PART II

_THE SYMPTOMS AND TREATMENT OF INDUSTRIAL POISONING_

In this section the most important diseases and symptoms of industrial poisoning will be described. In doing this—considering the mainly practical purpose of this book—theoretical toxicological details and any full discussion of disputed scientific points will be omitted.

I. INTRODUCTORY

Hitherto in this book we have intentionally followed the inductive method, from the particular to the general: we began by citing a number of important instances of industrial poisoning, but only now will endeavour be made to give a definition of the terms ‘poison’ and ‘poisoning.’

Attempts at such definitions are numerous; every old and new text-book of toxicology contains them. A few only hold good for our purpose. It is characteristic that Lewin, after attempting a definition of the conception ‘poisoning,’ himself rejects it and declares that he can see no practical disadvantage in the impossibility of defining this notion, because deductions based upon the knowledge of undoubted cases can never be dispensed with, even if a definition were possible: one justification the more for our inductive method.

But we will not quite dispense with a definition.

_Poisons are certain substances which are able chemically to act on an organism in such a way as to effect a permanent or transient injury to its organs and functions; an injury consequently to the health and well-being of the person affected; this injury we call poisoning._

In the present book we have refrained from including industrial infections among industrial poisonings, and the subject has been limited to poisoning in the restricted and current sense of the word.

An industrial poison is a poison employed, produced, or somehow occasioned in industrial occupation, which is brought about inadvertently, and consequently against the will of the person poisoned.

From a simple survey of the action of industrial poisons in general we may group them as follows:

1. Poisons which act _superficially_, i.e. which cause in the organs which they touch gross anatomical lesions (irritation, corrosion, &c.)—so-called contact-effect. To this class belong especially irritant and corrosive poisons.

2. _Blood_ poisons, i.e. poisons which are absorbed by the blood and change it; this change can affect either the blood colouring-matter, with which certain poisons form chemical compounds, or the blood corpuscles themselves can be altered or destroyed (for instance, poisons having a hæmolytic action).

3. Poisons with definite _internal_ action, so-called remote or specific effect. To this class belong the poisons which, after being absorbed into the system, act upon definite organs or tissues in a specific manner (nerve poisons, heart poisons, &c.).

It is indeed possible for one and the same poison to display two or all three of these modes of action.

The effect of poison depends upon an interaction of the poison and the organism, or its single organs. Selection as regards quality and quantity is a property of the organism as well as of the poison: the nature and amount of the poison taken in are determining factors on the one side, and on the other the constitution, size, and weight of the affected organism. The chemical constitution of the poisonous substance determines the qualitative property of the poison.

Further, certain physical properties of the poison determine its action, especially its form, solubility in water, and its power of dissolving fat. These affect its susceptibility to absorption, to which point we shall return shortly; the hygroscopic capacity of a poison produces a highly irritant and corrosive action.

Industrial poisons can be absorbed (1) as solid substances, (2) as liquids, and (3) as gases. Since industrial poisoning, as defined above, is of course neither desired nor intended by the sufferer, who unsuspectingly takes into his system poison used or developed in the factory, solid substances in finely divided condition—in the form of dust—can be considered as industrial poisons. Accordingly, industrial poisons can be classed as due to dust, gases, and liquids.

The poison may be introduced into the body through the functional activity of the organism by the lungs or alimentary tract, or it may penetrate the uninjured or injured surface of the skin.

Industrial poisons which contaminate the air of the factory are inhaled—these are consequently either poisonous dusts or gases and vapours.

As a rule, only industrial poisons in a liquid form enter through the skin, which may be either intact or wounded; gaseous poisons seldom do; poisons in the form of fat or dust can only pass through the skin after they have been first dissolved by the secretions of the skin or of a wound, so that they come to be absorbed in solution. Most frequently those liquid poisons which are capable of dissolving the fat of the skin are thus absorbed, and next, such liquids as have a corrosive effect, breaking down the resistance of the skin covering and producing an inflamed raw surface. But such poisons much more easily enter through the mucous membrane, as this naturally offers a much weaker resistance than the skin.

From a quantitative point of view it is especially the amount of poison actively assimilated which determines the effect. Every poison is without effect if assimilated in correspondingly small quantities. There is consequently a minimum poisonous dose, after which the poison begins to act; but this minimum dose can only be ascertained and specified when the qualitative properties and the weight of the organism are also taken into consideration; it has therefore a relative value. The strongest effect which a poison is able to produce is the destruction of the life functions of the organism, the fatal effect. This fatal dose, however, can only be determined relatively to the qualities of the organism in question.

Not only is the absolute quality of the poison of decisive significance, but the degree of concentration often influences its action, that is to say, the greater or less amount of effective poison contained in the substance conveying it into the organism; concentration plays an important part in many industrial poisons, especially, as is obvious, in corrosive poisons.

A further important point is the time which it takes to absorb the poison. The action of the poison—the whole expression of the symptoms of poisoning—is essentially influenced by this fact.

Usually gradual and repeated absorption of small quantities produces slow onset of symptoms, while sudden absorption of larger quantities of poison brings about rapid onset of illness. In the former case the poisoning is called _chronic_, in the latter, _acute_. Acute industrial poisoning is sometimes so sudden that the affected person cannot withdraw himself in time from the influence of the poison, nor prevent its entrance in considerable quantities into his system; this is often caused by the fact that the effect of the poison is so rapid that he is often suddenly deprived of power to move or of consciousness, and remains then exposed to the action of the poison until help comes. Such accidents are mostly caused by poisonous gases. Occasionally also considerable quantities of poison enter quite unnoticed into the body, such as odourless poisonous gases in breathing, or poisonous liquids through the skin. In chronic industrial poisoning unsuspected accumulation of poison takes place, until symptoms of illness ultimately reveal themselves; as the first stages of poisoning are not recognised in time by the person affected, he continues exposed to the influence of the poison for weeks, months, even years, until the chronic effect has reached its full development and becomes obvious. Such insidious industrial poisoning arises through the continual absorption into the lungs or stomach of small quantities of poisonous dust, gases, and vapours, during constant or frequent work in an atmosphere containing such gases; poisonous liquids also, by soiling hands and food, or by penetrating the skin, can produce slow industrial poisoning.

Industrial poisoning which in respect of its duration stands midway between acute and chronic is called sub-acute poisoning. This usually means that more frequent absorption of greater quantities of poison has taken place, though not in doses large enough to produce an immediately acute effect. This is important legally because industrial poisonings caused through the sudden absorption of poison in sufficient quantity to act immediately or to bring about subsequent symptoms of poisoning, are reckoned as accidents. Thus acute and many sub-acute industrial poisonings are accounted accidents. Chronic industrial poisonings, acquired gradually, count as illnesses. But as in certain cases it cannot be decided whether sudden or gradual absorption of the industrial poison is in question, this distinction is an unnatural one. It is also unnatural in the legal sense, for there is often no material reason for regarding as legally distinct cases of chronic and acute industrial poisoning. To this we shall refer later in discussing the question of insurance against industrial poisoning.

We have from the outset assumed that the effect of the poison depends not only on the nature of the poison itself, but also on that of the organism, considered both quantitatively and qualitatively.

Significant in a quantitative respect is the body weight of the organism, and the fatal dose of the poison must be ascertained and stated in connection with the body weight, calculated as a rule per kilo of the live weight.

The qualitative point of view must reckon with the differing susceptibility of organisms for poison. This varying susceptibility to the action of poison, the causes of which are very obscure, is called disposition.

Different species (of animals and men) exhibit often very different degrees of susceptibility towards one and the same poison; the differences in this respect are often very considerable, and one cannot simply transfer the experience experimentally gained from one species of animal to man or another species of animal, without further experiment. Besides disposition, sex, and still more age, often determine within the same species marked difference of susceptibility to a poison. Further, there is an individual disposition due to qualities peculiar to the individual, which makes some persons more than usually immune and others specially susceptible. Individuals weakened by illness are particularly susceptible to poisoning. Two diseases, in especial, favour the operation of poison, influencing disastrously the capacity for assimilating food, and reducing the general resisting power of the body; of these tuberculosis stands first.

Individual disposition plays in industrial poisoning a part which must not be under-estimated; it determines the possibility of acclimatisation to a poison; some individuals capable of resistance habituate themselves—often comparatively easily—to a poison, and become, up to a certain limit, immune against it, that is, they can tolerate a quantity which would be injurious to others not so accustomed. With other individuals, however, the opposite effect is apparent. Repeated exposure to the action of the poison leads to an increased susceptibility, so that acclimatisation is not possible. Innate hyper-sensitiveness of the individual towards a poison is called idiosyncrasy. Frequently, for example, this quality shows itself as hyper-sensitiveness of the skin towards the harmful action of certain poisons. A marked lowering in the sensitiveness, innate or acquired, of the organism towards a poison is called immunity.

The possibility of the absorption and action of a poison presupposes—speaking generally—its solubility, and indeed its solubility in the body juices.

In general, poison can be absorbed at very different points of the body; so far as industrial poisons are concerned, these are the mucous membrane of the respiratory passages, the mucous membrane of the digestive tract, and the skin, intact or broken. The rapidity of absorption depends on the nature of the poison, of the individual, and the channel of absorption. Of industrial poisons gases are relatively the most quickly absorbed; sometimes indeed so swiftly that the effect follows almost immediately.

Elimination of industrial poisons is effected principally by the kidneys, the intestinal canal, the respiratory organs, and, more rarely, the skin. Rapidity of elimination also depends on the nature of the poison and of the person poisoned.

If elimination is insufficient, or absorption takes place more quickly than excretion, the poison accumulates in the body, and has a cumulative effect which in chronic industrial poisonings plays a very important rôle. Under certain circumstances poisons are not thrown off, but stored up—fixed—in the body.

The poison absorbed in the body can act unchanged from the place where it is stored. A number of poisons, however, undergo in the organism chemical change through which the action of the poison is partly lessened, rarely increased. Among such changes and weakening of the poison are: oxidation, as, for example, of organic poisons into their final products (carbonic acid, water, &c.), oxidation of benzene into phenol, oxidation of sulphur dioxide into sulphuric acid, &c.; reduction in the case of metals, peroxides, &c.; neutralisation of acids by alkaline juices; chemical union (for instance, of aromatic compounds with sulphuric acid). The splitting up of albuminous bodies is not of importance in regard to industrial poisons.

GENERAL REMARKS ON THE TREATMENT OF INDUSTRIAL POISONINGS

Although in industrial poisoning the importance of treatment is small in comparison with that of preventive measures, in discussing particular forms of poisoning, full weight must be given to it; and in order to avoid repetition, certain points will be brought forward here.

Of the treatment of chronic industrial poisonings not much in general can be said; unfortunately, special treatment has often little chance. It will usually be of advantage to maintain the activity of the excretory organs. So far as there is question of poisons affecting metabolism and injuriously influencing the general state of nutrition, treatment aiming at improving the general health and strength offers hope of success. For nervous symptoms, especially paralysis, disturbance in sensation, &c., treatment generally suitable to nervous diseases can be tried (electro-therapeutics, baths, &c.). In treatment of acute industrial poisonings, which often demand the prompt intervention of laymen, ‘first aid’ is more hopeful.

The most important general rules of treatment arise in reference to irritant poisons which produce ulceration of the skin, and further in regard to those poisons which cause unconsciousness, especially blood poisons.

When an irritant poison is acting on the skin, the first object to be aimed at is naturally the immediate removal of the cause of corrosion by water, or, better still, neutralisation by an alkaline solution (for example, soda solution) in the case of corrosive acids, and weak acids (organic acids, acetic acid, citric acid) in the case of caustic action by alkalis. Such remedies must be at hand in factories as part of the equipment for first aid, where irritant poisonings can occur.

In those industrial poisonings which result in loss of consciousness, arrest of respiration and suffocation, attempts at resuscitation should at once be made. In these attempts at resuscitation, _artificial respiration_ is of the greatest importance; of course the sufferer must first be withdrawn from the influence of the poison, i.e. be brought into fresh air. Great care must be taken, especially where it is necessary to enter places filled with a poisonous atmosphere, to prevent the rescuers, as is often the case, themselves falling victims to the influence of the poison. They should be provided with suitable smoke helmets or breathing apparatus.

We will not describe the methods of resuscitation and artificial respiration universally enjoined; they can be found in every first-aid handbook.

Emphasis is laid on the great importance of _treatment by oxygen_ in cases of industrial poisoning through gaseous blood poisons, as this treatment is attended with good results. Apparatus for the administration of oxygen should be kept wherever there exists the possibility of such poisoning, especially in mines, smelting works, chemical factories, and chemical laboratories.

Oxygen treatment rests on the fact that by raising the pressure of the oxygen from 113 mm., as it is generally in ordinary air, to 675 mm., which is reached in presence of pure oxygen, the quantity of oxygen absorbed in the blood rises from 0·3 to 1·8 per 100 c.c. Further, the saturation of the hæmoglobin, the colouring matter of the blood, undergoes an increase of 2·4 per cent. This increase of oxygen in the blood can save life in cases where through poisoning a deficiency of oxygen has resulted.

The introduction of oxygen is done by special apparatus which acts essentially on the principle that during inhalation oxygen is pressed into the lungs which are below normal physiological pressure, while exhalation is effected by a deflating arrangement when the poisoned individual no longer breathes of his own accord. When natural breathing begins, the introduction of oxygen without special apparatus generally suffices.

Dräger’s _oxygen apparatus_ (fig. 30) consists of a small oxygen cylinder provided with a closing valve, a small manometer, a so-called ‘automatic’ reducing valve with an arrangement for opening and closing the oxygen supply, a bag to act as a receiver or economiser, a breathing mask, and a metal tube connecting the breathing mask with the other parts of the apparatus. The oxygen cylinder, when filled, contains about 180 litres of oxygen, and the manometer allows the manipulator to control at any time whatever oxygen it still contains. The automatic arrangement not only reduces the pressure but at the same time controls the supply of oxygen. This dose is fixed at three litres of oxygen per minute, so that the apparatus with the same oxygen cylinder will last for sixty minutes. The oxygen is not inhaled pure, but is mixed with atmospheric air according to need, and in order to make this possible the breathing mask is provided with a small hole through which atmospheric air finds entrance.

As the oxygen flows continuously from the cylinder waste during exhalation is prevented by the economiser, in which, during exhalation, the inflowing oxygen accumulates, to be absorbed again in inhalation. A small relief valve in the screw head of the bag prevents the entrance into it of exhaled air.

Another oxygen inhaling apparatus for resuscitating purposes, that of Siebe, Gorman & Co., is illustrated in figs. 31 and 32.

Dräger also constructs an apparatus called the ‘Pulmotor’ which simultaneously accomplishes the introduction of oxygen and artificial respiration.

Inflation and deflation are effected by an injector driven by compressed oxygen; this alternately drives fresh air enriched with oxygen into the lungs and then by suction empties them again. While with the mechanical appliances of resuscitation belonging to older systems the hand of the helper regulated the rate of breathing, in the case of the Pulmotor the lungs, according to their size, automatically fix the rate of breathing; as soon as the lungs are filled the apparatus of its own accord marks the moment for ‘deflation,’ and as soon as they are emptied of ‘inflation.’ This automatic reversal is effected by a little bellows which is connected with the air tubes. During inflation the same pressure is exerted in the bellows as in the lungs. As soon as the lungs are filled, the pressure in the bellows increases and it expands, its forward movement causing the reversal to deflation. When the lungs are emptied the bellows contracts, and through this contraction results the reversal to inflation.

If, in an exceptional case, the breathing for some reason does not act automatically, the hand of the helper can manipulate it by means of a backward and forward movement of a lever. According to choice, either a nose-mask or a mask covering both mouth and nose can be worn.

Combined with the regular apparatus for resuscitation is an ordinary apparatus for the inhalation of oxygen; by the simple altering of a lever, either the one or the other can be employed.

II. INDUSTRIAL POISONING IN PARTICULAR INDUSTRIES

After the foregoing general remarks we may now consider various points of view in regard to classification of industrial poisonings into groups:

(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.

_GROUP: MINERAL ACIDS, HALOGENS, INORGANIC HALOGEN COMPOUNDS, ALKALIS_

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.

MINERAL ACIDS

=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.

THE HALOGENS (CHLORINE, BROMINE, IODINE)

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

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.

ALKALIS

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.

_GROUP: METALS AND METAL-COMPOUNDS_

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, LEAD COMPOUNDS

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.

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 (ZINC ALLOYS)

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, MERCURY COMPOUNDS

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, MANGANESE COMPOUNDS

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, CHROME COMPOUNDS

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.

OTHER METALS AND METAL COMPOUNDS

=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.

_GROUP: ARSENIC, PHOSPHORUS_

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.

ARSENIC, OXIDES OF ARSENIC

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

_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.

Phosphoretted Hydrogen

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.

_GROUP: SULPHURETTED HYDROGEN, CARBON BISULPHIDE, AND CYANOGEN (NERVE POISONS)_

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.

SULPHURETTED HYDROGEN

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.

CARBON BISULPHIDE

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.

CYANOGEN AND CYANOGEN COMPOUNDS (CYANOGEN GAS, PRUSSIC ACID, CYANIDES)

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.

_GROUP: ARSENIURETTED HYDROGEN AND CARBONIC OXIDE (BLOOD POISONS)_

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.

ARSENIURETTED HYDROGEN

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)

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 (PHOSGENE)

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.

NICKEL CARBONYL

The effects of nickel carbonyl are described on pp. 186-8.

CARBONIC ACID

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.

_GROUP: HYDROCARBONS OF THE ALIPHATIC AND AROMATIC SERIES AND THEIR HALOGEN AND HYDROXYL SUBSTITUTION PRODUCTS_

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).

HYDROCARBONS OF MINERAL OIL

BENZINE, LIGROINE, PETROLEUM, PARAFFIN, VASELINE

_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.

Acute poisoning from inhalation of benzine fumes begins with headache, sickness, and attacks of giddiness resembling alcoholic intoxication. If very much has been inhaled, the patient quickly becomes unconscious, with occasionally muscular tremors, convulsions, difficulty in breathing, and cyanosis.

In cases of poisoning by inhalation of fumes of crude petroleum, these symptoms may be complicated by coughing, intense inflammation of the mucous membrane of the respiratory organs—congestion, bronchitis, bloodstained expectoration, and inflammation of the lungs. In workers who frequently remain long in an atmosphere filled with benzine fumes, further symptoms of chronic benzine poisoning show themselves—mental hebetude, pains in the limbs, trembling, weakness of the muscles, and other disturbances of the nervous system; in such cases these may really be signs of continued attacks of acute or sub-acute poisoning; many benzine workers are anæmic.

The treatment of acute benzine poisoning consists in oxygen inhalation, with simultaneous artificial respiration. Treatment of chronic derangement of health is symptomatic.

HYDROCARBONS OF THE AROMATIC SERIES

BENZENE AND ITS HOMOLOGUES

_Benzene_ (C₆H₆) is a characteristically smelling (aromatic) liquid which boils at 80·5° C. Acute benzene poisoning, which plays an important part as an industrial poisoning, is caused by inhalation of benzene fumes. The various kinds of benzol used commercially contain, besides benzene, alkyl benzenes, especially _toluene_ (methylbenzene, C₆H₅.CH₃, boiling-point 111° C.); _xylene_ (dimethylbenzene, C₆H₄[CH₃]₂, boiling-point 140° C.); _pseudocumene_ and _mesitylene_ (tri-methylbenzene, C₆H₃[CH₃]₃, boiling-point 169° or 163° C.); the regular presence of _thiophene_ (C₄H₄S, boiling-point 84° C.) in commercial benzol must also be taken into account. Industrial benzol poisoning arises, therefore, as a rule, not from the action of pure benzene vapour, but from fumes which contain a mixture of the compounds mentioned.

The course run by industrial benzol poisoning is often very acute, if large quantities are inhaled—death occurring suddenly, after a short illness with symptoms of vertigo. Gradual inhalation of lesser quantities gives rise to headache, giddiness, malaise, then twitchings appear which develop into convulsions, and lastly unconsciousness. In order to ascertain in what manner the various substances contained in commercial benzol share in the poisonous effect, experimental research seemed to me to be indispensable, especially as published statements so far gave no accurate data.

Two cases of industrial benzol poisoning have given rise to close experimental research upon the poisonous nature of benzene.

Lewin undertook experiments on animals; which he confined under bells and caused to inhale fumes of chemically pure and impure benzene. He mentions that even at comparatively low concentration poisoning results, and indeed more readily and certainly from the action of impure than pure benzene. Lewin found that when air was made to flow slowly first through benzene and then into the bell, symptoms of paralysis, convulsions, and unconsciousness showed themselves in from four to six minutes. After-effects by this means could not be observed. Lewin maintains, however, that in man even slight acute action of benzene can be followed by after-effects (giddiness, sickness, headache, distress in breathing, and oppression of the heart).

Santesson made researches upon the poisonous action of benzene in connection with occurrence of certain cases of poisoning through ‘impure benzol’ (coal-tar benzene) in a rubber tyre factory. In the factory mentioned nine young women were poisoned, of whom four died. The symptoms shown were lassitude, anæmia, giddiness, headache, vomiting, and fever. Post mortem, hæmorrhages and fatty degeneration of the endothelium of the bloodvessels and various organs were found. Experimental research showed that commercial benzol and chemically pure benzene had the same effect. Santesson did not succeed in his experiments on animals in producing chronic poisoning by inhalation of benzine and of benzene fumes (which two completely different poisons he does not distinguish strictly from each other, as is the case, unfortunately, with many other writers). My experimental researches upon the poisonous effect of pure benzene, pure toluene, cumene, thiophene, and the most important kinds of commercial benzol gave the following results:

For rabbits the limit of toxicity is a proportion of 0·015 to 0·016 per thousand pure benzene in the air, that is 0·015 to 0·016 c.c. benzene vapour per litre of air.

A concentration of 0·056-0·057 per thousand pure benzene in the air causes in rabbits at once—after one minute—twitching of the muscles; after eight minutes, convulsions; after ten minutes, deep narcosis; and after twenty-five minutes, coma. If the animal is taken out of the bell in time, even if it has shown marked symptoms, it recovers very quickly (in two to ten minutes) without manifesting any after effects. Even in animals repeatedly exposed to the poison sequelæ were not observed.

Dogs are somewhat more susceptible to pure benzene than rabbits; 0·024 per thousand causes after ten minutes severe convulsions, which after twenty minutes become continuous; 0·042 per thousand kills after twenty minutes (sudden death in a state of tetanus).

Cats are less sensitive than dogs and more sensitive than rabbits; 0·03-0·04 per thousand causes after ten minutes attacks of cramp and, after twenty minutes, convulsions; 0·05 per thousand at once brings on poisoning symptoms. As regards the character of the symptoms (cramps, convulsions, quick recovery, no after effects) the above statements apply to all three kinds of animals (rabbit, dog, and cat).

Chloral hydrate completely checks the convulsions and enables animals to tolerate higher concentrations of benzene for a longer time.

Benzene is thus to be counted among nerve irritant poisons. The convulsions are probably provoked by excitement of the motor centres in the brain.

In view of the fact that thiophene in a concentration of 0·03-0·05 per thousand in the air was borne by animals for an hour without producing any symptoms of poisoning, the proportion of thiophene in commercial benzol must be looked upon as practically non-injurious.

The so-called 90 _benzol_—a commercial benzol of which 90 per cent. distils at 100° C.—has naturally a somewhat weaker action, although, in respect of the poisoning symptoms produced, it is similar to that of pure benzene.

_Pure toluene_ (boiling-point 111° C.) and purified toluol (commercial product, boiling-point 109°-112° C.) produce, when inhaled, gradually increasing narcosis in the three kinds of animals referred to; they produce no symptoms of convulsions or spasms.

After the animals have been taken out of the bell, recovery is not so rapid as after benzine inhalation, but takes from half an hour to one hour. In rabbits and cats 0·046-0·05 per thousand produces after fifteen minutes staggering and paresis; after thirty minutes deep narcosis. The dog is again somewhat more susceptible, as little as 0·034 per thousand causing these symptoms in the same time.

‘Purified toluol’ (commercial product) acts somewhat less rapidly than pure toluene, but this small difference in effect need hardly be considered.

Other poisons were also investigated:—

_Solvent naphtha I_, a commercial product, of which 90 per cent. comes over at 160° C.; it contains little toluene, chiefly xylene, pseudocumene, and cumene.

_Solvent naphtha II_, of which 90 per cent. comes over at 175° C, it contains besides xylene, chiefly pseudocumene, mesitylene, cumene, &c.

The fumes of solvent naphtha I cause, when inhaled by rabbits, dogs, and cats, gradual narcosis, although not nearly so quickly as toluene at similar concentrations; recovery usually takes over an hour after the deeply narcotised animals have been removed from the bell. Rabbits and cats are affected in about equal degree. The dog is the more sensitive. Rabbits and cats can tolerate about 0·012-0·013 per thousand of the fumes of solvent naphtha I in the atmosphere for a long time without any symptoms. Only after breathing for fifty minutes air containing 0·0536 per thousand do they become narcotised. In the dog 0·036 per thousand causes narcosis only after thirty minutes.

With the fumes of solvent naphtha II I could not affect rabbits at all. The cat also, in spite of long inhalation of the heavy fumes, showed no marked symptoms of poisoning. In the dog gradual narcosis came about only after an hour’s inhalation of 0·048 per thousand.

The fumes of pure _xylene_ caused narcosis in rabbits after forty minutes’ inhalation of 0·05 per thousand in the atmosphere; after being taken out of the bell the animals recovered slowly (after half an hour to one hour).

_Cumene_ causes no symptoms after one hour’s inhalation in a concentration of 0·06 to 0·07 per thousand. This explains the effects of solvent naphtha I (in which xylene preponderates) and solvent naphtha II (in which pseudocumene, cumene, &c., preponderate). After effects were not observed.

Benzol and toluol fumes, and particularly those of solvent naphtha, exercise a distinctly irritant effect upon the mucous membrane, which, however, passes off without after effects.

Pure benzene, therefore, proved the most poisonous of the substances under investigation. When inhaled its effect (convulsions, with quick recovery) differs essentially from that of toluene, solvent naphtha, xylene, and cumene (gradual narcosis, slow recovery). The fumes of the various kinds of commercial benzol (solvent naphtha) boiling at a higher temperature are practically non-poisonous (solvent naphtha II). Pure benzene fumes are, however poisonous, even in very small quantities in the air. The limit for animals lies at 0·015-0·016 per thousand.

Lehmann has shown in a recent work that man, exposed to a mixture of benzene and air, absorbs 80 per cent. of the benzene.

Treatment of acute industrial benzene poisoning consists in severe cases of artificial respiration, with simultaneous administration of oxygen; in slight cases it is sufficient to bring the patient into fresh air.

_Naphthalene._—Naphthalene, which is insoluble in water, has irritant effect upon the mucous membrane and upon the skin when brought into contact with it.

Long continuance in an atmosphere containing naphthalene as dust or fumes causes headache, nausea, giddiness, &c.

HALOGEN SUBSTITUTION PRODUCTS

ALIPHATIC SERIES (NARCOTIC POISONS)

The halogen substitution products of the aliphatic series are not of much account as industrial poisons. They have generally a narcotic effect, that is, a paralysing effect upon the central nervous system, usually preceded by a short stage of excitement. This effect shows itself typically on inhalation of chloroform (methanetrichloride, CHCl₃), which however plays no part as an industrial poison. The narcotic effect of the other alkyl chlorides is less than that of chloroform. With carbon tetrachloride (CCl₄) the narcotic effect is only half that of chloroform; it causes, however, a more violent excitation; inhaling the fumes brings on nausea, coughing, sickness, headache, &c.

_Methylchloride_ (CH₃Cl) has a less narcotising effect. On the other hand it has a stronger local irritant action, which is indeed present also in chloroform, though not so apparent. This gas, as is well known, is used as a local anæsthetic in medicine.

Pure _methylene chloride_ (CH₂Cl₂) similarly is much less powerful than chloroform. Severe poisoning, alleged to have resulted from methylene chloride was caused by a mixture, called indeed methylene chloride, but composed of methylalcohol and chloroform.

Of the remaining halogen substitution products of methane, _methyl bromide_ (CH₃Br) and _methyl iodide_ (CH₃I) have given rise to industrial poisoning.

These poisons also act in the same way as the alkyl chlorides, but the excitement accompanying the narcosis is more marked—so far as the scanty observations allow conclusions to be drawn. The symptoms first show themselves in sickness, giddiness, hebetude, slowing of respiratory movements and of the heart’s action; convulsions or delirium ensue.

Treatment consists in artificial respiration or promotion of breathing by a plentiful supply of fresh air or oxygen; in pronounced narcosis stimulating remedies should be applied.

BENZENE SERIES

_Chlorobenzene_, and _nitro-_ and _dinitro-chlorobenzene_ and _benzoylchloride_, have given rise to industrial poisoning.

To chlorobenzene similar action is attributed as to benzene (headache, fainting, rapid breathing, cyanosis); changes in the blood (methæmoglobin formation) have also been observed.

Nitro- and dinitro-chlorobenzene are active poisons; the effect corresponds in general to that of nitro- and dinitrobenzene, but in addition the fumes or dust have markedly irritant action on the skin (dermatitis).

_Benzoylchloride_ (C₆H₅COCl), a colourless, pungent-smelling liquid, produces a violently irritant effect upon the mucous membrane, decomposing into hydrochloric acid and benzoic acid.

Treatment is analogous to that of benzene poisoning, and in cases of benzoyl chloride poisoning to that by hydrochloric acid.

It may be mentioned that chlorine rash is attributed to the action of chlorinated tar products (chlorobenzene compounds).

HYDROXYL SUBSTITUTION PRODUCTS

FATTY SERIES (ALCOHOLS)

The hydroxyl substitution products of the fatty series belong mainly to the narcotic poisons; the greater the molecular weight of the alcohol, the more marked is usually the narcotic effect. According to this propylalcohol is eighteen times as poisonous as ethylalcohol; butylalcohol and amylalcohol have from 36 to 120 times as great a narcotic effect as methylalcohol.

_Methylalcohol_ (wood spirit, CH₃OH) plays relatively the greatest part among alcohols as an industrial poison, because it is employed as a means of denaturing spirit. Its poisonous nature is relatively great, being very persistent. Industrial poisoning by methylalcohol is due to inhalation of the vapour and is rarely of a severe nature. The fumes have a strongly irritant effect upon the mucous membrane, giving rise to throat irritation, cough, hoarseness, and in severe cases bronchitis and inflammation of the conjunctiva of the eye. In addition inhalation of methylalcohol vapour causes headache, giddiness, nausea (inclination to vomit), and occasionally also twitchings and tremor.

The _higher alcohols_ (propyl-, butyl-, amyl-alcohol, C₃H₇.OH, C₄H₉.OH, and C₅H₁₁.OH) occur in fusel oil. They cause but slight (if any) industrial poisoning. Cases of more severe industrial poisoning through amylalcohol fumes have been described (in factories for smokeless powder), with symptoms of sickness, headache, giddiness, with fatal issue in some cases, preceded by severe nervous symptoms (convulsions or delirium).

Beyond speedy removal out of the dangerous atmosphere, probably no special treatment is needed in these cases of industrial poisoning from alcoholic vapour.

_GROUP: NITRO AND AMIDO COMPOUNDS OF THE ALIPHATIC AND AROMATIC SERIES (BLOOD POISONS WHICH FORM METHÆMOGLOBIN)_

Characteristic of the nitro and amido compounds of the aliphatic and aromatic series of the organic substances is their action upon the blood. The normal oxyhæmoglobin (blood-colouring matter) is changed into methæmoglobin, with which the oxygen is so firmly combined that the internal exchange of gases necessary to life becomes impossible. Methæmoglobin has a dark chocolate-brown colour and a clearly defined characteristic spectrum.

Of the poisons belonging to this group several are important. In so far as these substances are volatile—and this is generally the case with those causing industrial poisoning—effects are due to inhalation of fumes, but it is proved that the poisons of this group in liquid form can be absorbed by the intact skin, and this channel of absorption is characteristic of industrial poisoning. Severe poisoning results especially from wetting the skin by spilling on the clothes, &c.

The grey-blue discoloration of the mucous membrane, especially of the lips, is characteristic; sometimes also the skin is altered in colour. This discoloration is often noticed by others before the patient feels unwell. Soon the person affected has general nausea, vomiting, headache, giddiness, severe nervous symptoms, feeling of anxiety, and difficulty of breathing; in severe cases unconsciousness comes on, and death occurs with increasing cyanosis (lividity).

Treatment is naturally that which has been emphasised in the introductory words to Part II, which hold for all blood poisonings. In mild cases oxygen treatment has given good results. In all factories where such poisoning can occur provision should be made for immediate oxygen treatment. Besides this, the workers must be adequately instructed as to the danger and symptoms of poisoning, especially of the characteristic premonitory skin discoloration, in order to be able to assist their fellows.

NITROCOMPOUNDS

ALIPHATIC SERIES

_Nitro-glycerin_ (triple nitric acid ester of glycerin, C₃H₅.[NO₃]₃), the well-known oily explosive liquid, has also an irritant local effect. When absorbed into the body, in addition to methæmoglobin formation, it causes dilatation of the bloodvessels, slowing of the respiration and heart’s action, and attacks of suffocation. The general remarks upon this group apply here, but symptoms referable to central paralysis occur as the methæmoglobin formation is slow. Industrial poisoning arises through inhalation of gases containing nitro-glycerin and also by absorption through the skin. Statements as to its poisonous nature are very varied. Under certain conditions moistening the skin with small quantities of nitro-glycerin suffices to produce symptoms. Probably the susceptibility of different persons varies greatly.

_Amylnitrite_ (nitric acid amyl ester, C₅H₁₁NO₂), a characteristically smelling liquid, acts similarly. The fumes of amylnitrite, even when inhaled in small quantities, cause marked dilatation of the bloodvessels, through paralysis of the muscular walls of the bloodvessels, thus causing marked flushing of the face; the pulse becomes quick, then weak and slow.

NITRO AND AMIDO COMPOUNDS

AROMATIC SERIES

The substances of this group are important.

_Nitrobenzene_ (C₆H₅NO₂, named oil of mirbane), a yellowish liquid of characteristic smell, induces especially the formation of methæmoglobin in the blood; the effect upon the central nervous system (first excitation, then depression) is often absent. The description of the disease in general in the introductory words of this whole group is characteristic. Occasionally signs of asphyxia show themselves; sometimes there are twitchings, disturbance of the power of sensation, and convulsions; early discoloration of the mucous membrane and the skin, which assume a blue to grey-black colour, is characteristic.

Chronic poisoning is also attributed to nitrobenzene, showing itself in lassitude, headache, malaise, giddiness, and other disturbances of the nervous system.

_Nitrotoluene_ (C₆H₄CH₃NO₂), of which the ortho-compound acts most powerfully, and also _nitroxylene_ (C₆H₃[CH₃]₂NO₂) have similar but less marked effect.

The _dinitrobenzenes_ (C₆H₄[NO₂]₂) are stable bodies. Meta-dinitrobenzene inhaled as dust or otherwise, can produce marked poisoning symptoms essentially the same as those described. Especially characteristic is the early dark discoloration of the skin.

Symptoms resembling nitrobenzene poisoning in general are caused by _nitrophenols_ (C₆H₄.OH.NO₂), of which paranitrophenol is the most toxic; also by _dinitrophenols_ (C₆H₃[NO₂]₂OH), solid crystalline substances which melt at different temperatures, and the _mono-_ and _di-nitrochlorobenzenes_ (C₆H₄.Cl.NO₂ and C₆H₃.Cl[NO₂]₂). In cases of industrial poisoning by dinitrophenol, observed by Leymann, the workers were taken suddenly ill, with symptoms of collapse, pains in the chest, vomiting, distress of breathing, rapid pulse, and convulsions, and died within a few hours. At the autopsy a yellow substance was found with picric acid reaction which appeared to be di- or tri-nitrophenol. In other cases, some fatal, of industrial nitrochlorobenzene poisoning, also observed by Leymann, the typical grey-blue discoloration of the skin was obvious, and the chocolate-brown colour of the blood produced by methæmoglobin.

_Trinitrophenol_ (picric acid, C₆H₂[NO₂]₃OH) is a yellow crystalline compound with bitter taste; poisoning by this substance exhibits clearly strong local irritant action (upon skin, mucous membrane, and intestinal canal, and especially upon the kidneys), besides effect on the blood and central nervous system. Prolonged action of picric acid upon the skin causes inflammation. Absorption of picric acid dust causes inflammation of the mucous membrane of the respiratory passages and symptoms of gastric and intestinal catarrh as well as inflammation of the kidneys.

A jaundice-like discoloration of the skin and darkening of the urine are also characteristic; sometimes picric acid poisoning produces a rash resembling that of measles and scarlet fever.

_Nitronaphthalene_ (C₁₀H₇[NO₂]) and _nitronaphthol_ (C₁₀H₆.NO₂.OH) in addition to methæmoglobin formation have an irritant action. It is stated also that dulness of the cornea is produced.

_Azobenzenes_ also, which are to be considered as intermediate between nitrobenzene and aniline, form methæmoglobin (azobenzene, C₆H₅N = NH₅C₆).

_Aniline_ (amidobenzene, C₆H₅.NH₂), a colourless, oily liquid of aromatic smell, has only slight local irritant effect. In the frequent cases of industrial poisoning by ‘aniline oil’ or aniline hydrochloride, in which the aniline enters through the skin or is inhaled in the form of fume, there appear the typical symptoms common to this group, of the action upon the blood through methæmoglobin formation: headache, weakness, cyanosis, difficulty in breathing, &c., to which are added nervous symptoms such as convulsions and psychical disturbance, although these play a subordinate part in industrial poisoning. In severe cases the typical symptoms of air hunger are shown. Occasionally recovery only takes place gradually, and signs of irritation of the kidneys and inflammation of the urinary organs are seen. These symptoms occur only rarely in acute industrial poisoning, but are, however, in so far worthy of notice because of the frequent occurrence of tumours in the bladder among aniline workers. It is possible that here the irritant action of the urine which contains aniline plays a part. The tumours in the bladder operated upon, in some cases with success, were many of them non-malignant (papillomata), but some were carcinomata (cancerous new growths) running a malignant course, and recurring after operation. In the urine the aniline combines with sulphuric acid, and is partly excreted as paramidophenol sulphuric acid.

The treatment of aniline poisoning is the same as that for all the poisons of this group. In view of the occurrence of tumours of the bladder in aniline workers, they should be instructed to seek medical aid on the first indications of trouble, so that a careful cystoscopic examination may be made.

_Toluidine_ (C₆H₄.CH₃.NH₂), which is mixed with aniline for industrial use, produces the same symptoms with marked irritation of the renal organs.

Of the _nitroanilines_ (C₆H₄.NH₂.NO₂) _paranitroaniline_ is the most poisonous. Characteristic of the action of this compound is methæmoglobin formation, central paralysis and paralysis of the heart’s action.

Of the _benzenediamines_, _paraphenylene diamine_ (C₆H₄[NH₂]₂) may be regarded as an industrial poison. The irritant action of this substance is prominent; it induces skin affections, inflammation of the mucous membranes, more especially of the respiratory organs, and sometimes inflammation of the kidneys. They have been noted in workers using ursol as a dye; here, doubtless, the action of diimine (C₆H₄.NH.NH.) must be taken into account, which arises as an intermediate product and exercises a markedly irritant action. Further, the general effect of paraphenylene diamine is an irritant one upon the central nervous system.

_APPENDIX_

TURPENTINE, PYRIDINE BASES, ALKALOIDS

_Turpentine oil._.—Turpentine oil is a peculiar-smelling, colourless liquid of the composition C₁₀H₁₆; different reactions show that turpentine oil contains the aromatic nucleus (cymene). It is used in the manufacture of varnish, and thus can cause industrial poisoning by inhalation of fumes. Even from 3 to 4 mg. of vapour of turpentine oil per litre of air brings on severe symptoms. Turpentine oil acts as a local irritant, and when absorbed into the system has an exciting effect upon the central nervous system. Inhalation of large quantities of turpentine vapour cause rapid breathing, palpitation, giddiness, stupor, convulsions, and other nervous disturbances, pains in the chest, bronchitis, and inflammation of the kidneys. The last-mentioned symptom also arises from the chronic action of turpentine vapours.

_Pyridine._—Pyridine (C₅H₅N), a colourless liquid of peculiar odour, is employed as well as methylalcohol in denaturing alcohol. The disturbance of health observed in workers occupied with the denatured spirit are probably mainly due to the inhalation of fumes of methylalcohol. Pyridine is comparatively innocuous. Eczema, from which persons suffer who come into contact with denatured spirit, is ascribed to the action of pyridine. Larger doses produce a paralysing effect, but this need not be considered in its industrial use.

_Nicotine, tobacco._—According to various published statements, effects among tobacco factory workers are attributed to the nicotine contained in tobacco dust and to the aroma which fills the air. Nicotine in large doses has at first an exciting followed by a paralysing effect upon the central nervous system; it causes moreover contraction of the unstriped muscles and has a local irritant effect.

The symptoms of illness ascribed to nicotine are: conjunctivitis, catarrh of the air passages, palpitation, headache, want of appetite, and, particularly, tendency to abortion and excessive menstruation. Severe industrial poisoning due to nicotine has only been observed in workers who chewed tobacco leaves.

_Poisonous wood._—The symptoms of disease noticed in workers who manipulate certain kinds of wood are attributed by some writers to the presence of alkaloids. Such knowledge as we have of the illness due to them—they are evidently of the nature of poisoning—is referred to at the end of Part I.