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Title: Poisons: Their Effects and Detection
       A Manual for the Use of Analytical Chemists and Experts

Author: Alexander Wynter Blyth

Release Date: May 13, 2013 [EBook #42709]

Language: English

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Title page

POISONS:
THEIR EFFECTS AND DETECTION.


BY THE SAME AUTHOR.

Fourth Edition. At Press.

FOODS:

THEIR COMPOSITION AND ANALYSIS.

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 Chocolate—Alcohol—Brandy—Rum—Whisky—Gin—Arrack—Liqueurs—Beer—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 Record.

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


In Large 8vo, Handsome Cloth. 21s.

FORENSIC MEDICINE
AND
TOXICOLOGY.

By J. DIXON MANN, M.D., F.R.C.P.,
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.

“By far the MOST RELIABLE, MOST SCIENTIFIC, and MOST MODERN book on 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 Journal.


London: Charles Griffin & Co., Ltd., Exeter St., Strand.


POISONS:
THEIR EFFECTS AND DETECTION.
A MANUAL FOR THE USE OF ANALYTICAL
CHEMISTS AND EXPERTS.

WITH AN INTRODUCTORY ESSAY ON THE GROWTH OF MODERN TOXICOLOGY.

BY
ALEXANDER WYNTER BLYTH,
M.R.C.S., F.I.C., F.C.S., &c.,
BARRISTER-AT-LAW; PUBLIC ANALYST FOR THE COUNTY OF DEVON; AND MEDICAL OFFICER OF HEALTH AND PUBLIC ANALYST FOR ST. MARYLEBONE.

THIRD EDITION, REVISED AND ENLARGED.

With Tables and Illustrations.

LONDON:
CHARLES GRIFFIN AND COMPANY, LIMITED,
EXETER STREET, STRAND.
1895.

(All Rights Reserved.)
D. VAN NOSTRAND COMPANY,
NEW YORK.



[v]

PREFACE TO THE THIRD EDITION.

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 corrected.

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 chapter.

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.

The Court House, St. Marylebone, W.
June, 1895.



[vii]

CONTENTS.

  PART I.—INTRODUCTORY.  
  I. THE OLD POISON-LORE.  
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
  II. GROWTH AND DEVELOPMENT OF THE MODERN METHODS OF CHEMICALLY DETECTING POISONS.  
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

  PART II.  
  I. DEFINITION OF POISON.  
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,[viii] 22, 23
  II. CLASSIFICATION OF POISONS.  
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
  III. STATISTICS.  
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
  IV. THE CONNECTION BETWEEN TOXIC ACTION AND CHEMICAL COMPOSITION.  
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
  V. LIFE TESTS: OR THE IDENTIFICATION OF POISON BY EXPERIMENTS ON ANIMALS.  
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
  VI. GENERAL METHOD OF PROCEDURE IN SEARCHING FOR POISON.  
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
  VII. THE SPECTROSCOPE AS AN AID TO THE IDENTIFICATION OF CERTAIN POISONS.  
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

  PART III.—POISONOUS GASES: CARBON MONOXIDE—CHLORINE—HYDRIC SULPHIDE.[ix]  
  I. CARBON MONOXIDE.  
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
  II. CHLORINE.  
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
  III. HYDRIC SULPHIDE (SULPHURETTED HYDROGEN).  
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

  PART IV.—ACIDS AND ALKALIES.  
  Sulphuric Acid—Hydrochloric Acid—Nitric Acid—Acetic Acid—Ammonia—Potash—Soda—Neutral Sodium, Potassium, and Ammonium Salts.  
  I. SULPHURIC ACID.  
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,[x] 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
  II. HYDROCHLORIC ACID.  
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
  III. NITRIC ACID.  
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
  IV. ACETIC ACID.  
90. Symptoms and Detection, 110
  V. AMMONIA.  
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,[xi] 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
  VI. CAUSTIC POTASH AND SODA.  
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
  VII. NEUTRAL SODIUM, POTASSIUM, AND AMMONIUM SALTS.  
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,[xii] 127, 128

  PART V.—MORE OR LESS VOLATILE POISONOUS SUBSTANCES CAPABLE OF BEING SEPARATED BY DISTILLATION FROM NEUTRAL OR ACID LIQUIDS.  
  Hydrocarbons—Camphor—Alcohol—Amyl Nitrite—Ether—Chloroform and other Anæsthetics—Chloral—Carbon Bisulphide—Carbolic Acid—Nitro-Benzene—Prussic Acid—Phosphorus.  
  I. HYDROCARBONS.  
  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
  II. CAMPHOR.  
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
  III. ALCOHOLS.  
  1. Ethylic Alcohol.  
158. Chemical Properties of Alcohol—Statistics of Poisoning by Alcohol, 136
159. Criminal or Accidental Alcoholic Poisoning, 137
160. Fatal Dose,[xiii] 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
  IV. ETHER.  
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
  V. CHLOROFORM.  
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
  VI. OTHER ANÆSTHETICS.  
191. Methyl Chloride—Methene Dichloride, &c., 154
192. Pentane, 154
193. Aldehyde, 154
194. Paraldehyde, 154
  VII. CHLORAL.  
195. Chloral Hydrate; its Composition and Properties, 154, 155
196. Detection,[xiv] 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
  VIII. BISULPHIDE OF CARBON.  
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
  IX. THE TAR ACIDS—PHENOL—CRESOL.  
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,[xv] 183
  X. NITRO-BENZENE.  
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
  XI. DINITRO-BENZOL.  
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
  XII. HYDROCYANIC ACID.  
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
  XIII. PHOSPHORUS.  
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,[xvi] 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, 229-232
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

  PART VI.—ALKALOIDS AND POISONOUS VEGETABLE PRINCIPLES SEPARATED FOR THE MOST PART BY ALCOHOLIC SOLVENTS.  
  Division I.—Vegetable Alkaloids.  
  I. GENERAL METHOD OF TESTING AND EXTRACTING ALKALOIDS.  
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, 262-264
  II. LIQUID VOLATILE ALKALOIDS.[xvii]  
  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
  III. THE OPIUM GROUP OF ALKALOIDS.  
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, 296-298
357. Physiological Action, 298, 299
358. Physiological Action of Morphine Derivatives,[xviii] 299
359. Action on Man—(a) The Sudden Form; (b) the Convulsive Form; (c) a Remittent Form of Opium Poisoning—Illustrative Cases, 299-303
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
  IV. THE STRYCHNINE OR TETANUS-PRODUCING GROUP OF ALKALOIDS.  
  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,[xix] 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
  V. THE ACONITE GROUP OF ALKALOIDS.  
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
  VI. THE MYDRIATIC GROUP OF ALKALOIDS—ATROPINE—HYOSCYAMINE—SOLANINE—CYTISINE.  
  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,[xx] 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
  VII. THE ALKALOIDS OF THE VERATRUMS.  
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,[xxi] 397
  VIII. PHYSOSTIGMINE.  
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, 400
491. Physiological Action, 401
492. Post-mortem Appearances, 401
493. Separation of Physostigmine, 401, 402
494. Fatal Dose of Physostigmine, 402
  IX. PILOCARPINE.  
495. Alkaloids from the Jaborandi, 402
496. Pilocarpine, 402, 403
497. Tests, 403
498. Effects of Pilocarpine, 403, 404
  X. TAXINE.  
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
  XI. CURARINE.  
504. Commercial Curarine—Properties, 405-407
505. Physiological Effects, 407
506. Separation of Curarine, 407, 408
  XII. COLCHICINE.  
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
  XIII. MUSCARINE AND THE ACTIVE PRINCIPLES OF CERTAIN FUNGI.  
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 PhalloidesPhallin, 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,[xxii] 418
  Division II.—Glucosides.  
  I. DIGITALIS GROUP.  
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
  II. OTHER POISONOUS GLUCOSIDES ACTING ON THE HEART.  
  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 Digitalins.  
562. Erythrophlein, 436
  III. SAPONIN—SAPONIN SUBSTANCES.  
563. The Varieties of Saponins, 436, 437
564. Properties of Saponin,[xxiii] 437
565. Effects of Saponin, 437, 438
566. Action on Man, 438
567. Separation of Saponin, 438, 439
568. Identification of Saponin, 439
  Division III.—Certain Poisonous Anhydrides of Organic Acids.  
  I. SANTONIN.  
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
  II. MEZEREON.  
576. Cases of Poisoning by the Mezereon, 442
  Division IV.—Various Vegetable Poisonous Principles—not Admitting of Classification Under the Previous Three Divisions.  
  I. ERGOT OF RYE.  
577. Description of the Ergot Fungus, 442, 443
578. Chemical Constituents of Ergot—Ergotinine—EcbolineScleromucin—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
  II. PICROTOXIN, THE ACTIVE PRINCIPLE OF THE COCCULUS INDICUS.  
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
  III. THE POISON OF ILLICIUM RELIGIOSUM.  
595. Dr. Langaard’s Researches, 454
  IV. PICRIC ACID AND PICRATES.  
596. Properties of Picric Acid, 454
597. Effects of Picric Acid, 454, 455
598. Tests,[xxiv] 455
  V. CICUTOXIN.  
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
  VI. ÆTHUSA CYNAPIUM (FOOL’S PARSLEY).  
603. Dr. Harley’s Experiments, 457
  VII. ŒNANTHE CROCATA.  
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
  VIII. OIL OF SAVIN.  
607. Effects and Properties of Savin Oil, 459
608. Post-mortem Appearances, 460
609. Separation and Identification, 460
  IX. CROTON OIL.  
610. Chemical Properties of Croton Oil, 461
611. Dose—Effects—Illustrative Cases, 461
612. Post-mortem Appearances, 461
613. Chemical Analysis, 462
  X. THE TOXALBUMINS OF CASTOR OIL SEEDS AND ABRUS.  
614. The Toxalbumin of Castor Oil Seeds, 462
615. Toxalbumin of Abrus, 462, 463
  XI. ICTROGEN.  
616. Ictrogen, 463
  XII. COTTON SEEDS.  
617. Cotton Seeds as a Poison, 464
  XIII. LATHYRUS SATIVUS.  
618. Poisonous Qualities of Vetchlings, 464, 465
  XIV. ARUM—LOCUST-TREE—BRYONY—MALE FERN.  
619. Arum Maculatum, 465
620. The Black Bryony, 465
621. The Locust Tree, 465
622. Male Fern, 465, 466

  PART VII.—POISONS DERIVED FROM LIVING OR DEAD ANIMAL SUBSTANCES.  
  Division I.—Poisons Secreted by Living Animals.  
  I. POISONOUS AMPHIBIA.  
623. Poisonous Properties of the Skin of the Salamandra Maculosa—Salamandrine, &c., 467
624. Poison from the Toad,[xxv] 468
  II. THE POISON OF THE SCORPION.  
625. Various Species of Scorpions—Effects of the Scorpion Poison, 468
  III. POISONOUS FISH.  
626. Poisonous Fish—Illustrative Cases, 468-470
  IV. POISONOUS SPIDERS AND INSECTS.  
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
  V. SNAKE POISON.  
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
  Division II.—Ptomaines—Toxines.  
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
  Diamines.  
661. Rate of Formation of Diamines, 492
662. Ethylidenediamine, 492
663. Neuridine,[xxvi] 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
  Division III.—Food Poisoning.  
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

  PART VIII.—THE OXALIC ACID GROUP OF POISONS.  
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

  PART IX.—INORGANIC POISONS.[xxvii]  
  I. Precipitated from a Hydrochloric Acid Solution by Hydric Sulphide—Precipitate Yellow or Orange.  
  ARSENIC—ANTIMONY—CADMIUM.  
  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, 539-541
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, 554-560
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, 560-562
741. Imbibition of Arsenic after Death—Mason’s Case,[xxviii] 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,[xxix] 590, 591
  II. Precipitated by Hydric Sulphide in Hydrochloric Acid Solution—Black.  
  LEAD—COPPER—BISMUTH—SILVER—MERCURY.  
  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,[xxx] 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, 650
851. Elimination of Mercury, 650, 651
852. Tests for Mercury, 651, 652
853. The Detection of Mercury in Organic Substances and Fluids, 652-654
854. Estimation of Mercury—The Dry Method, 654
855. Volumetric Processes for the Estimation of Mercury, 654, 655
  III. Precipitated by Hydric Sulphide from a Neutral Solution.  
  ZINC—NICKEL—COBALT.  
  1. Zinc.  
856. Properties of Metallic Zinc, 655, 656
857. Carbonate of Zinc,[xxxi] 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
  IV. Precipitated by Ammonium Sulphide.  
  IRON—CHROMIUM—THALLIUM—ALUMINIUM—URANIUM.  
  1. Iron.  
875. Poisonous and Non-Poisonous Salts of Iron, 665
876. Ferric Chloride—Pharmaceutical Preparations of Ferric Chloride, 666
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,[xxxii] 678
899. Detection of Alumina, 678, 679
  5. Uranium.  
900. Poisonous Properties of Uranium Salts, 679
901. Detection and Estimation of Uranium, 679
  V. Alkaline Earths.  
  BARIUM.  
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

  APPENDIX.  
  Treatment, by Antidotes or Otherwise, of Cases of Poisoning.  
912. Instruments, Emetics, and Antidotes Proper for Furnishing an Antidote Bag, 685, 686
913. Poisons Arranged Alphabetically—Details of Treatment, 687-700
  Domestic Ready Remedies for Poisoning.  
914. The “Antidote Cupboard,” and How to Furnish it, 701

LIST OF ILLUSTRATIONS.

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

[1]

POISONS:
THEIR EFFECTS AND DETECTION.


PART I.—INTRODUCTORY.

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]

§ 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[3] 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[4] 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 practice.

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.[5] 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 development.

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.

[6]

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, Tiberius.

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[7] 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 healthy.

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

“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,[8] 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. 384.


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 business!


[7] Œuvres de Paré, 2nd ed., liv. xx. Des Vennes, chap. xliv. p. 507.


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[9] 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 households.[9]


[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[10] 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[11] 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 confession.[12]


[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][12] 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,[13] 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 schools.[18]


[17] De Rerum Proprietaribus.

[18] In the sixteenth century it was not considered proper to write upon poisons. Jerôme 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, 1558.


In the seventeenth century the Honourable Robert Boyle made some[14] 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 time.[19]


[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[15] 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, 1831.


§ 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,[16] 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 century.

§ 13.—BIBLIOGRAPHY OF THE CHIEF WORKS ON TOXICOLOGY (NINETEENTH CENTURY).

Anglada, Jos.—“Traité de Toxicologie Générale, &c.” Montpellier et Paris, 1835.

Autenrieth.—“Kurze Anleitung zur Auffindung der Gifte.” Freiburg, 1892.

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 Cyclopædia.)

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, 1881.

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.

[17]

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. 1876.

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, 1876.

Falck, C. Ph.—“Die Klinischwichtigen Intoxicationen.” (Handbuch der spec. Pathologie u. Therapie red. von R. Virchow, Bd. 2.) Erlangen, 1854.

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, 1890.

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, 1883.

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, 1877.

Hermann, L.—“Lehrbuch der experimentellen Toxicologie.” 8vo. Berlin, 1874.

Hoffmann, E. R.—“Lehrbuch der gerichtlichen Medicin.” 5th ed. Wien, 1890-91.

Husemann and A. Hilger.—“Die Pflanzenstoffe in chemischer, pharmakologischer, u. toxicologischer Hinsicht.” 2nd ed. Berlin, 1882.

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, 1869.

Lesser, Adolf.—“Atlas der gerichtlichen Medicin.” Berlin, 1883.

Loew, Oscar.—“Ein natürliches System der Gift-Wirkungen.” München, 1893.

Ludwig, E.—“Medicinische Chemie in Anwendung auf gerichtliche Untersuchungen.”

Mahon, A.—“Médecine Légale et Police Médicale.” Paris, 1807.

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

[18]

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, 1824.

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, 1869.

[19]

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.


[20]

PART II.

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 felony.”

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 intent.

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,[21] 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’ imprisonment.

[22]

“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 health.”[29]


[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[23] 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 poisons.


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:

A. Poisons causing Death immediately, or in a few minutes.

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 substances.

[24]

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.

D. Poisons more especially affecting the Nervous System.

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 scheme:

I. POISONS WHICH CAUSE COARSE ANATOMICAL CHANGES OF THE ORGANS.

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

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 dioxide.

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

II. BLOOD POISONS.

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[25] its decomposition products, such as hydric sulphide, hydric cyanide, and the cyanides and carbon monoxide.

III. POISONS WHICH KILL WITHOUT THE PRODUCTION OF COARSE ANATOMICAL CHANGE.

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.

IV. POISONOUS PRODUCTS OF TISSUE CHANGE.

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 ptomaines.


§ 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:

A.—POISONOUS GASES.

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

[26]

B.—ACIDS AND ALKALIES.

  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.

C.—POISONOUS SUBSTANCES CAPABLE OF BEING SEPARATED BY DISTILLATION FROM EITHER NEUTRAL OR ACID LIQUIDS.

  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.

D.—ALKALOIDS AND POISONOUS VEGETABLE PRINCIPLES SEPARATED FOR THE MOST PART BY ALCOHOLIC SOLVENTS.

DIVISION I.—Vegetable Alkaloids.
  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, igasurine.
  4. The aconite group of alkaloids.[27]
  5. The mydriatic group of alkaloids—atropine, hyoscyamine, solanin, cytisine.
  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.

DIVISION II.—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.

DIVISION III.—Certain Poisonous Anhydrides of the Organic 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.

DIVISION IV.—Various Vegetable Poisonous Principles not admitting of Classification under the previous Three Divisions.

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.

[28]

E.—POISONS DERIVED FROM LIVING OR DEAD ANIMAL SUBSTANCES.

DIVISION I.—Poisons Secreted by the Living.
  1. Poisonous amphibia.
  2. Poison of the scorpion.
  3. Poisonous fish.
  4. Poisonous insects—spiders, wasps, bees, beetles, &c.
  5. Snake poison.
DIVISION II.—Poisons formed in Dead Animal Matters.
  1. Ptomaines.
  2. Poisoning by putrid or changed foods—sausage poisoning.

F.—THE OXALIC ACID GROUP.

G.—INORGANIC POISONS.

DIVISION I.—Precipitated from a Hydrochloric Acid Solution by Hydric Sulphide—Precipitate, Yellow or Orange.
  • Arsenic, antimony, cadmium.
DIVISION II.—Precipitated by Hydric Sulphide in Hydrochloric acid Solution—Black.
  • Lead, copper, bismuth, silver, mercury.
DIVISION III.—Precipitated from a Neutral Solution by Hydric Sulphide.
  • Zinc, nickel, cobalt.
DIVISION IV.—Precipitated by Ammonia Sulphide.
  • Iron, chromium, thallium, aluminium.
DIVISION V.—Alkaline Earths.
  • Barium.

III.—Statistics.

§ 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.

[29]

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:

DEATHS FROM POISON IN ENGLAND AND WALES DURING THE TEN YEARS 1883-92.

  Accident or
Negligence.
Suicide. Murder. Total.
  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
Cautic Potash, 8 10 1 ... ... ... 9 10
Potassic Chlorate, 1 ... ... ... ... ... 1 ...
Potssic Bichromate, 2 2 7 3 ... ... 9 5
Potssic Bromide, 1 ... ... ... ... ... 1 ...
Potssic 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 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,[30] 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

[31]

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.

§ 21. The following table gives some German statistics of poisoning:

[32]

TABLE SHOWING THE ADMISSIONS INTO VARIOUS MEDICAL INSTITUTIONS[30] IN BERLIN OF PERSONS SUFFERING FROM THE EFFECTS OF POISON DURING THE THREE 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 Staatsarzneikunde.


  Males. Females. Total.
Charcoal Vapour, 77 78   155
Sulphuric Acid, 24 54   - 93
Hydrochloric Acid, 4 4
Nitric Acid, and Aqua Regia, 7 ...
Phosphorus, 13 28   41
Cyanide of Potassium, 29 3   - 38
Prussic Acid, 5 1
Oxalic Acid, and Oxalate of Potash, 11 8   19
Alcohol, 12 2   14
Arsenic, 7 5   12
Morphine, 8 1   - 12
Opium, 2 1
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[33] 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 follows:


[31] Étude Médico-Légale sur l’Empoisonnement, Paris, 1875.


Total accusations of Poisoning in the 21 years, 793
Results of the Poisoning:—
  Death, 280   - 872
  Illness, 346
  Negative, 246
Accused:—
  Men, 304   - 703
  Women, 399
Nature of Poison Employed:—
  Arsenic,   287
  Phosphorus,   267
  Copper -   Sulphate, 120   - 159
  Acetate (Verdigris), 39
  Acids -   Sulphuric Acid, 36   - 47
  Hydrochloric Acid, 8
  Nitric Acid, 3
  Cantharides, 30
  Nux Vomica, 5   - 12
  Strychnine, 7
  Opiates -   Opium, 6   - 10
Laudanum, 3
Sedative Water,[34] 1
  Salts of Mercury,   8
  Sulphate of Iron,   6
  Preparations of Antimony,   5
  Ammonia,   4
  Cyanides -   Prussic Acid, 2   - 4
Cyanide of Potassium, 2
  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.

[35]


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 acquainted.”[32]


[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[36] 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.


α Naphthylamine.

β Naphthylamine.

Acylic tetrahydro-α Naphthylamine.

Aromatic tetrahydro-β Naphthylamine.

α Naphthylamine.

β Naphthylamine.

Acylic tetrahydro-α Naphthylamine.

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 inactive.

§ 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

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[37] 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.

Pyrogallol.

Phloroglucin.

Pyrogallol.

Phloroglucin.

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 curare.

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-acetamido-phenol.

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 produced.

(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.

[38]

(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 substitution.

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 blood.

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 .

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

[39]

§ 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.

Allantoin.

Alloxantin.

Allantoin.

Alloxantin.

§ 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;[40] and amarin,[38] , 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, thus:

Xanthin.

Theobromin.

Xanthin.

Theobromin.

Caffein.

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[41] 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 ethylamine.

Neurine.

Choline.

Neurine.

Choline.

Vinylamine.

Ethylamine.

Vinylamine.

Ethylamine.

§ 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.

[42]

TABLE SHOWING THE RESULTS OF EXPERIMENTS ON FISH.

No. of
Experiments.
Metal. Limit of
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 Animals.

§ 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[43] 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[44] 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.

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[45] 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 death.

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[46] 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 β-tetrahydronaphthylamine.

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 directions.

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[47] 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 following:

Mercury pump

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[48] 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.

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.

Ether recovery apparatus

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.

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.[49] 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[50] 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.


AUTENRIETH’S GENERAL PROCESS.

§ 32. A general method of procedure has been published by W. Autenrieth.[43]


[43] Kurze Anleitung zur Auffindung der Gifte, Freiburg, 1892.


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

  1. Poisons capable of distillation from an acid aqueous solution.
  2. Organic substances which are not capable of distillation from acid solutions.
  3. Metallic poisons.

[51]

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 division.

I. SUBSTANCES SEPARATED BY DISTILLATION.

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.


II. ORGANIC POISONS NOT VOLATILE IN ACID SOLUTION.

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”).


III. METALS.

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[52] 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 sulphide.

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.


INVESTIGATION OF THE SULPHIDES SOLUBLE IN AMMONIUM SULPHIDE, VIZ., ARSENIC, ANTIMONY, TIN.

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 oxide.

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, Copper).


INVESTIGATION OF THE SULPHIDES INSOLUBLE IN SULPHIDE OF AMMONIUM, VIZ., MERCURY, LEAD, COPPER, CADMIUM.

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

[53]

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.


SEARCH FOR ZINC AND CHROMIUM.

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 “Zinc”).

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”).

INVESTIGATION OF THE RESIDUE (p. 52) AFTER THE TREATMENT OF THE ORIGINAL SUBSTANCE WITH HYDROCHLORIC ACID AND POTASSIC CHLORATE FOR PRESENCE OF SILVER CHLORIDE, LEAD AND BARIUM SULPHATES.

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[54] 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 Poisons.

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

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

Spectroscope

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[55
56]
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.


CURVES INDICATING THE POSITION OF ABSORPTION BANDS ON TREATING CERTAIN ALKALOIDS WITH REAGENTS.

Absorption bands

NOTES TO CURVES INDICATING ABSORPTION BANDS.

  1. Strychnine, treated with sulphuric acid and potassic dichromate (violet).
  2. Brucine, treated with potassic nitrate and sulphuric acid (clear red).
  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. Verarine, treate with sulpuric acid  (cherry-red).
  9. Verarine, treate with sulpuric acid  (carmine-red).
  10. Veratrine, Furfurol reaction (blue-violet).
  11. Sabadillin, treated with sulphuric acid (red).
  12. Veratroidine,eatedwith sulphric acid (brown-red).
  13. Jervine, Furfurol reaction (blue).
  14. Sabadine, ururol reation (blue).
  15. Sabadine, treated with sulphuric acid (cherry-red).
  16. Physostigmine,ed ith sulphric acid  (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, reatd with Froehe’s reagent  (violet-red).
  22. Chelidonin,treated with sulphate of vanadium (dark green).
  23. Solanin,in, treated with sulphuric acid and allowed to stand 4 hours (brown-red).
  24. Digitalin,n, treated with Erdmann’s reagent (red).
  25. Aniline, in, treated with sulphuric acid and potassic dichromate (blue).

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

  W.L.
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[57] in water, and present it for farther examination in a concentrated form, by the use of certain precipitating agents (see p. 61).

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[58] 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[59] 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 methæmoglobin.

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 hæmatin.

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 brown.[50]


[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[60] 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 dates:


[52] Compt. Rend. Soc. de Biol., v. 433.


Date. Content of
gas in CO.
Jan. 12, 1892, 24·7 per cent.
J 20, 23·5
J 28, 22·2
Feb. 8, 20·3
F 16, 15·5
F 26, 10·2
March 3, 6·3
Ma 14, 4·6
Ma 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[61] 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.

Hæmatin crystals

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[62] 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 1126 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] 13200 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[63] 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 blood-stain.


[64]

PART III.—POISONOUS GASES: CARBON MONOXIDE—CHLORINE—HYDRIC SULPHIDE.


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 CO.

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 gas.


[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,[65] 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.

[66]

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[67] 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[68] 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.


[69]

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 floor.

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[70] 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.

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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.


II.—Chlorine.

§ 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[72] 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 bleached.

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. 74.


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,[73] 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 laboratories.

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[74] 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.



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PART IV.—ACIDS AND ALKALIES.


SULPHURIC ACID—HYDROCHLORIC ACID—NITRIC ACID—ACETIC ACID—AMMONIA—POTASH—SODA—NEUTRAL SODIUM, POTASSIUM, AND AMMONIUM SALTS.


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[76] 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 ginger.

§ 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[77] employing sulphuric acid. The number of cases of poisoning in England and Wales for ten years is given in the following table:

DEATHS FROM SULPHURIC ACID IN ENGLAND AND WALES FOR THE TEN YEARS ENDING 1892.

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

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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. 181.


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[79] 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 6812 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[80] 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 investigation.

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[81] 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[82] inflammatory processes in the skin are similar to those noticed by Falck and Vietor in their experiments, already detailed (p. 79).

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[83] 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[84] 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[85] 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.

[86]

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 blackened.

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.


[87]


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., 1100th 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[88] 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 weighed.

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

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[89] 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[90] 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 blood.


[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. 237.

[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[91] 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 extract.

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[92] 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):

[93]

DEATHS FROM HYDROCHLORIC ACID IN ENGLAND AND WALES DURING THE TEN YEARS ENDING 1892.

Accident or Negligence.
Ages, Under
1
1-5 5-15 15-25 25-65 65 and
above
Total
Males, 1 16 2 ... 26 3 48
Females, ... 8 ... ... 9 1 18
Totals, 1 24 2 ... 35 4 66
Suicide.
Ages,   5-15 15-25 25-65 65 and
above
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[94] does not contain absolutely free hydrochloric acid, but that it is in loose combination with the pepsin.


[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.


[95]

§ 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 removed.


[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[96] 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[97] 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[98] 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 matter.[97]


[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.

[99]

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

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,[100] 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 acids.


[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 HCl.

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.


[101]

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 exposed.

The most accurate method of investigation for the purpose of separating chlorine from combination with organic matters is to cut out the stained[102] 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
Nitrate.
  Chlorine.   Silver
Chloride.
  Nitrogen
Pentoxide.
  Oxygen.
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[103] 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 deaths:

DEATHS IN ENGLAND AND WALES DURING THE TEN YEARS ENDING 1892 FROM NITRIC ACID.

Accident or Negligence.
Ages, 1-5 5-15 15-25 25-65 65 and
above
Total
Males, 6 2 1 9 ... 18
Females, 3 ... ... 4 ... 7
Totals, 9 2 1 13 ... 25
Suicide.
Ages,   15-25 25-65 65 and
above
Total
Males,   3 14 1 18
Females,   1 8 ... 9
Totals,   4 22 1 27

[104]

§ 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[105] 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[106] 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[107] 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;[108] 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 colour.

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 inflamed.

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 fluids.

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[109] 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 oxygen.

(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[110] 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 convulsions.

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.

[111]

V.—Ammonia.

§ 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 612 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.


[112]

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, 412 drms.; and oil of lemon, 612 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[113] 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 carbonate.

§ 98. Action on Human Beings and Animal Life.—The violence[114] 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 minutes.


[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[115] 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 liver.

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,[116] 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 together.

Potash (potassa caustica).—Hydrate of potassium (KHO), atomic weight 56, specific gravity 2·1.

Properties.—Pure hydrate of potassium is a compact, white solid,[117] 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 + 112H2O), 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;[118] 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[119] 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[120] 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[121] 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[122] 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 experience.


[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 water.

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[123] 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 grms.

§ 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[124] 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[125] 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 1212 ozs.) of a vegetable infusion.


[128] Annales d’Hygiène publique, 1881, p. 232.


This potion was administered to four children—viz., David, aged 212; Cousin, aged 312; Salmont, 212; and Guérin, 212. 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.

[126]

§ 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 grains).

§ 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 212 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[127] 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 chlorate.


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[128] 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.


[129]

PART V.—MORE OR LESS VOLATILE POISONOUS SUBSTANCES CAPABLE OF BEING SEPARATED BY DISTILLATION FROM NEUTRAL OR ACID LIQUIDS.


HYDROCARBONS—CAMPHOR—ALCOHOL—AMYL NITRITE—ETHER—CHLOROFORM AND OTHER ANÆSTHETICS—CHLORAL—CARBON DISULPHIDE—CARBOLIC ACID—NITRO-BENZENE—PRUSSIC ACID—PHOSPHORUS.


I.—Hydrocarbons.

1. PETROLEUM.

§ 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 ·650.

§ 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.


[130]

TABLE OF THE VARIETIES OF NAPHTHA.

Petroleum Naphtha. Shale Naphtha. Coal-tar Naphtha.
Contains at least 75 per cent. of heptane, C7H16, and other hydrocarbons of the marsh gas or paraffin series; the remainder apparently olefins, CnH2n, with distinct traces of benzene and its homologues. Contains at least 60 to 70 per cent. of heptylene, C7H14, and other hydrocarbons of the olefin series; the remainder paraffins. No trace of benzene or its homologues. Consists almost wholly of benzene, C6H6, and other homologous hydrocarbons, with a small percentage of light hydrocarbons in some samples.
Specific gravity at 15°, ·600. Specific gravity at 15°, ·718. Specific gravity ·876.
Distils between 65° and 100°. Distils between 65° and 100°. Distils between 80° and 120°.
Dissolves coal-tar pitch, but slightly; liquid, but little coloured even after prolonged contact. Behaves similarly to petroleum naphtha with regard to the solution of pitch. Readily dissolves pitch, forming a deep brown solution.
On shaking three measures of the sample with one measure of fused crystals of absolute carbolic acid, no solution. Liquids not miscible. When treated with fused carbolic acid crystals, the liquids mix perfectly. The liquids form a homogeneous mixture when treated with fused carbolic acid crystals.
Combines with 10 per cent. of its weight of bromine in the cold. Combines with upwards of 90 per cent. of its weight of bromine. Combines slowly with 30-40 per cent. of its weight of bromine.

§ 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[131] 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 time.


[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 benzoline.

[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.

2. COAL-TAR-NAPHTHA—BENZENE.

§ 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[132] 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 runnaphtha, 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 5090 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.


DETECTION AND SEPARATION OF BENZENE.

§ 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 follows:

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[133] 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 observed.

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.

3. TERPENES—ESSENTIAL OILS—OIL OF TURPENTINE.

§ 150. The terpenes are hydrocarbons of the general formula CnH2n-4. The natural terpenes are divided into three classes:

1. The true terpenes, formula (C10;H16)—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 class.

3. The colophene hydrocarbons, formula (C20H32), represented by colophony.

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 purity.

4. OIL OF TURPENTINE—SPIRIT OF TURPENTINE—“TURPS.”

§ 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[134] 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 investigated.


[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.



[135]

II.—Camphor.

§ 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 C10H10O; 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 internally.

§ 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. 1875.


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.


[136]

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 water.


III.—Alcohols.

1. ETHYLIC ALCOHOL.

§ 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)[137] were ascribed under the head of “accident or negligence” directly to alcohol.

CHART SHEWING DEATHS PER MILLION PERSONS LIVING, FROM INTEMPERANCE & FROM LIVER DISEASES.

Alcohol deaths
THE MEDICAL “OFFICERS OF HEALTH” CHART. ENT. AT STA. HALL.
Notes.
  Intemperance Solid line  
  Liver disease Dashed line  
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[138] 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 causes.


[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[139] 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[140] 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 fæces.

§ 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.

2. AMYLIC ALCOHOL.

§ 165. Amylic AlcoholFormula, 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.


[141]

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.


IV.—Ether.

§ 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.

[142]

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[143] 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.


V.—Chloroform.

CHLOROFORM, TRICHLOROMETHANE OR METHENYL CHLORIDE (CHCl3).

§ 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[144] 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[145] 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, litmus-paper.


[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 12 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[146] 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.

1. AS A LIQUID.

§ 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[147] 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.

[148]

§ 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 jaundice.

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 ecchymosis.


[164] Lehrbuch der ger. Medicin, 2te Aufl.


2. THE VAPOUR OF CHLOROFORM.

§ 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.[149] 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, 1882.


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 impossible.

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[150] 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 successful.

§ 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.[151] 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 inhalation.

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 insanity.

[152]

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 seldom.


[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 compass.

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.

[153]

(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 chloroform.[178]


[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.


[154]

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., 1893.


§ 193. Aldehyde (Acetaldehyde), Acetaldehyde, 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 movements.


VII.—Chloral.

§ 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,[155] 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 thus

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 present.

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[156] 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.

Chloral detector

[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[157] 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[158] 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[159] 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.


[160]

§ 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[161] 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 impurities.

[162]

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; 110 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 hydrate.[191]


[191] C. Schwarz, Pharm. Zeit., xxxiii. 419.


Dr. Frank Ogston[192] has recommended sulphide of ammonium to be[163] 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[164] 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 muscles.


[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[165] 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[166] 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.

[167]

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 operations.

§ 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[168] 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 meant.


DEATHS FROM CARBOLIC ACID IN ENGLAND AND WALES DURING THE TEN YEARS ENDING 1892.

Accident or Negligence.
Ages, 0-1 1-5 5-15 15-25 25-65 65 and
above
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
Suicide.
Ages,   15-25 25-65 65 and
above
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:

  Cases.
Taken instead of Tincture of Opium, 1
Taen instad of  Infusion of Senna, 3
Taen instad of  Mineral Water, 2
Taen instad of  other Mixtures, 3
Taen inwardly instead of applied outwardly, 3
  12

Of these 12, 8 died.

Again, 10 persons took carbolic acid in mistake for various alcoholic[169] 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.

[170]

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.[171] 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 212 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 212 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[172] 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 day.


[201] American Journal of Pharmacy, vol. li., 4th Ser.; vol. ix., 1879, p. 57.


[173]

§ 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 acids.

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[174] 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 adults.

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 increasing.


[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][175] that hydroquinone () (paradihydroxyl phenol) and pyrocatechin () (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 pigment.


[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[176] 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[177] 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 odour.



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[178] 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 160000 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 112 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), —There[179] 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
temperature.
201·0° Meta-oxybenzoic 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 112 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[180] 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[181] 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 follows:


[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[182] 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 are


[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 liquid.

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;

and

(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[183] 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.


X.—Nitro-Benzene.

§ 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[184] 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 insensibility.

An interesting case of poisoning by the vapour is recorded by Taylor.[222][185] 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.[186] 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 conditions.

In a case related by Stevenson,[224] in which so small a quantity as 1·74[187] 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 312 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[188] 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 emerald-green.


[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 time.


[189]

XI.—Dinitro-benzol.

§ 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 follows:

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 diamines.

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 meta-phenylene-diamine.

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[190] 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 recovered.

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.


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 624, left 636, both optic[191] 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 died.


[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.


  Dinitro-Bands.
  In Red. In Green.
  50-52 62-66 70-77
After NH4SO4, 53-55 62-66 70-77
Afer NH3, 54-58 60-65 70-77
Afer 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[192] 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 (triamido-phenol).


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.

[193]

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,[194] 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,[195] 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 212 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[196] 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:

DEATHS IN ENGLAND AND WALES DURING THE TEN YEARS 1883-1892 FROM PRUSSIC ACID AND POTASSIC CYANIDE.

Prussic Acid (Accident or Negligence).
Ages, 0-1 1-5 5-15 15-25 25-65 65 and
above
Total
Males, ... 1 1 1 12 1 16
Females, 1 1 ... 2 7 ... 11
Totals, 1 2 1 3 19 1 27
Cyanide of Potassium (Accident or Negligence).
Ages,   1-5 5-15 15-25 25-65 65 and
above
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
above
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
above
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,[197] 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[198] 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[199] 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[200] 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.


[201]

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[202] 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 m