Chapter XII: Part II: The Symptoms and Treatment of Industrial Poisoning (1)

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.

I Oxygen cylinder; A Valve on cylinder; B Manometer; C Key for opening and closing the flow of oxygen; F Economiser; H Facepiece.]

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).