3PIH₄ + PI₂. Chlorine inflames the gas, the
final result being hydric chloride and chloride of phosphorus, PH₃ + 8Cl
= 3ClH + PCl₅. One of the most important decompositions for our purpose
is the action of phosphine on a solution of nitrate of silver; there is
a separation of metallic silver, and nitric and phosphoric acids are
found in solution, thus--8AgNO₃ + PH₃ + 4OH₂ = 8Ag + 8HNO₃ + PO₄H₃. This
is, however, rather the end reaction; for, at first, there is a
separation of a black precipitate composed of phosphor-silver. The
excess of silver can be separated by hydric chloride, and the phosphoric
acid made evident by the addition of molybdic acid in excess.

§ 274. =The medicinal preparations of phosphorus= are not numerous; it
is usually prescribed in the form of pills, made by manufacturers of
coated pills on a large scale. The pills are composed of phosphorus,
balsam of Tolu, yellow wax, and curd soap, and 3 grains equal 1/30 grain
of phosphorus. There is also a _phosphorated oil_, containing about 1
part of phosphorus in 100; that of the French Pharmacopœia is made with
1 part of dried phosphorus dissolved in 50 parts of warm almond oil;
that of the German has 1 part in 80; the strength of the former is
therefore 2 per cent., of the latter 1·25 per cent. The medicinal dose
of phosphorus is from 1/100 to 1/30 grain.

§ 275. =Matches and Vermin Pastes.=--An acquaintance with the percentage
of phosphorus in the different pastes and matches of commerce will be
found useful. Most of the vermin-destroying pastes contain from 1 to 2
per cent. of phosphorus.

A phosphorus paste that was fatal to a child,[275] and gave rise to
serious symptoms in others, was composed as follows:--

[275] Casper’s 204th case.

                                Per cent.
  Phosphorus,                      1·4
  Flowers of sulphur,             42·2
  Flour,                          42·2
  Sugar,                          14·2

Three common receipts give the following proportions:--

                                Per cent.
  Phosphorus,                      1·5
  Lard,                           18·4
  Sugar,                          18·4
  Flour,                          61·7

                               Per cent.
  Phosphorus,                      1·2
  Warm water,                     26·7
  Rye flour,                      26·7
  Melted butter,                  26·7
  Sugar,                          18·7

                                Per cent.
  Phosphorus,                      1·6
  Nut oil,                        15·7
  Warm water,                     31·5
  Flour,                          31·5
  Sugar,                          19·7

A very common phosphorus paste, to be bought everywhere in England, is
sold in little pots; the whole amount of phosphorus contained in these
varies from ·324 to ·388 grm. (5 to 6 grains), the active constituent
being a little over 4 per cent. Matches differ much in composition. Six
matchheads, which had been placed in an apple for criminal purposes, and
were submitted to Tardieu, were found to contain 20 mgrms. of
phosphorus--_i.e._, ·33 grm. in 100. Mayet found in 100 matches 55
mgrms. of phosphorus. Gonning[276] analysed ten different kinds of
phosphorus matches with the following result:--Three English samples
contained in 100 matches 34, 33, and 32 mgrms. of phosphorus: a Belgian
sample, 38 mgrms.; and 5 others of unknown origin, 12, 17, 28, 32, and
41 mgrms. respectively. Some of the published formularies are as

[276] _Nederlandsch Tijdschr. voor Geneesk._, Afl. i., 1866.

  (1.) Glue,                 6 parts.
       Phosphorus,           4   „    or 14·4 per cent.
       Nitre,               10   „
       Red ochre,            5   „
       Blue smalts,          2   „

  (2.) Phosphorus,           9 parts, or 16·3 per cent.
       Gum,                 16   „
       Nitre,               14   „
       Smalts,              16   „

  (3.) Phosphorus,           4 parts, or 14·4 per cent.
       Glue,                 6   „
       Nitre,               10   „
       Red lead,             5   „
       Smalts,               2   „

  (4.) Phosphorus,          17 parts, or 17 per cent.
       Glue,                21   „
       Nitre,               38   „
       Red lead,            24   „

Phosphorus poisoning by matches will, however, shortly become very rare,
for those containing the ordinary variety of phosphorus are gradually
being superseded by matches of excellent quality, which contain no
phosphorus whatever.

§ 276. =Statistics.=--The following table gives the deaths for ten years
from phosphorus poisoning in England and Wales:--


                   ACCIDENT OR NEGLIGENCE.

  Ages,       1-5   5-15   15-25   25-65   65 and  Total
  Males,       11     1       2       8     ...      22
  Females,     15     2      11       5     ...      33
    Totals,    26     3      13      13     ...      55


  Ages,             5-15   15-25   25-65   65 and  Total
  Males,              1       6      20       1      28
  Females,            6      33      24       1      64
      Totals,         7      39      44       2      92

Phosphorus as a cause of death through accident or negligence occupies
the eighth place among poisons, and as a cause of suicide the ninth.

A far greater number of cases of poisoning by phosphorus occur yearly in
France and Germany than in England. Phosphorus may be considered as the
favourite poison which the common people on the Continent employ for the
purpose of self-destruction. It is an agent within the reach of anyone
who has 2 sous in his pocket, wherewith to buy a box of matches, but to
the educated and those who know the horrible and prolonged torture
ensuing from a toxic dose of phosphorus, such a means of exit from life
will never be favoured.

Otto Schraube[277] has collected 92 cases from Meischner’s work,[278]
and added 16 which had come under his own observation, giving in all 108
cases. Seventy-one (or 65 per cent.) of these were suicidal--of the
suicides 24 were males, 47 females (12 of the latter being prostitutes);
21 of the cases were those of murder, 11 were accidental, and in 3 the
cause was not ascertained. The number of cases in successive years, and
the kind of poison used, is given as follows:--

[277] Schmidt’s _Jahrbuch der ger. Med._, 1867, Bd. 186, S. 209-248.

[278] _Die acute Phosphorose und einige Reflexionen über die acute gelbe
Leberatrophie, &c., Inaug. Diss._, Leipzig, 1864.

                                      Phosphorus in    Phosphorus
  Number of Cases.    In the Years      Substance,      Matches.
                                       or as Paste.

         15            1798-1850           13               2
         36            1850-1860           15              21
         41            1860-1864            6              35
         16            1864-1867            5              11

Of the 108 cases, 18 persons recovered and 90 (or 83·3 per cent.) died.

Falck also has collected 76 cases of poisoning from various sources
during eleven years; 55 were suicidal, 5 homicidal[279] (murders), and
the rest accidental. Of the latter, 2 were caused by the use of
phosphorus as a medicine, 13 by accidents due to phosphorus being in the
house; in 1 case phosphorus was taken intentionally to try the effects
of an antidote.[280] With regard to the form in which the poison was
taken, 2 of the 76, as already mentioned, took it as prescribed by
physicians, the remaining 74 were divided between poisonings by
phosphorus paste (22) and matches (52) = 70 per cent. Of the 76 cases, 6
were children, 43 adult males, 13 adult females, and 14 adults, sex not
given. Of the 76 cases, 42, or 55·3 per cent., died--a much smaller rate
of mortality than that shown by Schraube’s collection.

[279] Dr. Dannenberg has shown by direct experiment that a poisonous
dose of phosphorus may be introduced into spirits or coffee, and the
mixture have but little odour or taste of phosphorus.--Schuchardt in
Maschka’s _Handbuch_.

[280] Géry, “_Ueber Terpentinessenz als Gegenmittel gegen Phosphor_,” in
_Gaz. Hebd. de Méd._, 2 sér., x. 2, 1873.

§ 277. =Fatal Dose.=--The smallest dose on record is that mentioned by
Lobenstein Lobel, of Jena, where a lunatic died from taking 7·5 mgrms.
(·116 grain). There are other cases clearly indicating that this small
quantity may produce dangerous symptoms in a healthy adult.

§ 278. =Effects of Phosphorus.=--Phosphorus is excessively poisonous,
and will destroy life, provided only that it enters the body in a fine
state of division, but if taken in coarse pieces no symptoms may follow,
for it has been proved that single lumps of phosphorus will go the whole
length of a dog’s intestinal canal without causing appreciable loss of
weight, and without destroying life.[281] Magendie injected _oleum
phosphoratum_ into the veins, and although the animals experimented on
exhaled white fumes, and not a few died asphyxiated, yet no symptoms of
phosphorus poisoning resulted--an observation confirmed by others--the
reason being that the phosphorus particles in a comparatively coarse
state of division were arrested in the capillaries of the lung, and may
be said to have been, as it were, outside the body. On the other hand,
A. Brunner,[282] working in L. Hermann’s laboratory, having injected
into the veins phosphorus in such a fine emulsion that the phosphorus
could pass the lung capillaries, found that there were no exhalations of
white fumes, but that the ordinary symptoms of phosphorus poisoning soon
manifested themselves. Phosphorus paste, by the method of manufacture,
is in a state of extreme sub-division, and hence all the phosphorus
pastes are extremely poisonous.

[281] Reveil, _Ann. d’Hygiène Publ._ (3), xii. p. 370.

[282] _Arch. f. d. Ges. Physiologie_, iii. p. 1.

§ 279. In a few poisons there is a difference, more or less marked,
between the general symptoms produced on man, and those noticeable in
the different classes of animals; but with phosphorus, the effects on
animals appear to agree fairly with those witnessed most frequently in
man. Tardieu (who has written perhaps the best and most complete
clinical record of phosphorus poisoning extant) divides the cases under
three classes, and to use his own words:--“I think it useful to
establish that poisoning by phosphorus in its course, sometimes rapid,
sometimes slow, exhibits in its symptoms three distinct forms--a common
form, a nervous form, and a hæmorrhagic form. I recognise that, in
certain cases, these three forms may succeed each other, and may only
constitute periods of poisoning; but it is incontestable that each of
them may show itself alone, and occupy the whole course of the illness
produced by the poison.”[283] Premising that the common form is a
blending of irritant, nervous, and hæmorrhagic symptoms, I adopt here in
part Tardieu’s division. The name of “hæmorrhagic form” may be given to
that in which hæmorrhage is the predominant feature, and the “nervous”
to that in which the brain and spinal cord are from the first affected.
There yet remain, however, a few cases which have an entirely anomalous
course, and do not fall under any of the three classes.

[283] _Étude Médico-Légale et Clinique sur l’Empoisonnement_, Paris,
1875, p. 483.

From a study of 121 recorded cases of phosphorus poisoning, I believe
the relative frequency of the different forms to be as follows:--The
common form 83 per cent., hæmorrhagic 10 per cent., nervous 6 per cent.,
anomalous 1 per cent. The “anomalous” are probably over-estimated, for
the reason that cases presenting ordinary features are not necessarily
published, but others are nearly always chronicled in detail.

§ 280. =Common Form.=--At the moment of swallowing, a disagreeable taste
and smell are generally experienced, and there may be immediate and
intense pain in the throat, gullet, and stomach, and almost immediate
retching and vomiting. The throat and tongue also may become swollen and
painful; but in a considerable number of cases the symptoms are not at
once apparent, but are delayed from one to six hours--rarely longer. The
person’s breath may be phosphorescent before he feels in any way
affected, and he may go about his business and perform a number of acts
requiring both time and mental integrity. Pain in the stomach (which, in
some of the cases, takes the form of violent cramp and vomiting)
succeeds; the matters vomited may shine in the dark, and are often
tinged with blood. Diarrhœa is sometimes present, sometimes absent;
sleeplessness for the first night or two is very common. The pulse is
variable, sometimes frequent, sometimes slow; the temperature in the
morning is usually from 36·0° to 36·5°, in the evening 37° to 38°.

The next symptom is jaundice. I have notes of the exact occurrence of
jaundice in 23 cases, as follows:--In 1 within twenty-four hours, in 3
within thirty-six hours, in 3 within two days, in 11 within three days,
in 1 within four days, in 1 within five days, in 1 within nine days, in
1 within eighteen days, and in 1 within twenty-seven days; so that in
about 78 per cent. jaundice occurred before the end of the third day.
Out of 26 cases, in which the patients lived long enough for the
occurrence of jaundice, in 3 (or 11 per cent.) it was entirely absent.
In 132 cases recorded by Lewin, Meischner, and Heisler, jaundice
occurred in 65, or about 49 per cent., but it must be remembered, that
in many of these cases the individual died before it had time to
develop. The jaundice having thoroughly pronounced itself, the system
may be considered as not only under the influence of the toxic action of
phosphorus, but as suffering in addition from all the accidents
incidental to the retention of the biliary secretion in the blood; nor
is there from this point any special difference between phosphorus
poisoning and certain affections of the liver--such, for example, as
acute yellow atrophy. There is retention of urine, sleeplessness,
headache, frequent vomiting, painful and often involuntary evacuations
from the bowels, and occasionally skin affections, such as urticaria or
erythema. The case terminates either by acute delirium with fever,
followed by fatal coma, or, in a few instances, coma comes on, and the
patient passes to death in sleep without delirium. In this common form
there is in a few cases, at the end of from twenty-four to thirty hours,
a remission of the symptoms, and a non-medical observer might imagine
that the patient was about to recover without further discomfort; but
then jaundice supervenes, and the course is as described. Infants often
do not live long enough for the jaundiced stage to develop, but die
within twenty-four hours, the chief symptoms being vomiting and

§ 281. =Hæmorrhagic Form.=--The symptoms set in as just detailed, and
jaundice appears, but accompanied by a new and terrible train of
events--viz., great effusion of blood. In some cases the blood has been
poured out simultaneously from the nose, mouth, bladder, kidneys, and
bowels. Among women there is excessive hæmorrhagia. The liver is found
to be swollen and painful; the bodily weakness is great. Such cases are
usually of long duration, and a person may die months after taking the
poison from weakness, anæmia, and general cachexia. In many of its
phases the hæmorrhagic form resembles scurvy, and, as in scurvy, there
are spots of purpura all over the body.

§ 282. =The nervous form= is less common than the two forms just
described. From the beginning, there are strange creeping sensations
about the limbs, followed by painful cramps, repeated faintings, and
great somnolence. Jaundice, as usual, sets in, erythematous spots appear
on the skin, and, about the fifth day, delirium of an acute character
breaks out, and lock-jaw and convulsions close the scene.

The following are one or two brief abstracts of anomalous cases in which
symptoms are either wanting, or run a course entirely different from any
of the three forms described:--

A woman, aged 20, took about 3 grains of phosphorus in the form of
rat-paste. She took the poison at six in the evening, behaved according
to her wont, and sat down and wrote a letter to the king. During the
night she vomited once, and died the next morning at six o’clock,
exactly twelve hours after taking the poison. There appear to have been
no symptoms whatever, save the single vomiting, to which may be added
that in the course of the evening her breath had a phosphorus odour and
was luminous.[284]

[284] Casper’s 205th case.

A girl swallowed a quantity of phosphorus paste, but there were no
marked symptoms until the fifth day, on which there was sickness and
purging. She died on the seventh day. A remarkable blueness of the
finger nails was observed a little before death, and was noticeable

[285] Taylor on _Poisons_, p. 277.

§ 283. =Sequelæ.=--In several cases in which the patients have recovered
from phosphorus poisoning, there have been observed paralytic
affections.[286] O. Bollinger has recorded a case in which paralysis of
the foot followed;[287] in another, published by Bettelheim,[288] there
were peculiar cerebral and spinal symptoms. Most of these cases are to
be explained as disturbance or loss of function from small hæmorrhages
in the nervous substance.

[286] See Gallavardin, _Les Paralyses Phosphoriques_, Paris, 1865.

[287] _Deutsches Archiv f. klin. Med._, Bd. 6, Hft. 1, S. 94, 1869.

[288] _Wiener Med. Presse_, 1868, No. 41.

§ 284. =Period at which the first Symptoms commence.=--The time when the
symptoms commence is occasionally of importance from a forensic point of
view. I find that out of 28 cases in which the commencement of evident
symptoms--_i.e._, pain, or vomiting, or illness--is precisely recorded,
in 8 the symptoms were described as either immediate or within a few
minutes after swallowing the poison; in 6 the symptoms commenced within
the hour; in 3 within two hours; in other 3 within four hours; and in 1
within six hours. One was delayed until the lapse of twelve hours, 1
from sixteen to eighteen hours, 1 two, and another five days. We may,
therefore, expect that in half the cases which may occur, the symptoms
will commence within the hour, and more than 80 per cent. within six

§ 285. =Period of Death.=--In 129 cases death took place as follows:--In
17 within twenty-four hours, in 30 within two days, in 103 within seven
days. Three patients lived eight days, 6 nine days, 13 ten days, 1
eleven days, 1 sixteen days, 1 seventeen days, and 1 survived eight
months. It hence follows that 79·8 per cent. of the fatal cases die
within the week.

§ 286. =Phosphorus Vapour.=--There are one or two cases on record of
acute poisoning by phosphorus in the form of vapour. The symptoms are
somewhat different from the effects produced by the finely-divided
solid, and in general terms it may be said that phosphorus vapour is
more apt to produce the rarer “nervous” form of poisoning than the solid

Bouchardat[289] mentions the case of a druggist who, while preparing a
large quantity of rat-poison in a close room, inhaled phosphorus vapour.
He fainted repeatedly, fell into a complete state of prostration, and
died within a week.

[289] _Annuaire de Thérap._, 1874, p. 109; Schuchardt in Maschka’s
_Handbuch_; also Schmidt’s _Jahrbuch_, 1846, Bd. 51, S. 101.

The following interesting case came under the observation of Professor
Magnus Huss:--A man, thirty-nine years old, married, was admitted into
the Seraphin-Lazareth, Stockholm, on the 2nd of February 1842. He had
been occupied three years in the manufacture of phosphorus matches, and
inhabited the room in which the materials were preserved. He had always
been well-conducted in every way, and in good health, until a year
previously, when a large quantity of the material for the manufacture of
the matches accidentally caught fire and exploded. In his endeavours to
extinguish the flames, he breathed a large quantity of the vapour, and
he fell for a time unconscious. The spine afterwards became so weak that
he could not hold himself up, and he lost, in a great measure, power
over his legs and arms. On admission, his condition was as follows:--He
could make a few uncertain and staggering steps, his knees trembled, his
arms shook, and if he attempted to grasp anything when he lay in bed,
there were involuntary twitchings of groups of muscles. There was no
pain; the sensibility of the skin was unchanged; he had formication in
the left arm; the spine was neither sensitive to pressure, nor unusually
sensitive to heat (as, _e.g._, to the application of a hot sponge); the
organs of special sense were not affected, but his speech was somewhat
thick. He lived to 1845 in the same condition, but the paralysis became
worse. There does not seem to have been any autopsy.

The effects of phosphorus vapour may be still further elucidated by one
of Eulenberg’s[290] experiments on a rabbit. The vapour of burning
phosphorus, mixed with much air, was admitted into a wooden hutch in
which a strong rabbit sat. After 5 mgrms. of phosphorus had been in this
manner consumed, the only symptoms in half an hour were salivation, and
quickened and somewhat laboured respiration. After twenty-four hours had
elapsed there was sudden indisposition, the animal fell as if lifeless,
with the hind extremities stretched out, and intestinal movements were
visible; there was also expulsion of the urine. These epileptiform
seizures seem to have continued more or less for twelve days, and then
ceased. After fourteen days the experiment was repeated on the same
rabbit. The animal remained exposed to the vapour for three-quarters of
an hour, when the epilepsy showed itself as before, and, indeed, almost
regularly after feeding. Between the attacks the respiration was slowed.
Eight weeks afterwards there was an intense icterus, which disappeared
at the end of ten weeks.

[290] _Gewerbe Hygiene_, p. 255.

§ 287. =Chronic phosphorus poisoning= has frequently been noticed in
persons engaged either in the manufacture of phosphorus or in its
technical application. Some have held that the symptoms are due to an
oxidation product of phosphorus rather than to phosphorus itself; but in
one of Eulenberg’s experiments, in which a dove was killed by breathing
phosphorus fumes evolved by phosphorus oil, phosphorus was chemically
recognised in the free state in the lungs. The most constant and
peculiar effect of breathing small quantities of phosphorus vapour is a
necrosis of the lower jaw. There is first inflammation of the periosteum
of the jaw, which proceeds to suppuration and necrosis of a greater or
smaller portion. The effects may develop with great suddenness, and end
fatally. Thus Fournier and Olliver[291] relate the case of a girl,
fourteen years old, who, after working four years in a phosphorus
manufactory, was suddenly affected with periostitis of the upper jaw,
and with intense anæmia. An eruption of purpuric spots ensued, and she
died comatose. There is now little doubt, that minute doses of
phosphorus have a specific action on the bones generally, and more
especially on the bones of the jaw. Wegner[292] administered small daily
doses to young animals, both in the state of vapour, and as a
finely-divided solid. The condition of the bones was found to be more
compact than normal, the medullary canals being smaller than in healthy
bone, the ossification was quickened. The formation of callus in
fractured limbs was also increased.

[291] _Gaz. hebd. de Méd._, 29, p. 461, 1868.

[292] Virchow’s _Arch. f. path. Anat._, lv. 11.

§ 288. =Changes in the Urinary Secretion.=--It has been before stated
that, at a certain period of the illness, the renal secretion is
scantier than in health, the urine diminishing, according to Lebert and
Wyss’s[293] researches, to one-half on the third, fourth, or fifth day.
It frequently contains albumen, blood, and casts. When jaundice is
present, the urine has then all the characters noticed in icterus;
leucin and tyrosin, always present in acute yellow atrophy of the liver,
have been found in small quantity in jaundice through phosphorus; lactic
acid is also present. The urea is much diminished, and, according to
Schultzen and Riess,[294] may be towards death entirely absent. Lastly,
it is said that there is an exhalation of either phosphorus vapour or
phosphine from such urine. In some cases the urine is normal, _e.g._, in
a case recorded by E. H. Starling, M.D., and F. G. Hopkins, B.Sc.
(_Guy’s Hospital Report_, 1890), in which a girl, aged 18, died on the
fifth day after taking phosphorus paste, the liver was fatty, and there
was jaundice; but the urine contained neither leucin nor tyrosin, and
was stated to be generally normal.

[293] _Archiv Générale de Méd._, 6 Sér., Tom. 12, 1868, p. 709.

[294] _Annalen der Charité_, Berlin.

§ 289. =Changes in the blood= during life have been several times
observed. In a case attended by M. Romellære of Brussels,[295] in which
a man took the paste from 300 matches, and under treatment by turpentine
recovered, the blood was frequently examined, and the leucocytes found
much increased in number. There is a curious conflict of evidence as to
whether phosphorus prevents coagulation of the blood or not. Nasse
asserted that phosphorated oil given to a dog fully prevented
coagulation; P. I. Liebreck[296] also, in a series of researches, found
the blood dark, fluid, and in perfect solution. These observations were
also supported by V. Bibra and Schuchardt.[297] Nevertheless, Lebert and
Wyss found the blood, whether in the veins or in extravasations, in a
normal condition. Phosphorus increases the fatty contents of the blood.
Ritter found that phosphorus mixed with starch, and given to a dog,
raised the fatty content from the normal 2 per 1000 up to 3·41 and 3·47
per 1000. Eug. Menard[298] saw in the blood from the jugular and portal
veins, as well as in extravasations, microscopic fat globules and fine
needle-shaped crystals soluble in ether.

[295] Tardieu, _op. cit._, Case 31.

[296] _Diss. de Venefico Phosphoreo Acuto_, Upsal, 1845.

[297] V. Bibra u. Geist, _Die Krankheiten der Arbeiter in den
Phosphorzundholz Fabriken_, 1847, S. 59, &c.; Henle u. v. Pfeuffer’s
_Zeitschr. f. ration. Med._, N. F., Bd. 7, Hft. 3, 1857.

[298] _Étude Expérimentale sur quelques lésions de l’Empoisonnement aigu
par le Phosphore (Thèse)_, Strasbourg, 1869.

§ 290. =Antidote--Treatment.=--After emptying the stomach by means of
emetics or by the stomach-pump, oil of turpentine in full medicinal
doses, say 2·5 c.c. (about 40 min.), frequently administered, seems to
act as a true antidote, and a large percentage of cases treated early in
this way recover.

§ 291. =Poisonous Effects of Phosphine (phosphuretted
hydrogen).=--Experiments on pigeons, on rats, and other animals, and a
few very rare cases among men, have shown that phosphine has an exciting
action on the respiratory mucous membranes, and a secondary action on
the nervous system. Eulenberg[299] exposed a pigeon to an atmosphere
containing 1·68 per cent. of phosphine. There was immediate unrest; at
the end of three minutes, quickened and laboured breathing (100 a
minute); after seven minutes, the bird lay prostrate, with shivering of
the body and wide open beak; after eight minutes, there was vomiting;
after nine minutes, slow breathing (34 per minute); after twelve
minutes, convulsive movements of the wings; and after thirteen minutes,
general convulsions and death.

[299] _Gewerbe Hygiene_, p. 273.

The membranes of the brain were found strongly injected, and there were
extravasations. In the mucous membrane of the crop there was also an
extravasation. The lungs externally and throughout were of a dirty
brown-red colour; the entire heart was filled with coagulated blood,
which was weakly acid in reaction.

In a second experiment with another pigeon, there was no striking
symptom save that of increased frequency of respiration and loss of
appetite; at the end of four days it was found dead. There was much
congestion of the cerebral veins and vessels, the mucous membrane of the
trachea and bronchi were weakly injected, and the first showed a thin,
plastic, diphtheritic-like exudation.

Dr. Henderson’s[300] researches on rats may also be noticed here. He
found that an atmosphere consisting entirely of phosphine killed rats
within ten minutes, an atmosphere with 1 per cent. in half an hour. The
symptoms observed were almost exactly similar to those noticed in the
first experiment on the pigeon quoted above, and the _post-mortem_
appearances were not dissimilar. With smaller quantities of the gas, the
first symptom was increased frequency of the respiration; then the
animals showed signs of suffering intense irritation of the skin,
scratching and biting at it incessantly; afterwards they became drowsy,
and assumed a very peculiar attitude, sitting down on all-fours, with
the back bent forward, and the nose pushed backwards between the
forepaws, so as to bring the forehead against the floor of the cage.
When in this position, the rat presented the appearance of a curled-up
hedgehog. Phosphine, when injected into the rectum, is also fatal; the
animals exhale some of the gas from the lungs, and the breath,
therefore, reduces solutions of silver nitrate.[301]

[300] _Journ. Anat. and Physiol._, vol. xiii. p. 19.

[301] Dybskowsky, _Med. Chem. Untersuchungen aus Hoppe-Seyler’s Labor.
in Tübingen_, p. 57.

Brenner[302] has recorded the case of a man twenty-eight years old, a
pharmaceutist, who is supposed to have suffered from illness caused by
repeated inhalations of minute quantities of phosphine. He was engaged
for two and a half years in the preparation of hypophosphites; his
illness commenced with spots before the eyes, and inability to fix the
attention. His teeth became very brittle, and healthy as well as carious
broke off from very slight causes. Finally, a weakness of the arms and
limbs developed in the course of nine months into complete locomotor

[302] _St. Petersburg Med. Zeitschr._, 4 Hft., 1865.

§ 292. Blood takes up far more phosphine than water. Dybskowsky found
that putting the coefficient of solubility of phosphine in pure water at
·1122 at 15°, the coefficient for venous blood was ·13, and for arterial
26·73; hence the richer the blood is in oxygen the more phosphine is
absorbed. It seems probable that the poisonous gas reacts on the
oxyhæmoglobin of the blood, and phosphorous acid is formed. This is
supported by the fact that a watery extract of such blood reduces silver
nitrate, and has been also found feebly acid. The dark blood obtained
from animals poisoned by phosphine, when examined spectroscopically, has
been found to exhibit a band in the violet.

§ 293. =Post-mortem Appearances.=--There are a few perfectly well
authenticated cases showing that phosphorus may cause death, and yet no
lesion be discovered afterwards. Thus, Tardieu[303] cites a case in
which a woman, aged 45, poisoned herself with phosphorus, and died
suddenly the seventh day afterwards. Dr. Mascarel examined the viscera
with the greatest care, but could discover absolutely no abnormal
conditions; the only symptoms during life were vomiting, and afterwards
a little indigestion. It may, however, be remarked that the microscope
does not seem to have been employed, and that probably a close
examination of the heart would have revealed some alteration of its
ultimate structure. The case quoted, by Taylor[304] may also be
mentioned, in which a child was caught in the act of sucking phosphorus
matches, and died ten days afterwards in convulsions. None of the
ordinary _post-mortem_ signs of poisoning by phosphorus were met with,
but the intestines were reddened throughout, and there were no less than
ten invaginations; but the case is altogether a doubtful one, and no
phosphorus may actually have been taken. It is very difficult to give in
a limited space anything like a full picture of the different lesions
found after death from phosphorus, for they vary according as to whether
the death is speedy or prolonged, whether the phosphorus has been taken
as a finely-divided solid, or in the form of vapour, &c. It may,
however, be shortly said, that the most common changes are fatty
infiltration of the liver and kidneys, fatty degeneration of the heart,
enlargement of the liver, ecchymoses in the serous membranes, in the
muscular, in the fatty, and in the mucous tissues. When death occurs
before jaundice supervenes, there may be little in the aspect of the
corpse to raise a suspicion of poison; but if intense jaundice has
existed during life, the yellow staining of the skin, and it may be,
spots of purpura, will suggest to the experienced pathologist the
possibility of phosphorus poisoning. In the mouth and throat there will
seldom be anything abnormal. In one or two cases of rapid death among
infants, some traces of the matches which had been sucked were found
clinging to the gums. The stomach may be healthy, but the most common
appearance is a swelling of the mucous membrane and superficial
erosions. Virchow,[305] who was the first to call attention to this
peculiar grey swelling of the intestinal mucous membrane under the name
of _gastritis glandularis_ or _gastradenitis_, shows that it is due to a
fatty degeneration of the epithelial cells, and that it is by no means
peculiar to phosphorus poisoning. The swelling may be seen in
properly-prepared sections to have its essential seat in the glands of
the mucous membrane; the glands are enlarged, their openings filled with
large cells, and each single cell is finely granular. Little centres of
hæmorrhage, often microscopically small, are seen, and may be the
centres of small inflammations; their usual situation is on the summit
of the rugæ. Very similar changes are witnessed after death from
septicæmia, pyæmia, diphtheria, and other diseases. The softening of the
stomach, gangrene, and deep erosions, recorded by the earlier authors,
have not been observed of late years, and probably were due to
_post-mortem_ changes, and not to processes during life. The same
changes are to be seen in the intestines, and there are numerous
extravasations in the peritoneum.

[303] _L’Empoisonnement_, p. 520.

[304] _Poisons_, 3rd ed., p. 276.

[305] Virchow’s _Archiv. f. path. Anat._, Bd. 31, Hft. 3, 399.

The liver shows of all the organs the most characteristic signs; a more
or less advanced fatty infiltration of its structure takes place, which
was first described as caused by phosphorus by Hauff in 1860.[306] It
is the most constant pathological evidence both in man and animal, and
seems to occur at a very early period, Munk and Leyden having found a
fatty degeneration in the liver far advanced in twenty-four hours[307]
after poisoning. In rats and mice poisoned with paste, I have found this
evident to the naked eye twelve hours after the fatal dose. The liver is
mostly large, but in a case[308] recorded in the _Lancet_, July 14,
1888, the liver was shrunken; it has a pale yellow (or sometimes an
intense yellow) colour; on section the cut surface presents a mottled
appearance; the serous envelopes, especially along the course of the
vessels, exhibit extravasations of blood. The liver itself is more
deficient in blood than in the normal condition, and the more bloodless
it is, the greater the fatty infiltration.

[306] Hauff collected 12 cases, and found a fatty liver in
11.--_Würtemb. Med. Corresp. Bl._, 1860, No. 34.

[307] _Die acute Phosphor-Vergiftung_, Berlin, 1865.

[308] This case, from the similarity of the pathological appearances to
those produced by yellow atrophy, deserves fuller notice:--“Frances A.
Cowley, aged 20, on her own admission, took some rat paste on Tuesday,
June 19th. Death ensued eleven days later. The initial symptoms were not
very marked. Nausea and vomiting continued with moderate severity for a
few days and then ceased. There ensued a feeling of depression. Towards
the end insensibility, icterus, and somewhat profuse metrorrhagia
supervened. At the necropsy the skin and conjunctivæ were observed of a
bright yellow colour. There was no organic disease save of a recent
nature, and entirely attributable to the action of the poison ingested.
The stomach contained about three-quarters of a pint of dark
claret-coloured fluid, consisting largely of blood derived from
capillary hæmorrhage from the mucous membrane. There was no solution of
continuity of the mucous membrane, which showed traces of recent
irritation. The whole surface presented a yellow icteric tint, except
the summits of some of the rugæ, which were of a bright pink colour.
There was also faint wrinkling of the mucous membrane. The upper part of
the small intestine was affected in much the same manner as the stomach.
The large intestine contained a quantity of almost colourless fæces. The
liver was shrunken, weighing only 26 ozs., and both on its outer and
sectional surface exactly resembled the appearances produced by acute
yellow atrophy, except that there were greater congestion and
interstitial hæmorrhage in patches. The lobules of the liver were in
many places unrecognisable; in others they stood in bold relief as
brilliant canary-yellow patches, standing in strong contrast to the deep
dark-red areas of congestion and extravasation. The gall-bladder
contained about 2 drachms of thin greyish fluid, apparently all but
devoid of bile. The urinary bladder was empty; the kidneys were
enlarged; the cortex was very pale and bile-stained, of greater depth
than natural, and of softer consistence. The spleen was not enlarged,
nor was it in the least degree softened. In addition to the bleeding
from the uterus noticed during life, there was capillary hæmorrhage into
the right lung and pleura, into the pericardium, and, as already
mentioned, into the stomach. The brain was healthy.”

In the Museum of the Royal College of Surgeons there is a preparation
(No. 2737) of the section of a liver derived from a case of phosphorus

A girl, aged 18, after two days’ illness, was admitted into Guy’s
Hospital. She confessed to having eaten a piece of bread coated with
phosphorus paste. She had great abdominal pain, and died on the seventh
day after taking the phosphorus. A few hours before her death she was
profoundly and suddenly collapsed. The liver weighed 66 ozs. The
outlines of the hepatic lobules were very distinct, each central vein
being surrounded by an opaque yellowish zone; when fresh the hue was
more uniform, and the section was yellowish-white in colour. A
microscopical examination of the hepatic cells showed them laden with
fat globules, especially in the central parts of the liver.

The microscopic appearances are also characteristic. In a case of
suicidal poisoning by phosphorus, in which death took place on the
seventh day, the liver was very carefully examined by Dr. G. F. Goodart,
who reported as follows:--

    “Under a low power the structure of the liver is still readily
    recognisable, and in this the specimen differs from slides of three
    cases of acute yellow atrophy that I have in my possession. The
    hepatic cells are present in large numbers, and have their natural
    trabecular arrangement. The columns are abnormally separated by
    dilated blood or lymph-spaces, and the individual cells are cloudy
    and ill-defined. The portal channels are everywhere characterised by
    a crowd of small nuclei which stain with logwood deeply. The
    epithelium of the smaller ducts is cloudy, and blocks the tubes in
    many cases. Under a high power (one-fifth) it is seen that the
    hepatic cells are exceedingly ill-defined in outline, and full of
    granules and even drops of oil. But in many parts, even where the
    cells themselves are hazy, the nucleus is still fairly visible. It
    appears to me that, in opposition to what others have described, the
    nuclei of the cells have in great measure resisted the degenerative
    process. The change in the cells is uniform throughout each lobule,
    but some lobules are rather more affected than others. The
    blood-spaces between the cells are empty, and the liver appears to
    be very bloodless. The portal canals are uniformly studded with
    small round nuclei or cells, which are in part, and might be said in
    great part, due to increase of the connective tissue or to a
    cirrhotic process. But I am more disposed to favour the view that
    they are due to migration from the blood-vessels, because they are
    so uniform in size, and the hepatic cells and connective tissue in
    their neighbourhood are undergoing no changes in the way of growth
    whatever. I cannot detect any fatty changes in the vessels, but some
    of the smaller biliary ducts contain some cloudy albuminous
    material, and their nucleation is not distinct. No retained biliary
    pigment is visible.”[309]

[309] “A Recent Case of Suicide,” by Herbert J. Capon, M.D.--_Lancet_,
March 18, 1882.

Oscar Wyss,[310] in the case of a woman twenty-three years old, who died
on the fifth day after taking phosphorus, describes, in addition to the
fatty appearance of the cells, a new formation of cells lying between
the lobules and in part surrounding the gall-ducts and the branches of
the portal vein and hepatic artery.

[310] Virchow’s _Archiv. f. path. Anat._, Bd. 33, Hft. 3, S. 432, 1865.

Salkowsky[311] found in animals, which he killed a few hours after
administering to them toxic doses of phosphorus, notable hyperæmia of
the throat, intestine, liver, and kidneys--both the latter organs being
larger than usual. The liver cells were swollen, and the nuclei very
evident, but they contained no fat, fatty drops being formed afterwards.

[311] _Ibid._, Bd. 34, Hft. 1 u. 2, S. 73, 1865.

§ 294. =The kidneys= exhibit alterations very similar and analogous to
those of the liver. They are mostly enlarged, congested, and flabby,
with extravasations under the capsule, and show microscopic changes
essentially consisting in a fatty degeneration of the epithelium. In
cases attended with hæmorrhage, the tubuli may be here and there filled
with blood. The fatty epithelium is especially seen in the contorted
tubes, and the walls of the vessels, both of the capsule and of the
malpighian bodies, also undergo the same fatty change. In cases in which
death has occurred rapidly, the kidneys have been found almost healthy,
or a little congested only. The pancreas has also been found with its
structure in part replaced by fatty elements.

Of great significance are also the fatty changes in the general muscular
system, and more especially in the heart. The muscular fibres of the
heart quickly lose their transverse striæ, which are replaced by drops
of fat. Probably this change is the cause of the sudden death not
unfrequently met with in phosphorus poisoning.

=In the lungs=, when the phosphorus is taken in substance, there is
little “naked-eye” change, but Perls,[312] by manometric researches, has
shown that the elasticity is always decreased. According to experiments
on animals, when the vapour is breathed, the mucous membrane is red,
congested, swollen, and has an acid reaction.

[312] Deutsch. _Archiv f. klin. Med._, vi. Hft. 1, S. 1, 1869.

=In the nervous system= no change has been remarked, save occasionally
hæmorrhagic points and extravasations.

§ 295. =Diagnostic Differences between Acute Yellow Atrophy of the Liver
and Fatty Liver produced by Phosphorus.=--O. Schultzen and O. L. Riess
have collected and compared ten cases of fatty liver from phosphorus
poisoning, and four cases of acute yellow atrophy of the liver, and,
according to them, the chief points of distinction are as follows:--In
phosphorus poisoning the liver is large, doughy, equally yellow, and
with the acini well marked; while in acute yellow atrophy the liver is
diminished in size, tough, leathery, and of a dirty yellow hue, the
acini not being well mapped out. The “phosphorus” liver, again, presents
the cells filled with large fat drops, or entirely replaced by them; but
in the “atrophy” liver, the cells are replaced by a finely-nucleated
detritus and through newly-formed cellular tissue. Yellow atrophy seems
to be essentially an inflammation of the intralobular connective tissue,
while in phosphorus poisoning the cells become gorged by an infiltration
of fat, which presses upon the vessels and lessens the blood supply,
and the liver, in consequence, may, after a time, waste.

There is also a clinical distinction during life, not only in the
lessening bulk of the liver in yellow atrophy, in opposition to the
increase of size in the large phosphorus liver, but also in the
composition of the renal secretion. In yellow atrophy the urine contains
so much leucine and tyrosin, that the simple addition of acetic acid
causes at once a precipitate. Schultzen and Riess also found in the
urine, in cases of yellow atrophy, _oxymandelic acid_ (C₈H₈O₄), but in
cases of phosphorus poisoning a nitrogenised acid, fusing at 184° to

According to Maschka, grey-white, knotty, fæcal masses are found in the
intestines in yellow atrophy, but never in cases of phosphorus
poisoning. In the latter, it is more common to find a slight intestinal
catarrh and fluid excreta.

§ 296. =The Detection of Phosphorus=.--The following are the chief
methods in use for the separation and detection of phosphorus:[313]--

[313] It has been recommended to dissolve the phosphorus out from
organic matters by carbon disulphide. On evaporation of the latter the
phosphorus is recognised by its physical properties. Such a method is of
but limited application, although it may sometimes be found useful. I
have successfully employed it in the extraction of phosphorus from the
crop of a fowl; but on this occasion it happened to be present in large

1. =Mitscherlich’s Process=.--The essential feature of this process is
simply distillation of free phosphorus, and observation of its luminous
properties as the vapour condenses in the condensing tube. The
conditions necessary for success are--(1) that the apparatus should be
in total darkness;[314] and (2) that there should be no substance
present, such as alcohol or ammonia,[315] which, distilling over with
the phosphorus-vapour, could destroy its luminosity. A convenient
apparatus, and one certain to be in all laboratories, is an ordinary
Florence flask, containing the liquid to be tested, fitted to a glass
Liebig’s condenser, supported on an iron sand-bath (which may, or may
not, have a thin layer of sand), and heated by a Fletcher’s low
temperature burner. The distillate is received into a flask. This
apparatus, if in darkness, works well; but should the observer wish to
work in daylight, the condenser must be enclosed in a box perfectly
impervious to light, and having a hole through which the luminosity of
the tube may be seen, the head of the operator and the box being covered
with a cloth. If there be a stream of water passing continuously
through the condenser, a beautiful luminous ring of light appears in the
upper part of the tube, where it remains fixed for some time. Should,
however, the refrigeration be imperfect, the luminosity travels slowly
down the tube into the receiver. In any case, the delicacy of the test
is extraordinary.[316] If the organic liquid is alkaline, or even
neutral, there will certainly be some evolution of ammonia, which will
distil over before the phosphorus, and retard (or, if in sufficient
quantity, destroy) the luminosity. In such a case it is well, as a
precaution, to add enough sulphuric acid to fix the ammonia, omitting
such addition if the liquid to be operated upon is acid.

[314] Any considerable amount of phosphorescence can, however, be
observed in twilight.

[315] Many volatile substances destroy the luminous appearance of
phosphorus vapour, _e.g._, chlorine, hydric sulphide, sulphur dioxide,
carbon disulphide, ether, alcohol, petroleum, turpentine, creasote, and
most essential oils. On the other hand, bromine, hydrochloric acid,
camphor, and carbonate of ammonia do not seem to interfere much with the

[316] Fresenius states that he and Neubauer, with 1 mgrm. of phosphorus
in 200,000, recognised the light, which lasted for half an
hour.--_Zeitschr. f. anal. Chem._, i. p. 336.

2. =The Production of Phosphine= (PH₃).--Any method which produces
phosphine (phosphuretted hydrogen), enabling that gas to be passed
through nitrate of silver solution, may be used for the detection of
phosphorus. Thus, Sonnenschein states that he has found phosphorus in
extraordinary small amount, mixed with various substances, by heating
with potash in a flask, and passing the phosphine into silver nitrate,
separating the excess of silver, and recognising the phosphoric acid by
the addition of molybdate of ammonia.[317]

[317] Sonnenschein, _Handbuch der gerichtlichen Chemie_, Berlin, 1869.

The usual way is, however, to produce phosphine by means of the action
on free phosphorus of nascent hydrogen evolved on dissolving metallic
zinc in dilute sulphuric acid. Phosphine is formed by the action of
nascent hydrogen on solid phosphorus, phosphorous acid, and
hypophosphorous acid; but no phosphine can be formed in this way by the
action of hydrogen on phosphoric acid.

Since it may happen that no free phosphorus is present, but yet the
first product (phosphorous acid) of its oxidation, the production of
phosphine becomes a necessary test to make on failure of Mitscherlich’s
test; if no result follows the proper application of the two processes,
the probability is that phosphorus has not been taken.

Blondlot and Dusart evolve hydrogen from zinc and dilute sulphuric acid,
and pass the gas into silver nitrate; if the gas is pure, there is of
course no reduction; the liquid to be tested is then added to the
hydrogen-generating liquid, and if phosphorous or hypophosphorous acids
be present, a black precipitate of phosphor-silver will be produced. To
prove that this black precipitate is neither that produced by SH₂, nor
by antimony nor arsenic, the precipitate is collected and placed in the
apparatus to be presently described, and the spectroscopic appearances
of the phosphine flame observed.

3. =Tests Dependent on the Combustion of Phosphine= (PH₃).--A hydrogen
flame, containing only a minute trace of phosphorus, or of the lower
products of its oxidation, acquires a beautiful green tint, and
possesses a characteristic _spectrum_. In order to obtain the latter in
its best form, the amount of phosphine must not be too large, or the
flame will become whitish and livid, and the bands lose their defined
character, rendering the spectrum continuous. Again, the orifice of the
tube whence the gas escapes must not be too small; and the best result
is obtained when the flame is cooled.

M. Salet has proposed two excellent methods for the observation of
phosphine by the spectroscope:--

(1) He projects the phosphorus-flame on a plane vertical surface,
maintained constantly cold by means of a thin layer of running water;
the green colour is especially produced in the neighbourhood of the cool

(2) At the level of the base of the flame, there is an annular space,
through which a stream of cold air is continually blown upwards. Thus
cooled, the light is very pronounced, and the band δ, which is almost
invisible in the ordinary method of examination, is plainly seen.[318]

[318] Consult _Spectres Lumineux_, par M. Lecoq de Boisbaudran, Paris,
1874. See also Christofle and Beilstrom’s “Abhandlung,” in _Fresenius’
Zeitschr. f. anal. Chem._, B. 2, p. 465, and B. 3, p. 147.

An apparatus (devised by Blondlot, and improved by Fresenius) for the
production of the phosphine flame in medico-legal research, is
represented in the following diagram:--


Several of the details of this apparatus may be modified at the
convenience of the operator. A is a vessel containing sulphuric acid; B
is partly filled with granulated zinc, and hydrogen may be developed at
pleasure; _c_ contains a solution of nitrate of silver; _d_ is a tube at
which the gas can be lit; _e_, a flask containing the fluid to be
tested, and provided with a tube _f_, at which also the gas issuing can
be ignited. The orifice should be provided with a platinum nozzle. When
the hydrogen has displaced the air, both tubes are lit, and the two
flames, being side by side, can be compared. Should any phosphorus come
over from the zinc (a possibility which the interposed silver nitrate
ought to guard against), it is detected; the last flask is now gently
warmed, and if the flame is green, or, indeed, in any case, it should be
examined by the spectroscope.[319]

[319] F. Selmi has proposed the simple dipping of a platinum loop into a
liquid containing phosphoric acid, and then inserting it into the tip of
a hydrogen flame.

§ 297. The spectrum, when fully developed, shows one band in the orange
and yellow between C and D, but very close to D, and several bands in
the green. But the bands δ, γ, α, and β are the most characteristic. The
band δ has its centre about the wave-length 599·4; it is easily
distinguished when the slit of the spectroscope is a little wide, but
may be invisible if the slit is too narrow. It is best seen by M.
Salet’s second process, and, when cooled by a brisk current of air, it
broadens, and may extend closer to D. The band γ has a somewhat decided
border towards E, while it is nebulous towards D, and it is, therefore,
very difficult to say where it begins or where it ends; its centre may,
however, be put at very near 109 of Boisbaudran’s scale, corresponding
to W. L. 560·5, if the flame is free. This band is more distinct than β,
but with a strong current of air the reverse is the case. The middle of
the important band α is nearly marked by Fraunhofer’s line E.
Boisbaudran gives it as coinciding with 122 of his scale W. L. 526·3. In
ordinary conditions (that is, with a free uncooled flame) this is the
brightest and most marked of all the bands. The approximate middle of
the band β is W. L. 510·6 (Boisbaudran’s scale 129·00).

=Lipowitz’s Sulphur Test.=--Sulphur has the peculiar property of
condensing phosphorus on its surface, and of this Lipowitz proposed to
take advantage. Pieces of sulphur are digested some time with the liquid
under research, subsequently removed, and slightly dried. When examined
in the dark, should phosphorus be present, they gleam strongly if rubbed
with the finger, and develop a phosphorus odour. The test is wanting in
delicacy, nor can it well be made quantitative; it has, however, an
advantage in certain cases, _e.g._, the detection of phosphorus in an
alcoholic liquid.

Scherer’s test, as modified by Hager,[320] is a very delicate and
almost decisive test. The substances to be examined are placed in a
flask with a little lead acetate (to prevent the possibility of any
hydric sulphide being evolved), some ether added, and a strip of
filter-paper soaked in a solution of silver nitrate is then suspended in
the flask; this is conveniently done by making a slit in the bottom of
the cork, and in the slit securing the paper. The closed flask is placed
in the dark, and if phosphorus is present, in a few minutes there is a
black stain. It may be objected that arsine will cause a similar
staining, but then arsine could hardly be developed under the
circumstances given. It is scarcely necessary to observe that the paper
must be wet.

[320] _Pharm. Central-halle_, 20, 353.

§ 298. =Chemical Examination of the Urine.=--It may be desirable, in any
case of suspected phosphorus poisoning, to examine the renal secretion
for leucin and tyrosin, &c. Leucin may be found as a deposit in the
urine. Its general appearance is that of little oval or round discs,
looking like drops of fat. It can be recognised by taking up one or more
of these little bodies and placing them in the author’s subliming cell
(see § 314). By careful heating it will sublime wholly on to the upper
cover. On now adding a little nitric acid to the sublimed leucin, and
drying, and then to the dried residue adding a droplet of a solution of
sodium hydrate, leucin forms an oily drop. Tyrosin also may occur as a
sediment of little heaps of fine needles. The best test for tyrosin is
to dissolve in hot water, and then add a drop of a solution of mercuric
nitrate and mercurous nitrate, when a rose colour is at once developed,
if the tyrosin is in very minute quantity; but if in more than traces,
there is a distinct crimson precipitate. To separate leucin and tyrosin
from the urine, the best process is as follows:--The urine is filtered
from any deposit, evaporated to a thin syrup, and decanted from the
second deposit that forms. The two deposits are mixed together and
treated with dilute ammonia, which will dissolve out any tyrosin and
leave it in needles, if the ammonia is spontaneously evaporated on a
watch-glass. The urine is then diluted and treated with neutral and
basic acetates of lead, filtered, and the lead thrown out of the
filtrate by hydric sulphide. The filtrate is evaporated to a syrup, and
it then deposits leucin mixed with some tyrosin. If, however, the syrup
refuses to crystallise, it is treated with cold absolute alcohol, and
filtered, the residue is then boiled up with spirit of wine, which
extracts leucin, and deposits it on cooling in a crystalline form. To
obtain oxymandelic acid, the mother liquor, from which leucin and
tyrosin have been extracted, is precipitated with absolute alcohol,
filtered, and then the alcoholic solution evaporated to a syrup. This
syrup is acidified by sulphuric acid, and extracted with ether; the
ether is filtered off and evaporated to dryness; the dry residue will be
in the form of oily drops and crystals. The crystals are collected,
dissolved in water, and the solution precipitated by lead acetate to
remove colouring-matters; after filtration it is finally precipitated
by basic acetate. On decomposition of the basic acetate, by suspending
in water and saturating with hydric sulphide, the ultimate filtrate on
evaporation deposits colourless, flexible needles of oxymandelic acid.
The nitrogenised acid which Schultzen and Riess obtained from urine in a
case of phosphorus poisoning, was found in an alcohol and ether
extract--warts of rhombic scales separating out of the syrupy residue.
These scales gave no precipitate with basic acetate, but formed a
compound with silver nitrate. The silver compound was in the form of
shining white needles, and contained 33·9 per cent. of silver; the acid
was decomposed by heat, and with lime yielded aniline. Its melting-point
is given at from 184° to 185°. The occurrence of some volatile substance
in phosphorus urine, which blackens nitrate of silver, and which is
probably phosphine, was first noticed by Selmi.[321] Pesci and Stroppa
have confirmed Selmi’s researches. It is even given off in the cold.

[321] _Giornale Internaz. della Scienza Med._, 1879, Nro. 5, p. 645.

§ 299. =The quantitative estimation of phosphorus= is best carried out
by oxidising it into phosphoric acid, and estimating as ammon. magnesian
phosphate. To effect this, the substances are distilled in an atmosphere
of CO₂ into a flask with water, to which a tube containing silver
nitrate is attached; the latter retains all phosphine, the former solid
phosphorus. If necessary, the distillate may be again distilled into
AgNO₃; and in any case the contents of the [U]-tube and flask are mixed,
oxidised with nitromuriatic acid, filtered from silver chloride, and the
phosphoric acid determined in the usual way.

In the case of a child poisoned by lucifer matches, Sonnenschein
estimated the free phosphorus in the following way:--The contents of the
stomach were diluted with water, a measured part filtered, and the
phosphoric acid estimated. The other portion was then oxidised by HCl
and potassic chlorate, and the phosphoric acid estimated--the difference
being calculated as free phosphorus.

§ 300. =How long can Phosphorus be recognised after Death?=--One of the
most important matters for consideration is the time after death in
which free phosphorus, or free phosphoric acids, can be detected. Any
phosphorus changed into ammon. mag. phosphate, or into any other salt,
is for medico-legal purposes entirely lost, since the expert can only
take cognisance of the substance either in a free state, as phosphine,
or as a free acid.

The question, again, may be asked in court--Does the decomposition of
animal substances rich in phosphorus develop phosphine? The answer to
this is, that no such reaction has been observed.

A case is related[322] in which phosphorus was recognised, although the
body had been buried for several weeks and then exhumed.

[322] _Pharm. Zeitsch. f. Russl._, Jahrg. 2, p. 87.

The expert of pharmacy of the Provincial Government Board of Breslau has
also made some experiments in this direction, which are worthy of
note:--Four guinea-pigs were poisoned, each by 0·023 grm. of phosphorus;
they died in a few hours, and were buried in sandy-loam soil, 0·5 metre
deep. Exhumation of the first took place four weeks after. The
putrefying organs--heart, liver, spleen, stomach, and all the
intestines--tested by Mitscherlich’s method of distillation, showed
characteristic phosphorescence for nearly one hour.

The second animal was exhumed after eight weeks in a highly putrescent
state. Its entrails, on distillation, showed the phosphorescent
appearance for thirty-five minutes.

The third animal was taken from the earth after twelve weeks, but no
free phosphorus could be detected, although there was evidence of the
lower form of oxidation (PO₃) by Blondlot’s method.

The fourth animal was exhumed after fifteen weeks, but neither free
phosphorus nor PO₃ could be detected.[323]

[323] _Vierteljahrsschrift für gerichtliche Medicin_, Jan. 7, 1876; see
also _Zeitschr. f. anal. Chemie_, 1872.

A man, as well as a cat, was poisoned by phosphorus. On analysis,
twenty-nine days after death, negative results were alone

It will thus be evident that there is no constant rule, and that, even
when decomposition is much advanced, an examination _may_ be



I.--General Methods of Testing and Extracting Alkaloids.

§ 301. =General Tests for Alkaloids.=--In order to ascertain whether an
alkaloid is present or not, a method of extraction must be pursued
which, while disposing of fatty matters, salts, &c., shall dissolve as
little as possible of foreign substances--such a method, _e.g._, as the
original process of Stas, or one of its modern modifications.

If to the acid aqueous solution finally obtained by this method a dilute
solution of soda be added, drop by drop, until it is rendered feebly
alkaline, _and no precipitate appear_, whatever other poisonous
plant-constituents may be present, all ordinary alkaloids[324] are

[324] In the case of morphine tartrate, this test will not answer. See
the article on Morphine.

In addition to this negative test, there are also a number of substances
which give well-marked crystalline or amorphous precipitates with

§ 302. These may be called “group reagents.” The chief members of the
group-reagents are--Iodine dissolved in hydriodic acid, iodine dissolved
in potassic iodide solution, bromine dissolved in potassic bromide
solution, hydrargo-potassic iodide, bismuth-potassic iodide, cadmic
potassic iodide; the chlorides of gold, of platinum, and mercury; picric
acid, gallic acid, tannin, chromate of potash, bichromate of potash,
phospho-molybdic acid, phospho-tungstic acid, silico-tungstic acid, and
Fröhde’s reagent. It will be useful to make a few general remarks on
some of these reagents.

=Iodine in hydriodic acid= gives either crystalline or amorphous
precipitates with nearly all alkaloids; the compound with morphine, for
example, is in very definite needles; with dilute solutions of
atropine, the precipitate is in the form of minute dots, but the
majority of the precipitates are amorphous, and all are more or less

=Iodine dissolved in a solution of potassic iodide= gives with alkaloids
a reddish or red-brown precipitate, and this in perhaps a greater
dilution than almost any reagent. When added to an aqueous solution, the
precipitates are amorphous, but if added to an alcoholic solution,
certain alkaloids then form crystalline precipitates; this, for example,
is the case with berberine and narceine. By treating the precipitate
with aqueous sulphurous acid, a sulphate of the alkaloid is formed and
hydriodic acid, so that by suitable operations the alkaloid may readily
be recovered from this compound. A solution of bromine in potassic
bromide solution also gives similar precipitates to the above, but it
forms insoluble compounds with phenol, orcin, and other substances.

=Mercuric potassic iodide= is prepared by decomposing mercuric chloride
with potassic iodide in excess. The proportions are 13·546 grms. of
mercuric chloride and 49·8 of potassic iodide, and water sufficient to
measure, when dissolved, 1 litre. The precipitates from this reagent are
white and flocculent; many of them become, on standing, crystalline.

=Bismuthic potassic iodide= in solution precipitates alkaloids, and the
compounds formed are of great insolubility, but it also forms compounds
with the various albuminoid bodies.

=Chloride of gold= forms with the alkaloids compounds, many of which are
crystalline, and most admit of utilisation for quantitative
determinations. Chloride of gold does not precipitate amides or ammonium
compounds, and on this account its value is great. The precipitates are
yellow, and after a while are partly decomposed, when the colour is of a

=Platinic chloride= also forms precipitates with most of the alkaloids,
but since it also precipitates ammonia and potassic salts, it is
inferior to gold chloride in utility.

§ 303. (1.) =Phosphomolybdic Acid as a Reagent for
Alkaloids.=--_Preparation_; Molybdate of ammonia is precipitated by
phosphate of soda; and the well-washed yellow precipitate is suspended
in water and warmed with carbonate of soda, until it is entirely
dissolved. This solution is evaporated to dryness, and the ammonia fully
expelled by heating. If the molybdic acid is fairly reduced by this
means, it is to be moistened by nitric acid, and the heating repeated.
The now dry residue is warmed with water, nitric acid added to strong
acid reaction, and the mixture diluted with water, so that 10 parts of
the solution contain 1 of the dry salt. The precipitates of the
alkaloids are as follows:--

  Aniline,                 Bright-yellow, flocculent.
  Morphine,                      „             „
  Narcotine,               Brownish-yellow,    „
  Quinine,                 Whitish-yellow,     „
  Cinchonine,                    „             „
  Codeine,                 Brownish-yellow, voluminous.
  Strychnine,              White-yellow,        „
  Brucine,                 Yelk-yellow, flocculent.
  Veratrine,               Bright-yellow,    „
  Jervine,                       „           „
  Aconitine,                     „           „
  Emetine,                       „           „
  Theine,                  Bright-yellow, voluminous.
  Theobromine,                   „             „
  Solanine,                Citron-yellow, pulverulent.
  Atropine,                Bright-yellow, flocculent.
  Hyoscyamine,                   „             „
  Colchicine,              Orange-yellow,      „
  Delphinine,              Grey-yellow, voluminous.
  Berberine,               Dirty-yellow, flocculent.
  Coniine,                 Bright-yellow, voluminous.
  Nicotine,                      „            „
  Piperine,                Brownish-yellow, flocculent.

(2.) =Silico-Tungstic Acid as a Reagent for Alkaloids.=--Sodium
tungstate is boiled with freshly precipitated gelatinous silica. To the
solution is added mercurous nitrate, which precipitates the yellow
mercurous silico-tungstate. This is filtered, well-washed, and
decomposed by an equivalent quantity of hydrochloric acid;
silico-tungstic acid then goes into solution, and mercurous chloride
(calomel) remains behind. The clear filtrate is evaporated to drive off
the excess of hydrochloric acid, and furnishes, on spontaneous
evaporation, large, shining, colourless octahedra of silico-tungstic
acid, which effloresce in the air, melt at 36°, and are easily soluble
in water or alcohol.

This agent produces no insoluble precipitate with any metallic salt.
Cæsium and rubidium salts, even in dilute solutions, are precipitated by
it; neutral solutions of ammonium chloride give with it a white
precipitate, soluble with difficulty in large quantities of water. It
precipitates solutions of the salts of quinine, cinchonine, morphine,
atropine, &c.; if in extremely dilute solution, an opalescence only is
produced: for instance, it has been observed that cinchonine
hydrochlorate in 1/200000, quinia hydrochlorate in 1/20000,
morphia hydrochlorate in 1/15285 dilution, all gave a distinct
opalescence.--_Archiv der Pharm._, Nov., Dr. Richard Godeffroy.

(3.) =Scheibler’s Method for Alkaloids: Phospho-Tungstic
Acid.=--Ordinary commercial sodium tungstate is digested with half its
weight of phosphoric acid, specific gravity 1·13, and the whole allowed
to stand for some days, when the acid separates in crystals. A solution
of these crystals will give a distinct precipitate with the most minute
quantities of alkaloids, 1/200000 of strychnine, and 1/100000 of
quinine. The alkaloid is liberated by digestion with barium hydrate (or
calcium hydrate); and if volatile, may be distilled off, if fixed,
dissolved out by chloroform. In complex mixtures, colouring-matter may
be removed by plumbic acetate, the lead thrown out by SH₂, and
concentrated, so as to remove the excess of SH₂.

§ 304. =Schulze’s reagent= is phospho-antimonic acid. It is prepared by
dropping a strong solution of antimony trichloride into a saturated
solution of sodic phosphate. The precipitation of the alkaloids is
effected by this reagent in a sulphuric acid solution.

§ 305. =Dragendorff’s reagent= is a solution of potass-bismuth iodide;
it is prepared by dissolving bismuth iodide in a hot solution of
potassium iodide, and then diluting with an equal volume of iodide of
potassium solution. On the addition of an acid solution of an alkaloid,
a kermes-red precipitate falls down, which is in many cases crystalline.

=Marm’s reagent= is a solution of potass-cadmium iodide. It is made on
similar principles.

=Potass-zinc iodide= in solution is also made similarly. The
precipitates produced in solutions of narceine and codeine are
crystalline and very characteristic.

§ 306. =Colour Tests.=--=Fröhde’s reagent= is made by dissolving 1 part
of sodic molybdate in 10 parts of strong sulphuric acid; it strikes
distinctive colours with many alkaloids.

=Mandelin’s reagent= is a solution of meta-vanadate of ammonia in mono-
or dihydrated sulphuric acid. The strength should be 1 part of the salt
to 200 of the acid. This reagent strikes a colour with many alkaloids,
and aids to their identification. It is specially useful to supplement
and correct other tests. The following table gives the chief colour
reactions, with the alkaloids. (See also p. 55 for the spectroscopic
appearances of certain of the colour tests.)


§ 307. =Stas’s Process.=--The original method of Stas[325] (afterwards
modified by Otto)[326] consisted in extraction of the organic matters by
strong alcohol, with the addition of tartaric acid; the filtered
solution was then carefully neutralised with soda, and shaken up with
ether, the ethereal solution being separated by a pipette. Subsequent
chemists proposed chloroform instead of ether,[327] the additional use
of amyl-alcohol,[328] and the substitution of acetic, hydrochloric, and
sulphuric for tartaric acid.

[325] _Annal d. Chem. u. Pharm._, 84, 379.

[326] _Ib._, 100, 44. _Anleitung zur Ausmittel. d. Gifte._

[327] Rodgers and Girwood, _Pharm. Journ. and Trans._, xvi. 497;
Prollin’s _Chem. Centralb._, 1857, 231; Thomas, _Zeitschr. für analyt.
Chem._, i. 517, &c.

[328] Erdmann and v. Ushlar, _Ann. Chem. Pharm._, cxx. pp. 121-360.


[329] Caustic potash also gives characteristic colours with certain
alkaloids. Out of seventy-two alkaloids (using 0·5 mgrm.), the following
alone gave characteristic colours when fused with KHO:--Quinine,
grass-green, and peculiar odour; quinidine, becoming yellower and
finally brown; cinchonine, at first brownish-red to violet, with green
edges, later, bluish-green; cinchonidine, blue passing into grey;
cocaine, greenish-yellow, turning to blue, and then dirty red on strong
heating.--W. Lenz, _Zeit. f. anal. Chem._, 25, 29-32.

  |  Name of  |Strong Sulphuric | Fröhde’s Reagent.|Mandelin’s Reagent.|
  |Substance. |     Acid.       |                  |                   |
  |           |                 |                  |                   |
  |Strychnine.|       ...       |        ...       |Violet-blue, then  |
  |           |                 |                  |lastly cinnabar-   |
  |           |                 |                  |red.               |
  |           |                 |                  |                   |
  |Brucine.   |Pale red.        |Red, then yellow. |Yellow-red to      |
  |           |                 |                  |orange, afterwards |
  |           |                 |                  |blood-red.         |
  |           |                 |                  |                   |
  |Curarine.  |Fine red.        |        ...       |        ...        |
  |           |                 |                  |                   |
  |Quinine.   |       ...       |Greenish.         |Weak orange, then  |
  |           |                 |                  |blue-green, lastly |
  |           |                 |                  |green-brown.       |
  |           |                 |                  |                   |
  |Atropine.  |       ...       |        ...       |Red, then yellow-  |
  |           |                 |                  |red, and lastly    |
  |           |                 |                  |yellow.            |
  |           |                 |                  |                   |
  |Aconitine. |       ...       |        ...       |         ...       |
  |           |                 |                  |                   |
  |Veratrine. |Yellow, then     |Gamboge-yellow,   |Yellow, orange,    |
  |           |orange, blood-   |then cherry-red.  |blood-red, lastly  |
  |           |red, lastly      |                  |carmine-red.       |
  |           |carmine-red.     |                  |                   |
  |           |                 |                  |                   |
  |Morphine.  |       ...       |Violet, green,    |Reddish, then      |
  |           |                 |blue-green, and   |blue-violet.       |
  |           |                 |yellow.           |                   |
  |           |                 |                  |                   |
  |Narcotine. |Yellow, then     |Green, then brown-|Cinnabar-red, then |
  |           |raspberry colour.|green, yellow,    |carmine-red.       |
  |           |                 |lastly red.       |                   |
  |           |                 |                  |                   |
  |Codeine.   |        ...      |Dirty green, then |Green-blue to blue.|
  |           |                 |blue, lastly      |                   |
  |           |                 |yellow.           |                   |
  |           |                 |                  |                   |
  |Papaverine.|        ...      |Green, then blue- |Blue-green to blue.|
  |           |                 |violet, lastly    |                   |
  |           |                 |cherry-red.       |                   |
  |           |                 |                  |                   |
  |Thebaine.  |Blood-red, then  |Orange, then      |Red to orange.     |
  |           |yellow-red.      |colourless.       |                   |
  |           |                 |                  |                   |
  |Narceine.  |Grey-brown, then |Brown, green, red,|Violet, then       |
  |           |blood-red.       |lastly blue.      |orange.            |
  |           |                 |                  |                   |
  |Nicotine.  |        ...      |Yellowish, then   |Transitory dark    |
  |           |                 |red.              |colour.            |
  |           |                 |                  |                   |
  |Coniine.   |        ...      |Yellow.           |        ...        |
  |           |                 |                  |                   |
  |Colchicine.|Intense yellow.  |Yellow to         |Blue-green, then   |
  |           |                 |green-yellow.     |brown.             |
  |           |                 |                  |                   |
  |Delphini-  |Red.             |Red-brown.        |Red-brown to brown.|
  |dine.      |                 |                  |                   |
  |           |                 |                  |                   |
  |Solanine.  |Red-yellow, then |Cherry-red,       |Yellow-orange,     |
  |           |brown.           |red-brown, yellow,|cherry-red, and    |
  |           |                 |yellow-green.     |lastly violet.     |

§ 308. =Selmi’s Process for Separating Alkaloids.=--A method of
separating alkaloids from an ethereal solution has been proposed by
Selmi.[330] The alcoholic extract of the viscera, acidified and
filtered, is evaporated at 65°; the residue taken up with water,
filtered, and decolorised by basic acetate of lead. The lead is thrown
out by sulphuretted hydrogen; the solution, after concentration,
repeatedly extracted with ether; and the ethereal solution saturated
with dry CO₂, which generally precipitates some of the alkaloids. The
ethereal solution is then poured into clean vessels, and mixed with
about half its volume of water, through which a current of CO₂ is passed
for twenty minutes; this may cause the precipitation of other alkaloids
not thrown down by dry CO₂. If the whole of the alkaloids are not
obtained by these means, the solution is dehydrated by agitation with
barium oxide, and a solution of tartaric acid in ether is added (care
being taken to avoid excess); this throws down any alkaloid still
present. The detection of any yet remaining in the viscera is effected
by mixing with barium hydrate and a little water, and agitating with
_purified_ amylic alcohol; from the alcohol the alkaloids may be
subsequently extracted by agitation with very dilute sulphuric acid.

[330] F. Selmi, _Gazett. Chim. Ital._, vj. 153-166, and _Journ. Chem.
Soc._, i., 1877, 93.

Another ingenious method (also the suggestion of Selmi) is to treat the
organic substance with alcohol, to which a little sulphuric acid has
been added, to filter, digest with alcohol, and refilter. The filtrates
are united, evaporated down to a smaller bulk, filtered, concentrated to
a syrup, alkalised by barium hydrate, and, after the addition of freshly
ignited barium oxide and some powdered glass, exhausted with dry ether;
the ether filtered, the filtrate digested with lead hydrate; the
ethereal solution filtered, evaporated to dryness, and finally again
taken up with ether, which, this time, should leave on evaporation the
alkaloid almost pure.

§ 309. =Dragendorff’s Process.=--To Dragendorff we owe an elaborate
general method of separation, since it is applicable not only to
alkaloids, but to glucosides, and other active principles derived from
plants. His process is essentially a combination of those already known,
and its distinctive features are the shaking up--(1) of the acid fluid
with the solvent, thus removing colouring matters and certain
non-alkaloidal principles; and (2) of the same fluid made alkaline. The
following is his method in full. It may be advantageously used when the
analyst has to search generally for vegetable poison, although it is, of
course, far too elaborate for every case; and where, from any
circumstance, there is good ground for suspecting the presence of one or
two particular alkaloids or poisons, the process may be much shortened
and modified.[331]

[331] Dragendorff’s _Gerichtlich-chemische Ermittelung von Giften_, St.
Petersburg, 1876, p. 141.

I. The substance, in as finely-divided form as possible, is digested for
a few hours in water acidified with sulphuric acid, at a temperature of
40° to 50°, and this operation is repeated two or three times, with
filtering and pressing of the substances; later, the extracts are
united. This treatment (if the temperature mentioned is not exceeded)
does not decompose the majority of alkaloids or other active substances;
but there are a few (_e.g._, solanine and colchicine) which would be
altered by it; and, if such are suspected, maceration at the common
temperature is necessary, with substitution of acetic for sulphuric

[332] When blood is to be examined, it is better to dry it, and then
powder and extract with water acidified with dilute sulphuric acid.
However, if the so-called volatile alkaloids are suspected, this
modification is to be omitted.

II. The extract is next evaporated until it begins to be of a syrupy
consistence; the residue mixed with three to four times its volume of
alcohol, macerated for twenty-four hours at about 34°, allowed to become
quite cool, and filtered from the foreign matters which have separated.
The residue is washed with alcohol of 70 per cent.

III. The filtrate is freed from alcohol by distillation, the watery
residue poured into a capacious flask, diluted (if necessary) with
water, and filtered. Acid as it is, it is extracted at the common
temperature, with frequent shaking, by freshly-rectified petroleum
ether; and, after the fluids have again separated, the petroleum ether
is removed, carrying with it certain impurities (colouring matter, &c.),
which are in this way advantageously displaced. By this operation
ethereal oils, carbolic acid, picric acid, &c., which have not been
distilled, besides piperin, may also be separated. The shaking up with
petroleum ether is repeated several times (as long as anything remains
to be dissolved), and the products are evaporated on several


                                                  with a powerful
                                                         _ethereal oil,
                                                    carbolic acid, &c._

  A. _It is yellowish_,   A. It is fixed.
  and with difficulty

  α. The crystals are     α. Concentrated sul-
  dissolved by concen-    phuric acid dissolves
  trated sulphuric        it immediately--
  acid, with the pro-     violet, and later
  duction of a clear      greenish-blue.
  yellow colour, pass-      _Constituents of the
  ing into brown and           black hellebore._

  β. The solution in sulphuric acid   β. It dissolves with a yellow
  remains yellow; potassic cyanide    colour, changing into fallow-
  and caustic potash colour it, on    brown.
  warming, blood-red.                    _Constituents of aconite plant
                      _Picric acid._  and products of the decomposition
                                                         of Aconitine._

      _Camphor and similar matters._                        _Capsicin._

It may be expected that the substances mentioned under the heads 1, 2,
and 3 will be, in general, fully obtained by degrees. This is not the
case, however, as regards piperin and picric acid.

IV. The watery fluid is now similarly shaken up with benzene, and the
benzene removed and evaporated. Should the evaporated residue show signs
of an alkaloid (and especially of theine), the watery fluid is treated
several times with a fresh mixture of benzene, till a little of the
last-obtained benzene extraction leaves on evaporation no residue. The
benzene extracts are now united, and washed by shaking with distilled
water; again separated and filtered, the greater part of the benzene
distilled from the filtrate, and the remainder of the fluid divided and
evaporated on several watch-glasses.

The evaporated residue may contain theine, colchicine, cubebin,
digitalin, cantharidin, colocynthin, elaterin, caryophylline, absinthin,
cascarillin, populin, santonin, &c., and traces of veratrine,
delphinine, physostigmine, and berberine.

A remnant of piperin and picric acid may remain from the previous
treatment with petroleum ether.


  1. IT IS CRYSTALLINE.               2. IT IS AMORPHOUS.

  CRYSTALS.                           RESIDUE.

  α. Sulphuric acid dissolves the     α. Sulphuric acid dissolves it at
  hair-like crystals without change   first yellow; the solution be-
  of colour; evaporation with chlo-   coming later red. Fröhde’s re-
  rine water, and subsequent treat-   agent does not colour it violet.
  ment with ammonia, gives a                                _Elaterin._
  murexide reaction.       _Theine._

  β. Sulphuric acid leaves the        β. Sulphuric acid dissolves red;
  rhombic crystals uncoloured. The    Fröhde’s reagent violet-red;[333]
  substance, taken up by oil, and     tannic acid does not precipitate.
  applied to the skin, produces a                            _Populin._
  blister.            _Cantharidin._

  γ. Sulphuric acid leaves the        γ. Sulphuric acid dissolves it
  scaly crystals at first un-         with a red colour; Fröhde’s
  coloured, then slowly develops a    reagent[334] a beautiful cherry-
  reddening. It does not blister.     red; tannic acid precipitates a
  Warm alcoholic potash-lye colours   yellowish-white.   _Colocynthin._
  it a transitory red.   _Santonin._

  δ. Sulphuric acid colours the       δ. Sulphuric acid colours it
  crystals almost black, whilst it    gradually a beautiful red, whilst
  takes itself a beautiful red        tannin does not precipitate.
  colour.                 _Cubebin._     _Constituents of the Pimento._


  α. _Piperin._                       α. Sulphuric acid dissolves it
                                      yellow; on the addition of nitric
                                      acid, this solution is green,
                                      quickly changing to blue and
                                      violet.             _Colchicine._

  β. _Picric Acid._                   β. Sulphuric acid dissolves with
                                      separation of a violet powder;
                                      caustic potash colours it red;
                                      sulphide of ammonia violet, and,
                                      by heating, indigo-blue.
                                                     _Chrysammic acid._

  γ. Caustic potash dissolves it
  purple.                 _Aloetin._

  CRYSTALS.                           which dissolves brown in concen-
                                      trated sulphuric acid; in
                                      Fröhde’s reagent, likewise, at
                                      first brown, then at the edge
                                      green, changing into blue-violet,
                                      and lastly violet.  _Constituents
                                           of wormwood, with absynthin,
                                          besides quassiin, menyanthin,
                                         ericolin, daphnin, cnicin, and

  α. Sulphuric acid dissolves it
  green-brown; bromine colours this
  solution red; dilution with water
  again green. The substance
  renders the heart-action of a
  frog slower.          _Digitalin._

  β. Sulphuric acid dissolves it
  orange, then brown, lastly red-
  violet. Nitric acid dissolves it
  yellow, and water separates as a
  jelly out of the latter solution.
  Sulphuric acid and bromine do not
  colour it red.        _Gratiolin._

  γ. Sulphuric acid dissolves it
  red-brown. Bromine produces in
  this solution red-violet
  stripes. It does not act on
  frogs.              _Cascarillin._

  solves it olive-green. The alcoholic solution gives with potassic
  iodide a colourless and green crystalline precipitate.    _Berberin._

[333] Fröhde’s reagent is described at page 239.

[334] Fröhde’s reagent is described at page 239.

V. As a complete exhaustion of the watery solution is not yet attained
by the benzene agency, another solvent is tried.


In chloroform the following substances are especially taken
up:--Theobromine, narceine, papaverine, cinchonine, jervine, besides
picrotoxin, syringin, digitalin, helleborin, convallamarin, saponin,
senegin, smilacin. Lastly, portions of the bodies named in Process IV.,
which benzene failed to extract entirely, enter into solution, as well
as traces of brucine, narcotine, physostigmine, veratrine, delphinine.
The evaporation of the chloroform is conducted at the ordinary
temperature in four or five watch-glasses.


[335] Chloroform removes small portions of acetate of aconitine from
acid solution, Dunstan and Umney, _J. C. S._, 1892, p. 338.


  A. _It gives in the sulphuric       A. _In acetic acid solution it
  acid solution evidence of an        renders the action of the frog’s
  alkaloid by its action towards      heart slower, or produces local
  iodine and iodide of potassium._    anæsthesia._

                                      _aa_. It does not produce local

  α. Sulphuric acid dissolves it      α. Sulphuric acid dissolves it
  without the production of colour,   red-brown, bromine produces a
  and chlorine and ammonia give no    beautiful purple colour, water
  murexide reaction.   _Cinchonine._  changes it into green, hydro-
                                      chloric acid dissolves it
                                      greenish-brown.      _Digitalin._

  β. Sulphuric acid dissolves it      β. Sulphuric acid dissolves it
  without colour, chlorine and        yellow, then brown-red; on ad-
  ammonia give, as with theine, a     dition of water this solution be-
  murexide reaction.  _Theobromine._  comes violet. Hydrochloric acid,
                                      on warming, dissolves it red.

                                      _bb_. It produces local anæsthe-

                                      α. Sulphuric acid dissolves it
                                      brown. The solution becomes, by
                                      extracting with water, violet,
                                      and can even be diluted with two
                                      volumes of water without losing
                                      its colour.            _Saponin._

                                      β. Sulphuric acid dissolves it
                                      yellow. On diluting with water
                                      the same reaction occurs as in
                                      the previous case, but more
                                      feebly.                _Senegin._

  γ. Sulphuric acid does not colour   γ. Sulphuric acid dissolves
  in the cold; on warming, the        brown, and the solution becomes
  solution becomes a blue violet.     red by the addition of a little
                       _Papaverine._  water. The action is very weak.

                                      _cc_. Sulphuric acid dissolves it
                                      with the production of a dirty
                                      red, hydrochloric acid, in the
                                      cold, with that of a reddish-
                                      brown colour, and the last solu-
                                      tion becomes brown on boiling.
                                        _Constituents of the hellebore,
                                                 particularly Jervine._

  δ. Sulphuric acid dissolves it in
  the cold with the production of a
  blue colour.  _Unknown impurities,
          many commercial samples of

  ε. Sulphuric acid dissolves it at
  first grey-brown; the solution
  becomes in about twenty-four
  hours blood-red. Iodine water
  colours it blue.       _Narceine._

  B. IT GIVES NO ALKALOID REACTION.   B. Is inactive, and becomes blue
                                      by sulphuric acid; by Fröhde’s
                                      reagent[336] dark cherry-red.
                                      Hydrochloric acid dissolves it
                                      red. The solution becomes, by
                                      boiling, colourless.  _Syringin._

  α. Sulphuric acid dissolves it
  with a beautiful yellow colour;
  mixed with nitre, then moistened
  with sulphuric acid, and lastly
  treated with concentrated soda-
  lye, it is coloured a brick-red.

  β. Sulphuric acid dissolves it
  with the production of a splendid
  red colour. The substance renders
  the heart-action of a frog slower.

[336] Described at p. 239.


in order to take up the rest of the chloroform, and the watery fluid is
saturated with ammonia. The watery solution of _aconitine_ and _emetine_
is liable to undergo, through free ammonia, a partial decomposition;
but, on the other hand, it is quite possible to obtain, with very small
mixtures of the substances, satisfactory reactions, even out of
ammoniacal solutions.


In the earlier stages Dragendorff advises the shaking up with petroleum
ether at about 40°, and the removal of the ether as quickly as possible
whilst warm. This is with the intention of separating by this fluid
strychnine, brucine, emetine, quinine, veratrine, &c. Finding, however,
that a full extraction by petroleum ether is either difficult or not
practicable, he prefers, as we have seen, to conclude the operation by
other agents, coming back again upon the ether for certain special
cases. Such are the volatile alkaloids; and here he recommends
treatment of the fluid by _cold_ petroleum ether, taking care _not_ to
hasten the removal of the latter. Strychnine and other fixed alkaloids
are then only taken up in small quantities, and the greater portion
remains for the later treatment of the watery fluid by benzene.

A portion of the petroleum ether, supposed to contain in solution
volatile alkaloids, is evaporated in two watch-glasses; to the one,
strong hydrochloric acid is added, the other being evaporated without
this agent. On the evaporation of the petroleum ether, it is seen
whether the first portion is crystalline or amorphous, or whether the
second leaves behind a strongly-smelling fluid mass, which denotes a
volatile alkaloid. If the residue in both glasses is without odour and
fixed, the absence of volatile acids and the presence of fixed
alkaloids, strychnine, emetine, veratrine, &c., are indicated.


  CRYSTALLINE.           AMORPHOUS.               ODOROUS.

  A. _The crystals are                            A. _On adding to the
  volatilised with                                watch-glass a little
  difficulty._                                    hydrochloric acid,
                                                  crystals are left

  _aa._ Sulphuric acid                            _aa._ Its solution is
  dissolves it without                            not precipitated by
  colour.                                         platin chloride.

  α. Potassic chromate   α. The purest sulphuric  α. The crystals of the
  colours this solution  acid dissolves it        hydrochloric compound
  a transitory blue,     almost without colour;   act on polarised
  then red.              sulphuric acid con-      light; and are mostly
          _Strychnine._  taining nitric acid,     needle-shaped and
                         red quickly becoming     columnar.    _Coniine
                         orange.                   and Methyl-Coniine._

  β. Potassic chromate   β. Sulphuric acid dis-   β. The crystals are
  does not colour it     solves it yellow,        cubical or tetra-
  blue; with chlorine    becoming deep red.       hedral.      _Alkaloid
  water and ammonia it              _Veratrine._         from Capsicum._
  gives a green colour.

                         γ. Sulphuric acid dis-
                         solves it brown-green;
                         Fröhde’s reagent red,
                         changing into green.

                                                  _bb_. The solution of
                                                  the hydrochlorate of
                                                  the alkaloid is pre-
                                                  cipitated by platin

  γ. Sulphuric acid                               B. The residue of the
  dissolves it yellow,                            hydrochlorate of the
  and the solution be-                            alkaloid is amor-
  comes gradually a                               phous, or, by further
  beautiful deep red.                             additions of HCl,
         _Sabadilline._                           becomes crystalline.

  δ. The crystals are
  easily volatilised.

                                                  _aa._ Its diluted
                                                  aqueous solution is
                                                  precipitated by
                                                  platin chloride.

                                                  α. The hydrochlorate
                                                  salt, being quickly
                                                  treated with Fröhde’s
                                                  reagent, gives after
                                                  about two minutes a
                                                  violet solution which
                                                  gradually fades.

                                                  β. The hydrochlorate
                                                  smells like nicotine,
                                                  and becomes by
                                                  Fröhde’s reagent
                                                  yellow, and after
                                                  twenty-four hours
                                                  pale red. _Nicotine._

                                                  γ. The hydrochlorate
                                                  is without odour, the
                                                  free base smells
                                                  faintly like aniline.

                                                  _bb._ The substance
                                                  is not precipitated
                                                  from a diluted solu-
                                                  tion by platin

                                                  α. Its petroleum
                                                  ether solution pro-
                                                  duces no turbidity
                                                  with a solution of
                                                  picric acid in petro-
                                                  leum ether; but it
                                                  leaves behind, when
                                                  mixed with the above,
                                                  crystals mostly of
                                                  three-sided plates.

                                                  β. The petroleum
                                                  ether solution gives,
                                                  on evaporation, when
                                                  treated similarly,
                                                  moss-like crystals.
                                                  The substance is made
                                                  blue by chloride of
                                                  lime, as well as by
                                                  diluted sulphuric
                                                  acid and bichromate
                                                  of potash. _Aniline._

                                                  γ. The alkaloid does
                                                  not smell like
                                                  methylamine, and is
                                                  not coloured by chlo-
                                                  ride of lime, sul-
                                                  phuric acid, or chro-
                                                  mate of potash.
                                                  _Volatile alkaloid of
                                                          the Pimento._


In most cases petroleum ether, benzene, and chloroform are more easily
separated from acid watery fluids than from ammoniacal, benzene and
chloroform causing here a difficulty which has perhaps deterred many
from using this method. Dragendorff, however, maintains that he has
never examined a fluid in which he could not obtain a complete
separation of the benzene and water. If the upper benzene layer is fully
gelatinous and emulsive, the under layer of water is to be removed with
a pipette as far as possible, and the benzene with a few drops of
absolute alcohol and filtration. As a rule, the water goes through first
alone, and by the time the greater part has run through, the jelly in
the filter, by dint of stirring, has become separated from the benzene,
and, finally, the jelly shrinks up to a minimum, and the clear benzene
filters off. Dragendorff filters mostly into a burette, from which
ultimately the benzene and the water are separated.

The principal alkaloids which are dissolved in benzene are--strychnine,
methyl and ethyl strychnine, brucine, emetine, quinine, cinchonine,
atropine, hyoscyamine, physostigmine, aconitine, nepalin, the alkaloid
of the _Aconitum lycoctonum_, aconellin, napellin, delphinine,
veratrine, sabatrin, sabadilline, codeine, thebaine, and narcotine.


  TALLINE.                            PHOUS.

  _a._ Sulphuric acid dissolves it    _a._ Pure sulphuric acid dis-
  without colour, the solution        solves it either whitish-red or
  being coloured neither on stand-    yellowish.
  ing nor on the addition of nitric

  _aa._ It dilates the pupil of a

  α. Platin chloride does not pre-    α. The solution becomes by nitric
  cipitate the aqueous solution.      acid immediately red, then quickly
  The sulphuric acid solution gives,  orange.                _Brucine._
  on warming, a peculiar smell.

  β. Platin chloride applied to the   β. The solution becomes by little
  solution precipitates.              and little brownish-red. The sub-
                     _Hyoscyamine._   stance is coloured red by chlo-
                                      ride of lime solution, and it
                                      contracts the pupil.

  _bb._ It does not dilate the

  α. The sulphuric acid solution
  becomes blue by chromate of

  αα. The substance applied to a
  frog produces tetanus.

  ββ. It lowers the number of res-
  pirations in a frog.    _Ethyl and
                 Methyl Strychnine._

  β. Sulphuric acid and bichromate
  of potash do not colour it blue.

  αα. The sulphuric acid watery so-
  lution is fluorescent, and be-
  comes green on the addition of
  chlorine water and ammonia.
           _Quinine and Cinchonine._

  (The last is more difficult to
  dissolve in petroleum ether than

  ββ. The solution is not fluores-
  cent.                _Cinchonine._

  _b._ Sulphuric acid dissolves it    _b._ Pure sulphuric acid dis-
  at first colourless; the solution   solves it yellow, and the solu-
  takes on standing a rose or         tion becomes later beautiful red
  violet-blue; on addition of         (with delphinine, more quickly a
  nitric acid, a blood-red or brown   darker cherry-red.)

  α. A solution in diluted sulphuric  α. The hydrochloric acid solution
  acid becomes, on heating, deep      gradually becomes red on heating.
  blood-red, and, when cooled,
  violet, with nitric acid. The
  aqueous solution is precipitated
  by ammonia.           _Narcotine._

                                      αα. The substance acts on a
                                      frog, causing, in large doses,
                                      tetanus.             _Veratrine._

                                      ββ. It is almost without action
                                      on frogs.             _Sabatrin._

  β. The solution in diluted sul-     β. The hydrochloric acid solution
  phuric acid becomes, on heating,    does not, on heating, become red.
  a beautiful blue. Excess of ammo-                       _Delphinine._
  nia does not precipitate in a
  diluted watery solution.

  _c._ Sulphuric acid dissolves it    _c._ Pure sulphuric acid dis-
  with the production of a yellow     solves it yellow, and the solu-
  colour.                             tion becomes later red-brown, and
                                      gradually violet-red.

  α. The solution remains yellow      α. The substance even in small
  on standing.          _Acolyctin._  doses paralyses frogs, and
                                      dilates the pupil of a cat’s eye.
                                      Ether dissolves it with diffi-
                                      culty.                 _Nepalin._

  β. It becomes beautifully red.      β. It is easily soluble in ether,
                      _Sabadilline._  its effects are not so marked,
                                      and it does not dilate the pupil.

                                      γ. Its effects are still feeble;
                                      it does not dilate the pupil, and
                                      is with difficulty dissolved by
                                      ether.                _Napellin._

  _d._ Sulphuric acid dissolves it    _d._ Sulphuric acid dissolves it
  with an immediate deep red-brown    with a dark green colour, and the
  colour.                _Thebaine._  solution becomes, even after a
                                      few seconds, a beautiful blood-
                                      red.   _Alkaloidal substances out
                                          of the  Aconitum lycoctonum._

  _e._ Sulphuric acid dissolves it    _e._  Sulphuric acid dissolves it
  immediately blue.      _Substances  brown-green, and Fröhde’s reagent
       accompanying the Papaverins._  red, becoming beautifully green.


This extracts the remainder of the cinchonine and papaverine, narceine,
and a small portion of morphine, as well as an alkaloid from the


  _aa._ The solution, on warming, is only slightly coloured.

  α. But, after it is again cooled, it strikes with nitric acid a
  violet-blue; chloride of iron mixed with the substance gives a blue
  colour; Fröhde’s reagent also dissolves it violet.        _Morphine._

  β. It is not coloured by nitric acid; it is also indifferent to
  chloride of iron.                                       _Cinchonine._

  _bb._ The solution becomes by warming violet-blue.      _Papaverine._

  γ. Sulphuric acid dissolves it greenish-brown, and the solution
  becomes, on standing, blood-red.                          _Narceine._

  δ. Sulphuric acid dissolves it a violet-blue. _Alkaloidal constituent
                                                     of the Celandine._


From this process, besides morphine and solanine, as well as salicin,
the remnants of the convallamarin, saponin, senegin, and narceine are
also to be expected.


  _a._ Sulphuric acid dissolves it without colour in the cold.
                                                _Morphine_ (see above).

  _b._ Sulphuric acid dissolves it with the production of a clear
  yellow-red and the solution becomes brownish. Iodine water colours it
  a deep brown. The alcoholic solution gelatinises.         _Solanine._

  _c._ Sulphuric acid dissolves it green-brown, becoming red.
                                                _Narceine_ (see above).

  _d._ Sulphuric acid dissolves it yellow, then brown-red, becoming
  violet on dilution with water. Hydrochloric acid dissolves it, and it
  becomes red on warming. It stops the heart-action in the systole.

  _e._ Hydrochloric acid dissolves it for the most part without colour.

  _f._ As the foregoing, but acting more feebly.             _Senegin._

  _g._ Sulphuric acid dissolves it immediately a pure red. On warming
  with sulphuric acid and bichromate of potash, a smell of salicylic
  acid is developed.                                         _Salicin._


The residue of the first chloroform extract lessens the number of
respirations of a frog; the residue of the second and third chloroform
extract becomes, by sulphuric acid and bichromate of potash, blue,
passing into a permanent red.

  Another portion of this residue becomes red on warming with diluted
  sulphuric acid.                                           _Curarine._


§ 310. A shorter process, recommended conditionally by Dragendorff, for
brucine, strychnine, quinine, cinchonine, and emetine, is as follows:--

The substance, if necessary, is finely divided, and treated with
sulphuric acid (dilute) until it has a marked acid reaction. To every
100 c.c. of the pulp (which has been diluted with distilled water to
admit of its being filtered later), at least 5 to 10 c.c. of diluted
sulphuric acid (1 : 5) are added. It is digested at 50° for a few hours,
filtered, and the residue treated again with 100 c.c. of water at 50°.
This extract is, after a few hours, again filtered; both the filtrates
are mixed and evaporated in the water-bath to almost the consistency of
a thin syrup. The fluid, however, must not be concentrated too much, or
fully evaporated to dryness. The residue is now placed in a flask, and
treated with three to four times its volume of alcohol of 90 to 95 per
cent.; the mixture is macerated for twenty-four hours, and then
filtered. The filtrate is distilled alcohol-free, or nearly so, but a
small amount of alcohol remaining is not objectionable. The watery fluid
is diluted to about 50 c.c., and treated with pure benzene; the mixture
is shaken, and after a little time the benzene removed--an operation
which is repeated. After the removal the second time of the benzene, the
watery fluid is made alkaline with ammonia, warmed to 40° or 50°, and
the free alkaloid extracted by twice shaking it up with two different
applications of benzene. On evaporation of the latter, if the alkaloid
is not left pure, it can be dissolved in acid, precipitated by ammonia,
and again extracted by benzene.

    § 311. =Scheibler’s Process=.--A method very different from those
    just described is one practised by Scheibler. This is to precipitate
    the phosphotungstate of the alkaloid, and then to liberate the
    latter by digesting the precipitate with either hydrate of barium or
    hydrate of calcium, dissolving it out by chloroform, or, if
    volatile, by simple distillation. The convenience of Scheibler’s
    process is great, and it admits of very general application. In
    complex mixtures, it will usually be found best to precede the
    addition of phosphotungstic acid[337] by that of acetate of lead, in
    order to remove colouring matter, &c.; the excess of lead must in
    its turn be thrown out by SH₂, and the excess of SH₂ be got rid of
    by evaporation. Phosphotungstic acid is a very delicate test for the
    alkaloids, giving a distinct precipitate with the most minute
    quantities (1/200000 of strychnine and 1/100000 of quinine). A very
    similar method is practised by Sonnenschein and others with the aid
    of phospho-molybdic acid. The details of Scheibler’s process are as

[337] The method of preparing this reagent is as follows:--Ordinary
commercial sodium tungstate is treated with half its weight of
phosphoric acid, specific gravity, 1·13, and then allowed to stand for
some days. Phosphotungstic acid separates in crystals.

    The organic mixture is repeatedly extracted by water strongly
    acidified with sulphuric acid; the extract is evaporated at 30° to
    the consistence of a thin syrup; then diluted with water, and, after
    several hours’ standing, filtered in a cool place. To the filtered
    fluid phosphotungstic acid is added in excess, the precipitate
    filtered, washed with water to which some phosphotungstic acid
    solution has been added, and, whilst still moist, rinsed into a
    flask. Caustic baryta or carbonate of potash is added to alkaline
    reaction, and after the flask has been connected with bulbs
    containing HCl, it is heated at first slowly, then more strongly.
    Ammonia and any volatile alkaloids are driven over into the acid,
    and are there fixed, and can be examined later by suitable methods.
    The residue in the flask is carefully evaporated to dryness (the
    excess of baryta having been precipitated by CO₂), and then
    extracted by strong alcohol. On evaporation of the alcohol, the
    alkaloid is generally sufficiently pure to be examined, or, if not
    so, it may be obtained pure by re-solution, &c.

The author has had considerable experience of Scheibler’s process, and
has used it in precipitating various animal fluids, but has generally
found the precipitate bulky and difficult to manage.

    § 312. =Grandval and Lajoux’s Method=.[338]--The alkaloids are
    precipitated from a solution slightly acidified by hydrochloric or
    sulphuric acid by a solution of hydrarg-potassium iodide. The
    precipitate is collected on a filter, washed and then transferred to
    a flask; drop by drop, a solution of sodium sulphide is added; after
    each addition the suspended precipitate is shaken and allowed to
    stand for a few minutes, and a drop of the liquid taken out and
    tested with lead acetate; directly a slight brown colour appears,
    sufficient sodic sulphide has been added. The liquid is now left for
    half-an-hour, with occasional shaking. Then sulphuric acid is added
    until it is just acid, and the liquid is filtered and the mercury
    sulphide well washed. In the filtrate will be the sulphate of any
    alkaloid in solution; this liquid is now made alkaline with soda
    carbonate and shaken up, as in Dragendorff’s process, with
    appropriate solvents; such, for example, as ether, or chloroform, or
    acetone, or amylic alcohol, according to the particular alkaloid the
    analyst is searching for, and the solvent finally separated and
    allowed to evaporate, when the alkaloid is found in the residue.

[338] “Dosage des alcaloides à l’aide de l’iodure double de mercure et
de potassium,” par MM. A. Grandval et Henri Lajoux, _Journ. de
Pharmacie_, 5 sér. t. xxviii. 152-156.

    § 313. =Identification of the Alkaloids=.--Having obtained, in one
    way or other, a crystalline or amorphous substance, supposed to be
    an alkaloid, or, at all events, an active vegetable principle, the
    next step is to identify it. If the tests given in Dragendorff’s
    process have been applied, the observer will have already gone a
    good way towards the identification of the substance; but it is, of
    course, dangerous to trust to one reaction.

    In medico-legal researches there is seldom any considerable quantity
    of the material to work upon. Hence the greatest care must be taken
    from the commencement not to waste the substance in useless tests,
    but to study well at the outset what--by the method of extraction
    used, the microscopic appearance, the reaction to litmus paper, and
    the solubility in different menstrua--it is likely to be. However
    minute the quantity may be, it is essential to divide it into
    different parts, in order to apply a variety of tests; but as any
    attempt to do this on the solid substance will probably entail loss,
    the best way is to dissolve it in a watch-glass in half a c.c. of
    alcohol, ether, or other suitable solvent. Droplets of this solution
    are then placed on watch-glasses or slips of microscopic glass, and
    to these drops, by the aid of a glass rod, different reagents can be
    applied, and the changes watched under the microscope as the drops
    slowly evaporate.

§ 314. =Sublimation of the Alkaloids.=--A very beautiful and elegant aid
to the identification of alkaloids, and vegetable principles generally,
is their behaviour towards heat.

Alkaloids, glucosides, the organic acids, &c., when carefully heated,
either--(1) sublime wholly without decomposition (like theine, cytisin,
and others); or (2) partially sublime with decomposition; or (3) are
changed into new bodies (as, for example, gallic acid); or (4) melt and
then char; or (5) simply char and burn away.

Many of these phenomena are striking and characteristic, taking place at
different temperatures, subliming in characteristic forms, or leaving
characteristic residues.

One of the first to employ sublimation systematically, as a means of
recognition of the alkaloids, &c., was Helwig.[339] His method was to
place a small quantity (from ½ to 1/4000 of a mgrm.) in a depression on
platinum foil, cover it with a slip of glass, and then carefully heat by
a small flame. After Helwig, Dr. Guy[340] greatly improved the process
by using porcelain discs, and more especially by the adoption of a
convenient apparatus, which may be termed “the subliming cell.” It is
essentially composed of a ring of glass from ⅛ to ⅔ of an inch in
thickness, such as may be obtained by sections of tubing, the cut
surfaces being ground perfectly smooth. This circle is converted into a
closed cell by resting it on one of the ordinary thin discs of glass
used as a covering for microscopic purposes, and supporting a similar
disc. The cell was placed on a brass plate, provided with a nipple,
which carried a thermometer, and was heated by a small flame applied
midway between the thermometer and the cell; the heat was raised very
gradually, and the temperature at which any change took place was noted.
In this way Dr. Guy made determinations of the subliming points of a
large number of substances, and the microscopic appearances of the
sublimates were described with the greatest fidelity and accuracy. On
repeating with care Dr. Guy’s determinations, however, I could in no
single instance agree with his subliming points, nor with the apparatus
he figures and describes could two consecutive observations exactly
coincide. Further, on examining the various subliming temperatures of
substances, as stated by different authors, the widest discrepancies
were found--differences of 2 or even 3 degrees might be referred to
errors of observation, a want of exact coincidence in the thermometers
employed, and the like; but to what, for example, can we ascribe the
irreconcilable statements which have been made with regard to theine?
According to Strauch, this substance sublimes at 177°; according to
Mulder, at 184·7°. But that both of these observations deviate more than
70° from the truth may be proved by any one who cares to place a few
mgrms. of theine, enclosed between two watch-glasses, over the
water-bath; in a few minutes a distinct sublimate will condense on the
upper glass, and, in point of fact, theine will be found to sublime
several degrees below 100°.

[339] _Das Mikroskop in der Toxicologie_.

[340] _Pharm. Journ. Trans_. (2), viij. 719; ix. 10, 58. _Forensic
Medicine_, London, 1875.

Since this great divergency of opinion is not found either in the
specific gravity, or the boiling-points, or any of the like
determinations of the physical properties of a substance, it is
self-evident that the processes hitherto used for the determination of
subliming points are faulty. The sources of error are chiefly--

(1.) Defects in the apparatus employed--the temperature read being
rather that of the metallic surface in the immediate vicinity of the
thermometer than of the substance itself.

(2.) The want of agreement among observers as to what should be called a
sublimate--one considering a sublimate only that which is evident to the
naked eye, another taking cognisance of the earliest microscopic film.

(3.) No two persons employing the same process.

With regard to the apparatus employed, I adopt Dr. Guy’s subliming cell;
but the cell, instead of resting on a metallic solid, floats on a
metallic fluid. For any temperature a little above 100° this fluid is
mercury, but for higher temperatures fusible metal is preferable.

[Illustration: SUBLIMING CELL.]

The exact procedure is as follows:--A porcelain crucible (_a_ in fig.),
about 3 inches in diameter, is nearly filled with mercury or fusible
metal, as the case may be; a minute speck (or two or three crystals of
the substance to be examined) is placed on a thin disc of microscopic
covering glass, floated on the liquid, and the cell is completed by the
glass ring and upper disc. The porcelain crucible is supported on a
brass plate (_b_), fixed to a retort-stand in the usual way, and
protected from the unequal cooling effects of currents of air by being
covered by a flask (_c_), from which the bottom has been removed. The
neck of the flask conveniently supports a thermometer, which passes
through a cork, and the bulb of the thermometer is immersed in the bath
of liquid metal. In the first examination of a substance the temperature
is raised somewhat rapidly, taking off the upper disc with a forceps at
every 10° and exchanging it for a fresh disc, until the substance is
destroyed. The second examination is conducted much more slowly, and the
discs exchanged at every 4° or 5°, whilst the final determination is
effected by raising the temperature with great caution, and exchanging
the discs at about the points of change (already partially determined)
at every half degree. All the discs are examined microscopically. The
most convenient definition of a sublimate is this--the most minute
films, dots, or crystals, which can be observed by ¼-inch power, and
which are obtained by keeping the subliming cell at a definite
temperature for 60 seconds. The commencement of many sublimates assumes
the shape of dots of extraordinary minuteness, quite invisible to the
unaided eye; and, on the other hand, since the practical value of
sublimation is mainly as an aid to other methods for the recognition of
substances, if we go beyond _short_ intervals of time, the operation,
otherwise simple and speedy, becomes cumbersome, and loses its general

There is also considerable discrepancy of statement with regard to the
melting-point of alkaloidal bodies; in many instances a viscous state
intervenes before the final complete resolution into fluid, and one
observer will consider the viscous state, the other complete fluidity,
as the melting-point.

In the melting-points given below, the same apparatus was used, but the
substance was simply placed on a thin disc of glass floating on the
metallic bath before described (the cell not being completed), and
examined from time to time microscopically, for by this means alone can
the first drops formed by the most minute and closely-adherent crystals
to the glass be discovered.

=Cocaine= melts at 93°, and gives a faint sublimate at 98°; if put
between two watch-glasses on the water-bath, in fifteen minutes there is
a good cloud on the upper glass.

=Aconitine= turns brown, and melts at 179° C.; it gives no
characteristic sublimate up to 190°.

=Morphine=, at 150°, clouds the upper disc with nebulæ; the nebulæ are
resolved by high magnifying powers into minute dots; these dots
gradually become coarser, and are generally converted into crystals at
188°; the alkaloid browns at or about 200°.

=Thebaine= sublimes in theine-like crystals at 135°; at higher
temperatures (160° to 200°), needles, cubes, and prisms are observed.
The residue on the lower disc, if examined before carbonisation, is
fawn-coloured with non-characteristic spots.

=Narcotine= gives no sublimate; it melts at 155° into a yellow liquid,
which, on raising the temperature, ever becomes browner to final
blackness. On examining the residue before carbonisation, it is a rich
brown amorphous substance; but if narcotine be heated two or three
degrees above its melting-point, and then cooled slowly, the residue is
crystalline--long, fine needles radiating from centres being common.

=Narceine= gives no sublimate; it melts at 134° into a colourless
liquid, which undergoes at higher temperatures the usual transition of
brown colours. The substance, heated a few degrees above its
melting-point, and then allowed to cool slowly, shows a straw-coloured
residue, divided into lobes or drops containing feathery crystals.

=Papaverine= gives no sublimate; it melts at 130°. The residue, heated a
little above its melting-point, and then slowly cooled, is amorphous, of
a light-brown colour, and in no way characteristic.

=Hyoscyamine= gives no crystalline sublimate; it melts at 89°, and
appears to volatilise in great part without decomposition. It melts into
an almost colourless fluid, which, when solid, may exhibit a network not
unlike vegetable parenchyma; on moistening the network with water,
interlacing crystals immediately appear. If, however, hyoscyamine be
kept at 94° to 95° for a few minutes, and then slowly cooled, the edges
of the spots are arborescent, and the spots themselves crystalline.

=Atropine= (daturine) melts at 97°; at 123° a faint mist appears on the
upper disc. Crystals cannot be obtained; the residue is not

=Solanine.=--The upper disc is dimmed with nebulæ at 190°, which are
coarser and more distinct at higher temperatures; at 200° it begins to
brown, and then melts; the residue consists of amber-brown,
non-characteristic drops.

=Strychnine= gives a minute sublimate of fine needles, often disposed in
lines, at 169°; about 221° it melts, the residue (at that temperature)
is resinous.

=Brucine= melts at 151° into a pale yellow liquid, at higher
temperatures becoming deep-brown. If the lower disc, after melting, be
examined, no crystals are observed, the residue being quite transparent,
with branching lines like the twigs of a leafless tree; light mists,
produced rather by decomposition than by true sublimation, condense on
the upper disc at 185°, and above.

=Saponin= neither melts nor sublimes; it begins to brown about 145°, is
almost black at 185°, and quite so at 190°.

=Delphinine= begins to brown about 102°; it becomes amber at 119°, and
melts, and bubbles appear. There is no crystalline sublimate; residue
not characteristic.

=Pilocarpine= gives a distinct crystalline sublimate at 153°; but thin
mists, consisting of fine dots, may be observed as low as 140°.
Pilocarpine melts at 159°; the sublimates at 160° to 170° are in light
yellow drops. If these drops are treated with water, and the water
evaporated, feathery crystals are obtained; the residue is resinous.

=Theine= wholly sublimes; the first sublimate is minute dots, at 79°; at
half a degree above that very small crystals may be obtained; and at
such a temperature as 120°, the crystals are often long and silky.

=Theobromine= likewise wholly sublimes; nebulæ at 134°, crystals at
170°, and above.

=Salicin= melts at 170°; it gives no crystalline sublimate. The melted
mass remains up to 180° almost perfectly colourless; above that
temperature browning is evident. The residue is not characteristic.

=Picrotoxin= gives no crystalline sublimate. The lowest temperature at
which it sublimes is 128°; the usual nebulæ then make their appearance;
between 165° and 170° there is slight browning; at 170° it melts. The
residue, slowly cooled, is not characteristic.

=Cantharidin= sublimes very scantily between 82° and 83°; at 85° the
sublimate is copious.

The active principles of plants may, in regard to their behaviour to
heat, be classed for practical purposes into--

  1. Those which give a decided crystalline sublimate:
     (_a._) Below 100°, _e.g._, cocaine, theine, thebaine, cantharidin.
     (_b._) Between 100° and 150°, _e.g._, quinetum.
     (_c._) Between 150° and 200°, _e.g._, strychnine, morphine,
  2. Those which melt, but give no crystalline sublimate:
     (_a._) Below 100°, _e.g._, hyoscyamine, atropine.
     (_b._) Between 100° and 150°, _e.g._, papaverine.
     (_c._) Between 150° and 200°, _e.g._, salicin.
     (_d._) Above 200°, _e.g._, solanine.
  3. Those which neither melt nor give a crystalline sublimate, _e.g._,

§ 315. =Melting-point.=--The method of sublimation just given also
determines the melting-point; such a determination will, however, seldom
compare with the melting-points of the various alkaloids as given in
text-books, because the latter melting-points are not determined in the
same way. The usual method of determining melting-points is to place a
very small quantity in a glass tube closed at one end; the tube should
be almost capillary. The tube is fastened to a thermometer by means of
platinum wire, and then the bulb of the thermometer, with its attached
tube, is immersed in strong sulphuric acid or paraffin, contained in a
flask. The thermometer should be suspended midway in the liquid and heat
carefully applied, so as to raise the temperature gradually and equably.
It will be found that rapidly raising the heat gives a different
melting-point to that which is obtained by slowly raising the heat.
During the process careful watching is necessary: most substances change
in hue before they actually melt. A constant melting-point, however
often a substance is purified by recrystallisation, is a sign of purity.

§ 316. =Identification by Organic Analysis.=--In a few cases (and in a
few only) the analyst may have sufficient material at hand to make an
organic analysis, either as a means of identification or to confirm
other tests. By the vacuum process described in “Foods,” in which carbon
and nitrogen are determined by measuring the gases evolved by burning
the organic substance in as complete a vacuum as can be obtained, very
minute quantities of a substance can be dealt with, and the carbon and
nitrogen determined with fair accuracy. It is found in practice that the
carbon determinations appear more reliable than those of the nitrogen,
and there are obvious reasons why this should be so.

Theoretically, with the improved gas-measuring appliances, it is
possible to measure a c.c. of gas; but few chemists would care to create
a formula on less than 10 c.c. of CO₂. Now, since 10 c.c. of CO₂ is
equal to 6·33 mgrms. of carbon, and alkaloids average at least half
their weight of carbon, it follows that 12 mgrms. of alkaloid represent
about the smallest quantity with which a reliable single combustion can
be made.

The following table gives a considerable number of the alkaloids and
alkaloidal bodies, arranged according to their content in carbon:--


                              Carbon.    Nitrogen.

  Asparagin,                   36·36       21·21
  Methylamine,                 38·71       45·17
  Betaine,                     44·44       10·37
  Theobromine,                 46·67       31·11
  Theine,                      49·48       28·86
  Indican,                     49·60        2·22
  Muscarine,                   50·42       11·77
  Lauro-cerasin,               52·47        1·53
  Amanitine,                   57·69       13·46
  Narceine,                    59·63        3·02
  Colchicine,                  60·53        4·15
  Oxyacanthine,                60·57        4·42
  Solanine,                    60·66        1·68
  Trimethylamine,              61·02       23·73
  Jervine,                     61·03        5·14
  Sabadilline,                 61·29        3·46
  Aconitine,                   61·21        2·16
  Nepaline,                    63·09        2·12
  Colchicein,                  63·44        4·38
  Veratroidine,                63·8         3·1
  Narcotine,                   63·92        3·39
  Veratrine,                   64·42        2·91
  Delphinine,                  64·55        3·42
  Physostigmine,               65·49       15·27
  Rhœadine,                    65·79        3·65
  Cocaine,                     66·44        4·84
  Gelsemine,                   67·00        7·10
  Conhydrine,                  67·12        9·79
  Staphisagrine,               67·5         3·6
  Chelidonine,                 68·06       12·34
  Atropine, Hyoscyamine,       70·58        4·84
  Sanguinarine,                70·59        4·33
  Papaverine,                  70·79        4·13
  Delphinoidine,               70·9         3·9
  Morphine and Piperine,       71·58        4·91
  Berberine,                   71·64        4·18
  Codeine,                     72·24        4·68
  Thebaine,                    73·31        4·50
  Cytisine,                    73·85       12·92
  Nicotine,                    74·08       17·28
  Quinine,                     75·02        8·64
  Coniine,                     76·81       11·20
  Strychnine,                  77·24        8·92
  Curarine,                    81·51        5·28

§ 317. =Quantitative Estimation of the Alkaloids.=--For medico-legal
purposes the alkaloid obtained is usually weighed directly, but for
technical purposes other processes are used. One of the most convenient
of these is titration with normal or decinormal sulphuric acid, a method
applicable to a few alkaloids of marked basic powers--_e.g._, quinine is
readily and with accuracy estimated in this way, the alkaloid being
dissolved in a known volume of the acid, and then titrated back with
soda. If a large number of observations are to be made, an acid may be
prepared so that each c.c. equals 1 mgrm. of quinine. A reagent of
general application is found in the so-called _Mayer’s reagent_, which
consists of 13·546 grms. of mercuric chloride, and 49·8 grms. of iodide
of potassium in a litre of water. Each c.c. of such solution

  Of Strychnine,   ·0167  grm.
   „ Brucine,      ·0233   „
   „ Quinine,      ·0108   „
   „ Cinchonine,   ·0102   „
   „ Quinidine,    ·0120   „
   „ Atropine,     ·0145   „
   „ Aconitine,    ·0268   „
   „ Veratrine,    ·0269   „
   „ Morphine,     ·0200   „
   „ Narcotine,    ·0213   „
   „ Nicotine,     ·00405  „
   „ Coniine,      ·00416  „

The final reaction is found by filtering, from time to time, a drop on
to a glass plate, resting on a blackened surface, and adding the test
until no precipitate appears. The results are only accurate when the
strength of the solution of the alkaloid is about 1 : 200; so that it is
absolutely necessary first to ascertain approximatively the amount
present, and then to dilute or concentrate, as the case may be, until
the proportion mentioned is obtained.

A convenient method of obtaining the sulphate of an alkaloid for
quantitative purposes, and especially from organic fluids, is that
recommended by Wagner. The fluid is acidulated with sulphuric acid, and
the alkaloid precipitated by a solution of iodine in iodide of
potassium. The precipitate is collected and dissolved in an aqueous
solution of hyposulphite of soda. The filtered solution is again
precipitated with the iodine reagent, and the precipitate dissolved in
sulphurous acid, which, on evaporation, leaves behind the pure sulphate
of the base.

It is also very useful for quantitative purposes to combine an alkaloid
with gold or platinum, by treating the solution with the chlorides of
either of those metals--the rule as to selection being to give that
metal the preference which yields the most insoluble and the most
crystallisable compound.

The following table gives the percentage of gold or platinum left on
ignition of the double salt:--

                          Gold.   Platinum.

  Atropine,               31·57      ...
  Aconitine               20·0       ...
  Amanitine,              44·23      ...
  Berberine,              29·16     18·11
  Brucine,                 ...      16·52
  Cinchonine,              ...      27·36
  Cinchonidine,            ...      27·87
  Codeine,                 ...      19·11
  Coniine,                 ...      29·38
  Curarine,                ...      32·65
  Delphinine,             26·7       ...
  Delphinoidine,          29·0      15·8
  Emetine,                 ...      29·7
  Hyoscyamine,            34·6       ...
  Morphine,                ...      19·52
  Muscarine,              43·01      ...
  Narcotine,              15·7      15·9
  Narceine,                ...      14·52
  Nicotine,                ...      34·25
  Papaverine,              ...      17·82
  Pilocarpine,            35·5      23·6 to 25·2.
  Piperine,                ...      12·7
  Quinine,                40·0      26·26
  Strychnine,             29·15     18·16
  Thebaine,                ...      18·71
  Theine,                 37·02     24·58
  Theobromine,             ...      25·55
  Veratrine,              21·01      ...

II.--Liquid Volatile Alkaloids.



§ 318. The _Conium maculatum_, or spotted hemlock, is a rather common
umbelliferous plant, growing in waste places, and flowering from about
the beginning of June to August. The stem is from three to five feet
high, smooth, branched, and spotted with purple; the leaflets of the
partial involucres are unilateral, ovate, lanceolate, with an attenuate
point shorter than the umbels; the seeds are destitute of vittæ, and
have five prominent crenate wavy ridges. The whole plant is fœtid and
poisonous. Conium owes its active properties to a volatile liquid
alkaloid, _Coniine_, united with a crystalline alkaloid, _Conhydrine_.

§ 319. =Coniine= (=conia=, =conicine=), (C₈H₁₇N)--specific gravity 0·862
at 0°; melting-point, -2·5°; boiling-point, 166·6°. Pure coniine has
been prepared synthetically by Ladenburg, and found to be
propyl-piperidine C₅H₁₀NC₃H₇, but the synthetically-prepared piperidine
has no action on polarised light. By uniting it with dextro-tartaric
acid, and evaporating, it is possible to separate the substance into
dextro-propyl-piperidine and lævo-propyl-piperidine. The former is in
every respect identical with coniine from hemlock; it is a clear, oily
fluid, possessing a peculiarly unpleasant, mousey odour. One part is
soluble in 150 parts of water,[341] in 6 parts of ether, and in almost
all proportions of amyl alcohol, chloroform, and benzene. It readily
volatilises, and, provided air is excluded, may be distilled unchanged.
It ignites easily, and burns with a smoky flame. It acts as a strong
base, precipitating the oxides of metals and alkaline earths from their
solutions, and it coagulates albumen. Coniine forms salts with
hydrochloric acid (C₈H₁₅N.HCl), phosphoric acid, iodic acid, and oxalic
acid, which are in well-marked crystals. The sulphate, nitrate, acetate,
and tartrate are, on the other hand, non-crystalline.

[341] The saturated watery solution of coniine at 15°, becomes cloudy if
gently warmed, and clears again on cooling.

If coniine is oxidised with nitric acid, or bichromate of potash, and
diluted sulphuric acid, butyric acid is formed; and since the latter has
an unmistakable odour, and other characteristic properties, it has been
proposed as a test for coniine. This may be conveniently performed
thus:--A crystal of potassic bichromate is put at the bottom of a
test-tube, and some diluted sulphuric acid with a drop of the supposed
coniine added. On heating, the butyric acid reveals itself by its odour,
and can be distilled into baryta water, the butyrate of baryta being
subsequently separated in the usual way, and decomposed by sulphuric
acid, &c.

Another test for coniine is the following:--If dropped into a solution
of alloxan, the latter is coloured after a few minutes an intense
purple-red, and white needle-shaped crystals are separated, which
dissolve in cold potash-lye into a beautiful purple-blue, and emit an
odour of the base.[342] Dry hydrochloric acid gives a purple-red, then
an indigo-blue colour, with coniine; but if the acid is not dry, there
is formed a bluish-green crystalline mass. This test, however, is of
little value to the toxicologist, the pure substance alone responding
with any definite result.

[342] Schwarzenbach, _Vierteljahrsschr. f. prakt. Pharm._, viij. 170.

The ordinary precipitating agents, according to Dragendorff, act as

  Potass bismuth iodide.
    1 : 2000, a strong orange precipitate.
    1 : 3000. The drop of the reagent is surrounded with a muddy border.
    1 : 4000. The drop of the reagent is surrounded with a muddy border.
    1 : 5000, still perceptible.
    1 : 6000. The last limit of the reaction.

Phosphomolybdic acid gives a strong yellow precipitate; limit, 1 : 5000.

Potass. mercuric iodide gives a cheesy precipitate; limit, 1 : 1000 in
neutral, 1 : 800 in acid, solutions.

Potass. cadmic iodide gives an amorphous precipitate, 1 : 300. The
precipitate is soluble in excess of the precipitant. (Nicotine, under
similar circumstances, gives a crystalline precipitate.)

Flückiger recommends the following reaction:[343]--“Add to 10 drops of
ether in a shallow glass crystallising dish 2 drops of coniine, and
cover with filter paper. Set upon the paper a common-sized watch-glass
containing bromine water, and invert a beaker over the whole
arrangement. Needle-shaped crystals of coniine hydro-bromine soon form
in the dish as well as in the watch-glass.” Hydrochloric acid, used in
the same way, instead of bromine water, forms with coniine microscopic
needles of coniine hydrochlorate; both the hydro-bromide and the
hydrochlorate doubly refract light. Nicotine does not respond to this

[343] _Reactions_, by F. A. Flückiger, Detroit, 1893.

Coniine forms with carbon disulphide a thiosulphate and a sulphite. If
carbon disulphide, therefore, be shaken with an aqueous solution of
coniine, the watery solution gives a brown precipitate with copper
sulphate, colours ferric chloride solution dark brown red, and gives a
milky opalescence with dilute acids. If coniine itself is added to
carbon disulphide, there is evolution of heat, separation of sulphur,
and formation of thiosulphate. Nicotine does not respond to this

§ 320. =Other Coniine Bases.=--Methyl- and ethyl-coniine have been
prepared synthetically, and are both similar in action to coniine, but
somewhat more like curarine. By the reduction of coniine with zinc dust
conyrine (C₈H₁₁N) is formed; between coniine and conyrine stands
coniceine (C₈H₁₅NO). De Coninck has made synthetically by the addition
of 6 atoms of hydrogen to β collidine, a new fluid alkaloid (C₈H₁₁N + 6H
= C₈H₁₇N), which he has called _isocicutine_: it has the same formula as
coniine. Paraconiine Schiff prepared synthetically from ammonia and
normal butyl aldehyde; it has the formula C₈H₁₅N, and therefore differs
from coniine in containing two atoms less of hydrogen. All the above
have a similar physiological action to coniine. α-stillbazoline
(C₁₁H₁₉N), prepared by Baurath from benzaldehyde and picoline, is
analogous to coniine, and according to Falck has similar action, but is
more powerful.

§ 321. =Pharmaceutical Preparations.=--The percentage of coniine in the
plant itself, and in pharmaceutical preparations, can be approximately
determined by distilling the coniine over, in a partial vacuum,[344]
and titrating the distillate with Mayer’s reagent, each c.c. = about
·00416 grm. of coniine. It appears to be necessary to add powdered
potassic chloride and a small quantity of diluted sulphuric acid before
titrating, or the precipitate does not separate. In any case, the end of
the reaction is difficult to observe.[345]

[344] This is easily effected by uniting a flask containing the
alkaloidal fluid, air-tight, with a Liebig’s condenser and a receiver,
the latter being connected with Bunsen’s water-pump, or one of the
numerous exhausting apparatuses now in use in every laboratory.

[345] Dragendorff, _Die Chemische Werthbestimmung einiger starkwirkender
Droguen_, St. Petersb., 1874.

The fresh plant is said to contain from about ·04 to ·09 per cent., and
the fruit about 0·7 per cent. of coniine.

The officinal preparations are--the leaves, the fruit, a tincture of the
fruit, an extract of the leaves, the juice of the leaves (_Succus
conii_), a compound hemlock pill (composed of extract of hemlock,
ipecacuanha, and treacle), an inhalation of coniine (_Vapor conii_), and
a poultice (_Cataplasma conii_) made with the leaves.

§ 322. =Statistics of Coniine Poisoning.=--F. A. Falck[346] has been
able to collect 17 cases of death recorded in medical literature, up to
the year 1880, from either coniine or hemlock. Two of these cases were
criminal (murders), 1 suicidal, 2 cases in which coniine had been used
medicinally (in one instance the extract had been applied to a cancerous
breast; in the other, death was produced from the injection of an
infusion of hemlock leaves). The remaining 12 were cases in which the
root, leaves, or other portions of the plant had been ignorantly or
accidentally eaten.

[346] _Prakt. Toxicologie_, p. 273.

§ 323. =Effects on Animals.=--It destroys all forms of animal life. The
author made some years ago an investigation as to its action on the
common blow-fly. Droplets of coniine were applied to various parts of
blow-flies, which were then placed under glass shades. The symptoms
began within a minute by signs of external irritation, there were rapid
motions of the wings, and quick and aimless movements of the legs.
Torpor set in speedily, the buzz soon ceased, and the insects lay on
their sides, motionless, but for occasional twitching of the legs. The
wings, as a rule, became completely paralysed before the legs, and death
occurred at a rather variable time, from ten minutes to two hours. If
placed in a current of air in the sun, a fly completely under the
influence of coniine may recover. Coniine causes in frogs, similar to
curarine, peripheral paralysis of the motor nerves, combined with a
transitory stimulation, and afterwards a paralysis of the motor centres;
in frogs the paralysis is not preceded by convulsions. Dragendorff
experimented on the action of coniine when given to five cats, the
quantities used being ·05 to ·5 grm. The symptoms came on almost
immediately, but with the smaller dose given to a large cat, no effect
was witnessed until twenty-five minutes afterwards; this was the longest
interval. One of the earliest phenomena was dilatation of the pupil,
followed by weakness of the limbs passing into paralysis, the hinder
legs being affected prior to the fore. The respiration became troubled,
and the frequency of the breathing diminished; the heart in each case
acted irregularly, and the sensation generally was blunted; death was
preceded by convulsions. In the cases in which the larger dose of ·4 to
·5 grm. was administered, death took place within the hour, one animal
dying in eight minutes, a second in eighteen minutes, a third in twenty
minutes, and a fourth in fifty-eight minutes. With the smaller dose of
·051 grm. given to a large cat, death did not take place until eight
hours and forty-seven minutes after administration.

§ 324. =Effects on Man.=--In a case recorded by Bennet,[347] and quoted
in most works on forensic medicine, the symptoms were those of general
muscular weakness deepening into paralysis. The patient had eaten
hemlock in mistake for parsley; in about twenty minutes he experienced
weakness in the lower extremities, and staggered in walking like a
drunken man; within two hours there was perfect paralysis of both upper
and lower extremities, and he died in three and a quarter hours. In
another case, related by Taylor, the symptoms were also mainly those of
paralysis, and in other instances stupor, coma, and slight convulsions
have been noted.

[347] _Edin. Med. and Surg. Journ._, July 1845, p. 169.

§ 325. =Physiological Action.=--It is generally agreed that coniine
paralyses, first the ends of the motor nerves, afterwards their trunks,
and lastly, the motor centre itself. At a later period the sensory
nerves participate. In the earlier stage the respiration is quickened,
the pupils contracted, and the blood-pressure increased; but on the
development of paralysis the breathing becomes slowed, the capillaries
relaxed, and the blood-pressure sinks. Death takes place from cessation
of the respiration, and not primarily from the heart, the heart beating
after the breathing has stopped. Coniine is eliminated by the urine, and
is also in part separated by the lungs, while a portion is, perhaps,
decomposed in the body.

§ 326. =Post-mortem Appearances.=--There is nothing characteristic in
the appearances after death.

=Fatal Dose.=--The fatal dose of coniine is not accurately known; it is
about 150 mgrms. (2·3 grains). In the case of Louise Berger, 10 to 15
drops appear to have caused death in a few minutes. The auto-experiments
of Dworzak, Heinrich, and Dillaberger would indicate that one drop may
cause unpleasant symptoms. Albers, in the treatment of a woman suffering
from cancer of the breast, witnessed convulsions and loss of
consciousness from a third dose of 4 mgrms. (·06 grain); and Eulenberg,
its full narcotic effects on a child after subcutaneous injection of 1
mgrm. (·015 grain).

§ 327. =Separation of Coniine from Organic Matters or Tissues.=--The
substances are digested with water, acidulated with H₂SO₄, at a
temperature not exceeding 40°, and then filtered. If the filtrate should
be excessive, it must be concentrated; alcohol is then added, the liquid
refiltered, and from the filtrate the alcohol separated by distillation.

On cooling, the acid fluid is agitated with benzene, and the latter
separated in the usual way. The fluid is now alkalised with ammonia, and
shaken up once or twice with its own volume of petroleum ether; the
latter is separated and washed with distilled water, and the alkaloid is
obtained almost pure. If the petroleum ether leaves no residue, it is
certain that the alkaloid was not present in the contents of the stomach
or intestine.

The affinity of coniine with ether or chloroform is such, that its
solution in either of these fluids, passed through a _dry_ filter,
scarcely retains a drop of water. In this way it may be conveniently
purified, the impurities dissolved by water remaining behind.

In searching for coniine, the stomach, intestines, blood, urine, liver,
and lungs are the parts which should be examined. According to
Dragendorff, it has been discovered in the body of a cat six weeks after

Great care must be exercised in identifying any volatile alkaloid as
coniine, for the sources of error seem to be numerous. In one case[348]
a volatile coniine-like ptomaine, was separated from a corpse, and
thought to be coniine; but Otto found that in its behaviour to platinic
chloride, it differed from coniine; it was very poisonous--·07 was fatal
to a frog, ·44 to a pigeon, in a few minutes. In the seeds of _Lupinus
luteus_ there is a series of coniine-like substances,[349] but they do
not give the characteristic crystals with hydrochloric acid.

[348] Otto, _Anleitung z. Ausmittlung d. Gifte_, 1875.

[349] Sievert, _Zeitschrift für Naturwissenschaften_.


§ 328. The different forms of tobacco are furnished by three species of
the tobacco plant, viz., _Nicotianum tabacum_, _N. rustica_, and _N.

Havanna, French, Dutch, and the American tobaccos are in the main
derived from _N. tabacum_; Turkish, Syrian, and the Latakia tobaccos are
the produce of _N. rustica_. There seems at present to be little of _N.
persica_ in commerce.

All the species of tobacco contain a liquid, volatile, poisonous
alkaloid (_Nicotine_), probably united in the plant with citric and
malic acids. There is also present in tobacco an unimportant camphor
(_nicotianin_). The general composition of the plant may be gathered
from the following table:--


  Nicotine,                                          0·060
  Concrete volatile oil,                             0·010
  Bitter extractive,                                 2·870
  Gum with malate of lime,                           1·740
  Chlorophyl,                                        0·267
  Albumen and gluten,                                1·308
  Malic acid,                                        0·510
  Lignine and a trace of starch,                     4·969
  Salts (sulphate, nitrate, and malate of potash, }
  chloride of potassium, phosphate and malate     }  0·734
  of lime, and malate of ammonia,)                }
  Silica,                                            0·088
  Water,                                            88·280

§ 329. =Quantitative Estimation of Nicotine in Tobacco.=--The best
process (although not a perfectly accurate one) is the following:--25
grms. of the tobacco are mixed with milk of lime, and allowed to stand
until there is no odour of ammonia; the mixture is then exhausted by
petroleum ether, the ether shaken up with a slight excess of normal
sulphuric acid, and titrated back by baryta water; the sulphate of
baryta may be collected and weighed, so as to control the results. With
regard to the percentage of nicotine in commercial tobacco, Kosutany
found from 1·686 to 3·738 per cent. in dry tobacco; Letheby, in six
samples, from 1·5 to 3·2 per cent.; whilst Schlössing gives for Havanna
2 per cent., Maryland 2·29 per cent., Kentucky 6·09 per cent., Virginian
6·87 per cent., and for French tobacco, quantities varying from 3·22 to
7·96 per cent. Again, Lenoble found in Paraguay tobacco from 1·8 to 6
per cent.; and Wittstein, in six sorts of tobacco in Germany, 1·54 to
2·72 per cent.

Mr. Cox[350] has recently determined the amount of nicotine in a number
of tobaccos. The results are tabulated in the following table as

[350] _Pharm. Journ._, Jan. 20, 1894.


  Variety examined.                      Nicotine
                                         per cent.

   1. Syrian leaves (_a_),                  ·612
   2. American chewing,                     ·935
   3. Syrian leaves (_b_),                 1·093
   4. Chinese leaves,                      1·902
   5. Turkish (coarse cut),                2·500
   6. Golden Virginia (whole strips),      2·501
   7. Gold Flake (Virginia),               2·501
   8. “Navy-cut” (light coloured),         2·530
   9. Light returns (Kentucky),            2·733
  10. “Navy-cut” (dark “all tobacco”),     3·640
  11. Best “Birds-eye,”                    3·931
  12. Cut Cavendish (_a_),                 4·212
  13. “Best Shag” (_a_),                   4·907
  14. “Cut Cavendish” (_b_),               4·970
  15. “Best Shag” (_b_),                   5·000
  16. French tobacco,                      8·711
  17. Algerian tobacco (_a_),              8·813
  18. Algerian tobacco (_b_),              8·900

It is therefore obvious that the strength of tobacco in nicotine varies
between wide limits.

Twenty-five grammes (or more or less, according to the amount of the
sample at disposal) of the dried and powdered tobacco were intimately
mixed with slaked lime, and distilled in a current of steam until the
condensed steam was no longer alkaline; the distillate was slightly
acidulated with dilute H₂SO₄, and evaporated to a conveniently small
bulk. This was made alkaline with soda, and agitated repeatedly with
successive portions of ether. The separated batches of ethereal solution
of nicotine were then mixed and exposed to the air in a cool place. This
exposure to the air carries away ammonia, if any be present, as well as

Water was added to the ethereal residue, and the amount of nicotine
present determined by decinormal H₂SO₄, using methyl-orange as an
indicator. One c.c. of decinormal H₂SO₄ represents 0·0162 gramme of
nicotine (C₁₀H₁₄N₂).

§ 330. =Nicotine= (C₁₀H₁₄N₂).--Hexahydro dipyridyl (C₅H₄N)₂H₆, when
pure, is an oily, colourless fluid, of 1·0111, specific gravity at
15°.[351] It evaporates under 100° in white clouds, and boils at about
240°, at which temperature it partly distils over unchanged, and is
partly decomposed--a brown resinous product remaining. It volatilises
with aqueous and amyl alcohol vapour notably, and is not even fixed at
-10°. It has a strong alkaline reaction, and rotates a ray of polarised
light to the right. Its odour, especially on warming, is strong and
unpleasantly like tobacco, and it has a sharp caustic taste. It absorbs
water exposed to the air, and dissolves in water in all proportions,
partly separating from such solution on the addition of a caustic
alkali. The aqueous solution acts in many respects like ammonia,
saturating acids fully, and may therefore be in certain cases estimated
with accuracy by titration, 49 parts of H₂SO₄ corresponding to 162 of
nicotine. It gives on oxidation nicotinic acid = m(β) pyridincarbo acid
C₅H₄N(COOH), and by oxidation with elimination of water dipyridyl
(C₅H₄N)₂, and through reduction dipiperydil (C₅H₁₀N)₂.

[351] J. Skalweit, _Ber. der. deutsch. Chem. Gesell._, 14, 1809.

Alcohol and ether dissolve nicotine in every proportion; if such
solutions are distilled, nicotine goes over first. The salts which it
forms with hydrochloric, nitric, and phosphoric acids crystallise with
difficulty; tartaric and oxalic acid form white crystalline salts, and
the latter, oxalate of nicotine, is soluble in alcohol, a property which
distinguishes it from the oxalate of ammonia. The best salts are the
oxalate and the acid tartrate of nicotine, from which to regenerate
nicotine in a pure state.

Hydrochloride of nicotine is more easily volatilised than the pure base.
Nicotine is precipitated by alkalies, &c., also by many oxyhydrates,
lead, copper, &c. By the action of light, it is soon coloured yellow and
brown, and becomes thick, in which state it leaves, on evaporation, a
brown resinous substance, only partly soluble in petroleum ether.

A very excellent test for nicotine, as confirmatory of others, is the
beautiful, long, needle-like crystals obtained by adding to an ethereal
solution of nicotine a solution of iodine in ether. The crystals require
a few hours to form.

Chlorine gas colours nicotine blood-red or brown; the product is soluble
in alcohol, and separates on evaporation in crystals.

Cyanogen also colours nicotine brown; the product out of alcohol is not
crystalline. Platin chloride throws down a reddish crystalline
precipitate, soluble on warming; and gallic acid gives a flocculent
precipitate. A drop of nicotine poured on dry chromic acid blazes up,
and gives out an odour of tobacco camphor; if the ignition does not
occur in the cold, it is produced by a gentle heat. It is scarcely
possible to confound nicotine with ammonia, by reason of its odour; and,
moreover, ammonia may always be excluded by converting the base into the
oxalate, and dissolving in absolute alcohol.

On the other hand, a confusion between coniine and nicotine is apt to
occur when small quantities only are dealt with. It may, however, be
guarded against by the following tests:--

(1.) If coniine be converted into oxalate, the oxalate dissolved in
alcohol, and coniine regenerated by distillation (best in _vacuo_) with
caustic lye, and then hydrochloric acid added, a crystalline
hydrochlorate of coniine is formed, which doubly refracts light, and is
in needle-shaped or columnar crystals, or dendritic, moss-like forms.
The columns afterwards become torn, and little rows of cubical,
octahedral, and tetrahedral crystals (often cross or dagger-shaped) grow
out of yellow amorphous masses. Crystalline forms of this kind are rare,
save in the case of dilute solutions of chloride of ammonium (the
presence of the latter is, of course, rendered by the treatment
impossible); and nicotine does not give anything similar to this

(2.) Coniine coagulates albumen; nicotine does not.

(3.) Nicotine yields a characteristic crystalline precipitate with an
aqueous solution of mercuric chloride; the similar precipitate of
coniine is amorphous.

(4.) Nicotine does not react with CS₂ to form thiosulphate (see p. 266).

§ 331. =Effects on Animals.=--Nicotine is rapidly fatal to all animal
life--from the lowest to the highest forms. That tobacco-smoke is
inimical to insect-life is known to everybody; very minute quantities in
water kill infusoria. Fish of 30 grms. weight die in a few minutes from
a milligram of nicotine; the symptoms observed are rapid movements, then
shivering and speedy paralysis, with decreased motion of the gills, and
death. With frogs, if doses not too large are employed, there is first
great restlessness, then strong tetanic convulsions, and a very peculiar
position of the limbs; the respiration after fatal doses soon ceases,
but the heart beats even after death. Birds also show tetanic
convulsions followed by paralysis and speedy death. The symptoms
witnessed in mammals poisoned by nicotine are not essentially
dissimilar. With large doses the effect is similar to that of prussic
acid--viz., a cry, one or two shuddering convulsions, and death. If the
dose is not too large, there is trembling of the limbs, excretion of
fæces and urine, a peculiar condition of stupor, a staggering gait, and
then the animal falls on its side. The respiration, at first quickened,
is afterwards slowed, and becomes deeper than natural; the pulse, also,
with moderate doses, is first slowed, then rises in frequency, and
finally, again falls. Tetanic convulsions soon develop, during the
tetanus the pupils have been noticed to be contracted, but afterwards
dilated, the tongue and mouth are livid, and the vessels of the ear
dilated. Very characteristic of nicotine poisoning as witnessed in the
cat, the rabbit, and the dog, is its peculiarly violent action, for
after the administration of from one to two drops, the whole course from
the commencement of symptoms to the death may take place in five
minutes. F. Vas has drawn the smoke of tobacco from an immense pipe, and
condensed the products; he finds the well-washed tarry products without
physiological action, but the soluble liquid affected the health of
rabbits,--they lost weight, the number of the blood corpuscles was
decreased, and the hæmoglobin of the blood diminished.[352]

[352] _Archiv. f. Exper. Pathol. u. Pharm._, Bd. 33.

The larger animals, such as the horse, are affected similarly to the
smaller domestic animals. A veterinary surgeon, Mr. John Howard, of
Woolwich,[353] has recorded a case in which a horse suffered from the
most violent symptoms of nicotine-poisoning, after an application to his
skin of a strong decoction of tobacco. The symptoms were trembling,
particularly at the posterior part of the shoulders, as well as at the
flanks, and both fore and hind extremities; the superficial muscles were
generally relaxed and felt flabby; and the pupils were widely dilated.
There was also violent dyspnœa, the respirations being quick and short,
pulse 32 per minute, and extremely feeble, fluttering, and indistinct.
When made to walk, the animal appeared to have partly lost the use of
his hind limbs, the posterior quarter rolling from side to side in an
unsteady manner, the legs crossing each other, knuckling over, and
appearing to be seriously threatened with paralysis. The anus was very
prominent, the bowels extremely irritable, and tenesmus was present. He
passed much flatus, and at intervals of three or four minutes, small
quantities of fæces in balls, partly in the liquid state, and coated
with slimy mucus. There was a staring, giddy, intoxicated appearance
about the head and eyes, the visible mucous membrane being of a dark-red
colour. A great tendency to collapse was evident, but by treatment with
cold douches and exposure to the open air, the horse recovered.

[353] _Veter. Journal_, vol. iii.

In a case occurring in 1863, in which six horses ate oats which had been
kept in a granary with tobacco, the symptoms were mainly those of
narcosis, and the animals died.[354]

[354] _Annales Vétérinaires_, Bruxelles, 1868.

§ 332. =Effects on Man.=--Poisoning by the pure alkaloid nicotine is so
rare that, up to the present, only three cases are on record. The first
of these is ever memorable in the history of toxicology, being the first
instance in which a pure alkaloid had been criminally used. The
detection of the poison exercised the attention of the celebrated
chemist Stas. I allude, of course, to the poisoning of M. Fougnies by
Count Bocarmé and his wife. For the unabridged narrative of this
interesting case the reader may consult Tardieu’s _Étude Médico-Légale
sur L’Empoisonnement_.

Bocarmé actually studied chemistry in order to prepare the alkaloid
himself, and, after having succeeded in enticing his victim to the
chateau of Bitremont, administered the poison forcibly. It acted
immediately, and death took place in five minutes. Bocarmé now attempted
to hide all traces of the nicotine by pouring strong acetic acid into
the mouth and over the body of the deceased. The wickedness and cruelty
of the crime were only equalled by the clumsy and unskilful manner of
its perpetration. The quantity of nicotine actually used in this case
must have been enormous, for Stas separated no less than ·4 grm. from
the stomach of the victim.

The second known case of nicotine-poisoning was that of a man who took
it for the purpose of suicide. The case is related by Taylor. It
occurred in June 1863. The gentleman drank an unknown quantity from a
bottle; he stared wildly, fell to the floor, heaving a deep sigh, and
died quietly without convulsion. The third case happened at
Cherbourg,[355] where an officer committed suicide by taking nicotine,
but how much had been swallowed, and what were the symptoms, are equally
unknown, for no one saw him during life.

[355] _Ann. d’Hygiène_, 1861, x. p. 404.

Poisoning by nicotine, pure and simple, then is rare. Tobacco-poisoning
is very common, and has probably been experienced in a mild degree by
every smoker in first acquiring the habit. Nearly all the fatal cases
are to be ascribed to accident; but criminal cases are not unknown.
Christison relates an instance in which tobacco in the form of snuff was
put into whisky for the purpose of robbery. In 1854, a man was accused
of attempting to poison his wife by putting snuff into her ale, but
acquitted. In another case, the father of a child, ten weeks old, killed
the infant by putting tobacco into its mouth. He defended himself by
saying that it was applied to make the child sleep.

In October 1855,[356] a drunken sailor swallowed (perhaps for the
purpose of suicide) his quid of tobacco, containing from about half an
ounce to an ounce. He had it some time in his mouth, and in half an hour
suffered from frightful tetanic convulsions. There was also diarrhœa;
the pupils were dilated widely; the heart’s action became irregular; and
towards the end the pupils again contracted. He died in a sort of
syncope, seven hours after swallowing the tobacco.

[356] _Edin. Med. Journ._, 1855.

§ 333. In 1829 a curious instance of poisoning occurred in the case of
two girls, eighteen years of age, who suffered from severe symptoms of
tobacco-poisoning after drinking some coffee. They recovered; and it was
found that tobacco had been mixed with the coffee-berries, and both
ground up together.[357]

[357] Barkhausen, _Pr. Ver. Ztg._, v. 17, p. 83, 1838.

Accidents have occurred from children playing with old pipes. In
1877[358] a child, aged three, used for an hour an old tobacco-pipe, and
blew soap bubbles with it. Symptoms of poisoning soon showed themselves,
and the child died in three days.

[358] _Pharm. Journ._ [3], 377, 1877.

Tobacco-juice, as expressed or distilled by the heat developed in the
usual method of smoking, is very poisonous. Sonnenschein relates the
case of a drunken student, who was given a dram to drink, into which his
fellows had poured the juice from their pipes. The result was fatal.
Death from smoking is not unknown.[359] Helwig saw death follow in the
case of two brothers, who smoked seventeen and eighteen German pipefuls
of tobacco. Marshall Hall[360] records the case of a young man, nineteen
years of age, who, after learning to smoke for two days, attempted two
consecutive pipes. He suffered from very serious symptoms, and did not
completely recover for several days. Gordon has also recorded severe
poisoning from the consecutive smoking of nine cigars. The external
application of the leaf may, as already shown in the case of the horse,
produce all the effects of the internal administration of nicotine. The
old instance, related by Hildebrand, of the illness of a whole squadron
of hussars who attempted to smuggle tobacco by concealing the leaf next
to their skin, is well known, and is supported by several recent and
similar cases. The common practice of the peasantry, in many parts of
England, of applying tobacco to stop the bleeding of wounds, and also as
a sort of poultice to local swellings, has certainly its dangers. The
symptoms--whether nicotine has been taken by absorption through the
broken or unbroken skin, by the bowel, by absorption through smoking, or
by the expressed juice, or the consumption of the leaf itself--show no
very great difference, save in the question of time. Pure nicotine acts
with as great a rapidity as prussic acid; while if, so to speak, it is
entangled in tobacco, it takes more time to be separated and absorbed;
besides which, nicotine, taken in the concentrated condition, is a
strong enough base to have slight caustic effects, and thus leaves some
local evidences of its presence. In order to investigate the effects of
pure nicotine, Dworzak and Heinrich made auto-experiments, beginning
with 1 mgrm. This small dose produced unpleasant sensations in the mouth
and throat, salivation, and a peculiar feeling spreading from the region
of the stomach to the fingers and toes. With 2 mgrms. there was
headache, giddiness, numbness, disturbances of vision, torpor, dulness
of hearing, and quickened respirations. With 3 to 4 mgrms., in about
forty minutes there was a great feeling of faintness, intense
depression, weakness, with pallid face and cold extremities, sickness,
and purging. One experimenter had shivering of the extremities and
cramps of the muscles of the back, with difficult breathing. The second
suffered from muscular weakness, fainting, fits of shivering, and
creeping sensations about the arms. In two or three hours the severer
effects passed away, but recovery was not complete for two or three
days. It is therefore evident, from these experiments and from other
cases, that excessive muscular prostration, difficult breathing, tetanic
cramps, diarrhœa, and vomiting, with irregular pulse, represent both
tobacco and nicotine poisoning. The rapidly-fatal result of pure
nicotine has been already mentioned; but with tobacco-poisoning the case
may terminate lethally in eighteen minutes. This rapid termination is
unusual, with children it is commonly about an hour and a half, although
in the case previously mentioned, death did not take place for two days.

[359] The question as to whether there is much nicotine in tobacco-smoke
cannot be considered settled; but it is probable that most of the
poisonous symptoms produced are referable to the pyridene bases of the
general formula (C_{n}H_{2n-5}N). Vohl and Eulenberg (_Arch. Pharmac._,
2, cxlvi. p. 130) made some very careful experiments on the smoke of
strong tobacco, burnt both in pipes and also in cigars. The method
adopted was to draw the smoke first through potash, and then through
dilute sulphuric acid. The potash absorbed prussic acid, hydric
sulphide, formic, acetic, propionic, butyric, valeric, and carbolic
acids; while in the acid the bases were fixed, and these were found to
consist of the whole series of pyridene bases, from pyridene (C₅H₅N),
boil. point 117°, picoline (C₆H₇N), boil. point 133°, lutidine (C₇H₉N),
boil. point 154°, upwards. When smoked in pipes, the chief yield was
pyridene; when in cigars, collidine (C₈H₁₁N); and in general,
pipe-smoking was found to produce a greater number of volatile bases.
The action of these bases has been investigated by several observers.
They all have a special action on the organism, and all show an increase
in physiological activity as the series is ascended. The lowest produce
merely excitement from irritation of the encephalic nervous centres, and
the highest, paralysis of those centres. Death proceeds from gradual
failure of the respiratory movements, leading to asphyxia--(Kendrick and
Dewar, _Proc. Roy. Soc._, xxii. 442; xxiii. 290). The most recent
experimental work is that of A. Gautier; he found that tobacco smoked in
a pipe produced basic compounds, a large quantity of nicotine, and a
higher homologue of nicotine, C₁₁H₁₆N₂, which pre-exists in tobacco
leaves, and a base C₆H₉NO, which seems to be a hydrate of
picoline--(_Compt. Rend._, t. cxv. p. 992, 993). The derivatives of the
pyridene series are also active. The methiodides strongly excite the
brain and paralyse the extremities. A similar but more energetic action
is exerted by the ethyl and allyl derivatives; the iodyallyl derivatives
are strong poisons. Methylic pyridene carboxylate is almost inactive,
but the corresponding ammonium salt gives rise to symptoms resembling
epilepsy--(Ramsay, _Phil. Mag._, v. 4, 241). One member of the pyridene
series β-lutidine has been elaborately investigated by C. Greville
Williams and W. H. Waters--(_Proc. Roy. Soc._, vol. xxxii. p. 162,
1881). They conclude that it affects the heart profoundly, causing an
increase in its tonicity, but the action is almost confined to the
ventricles. The auricles are but little affected, and continue to beat
after the ventricles have stopped. The rate of the heart’s beat is
slowed, and the inhibitory power of the vagus arrested. By its action on
the nervous cells of the spinal cord, it in the first place lengthens
the time of reflex action, and then arrests that function. Finally, they
point out that it is antagonistic to strychnine, and may be successfully
employed to arrest the action of strychnine on the spinal cord.

[360] _Edin. Med. and Surg. Jour._, xii., 1816.

§ 334. =Physiological Action.=--Nicotine is absorbed into the blood and
excreted unchanged, in part by the kidneys and in part by the saliva
(_Dragendorff_). According to the researches of Rosenthal and
Krocker,[361] nicotine acts energetically on the brain, at first
exciting it, and then lessening its activity; the spinal marrow is
similarly affected. The convulsions appear to have a cerebral origin;
paralysis of the peripheral nerves follows later than that of the nerve
centres, whilst muscular irritability is unaffected. The convulsions are
not influenced by artificial respiration, and are therefore to be
considered as due to the direct influence of the alkaloid on the nervous
system. Nicotine has a striking influence on the respiration, first
quickening, then slowing, and lastly arresting the respiratory
movements: section of the vagus is without influence on this action.
The cause of death is evidently due to the rapid benumbing and paralysis
of the respiratory centre. Death never follows from heart-paralysis,
although nicotine powerfully influences the heart’s action, small doses
exciting the terminations of the vagus in the heart, and causing a
slowing of the beats. Large doses paralyse both the controlling and
exciting nerve-centres of the heart; the heart then beats fast,
irregularly, and weakly. The blood-vessels are first narrowed, then
dilated, and, as a consequence, the blood-pressure first rises, then
falls. Nicotine has a special action on the intestines. As O. Nasse[362]
has shown, there is a strong contraction of the whole tract, especially
of the small intestine, the lumen of which may be, through a continuous
tetanus, rendered very small. This is ascribed to the peripheral
excitation of the intestinal nerves and the ganglia. The uterus is also
excited to strong contraction by nicotine; the secretions of the bile
and saliva are increased.

[361] _Ueber die Wirkung des Nicotines auf den thierischen Organismus_,
Berlin, 1868.

[362] _Beiträge zur Physiologie der Darmbewegung, Leipsic_, 1866.

§ 335. =Fatal Dose.=--The fatal dose for dogs is from ½ to 2 drops; for
rabbits, a quarter of a drop; for an adult not accustomed to tobacco the
lethal dose is probably 6 mgrms.

§ 336. =Post-mortem Appearances.=--There seem to be no appearances so
distinctive as to be justly ascribed to nicotine or tobacco-poisoning
and no other.

A more or less fluid condition of the blood, and, generally, the signs
of death by the lungs, are those most frequently found. In
tobacco-poisoning, when the leaves themselves have been swallowed, there
may be some inflammatory redness of the stomach and intestine.

§ 337. =Separation of Nicotine from Organic Matters, &c.=--The process
for the isolation of nicotine is precisely that used for coniine (see p.
269). It appears that it is unaltered by putrefaction, and may be
separated and recognised by appropriate means a long time after death.
Orfila detected it in an animal two or three months after death; Melsens
discovered the alkaloid unmistakably in the tongues of two dogs, which
had been buried in a vessel filled with earth for seven years; and it
has been found, by several experiments, in animals buried for shorter
periods. Nicotine should always be looked for in the tongue and mucous
membrane of the mouth, as well as in the usual viscera. The case may be
much complicated if the person supposed to be poisoned should have been
a smoker; for the defence would naturally be that there had been either
excessive smoking or chewing, or even swallowing accidentally a quid of
tobacco.[363] A ptomaine has been discovered similar to nicotine.
Wolckenhaar separated also an alkaloid not unlike nicotine from the
corpse of a woman addicted to intemperate habits; but this base was not
poisonous, nor did it give any crystals when an ethereal solution was
added to an ether solution of iodine. It will be well always to support
the chemical evidence by tests on animal life, since the intensely
poisonous action of nicotine seems not to be shared by the nicotine-like

[363] In an experiment of Dragendorff’s, nicotine is said to have been
detected in 35 grms. of the saliva of a person who had half an hour
previously smoked a cigar.

3. PITURIE.[364]

[364] See “The Alkaloid from Piturie,” by Prof. Leversidge, _Chem.
News_, March 18 and 25, 1881.

    § 338. Piturie (C₆H₈N) is a liquid, nicotine-like alkaloid, obtained
    from the _Duboisia hopwoodii_, a small shrub or tree belonging to
    the natural order _Solanaceæ_, indigenous in Australia. The natives
    mix piturie leaves with ashes from some other plant, and chew them.
    Piturie is obtained by extracting the plant with boiling water
    acidified with sulphuric acid, concentrating the liquid by
    evaporation, and then alkalising and distilling with caustic soda,
    and receiving the distillate in hydrochloric acid. The solution of
    the hydrochlorate is afterwards alkalised and shaken up with ether,
    which readily dissolves out the piturie. The ether solution of
    piturie is evaporated to dryness in a current of hydrogen, and the
    crude piturie purified by distillation in hydrogen, or by changing
    it into its salts, and again recovering, &c. It is clear and
    colourless when pure and fresh, but becomes yellow or brown when
    exposed to air and light. It boils and distils at 243° to 244°. It
    is soluble in all proportions in alcohol, water, and ether; its
    taste is acrid and pungent; it is volatile at ordinary temperatures,
    causing white fumes with hydrochloric acid; it is very irritating to
    the mucous membranes, having a smell like nicotine at first, and
    then, when it becomes browner, like pyridine. It forms salts with
    acids, but the acetate, sulphate, and hydrochlorate are varnish-like
    films having no trace of crystallisation; the oxalate is a
    crystalline salt. Piturie gives precipitates with mercuric chloride,
    cupric sulphate, gold chloride, mercur-potassic iodide, tannin, and
    an alcoholic solution of iodine. If an ethereal solution of iodine
    is added to an ethereal solution of piturie, a precipitate of
    yellowish-red needles, readily soluble in alcohol, is deposited. The
    iodine compound melts at 110°, while the iodine compound of nicotine
    melts at 100°. Piturie is distinguished from coniine by its aqueous
    solution not becoming turbid either on heating or on the addition of
    chlorine water; it differs from picoline in specific gravity,
    picoline being ·9613 specific gravity at 0°, and piturie sinking in
    water; it differs from aniline by not being coloured by chlorinated
    lime. From nicotine it has several distinguishing marks, one of the
    best being that it does not change colour on warming with
    hydrochloric acid and the addition to the mixture afterwards of a
    little nitric acid. The physiological action seems to be but little
    different from that of nicotine. It is, of course, poisonous, but as
    yet has no forensic importance.


    § 339. In 1851 Stenhouse[365] separated a poisonous volatile
    alkaloid from _Spartium scoparium_, the common broom, to which he
    gave the name of sparteine. At the same time a crystalline
    non-poisonous substance, _scoparin_, was discovered.

[365] _Phil. Trans._, 1851.

    Sparteine is separated from the plant by extraction with sulphuric
    acid holding water, and then alkalising the acid solution and
    distilling: it has the formula (C₁₅H₂₆N₂), and belongs to the class
    of tertiary diamines. It is a clear, thick, oily substance, scarcely
    soluble in water, to which it imparts a strong, alkaline reaction;
    it is soluble in alcohol, in ether, and chloroform; insoluble in
    benzene and in petroleum; it boils at 288°. Sparteine neutralises
    acids fully, but the oxalate is the only one which can be readily
    obtained in crystals. It forms crystalline salts with platinic
    chloride, with gold chloride, with mercuric chloride, and with zinc
    chloride. The picrate is an especially beautiful salt, crystallising
    in long needles, which, when dried and heated, explode. On sealing
    sparteine up in a tube with ethyl iodide and alcohol, and heating to
    100° for an hour, ethyl sparteine iodide separates in long,
    needle-like crystals, which are somewhat insoluble in cold alcohol.

    =Effect on Animals.=--A single drop kills a rabbit; the symptoms are
    similar to those produced by nicotine, but the pupils are

[366] To the nicotine group, gelsemine (C₂₄H₂₈N₂O₄) and oxalathylin
(C₆H₁₀N₂) also belong, in a physiological sense, but gelsemine, like
sparteine, dilates the pupil.


    § 340. =Properties.=--Aniline or amido-benzol (C₆H₅NH₂) is made by
    the reduction of nitro-benzol. It is an oily fluid, colourless when
    quite pure, but gradually assuming a yellow tinge on exposure to the
    air. It has a peculiar and distinctive smell. It boils at 182·5°,
    and can be congealed by a cold of 8°. It is slightly soluble in
    water, 100 parts of water at 16° retaining about 3 of aniline, and
    easily soluble in alcohol, ether, and chloroform. It does not blue
    red-litmus paper, but nevertheless acts as a weak alkali, for it
    precipitates iron from its salts. It forms a large number of
    crystalline salts. The hydrochloride crystallises in white plates,
    and has a melting-point of 192°. The platinum compound has the
    formula of (C₆H₅NH₂HCl)₂PtCl₄, and crystallises in yellow needles.

    § 341. =Symptoms and Effects.=--Aniline, like picric acid,
    coagulates albumin. Aniline is a blood poison; it produces, even
    during life, in some obscure way, methæmoglobin, and it
    disintegrates the red blood corpuscles; both these effects lessen
    the power of the blood corpuscles to convey oxygen to the tissues,
    hence the cyanosis observed so frequently in aniline poisoning is
    explained. Engelhardt[367] has found that aniline black is produced;
    in every drop of blood there are fine black granules, the total
    effect of which produce a pale blue or grey-blue colour of the skin.
    Aniline has also an action on the central nervous system, at first
    stimulating, and then paralysing. Schmiedeberg finds that
    para-amido-phenol-ether-sulphuric acid is produced, and appears in
    the urine as an alkali salt; a small quantity of fuchsine is also
    produced, and has been found in the urine. Some aniline may be
    excreted unchanged.

[367] _Beiträge zur Tox. des Anilins. Inaug.-Diss._, Dorpat, 1888.

    The symptoms are giddiness, weakness, cyanosis, blueness of the
    skin, sinking of the temperature, and dilatation of the pupil. The
    pulse is small and frequent, the skin moist and cold. The patient
    smells of aniline. Towards the end coma and convulsions set in. The
    urine may be brown to brown-black, and may contain hyaline
    cylinders. The blood shows the spectrum of methæmoglobin, and has
    the peculiarities already mentioned. Should the patient recover,
    jaundice often follows. The outward application of aniline produces

    Chronic poisoning by aniline is occasionally seen among workers in
    the manufacture of aniline. Headache, loss of muscular power,
    diminished sensibility of the skin, vomiting, loss of appetite,
    pallor, eruptions on the skin, and general malaise are the chief
    symptoms. The perspiration has been noticed to have a reddish

    Cases of aniline poisoning are not common; Dr. Fred. J. Smith has
    recorded one in the _Lancet_ of January 13, 1894.[368] The patient,
    a woman, 42 years of age, of alcoholic tendencies, swallowed, 13th
    December 1893, at 1.40 P.M., about 3 ounces of marking ink, the
    greatest part of which consisted of aniline; in a very little while
    she became unconscious, and remained so until death. At 3 P.M. her
    lips were of a dark purple, the general surface of the skin was
    deadly white, with a slight bluish tinge; the pupils were small and
    sluggish, the breathing stertorous, and the pulse full and slow--60
    per minute. The stomach was washed out, ether injected, and oxygen
    administered, but the patient died comatose almost exactly twelve
    hours after the poison had been taken.

[368] See also a case reported by K. Dehio, in which a person drank 10
grms. and recovered, _Ber. klinis. Wochen._, 1888, Nr. 1.

    The _post-mortem_ examination showed slight congestion of the lungs;
    the heart was relaxed in all its chambers, and empty of blood; it
    had a peculiar green-blue appearance. All the organs were healthy.
    The blood was not spectroscopically examined.

    § 342. =Fatal Dose.=--This is not known, but an adult would probably
    be killed by a single dose of anything over 6 grms. Recovery under
    treatment has been known after 10 grms.; the fatal dose for rabbits
    is 1-1·5 grms., for dogs 3-5 grms.

    § 343. =Detection of Aniline.=--Aniline is easily separated and
    detected. Organic fluids are alkalised by a solution of potash, and
    distilled. The organs, finely divided, are extracted with water
    acidulated with sulphuric acid, the fluid filtered, and then
    alkalised and distilled. The distillate is shaken up with ether, the
    ether separated and allowed to evaporate spontaneously. Any aniline
    will be in the residue left after evaporation of the ether, and may
    be identified by the following tests:--An aqueous solution of
    aniline or its salts is coloured blue by a little chloride of lime
    or hypochlorite of soda; later on the mixture becomes red. The blue
    colour has an absorption band, when examined spectroscopically,
    extending from W.L. 656 to 560, and therefore in the red and yellow
    from Fraunhofer’s line C, and overlapping D. Another test for
    aniline is the addition of kairine, hydrochloric acid, and sodium
    nitrite, which strikes a blue colour.

III.--The Opium Group of Alkaloids.

§ 344. =General Composition.=--Opium contains a larger number of basic
substances than any plant known. The list reaches at present to 18 or 19
nitrogenised bases, and almost each year there have been additions. Some
of these alkaloids exist in very small proportion, and have been little
studied. Morphine and narcotine are those which, alone, are
toxicologically important. Opium is a gummy mass, consisting of the
juice of the incised unripe fruit of the _Papaver somniferum_ hardened
in the air. The following is a nearly complete list of the constituents
which have been found in opium:--

  Morphine, C₁₇H₁₉NO₃.
  Narcotine, C₂₂H₂₃NO₇.
  Narceine, C₂₃H₂₉NO₉.
  Apomorphine, C₁₇H₁₇NO₂ } By dehydration of morphine and codeine
  Apocodeine, C₁₈H₁₉NO₂  } respectively.
  Pseudomorphine, C₁₇H₁₉NO₄.
  Codamine, C₂₀H₂₅NO₄.
  Ladanine, C₂₀H₂₅NO₄.
  Ladanosine, C₂₁H₂₇NO₄.
  Protapine, C₂₀H₁₉NO₅.
  Cryptopine, C₂₁H₂₃NO₅.
  Lanthopine, C₂₃H₂₅NO₄.
  Hydrocotarnine, C₁₂H₁₅NO₃.
  Opianine, C₂₁H₂₁NO₇.
  Cnoscopine, C₃₄H₃₆N₂O₁₁.
  Rhœadine, C₂₀H₂₁NO₇.
  Codeine, C₁₈H₂₁NO₃.
  Thebaine, C₁₉H₂₁NO₃.
  Papaverine, C₂₀H₂₁NO₄.
  Meconidine, C₂₁H₂₃NO₄.
  Meconin, C₁₀H₁₀O₄.
  Meconic acid, C₇H₄O₇.
  Thebolactic acid.
  Gummy matters--Vegetable mucus.
  Ash, containing the usual constituents.

The various opiums differ, the one from the other, in the percentages of
alkaloids, so that only a very general statement of the mean composition
of opium can be made. The following statement may, however, be accepted
as fairly representative of these differences:--

                                            Per cent.
  Morphine,                                  6 to 15
  Narcotine,                                 4 to  8
  Other alkaloids,                           5 to  2
  Meconin,                                   Under 1
  Meconic acid,                              3 to  8
  Peculiar resin and caoutchouc,             5 to 10
  Fat,                                       1 to  4
  Gum and soluble humoid acid matters,      40 to 50
  Insoluble matters and mucus,              18 to 20
  Ash,                                       4 to  8
  Water,                                     8 to 30

The general results of the analysis of 12 samples of Turkey opium,
purchased by Mr. Bott,[369] from leading druggists in London, Dublin,
and Edinburgh, are as follows:--

[369] _Year Book of Pharmacy_, 1876.

=Water.=--Highest, 31·2; lowest, 18·4; mean, 22·4 per cent.

=Insoluble Residue.=--Highest, 47·9; lowest, 25·45; mean, 32·48 per

=Aqueous Extract.=--Highest, 56·15; lowest, 20·90; mean, 45·90 per cent.

=Crude Morphine= (containing about 7/10 of pure morphine).--Highest,
12·30; lowest, 6·76; mean, 9·92 per cent., which equals 12·3 per cent.
of the dried drug.

=Persian Opium=, examined in the same way, varied in crude morphine from
2·1 to 8·5 per cent.; Malwa, from 5·88 to 7·30. In 18 samples of
different kinds of opium, the mean percentage of crude morphine was 8·88
per cent. (11 per cent. of the dried opium). According to Guibourt,
Smyrna opium, dried at 100°, yields 11·7 to 21·46 per cent., the mean
being 12 to 14 per cent.; Egyptian, from 5·8 to 12 per cent.; Persian,
11·37 per cent. In East Indian Patna opium, for medical use, he found
7·72; in a sample used for smoking, 5·27 per cent.; in Algerian opium,
12·1 per cent.; in French opium, 14·8 to 22·9 per cent.

§ 345. =Action of Solvents on Opium.=--The action of various solvents on
opium has been more especially studied by several scientists who are
engaged in the extraction of the alkaloids.

=Water= dissolves nearly everything except resin, caoutchouc, and woody
fibre. Free morphine would be left insoluble; but it seems always to be
combined with meconic and acetic acids. The solubility of free narcotine
in water is extremely small.

=Alcohol= dissolves resin and caoutchouc, and all the alkaloids and
their combinations, with meconic acid, &c.

=Amylic Alcohol= dissolves all the alkaloids, if they are in a free
state, and it also takes up a little of the resin.

=Ether, Benzene, and Carbon Sulphide= do not dissolve the resin, and
only slightly morphine, if free; but they dissolve the other free
alkaloids as well as caoutchouc.

=Acids= dissolve all the alkaloids and the resin.

=Fixed Alkalies=, in excess, dissolve in part resin; they also dissolve
morphine freely; narcotine remains insoluble.

=Lime Water= dissolves morphine, but is a solvent for narcotine only in
presence of morphine.

=Ammonia= dissolves only traces of morphine; but narceine and codeine
readily. It does not dissolve the other alkaloids, nor does it dissolve
the resin.

§ 346. =Assay of Opium.=--The following processes may be described:--

=Process of Teschemacher and Smith.=--This process, with a few
modifications, is as follows:--10 grms. of opium are as completely
exhausted with proof spirit at a boiling temperature as possible. The
resulting alcoholic extract is treated with a few drops of ammonium
oxalate solution, and the solution is almost neutralised with ammonia.
The solution is concentrated to one-third, cooled, and filtered. The
filtrate is farther concentrated to 5 c.c., and transferred to a small
flask, it is washed into this flask by 4 c.c. of water, and 3 c.c. of 90
per cent. alcohol; next 2 c.c. solution of ammonia (sp. gr. 0·960) and
25 c.c. of dry ether are added. The flask is corked, shaken, and then
allowed to rest over-night.

The ether is decanted as completely as possible. Two filter papers are
taken and counterpoised--that is to say, they are made precisely the
same weight. The filters are placed one inside the other, and the
precipitate collected on the inner one; the precipitate is washed with
morphinated water--that is to say, water in which morphine has been
digested for some days. The filter papers with their contents are washed
with benzene and dried, the outer paper put on the pan of the balance
carrying the weights, and the inner filter with the precipitate weighed.
The precipitate is now digested with a known volume of decinormal acid,
and then the excess of acid ascertained by titration with decinormal
alkali, using either litmus or methyl orange; each c.c. of decinormal
acid is equal to 30·3 mgrms. of morphine.[370]

[370] _Pharm. Journal_, xix. 45, 82; xxii. 746. Wright and Farr,
_Chemist and Druggist_, 1893, i. 78.

=Dott’s Process.=--Dott has recently proposed a new process, which he
states has given good results. The process is as follows:--10 grammes
of powdered opium are digested with 25 c.c. water; 1·8 gramme barium
chloride dissolved in about 12 c.c. water is then added, the solution
made up to 50 c.c., well mixed, and after a short time filtered. 22 c.c.
(representing 5 grammes opium) are mixed with dilute sulphuric acid in
quantity just sufficient to precipitate the barium. About 1 c.c. is
required, and the solution should be warmed to cause the precipitate to
subside, and the solution to filter clear. To this filtered solution a
little dilute ammonia, about 0·5 c.c. is added to neutralise the free
acid, and the solution concentrated to 6 or 7 c.c., and allowed to cool.
1 c.c. spirit and 1 c.c. ether are then added, and next ammonia in
slight excess. The ammonia should be added gradually until there is no
further precipitation, and a perceptible odour of ammonia remains after
well stirring and breaking down any lumps with the stirring rod. After
three hours the precipitate is collected on counterpoised filters and
washed. Before filtering, it should be noted that the solution has a
faint odour of ammonia: if not, one or two drops of ammonia solution
should be added. The dried precipitate is washed with benzene or
chloroform, dried, and weighed. It is then titrated with _n_/10 acid,
until the morphine is neutralised, as indicated by the solution
reddening litmus paper.[371]

[371] Other methods of opium assay have been published: see Mr. A. B.
Prescott’s method (_Proceedings of Amer. Pharm. Assoc._, 1878); Allen
(_Commercial Org. Analysis_, vol. ii. p. 473); E. R. Squibb’s
modification of Flückiger’s method (_Pharm. Journ._ (3), xii. p. 724); a
rapid mode of opium assay, MM. Portes and Lanjlois (_Journ. de Pharm. et
de Chim._, Nov. 1881); _Year Book of Pharmacy_, 1882.

To the above may be added--(1.) _Schacht’s Method._--5 to 10 grms. of
dry, finely-powdered opium are digested with sufficient distilled water
to make a thin pulp. After twenty-four hours the whole is thrown on a
weighed filter, and washed until the washings are almost colourless and
tasteless. The portion insoluble in water is dried at 100° and weighed;
in good opium this should not exceed 40 per cent. The filtrate is
evaporated until it is about one-fifth of the weight of the opium taken
originally; cooled, filtered, and treated with pure animal charcoal,
until the dark brown colour is changed into a brownish-yellow. The
liquid is then refiltered, precipitated with a slight excess of ammonia,
allowed to stand in an open vessel until all odour of ammonia
disappears, and at the same time frequently stirred, in order that the
precipitate may not become crystalline--a form which is always more
difficult to purify. The precipitate is now collected on a tared filter,
washed, dried, and weighed. With an opium containing 10 per cent. of
morphine, its weight is usually 14 per cent. A portion of the
precipitate is then detached from the filter, weighed, and exhausted,
first with ether, and afterwards with boiling alcohol (0·81 specific
gravity). Being thus purified from narcotine, and containing a little
colouring-matter only, it may now be dried and weighed, and the amount
of morphine calculated, on the whole, from the data obtained.

(2.) _Fleury_ has proposed a titration by oxalic acid as follows:--2
grms. of the powdered opium are macerated a few hours with 8 c.c. of
aqueous oxalate of ammonia, brought on a filter, and washed with 5 c.c.
of water. To the filtrate an equal volume of 80 per cent. alcohol and
ammonia to alkaline reaction is added; and, after standing twenty-four
hours in a closed flask, it is filtered, and the flask rinsed out with
some c.c. of 40 per cent. alcohol. The filter, with its contents, after
drying, is placed in the same flask (which should not be cleansed), a
few drops of alcoholic logwood solution are added, with an excess of
oxalic acid solution of known strength, the whole being made up to 100
c.c. This is divided into two parts, and the excess of acid titrated
back with diluted soda-lye. If the oxalic acid solution is of the
strength of 4·42 grms. to the litre, every c.c. of the oxalic acid
solution which has become bound up with morphine, corresponds to 0·02
grm. of morphine.

§ 347. =Medicinal and other Preparations of Opium.=--The chief mixtures,
pills, and other forms, officinal and non-officinal, in which opium may
be met with, are as follows:--


=Compound Tincture of Camphor=, P. B. (Paregoric).--Opium, camphor,
benzoic acid, oil of anise, and proof spirit: the opium is in the
proportion of about 0·4 per cent., or 1 grain of opium in 240 minims.

=Ammoniated Tincture of Opium= (Scotch paregoric).--Strong solution of
ammonia, rectified spirit, opium, oil of anise, saffron, and benzoic
acid. Nearly 1 per cent. or 1 grain of opium in every 96 minims.

  =The Compound Powder of Kino=, P. B.
    Opium,                     5 per cent.
    Cinnamon,                 20     „
    Kino,                     75     „

  =The Compound Powder of Opium=, P. B.
    Opium,                    10·00 per cent.
    Black Pepper,             13·33     „
    Ginger,                   33·33     „
    Caraway Fruit,            40·00     „
    Tragacanth,                3·33     „

  =Pill of Lead and Opium=, P. B.
    Acetate of Lead,          75·0 per cent.
    Opium,                    12·5     „
    Confection of Roses,      12·5     „

=Tincture of Opium= (=Laudanum=).--Opium and proof spirit. One grain of
opium in 14·8 min.--that is, about 6·7 parts by weight in 100 by

The amount of opium actually contained in laudanum has been investigated
by Mr. Woodland,[372] from fourteen samples purchased from London and
provincial chemists. The highest percentage of extract was 5·01, the
lowest 3·21, the mean being 4·24; the highest percentage of morphine was
·70 per cent., the lowest ·32, the mean being ·51 per cent. It is,
therefore, clear that laudanum is a liquid of very uncertain strength.

[372] _Year Book of Pharmacy_, 1882.

=Aromatic Powder of Chalk and Opium.=--Opium 2·5 per cent., the rest of
the constituents being cinnamon, nutmeg, saffron, cloves, cardamoms, and

=Compound Powder of Ipecacuanha= (Dover’s Powder).

  Opium,                   10 per cent.
  Ipecacuanha,             10     „
  Sulphate of Potash,      80     „

=Confection of Opium= (=Confectio opii=) is composed of syrup and
compound powder of opium; according to its formula, it contains 2·4 per
cent. of opium by weight.

=Extract of Opium= contains the solid constituents capable of extraction
by water; it should contain 20 per cent. of morphine, and is therefore
about double the strength of dry powdered opium.

=Liquid Extract of Opium= has been also examined by Mr. Woodland:[373]
ten samples yielded as a mean 3·95 per cent. of dry extract, the highest
number being 4·92 per cent., the lowest 3·02. The mean percentage of
morphine was ·28 per cent., the highest amount being ·37, and the lowest
·19 per cent.

[373] _Op. cit._

=Liniment of Opium= is composed of equal parts of laudanum and soap
liniment; it should contain about 0·0375 per cent. morphine.

=The Compound Soap-pill= is made of soap and opium, one part of opium in
every 5·5 of the mass--_i.e._, about 18 per cent.

=Ipecacuanha and Morphine Lozenges=, as the last, with the addition of
ipecacuanha; each lozenge contains 1/36 grain (1·8 mgrms.) morphine
hydrochlorate, 1/12 grain (5·4 mgrms.) ipecacuanha.

=Morphia Suppositories= are made with hydrochlorate of morphine,
benzoated lard, white wax, and oil of theobroma; each suppository
contains ½ grain (32·4 mgrms.) of morphine salt.

=Opium Lozenges= are composed of opium extract, tincture of tolu, sugar,
gum, extract of liquorice, and water. Each lozenge contains 1/10 grain
(6·4 mgrms.) of extract of opium, or about 1/50 grain (1·3 mgrm.)

=The Ointment of Galls and Opium= contains one part of opium in 14·75
parts of the ointment--_i.e._, opium 6·7 per cent.

=Opium Wine=, P. B.--Sherry, opium extract, cinnamon, and cloves. About
5 of opium extract by weight in 100 parts by measure (22 grains to the

=Solutions of Morphine=, both of the acetate and hydrochlorate, P. B.,
are made with a little free acid, and with rectified spirit. The
strength of each is half a grain in each fluid drachm (·0324 grm. in
3·549), or ·91 part by weight in 100 by measure.

=Solution of Bimeconate of Morphine.=--One fluid oz. contains 5½ grains
of bimeconate of morphine.

=Morphia Lozenges= are made with the same accessories as opium lozenges,
substituting morphine for opium; each lozenge contains 1/36 grain of
hydrochlorate of morphia (1·8 mgrm.).

=Syrup of Poppies.=--The ordinary syrup of poppies is sweetened
laudanum. It should, however, be what it is described--viz., a syrup of
poppy-heads. As such, it is said to contain one grain of extract of
opium to the ounce.


    =Godfrey’s Cordial= is made on rather a large scale, and is variable
    in strength and composition. It usually contains about 1½ grains of
    opium in each fluid ounce,[374] and, as other constituents:
    sassafras, molasses or treacle, rectified spirit, and various
    flavouring ingredients, especially ginger, cloves, and coriander;
    aniseed and caraways may also be detected.

[374] If made according to Dr. Paris’ formula, 1⅙ grains in an ounce.

    =Grinrod’s Remedy for Spasms= consists of hydrochlorate of morphine,
    spirit of sal-volatile, ether, and camphor julep; strength, 1 grain
    of the hydrochlorate in every 6 ounces.

    =Lemaurier’s Odontalgic Essence= is acetate of morphine dissolved in
    cherry-laurel water; strength, 1 grain to the ounce.

    =Nepenthe= is a preparation very similar to _Liq. Opii sedativ._,
    and is of about the same strength as laudanum.[375]

[375] It may be regarded as a purified alcoholic solution of meconate of
morphia, with a little excess of acid, and of about the same strength as

    =Black Drop= (known also by various names, such as Armstrong’s Black
    Drop) is essentially an acetic acid solution of the constituents of
    opium. It is usually considered to be of four times the strength of
    laudanum. The wholesale receipt for it is: Laudanum, 1 oz., and
    distilled vinegar 1 quart, digested for a fortnight. The original
    formula proposed by the Quaker doctor of Durham, Edward Tunstall,
    is--Opium, sliced, ½ lb.; good verjuice,[376] 3 pints; and nutmeg,
    1½ oz.; boiled down to a syrup thickness; ¼ lb. of sugar and 2
    teaspoonfuls of yeast are then added. The whole is set in a warm
    place for six or eight weeks, after which it is evaporated in the
    open air until it becomes of the consistence of a syrup. It is
    lastly decanted and filtered, a little sugar is added, and the
    liquid made up to 2 pints.

[376] Verjuice is the juice of the wild crab.

    =“Nurse’s Drops”= seem to be composed of oil of caraway and

    =Powell’s Balsam of Aniseed=, according to evidence in the case of
    _Pharmaceutical Society v. Armson_ (_Pharm. Journ._, 1894), contains
    in every oz. 1/10 grain of morphine.

    =Dalby’s Carminative=--

  Carbonate of magnesia,                                40  grains.
  Tincture of castor, and compound tincture  of cardamoms,
  of each                                               15  drops.
  Laudanum,                                              5    „
  Oil of aniseed,                                        3    „
  Oil of nutmeg,                                         2    „
  Oil of peppermint,                                     1    „
  Peppermint water,                                      2  fl. ounces

    Dose, from a half to one teaspoonful. Another recipe has no
    laudanum, but instead syrup of poppies.

    =Chlorodyne=--Brown’s Chlorodyne is composed of--

  Chloroform,                                            6  drachms.
  Chloric ether,                                         1     „
  Tincture of capsicum,                                   ½    „
  Hydrochlorate of morphine,                             8  grains.
  Scheele’s prussic acid,                               12  drops
  Tincture of Indian hemp,                               1  drachm.
  Treacle,                                               1     „

    =Atkinson’s Infant Preserver=--

  Carbonate of magnesia,                                 6  drachms.
  White sugar,                                           2  ounces
  Oil of aniseed,                                       20  drops.
  Spirit of sal-volatile,                                2½ drachms.
  Laudanum,                                              1     „
  Syrup of saffron,                                      1  ounce.
  Caraway water, to make up,                             1  pint.

    =Boerhave’s Odontalgic Essence=--

  Opium,                                                  ½ drachm.
  Oil of cloves,                                         2    „
  Powdered camphor,                                      5    „
  Rectified spirit,                                      1½ fl. ounce.

§ 348. =Statistics.=--During the ten years 1883-1892 no less than 1424
deaths in England and Wales were attributed to some form or other of
opium or its active constituents; 45 of these deaths were ascribed to
various forms of soothing syrup or to patent medicines containing opium
or morphine; 876 were due to accident or negligence; 497 were suicidal
and 6 were homicidal deaths. The age and sex distribution of the deaths
ascribed to accident and those ascribed to suicide are detailed in the
following tabular statement:--



  Ages,        0-1  1-5  5-15  15-25  25-65  65 and  Total
  Males,        72   27    1     16    302     85     503
  Females,      50   23    4     21    189     86     373
    Total,     122   50    5     37    491    171     876


  Ages,                  5-15  15-25  25-65  65 and  Total
  Males,                   1     26    269     34     330
  Females,               ...     24    126     17     167
  Total,                   1     50    395     51     497

Of European countries, England has the greatest proportional number of
opium poisonings. In France, opium or morphine poisoning accounts for
about 1 per cent. of the whole; and Denmark, Sweden, Switzerland,
Germany, all give very small proportional numbers; arsenic, phosphorus,
and the acids taking the place of opiates. The more considerable
mortality arises, in great measure, from the pernicious practice--both
of the hard-working English mother and of the baby-farmer--of giving
infants various forms of opium sold under the name of “_soothing
syrups_,” “_infants’ friends_,” “_infants’ preservatives_,” “_nurses’
drops_” and the like, to allay restlessness, and to keep them during the
greater part of their existence asleep. Another fertile cause of
accidental poisoning is mistakes in dispensing; but these mistakes seem
to happen more frequently on the Continent than in England. This is in
some degree due to the decimal system, which has its dangers as well as
its advantages, _e.g._:--A physician ordered ·5 decigrm. of morphine
acetate in a mixture for a child, but omitted the decimal point, and the
apothecary, therefore, gave ten times the dose desired, with fatal
effect. Again, morphine hydrochlorate, acetate, and similar soluble
salts are liable to be mistaken for other white powders, and in this way
unfortunate accidents have occurred--accidents that, with proper
dispensing arrangements, should be impossible.

§ 349. =Poisoning of Children by Opium.=--The drugging of children by
opium--sometimes with a view to destroy life, sometimes merely for the
sake of the continual narcotism of the infant--is especially rife in
India.[377] A little solid opium is applied to the roof of the mouth, or
smeared on the tongue, and some Indian mothers have been known to
plaster the nipples with opium, so that the child imbibes it with the
milk. Europeans, again and again, have discovered the native nurses
administering opiates to the infants under their care, and it is feared
that in many cases detection is avoided.

[377] See Dr. Chevers’s _Jurisprudence_, 3rd ed., 232 _et seq._

The ignorant use of poppy-tea has frequently caused the death of young
children; thus in 1875 an inquest was held at Chelsea on the body of a
little boy two years and a half old. He had been suffering from
whooping-cough and enlargement of the bowels, and poppy-tea was by the
advice of a neighbour given to him. Two poppy-heads were used in making
a quart of tea, and the boy, after drinking a great portion of it, fell
into a deep sleep, and died with all the symptoms of narcotic poisoning.

§ 350. =Doses of Opium and Morphia.=--Opium in the solid state is
prescribed for adults in quantities not exceeding 3 grains, the usual
dose being from 16·2 mgrms. to 64·8 mgrms. (¼ to 1 grain). The extract
of opium is given in exactly the same proportions (special
circumstances, such as the habitual use of opium, excepted); the dose of
all the compounds of opium is mainly regulated by the proportion of
opium contained in them.

The dose for children (who bear opium ill) is usually very small; single
drops of laudanum are given to infants at the breast, and the dose
cautiously increased according to age. Most practitioners would consider
half a grain a very full dose, and, in cases requiring it, would seldom
prescribe at first more than 1/16 to ¼ grain.

The dose of solid opium for a horse is from 1·77 grm. to 7·08 grms. (½
drachm to 2 drachms); in extreme cases, however, 4 drachms (14·16 grms.)
have been given.

The dose for large cattle is from ·648 grm. to 3·88 grms. (10 to 60
grains); for calves, ·648 grm. (10 grains); for dogs it is greatly
regulated by the size of the animal, 16·2 to 129·6 mgrms. (¼ grain to 2

=Fatal Dose.=--Cases are recorded of infants dying from extremely small
doses of opium, _e.g._, ·7, 4·3, and 8·1 mgrms. (1/90, 1/15, and ⅛ of a
grain); but in such instances one cannot help suspecting some mistake.
It may, however, be freely conceded that a very small quantity might be
fatal to infants, and that 3 mgrms. given to a child under one year
would probably develop serious symptoms.

The smallest dose of solid opium known to have proved fatal to adults
was equal to 259 mgrms. (4 grains) of crude opium (_Taylor_), and the
smallest dose of the tincture (laudanum), 7·0 c.c. (2 drachms),
(_Taylor_); the latter is, however, as already shown, uncertain in its

A dangerous dose (save under special circumstances) is:--For a horse,
14·17 grms. (4 drachms); for cattle, 7·04 grms. (2 drachms); for a dog
of the size and strength of a foxhound, 204 mgrms. (3 grains).

Enormous and otherwise fatal doses may be taken under certain conditions
by persons who are not opium-eaters. I have seen 13 cgrms. (2 grains) of
morphine acetate injected hypodermically in a strong man suffering from
rabies with but little effect. Tetanus, strychnine, convulsions, and
excessive pain all decrease the sensibility of the nervous system to

§ 351. =General Method for the Detection of Opium.=--It is usually laid
down in forensic works that, where poisoning by opium is suspected, it
is sufficient to detect the presence of meconic acid in order to
establish that of opium. In a case of adult poisoning there is generally
substance enough available to obtain one or more alkaloids, and the
presence of opium may, without a reasonable doubt, be proved, if meconic
acid (as well as either morphine, narcotine, thebaine, or other opium
alkaloid) has been detected. Pills containing either solid opium or the
tincture usually betray the presence of the drug by the odour, and in
such a case there can be no possible difficulty in isolating morphine
and meconic acid, with probably one or two other alkaloids. The method
of extraction from organic fluids is the same as before described, but
it may, of course, be modified for any special purpose. If opium, or a
preparation of opium, be submitted to Dragendorff’s process (see p.
242), the following is a sketch of the chief points to be noticed.

If the solution is _acid_--

(1.) =Benzene= mainly extracts _meconin_, which dissolves in sulphuric
acid very gradually (in twenty-four to forty-eight hours), with a green
colour passing into red. Meconin has no alkaloidal reaction.

(2.) =Amyl alcohol= dissolves small quantities of _meconic acid_,
identified by striking a blood-red colour with ferric chloride.

If now the amyl alcohol is removed with the aid of petroleum ether, and
the fluid made alkaline by ammonia--

(1.) =Benzene= extracts _narcotine_, _codeine_, and _thebaine_. On
evaporation of the benzene the alkaloidal residue may be dissolved in
water, acidified with sulphuric acid, and after filtration, on adding
ammonia _in excess_, _thebaine and narcotine_ are precipitated,
_codeine_ remaining in solution. The dried precipitate, if it contain
thebaine, becomes blood-red when treated with cold concentrated
sulphuric acid, while narcotine is shown by a violet colour developing
gradually when the substance is dissolved in dilute sulphuric acid 1 :
5, and gently warmed. The codeine in the ammoniacal solution can be
recovered by shaking up with benzene, and recognised by the red colour
which the solid substance gives when treated with a little sugar and
sulphuric acid.

(2.) =Chloroform= especially dissolves the _narceine_, which, on
evaporation of the chloroform, may be identified by its general
characters, and by its solution in Fröhde’s reagent becoming a beautiful
blue colour. Small quantities of morphine may be extracted with codeine.

(3.) =Amyl alcohol= extracts from the alkaline solution morphine,
identified by its physical characters, by its forming a crystalline
precipitate with iodine and hydriodic acid, and the reaction with iodic
acid to be described.

§ 352. =Morphine= (C₁₇H₁₇NO(OH)₂ + H₂O).--Morphine occurs in commerce as
a white powder, sp. gr. 1·205, usually in the form of more or less
perfect six-sided prisms, but sometimes in that of white silky needles.
When heated in the subliming cell (described at pp. 257-8), faint
nebulæ, resolved by high microscopic powers into minute dots, appear on
the upper disc at 150°. As the temperature is raised the spots become
coarser, and at 188° distinct crystals may be obtained, the best being
formed at nearly 200°, at which temperature morphine begins distinctly
to brown, melt, and carbonise. At temperatures below 188°, instead of
minute dots, the sublimate may consist of white circular spots or
foliated patterns. One part of morphine, according to P. Chastaing, is
soluble at a temperature of 3° in 33,333 parts of water; at 22°, in 4545
parts; at 42°, 4280; and at 100°, 4562. It is scarcely soluble in ether
or benzene. Absolute alcohol, according to Pettenkofer, dissolves in the
cold one-fortieth of its weight; boiling, one-thirtieth. Amyl alcohol,
in the cold, dissolves one-fourth per cent., and still more if the
alkaloid be thrown out of an aqueous acid solution by ammonia in the
presence of amyl alcohol; for under such circumstances the morphine has
no time to become crystalline. According to Schlimpert, 1 part of
morphine requires 60 of chloroform for solution; according to
Pettenkofer, 175.

Morphine is easily soluble in dilute acids, as well as in solutions of
the caustic alkalies and alkaline earths; carbonated alkalies and
chloride of ammonium also dissolve small quantities. The acid watery,
and the alcoholic solutions, turn the plane of polarisation to the left;
for sulphuric, nitric, and hydrochloric acids [α]_r_ = 89·8°; in
alkaline solution the polarisation is less, [α]_r_ = 45·22°. It is
alkaline in reaction, neutralising acids fully; and, in fact, a
convenient method of titrating morphine is by the use of a centinormal
sulphuric acid--each c.c. equals 2·85 mgrms. of anhydrous morphine.

§ 353. The salts of morphine are for the most part crystalline, and are
all bitter, neutral, and poisonous. They are insoluble in amylic
alcohol, ether, chloroform, benzene, or petroleum ether.

=Morphine meconate= is one of the most soluble of the morphine salts; it
is freely soluble in water. Of all salts this is most suitable for
subcutaneous injection; it is the form in which the alkaloid exists in

=Morphine hydrochlorate= (C₁₇H₁₉NO₃HCl) crystallises in silky fibres; it
is readily soluble in alcohol, and is soluble in cold, more freely in
boiling water. The purest morphine hydrochlorate is colourless, but that
which is most frequently met with in commerce is fawn or buff-coloured.

=Morphine acetate= is a crystallisable salt, soluble in water or
alcohol; it is in part decomposed by boiling the aqueous solution, some
of the acetic acid escaping.

=Morphine Tartrates.=--These are readily soluble salts, and it is
important to note that the morphine might escape detection, if the
expert trusted alone to the usual test of an alkaloidal salt giving a
precipitate when the solution is alkalised by the fixed or volatile
alkalies; for the tartrates of morphine do not give this reaction, nor
do they give any precipitate with calcic chloride. By adding a solution
of potassium acetate in spirit, and also alcohol and a little acetic
acid to the concentrated solution, the tartrate is decomposed, and acid
tartrate of potassium is precipitated in the insoluble form; the
morphine in the form of acetate remains in solution, and then gives the
usual reactions.

The solubility of morphine salts in water and alcohol has been
investigated by Mr. J. U. Lloyd. His results are as follows:--

  =Morphine Acetate.=

   11·70 parts of water by weight at 15·0° dissolve 1 part of morphine
   61·5  parts of water by weight at 100° dissolve 1 part of morphine
   68·30 parts of alcohol by weight (·820 specific gravity) at 15·0°
         dissolve 1 part of morphine acetate.
   13·30 parts of alcohol by weight (·820 specific gravity) at 100°
         dissolve 1 part of morphine acetate.

  =Morphine Hydrochlorate.=

   23·40 parts of water dissolve at 15° 1 morphine hydrochlorate.
     ·51 part of water dissolves at 100° 1 morphine hydrochlorate.
   62·70 parts of alcohol (·820 specific gravity) dissolve at 15° 1
         morphine hydrochlorate.
   30·80 parts of alcohol (·820 specific gravity) dissolve at 100° 1
         morphine hydrochlorate.

  =Morphine Sulphate.=

   21·60 parts of water at 15° dissolve 1 morphine sulphate.
     ·75 part of water at 100° dissolves 1 morphine sulphate.
  701·5  parts of alcohol (·820) at 15° dissolve 1 morphine sulphate.
  144·00 parts of alcohol (·820) at 100° dissolve 1 morphine sulphate.

§ 354. =Constitution of Morphine.=--The chief facts bearing on the
constitution of morphine are as follows:--

It certainly contains two hydroxyl groups, because by the action of
acetic anhydride, acetyl morphine and diacetyl morphine,
C₁₇H₁₈(CH₃CO)NO₃ and C₁₇H₁₇(CH₃CO)₂NO₃ are produced. The formation of
the monomethyl ether of morphine (codeine), C₁₇H₁₇(OH)(OCH₃)NO, is also
a testimony to the existence of hydroxyl groups. One of the hydroxyl
groups has phenolic functions, the other alcoholic functions. By
suitable oxidation morphine yields trinitrophenol (picric acid), and by
fusion with an alkali, protocatechuic acid; both of these reactions
suggest a benzene ring. On distilling with zinc dust phenanthrene,
pyridine, pyrrol, trimethylamine, and ammonia are formed; evidence of a
pyridine nucleus. If morphine is mixed with 10 to 15 times its weight of
a 20 per cent. solution of potash, and heated at 180° for from four to
six hours, air being excluded, a phenol-like compound is formed, and a
volatile amine, ethylmethylamine (the amine boils at 34° to 35°, and its
hydrochloride melts at 133°). This reaction is interpreted by Z. H.
Skrauk[378] and L. Wiegmann to indicate that the nitrogen is directly
connected with two alkyl groups--that is, ethyl and methyl.

[378] _Monatsb._, x. 110-114.

G. N. Vis,[379] after a careful review of the whole of the reactions of
morphine, has proposed the following constitutional formula as the one
that agrees best with the facts:--

  |       |   |   |                 |  |
  CH--CH--CH--O   NMe--CH₂--CH(OH)--C--CH--CH

[379] _J. pr. Chemie_ (2), xlvii. 584. Knorr’s formula is--

         /      |       \
  OH.C₁₀H₅       |        >
         \      |       /

_Ber._, xxii. 1113-1119.

§ 355. =Tests for Morphine.=--(1.) One hundredth of a milligrm. of pure
morphine gives a blue colour to a paste of ammonium molybdate in
sulphuric acid; 20 mgrms. of ammonium molybdate are rubbed with a glass
rod in a porcelain dish, and well mixed with 5 drops of pure strong
sulphuric acid and the morphine in a solid form applied; titanic acid
and tungstates give similar reactions.

(2.) Morphine possesses strong reducing properties; a little solid
morphine dissolved in a solution of ferric chloride gives a Prussian
blue precipitate when ferridcyanide solution is added. A number of
ptomaines and other substances also respond to this test, so that in
itself it is not conclusive.

(3.) =Iodic Acid Test.=--The substance supposed to be morphine is
converted into a soluble salt by adding to acid reaction a few drops of
hydrochloric acid, and then evaporating to dryness. The salt thus
obtained is dissolved in as little water as possible--this, as in
toxicological researches only small quantities are recovered, will
probably be but a few drops. A little of the solution is now mixed with
a very small quantity of starch paste, and evaporated to dryness at a
gentle heat in a porcelain dish. After cooling, a drop of a solution of
1 part of iodic acid in 15 of water is added to the dry residue; and if
even the 1/20000 of a grain of morphine be present, a blue colour will
be developed.

Another way of working the iodic acid test is to add the iodic acid
solution to the liquid in which morphine is supposed to be dissolved,
and then shake the liquid up with a few drops of carbon disulphide. If
morphine be present, the carbon disulphide floats to the top distinctly
coloured pink. Other substances, however, also set free iodine from
iodic acid, and it has, therefore, been proposed to distinguish morphine
from these by the after addition of ammonia. If ammonia is added to the
solution, which has been shaken up with carbon disulphide, the pink or
red colour of the carbon disulphide is deepened, if morphine was
present; on the contrary, if morphine was _not_ present, it is either
discharged or much weakened.

=Other Reactions.=--There are some very interesting reactions besides
the two characteristic tests just mentioned. If a saturated solution of
chloride of zinc be added to a little solid morphine, and heated over
the water-bath for from fifteen minutes to half-an-hour, the liquid
develops a beautiful and persistent green colour. This would be an
excellent test for morphine were it not for the fact that the colour is
produced with only pure morphine. For example, I was unable to get the
reaction from morphine in very well-formed crystals precipitated from
ordinary laudanum by ammonia, the least trace of resinous or
colouring-matter seriously interfering. By the action of nitric acid on
morphine, the liquid becomes orange-red, and an acid product of the
formula C₁₀H₉NO₉ is produced, which, when heated in a closed tube with
water at 100°, yields trinitrophenol or picric acid. This interesting
reaction points very decidedly to the phenolic character of morphine. On
adding a drop of sulphuric acid to solid morphine in the cold, the
morphine solution becomes of a faint pink; on gently warming and
continuing the heat until the acid begins to volatilise, the colour
changes through a series of brownish and indefinite hues up to black. On
cooling and treating the black spot with water, a green solution is
obtained, agreeing in hue with the same green produced by chloride of
zinc. Vidali[380] has proposed the following test:--Morphine is
dissolved in strong sulphuric acid, and a little arsenate of sodium is
added; on gently warming, a passing blue colour develops; on raising the
temperature higher, the liquid changes into green, then into blue, and
finally again into green. Codeine acts very similarly. The following
test originated with Siebold (_American Journal of Pharmacy_, 1873, p.
544):--The supposed morphine is heated gently with a few drops of
concentrated sulphuric acid and a little pure potassic perchlorate. If
morphine be present the liquid immediately takes a pronounced brown
colour--a reaction said to be peculiar to morphine, and to succeed with
1/10 of a mgrm. In order to obtain absolutely pure perchlorate, potassic
perchlorate is heated with hydrochloric acid so long as it disengages
chlorine; it is then washed with distilled water, dried, and preserved
for use. There is also a test known as “Pellagri’s”; it depends on the
production of apomorphine. The suspected alkaloid is dissolved in a
little strong hydrochloric acid, and then a drop of concentrated
sulphuric acid is added, and the mixture heated for a little time from
100° to 120°, until it assumes a purple-black colour. It is now cooled,
some hydrochloric acid again added, and the mixture neutralised with
sodic carbonate. If morphine be present, on the addition of iodine in
hydriodic acid, a cherry-red colour is produced, passing into green.
Morphine and codeine are believed alone to give this reaction.

[380] D. Vidali, _Bull. Farmaceut._, Milano, 1881, p. 197; D. E. Dott,
_Year Book of Pharmacy_, 1882.

The acetate of morphine, and morphine itself, when added to ferric
chloride solution, develop a blue colour. When 1 molecule of morphine is
dissolved in alcohol, containing 1 molecule of sodium hydroxide, and 2
vols. of methyl iodide are added, and the mixture gently heated, a
violent reaction sets in and the main product is codeine methiodide
(C₁₇H₁₈NO₂OCH,MeI). If only half the quantity of methyl iodide is added,
then free codeine is in small quantity produced; if ethyl iodide be
substituted for methyl, a new base is formed homologous with
codeine--codeine is therefore the methyl ether of morphine. If morphine
is heated with iodide of methyl and absolute alcohol in a closed tube
for half an hour at 100°, methyl iodide of morphine is obtained in
colourless, glittering, quadratic crystals, easily soluble in water
(C₁₇H₁₉NO₃MeI + H₂O); similarly the ethyl iodide compound can be

If morphine is heated for from two to three hours in a closed tube with
dilute hydrochloric acid, water is eliminated--

  (C₁₇H₁₉NO₃ = C₁₇H₁₇NO₂ + H₂O),

and the hydrochlorate of apomorphine is produced. This succeeds when
even ½ mgrm. is heated with 1/10 c.c. of strong HCl, and the tests for
apomorphine applied.

If concentrated sulphuric acid be digested on morphine for twelve to
fifteen hours (or heated for half an hour at 100°), on adding to the
cooled violet-coloured solution either a crystal of nitrate of potash or
of chlorate of potash, or a drop of dilute nitric acid, a beautiful
violet-blue colour is produced, which passes gradually into a dark
blood-red. 1/100 of a mgrm. will respond distinctly to this test.
Fröhde’s reagent strikes with morphine a beautiful violet colour,
passing from blue into dirty green, and finally almost vanishing. 1/200
of a mgrm. will respond to the test, but it is not itself conclusive,
since papaverine and certain glucosides give an identical reaction.

§ 356. =Symptoms of Opium and Morphine Poisoning.=--The symptoms of
opium and morphine poisoning are so much alike, that clinically it is
impossible to distinguish them; therefore they may be considered

=Action on Animals--Frogs.=--The action of morphine or opium on frogs is
peculiar: the animal at first springs restlessly about, and then falls
into a condition extremely analogous to that seen in strychnine
poisoning, every motion or external irritation producing a tetanic
convulsion. This condition is, however, sometimes not observed. The
tetanic stage is followed by paralysis of reflex movements and cessation
of breathing, the heart continuing to beat.

=Dogs.=--0·2 to 0·5 grm. of morphine meconate, or acetate, injected
directly into the circulation of a dog, shows its effects almost
immediately. The dog becomes uneasy, and moves its jaws and tongue as if
some peculiar taste were experienced; it may bark or utter a whine, and
then in a minute or two falls into a profound sleep, which is often so
deep that while it lasts--usually several hours--an operation may be
performed. In whatever attitude the limbs are placed, they remain. The
respiration is rapid and stertorous, and most reflex actions are
extinguished. Towards the end of the sleep, any sudden noise may startle
the animal, and when he wakes his faculties are evidently confused. A
partial paralysis of the hind legs has often been noticed, and then the
dog, with his tail and pelvis low, has something the attitude of the
hyena. Hence this condition (first, I believe, noticed by Bernard) has
been called the “hyenoid” state. If the dose is larger than 2 to 3 grms.
(31 to 46 grains), the symptoms are not dissimilar, save that they
terminate in death, which is generally preceded by convulsions.[381]

[381] MM. Grasset and Amblard have studied the action of morphine in
causing convulsions in the mammalia. They found that if small doses of
hydrochlorate of morphine (from 1 to 15 centigrammes) are administered
to dogs, the brief sleep which is produced may be accompanied by partial
muscular contractions (in one paw, for instance), which are renewed at
variable intervals. Then occur true convulsive shocks in the whole body
or in the hind limbs. After an interval, the phenomena recur in more
intense degree, and are followed by true convulsions. Regularly, ten or
sixteen times a minute, at each inspiration, the hind limbs present a
series of convulsive movements, which may become general. Sometimes they
are excited by external stimulation, but they are usually spontaneous.
The sleep may continue profound during this convulsive period, or it may
become distinctly lighter. These convulsive phenomena may continue, with
intervals, for an hour. Differences are observed with different animals;
but the chief characters of the phenomena are as described. In certain
animals, and with small doses, there may be a brief convulsive phase at
the commencement of the sleep, but it is much less constant than the
later period of spasm. These convulsions, the authors believe, have not
previously been described, except as a consequence of very large doses,
amounting to grammes. The period of cerebral excitement, described by
Claude Bernard as occurring at the commencement of the sleep from
morphine, is a phenomenon of a different order. The conclusions drawn
from the experiments are--(1) That morphia is not diametrically opposed
to thebaine, as is often stated, since it has, to a certain degree, the
convulsive properties of the latter alkaloid. (2) That the excitomotor
action of opium cannot be exclusively attributed to the convulsive
alkaloids, but is, in fact, due to those which are soporific. According
to the ordinary composition of opium, 5 centigrammes of morphine
represent about a milligramme of thebaine. But these experiments show
that the quantity of morphine has a much more powerful convulsive action
than a milligramme of thebaine. (3) There is not the supposed antagonism
between the action of morphine on the frog and on the mammalia. (4) The
researches hitherto undertaken on the antagonism between morphine and
other agents need to be repeated, and a separate study made of the
substances which antagonise the convulsive and soporific action.

=Goats.=--According to Guinard, goats are proof against the narcotic
influence of morphine. Large doses kill goats, but death is caused by
interference with the respiratory function. A young goat weighing 30
kilos, showed little effect beyond a slightly increased cerebral
excitability after two doses of 8 and 8·5 grms. respectively of morphine
hydrochlorate had been administered by intravenous injection, the second
being given an hour and a half after the first. To the same animal two
days afterwards 195 grms. were administered in the same way, yet the
goat recovered. The lethal dose for a goat seems to be no less than 1000
times that which will produce narcotism in man, and lies somewhere
between 0·25 to 0·30 per kilo. of the body weight.[382]

[382] _Compt. Rend._, t. cxvi. pp. 520-522.

=Cats and the Felidæ.=--According to Guinard,[383] morphine injected
subcutaneously or intravenously into cats, in doses varying from 0·4
mgrm. to 90 mgrms. per kilo., never produces sleep or narcotic
prostration. On the contrary, it causes a remarkable degree of
excitement, increasing in intensity with the dose given. This excitement
is evidently accompanied by disorder in the functions of the brain, and
if the dose is large convulsions set in, ending in death. According to
Milne-Edwards, the same symptoms are produced in lions and tigers.

[383] _Compt. Rend._, t. cxi. pp. 981-983. The _bovine_ animals also get
excited, and no narcotic effect is produced by dosing them with
morphine.--_Compt. Rend. Soc. de Biologie_, t. iv., v.

=Birds=, especially pigeons, are able to eat almost incredible
quantities of opium. A pigeon is said[384] to have consumed 801 grains
of opium, mixed with its food, in fourteen days. The explanation of this
is that the poison is not absorbed; for subcutaneous injections of salts
of morphine act rapidly on all birds hitherto experimented upon.

[384] Hermann’s _Lehrbuch der exper. Toxicologie_, p. 374.

§ 357. =Physiological Action.=--From experiments on animals, the
essential action of morphine on the nervous and arterial systems has in
some measure been examined. There is no very considerable action on the
heart. The beats are first accelerated, then diminished in frequency;
but very large doses introduced directly into the circulation at once
diminish the pulsations, and no acceleration is noticed. The slowing may
go on to heart-paralysis. The slowing is central in its origin, for on
the vagi being cut, morphine always quickens. With regard to the
peripheric ends of the vagi, small doses excite, large paralyse. If all
the nerves going to the heart are divided, there is first a considerable
acceleration, and then a slowing and weakening of the pulsations. The
arterial blood-pressure, at first increased, is afterwards diminished.
This increase of blood-pressure is noticed during the acceleration of
the pulse, and also during some portion of the time during which the
pulse is slowed. Stockman and D. B. Dott,[385] experimenting on rabbits
and frogs, consider that a medium dose of morphine first of all
depresses the spinal cord and then excites it, for tetanus follows. If
morphine is in sufficient quantity thrown into the circulation then
tetanus at once occurs. It would thus appear that depression and
stimulation is entirely a matter of dosage. Gescheidlen, in his
researches on the frog, found the motor nerves at first excited, and
then depressed. When the doses were large, there was scarcely any
excitement, but the reverse effect, in the neighbourhood of the place of
application. According to other observers, the function of the motor
nerves may be annihilated.[386] According to Meihuizen, reflex action,
at first much diminished, is later, after several hours, normal, and
later still again increased. The intestinal movements are transitorily
increased. In the dog there has been noticed a greater flow of saliva
than usual, and the flow of bile from the gall-bladder is diminished.
The pupils in animals are mostly contracted, but, if convulsions occur
towards death, they are dilated.

[385] _Brit. Med. Journ._ (2), 1890, 189-192.

[386] _Arch. f. d. Ges. Physiol._, vii. p. 201.

§ 358. =Physiological Effect of Morphine Derivatives.=--By introducing
methyl, or amyl, or ethyl, into the morphine molecule, the narcotic
action is diminished, while the tetanic effects are increased. Acetyl,
diacetyl, benzoyl, and dibenzoyl morphine, morphine sulphuric ether, and
nitrosomorphine are all weaker narcotics than morphine, but, on the
other hand, they depress the functions of the spinal cord and bring on,
in large doses, tetanus.

The introduction of two methyl groups into morphine, as in
metho-codeine, C₁₇H₁₇MeNO(OH)-Me, entirely alters the physiological
effect. This compound has an action on voluntary muscle causing gradual

The chlorine derivatives, trichlormorphine and chlorcodeine, have the
characteristic action of the morphine group on the central nervous
system and, in addition, act energetically as muscle poisons, soon
destroying the contractile power of the voluntary muscles with which
they first come into contact at the place of injection, and more
gradually affecting the other muscles of the body.[387]

[387] R. Stockman and Dott, _Brit. Med. Journ._ (2), 1890, 189-192.

§ 359. =Action on Man.=--There are at least three forms of opium
poisoning:--(1) _The common form_, as seen in about 99 per cent. of
cases; (2) A very _sudden form_, in which death takes place with fearful
rapidity (the _foudroyante_ variety of the French);[388] and (3) a very
rare entirely _abnormal form_, in which there is no coma, but

[388] Tardieu, _Étude Méd. Légale sur l’Empoisonnement._

In the _common form_ there are three stages, viz.:--(1) Excitement; (2)
Narcosis; (3) Coma. In from half an hour to an hour[389] the first
symptoms commence, the pulse is quickened, the pupils are contracted,
the face flushes, and the hands and feet reddened,--in other words, the
capillary circulation is active. This stage has some analogy to the
action of alcohol; the ideas mostly flow with great rapidity, and
instead of a feeling of sleepiness, the reverse is the case. It,
however, insensibly, and more or less rapidly, passes into the next
stage of heaviness and stupor. There is an irresistible tendency to
sleep; the pulse and the respiration become slower; the conjunctivæ are
reddened; the face and head often flushed. In some cases there is great
irritability of the skin, and an eruption of nettle-rash. If the poison
has been taken by the mouth, vomiting may be present. The bowels are
usually--in fact almost invariably--constipated. There is also some loss
of power over the bladder.

[389] In a remarkable case related by Taylor, a lady took a large dose
(supposed to be 1½ oz.) of laudanum, and there were no symptoms for four
and a half hours. She died in twenty-two hours.

In the next stage, the narcosis deepens into dangerous coma; the patient
can no longer be roused by noises, shaking, or external stimuli; the
breathing is loud and stertorous; the face often pale; the body covered
with a clammy sweat. The pupils are still contracted, but they may in
the last hours of life dilate: and it is generally agreed that, if a
corpse is found with the pupils dilated, this circumstance, taken in
itself, does not contra-indicate opium or morphine poisoning. Death
occasionally terminates by convulsion.

The _sudden form_ is that in which the individual sinks into a deep
sleep almost immediately--that is, within five or ten minutes--and dies
in a few hours. In these rapid cases the pupils are said to be
constantly dilated.

Examples of the _convulsive form_ are to be sought among opium-eaters,
or persons under otherwise abnormal conditions.

A man, forty years old, who had taken opiates daily since his
twenty-second year--his dose being 6 grms. (92·4 grains) of solid
opium--when out hunting, of which sport he was passionately fond, took
cold, and, as a remedy, administered to himself three times his
accustomed dose. Very shortly there was contraction of the left arm,
disturbance of vision, pain in the stomach, faintness, inability to
speak, and unconsciousness which lasted half an hour. Intermittent
convulsions now set in, and pains in the limbs. There was neither
somnolence nor delirium, but great agitation; repeated vomiting and
diarrhœa followed. After five hours these symptoms ceased; but he was
excessively prostrate.[390] There was complete recovery.

[390] Demontporcellet, _De l’Usage Quotidien de l’Opium_, Paris, 1874.

One may hazard a surmise that, in such a case, tolerance has been
established for morphine, but not for other morphine alkaloids in the
same degree, and that the marked nervous symptoms were in no small
degree the effect of some of the homologous alkaloids, which, in such an
enormous dose, would be taken in sufficient quantity to have a
physiological action.

There are several instances of a relapsing or remittent form of
poisoning--a form in which the patient more or less completely recovers
consciousness, and then sinks back into a fatal slumber. One of the best
known is the case of the Hon. Mrs Anson (January 1859), who swallowed an
ounce and a half of laudanum by mistake. After remaining in a comatose
condition for more than nine hours, she revived. The face became
natural, the pulse steady. She was able to recognise her daughter, and
in a thick voice to give an account of the mistake. But this lasted only
ten minutes, when she again became comatose, and died in fourteen

[391] Taylor, _op. cit._

In a Swedish case quoted by Maschka,[392] a girl, nine years old, in
weak health and suffering from slight bronchitis, had been given a
non-officinal acetate of morphia lozenge, which was supposed to contain
5 mgrms. (·075 grain) of morphine acetate. She took the lozenge at eight
in the evening; soon slept, woke at ten, got out of bed, laughed,
talked, and joked with the nurse, again got into bed, and very quickly
fell asleep. At four A.M. the nurse came and found her breathing with a
rattling sound, and the physician, who arrived an hour later, found the
girl in a state of coma, with contracted pupils, breathing stertorously,
and the pulse scarcely to be felt. Despite all attempts to rouse the
patient, she died at eight in the morning, twelve hours after taking the

[392] Maschka’s _Handbuch_, Band ii. p. 438; also Svenska, _Läk-Sällsk.
Förhandl._, Apr. 1, p. 90; Apr. 8, p. 160, 1873. For other cases see
Nasmyth, _Edin. Med. Journ._, Dec. 1878; Kirby, _Dub. Med. Press_, Dec.
24, 1845; W. Boyd Muschet, _Med. Times and Gaz._, March 20, 1858.

The _post-mortem_ examination showed some hyperæmia of the brain and
serous effusion in the ventricles, and there was also tubercle in the
pleura. Three lozenges similar to the one taken by the patient were
chemically investigated by Hamberg, who found that the amount of acetate
was very small, and that the lozenges, instead of morphine acetate,
might be considered as prepared with almost pure morphine; the content
in the three of morphine being respectively 35, 37, and 42 mgrms. (that
is, from half a grain to three-fifths of a grain). There was a
difference of opinion among the experts as to whether in this case the
child died from morphine poisoning or not--a difference solely to be
attributed to the waking up of the child two hours after taking the
poison. Now, considering the great probability that a large dose for a
weakly child of that age had been taken, and that this is not the only
case in which a relapse has occurred, it seems just to infer that it was
really a case of poisoning.

As unusual symptoms (or rather sequelæ) may be noted in a few cases,
hemiplegia, which soon passes off; a weakness of the lower extremities
may also be left, and inability to empty the bladder thoroughly; but
usually on recovery from a large dose of opium, there is simply
heaviness of the head, a dry tongue, constipation, and loss of appetite.
All these symptoms in healthy people vanish in a day or two. There have
also been noticed slight albuminuria, eruptions on the skin, loss of
taste, and numbness of parts of the body.

Opium, whether taken in substance, or still more by subcutaneous
injection, in some individuals constantly causes faintness. In my own
case, I have several times taken a single grain of opium to relieve
either pain or a catarrh; almost invariably within an hour afterwards
there has been great coldness of the hands and feet, lividity of the
face, a feeling of deadly faintness followed by vomiting; this stage
(which has seldom lasted more than half an hour) passed, the usual
narcotic effects have been produced.

Some years ago I injected one-sixth of a grain of morphine hydrochlorate
subcutaneously into an old gentleman, who was suffering from acute
lumbago, but was otherwise healthy, and had no heart disease which could
be detected; the malady was instantly relieved, and he called out, “I am
well; it is most extraordinary.” He went out of the front door, and
walked some fifty yards, and then was observed to reel about like a
drunken man. He was supported back and laid in the horizontal posture;
the face was livid, the pulse could scarcely be felt, and there was
complete loss of consciousness. This state lasted about an hour, and
without a doubt the man nearly died. Medical men in practice, who have
been in the habit of using hypodermic injections of morphine, have had
experiences very similar to this and other cases, and although I know of
no actual death, yet it is evident that morphine, when injected
hypodermically even in a moderate dose, may kill by syncope, and within
a few minutes.[393] Absorption by hypodermic administration is so rapid
that by the time, or even before the needle of the syringe is withdrawn,
a contraction of the pupil may be observed.

[393] See a case of morphia poisoning by hypodermic injection, and
recovery, by Philip E. Hill, M.R.C.S., _Lancet_, Sept. 30, 1882. In this
instance a third of a grain introduced subcutaneously caused most
dangerous symptoms in a gardener, aged 48.

Opium or morphine is poisonous by whatever channel it gains access to
the system, the intestinal mucous membrane absorbs it readily, and
narcotic effects may be produced by external applications, whether a
wound is present or not. A case of absorption of opium by a wound is
related in Chevers’s _Jurisprudence_.[394] A Burman boy, about nine or
ten years of age, was struck on the forehead by a brick-bat, causing a
gaping wound about an inch long; his parents stuffed the wound with
opium. On the third day after the accident, and the opium still
remaining in the wound, he became semi-comatose, and, in short, had all
the symptoms of opium narcosis; with treatment he recovered. The
unbroken skin also readily absorbs the drug. Tardieu states that he had
seen 30 grms. of laudanum, applied on a poultice to the abdomen, produce
death. Christison has also cited a case in which a soldier suffered from
erysipelas, and died in a narcotic state, apparently produced from the
too free application of laudanum to the inflamed part.

[394] Third ed., p. 228.

To these cases may be added the one cited by Taylor, in which a druggist
applied 30 grains of morphine to the surface of an ulcerated breast, and
the woman died with all the symptoms of narcotic poisoning ten hours
after the application--an event scarcely surprising. It is a curious
question whether sufficient of the poison enters into the
secretions--_e.g._, the milk--to render it poisonous. An inquest was
held in Manchester, Nov. 1875, on the body of a male child two days old,
in which it seemed probable that death had occurred through the mother’s
milk. She was a confirmed opium-eater, taking a solid ounce per week.

§ 360. =Diagnosis of Opium Poisoning.=--The diagnosis is at times
between poisoning by opium or other narcotic substances, at others,
between opium and disease. Insensibility from chloral, from alcohol,
from belladonna or atropine, and from carbon oxide gas, are all more or
less like opium poisoning. With regard to chloral, it may be that only
chemical analysis and surrounding circumstances can clear up the matter.
In alcohol poisoning, the breath commonly smells very strongly of
alcohol, and there is no difficulty in separating it from the contents
of the stomach, &c., besides which the stomach is usually red and
inflamed. Atropine and belladonna invariably dilate the pupil, and
although just before death opium has the same effect, yet we must hold
that mostly opium contracts, and that a widely-dilated pupil during life
would, _per se_, lead us to suspect that opium had not been used,
although, as before mentioned, too much stress must not be laid upon the
state of the pupils. In carbon oxide, the peculiar rose-red condition of
the body affords a striking contrast to the pallor which, for the most
part, accompanies opium poisoning. In the rare cases in which
convulsions are a prominent symptom, it may be doubtful whether opium or
strychnine has been taken, but the convulsions hitherto noticed in opium
poisoning seem to me to have been rather of an epileptiform character,
and very different from the effects of strychnine. No rules can be laid
down for cases which do not run a normal course; in medicine such are
being constantly met with, and require all the care and acumen of the
trained observer. Cases of disease render a diagnosis often extremely
difficult, and the more so in those instances in which a dose of
laudanum or other opiate has been administered. In a case under my own
observation, a woman, suffering from emphysema and bronchitis, sent to a
chemist for a sleeping draught, which she took directly it arrived. A
short time afterwards she fell into a profound slumber, and died within
six hours. The draught had been contained in an ounce-and-a-half bottle;
the bottle was empty, and the druggist stated in evidence that it only
contained 20 minims of laudanum, 10 grains of potassic bromide, and
water. On, however, diluting the single drop remaining in the bottle,
and imitating its colour with several samples of laudanum diluted in the
same way, I came to the conclusion that the quantity of laudanum which
the bottle originally contained was far in excess of that which had been
stated, and that it was over 1 drachm and under 2 drachms. The body was
pallid, the pupils strongly contracted, the vessels of the brain
membranes were filled with fluid blood, and there was about an ounce of
serous fluid in each ventricle. The lungs were excessively
emphysematous, and there was much secretion in the bronchi; the liver
was slightly cirrhotic. The blood, the liver, and the contents of the
stomach were exhaustively analysed with the greatest care, but no trace
of morphine, narcotine, or meconic acid could be separated, although the
woman did not live more than six hours after taking the draught. I gave
the opinion that it was, in the woman’s state, improper to prescribe a
sedative of that kind, and that probably death had been accelerated, if
not directly caused, by opium.

Deaths by apoplexy will only simulate opium-poisoning during life; a
_post-mortem_ examination will at once reveal the true nature of the
malady. In epilepsy, however, it is different, and more than once an
epileptic fit has occurred and been followed by coma--a coma which
certainly cannot be distinguished from that produced by a narcotic
poison. Death in this stage may follow, and on examining the body no
lesion may be found.

§ 361. =Opium-eating.=--The consumption of opium is a very ancient
practice among Eastern nations, and the picture, drawn by novelist and
traveller, of poor, dried-up, yellow mortals addicted to this vice, with
their faculties torpid, their skin hanging in wrinkles on their wasted
bodies, the conjunctivæ tinged with bile, the bowels so inactive that
there is scarcely an excretion in the course of a week, the mental
faculties verging on idiocy and imbecility, is only true of a percentage
of those who are addicted to the habit. In the _British Medical Journal_
for 1894, Jan. 13 and 20, will be found a careful digest of the
evidence collated from 100 Indian medical officers, from which it
appears that opium is taken habitually by a very large number of the
population throughout India, those who are accustomed to the drug taking
it in quantities of from 10 to 20 grains in the twenty-four hours; so
long as this amount is not exceeded they do not appear to suffer
ill-health or any injurious effect. The native wrestlers even use it
whilst training. The habitual consumption of opium by individuals has a
direct medico-legal bearing. Thus in India, among the Rajpoots, from
time immemorial, infused opium has been the drink both of reconciliation
and of ordinary greeting, and it is no evidence of death by poison if
even a considerable quantity of opium be found in the stomach after
death, for this circumstance taken alone would, unless the history of
the case was further known, be considered insufficient proof. So, again,
in all climates, and among all races, it is entirely unknown what
quantity of an opiate should be considered a poisonous dose for an
opium-eater. Almost incredible quantities have, indeed, been consumed by
such persons, and the commonly-received explanation, that the drug, in
these cases, passes out unabsorbed, can scarcely be correct, for Hermann
mentions the case of a lady of Zurich who daily injected subcutaneously
1 to 2 grms. (15-31 grains) of a morphine salt. In a case of uterine
cancer, recorded by Dr. W. C. Cass,[395] 20 grains of morphine in the
twelve hours were frequently used subcutaneously; during thirteen months
the hypodermic syringe was used 1350 times, the dose each time being 5
grains. It is not credible that an alkaloid introduced into the body
hypodermically should not be absorbed.

[395] _Lancet_, March 25, 1882. See also Dr. Boulton’s case, _Lancet_,
March 18, 1882.

Opium-smoking is another form in which the drug is used, but it is an
open question as to what poisonous alkaloids are in opium smoke. It is
scarcely probable that morphine should be a constituent, for its
subliming point is high, and it will rather be deposited in the cooler
portion of the pipe. Opium, specially prepared for smoking, is called
“Chandoo”; it is dried at a temperature not exceeding 240°. H.
Moissan[396] has investigated the products of smoking chandoo, but only
found a small quantity of morphine. N. Gréhant and E. Martin[397] have
also experimented with opium smoke; they found it to have no appreciable
effect on a dog; one of the writers smoked twenty pipes in succession,
containing altogether 4 grms. of chandoo. After the fourth pipe there
was some headache, at the tenth pipe and onwards giddiness. Half an hour
after the last pipe the giddiness and headache rapidly went off. In any
case, opium-smoking seems to injure the health of Asiatics but little.
Mr. Vice-Consul King, of Kew-Kiang, in a tour through Upper Yangtse and
Stechnan, was thrown much into the company of junk sailors and others,
“almost every adult of whom smoked more or less.” He says:--“Their work
was of the hardest and rudest, rising at four and working with hardly
any intermission till dark, having constantly to strip and plunge into
the stream in all seasons, and this often in the most dangerous parts.
The quantity of food they eat was simply prodigious, and from this and
their work it seems fairly to be inferred that their constitution was
robust. The two most addicted to the habit were the pilot and the ship’s
cook. On the incessant watchfulness and steady nerve of the former the
safety of the junk and all on board depended, while the second worked so
hard from 3 A.M. to 10 P.M., and often longer, and seemed so independent
of sleep or rest, that to catch him seated or idle was sufficient cause
for good-humoured banter. This latter had a conserve of opium and sugar
which he chewed during the day, as he was only able to smoke at night.”

[396] _Compt. Rend._, cxv. 988-992.

[397] _Compt. Rend._, 1012-1014.

§ 362. =Treatment of Opium or Morphine Poisoning.=--The first thing to
be done is doubtless to empty the stomach by means of the flexible
stomach tube; the end of a sufficiently long piece of indiarubber tubing
is passed down into the pharynx and allowed to be carried into the
stomach by means of the natural involuntary movements of the muscles of
the pharynx and gullet; suction is then applied to the free end and the
contents syphoned out; the stomach is, by means of a funnel attached to
the tube, washed out with warm water, and then some coffee administered
in the same way.

Should morphine have been taken, and permanganate of potash be at hand,
it has been shown that under such circumstances potassic permanganate is
a perfect antidote, decomposing at once any morphine remaining in the
stomach, but it, of course, will have no effect upon any morphine which
has already been absorbed. In a case of opium poisoning, reported in the
_Lancet_ of June 2, 1894, by W. J. C. Merry, M.B., inhalations of
oxygen, preceded by emptying the stomach and other means, appeared to
save a man, who, three hours before the treatment, had drank 2 ozs. of
chlorodyne. It is also the received treatment to ward off the fatal
sleep by stimulation; the patient is walked about, flicked with a towel,
made to smell strong ammonia, and so forth. This stimulation must,
however, be an addition, but must never replace the measures first

§ 363. =Post-mortem Appearances.=--There are no characteristic
appearances after death save hyperæmia of the brain and blood-vessels of
the membranes, with generally serous effusion into the ventricles. The
pupils are sometimes contracted, sometimes dilated, the dilatation
occurring, as before mentioned, in the act of dying. The external
surface of the body is either livid or pale. The lungs are commonly
hyperæmic, the bladder full of urine; still, in not a few cases, there
is nothing abnormal, and in no single case could a pathologist, from the
appearance of the organs only, declare the cause of death with

§ 364. =Separation of Morphine from Animal Tissues and
Fluids.=--Formerly a large proportion of the opium and morphine cases
submitted to chemical experts led to no results; but owing to the
improved processes now adopted, failure, though still common, is less
frequent. The constituents of opium taken into the blood undergo partial
destruction in the animal body, but a portion may be found in the
secretions, more especially in the urine and fæces. First
Bouchardat[398] and then Lefort[399] ascertained the excretion of
morphine by the urine after medicinal doses; Dragendorff and Kauzmann
showed that the appearance of morphine in the urine was constant, and
that it could be easily ascertained and separated from the urine of men
and animals; and Levinstein[400] has also shown that the elimination
from a single dose may extend over five or six days. The method used by
Dragendorff to extract morphine from either urine or blood is to shake
the liquid (acidified with a mineral acid) several times with amyl
alcohol, which, on removal, separates urea and any bile acids. The
liquid thus purified is then alkalised, and shaken up with amyl alcohol,
and this amyl alcohol should contain any morphine that was present. On
evaporation it may be pure enough to admit of identification, but if
not, it may be redissolved and purified on the usual principles.
Considerable variety of results seems to be obtained by different
experimenters. Landsberg[401] injected hypodermically doses of ·2 to ·4
grm. of morphine hydrochlorate into dogs, making four experiments in
all, but failed to detect morphine in the urine. A large dose with 2·4
mgrms. of the salt gave the same result. On the other hand, ·8 grm. of
morphine hydrochlorate injected direct into the jugular vein, was partly
excreted by the kidneys, for 90 c.c. of the urine yielded a small
quantity of morphine. Voit, again, examined the urine and fæces of a man
who had taken morphine for years; he could detect none in the urine, but
separated morphine from the fæces.[402] Morphine may occasionally be
recognised in the blood. Dragendorff[403] found it in the blood of a cat
twenty-five minutes after a subcutaneous dose, and he also separated it
from the blood of a man who died of morphine poisoning in six hours.
Haidlen[404] recognised morphine in the blood of a suicide who had taken
opium extract.

[398] _Bull. Gén. de Thérap._, Dec. 1861.

[399] _Journ. de Chim._, xi. 93, 1861.

[400] _Berl. klin. Wochenschr._, 1876, 27.

[401] _Pflüger’s Archiv._, 23, 433, 413-433. _Chem. Soc. Journ._, May
1882, 543.

[402] _Arch. Pharm._, pp. [3], vii. pp. 23-26.

[403] Kauzmann, _Beiträge für den gerichtlich-chemischen Nachweis des
Morphia u. Narcotins_, Dissert., Dorpat, 1868. Dragendorff, _Pharm.
Zeitschr. f. Russland_, 1868, Hft. 4.

[404] _Würtbg. Correspondenzbl._, xxxiv. 16, 1863.

On the other hand, in a case recorded at p. 304, where a woman died in
six hours from a moderate dose, probably of laudanum, although the
quantity of blood operated upon was over a pound in weight, and every
care was taken, the results were entirely negative. In poisoning by
laudanum there may be some remaining in the stomach, and also if large
doses of morphine have been taken by the mouth; but when morphine has
been administered hypodermically, and in all cases in which several
hours have elapsed, one may almost say that the organ in which there is
the least probability of finding the poison is the stomach. It may, in
some cases, be necessary to operate on a very large scale;--to examine
the fæces, mince up the whole liver, the kidney, spleen, and lungs, and
treat them with acid alcohol. The urine will also have to be examined,
and as much blood as can be obtained. In cases where all the evidence
points to a minute quantity (under a grain) of morphine, it is decidedly
best to add these various extracts together, to distil off the alcohol
at a very gentle heat, to dry the residue in a vacuum, to dissolve again
in absolute alcohol, filter, evaporate again to dryness, dissolve in
water, and then use the following process:--

§ 365. =Extraction of Morphine.=--To specially search for morphine in
such a fluid as the urine, it is, according to the author’s experience,
best to proceed strictly as follows:--The urine is precipitated with
acetate of lead, the powdered lead salt being added to the warm urine
contained in a beaker on the water-bath, until a further addition no
longer produces a precipitate; the urine is then filtered, the lead
precipitate washed, and the excess of lead thrown down by SH₂; the lead
having been filtered off, and the precipitate washed, the urine is
concentrated down to a syrup in a vacuum. The syrup is now placed in a
separating tube (if not acid, it is acidified with hydrochloric acid),
and shaken up successively with petroleum ether, chloroform, ether, and,
lastly, with amylic alcohol (the latter should be warm); finally, the
small amount of amylic alcohol left dissolved in the liquid is got rid
of by shaking it up with petroleum ether. To get rid of the last traces
of petroleum ether, it may be necessary to turn the liquid into an
evaporating dish, and gently heat for a little time over the water-bath.
The acid liquid is now again transferred to the separating tube, and
shaken up with ether, after being made alkaline with ammonia; this will
remove nearly all alkaloids save morphine,--under the circumstances, a
very small quantity of morphine may indeed be taken up by the ether, but
not the main bulk. After separating the ether, the liquid is again made
slightly acid, so as to be able to precipitate morphine in the presence
of the solvent; the tube is warmed on the water-bath, at least its own
bulk of hot amylic alcohol added and the liquid made alkaline, and the
whole well shaken. The amylic alcohol is removed in the usual way, and
shaken with a small quantity of decinormal sulphuric acid; this washes
out the alkaloid from the amyl alcohol, and the same amyl alcohol can be
used again and again. It is best to extract the liquid for morphine at
least thrice, and to operate with both the solution and the amyl hot.
The decinormal acid liquid is made slightly alkaline with ammonia, and
allowed to stand for at least twelve hours; any precipitate is collected
and washed with ether, and then with water; the alkaline liquid from
which the morphine has been separated is concentrated to the bulk of 5
c.c. on the water bath, and again allowed to stand for twelve hours; a
little more morphine may often in this way be obtained.

The author in some test experiments, in which weighed small quantities
of morphine (60-80 mgrms.) were dissolved in a little decinormal
sulphuric acid, and added to large quantities of urine, found the
process given to yield from 80 to 85 per cent. of the alkaloid added,
and it was always recovered in fine crystals of a slight brown tint,
which responded well to tests.

Various other methods were tried, but the best was the one given; the
method not only separates the alkaloid with but little loss, but also in
a sufficiently pure state to admit of identification.

From the tissues the alkaloid may be dissolved out by the general method
given at p. 239, and the ultimate aqueous solution, reduced to a bulk of
not more than 25 c.c., treated by the ethereal solvents in the way just

§ 366. =Narcotine= (C₂₂H₂₃NO₇) crystallises out of alcohol or ether in
colourless, transparent, glittering needles, or groups of needles,
belonging to the orthorhombic system.

It is only slightly soluble in boiling, and almost insoluble in cold
water. One part requires 100 parts of cold, and 20 of boiling 84 per
cent. alcohol; 126 parts of cold, 48 of boiling ether (specific gravity
0·735); 2·69 parts of chloroform; 400 of olive oil; 60 of acetic ether;
300 of amyl alcohol; and 22 parts of benzene, for solution. The neutral
solution of narcotine turns the plane of polarisation to the left [α]_r_
= 130·6; the acid solution to the right. Narcotine has no effect on red
litmus paper.

Narcotine gives no crystalline sublimate; its behaviour in the subliming
cell is described at p. 259. Its melting-point, taken in a tube, is
about 176°.

=Behaviour of Narcotine with Reagents.=--Narcotine, dissolved in dilute
hydrochloric acid, and then treated with a little bromine, gives a
yellow precipitate, which on boiling is dissolved; by gradually adding
solution of bromine and boiling, a fine rose colour is produced,
readily destroyed by excess of bromine. This is perhaps the best test
for the presence of narcotine. Concentrated sulphuric acid dissolves
narcotine; the solution in the cold is at first colourless, after a few
minutes yellow, and in the course of a day or longer the tints gradually
deepen. If the solution is warmed, it first becomes orange-red, then at
the margin violet-blue; and if heated until hydric sulphate begins to
volatilise, the colour is an intense red-violet. If the heating is not
carried so far, but the solution allowed to cool, a delicate cherry-red
hue slowly develops. If the sulphuric acid solution contains 1 : 2000 of
the alkaloid, this test is very evident; with 1 : 40,000, the colour is
only a faint carmine.--_A. Husemann._

A solution of narcotine in pure sulphuric acid, to which a drop of
nitric acid has been added, becomes of a red colour; if the solution is
warmed to 150°, hypochlorite of soda develops a carmine-red; and
chloride of iron, first a violet, then a cherry-red. The precipitants of
narcotine are--phosphomolybdic acid, picric acid, sulphocyanide of
potash, potassio cadmic iodide, mercuric chloride, platinic chloride,
auric chloride, and several other reagents.

From the brown mass left after heating narcotine above 200°,
hydrochloric acid extracts a small portion of a base but little studied.
The residue consists of humopic acid (C₄₀H₁₉O₁₄), which can be obtained
by dissolving in caustic potash, precipitating with HCl, dissolving the
precipitate in boiling alcohol, and finally throwing it down by water.

§ 367. =Effects.=--Narcotine in itself has toxic action only in rather
large doses; from 1 to 2 grms. have been given to man, and slight
hypnotic effects have followed. It is poisonous in very large doses; an
ordinary-sized cat is killed by 3 grms. The symptoms are mainly

§ 368. =Codeine= (=Codomethylene=), C₁₇H₁₇OCH₃(OH)NO + H₂O, is the
methyl of morphine; it is an alkaloid contained in opium in small
quantity only. Mulder, indeed, quotes ·66 to ·77 per cent. as present in
Smyrna opium, but Merck and Schindler give ·25 per cent. Schindler found
in Constantinople, ·5 per cent.; and Merck, in Bengal, ·5 per cent.

Codeine crystallises out of dry ether in small, colourless, anhydrous,
crystals; but crystallised slowly from an aqueous solution, the crystals
are either in well-defined octahedra, or in prisms, containing one atom
of water, and melting in boiling-water to an oily fluid. The anhydrous
crystals have a melting-point of 150°, and solidify again on cooling.
Its watery solution is alkaline to litmus paper.

It requires 80 parts of cold, 17 of boiling water, 10 parts of benzole,
and 7 parts of amyl alcohol respectively, for solution. Alcohol,
benzene, ether, carbon disulphide, and chloroform freely dissolve it,
but in petroleum ether it is almost insoluble. Further, it is also
soluble in aqueous ammonia, and in dilute acids, but insoluble in
excess of caustic potash or soda, and may thus be thrown out of an
aqueous solution. A solution of codeine turns the plane of polarisation
to the left, [α]_r_ = 118·2°.

Concentrated sulphuric acid dissolves codeine without colour, but after
eight days the solution becomes blue; this reaction is quicker if the
acid contains a trace of nitric acid. If the sulphuric acid solution be
warmed to 150°, and a drop of nitric acid be added after cooling, a
blood-red colour is produced. Fröhde’s reagent produces a dirty green
colour, soon becoming Prussian blue, and terminating after twenty-four
hours in a pale yellow.

Cyanogen gas, led into an alcoholic solution of codeine, gives first a
yellow and then a brown colour; lastly, a crystalline precipitate falls.
On warming with a little sulphuric acid and ferric chloride, a blue
colour is produced. This blue colour is apparently common to all ethers
of the codeine class.

Of the group reagents, the following precipitate solutions of
codeine:--Mercuric potassium iodide, mercuric chloride, mercuric
bromide, picric acid, and tannin solutions. The following do not
precipitate:--Mercuric cyanide and potassium ferrocyanide solutions.
Potassium dichromate gives no immediate precipitate, but crystals form
on long standing. It does not give the reaction with iodic acid like
morphine; it is distinguished from narceine by dropping a small particle
of iodine into the aqueous solution, the iodine particle does not become
surrounded with fine crystals.

§ 369. =Effects.=--The physiological action of codeine on animals has
been investigated by Claude Bernard, Magendie, Crum Brown and Fraser,
Falck, and a large number of others.[405] It has also been administered
to man, and has taken in some degree the place of morphine. Claude
Bernard showed that, when given to dogs in sufficient quantity to
produce sleep, the sleep was different in some respects to that of
morphine sleep, especially in its after-effects. Thus, in his usual
graphic way, he describes the following experiment:--“Two young dogs,
accustomed to play together, and both a little beyond the average size,
received in the cellular tissue of the axillæ, by the aid of a
subcutaneous syringe, the one 5 centigrammes of morphine hydrochloride,
the other 5 centigrammes of codeine hydrochloride. At the end of a
quarter of an hour both dogs showed signs of narcosis. They were placed
on their backs in the experimental trough, and slept tranquilly for
three or four hours. When the animals woke, they presented the most
striking contrast. The morphine dog ran with a hyena-like gait
(_démarche hyénoid_), the eye wild, recognising no one, not even his
codeine comrade, who vainly bit him playfully, and jumped sportively on
his back. It was not until the next day that the morphine dog regained
his spirits and usual humour. A couple of days after, the two dogs being
in good health, I repeated the same experiment, but in an inverse
order--that is to say, I gave the codeine to that which previously had
the morphine, and _vice versâ_. Both dogs slept about as long as the
first time; but on waking the attitudes were completely reversed, just
as the administration of the two substances had been. The dog which, two
days before, after having been codeinised, woke lively and gay, was now
bewildered and half paralysed at the end of his morphine sleep; whilst
the other was wide awake and in the best spirits.”

[405] _Ann. Chem. Phys._ [5], 27, pp. 273-288; also, _Journ. Chem.
Soc._, No. ccxliv., 1883, p. 358.

Subsequent experimenters found what Bernard does not mention--viz., that
codeine produced epileptiform convulsions. Falck made some very careful
experiments on pigeons, frogs, and rabbits. To all these in high enough
doses it was fatal. Falk puts the minimum lethal dose for a rabbit at
51·2 mgrms. per kilo. Given to man, it produces a sleep very similar to
that described by Claude Bernard--that is, a sleep which is very
natural, and does not leave any after-effect. Therefore it is declared
to be the best alkaloid of a narcotic nature to give when lengthened
slumber is desired, more especially since it does not confine the
bowels, nor has it been found to produce any eruption on the skin.
Before it has a full narcotic effect, vomiting has often been excited,
and in a few cases purging. The maximum dose for an adult is about ·1
grm. (1·5 grain); three times this quantity, ·3 grms. (4-5 grains),
would probably produce unpleasant, if not dangerous, symptoms.[406]

[406] For further details as to the action of codeine, the reader is
referred to L. O. Wach’s monograph, _Das Codein_ (1868), which contains
reference to the earlier literature. See also Harley, _The Old Vegetable
Neurotics_, London.

    § 370. =Narceine=, C₂₃H₂₇NO₈ + 3H₂O.--Two of the three molecules of
    water are expelled at 100°, the other molecule requires a higher
    temperature; anhydrous narceine is hygroscopic, and melts in a tube
    at about 140°; when exposed to air it unites with one molecule of
    water, and then melts at about 160°.

    The constitution of narceine is probably that of a substituted
    phenylbenzylketone, and the following structural formula has been
    attributed to it:[407]--

[407] M. Freund and G. B. Frankforter, _Annalen_, 277, pp. 20-58.

      3       I:2   4  1’         2’
  3 or 6/ \
     OMe   CH₂
        \ /

    It therefore contains three methoxyl groups.

    Narceine forms good crystals, the form being that of long,
    four-sided rhombic prisms or fine bushy united needles.

    Narceine hydrochloride crystallises with 5½H₂O and with 3H₂O; the
    anhydrous salt melts at 190°-192°. The platinochloride is a definite
    salt, m.p. 190°-191°; it decomposes at 195°-196°. The nitrate forms
    good crystals, which decompose at 97°. Narceine also forms
    crystalline salts with potassium and sodium; these may be obtained
    by heating the base at 60°-70° with a 33 per cent. of NaHO or KHO.

    The potassium compound melts at 90°, the sodium at 159°-160°. The
    alkaloid is regenerated when the alkali salts are treated with acids
    or with CO₂. Crude narceine may be purified by means of the sodium
    salt; the latter is dissolved in alcohol and precipitated with

    It is soluble in alcohol, but almost insoluble in alcohol and ether,
    or benzene and ether; it is slightly soluble in ether, carbon
    disulphide, and chloroform. It has no reaction on moist litmus

    Benzole and petroleum ether extract narceine neither from acid nor
    alkaline solutions; chloroform extracts narceine both from acid and
    from alkaline solutions, the latter in small proportion only.
    Narceine turns the plane of polarisation to the left, [α]_r_ =
    66·7°. Narceine may be separated from narcotine by the addition of
    ammonia to the acid aqueous solution; narcotine is fully
    precipitated by ammonia, but narceine is left in solution.

    In the subliming cell it melts at 134°, but gives no crystalline
    sublimate. The tube melting-point of the trihydrate is 170°. The
    melted substance is at first colourless; but on raising the
    temperature, the usual transitions of colour through different
    shades of brown to black are observed. If melted, and kept a few
    degrees above its melting-point, and then cooled slowly, the residue
    is straw-coloured, divided into lobes, most of which contain
    feathery crystals.

    At high temperatures narceine develops a herring-like odour; the
    residue becomes darkish blue with iron chloride. Concentrated nitric
    acid dissolves it with a yellow colour; on heating, red vapours are
    produced; the fluid contains crystals of oxalic acid, and develops
    with potash a volatile base. Concentrated sulphuric acid colours
    pure narceine brown; but if impure, a blood-red or blue colour may
    be produced. It does not reduce iron salts.

    Fröhde’s reagent colours it first brown-green, then red, passing
    into blue. Narceine forms precipitates with bichromate of potash,
    chloride of gold, bichloride of platinum, and several other
    reagents. The one formed by the addition of potassio zinc iodide is
    in hair-like crystals, which after twenty-four hours become blue.

    Weak iodine solution colours narceine crystals a black-blue; they
    dissolve in water at 100° without colour, but on cooling again
    separate with a violet or blue colour. If on a saturated solution of
    narceine a particle of iodine is strewn, fine needle-like grey
    crystals form around the iodine. A drop of “Nessler” solution, added
    to solid narceine, at once strikes a brown colour; on diluting the
    drop with a little water, beautiful little bundles of crystals

    The following group reagents precipitate narceine:--picric acid,
    tannin solution, and potassium dichromate on long standing. The
    following give no precipitate:--mercuric cyanide, mercuric potas.
    iodide, mercuric chloride, mercuric bromide, and potas. ferrocyanide

    § 371. =Effects.=--The physiological action of narceine has been
    variously interpreted by different observers. Claude Bernard[408]
    thought it the most somniferous of the opium alkaloids. He said that
    “the narceinic sleep was characterised by a profound calm and
    absence of the excitability of morphine, the animals narcotised by
    narceine on awaking returning to their natural state without
    enfeeblement of the hind limbs or other sequelæ.” It has been amply
    confirmed that narceine possesses somniferous properties, but
    certainly not to the extent that Bernard’s observations led
    physiologists to expect. In large doses there is some irritation of
    the stomach and intestines, and vomiting occurs, and even diarrhœa;
    moderate doses induce constipation. The maximum medicinal dose may
    be put at ·14 grm. (or 2·26 grains), and a probably dangerous dose
    would be three times that quantity.[409]

[408] _Compt. Rend._, lix. p. 406, 1864.

[409] See J. Bouchardat, _La Narcéine_, Thèse, Paris, 1865; Harley, _The
Old Vegetable Neurotics_, Lond.; Ch. Liné, _Études sur la Narcéine et
son Emploi Thérapeutique_, Thèse, Paris, 1865; also, Husemann’s
_Planzenstoffe_, in which these and other researches are summarised.

    § 372. =Papaverine= (C₂₁H₂₁NO₄) crystallises from alcohol in white
    needles or scales. It possesses scarcely any alkaline reaction, but
    its salts have an acid reaction; it has but little effect on a ray
    of polarised light. It is almost insoluble in water; it is easily
    soluble in acetone, amyl alcohol, alcohol, and chloroform. One part
    of the alkaloid is dissolved in 36·6 of benzene, and in 76 parts of
    amyl alcohol. Petroleum ether dissolves it by the aid of heat, but
    the alkaloid separates in crystals on cooling. Chloroform extracts
    it from either acid or alkaline solutions. Papaverine gives no
    crystalline sublimate. The melting-point of pure samples in a tube
    is 147°, with scarcely any colour; it solidifies again to crystals
    on cooling; in the subliming cell it melts at 130°, and decomposes
    about 149°; the vapours are alkaline; the residue is amorphous,
    light brown, and is not characteristic. Concentrated sulphuric acid
    colours it a deep violet-blue, and dissolves it to a violet, slowly
    fading. This solution, by permanganate of potash, is first green and
    then grey. Fröhde’s reagent gives a beautiful violet colour, which
    becomes blue, and vanishes after twenty-four hours. Diluted
    solutions of salts of papaverine are not precipitated by
    phosphomolybdic acid. It is precipitated by ammonia, by the caustic
    and carbonated alkalies, by potassic-cadmic iodide, iodine in
    hydriodic acid, and by alkaloidal reagents generally--save by the
    important exception mentioned above. A solution in amyl alcohol is
    also precipitated by bromine; the precipitate is crystalline. An
    alcoholic solution of platinic chloride also separates papaverine
    platin chloride in crystals. An alcoholic solution of iodine, added
    to an alcoholic solution of papaverine, separates in a little time
    crystals of the composition C₂₁H₂₁NO₄I₃. From the mother-liquor, by
    concentration, can be obtained needles of another iodine
    combination, C₂₁H₂₁NO₄I₅; the latter heated above 100° parts with
    free iodine. These compounds with iodine are decomposed by ammonia
    and potash, papaverine separating. The decomposition may be watched
    under the microscope. Nitric acid precipitates from a solution of
    the sulphate a white nitrate soluble in excess; the precipitate does
    not appear at once, but forms in the course of an hour; it is at
    first amorphous, but subsequently crystalline; this, with its
    physical properties, is a great assistance to identification.

    § 373. =Effects.=--Claude Bernard ranked papaverine with the
    convulsants; probably the papaverine he had was impure. In any case,
    subsequent observations have shown that it is to be classed rather
    with the hypnotic principles of opium. Leidesdorf[410] administered
    it to the insane, and noted slowness of the pulse, muscular
    weakness, and drowsiness to follow. The doses were given
    subcutaneously (·42 grm. of the hydrochloride). Baxt,[411]
    experimenting with the frog, found that a milligramme caused deep
    sleep and slowing of the heart’s action. This action on the heart is
    witnessed also on the recently-removed frog’s heart. Guinea-pigs,
    and other small animals poisoned by strychnine or thebaine, and then
    given papaverine, did not seem to be so soon affected with tetanus
    as when no such remedy was administered. The fatal dose of
    papaverine for a man is unknown. I should conjecture that the least
    quantity that would cause dangerous symptoms would be 1 grm. (15·4

[410] _Ztschr. d. Wien. Aerzte_, pp. 13, 115, 1868.

[411] _Arch. Anat. Phys._, p. 70, 1869.

    § 374. =Thebaine=, C₁₇H₁₅NO(OCH₃)₂.--Opium seldom contains much more
    than 1 per cent. of this alkaloid. It usually forms needles or short
    crystals. It is alkaline, and by rubbing becomes negatively
    electric. It is almost insoluble in water, aqueous ammonia, and
    solutions of the alkalies. It requires 10 parts of cold alcohol for
    solution, and dissolves readily in hot. Ether, hot or cold, is also
    a good solvent. 100 parts of benzene are required for 5·27 parts of
    thebaine, and 100 of amyl alcohol for 1·67 parts. Chloroform
    dissolves thebaine with difficulty out of both acid and alkaline
    solutions; petroleum ether extracts it from neither. Thebaine melts
    in a tube at 193°, sublimes at 135°. The sublimate is in min