(1) Toxicological, based on the action of the poisons.
(2) Chemical, based on the chemical composition of the poisons.
(3) Physical, based on the varying density of the poisons. (Division into solid (in form of dust), gaseous, and liquid poisons.)
To which may be added:
(4) Classification according to the source of the poisoning and therefore according to industry, upon which Part I is mainly based.
In this section (Part II) a system is adopted which takes into consideration as far as possible all the principles of division mentioned above, in order to classify industrial poisonous substances in such a manner that general practical conclusions can be clearly drawn, and supervision rendered easy.
Common to this group is a strong corrosive and irritant effect, varying however in degree; as gases this group corrode or inflame the mucous membrane of the respiratory passages, and in liquid form or in solution, the skin.
Besides this superficial effect single members of this group, especially those containing nitrogen, produce a remote effect upon the blood.
After absorption of the acids a decrease in the alkalinity of the blood can take place and in its power to take up carbonic acid, thus vitally affecting the interchange of gases in the body, and producing symptoms of tissue suffocation.
As regards treatment in the case of acids and alkalis, neutralisation has been already mentioned; further, oxygen treatment may be recommended in cases where the blood has been injuriously affected. In cases of poisoning through breathing in acid vapours, inhalation of extremely rarefied vapour of ammonia or of a spray of soda solution (about 1 per cent.) is advisable.
Hydrochloric Acid (HCl) is a colourless, pungently smelling gas which gives off strong white fumes. Experiments on animals, carefully carried out by Leymann, produced the following symptoms.
Even in a concentration of 2-5 per thousand clouding of the cornea ensues, and after about an hour inflammation of the conjunctiva, violent running from every exposed mucous membrane with marked reddening, and frequently inflammation (necrosis) of the septum of the nose; the lungs are distended with blood, here and there hæmorrhages occur in the respiratory and also in the digestive tracts. The animal dies of œdema (swelling) of the lungs and hæmorrhage into the lungs if exposed long enough to the action of HCl, even though (according to Lehmann) there may not be accumulation of HCl in the blood; the chief effect is the irritant one; 1·5-5 per thousand parts HCl in the air suffices, after three or four hours’ exposure, to affect smaller animals (rabbits) so much that they die during the experiment or shortly after it. Man can tolerate an atmosphere containing 0·1 to 0·2 per thousand HCl; a somewhat greater proportion of HCl produces bronchial catarrh, cough, &c.
The solution of hydrochloric acid in water is about 40 per cent. Simply wetting the skin with concentrated solution of hydrochloric acid does not generally have an irritant effect unless persisted in for some time; the action of the acid, when continued, has a marked effect upon the mucous membranes and upon the eyes.
The same treatment already recommended in the introductory remarks on poisoning by inhalation of acid fumes in general applies.
Hydrofluoric Acid (HFl), a pungently smelling, colourless gas, causes even in weak solutions (0·02 per cent.) irritant symptoms (catarrh of the mucous membrane of the respiratory organs, lachrymation, &c.). Stronger solutions set up obstinate ulcers, difficult to heal, in the mucous membrane and the skin.
Silico-fluoric Acid (H₂SiFl₆) produces an analogous though somewhat less marked corrosive action.
As regards treatment the reader is again referred to the introductory sentences on this group.
Sulphur Dioxide (SO₂) is a colourless, pungently smelling gas which, acting in low concentration or for a short period, causes cough and irritation of the mucous membrane of the respiratory passages and of the eyes; acting for a longer period, it sets up inflammation of the mucous membrane, bronchial catarrh, expectoration of blood, and inflammation of the lungs.
As Ogata and Lehmann have proved by experiments—some of them made on man—a proportion of 0·03-0·04 per thousand of sulphur dioxide in the air has a serious effect on a person unaccustomed to it, while workmen used to this gas can tolerate it easily.
As sulphur dioxide probably does not affect the blood, treatment by oxygen inhalation is useless. Otherwise the treatment spoken of as applying to acid poisonings in general holds good.
Sulphuric Acid (H₂SO₄). Concentrated sulphuric acid occasionally splashes into the eye or wets the skin, causing severe irritation and corrosion, unless the liquid is quickly washed off or neutralised. If the action of the acid persists, the corrosive effect becomes deepseated and leads to disfiguring scars.
Nitrous Fumes, Nitric Acid.—Nitric oxide (NO) oxidises in the air with formation of red fumes composed of nitrogen trioxide (N₂O₃) and nitrogen peroxide (NO₂). These oxides are contained in the gases evolved from fuming nitric acid and where nitric acid acts upon metals, organic substances, &c.
Industrial poisoning by nitrous fumes is dangerous; unfortunately it frequently occurs and often runs a severe, even fatal, course; sometimes numerous workers are poisoned simultaneously. The main reason why nitrous fumes are so dangerous is because their effect, like that of most other irritant gases, is not shown at once in symptoms of irritation, such as cough, cramp of the glottis, &c., which would at least serve as a warning to the affected person; on the contrary, generally no effect at all is felt at first, especially if the fumes are not very concentrated. Symptoms of irritation usually appear only after some hours’ stay in the poisonous atmosphere. By this time a relatively large quantity of the poisonous gas has been absorbed, and the remote effect on the blood induced.
The first symptoms of irritation (cough, difficulty of breathing, nausea, &c.) generally disappear when the affected person leaves the charged atmosphere, and he then often passes several hours without symptoms, relatively well. Later severe symptoms supervene—often rather suddenly—difficulty of breathing, fits of suffocation, cyanosis, and copious frothy blood-stained expectoration with symptoms of inflammation of the bronchial tubes and lungs. These attacks may last a longer or shorter time, and in severe cases can lead to death; slight cases end in recovery, without any sequelæ.
In poisoning by nitrous acid fumes, oxygen inhalation, if applied in time, undoubtedly holds out hope of success, and should always be tried. Chloroform has been repeatedly recommended as a remedy. Probably its inhalation produces no actual curative effect, but only an abatement of the symptoms through the narcosis induced.
Nitric acid (HNO₃) in solution has an irritant corroding action if, when concentrated, it comes into contact with the skin or mucous membrane.
Chlorine (Cl) is a yellow-green, pungently smelling gas, Bromine (Br) a fuming liquid, and Iodine (I) forms crystals which volatilise slightly at ordinary temperatures.
According to Lehmann’s experiments on animals the effect of chlorine gas and bromine fumes is completely similar. Lehmann and Binz assume that chlorine has a twofold effect: (1) narcotic, paralysing the outer membrane of the brain, and (2) the well-known irritant action upon the mucous membrane, producing a general catarrh of the air passages, and inflammation of the lungs; it is, however, only the latter which causes menace to life. Other writers do not mention the narcotic effect upon the brain and assume that the halogens when brought into contact with the mucous membrane are quickly converted into halogen hydrides, and, as such, produce a corrosive effect. According to Lehmann, even 0·01 per thousand Cl or Br in the air is injurious, even 0·1 per thousand produces ulceration of the mucous membrane, and one or two hours’ exposure to the poison endangers life. Lehmann has further tested (on dogs) acclimatisation to chlorine, and finds that after a month the power of resistance to chlorine appears to be increased about ten times. In a further series of experiments the same author has proved that even the smallest quantities of chlorine present in the atmosphere are completely absorbed in breathing.
Continued or frequent action of chlorine upon the organism produces symptoms which have been described as chronic chlorine poisoning—such as anæmia and indigestion, in addition to catarrhal and nervous symptoms. Further, in factories where chlorine is produced by the electrolytic process, workers were found to be suffering from the so-called chlorine rash (first observed by Herxheimer). This skin disease consists in an inflammation of the glands of the skin, with occasional development of ulcers and scars. Severe cases are accompanied by digestive disturbance. Bettmann, Lehmann, and others maintain that it is not caused by chlorine alone, but by chlorinated tar products, which are formed in the production of chlorine and hydrochloric acid.
In acute cases of chlorine poisoning oxygen treatment should be tried, but in any case the patient should have free access to pure air. Approved remedies are inhalation of soda spray or very dilute ammonia, or of a vapourised solution of sodium hypochlorite. If the patient is in great pain, he may be allowed to inhale cocaine solution (0·2 per cent.).
The administration of arsenic (solutio arsenicalis) is recommended, especially in cases of acne. In general the usual treatment for diseases of the skin is followed; salicylic acid lotions, sulphur baths, and sulphur ointments may be made use of.
Chlorides.—Chlorides of Phosphorus, Phosphorus-trichloride (PCl₃), and Phosphorus oxychloride (POCl₃), are strong-smelling liquids, fuming in the air, and when brought into contact with water decomposing into phosphorous acid and hydrochloric acid. These halogen compounds of phosphorus have a violently irritant action upon the respiratory organs and the eyes, in that they decompose on the mucous membrane into hydrochloric acid and an oxyacid of phosphorus. Inhalation of the fumes of these compounds causes cough, difficulty of breathing, inflammation of the respiratory passages, and blood-stained expectoration.
Treatment is similar to that for acid poisoning in general and hydrochloric acid in particular.
Similar to that of the chlorides of phosphorus is the action of chlorides of sulphur, of which sulphur monochloride (S₂Cl)₂ is of industrial hygienic importance as it is employed in the vulcanising of indiarubber. It is a brown, oily, fuming liquid, which, mixed with water or even in damp air, decomposes into sulphur dioxide and hydrochloric acid. The fumes of sulphur monochloride have therefore a marked irritant effect, like that of hydrochloric acid and sulphur dioxide. The action of sulphur chloride was thoroughly studied by Lehmann. Industrial poisoning by sulphur chloride is mentioned by Leymann and also in the reports of the Prussian factory inspectors for 1897. The latter case ended fatally owing to the ignorance of the would-be rescuers: a workman had spilt trichloride of phosphorus upon his clothes, and the by-standers, not knowing its dangerous action when combined with water, poured water on him.
Treatment is similar to that of poisoning from hydrochloric acid or sulphur dioxide.
Chloride of zinc (zinc chloride, ZnCl₂) likewise has corroding and irritant action upon the mucous membrane of the respiratory organs.
Ammonia (NH₃) is a colourless, pungent-smelling gas which dissolves to the extent of about 33 per cent. in water. Inhaled, it first produces violent reflex coughing, then irritation and corrosion of the mucous membrane of the respiratory organs, and finally death through suffocation (spasm of the glottis) if exposure to its action has lasted a sufficiently long time. Microscopic sections exhibit a diphtheritic appearance of the mucous membrane, and inflammation of the lungs. The effects upon the central nervous system (irritation of the medulla and spinal cord) which are peculiar to ammonia compounds need not be considered, as the corrosion of the respiratory passage is sufficient alone to cause death. When the action of the gas is less intense, the patient rallies from the first stage, but often severe symptoms come on later affecting the lungs.
Lehmann in experiments upon himself could tolerate as much as 0·33 per thousand NH₃ for thirty minutes; he found in gas works (with fairly marked odour) hardly more than 0·1 per thousand NH₃ in the atmosphere, and considers 0·5 per thousand distinct evidence of excess. He found that he could produce in dogs acclimatisation up to 1·0 per thousand NH₃ (five times as much as could at first be borne). About 88 per cent. of the ammonia contained in the air is absorbed in breathing; ammonia is said to exercise also a reducing action upon the oxygen of the blood (oxyhæmoglobin).
Chronic poisoning by ammonia can hardly be said to occur. In those who clean out sewers and drains, the inflammation of the eyes and digestive disturbance attributed partly to ammonia are probably due more to the action of sulphur compounds—ammonium sulphide and sulphuretted hydrogen. Irritation due to solution of ammonia does not come into account in industrial employment.
As regards treatment, fresh air or administration of oxygen is most likely to be successful. Inhalation also of very dilute acetic acid vapour, steam, or spray of sodium carbonate is advocated.
The alkaline hydroxides (potassium and sodium hydroxide, KOH, NaOH) have an albumen-dissolving and therefore caustic effect. Industrially it occurs in the caustic action of concentrated (often hot) lyes upon the skin or upon the eye—through splashing. Quicklime (CaO) has also a caustic action, producing inflammation of the skin or eyes (especially in those engaged in the preparation of mortar).
Under this head comes also the effect upon the respiratory passages—described by several authors—caused in the production of artificial manure discussed at length in Part I.
As regards treatment of the irritant effect of alkalis, what has been said as to corrosives in general applies here (rinsing with water or weak organic acids), and in inflammation of the eye caused by lime a drop of castor oil is recommended.
The various substances of this group differ markedly in their action. Under this heading come principally chronic metal poisonings, characterised by a general, often very intense, disturbance of nutrition, which justifies their delineation as ‘metabolic poisons’; among these poisons also are included certain others which produce chronic poisoning accompanied by severe disturbance of the peripheral and central nervous system.
The corrosive action common to the metal oxides (when acting in a concentrated condition), attributable to the formation of insoluble albuminates, need not, in industrial poisoning, be taken so much into account. The corrosive effect is characteristic only of the compounds, especially of the acid salts of chromium, which, as an acid-forming element, may be classed in the preceding group. Disturbance of health in workmen handling nickel compounds are also ascribed to the corrosive action of these substances.
Lead poisoning is the most frequent and important chronic industrial poisoning; the symptoms are very varied and associated with the most different groups of organs. We shall describe the typical course of a case of industrial lead poisoning, laying stress, however, on the fact that numerous cases follow an irregular course, in that special symptoms or complications of symptoms are in some especially accentuated, while in others they become less marked or are absent altogether.
A premonitory indication of chronic lead poisoning is a blue line on the gum, indicated by a slate gray or bluish black edging to the teeth, the appearance of which is usually accompanied by an unpleasant sweetish taste in the mouth. The cause of this blue line was for some time disputed. It is obviously due to the formation and deposit of sulphide of lead through the action of sulphuretted hydrogen arising from decomposition in the mouth cavity. At the same time a general feeling of malaise and weakness often comes on, occasionally accompanied by tremor of the muscles and disinclination for food, at which stage the sufferer consults the doctor. Frequently he complains also of pains in the stomach, not difficult to distinguish from the lead colic to be described later. Usually the patient already exhibits at this stage general emaciation and marked pallor.
The blue line was formerly considered a characteristic early indication of lead poisoning; but it has now been proved that occasionally it is absent even in severe attacks. But although the blue line may fail as an ‘initial symptom,’ it will nevertheless be a valuable aid to the practitioner in the recognition of lead poisoning. It is worth while to mention the fact that other metallic poisons produce a very similar ‘line,’ especially mercury, also iron and silver (as in the case of argyria); it has been stated that the blue line can be simulated by particles of charcoal on the gum. The pallor of the patient at the commencement of lead poisoning drew attention to the condition of the blood. The diminution in the amount of hæmoglobin often met with, which under certain circumstances is accompanied by diminution of the red blood cells, offers nothing characteristic. On the other hand, structural changes in the red blood cells—presence of basophil granules in them—are asserted by a number of writers to be characteristic of the first stages of lead poisoning. The basophil granules are believed to be due to regenerative changes in the nucleus. But these changes are also found in pernicious anæmia, cancer, leucæmia, anæmia, tuberculosis, &c.; also in a number of poisonings such as phenylhydrazine, dinitrobenzene, corrosive sublimate, and others; they are therefore the less characteristic of chronic lead poisoning, as occasionally they cannot be found in actual lead poisoning, a point upon which I have convinced myself in the case both of men and animals. Still, the appearance of much basophilia in the red blood cells is a valuable aid to diagnosis, especially as the method of staining to demonstrate them is simple.
Other anomalies of the blood observed in lead poisoning may here be mentioned. Glibert found a striking diminution in the elasticity of the red blood corpuscles, and experiments I have made point to the fact that the power of resistance of the red blood corpuscles to chemically acting hæmolytic agents, such as decinormal soda solution, is considerably reduced.
The pulse is generally hard and of high tension, especially during the attacks of colic. Further, cramp of the bloodvessels (also in the retinal arteries) has been observed. To these functional disturbances in the circulation are added sometimes definite changes in the vessel wall. Later, obliterative arteritis comes on (in the brain arteries), and arteriosclerosis.
The most important symptom of fully developed lead poisoning is colic, which is usually preceded by the initial symptoms described (especially the gastric symptoms), but not always so, as occasionally colic sets in without any warning. The colic pains often set in with marked vehemence. They radiate from the navel on all sides, even through the whole body; the abdomen is contracted and as hard as a board. Pressure on the lower part diminishes the pain somewhat, so that the sufferer often involuntarily lies flat on his stomach. During the attack the pulse is often remarkably slow. Constipation occurs, and often does not yield to purgatives. The attacks last sometimes for hours, occasionally for days, or the pains can (with remissions) even distress the patient for weeks. The frequency of attacks is also very variable. Occasionally one attack follows another, often there are intervals of weeks, even years, according to the severity of the poisoning and duration of exposure. If the patient is removed from the injurious action of lead, as a rule recovery soon ensues.
Fig. 34.—Paralysis of the Ulnar Nerve in Lead Poisoning
Fig. 34a.—Different Types of Paralysis of the Radial Nerve in Hungarian Potters poisoned by Lead (after Chyzer)
Often with the colic, or at any rate shortly after it, appear lead tremor and arthralgia, paroxysmal pain mostly affecting the joints, but occasionally also the muscles and bones. They are often the precursor of severe nervous symptoms which affect the peripheral and central nervous system. In a lead poisoning case running a typical course the predominant feature is the peripheral motor paralysis of the extensors of the forearms. Next the muscles supplied by the radial and ulnar nerves are affected. Often the progress of the paralysis is typical; it begins with paralysis of the extensor digitorum communis, passes on to the remaining extensors, then to the abductor muscles of the hand; the supinator longus and triceps escape. Sometimes the shoulder muscles are attacked; also paralysis in the region supplied by the facial nerve and of the lower extremities is observed. It appears plausible that overstrain of single groups of muscles plays a decisive part; this seems proved by the fact that paralysis first affects, among right-handed people, the right hand (especially of painters), but in the case of left-handed, the left hand; and among children the lower extremities are often attacked first. Disturbance of sight increasing to amaurosis is often an indication of severe brain symptoms. The view of some writers that the cause of the sight disturbance lies in vasomotor influences (cramp of the bloodvessels) is very probable, and supports the view that the brain symptoms are entirely due to diseases of the arteries (arteritis). These symptoms are distinguished by the collective name of saturnine encephalopathy; they include apoplexy, hemiplegia, epilepsy, delirium, and mania. The brain symptoms may cause death.
As later symptoms of lead poisoning may be mentioned lead gout and kidney disease (lead nephritis). The genesis of both these diseases is much disputed. It seems to be proved that the gout is true gout (with presence of tophi) and that the contracted kidney is indistinguishable from ordinary chronic Bright’s disease.
The kidney symptoms suggest that a regular excretion of lead through the urine takes place which, if it were a fact, would have been an important aid to diagnosis. But often analysis of urine for presence of lead is negative. Excretion of lead by the skin is scarcely to be credited, although occasionally affirmed. Elimination of lead is effected mainly through the intestines (probably for the most part as sulphide of lead).
All lead compounds more or less are to be regarded as poisonous, although the intensity of the action depends on the amount absorbed. For this its solubility in water or in weak acids (hydrochloric acid of the gastric juice) is the simplest test. According to this acetate of lead, lead chloride, carbonate of lead (white lead), oxide of lead (lead dross), minium (red oxide of lead) are relatively the most poisonous. Lead sulphate and lead iodide are to be regarded as relatively less poisonous, although by no means innocuous. The least poisonous, if not altogether innocuous, is sulphide of lead, because it is an insoluble lead compound.
Treatment of lead poisoning ought to aim first and foremost at the elimination of lead from the body. But unfortunately such attempts have had little success. Treatment of symptoms is all that for the most part is possible. Administration of iodide of potassium to assist the excretion of lead has not been found the success which many anticipated. This remedy however, can be tried; better results are to be expected from careful regulation of the bowels by means of purgatives. During colic administration of opium or morphia may be advisable to relieve pain and overcome the probable cramp of the intestinal muscles. The cautious administration of atropine (occasionally with cocaine) also serves the same purpose. Hot compresses and mustard plasters may be applied, and liquid diet should be given. Lead cachexia must be treated by strengthening diet. Electrical treatment for lead paralysis is advocated. From baths (sulphur baths) nothing more is to be expected than a bracing effect—elimination of lead through increased diaphoresis is hardly to be hoped for.
Zinc (Zn) melts at 412° C. and distills at about 900° C.; exposed to the air it burns, when heated, into zinc oxide. Older writers, when investigating gastric and intestinal diseases and affections of the nervous system observed in zinc smelters, regarded them as the result of chronic zinc poisoning; but it may now be accepted as certain that these symptoms are due to the lead always present in the zinc.
On the other hand so-called brass-founders’ ague may be regarded as a form of acute industrial zinc poisoning. Brass-founders’ ague occurs exclusively in brass casters, and not in zinc workers. Sigel and Lehmann have shown that founders’ ague is also caused by pure zinc if this is heated so strongly that it burns.
Premonitory symptoms often occur before the onset of the disease; usually they appear early, soon after casting has begun. The workman has general malaise accompanied by slight cough, nausea, throat irritation, &c., but these symptoms mostly disappear, returning again after a few hours with renewed violence, often in the evening before going to bed. Frequently, trembling sets in rather suddenly, often accompanied by headache, nausea, and muscular pains, and soon develops into a pronounced shivering fit, lasting generally about a quarter of an hour, but in severe cases for several hours (with intervals). At the same time the breathing is hurried and the heart’s action quickened (asthma and palpitation). Often the temperature rises as high as 104° F. The attack ends with profuse perspiration, and the patient sinks exhausted to sleep, awaking in the morning generally quite restored or with but slight signs of fatigue; only rarely is he unable to resume work.
It is noteworthy that some workmen are extraordinarily susceptible to brass-founders’ ague, and are attacked again and again, while others remain completely immune, so that idiosyncrasy and immunity both play a part. Workmen who are susceptible to the disease, yet without marked disposition (idiosyncrasy) towards it, can become acclimatised to the poison. Lehmann has succeeded in artificially producing an attack in a brass-caster who was highly susceptible. The symptoms in him were the result of work with pure zinc in a burning condition. The proof, therefore, is clear that brass-founders’ ague is due to zinc, and not, as some authors have supposed, to copper or the simultaneous action of both metals. The symptoms are produced through inhalation of zinc oxide, not zinc fumes.
Lehmann conjectures that brass-founders’ ague may be a secondary fever due to absorption into the system of the remains of cells in the respiratory tract that have been killed by the action of the zinc.
The treatment can only be symptomatic; as the attack is so transient, medical attendance is hardly necessary.
Mercury (Hg), on account of its volatility, is classed among industrial poisons. Although boiling at 360° C. it is volatile even at ordinary temperature. Industrial mercurial poisoning is caused by the frequent inhalation of small quantities of vapour, sometimes, but more rarely, of dust containing mercury, and assumes usually a chronic form.
Industrial mercurial poisoning often begins with inflammation of the mucous membrane of the mouth and gums. There is increased flow of saliva, a disagreeable metallic taste in the mouth, and foul breath. This may be limited to a simple inflammation of the gum, or go on to ulceration with falling out of teeth, or even to gangrene of the gum and mucous membrane inside the mouth. Gastric attacks also occur in the early stages; occasionally, however, they are absent.
The main symptoms of chronic mercurial poisoning are nervous and psychical derangement, to which in severe cases are added general disturbance of digestion and loss of strength.
Sometimes, after repeated attacks, more or less severe, a cachectic condition is induced, showing itself in general emaciation, decrease of strength, atrophy of the muscles, anæmia, and disturbed digestion, which—often intensified by some intercurrent disease, such as tuberculosis—lead to death. Slight cases of mercurialism recover, leaving no evil results, if the patient is removed in time from the influence of the poison.
The treatment of chronic mercury poisoning is symptomatic. To allay the inflammation of the mucous membrane of the mouth the patient should use a mouth wash of potassium chlorate and peroxide of hydrogen; the general condition should be raised by strengthening, unstimulating food; for the nervous symptoms baths and electricity should be tried; and for very marked erythism and tremor recourse to narcotics may be necessary.
Industrial mercurial poisoning is produced not only by metallic mercury but also by many compounds, of which industrially the oxides are the most important. Nitrate of mercury (Hg₂(NO₃)₂) comes into account in the treatment of fur. Mercury cyanide (HgCy₂) deserves mention, as small quantities cause mercurial and large quantities cyanogen poisoning.
Manganese (Mn) or manganese compounds are used industrially in fine powder; continuous absorption of dust containing manganese produces chronic manganese poisoning. Instances of such poisoning are not very numerous; altogether about twenty cases have been described. Recent publications agree in asserting that only the dust rich in manganese protoxide is dangerous.
Industrial manganese poisoning runs its course extraordinarily slowly, and resembles chronic poisoning by other heavy metals, such as lead and mercury, in that nervous and psychical symptoms, rather than digestive, are prominent. Sometimes—but not always—the disease is introduced or accompanied by psychical symptoms, both of excitement and depression (hilarity, laughing, or depression and weeping). In the course of the disease nervous disturbances arise, deafness, tingling, paralysis and paræsthesia, in the arms and legs, giddiness, difficulty of walking, tremor, increased knee-jerks and difficulty in speech. Often at the same time swelling of the lower extremities (œdema) and loss of strength (cachexia, marasmus) come on. Slight cases make a good recovery. An interesting case of illness is described by Jaksch as manganophobia, in which the symptoms were simulated, and were brought on solely by the fear of manganese poisoning.
As regards treatment, electricity, massage, and baths are advocated to allay the nervous symptoms, as in the case of chronic metal poisoning and suitable strengthening food.
Chromium trioxide (CrO₃) dissolves in water, forming chromic acid (H₂CrO₄); of the salts of chromic acid the neutral and acid alkaline salts concern our inquiry. These are normal and acid sodium or potassium chromate (K₂CrO₄ and K₂Cr₂O₇). Chromate of lead (PbCrO₄) can cause lead poisoning.
Poisoning can be produced by dust and by alkaline chromates, the latter, when hot, giving off steam which, as has been proved, contains excessively fine chrome particles. Chrome compounds attack especially the surface of the body, the skin and the mucous membrane.
The bichromate and chromate dust produce ulcers where slight injuries to the skin already exist. The ulcers develop slowly, and have a smooth, heaped-up, undermined edge; deep-seated, they can even pierce to the bone; they heal with great difficulty. Naturally they occur most frequently on the uncovered parts of the body, especially on the arms and hands. Characteristic also is an analogous ulceration attacking the mucous membrane of the nose, from which hardly any chrome worker (especially if brought into contact with chromate dust) is free. Perforation and destruction of the cartilaginous septum of the nose is very common. Ulcers on the mucous membrane at the entrance of the throat (on tonsils and palate or in the larynx) have been occasionally observed.
Absorption of small quantities of chrome compounds into the body are said to cause disturbances of digestion of an inflammatory character, and especially inflammation of the kidneys.
The treatment of chrome ulcers is similar to that of other chronic ulcers. An antidote for industrial chrome poisoning is not known.
Nickel Salts.—Of late years in nickel-plating establishments an eczematous inflammation of the skin has been described affecting first of all the hands, and occasionally spreading over the arms and even the whole body. The skin becomes inflamed, and vesicles appear on the affected part. Some persons are extraordinarily susceptible to this disease, others only become so after having worked for years quite unaffected, and are then obliged to give up their occupation. Probably the action of nickel salts (especially nickel sulphate) used in electrolytic baths causes the disease. But it was in fact traced by several writers to contact with benzene, petroleum, and lime by the workmen. The simultaneous action of these substances upon the skin would no doubt encourage its appearance. The application to the skin of vaseline or cream is recommended. Careful cleanliness and attention to the skin is on the whole by far the most reliable protection.
[Nickel carbonyl (Ni(CO)₄).—Mond, Langer, and Quincke in 1890 discovered that, on passing a current of carbon monoxide over finely divided (pyrophoric) metallic nickel, a gaseous compound of nickel and carbon monoxide was formed. When heated to 150° C. the gas decomposes into its constituents and metallic nickel is deposited.
Nickel carbonyl is a clear, pale straw-coloured liquid, volatilising at room temperature. It has a peculiar soot-like smell detectable when present to the extent of about 1 vol. in 2,000,000, while the Bunsen flame becomes luminous when nickel carbonyl is present in the air to the extent of 1 vol. in 400,000—two facts of great importance in detecting escape of the gas in the manufacture of pure nickel by the Mond process.
Occurrence of poisoning by nickel carbonyl.—At the first introduction of the process about 1902, before the dangerous properties of the gas had been sufficiently recognised, some twenty-five men were poisoned, of whom three died. Poisoning only occurred when, as a result of the breakdown of the automatic working of the plant, hand labour took the place of machinery.
This very rare form of poisoning has been very fully investigated by H. W. Armit (Journ. of Hygiene, 1907, p. 526, and 1908, p. 565). The symptoms in man, he says, were transient headache and giddiness and at times dyspnœa, quickly passing off on removal to fresh air. After from twelve to thirty-six hours the dyspnœa returned, cyanosis appeared, and the temperature began to be raised. Cough with more or less blood-stained sputum appeared on the second day. The pulse rate became increased, but not in proportion to the respiratory rate. The heart remained normal. Delirium of varying types frequently occurred. Death took place in the fatal cases between the fourth and eleventh days. The chief changes found post mortem were hæmorrhages in the lungs, œdema of the lungs, and hæmorrhages in the white matter of the brain, while some doubt exists as to whether any blood changes were present.
Precisely analogous results were found in experiments on animals (rabbits, cats, and dogs).
The points Armit investigated experimentally were (1) Is the carbon monoxide of the compound wholly or partly responsible for the symptoms, or (2), is nickel carbonyl absorbed as such, or (3), is it the nickel of the compound which produces the symptoms? His conclusions are that the poisonous effects of nickel carbonyl are entirely due to the nickel of the compound. The peculiar toxicity is due to the fact that, being introduced in a gaseous form, the nickel is deposited as a slightly soluble compound in a very fine state of subdivision over the immense area of the respiratory surface. Nickel carbonyl when mixed with air cannot be absorbed as such by an animal as it becomes split up into the nickel containing substance (possibly hydrated basic carbonate of nickel) and carbon monoxide before or soon after reaching the alveoli of the lungs. The nickel is dissolved from the respiratory surface by the tissue fluids and is then taken up by the blood. The hæmorrhages found after death follow as the result of fatty degeneration of the vessel walls which is the specific pathological change set up by nickel.]
Copper.—Symptoms which have been described by some writers as chronic industrial copper poisoning are probably due to admixtures of other poisonous metals, especially lead and arsenic. Although some copper workers, especially those careless of cleanliness, exhibit hair and teeth coloured by the action of copper compounds (green tinge on hair and edge of teeth), symptoms of illness traceable to copper are not demonstrable.
Brass-founders’ fever, which by some earlier writers was ascribed to copper or combined copper and zinc action, is traceable to zinc (see Zinc).
Ferro-silicon.—The illnesses due to this are phosphoretted or arseniuretted hydrogen poisoning (see pp. 191 and 197).
Silver and Silver Compounds.—Gradual absorption of small quantities of a solution of silver may produce industrial argyria, often beginning with the appearance of a black edge to the gums and darkening of the hair and nails, followed by black spots on the skin which in severe cases coalesce, so that the whole or almost the whole surface of the body becomes black and glossy.
Argyria is due to the absorption of silver compounds into the circulation, and subsequent deposition of the reduced silver in the body (liver, kidneys, spinal cord, &c.). The black colouring of the skin is caused by the action of light.
No interference with health worth mentioning is observed.
The poisons (gradually absorbed) belonging to this group are mainly such as affect metabolism; they impair the processes essential to metabolism (in especial the oxidation processes) and cause severe damage to the cells, through destruction of albumen. The poisons of this group also have a paralysing effect upon the central nervous system.
Generally speaking the effects produced by the poisons of this group vary considerably. Among the arsenic compounds arseniuretted hydrogen, which is supremely a blood poison, must be excluded from the group and included among the blood poisons.
Pure metallic arsenic (As) is considered innocuous. Oxides of arsenic especially are held to be industrial poisons such as arsenic trioxide (As₂O₃), the anhydride of arsenious acid (H₃AsO₃), a white powder, which is known under the name of white arsenic; arsenic acid (H₃AsO₄), which forms crystals easily soluble in water, and the salts of these acids, especially copper arsenite, formerly employed in the production of dyes, and also arsenic chloride (arsenic trichloride, AsCl₃). Arseniuretted hydrogen will be treated separately as it has a completely different poisonous effect from that of the oxidic compounds of arsenic. Arsenic sulphides (realgar, AsS₂, and orpiment, AsS₃) are regarded as innocuous in consequence of their insolubility in a pure state. But it may be remarked that arsenic sulphides (sulphur arsenic ores) which are used industrially, and even metallic arsenic, are to be considered poisonous, as they contain oxidic arsenic compounds in great quantity.
Chronic arsenical poisoning is caused by gradual absorption through the respiratory or digestive tracts of small quantities of the oxidic arsenic compounds either in solution or as dust or fumes.
The disease usually begins with digestive derangement which shows itself in more or less severe gastric and intestinal catarrh (loss of appetite, vomiting and diarrhœa); sometimes there are severe affections of the respiratory tract,—pharyngeal and bronchial catarrhs; often the illness is accompanied by skin affections of various kinds, rashes, pustular eczema, loosening of the nails, abscesses, dark pigmentation of particular parts of the skin, and other symptoms. The nervous symptoms vary much according to the severity of the disease; first of all, deafness and feeling of pins and needles, or loss of sensation (paræsthesia and anæsthesia) of the extremities. Further, rheumatic joint pains, weakness of the extremities and characteristic symptoms of paralysis occur, with accompanying atrophy of the muscles, and gradual loss of energy leading to total incapacity for work. Severe cases end in general exhaustion and loss of strength, with signs of severe injury to the central nervous system, such as epileptic fits, mental hebetude, &c.
Phosphorus (P) is polymorphic; red (amorphous) phosphorus is innocuous, while white or yellow is poisonous. Phosphorus at various stages of oxidation is little if at all poisonous. White phosphorus is volatile and fumes in the air—the fumes consisting of phosphorus, phosphoric and phosphorous acids.
Chronic industrial phosphorus poisoning is produced by continued inhalation of the fumes of white phosphorus resulting in inflammation of the periosteum of the bone, with which necrosis and formation of new bone are associated. It attacks especially the lower jawbone (ossifying periostitis). The inflammation begins with increased flow of saliva, painful swelling of the gums, which, as it increases, brings about the death of the jawbone (necrosis, phosphorus necrosis). This becomes covered again with newly formed bone substance from the periosteum. The process ends with the formation of a fistula (a passage filled with pus), which discharges outwards, and through which the dead bone (sequestrum) is eventually cast off. Occasionally the process attacks the upper jaw, rarely other bones.
With these characteristic symptoms of phosphorus necrosis, derangement of nutrition together with anæmia, indigestion and bronchial catarrh, may be associated. Further, a general brittleness of the bones (fragilitas ossium) is observed with the result that the long bones of the leg or arm sometimes break at relatively small exertion of force; such cases from Bohemia came lately under my notice.
Some authorities regard caries of the teeth as the pre-disposing cause of phosphorus necrosis; according to this view the carious teeth constitute the means of entrance for the poison. Opposed to this so-called ‘local’ theory is the view that chronic phosphorus poisoning is a ‘general’ one. The truth may lie midway. On the one hand phosphorus necrosis probably arises partly from the general poisonous action of the phosphorus, and on the other from local inflammation which leads to the occurrence of local symptoms. The general symptoms of chronic phosphorus poisoning described above support this view, especially the effect observed on the bones of the skeleton. This view is also strengthened by the fact that workmen with perfectly sound teeth, who had been exposed to phosphorus fumes for many years, were attacked by necrosis only when traumatic inflammation produced by chance injury was set up.
The treatment of phosphorus necrosis is surgical. Formerly the treatment recommended was to wait for formation of new bone and exfoliation of the dead bone (expectant treatment); the necrosed portions of bone were then extracted through the fistula. Recently early operative interference has succeeded in preserving the periosteum which enabled the new bone to form.
Industrial poisoning by gaseous phosphoretted hydrogen (PH₃) calls for attention in connection with the preparation and employment of calcium carbide (acetylene) and also of ferro-silicon.
Phosphoretted hydrogen is a dangerous poison. Even 0·025 per cent. in the air is harmful to animals after a time; 0·2 per cent. PH₃ in the air quickly causes death.
The poison produces changes in the lungs, though without injuring the respiratory passages by corrosion, and finally has a paralysing effect upon the central nervous system. It has no effect upon the blood. An autopsy on a person who has died of phosphoretted hydrogen poisoning reveals as a rule no characteristic sign, except centres of inflammation in the lungs.
The symptoms of phosphoretted hydrogen poisoning are—difficulty of breathing, cough, fainting fits, noises in the ears, and nausea; in severe cases coma and death. Slight cases soon recover without after-effects.
In this group are comprised industrial poisons the principal effect of which is upon the nervous system, especially the central nervous system. The chemical composition of the separate members of the group differs much.
Industrial poisoning by pure sulphuretted hydrogen (SH₂), the well-known colourless, nauseous-smelling gas, occurs comparatively rarely. Poisoning is generally acute, but chronic illness in workers has been traced back to inhalation of the gas.
This poison exerts a paralysing action upon the central nervous system and is slightly irritating to the mucous membranes and respiratory organs.
Its action can be described as follows: When absorbed into the blood union of the poison with the alkaline constituents takes place with formation of an alkaline sulphide. Presence of only slight quantities of sulphuretted hydrogen in the air acts injuriously. Lehmann has shown that about 0·15 to 0·2 per thousand sulphuretted hydrogen is not without effect, and that prolonged inhalation of 0·5 per thousand becomes dangerous. Continued exposure to the poison seems only to increase susceptibility to its action. An almost complete absorption of the whole of the sulphuretted hydrogen present in the air breathed takes place.
Continued inhalation of small quantities of sulphuretted hydrogen produces irritation of the mucous membrane, cough, and lacrymation; headache, giddiness, nausea, and mental dulness soon ensue; occasionally also symptoms of intestinal catarrh follow; if at this stage—or after a longer exposure to the action of a smaller amount—the patient is withdrawn from its further influence, there still continue for some time symptoms of irritation of the mucous membrane (such as inflammation of the conjunctiva and of the respiratory passages).
Further exposure or absorption of greater amounts induces general discomfort and passes on to a second stage of convulsions and delirium.
Inhalation of a large dose of sulphuretted hydrogen causes almost instantaneous death; the affected person falls dead—often without a sound—as if struck by a blow; occasionally a short stage of unconsciousness, with symptoms of suffocation, precede death.
This acute form often occurs, especially in acute sewer gas poisoning. Besides this, a sub-acute form of sewer gas poisoning is recognised which is attributable, in part at least, to the action of sulphuretted hydrogen, the prominent symptoms being irritation of the mucous membranes and of the intestinal canal. In other severe cases symptoms of the central nervous system preponderate (headache, giddiness, and delirium). These forms of poisoning can be caused not only by sulphuretted hydrogen, but also by other poisonous gases which are found in drains or sewers.
As regards treatment, continued inhalation of oxygen, supported by artificial respiration, is often, in serious cases, effective. In severe poisonings also saline injections and bleeding may be advocated. Other symptoms (catarrh, &c.) must be treated symptomatically.
Pure carbon bisulphide (CS₂) is a colourless, peculiar-smelling liquid which boils at 46° C.
As Lehmann has shown, even 1·5 to 3·0 mg. CS₂ per litre of air produces distress—with acute symptoms of poisoning (congestion, giddiness, sickness, &c.).
Industrial carbon bisulphide poisoning is, however, chronic in nature and induced by continuous inhalation of small quantities of the fumes. To understand the action of carbon bisulphide, its capacity for dissolving fats and fatty substances must be taken into account. Its injurious effect extends to the nerve tissues (central and peripheral nervous system) and the glandular tissues.
Throughout chronic industrial carbon bisulphide poisoning, which has been described fully by Delpech, Laudenheimer, and others, nervous and psychical symptoms predominate, together with severe chronic digestive derangement.
The patient after exposure for some time suffers from violent headache, giddiness, and sickness; he has sensations of cold, pains in the limbs, a feeling of ‘needles and pins,’ and itching in different parts of the body. Gradually a condition of general excitement develops. Sleeplessness, cramps, and palpitation set in. At the same time the nervous system becomes involved—hypersensitiveness, loss of sensation or complete numbness of some parts of the skin, diminution of muscular power, disturbances of movement, twitching, violent trembling, wasting of the muscles, and paralysis; the sight also is sometimes affected. The stage of excitement, in which the patient often becomes strikingly loquacious without cause, passes gradually, as the nervous symptoms develop, into the stage of depression; sometimes this takes weeks and months; excitement and gaiety give place to deep depression; other symptoms appear—weakness of memory, mental dulness, and difficulty in speaking. The powers of sensation become affected, paralysis increases, and digestive disturbances, anæmia, and general loss of strength are manifest. Occasionally definite mental disease (psychosis, mania, melancholia, dementia, &c.) develops.
Certain cases of chronic carbon bisulphide poisoning in indiarubber workers have come under my notice, and some remarks concerning them may be of interest. The characteristic symptoms are essentially as follows: the invalid appears in the consulting-room in a bent position, leaning upon a stick with head and hands shaking. The gait is clumsy (spastic-paralysis) so that the patient ‘steps’ rather than walks. When seated, the tremor ceases to some extent, but in purposive movements increases rapidly, involving the whole body, so that an exact systematic examination becomes impossible, and the invalid sinks back into the chair exhausted and bathed in perspiration. He complains of cold in the extremities. He looks pale; the skin of the upper extremities is totally without feeling, as also is the upper part of the feet; the skin of the head is hypersensitive; the muscular strength of the arms is almost lost; testing the strength brings on marked shaking, followed by a fainting-fit caused by exhaustion. The extremities of the patient are cyanotic (livid); the knee jerks are exaggerated. The patient suffers from indigestion, constipation, headache, and giddiness; he is irritable, and depressed; his memory is weak; mental derangement cannot be proved.
Chronic carbon bisulphide poisoning is rarely fatal. Slight cases end in recovery after more or less long continuance; in severe cases improvement occasionally takes place, but serious nervous disturbance (paralysis, weakness of the muscles, deterioration of intellect) usually persists.
Treatment is symptomatic, aiming especially at relieving the nervous symptoms and improving the state of nutrition. If psychical disturbances are prominent, treatment in an institution is necessary.
Industrial cyanogen poisoning is not frequent. Cyanogen gas (C₂N₂, existing in small quantities in furnace gas, illuminating gas, and other kinds of gas) and especially hydrocyanic acid (CNH, prussic acid) are considered industrial poisons; the latter is a very unstable, colourless, pungent-smelling liquid, boiling at 27° C. Among the cyanides employed industrially and having an effect similar to that of prussic acid must be mentioned cyanide of potassium and cyanide of sodium (KCN and NaCN), cyanide of silver (AgCN) and cyanide of mercury (Hg[CN]₂).
Cyanogen and cyanogen compounds are extraordinarily powerful poisons. The minimum dose lies, as Lehmann has proved by experiments on animals, at about 0·05 per thousand of hydrocyanic acid in the atmosphere breathed; 1-5 mg. per kg. weight is fatal to animals; to man about 60 mg. would be fatal.
The poisonous action of cyanogen and cyanogen compounds depends upon their power of preventing absorption of oxygen from the blood by the tissues with the result that the venous blood flowing to the heart retains the bright red colour which otherwise only arterial blood exhibits. This effect is due to cessation of the gaseous exchange in the body, and results in tissue suffocation. At the same time these poisons have at first an exciting and then a paralysing effect upon the central nervous system. In severe poisoning the nerve effect is masked by the effect upon the exchange of gases in the blood, since this quickly leads to death.
Most of the cases of industrial poisoning under this heading result from inhalation; absorption of liquid cyanogen compounds through the skin can rarely come into consideration.
If large quantities of hydrocyanic acid have been inhaled, death ensues very quickly. The person affected falls down suddenly, breathes with difficulty, the pulse soon becomes imperceptible, and after a more or less long stage of deep unconsciousness (coma) life becomes extinct.
In slight cases of poisoning the patient feels a sensation of irritation in the throat, giddiness, sickness, and difficulty in breathing; occasionally such disturbances persist for some time.
Some writers have described symptoms in workers manipulating prussic acid and cyanides, which they believe to be due to chronic prussic acid poisoning. Complaint is made of oppression of the chest, throat irritation, giddiness, difficulty in breathing, palpitation, hebetude, exhaustion, and nausea and vomiting; in certain instances the attack, aggravated by exhaustion and weakness, culminates in death. It is a question whether such poisonings are chronic in the true sense of the word. In view of the mode of action of hydrocyanic acid, such cases of sickness should rather be accounted acute or sub-acute poisonings through repeated action of small quantities of the poison.
It may be mentioned that in persons working with alkaline cyanides (especially in electro-plating) skin affections occasionally occur; these are traceable to the caustic effect of alkaline cyanides.
Treatment by oxygen inhalation with simultaneous artificial respiration holds out most prospect of success. This holds good for acute poisoning by the other poisons belonging to this group. Besides this, saline injections and bleeding are recommended, and also the administration of an infusion of sodium thiosulphate solution.
Included in this group, as in the former one, are substances chemically very different from each other, but of which the action is especially on the blood. Besides this common effect, these substances also produce various other effects, such as local irritation, effect on the nervous system, &c. The industrial blood poisons, which according to their chemical constitution are classed among the aliphatic and the aromatic series of organic compounds, will, for the sake of clearness, be discussed in the following chapters.
Acute arseniuretted hydrogen poisoning, produced by inhalation of relatively very small quantities of arseniuretted hydrogen gas (AsH₃) is in most cases industrial in origin. The absorption of an amount corresponding to about 0·01 mg. arsenic suffices to produce severe poisoning symptoms. The poisonous effect results chiefly from action upon the red blood corpuscles, which are dissolved (hæmolysis). Arseniuretted hydrogen is therefore a genuine blood poison. The effect upon the blood, if not immediately fatal to life, is to cause the dissolved blood-colouring matter to pass into the tissues where, though some is deposited, most goes to, and acts injuriously on, the organs, especially the liver, spleen, and kidneys. In cases running at once a fatal course, the impoverishment of the blood caused by the lack of colouring matter necessary to internal respiration produces tissue suffocation, which is therefore the primary cause of death. In cases not immediately fatal, the injury to the functions of the organs alluded to (for instance, cessation of the functions of the kidneys, &c.) may lead to death secondarily.
Symptoms of the disease appear often only some time after the poisoning has set in, and begin with general malaise, sickness, collapse, fainting fits, and difficulty of breathing; after some hours the characteristic signs follow—the urine becomes dark red to black, containing quantities of blood colouring matter and dissolved constituents of the blood, and later also bile colouring matter, so that a coppery jaundice comes on if the illness is prolonged. The region of the liver, spleen, and kidneys is painful. Severe cases often end fatally during the first stage of the illness, more rarely later, with increased difficulty of breathing; sometimes death occurs after a preceding comatose stage marked by convulsions and delirium. In slighter poisoning cases the symptoms abate in a few days and recovery follows.
The treatment of arseniuretted hydrogen poisoning is similar to that adopted in the case of all other blood poisonings: in addition, if possible, direct transfusion of blood from the artery of the giver into the vein of the receiver, liquid nourishment, saline injections, and, above all, prolonged oxygen inhalation.
Carbonic oxide (CO) is a colourless, odourless gas which frequently causes both acute and, it is said, chronic industrial poisoning.
Carbonic oxide is a very poisonous gas; even as little as 0·5 per thousand in the atmosphere breathed has a poisonous effect; about 2-3 per thousand can be dangerous to life.
Its poisonous effect results from its power of combining with the blood-colouring matter or hæmoglobin to form carboxy-hæmoglobin; the affinity of carbonic oxide for the hæmoglobin of the blood is more than 200 times greater than that of oxygen, so that, however small the amount of carbonic oxide in the air, it is inevitably absorbed by the blood and retained. The blood so altered, assumes a cherry-red colour, is unable to effect the necessary exchange of gases for internal respiration, and in consequence of the lack of oxygen suffocation ensues.
Without doubt, however, carbonic oxide has also an immediate effect upon the central nervous system (first excitation, followed quickly by paralysis). It is maintained also that besides the action upon the hæmoglobin it favours coagulation of the blood through the disintegration of the blood corpuscles. The last-mentioned action is thought to account for the sequelæ of carbonic oxide poisoning, but they can also naturally be accounted for by the direct effect of the poison.
Onset of symptoms is very sudden if a large quantity of pure carbonic oxide is inhaled. The affected person immediately falls down unconscious and succumbs after drawing a few breaths with difficulty.
In less acute cases the illness begins with premonitory symptoms, generally headache, sickness, giddiness, sleepiness, though in cases of fairly rapid absorption these are absent, and are naturally absent also when the poisoning creeps upon the affected persons while asleep, as occasionally happens in cabins, &c., in factories. If the poisoning continues, increasing mental dulness, accompanied by nausea and vomiting, leads sometimes to a short stage of seemingly drunken excitement, which preludes deep unconsciousness during which there is often a convulsive stage, followed by complete loss both of sensation and of reflex action; the breathing becomes shallow and intermittent, the pulse small and irregular, and finally death ensues. Occasionally in the stage of unconsciousness, death is hastened by entrance of vomited matter into the respiratory passages. Bright red patches are seen on the body after death.
If persons affected by severe carbonic oxide poisoning are withdrawn from the poisonous atmosphere after having reached the stage of unconsciousness, they may recover, but often with difficulty; not infrequently—in spite of suitable treatment—death occurs some considerable time later from the symptoms described above. Still, in many cases, under the influence of right treatment, gradual recovery has been brought about, even after long unconsciousness accompanied by repeated convulsions. In the rescued the symptoms described as characteristic of the first stage often continue for at least a day. Further, they are liable to a number of serious after effects, such as severe inflammation of the lungs due to infection by the entrance of vomited matter into the air passages, skin affections (rashes), and especially severe nervous and mental affections. Frequently these develop from centres of softening in the brain or from inflammation of the peripheral nerves (neuritis); occasionally the poisoning may really only be the predisposing cause for the outbreak of an existing psychical disease. It is not our task to enumerate all the extremely varied disturbances which are observed after carbonic acid gas poisoning. Neuralgias and paralyses have been described as associated with the peripheral nerve symptoms over areas supplied by different nerves; various forms of diseases of the brain and spinal cord (poliomyelitis, paralysis, sclerosis, &c.); and finally a series of psychoses (neurasthenia, melancholia, mania, &c.), occasionally passing into dementia and imbecility. Glycosuria (sugar in the urine) has also been noted as a sequela.
Chronic carbonic oxide poisoning, arising from continued inhalation of small quantities of the gas, sets in usually with symptoms similar to those of acute carbonic oxide poisoning; if the worker continues exposed to danger, severe symptoms may arise which point to marked alteration of the blood and later also of the digestion and bodily functions. Under certain circumstances severe nervous and mental affections are said to occur similar to those which we have mentioned as sequelæ of acute carbonic oxide poisoning (convulsions, disturbances of mental activity, symptoms which resemble progressive muscular atrophy, &c.).
In acute carbonic oxide poisoning oxygen inhalation indefatigably continued and supported by artificial respiration is often successful. The serious danger from this form of poisoning renders it very necessary that in all premises where there is risk provision should be made for the administration of oxygen. The sequelæ can of course only be treated symptomatically.
Oxychloride of carbon (COCl₂), also called phosgene, is, at the ordinary temperature, a colourless gas with a disagreeable smell. This decomposes in moist air into carbonic oxide, hydrochloric acid, or chlorine, and produces a strongly irritant local effect upon the mucous membranes. Industrial poisoning by phosgene is characterised by great difficulty in breathing and inflammation of the respiratory tract (bronchitis and bloodstained expectoration).
Several cases have been treated successfully by oxygen inhalation.
The effects of nickel carbonyl are described on pp. 186-8.
Carbonic acid (CO₂), a colourless gas, is heavier than air (specific weight, 1·526), and therefore, wherever it collects, sinks to the ground. Carbonic acid is only very slightly poisonous; about 10 per cent. carbonic acid in the air causes asphyxia. The extinguishing of a candle flame will serve as an indication that the amount of carbonic acid in the atmosphere has reached this point. Cases of industrial carbonic acid asphyxia are sudden; they do not occur frequently.
The gradual action of the gas when mixed with air produces first a tingling sensation on the surface of the body, reddening of the face, irritation of the mucous membrane and the respiratory organs, after which succeed difficulty in breathing, palpitation, fainting, and unconsciousness.
Sudden and fatal poisoning occurs industrially. Upon entering places filled with carbonic acid gas the affected person falls down dead almost immediately. These are cases of asphyxia, in which the lack of oxygen certainly plays the greatest part. If those affected by acute carbonic acid poisoning are removed in time out of the dangerous atmosphere they usually recover quickly.
Oxygen inhalations and artificial respiration are to be applied in severer cases. There are no sequelæ.
The industrial poisons comprised in this group have as their principal general effect injurious action upon the functions of the central nervous system (paralysis or causing excitation) which is prominent in most of the cases of industrial poisoning caused by these substances. This effect is most marked in the case of the readily volatile (low boiling) hydrocarbons, while those less volatile and boiling at a higher temperature often have collateral effects (such as local irritation). The characteristic poisonous effect caused by the chlorine and hydroxyl-substitution products (chloroform and alcohol group) is also mainly on the central nervous system (narcosis).
Mineral oil (crude petroleum) has, according to its origin, differing composition. Thus in American mineral oil hydrocarbons of the methane series preponderate; in the Russian, hydrocarbons of the aromatic series. Reference has been made in Part I. to this point, as well as to the separation of crude petroleum into its different fractions.
The injury to health produced by crude petroleum and its derivatives is of two kinds. Direct contact with liquid petroleum and the semi-liquid and solid deposit after distillation (paraffin) cause local injury to the skin. Inhalation of the volatile constituents of raw petroleum causes symptoms affecting mainly the central nervous system. They have moreover a markedly irritating effect upon the mucous membrane of the respiratory organs. These substances clearly exhibit the characteristic we have referred to, namely, that the hydrocarbons boiling at low temperature act as nerve poisons, whereas those boiling at a higher temperature produce a local irritant effect.
The skin affections take the form of inflammation of the hair follicles (acne), eruptions with characteristic formation of vesicles, and pimples and pustules which precede the deep-seated formation of ulcers, abscesses, &c.
In paraffin workers the acne-like skin inflammations are known as ‘paraffin eczema.’ They develop sometimes into cancer of the skin (warty and epitheliomatous growths).
In the general poisoning produced by inhalation of petroleum fumes the effect upon the central nervous system is all the more plainly and clearly marked when the irritant effect of the hydrocarbons boiling at higher temperature is slight or absent; that is, in the case of poisoning which arises solely from industrial products of low boiling hydrocarbons; among these benzine is included.