The Project Gutenberg EBook of Poisons: Their Effects and Detection, by 
Alexander Wynter Blyth

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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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[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.

[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 Phalloides—Phallin,	417
522.	Post-mortem Appearances,	417, 418
523.	The Agaricus Pantherinus—The Agaricus Ruber—Ruberine—Agarythrine,	418
524.	The Boletus Satanus, or Luridus,	418
525.	Occasional Effects of the Common Morelle,[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—Ecboline—Scleromucin—Sclerotic Acid—Sclererythrin—Scleroidin—Sclerocrystallin—Sphacelic Acid—Cornutin,	443-445
579.	Detection of Ergot in Flour,	445
580.	Pharmaceutical Preparations,	445
581.	Dose,	446
582.	Ergotism—Historical Notice of Various Outbreaks,	446, 447
583.	Convulsive Form of Ergotism,	447
584.	Gangrenous Form of Ergotism—The Wattisham Cases,	447, 448
585.	Symptoms of Acute Poisoning by Ergot,	448
586.	Physiological Action, as shown by Experiments on Animals,	448-450
587.	Separation of the Active Principles of Ergot,	450
	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

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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.

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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.

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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]

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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.

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§ 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]

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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]

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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!

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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]

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§ 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.

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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]

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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]

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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.

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“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]

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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.

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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]

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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]

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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:—

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§ 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.

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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]

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§ 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).

[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]—

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“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.

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“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]

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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]

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§ 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.

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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.

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§ 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.

II. BLOOD POISONS.

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

IV. POISONOUS PRODUCTS OF TISSUE CHANGE.

---

§ 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.

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.

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.

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

Ergot, picrotoxin, the poison of Illicium religiosum, cicutoxin, Æthusa cynapium, Œnanthe crocata, croton oil, savin oil, the toxalbumins of castor oil and Abrus.

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

[28]

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

F.—THE OXALIC ACID GROUP.

G.—INORGANIC POISONS.

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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
Cau„tic Potash,	8	10	1	...	...	...	9	10
Potassic Chlorate,	1	...	...	...	...	...	1	...
Pot„ssic Bichromate,	2	2	7	3	...	...	9	5
Pot„ssic Bromide,	1	...	...	...	...	...	1	...
Pot„ssic 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.

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	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.

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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:—

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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]

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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]

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---

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]

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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

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---

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.

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.

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---

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]

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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.

§ 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.”

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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 .

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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:—

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

Loew[39] makes the following generalisations:—

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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.

§ 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.”

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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

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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.

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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.

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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.

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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:—

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.

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.

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AUTENRIETH’S GENERAL PROCESS.

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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.

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.

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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

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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.

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§ 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.

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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]

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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]

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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:—

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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.

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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.

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]

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

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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.