Wrought iron is made by treating pig iron in refinery and puddling furnaces; in these much of the carbon is removed as carbon monoxide, and from the puddling furnace the iron is obtained as a pasty mass which can be worked into bars, rods, or plates.

Steel is made in various ways. The Acid Bessemer process consists in forcing compressed air in numerous small streams through molten cast iron, in iron vessels (converters) which are lined with ganister, a silicious sandstone. These can be rotated on trunnions. Basic Bessemer steel is made in similar converters by the Thomas-Gilchrist or basic process, which can be applied to pig irons containing phosphorus. The latter is removed by giving the converter a basic lining of calcined magnesium limestone mixed with tar.

In the Martin process steel is obtained by melting together pig iron with steel scrap, wrought iron scrap, &c., on the hearth of a Siemens regenerative furnace with a silicious lining.

In iron smelting the most important danger is from blast furnace gas rich in carbonic oxide. Sulphur dioxide, hydrocyanic acid, and arseniuretted hydrogen gas may possibly be present.

When work was carried out in blast furnaces with open tops the workers engaged in charging ran considerable risk. But as the blast furnace gas is rich in carbonic oxide and has high heating capacity these gases are now always led off and utilised; the charging point is closed by a cup (Parry’s cup and cone charger) and only opened from time to time mechanically, when the workers retire so far from the opening as to be unaffected by the escaping gas. The gas is led away (fig. 29) through a side opening into special gas mains, is subjected to a purifying process in order to rid it of flue dust, and then used to heat the blast, fire the boilers, or drive gas engines.

Severe blast furnace gas poisoning, however, does occur in entering the mains for cleaning purposes. Numerous cases of the kind are quoted in the section on Carbonic oxide poisoning.

The gases evolved on tapping and slag running can also act injuriously, and unpleasant emanations be given off in granulating the slag (by receiving the fluid slag in water).

In the puddling process much carbonic oxide is present. Other processes, however, can scarcely give rise to poisoning.

The basic slag produced in the Thomas-Gilchrist process is a valuable manure on account of the phosphorus it contains; it is ground in edge runners, and then reduced to a very fine dust in mills and disintegrators. This dust has a corrosive action already referred to in the chapter on Phosphorus and Artificial Manures.

The poisoning caused by ferro-silicon is of interest. Iron with high proportion of silicon has been made in recent years on a large scale for production of steel. Some 4000 tons of ferro-silicon are annually exported to Great Britain from France and Germany. It is made by melting together iron ore, quartz, coke, and lime (as flux) at very high temperature in electrical furnaces. The coke reduces the quartz and ore to silicon and metal with the production of ferro-silicon. Certain grades, namely those with about 50 per cent. silicon, have the property of decomposing or disintegrating into powder on exposure for any length of time to the air, with production of very poisonous gases containing phosphoretted and arseniuretted hydrogen. The iron and quartz often contain phosphates, which in presence of carbon and at the high temperature of the electrical furnace would no doubt be converted into phosphides combining with the lime to form calcium phosphide; similarly any arsenic present would yield calcium arsenide. These would be decomposed in presence of water and evolve phosphoretted and arseniuretted hydrogen gas. In addition to its poisonous properties it has also given rise to explosions.

[In January 1905 fifty steerage passengers were made seriously ill and eleven of them died. In 1907 five passengers died on a Swedish steamer as the result of poisonous gases given off from ferro-silicon, and more recently five lives were lost on the steamer Aston carrying the material from Antwerp to Grimsby.[C] This accident led to full investigation of the subject by Dr. Copeman, F.R.S., one of the Medical Inspectors of the Local Government Board, Mr. S. R. Bennett, one of H.M. Inspectors of Factories, and Dr. Wilson Hake, Ph.D., F.I.C., in which the conclusions arrived at are summarised as follows:

The suggested regulations are printed on p. 291.]

ZINC

Industrial poisoning from zinc is unknown. The chronic zinc poisoning among spelter workers described by Schlockow with nervous symptoms is undoubtedly to be attributed to lead.

COPPER: BRASS

Occurrence of brass-founder’s ague.—Opinion is divided as to whether pure copper is poisonous or not. Lehmann has at any rate shown experimentally that as an industrial poison it is without importance.

Occurrence, however, of brass-founder’s ague is undoubtedly frequent. Although neither pure zinc nor pure copper give rise to poisoning, yet the pouring of brass (an alloy of zinc and copper) sets up a peculiar train of symptoms. As the symptoms are transient, and medical attendance is only very rarely sought after, knowledge of its frequency is difficult to obtain.

Sigel,1 who has experimented on himself, believes that the symptoms result from inhalation of superheated zinc fumes. In large well-appointed brass casting shops (as in those of Zeiss in Jena) incidence is rare.

Lehmann2 very recently has expressed his decided opinion that brass-founder’s ague is a zinc poisoning due to inhalation of zinc oxide and not zinc fumes. This conclusion he came to as the result of experiments on a workman predisposed to attacks of brass-founder’s ague. Lehmann’s surmise is that the symptoms are due to an auto-intoxication from absorption of dead epithelial cells lining the respiratory tract, the cells having been destroyed by inhalation of the zinc oxide. He found that he could produce typical symptoms in a worker by inhalation of the fumes given off in burning pure zinc.

Metal pickling.—The object of metal dipping is to give metal objects, especially of brass (buckles, lamps, electric fittings, candlesticks, &c.), a clean or mat surface and is effected by dipping in baths of nitric, hydrochloric, or sulphuric acid. Generally after dipping in the dilute bath the articles go for one or two minutes into strong acid, from which injurious fumes, especially nitrous fumes, develop with occasionally fatal effect (see the chapter on Nitric Acid). Unfortunately, there are no references in the literature of the subject as to the frequency of such attacks.

Recovery of gold and silver has been already referred to in the chapters on Mercury, Lead, and Cyanogen.

Mention must be made of argyria. This is not poisoning in the proper sense of the word, as injury to health is hardly caused. Argyria results from absorption of small doses of silver salts which, excreted in the form of reduced metallic silver, give the skin a shiny black colour. Cases are most frequently seen in silverers of glass pearls who do the work by suction. Local argyria has been described by Lewin in silvering of mirrors and in photographers.

III. OCCURRENCE OF INDUSTRIAL POISONING IN VARIOUS INDUSTRIES

The most important facts have now been stated as to the occurrence of poisoning in industry, and there remain only a few gaps to fill in and to survey briefly the risks in certain important groups of industry.

TREATMENT OF STONE AND EARTHS

Lime Burning: Glass Industry

Lead poisoning in the ceramic industry (earthenware, porcelain, glass, polishing of precious stones, &c.) has been dealt with in detail in the chapter on Lead. There is further the possibility of chrome-ulceration, of arsenic poisoning, and conceivably also of manganese. Further, poisoning by carbonic oxide and carbon dioxide may occur from the escape of furnace gases where hygienic conditions are bad. In charging lime kilns poisoning by carbonic oxide has occurred. The report of the Union of Chemical Industry in 1906 describes the case of a workman who was assisting in filling the kiln with limestone. As the furnace door was opened for the purpose gas escaped in such amount as to render him unconscious. He was picked up thirty minutes later, but efforts at resuscitation failed.

Carbonic oxide poisoning, again, may arise from the use of Siemens regenerative furnaces, especially glass furnaces: details are given in the chapter on Illuminating Gas.

Hydrofluoric acid is present as an industrial poison in glass etching (see Fluorine Compounds). Persons employed in this process suffer from inflammation of the respiratory tract and ulceration of the skin of the hands. I could not find any precise statement as to the frequency of the occurrence of such injuries. Use of sand-blasting to roughen the surface of glass has to some extent taken the place of etching by hydrofluoric acid.

TREATMENT OF ANIMAL PRODUCTS

In tanning use of arsenic compounds for detaching the wool from skins and of gas lime for getting rid of hair may cause injury to health. With the latter there is possibility of the action of cyanogen compounds (see the chapters on Arsenic and Cyanogen).

PREPARATION OF VEGETABLE FOOD STUFFS AND THE LIKE

In fermentation processes as in breweries and the sugar industry accumulations of carbonic acid gas occur, and suffocation from this source has been repeatedly described. Mention in this connection should be made of the use of salufer containing some 2 per cent. of silicofluoric acid as a preservative and antiseptic in beer brewing. In the sulphuring of hops, wine, &c., the workers may run risk from the injurious action of sulphur dioxide. Arsenic in the sulphuric acid used for the production of dextrine may set up industrial poisoning. Poisoning from ammonia gas can occur in cold storage premises. Industrial poisoning from tobacco is not proved, but the injurious effect of the aroma and dust of tobacco—especially in women—in badly arranged tobacco factories is probable.

WOOD WORKING

Injurious woods.—In recent literature there are several interesting references to injury to health from certain poisonous kinds of wood—skin affections in workers manipulating satinwood, and affections of the heart and general health in workers making shuttles of African boxwood. Details of these forms of poisoning are reported from England and Bavaria. The wood used for making the shuttles was West African boxwood (Gonioma Kamassi). It appears that the wood contains an alkaloidal poison which affects the heart’s action. The workers suffered from headache, feeling of sleepiness, lachrymation, coryza, difficulty of breathing, nausea, and weakness. Four workers had to give up the work because of the difficulty in breathing. Inquiry was made by Dr. John Hay of Liverpool in 1908 and by the medical inspector of factories in 1905. The following table shows the symptoms found:

The later inquiry shows considerable diminution in the amount of complaint as to respiratory trouble. This may have been due to the improved conditions of working, freely acknowledged by the men. Men were examined who had complained of the effects of the wood in 1905, and had continued uninterruptedly at the same kind of work during the interval without any obvious further injury to their health, although they preferred working on other woods.

East Indian boxwood had to be discarded in the shuttle trade owing to its irritant action on the eyes. Sabicu wood from Cuba was stated to give off ‘a snuffy dust under the machine and hand planes, the effect of which upon the worker is to cause a running at the eyes and nose, and a general feeling of cold in the head. The symptoms pass off in an hour or so after discontinuance of work.’ Reference was made in the report for 1906 to eczematous eruptions produced by so-called Borneo rosewood, a wood used owing to its brilliant colour and exquisite grain in fret-saw work. The Director of the Imperial Institute experimented with this wood, but failed to discover injurious properties in it. At the same time experiments with the wood and sawdust of East and West Indian satinwood were undertaken, but also without result.

From inquiries subsequently made it appeared that much confusion existed as to the designation ‘satinwood,’ as under this name were classed both East and West Indian satinwood and also satin walnut. The evidence was clear that East Indian satinwood was more irritating than West Indian. Satin walnut wood is apparently harmless. In the shipbuilding yards of East London, Glasgow, and Bristol affections of the skin were recognised, but susceptibility to the wood varied. One man asserted that merely laying a shaving on the back of his hand would produce a sore place. The injurious effects here seem to disappear quickly. Exhaust ventilation is applied, but there is a tendency to give up the use of the wood.

Isolated cases of illness have been ascribed to working teak and olive wood. In Sheffield the following are held to be irritating: ebony, magenta rosewood, West Indian boxwood, cocos wood. Some kinds of mahogany are said to affect the eyes and nose.

Use of methylated spirit in polishing furniture is said to lead to injury to health although not to set up actual poisoning. Lead poisoning can occur from the sand-papering of coats of paint applied to wood.

In impregnating wood with creosote and tar the effects on the skin noted in the chapter on Tar are observed.

TEXTILE INDUSTRY

In getting rid of the grease from animal wool carbon bisulphide or benzine may be used.

The process of carbonising in the production of shoddy may give rise to injury to health from acid fumes. Lead poisoning used to be caused by the knocking together of the leaden weights attached to the Jacquard looms. This is a thing of the past, as now iron weights are universal.

Opportunity for lead poisoning is given in the weighting of yarn—especially of silk with lead compounds.

In bleaching use of chlorine and sulphur dioxide has to be borne in mind.

In chemical cleaning poisoning by benzine may occur.

In dyeing and printing use of poisonous colours is lessening, as they have been supplanted by aniline colours. On occurrence of aniline poisoning in aniline black dyeing see the section on Aniline. Use of lead colours and of chromate of lead are dealt with in special sections.

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:

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: