Physiological Properties of Arsenic

Arsenicals have long been considered the most important of toxic inorganic compounds and it is not surprising that, to the lay mind, the name itself suggests poison. In spite of the ease with which it may be detected if suspicion is aroused, the deliberate use of white arsenic as a homicidal poison is still prevalent, especially in Europe, probably owing to the ease with which it may be administered, its resemblance to flour, and the fact that it is odourless and practically tasteless; moreover, it has been easily obtainable, both directly and surreptitiously, from sources such as fly-papers, insect powders and weed-killers. The incidence of arsenical poisoning was greatly reduced by the Arsenic Act of 1851, which restricted the sale of white arsenic and prescribed its admixture with soot or indigo if sold in quantities of less than 10 lbs.; prior to this 34 per cent, of all cases of poisoning in England were due to this substance. This act was repealed by the Pharmacy and Poisons Act of 1933, which stipulated rules for colouring of arsenic, provision being made for the addition of a dye to arsenical poisons.

Accidental poisoning, however, provides a more important problem, and the widespread distribution of arsenic, its frequent occurrence as a by-product in industry, and its use for a great variety of purposes, constitute a source of danger. The most frequent sources of arsenical poisoning are food contamination and occupational contact. An outbreak affecting 6000 persons, including 70 fatal cases, occurred in Lancashire in 1900 and was traced to beer made from glucose in the preparation of which arsenical sulphuric acid had been employed. Confectionery and many food ingredients have been found to be similarly contaminated, but modern methods of sulphuric acid manufacture have considerably lessened the likelihood of contamination from this source. An interesting case of cocoa to which potassium carbonate had been added to improve its solubility is cited by Monier-Williams; the carbonate had been made by calcining the residues left after cleaning wool from sheep which had been washed with arsenical insecticide.

The amounts present vary within wide limits and the element appears to be in a form only slightly toxic, but there may be sufficient to affect a person who cannot tolerate arsenic.

Cases of poisoning by drinking water contaminated with arsenic have been reported.

In prepared foods there is a permissible limit to the amount of arsenic which may be present; this limit, 0.01 grain per lb., was recommended by a Royal Commission in 1903 and is generally accepted, although it is not laid down by Statute.

Pollution of the atmosphere is a frequent cause of trouble; thus in 1929 the cattle dipping truck yards at Julia Creek, Queensland, were removed owing to contamination of the town atmosphere, dust samples from which disclosed 10 to 12 parts of arsenic per million. Chronic poisoning has also resulted from the inhalation of the fumes liberated on burning " mosquito incense " made from orpiment and sawdust. A systematic clinical and X-ray examination of furnace workers at the arsenic works at Freiberg, Saxony, revealed that the majority suffered from pustular and eczematous conditions of the skin and 80 per cent, showed ulceration and perforation of the septum of the nose, in spite of the provision of sponge respirators and protective clothing; arsenic was present in the hair and nails.

All the organic arsenicals which find important therapeutic application in certain blood diseases and syphilis are synthetic products and are only feebly poisonous. In time, however, arsenious acid may be formed in the tissues and cause typical symptoms of poisoning.

The important inorganic toxic compounds to be considered in the following pages are arsine, arsenic trichloride, white arsenic, arsenites and arsenates and arsenic sulphides. Metallic arsenic itself is not poisonous, and the intravenous injection of a colloidal solution of this substance has been found to benefit greatly a case of bone sarcoma of the femur which did not respond to X-ray treatment.

Arsenic trihydride, or arsine, is a powerful blood poison, 1 part in 20,000 parts of air being sufficient to produce symptoms. Inhalation of the gas appears to cause a lysis of the red corpuscles, haemoglobin being excreted in the urine; symptoms of suffocation result, the anaemia may affect the kidneys and jaundice result; the victim suffers severe pain in the lower chest and upper abdominal regions, accompanied by rigor and spasms, and finally collapse and death occur about the ninth day. The usual effects of arsenical poisoning may also be present, but the gastro-intestinal symptoms may be slight or absent. The treatment consists in administering oxygen, repeated blood transfusions and saline injections.

Experiments show that arsine acts on the red blood cells only where oxidative processes are occurring. Thus if oxygen is removed from a suspension of the red corpuscles by a current of an inert gas such as hydrogen or nitrogen, or by reduction with sodium sulphite or a culture of paramcecia, haemolysis does not occur. In arsine-hsemolysis the oxygen is supplied by the oxyhemoglobin. Arsenites and arsenates do not act thus on the blood elements. Following inhalation by cats, dogs and rabbits, Thauer found arsenic in the non-hsemolysed blood corpuscles but not in the plasma. Methsemoglobin formation is noticeable. The arsenic content of the organs was relatively low, the highest occurring in the spleen (from blood degradation), liver and kidney. Rapid excretion, mainly in the urine, occurs. The animals were not all equally susceptible to the poison.

The chemist Gehlen, after inhaling the gas, died on the ninth day, and many cases have occurred of men being overcome by the impure gas generated in industrial processes. Among recent cases recorded are those in which the gas resulted from the sprinkling of water on to the dross, containing aluminium arsenide, remaining after tin refining, and when the zinc slimes, from the recovery of gold by the cyanide process, were treated with sulphuric acid. The distribution of the arsenic (in parts per million) in the bodies of two fatal cases from the latter cause was as follows: brain 1.4, 1.0; lungs 2.59, 2.3; stomach and contents 0.1, 0.3; spleen 0.48, 2.2; kidney 0.36, 1.3; liver 6.90, 4.4.

Very dilute crude sulphuric acid in contact with iron or steel, in the presence of reducible arsenic compounds, may generate arsine even at ordinary temperatures. Sufficient arsenic may be derived from impurities in either the acid or the metal, and the presence of small quantities of nitric acid in technical sulphuric acid does not prevent the reaction. The use of acid containing more than 1 p.p.m. of As₂O₃ should be avoided. A German patent suggests that a safeguard in treating industrial materials containing arsenic with acid is always to carry out the operation in the presence of an oxidising agent such as chlorine water.

There is evidence that repeated exposure to low concentrations of arsine results in a cumulative effect, leading to severe poisoning. Following exposure there is generally a delay in the onset of symptoms and it is difficult to state with certainty the concentration which it is safe to breathe; but it has been concluded from available data that the permissible concentration for an unprotected person for a single period of 4 to 6 hours' exposure should not exceed 1 in 200,000 (0.0005 per cent.).

Numerous cases of poisoning have occurred attributed to wall-papers containing an arsenical pigment such as Schweinfurt Green or Scheele's Green. The use of these pigments for colouring papers and boards is now discontinued and, in England, more than 2 to 3 parts of arsenic per million is rarely present, there beings a provisional agreement that not more than 10 parts per million is permissible, while in certain continental countries the permissible limit is 5 mg. per sq. m. The symptoms arising from this source are sneezing, lachrymation and cough, nausea, sickness and diarrhoea, dry throat and tongue with thirst, colic pains, cramps and spasms, depression and extreme weakness. In most wall-paper cases the poisonous effects were first attributed to the presence in the air of arsenical dust, but it has been shown that the action of moisture and organic matter such as starch paste and gelatin on free arsenious acid may produce a volatile compound presumed to be an alkylarsine, and after removal of all dust from such air, passage through aqueous silver nitrate shows that arsenic is still present. Gosio discovered that, in the presence of organic matter containing arsenic, certain moulds, under suitable conditions, were able to synthesise volatile arsenic compounds having an intense garlic odour. The most active organisms are Penicillium brevieaule and Penicillium divaricatum, and the action of the first is used for the detection of small quantities of arsenic in organic matter, the test being known as Abba's test. The presence of carbohydrate appears to be necessary. With the Penicillium divaricatum it is possible to detect as little as 0.00008 per cent, of arsenic. Compounds of selenium and tellurium similarly yield volatile compounds by the action of such organisms and, in the latter case, the odour resembles that due to arsenic. The nature of the volatile compound has not been conclusively demonstrated, being variously described as arsine, diethylarsine, trimethylarsine and diethylcacodyl oxide; possibly more than one such compound may be produced. Lerrigo experimented with garden soils to which arsenic had been added, but was unable to show that volatile compounds were produced by the agency of soil bacteria.

In the investigation of a number of eases of fatal poisoning attributed to wall coverings, the evidence has led to the plaster as being the source of the trouble. Thus, in a case in which two children died at Cinderford, Forest of Dean, in 1932, the paper from a dry part of the wall contained 8.3 parts As₂O₃ per million, a sample where mould was most pronounced 2.3 parts, an unused roll of wall-paper purchased when the wall was papered 4.4 parts, and the plaster (composed of coke breeze and cement) 91 parts. It was concluded that the arsenic present in the paper was an impurity and that that present in the plaster dissolved in moisture coming through the wall from a bank of soil outside and was converted to a volatile compound by the mould on the paper. The arsenic in the air could not be detected by simple aspiration, but filter papers saturated with silver nitrate placed near the walls for 7 and 9 days collected sufficient to be detected by the electrolytic Marsh test. In another case, where the odour of alkylarsines was reported, the outer papers gave a negative test for arsenic, but older paper beneath gave a strong positive test, the arsenic being almost completely soluble in water. It was revealed, however, that the paperhanger, 15 years previously, had mixed rat poison with the paste in order to prevent mice from gnawing the paper! Re-papering from time to time had evidently furnished nutrient material for the fungi which converted the arsenic to volatile compounds.

According to Foulkes, experiments with arsine for war purposes suggested that the toxicity was less than usually supposed. A pig in a trench exposed to a high concentration of the gas appeared unaffected, and of two officers who entered the trench, which smelt very strongly of garlic, one only suffered ill-effects. Such compounds as diphenyl-chlorarsine and diphenylamine-chlorarsine were employed during the Great War as lachrymators, sternutators and respiratory irritants, one part of the latter in 25 million of air being sufficient to produce intolerable conditions; chloroform gave immediate relief and the effects were only temporary.

Arsenic trichloride is highly toxic and inhalation of the fumes rapidly causes acute arsenical poisoning, the symptoms including laryngeal obstruction, dyspnoea and convulsions. During the Great War, shells containing the compound mixed with hydrogen cyanide and other ingredients were employed. The following relative toxicities have been given: Cl₂ 1, AsCl₃ 1.5, COCl₂ 5.5, but there is considerable divergence of opinion as to the relative values of chlorine and phosgene, Haber and others putting the lethal value of the latter at 17 to 19 times that of the former.

A series of epidemics among fisherfolk on the shores of the Gulf of Dantzig in 1924-25, known as "Haff sickness," was supposed to be due to poisoning resulting from the presence in the atmosphere of arsenious chloride. The possible source of the latter was the waste liquors from cellulose factories in the neighbourhood, being derived either from the sulphurous acid prepared from arsenical pyrites containing sodium chloride or from the action of algae on the arsenical trade waste. The findings of the Government Laboratory, established to investigate the problem, did not, however, confirm arsenical poisoning.

Application of liquid arsenious chloride to the skin also causes acute poisoning. The immediate result is necrosis; this may be considerably retarded by washing within one minute of the application, but after five minutes washing has no effect. The arsenic is rapidly absorbed by the tissues, and after a few hours, if death ensues, the element can be recovered from most of the tissues and organs of the body, especially the brain, liver and kidneys.

Arsenious chloride destroys the underground stems of some species of creeping perennials. It is very effective, even in very dilute solution, in destroying the growth of many annual weeds, including puncture vine, if applied before the seeds mature. Vegetation sprayed with arsenious chloride is repulsive to grazing animals and they avoid it, whereas vegetation sprayed with arsenites is attractive and is so toxic that it may cause death.

Arsenious oxide, or white arsenic, is an extremely powerful poison, especially when in solution. It acts as a severe gastro-intestinal irritant. As little as 0.13 g. has proved fatal, but 0.19 g. is probably the least quantity likely to cause death. The limit of toxicity in aqueous solution is 0.2 mg. As₂O₃ per litre.

The effects when taken in powder form vary considerably with the state of division, and cases are on record in which recovery has taken place after taking such large amounts as 15 to 42 g. Such large doses have generally been taken on a full stomach and have promptly been rejected with food by the brisk action of the bowels. But the toxicity of arsenious oxide depends upon its rate of solution, and this depends on the grain size. The toxic dose of potassium arsenite for man has been estimated to be 0.84 g. For a dog the dangerous dose of white arsenic is 0.32 to 0.65 g., for a horse 1.94 g. and for a cow 0.65 g. The fatal dose is dependent to some extent on body weight and, expressed in g. per kg. of body weight, the fatal doses of the finely powdered oxide taken through the mouth are estimated to be: for rabbits 0.2, for rats 0.1 and for chickens 0.075; while if taken in the form of a solution the quantities are respectively 0.015 to 0.020, 0.075 and 0.0667. For a sheep 0.86 g. of sodium arsenite is fatal, but half that quantity is non-toxic.

It is well known that white arsenic can be taken in small quantities with apparently good effects. Thus, the arsenic eating of the Styrian peasants is said to improve the respiration and to enable them to endure fatigue better in mountain climbing; the skin is improved and the body well developed, and the arsenic eater appears to be exempt from infectious diseases. The arsenic acts as a stimulant and causes an increased flow of the gastric juice. The doses taken are at first small, but are gradually increased to about 0.3 g. or more; Knapp records having witnessed the swallowing of 0.486 g. (7.5 grains). There is doubt, however, as to whether the arsenic eaten by these peasants is comparable in toxicity with ordinary white arsenic. It is obtained from the flues of local smelting furnaces, being known as hidrach, and is probably a coarse-grained, comparatively insoluble form of arsenic. Moreover, it has not been demonstrated that habituation to arsenic is possible. The peasants can discontinue taking it only by gradually diminishing the doses; if the doses are suddenly stopped, intense pain and sickness occur, often with fatal results. In the same way the improved condition of horses, to which arsenic has been daily administered for show purposes, soon disappears when the stimulant is withdrawn. Moreover, the practice of thus feeding animals results in reduced respiratory activity and impaired reproductive functions. The practice of arsenic eating also exists in parts of India.

The symptoms of acute poisoning by white arsenic usually appear in less than one hour. The victim may complain of a burning taste when taking it. He experiences a burning pain at the pit of the stomach, which is increased by pressure; nausea, faintness and uncontrollable vomiting follows, the latter being renewed by the act of swallowing. The pain becomes more diffuse, with diarrhoea, tenesmus and dysuria. There is a sense of constriction in the throat, intense thirst, headache, restlessness and rapid but weak pulse, cramps in the legs and convulsive twitchings of the extremities. In most cases the mind remains clear until there is complete collapse or coma. Death may follow after a few hours.

Chronic poisoning, which usually results from repeated small doses as in industry or by deliberate poisoning, but may be the result of one large dose, causes chronic ill-health, which appears to be due to mild gastro-enteritis. The victim loses appetite, loathes food and suffers nausea and general malaise. There is occasional vomiting, diarrhoea and increasing prostration. The effect of the poison on the liver may cause jaundice, the mucous membranes become inflamed causing conjunctivitis, running of the eyes, coughing and bronchial catarrh. Skin eruptions and various nervous symptoms, including peripheral neuritis, may occur, and the condition becomes such that the person may die from sheer exhaustion or, if death occurs by the administration of a larger final dose, arsenical poisoning may not be suspected.

Although the symptoms enumerated above are typical, different cases may present very different and perplexing features, for whereas in one case these symptoms may be present in an aggravated form, in another they may be absent or nearly so. The pulse may be very frequent (90 to 140) or almost imperceptible (30 to 45). The taking of the poison may be followed by immediate collapse with little pain, vomiting or diarrhoea, and one case is recorded where death occurred in four hours after profound sleep. The nervous symptoms, which are especially marked in chronic cases, show a similar variation and, in a consideration of 25 cases, the incidence was as follows: extreme restlessness 5, debility 10, coma 3, delirium 3, mind unimpaired 6, cramp in legs 9 (and arms 4), convulsions 6, tetanus 2, hysteria 1, epilepsy 2, tetanus, coma and delirium, successively, 2; death in convulsions 3, in one case after horrible laughter. The nervous symptoms may persist for a considerable time; periodic epilepsy, for example, has been observed after two years.

White arsenic is not considered to be a cumulative poison, and although it is absorbed by almost every part of the body, elimination proceeds slowly and almost at once, arsenic being detectable in the urine and faeces within half an hour. The amount excreted varies directly with the dose, but the rate varies greatly with the individual. It must be remembered, however, that excretion of arsenic occurs with normal persons, and the following variation has been observed in the urine of a large number of persons fed on the same diet: in 16 per cent, no arsenic present; in 43 per cent. 0.01 to 0.06 mg. As per litre; in 33 per cent. 0.07 to 0.20 mg. As per litre; and in 8 per cent. 0.21 to 0.69 mg. As per litre. The periodic variation of the arsenic content in the blood of women has been mentioned previously. Considerable quantities of arsenic may thus appear in the excretions of individuals without discoverable cause; this is especially so in persons with jaundice, and arsenic is thought to be a contributory factor in many cases of acute yellow atrophy of the liver. Also abnormal urinary arsenic accompanies many skin conditions, such as eczema, scleroderma, leucoderma, psoriasis and pemphigus, and in some cases of eczema arsenic appears to be the exciting cause.

The fatal period in poisoning by white arsenic varies considerably and may be a few hours or days, or many weeks; in most fatal cases death occurs in 6 to 24 hours.

A post-mortem examination usually reveals the stomach in a state of acute inflammation and, if the arsenic was taken in solid form, small white or yellowish patches, consisting of a paste of arsenious acid and coagulable lymph, adhere to the mucous membrane forming centres of intense inflammation. The stomach may contain brown clotted matter, sometimes yellow owing to partial conversion to sulphide. The inflammation may affect the whole intestinal canal, but is most conspicuous in the lower bowel. The gullet and sometimes the throat and mouth may be inflamed. There may also be inflammation of the bladder, livid spots on the skin, and congestion of the brain. On the other hand, inflammation of the lining of the stomach may be completely absent. The arsenic is eliminated by the bowels, kidneys, and to some extent by the skin and hair. That which is absorbed is found after death mainly in the liver and, to a less extent, in the kidneys and other soft organs. Thus, in a case of suicide, analysis of the viscera gave: - liver 5.6, kidneys 2.0, heart 2.5, stomach 4.0, small intestine 4.5 mg. As per kg.; while in a case of acute poisoning, in which 3 to 4 times the lethal dose had been taken, the following contents were found: - liver 10, kidneys 7.5, heart 3, spleen 3, lung 7.5, blood 4, stomach 16, intestines near the duodenum 11, central portion 14, extremity 18, liquid content of stomach and intestines 14.5, brain 0.5 mg. As per kg. But in chronic poisoning the arsenic permeates even to the hair and nails. The normal content of arsenic in human hair is 0.01 to 0.03 mg. per 100 g., and in the nails traces of this order may or may not occur, whereas the amount gradually increases after assimilation of arsenic. Nail clippings from such a person showed 2 to 13 mg. per 100 g. Moreover, characteristic nailbands appear after about 2 months when sublethal poisoning due to a few large doses has occurred. The accumulation of arsenic in the hair may be made use of to determine whether one or many doses have been taken; if the stomach contains large quantities of arsenic, whereas only a little is found in the hair, the case is one of acute poisoning.

Absorption of arsenic by the bones also occurs to a considerable extent, and their arsenic content, whether death occurs after a few hours or only after some days, may give valuable information where suspicion of poisoning exists. Thus in the case of a man who died 8 days after ingesting the poison, 110 mg. of arsenic were found in the bones, about half being present in the bones of the arms and legs and about 20 per cent, in the flat bones of the skull; but in the case of a woman who died after 12 hours, out of a total of 1907 mg. found in the body only 3.2 mg. occurred in the bones, but this amount was more than was found in any other portion of the body (except the skin) not in direct contact with the alimentary canal. In experiments on dogs to which arsenic had been administered, Popp showed that the amount of arsenic in the calcined bones was about one-sixth of the amount found in the bones before cremation, and less than one-thousandth of the total amount in the whole body before cremation.

Arsenic has been credited with retarding the decomposition of the body. This does not appear to be true in cases of acute poisoning, although the stomach may be preserved when the surrounding parts are in a state of advanced decay; in chronic cases, where the arsenic has pervaded the tissues, preservation may occur.

The toxic action of white arsenic has been attributed to its inhibitory action on the oxidative processes, partly owing to the effect of the change of on the enzyme concerned. Small quantities of arsenious acid reduce the power of suitably prepared extracts of animal tissues to oxidise reduced phenolphthalein. The oxidation of tartaric acid at the ordinary temperature and at 37.5° C. is inhibited by arsenious acid, as also is the respiration and fermentation of yeast, but the latter inhibition is minimised by the presence of sugar, the effect increasing with the sugar concentration. It has been observed that arsenites have a retarding effect on many oxidation-reduction systems, such as (1) acetaldehyde and colloidal platinum, (2) acetaldehyde, glycocoll and phosphate, (3) hypoxanthine-xanthine oxidase of rat or mouse skin; arsenates are comparatively inactive. In the respiration of minced heart muscle and minced liver tissue, a co-enzyme takes part which assists in the oxidation or dehydrogenation of lactic acid, and the action is poisoned by arsenious oxide, which inhibits the whole respiratory process. Parfentjev found that there was no disturbance of the fermentative processes in the acute poisoning of rabbits per os. Underhill and Dimick observed that subcutaneous injection of the oxide into dogs increased the ethereal sulphate and neutral sulphur fraction of the urinary sulphur, but no consistent variations could be detected when administered by mouth. The solubility of arsenic in aqueous solutions (5 to 7 per cent.) of glucose or sucrose is very much less than in water, and Cohen suggests that the variable toxicity of the oxide to animals may be due to differences in the concentration of sugars in the alimentary tract. Experiments on rabbits show that there is an increase in the non-protein nitrogen of the blood due to increase in carbamide nitrogen. There is also an increase in the sugar content of the blood at the expense of the glycogen of the liver, causing hyperglycemia; some of the glycogen may also constitute the source of the lactic acid which appears in appreciable proportion in the blood in cases of arsenical poisoning.

The first step in the treatment of arsenical poisoning is to wash out the stomach thoroughly, using mild emetics such as ipecacuanha, mustard or common salt, aided by copious draughts of warm milk and water. The usual antidote is freshly precipitated ferric hydroxide given moist; this renders the arsenious acid insoluble and is effective if administered while the poison is still in the stomach, but less so if the arsenic was taken in the solid state or if it adheres to the stomach lining. It is not a true antidote as it does not act unless it is in contact with the poison. Alternatives which may be used, though not with such good effect, are dialysed iron, magnesium hydroxide, and animal charcoal. Intravenous injections of sodium thiosulphate, in doses of 0.6 to 1.0 g., have been recommended and, although it is not an antidote, this substance appears to have good effect in cases of both acute and chronic poisoning, in the latter case preventing damage to the kidneys. It diminishes the rate of arsenic excretion, and its action probably depends on the formation of an insoluble compound.

The toxicity due to local or absorptive action of solid arsenious oxide is considerably decreased by boric acid, probably because the solubility of the former, which is dependent on H⁺-ion concentration, is much less in the aqueous boric acid than in water; with dissolved arsenious oxide the boric acid causes a retardation but no alleviation of the toxic action.

Other treatment is determined by the symptoms, stimulants being necessary in cases of collapse or anodynes if the nervous condition so requires; small quantities of iced water for the intense thirst; castor oil and milk if diarrhoea is ineffectual and painful. The patient needs to be kept warm and hot blankets should be applied to the feet and abdomen.

Arsenious oxide in dilute solution is not absorbed by the unbroken skin, but absorption occurs from concentrated solution. The action is not directly on the cells of the horny layer of the epithelium, but primarily on the capillaries.

Arsenites, as already indicated, and arsenates are also poisonous, the effects resembling those of white arsenic. The employment of these compounds in England is now severely restricted, and the manufacture of such pigments as Scheele's Green and Schweinfurt or Emerald Green has practically ceased, although the latter is still produced for use as an insecticide or fungicide and for high-class decorative and artistic work; it is also employed in the manufacture of " antifouling paints" for ships' bottoms. Formerly, persons engaged in such industries as colour printing and the making of artificial flowers, fruit and leaves, in which these colours were used, frequently suffered from catarrh, sore throat and skin rashes, and the more intense symptoms were liable, to occur.

The poisonous action is influenced by the solubility of the compound in water. Lethal doses of sodium arsenate for goats and rabbits are found to be approximately 0.11 and 0.05 g. per kg. body weight, and the following doses which produced death of sheep not earlier than the second day have been observed, the figures in brackets being nontoxic doses: sodium arsenite, 0.86 g. (0.43 g.); arsenic acid, 0.86 g. (0.43 g.); lead arsenate, 3.9 g. (2.6 g.); emerald green, 1.3 g.

An examination of the effect of arsenate on the blood glucolysis of dogs and rabbits has shown that in the former case the glucolysis is diminished but in the latter it is accelerated. The inorganic phosphates of the glucolysing blood invariably increase owing to stimulation of the blood phosphatases, the effect being directly proportional to the arsenate concentration. Braunstein states that the action of the arsenate is to impede the esterification of hexose with phosphate, this esterification not being a necessary condition of glycolysis but only an accompanying connected phenomenon.

The sulphides of arsenic are not poisonous when pure, but as they are frequently contaminated with arsenious oxide the usual symptoms may result from their ingestion. The yellow trisulphide is occasionally found adhering to the wall of the stomach after death owing to the action of hydrogen sulphide on arsenious oxide. It was observed by Ossikowsky that during the decomposition of organic substances, easily oxidisable compounds, if present, become oxidised, and that under such conditions arsenious sulphide yields arsenious oxide and small quantities of arsenic pentoxide; the oxidation is facilitated by the presence of water and heat. In cases of poisoning attributed to the sulphide, the oxidation products have appeared more or less quickly, according to conditions, and have contributed to the ill-effects.

Colloidal arsenious sulphide, in whatever way it may be administered to rabbits, dogs or guinea-pigs, changes its state of dispersion, becoming granular, and poisonous effects ensue.