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.
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.
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.
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).
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.
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.
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.
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.
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.
In discussing preventive measures against industrial poisoning the deductive method from the general to the particular will be followed. The numerous instances of poisoning mentioned in Part I afford a practical basis on which to formulate general rules before passing on to describe special measures. Technical details will be omitted, as they must be left to the technical expert whose business it is to draw up the plans as a whole and to modify them according to the requirements of individual cases.
In the effort to control industrial poisoning and disease it is necessary to insist absolutely on the concerted action of all concerned. In this co-operation every one is called who through his knowledge and sphere of activity is in a position to assist.
The medical man comes in with his special knowledge of the action of poisons as toxicologist, as practising physician (especially as works surgeon and doctor of the sick insurance society), and also in an official capacity as appointed surgeon or medical officer of health; the technical expert comes in as engineer, as manager, as foreman, and as factory inspector. But above all the interest and active co-operation of employers and employed are needed as well as the organisations of both. That the workers should understand and co-operate is essential for the success of preventive measures, and subsequently it will be shown in what direction this co-operation is most necessary.
To make possible such co-operation interest must be aroused and suitable information and teaching supplied to the parties concerned. Medical men and practical workers require to receive instruction in industrial hygiene, and teaching on this subject should be arranged for in secondary and technical schools. Medical men and others who, as officials and insurance doctors, are brought constantly into touch with industrial workers should have opportunity—by means of special courses and lectures—to keep pace with advancing knowledge in this direction. Beside these there are, as educative organisations, special Institutes of Industrial Hygiene and special hospitals for treatment of diseases of occupation which bring together the patients and the teaching staff and so facilitate pursuit of knowledge and research. A beginning of this kind has already been made by the Industrial Hygiene Institute, Frankfurt a.-Main, and the hospital for diseases of occupation at Milan, showing that the ideas are attainable. International agencies which unite all circles interested in the subject irrespective of profession or nationality in common interchange of thought and discussion are of great significance for uniform development of needful preventive measures; international congresses, often in connection with exhibitions, have given valuable stimulus and have been the starting-point of permanent international societies, unions, and organisations. The significance for our inquiry of these international efforts will be more closely considered in the following pages.
Experience and inquiry in the field of industrial poisoning led to a series of demands which, supported as they were by a general movement for the protection of workers, were soon followed by regulations and legislative action. For a long time efforts have been directed to treat industrial disease and poisoning in the same way as has been done in the case of industrial accidents. The question, however, is attended with much greater difficulty. On the other hand, uniform international regulation of questions affecting prevention of disease is called for both on humanitarian and economic grounds.
The idea of international legislation for the protection of workers was first mooted about the year 1870. The possibility and need of such intervention was much discussed and interest in it kept constantly alive, especially in Switzerland, until the organisations of the workers took up the idea. Several attempts failed. In France in 1883 a proposal of the Socialist party aiming at international agreement on the subject of protection of the workers was rejected. In 1885 (in opposition to Hertling) Prince Bismarck expressed himself strongly against the possibility of such international protection. But the stone, once set rolling, could not be stayed. In the years 1886, 1887, and 1888 the French and English trade unions, as well as the Swiss Federal Council, took up the question afresh. These endeavours at last took tangible shape in the first International Conference for the protection of workers held in Berlin in March 1890. This date remains a landmark in the history of the subject, but not until ten years later—1900—did the Congress held in Paris for the international legal protection of workers lead to the establishment of what had been repeatedly urged, namely, creation of an International Bureau. This was inaugurated at Basle in 1901 and forms the headquarters of the National Associations for Labour Legislation called into being in various countries.
This International Association meets regularly in conference, as in Cologne (1902), Berne (1905), Lucerne (1908), Lugano (1910), and Zurich (1912). The questions raised in the International Labour Bureau, which receives financial aid from a number of States, are fully and scientifically discussed with the object of finding a basis on which to bring into agreement the divergent laws of the different countries. A further task of this strictly scientific institution is the collection and publication of literature bearing on the protection of workers in one and another country, distribution of information, and the editing of reports and memoranda. The question of prevention of industrial poisoning has always taken a foremost place in the programme of the International Association and in the agenda of the International Labour Bureau. At its first meeting a resolution was adopted advocating the prohibition of the use of white phosphorus and white lead, and the Labour Bureau in Basle was instructed to take the necessary steps. Special, if not prohibitive, economical considerations foreshadowed difficulties—all the greater because the matter at issue concerned prohibition of articles playing a part in the markets of the world. Just on that account international treatment of such questions is necessary, since a peaceful and orderly solution can only be arrived at on such lines. International effort endeavours here to press with equal weight on the countries competing with one another commercially, so that in the protection of the workers economic adjustment is sought in order that efforts based on humanitarian grounds shall not at the same time cause economic disadvantages, the aim being to produce general welfare and not merely protection of one class at the expense of another.
Through these international agreements between various countries success in the direction aimed at is hopeful, and indeed to a certain extent—as in the phosphorus and lead questions—actually attained. Thus, for example, Germany and Italy were in a position to enforce prohibition of the use of white phosphorus early, while their neighbour Austria, on account of commercial and political considerations and the conditions of the home lucifer match industry, has only recently decided on prohibition.
As international agreement for the protection of workers is advisable on economic grounds, so also is it reasonable and just from purely humanitarian reasons that workers, without reference to civil condition or nationality, should be equally protected. On this point it is proposed to take a vote and to press only for those reforms which are thoroughly sound and recognised as necessary.
The first step in such a comprehensive attack is precise knowledge of the extent and source of origin of the particular forms of industrial poisoning and disease and the collection of reliable statistics. This suggested the obligation to notify such cases to the proper authorities in the same way as is now done in the case of infectious disease. A motion to this effect had already been passed at the Conference of the International Association for Labour Legislation held in Basle, and a request was made to the Labour Bureau to prepare a list of the diseases and poisonings in question. To them we shall refer later, but a schedule is necessary as a basis to work upon. Yet even when this is done there are obviously great difficulties to be overcome in carrying out the requirement of notification when the aim is kept in mind of collecting complete statistical data for controlling the conditions giving rise to industrial disease. The proposal of the International Association seeks to make notification obligatory on the part both of the medical practitioner in attendance and the occupier, and in connection with this to secure the co-operation of the Sick Insurance Society.[D] The proposal to require the appointed surgeons and surgeons of the Insurance Society to notify all cases is hardly feasible in view of their dependent position. Nor can the obligation on the occupiers lead to the desired result because of their lack of medical knowledge and the fact that by notifying they might be forced to act to their own disadvantage. A successful effort in this direction is recorded in Saxony, where lead poisoning was first made a notifiable disease, and later the general duty of notification of industrial poisoning was prescribed by Order dated March 4, 1901.
| Disease and Industry. (1) |
Reported Cases.[E] | ||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1912. (2) |
1911. (3) |
1910. (4) |
1909. (5) |
1908. (6) |
1907. (7) |
1906. (8) |
1905. (9) |
1904. (10) |
1903. (11) |
1902. (12) |
1901. (13) |
1900. (14) |
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| Lead Poisoning | 587 | 44 | 669 | 37 | 505 | 38 | 553 | 30 | 646 | 32 | 578 | 26 | 632 | 33 | 592 | 23 | 597 | 26 | 614 | 19 | 629 | 14 | 863 | 34 | 1058 | 38 | |
| 1. | Smelting of metals | 56 | 7 | 48 | 3 | 34 | 5 | 66 | 5 | 70 | 2 | 28 | 2 | 38 | 1 | 24 | 1 | 33 | 1 | 37 | 2 | 28 | 54 | 3 | 34 | 1 | |
| 2. | Brass works | 5 | 9 | 1 | 7 | 5 | 6 | 9 | 1 | 11 | 5 | 1 | 10 | 1 | 15 | 5 | 6 | 1 | 3 | ||||||||
| 3. | Sheet lead and lead piping | 6 | 12 | 4 | 9 | 2 | 14 | 6 | 7 | 9 | 7 | 11 | 12 | 17 | 17 | 1 | |||||||||||
| 4. | Plumbing and soldering | 35 | 5 | 37 | 2 | 25 | 1 | 28 | 27 | 20 | 2 | 16 | 4 | 24 | 2 | 21 | 3 | 26 | 23 | 1 | 23 | 9 | |||||
| 5. | Printing | 37 | 32 | 2 | 33 | 4 | 21 | 1 | 30 | 2 | 26 | 3 | 16 | 2 | 19 | 4 | 15 | 13 | 2 | 19 | 23 | 1 | 18 | 2 | |||
| 6. | File cutting | 13 | 18 | 2 | 9 | 1 | 8 | 9 | 2 | 10 | 15 | 12 | 20 | 4 | 24 | 2 | 27 | 1 | 46 | 7 | 40 | 3 | |||||
| 7. | Tinning | 15 | 11 | 13 | 17 | 22 | 10 | 25 | 18 | 1 | 14 | 1 | 10 | 14 | 11 | 10 | 5 | ||||||||||
| 8. | White lead | 23 | 41 | 2 | 34 | 1 | 32 | 2 | 79 | 3 | 71 | 108 | 7 | 90 | 116 | 2 | 109 | 2 | 143 | 1 | 189 | 7 | 358 | 6 | |||
| 9. | Red lead | 3 | 13 | 1 | 10 | 10 | 12 | 7 | 6 | 10 | 11 | 6 | 13 | 14 | 19 | ||||||||||||
| 10. | China and earthenware | 80 | 14 | 92 | 6 | 77 | 11 | 58 | 5 | 117 | 12 | 103 | 9 | 107 | 4 | 84 | 3 | 106 | 4 | 97 | 3 | 87 | 4 | 106 | 5 | 200 | 3 |
| 10a. | Litho-transfers | 1 | 1 | 1 | 1 | 1 | 2 | 10 | 5 | 5 | 3 | 3 | 2 | 7 | 10 | ||||||||||||
| 11. | Glass cutting and polishing | 1 | 1 | 5 | — | 4 | 2 | 3 | 1 | 4 | 4 | 1 | 3 | — | 4 | 8 | 2 | 11 | 3 | 7 | |||||||
| 12. | Vitreous Enamelling | 5 | 19 | 1 | 17 | 7 | 7 | 6 | 4 | 2 | 3 | 4 | 3 | 1 | 9 | 11 | |||||||||||
| 13. | Electric accumulators | 38 | 1 | 24 | 1 | 31 | 27 | 2 | 25 | 1 | 21 | 26 | 27 | 1 | 33 | 28 | 16 | 1 | 49 | 1 | 33 | ||||||
| 14. | Paints and colours | 19 | 21 | 17 | 1 | 39 | 2 | 25 | 35 | 1 | 37 | 57 | 1 | 32 | 1 | 39 | 1 | 46 | 56 | 56 | 1 | ||||||
| 15. | Coach building | 84 | 7 | 104 | 5 | 70 | 6 | 95 | 6 | 70 | 3 | 70 | 3 | 85 | 7 | 56 | 3 | 49 | 4 | 74 | 5 | 63 | 1 | 65 | 4 | 70 | 5 |
| 16. | Ship building | 34 | 2 | 36 | 6 | 21 | 2 | 27 | 1 | 15 | 22 | 1 | 26 | 1 | 32 | 2 | 48 | 24 | 1 | 15 | 1 | 28 | 1 | 32 | 2 | ||
| 17. | Paint used in other industries | 48 | 3 | 56 | 1 | 51 | 3 | 42 | 47 | 1 | 49 | 2 | 37 | 3 | 49 | 2 | 27 | 3 | 46 | 1 | 44 | 1 | 61 | 50 | 5 | ||
| 18. | Other industries | 84 | 2 | 88 | 4 | 47 | 3 | 52 | 2 | 78 | 5 | 56 | 2 | 66 | 2 | 70 | 1 | 53 | 3 | 40 | 64 | 89 | 1 | 86 | 4 | ||
| Phosphorus Poisoning | — | — | — | 3 | 1 | 1 | 1 | — | 3 | 1 | 1 | 1 | — | 1 | 2 | 4 | 3 | ||||||||||
| Arsenic Poisoning | 5 | 10 | 1 | 7 | 4 | 23 | 1 | 9 | 2 | 5 | 1 | 5 | 5 | 5 | 12 | 1 | 22 | 3 | |||||||||
| Mercurial Poisoning | 17 | 12 | 10 | 1 | 9 | 10 | 7 | 4 | 8 | 3 | 8 | 8 | 18 | 9 | |||||||||||||
| Anthrax | 47 | 64 | 11 | 51 | 9 | 56 | 12 | 47 | 7 | 58 | 11 | 67 | 22 | 59 | 18 | 50 | 10 | 47 | 12 | 38 | 9 | 39 | 10 | 37 | 7 | ||
| Wool | 31 | 6 | 35 | 10 | 28 | 3 | 28 | 3 | 18 | 3 | 23 | 3 | 24 | 8 | 34 | 12 | 12 | 1 | 20 | 5 | 12 | 2 | 6 | 4 | 9 | 2 | |
| Horsehair | 7 | 8 | 1 | 6 | 1 | 8 | 2 | 10 | 17 | 4 | 10 | 4 | 7 | 1 | 12 | 4 | 7 | 1 | 10 | 2 | 9 | 1 | 12 | 3 | |||
| Handling of hides and skins | 8 | 20 | 14 | 3 | 18 | 6 | 13 | 1 | 12 | 2 | 19 | 7 | 17 | 4 | 18 | 3 | 12 | 1 | 11 | 5 | 20 | 5 | 9 | 1 | |||
| Other industries | 1 | 1 | 3 | 2 | 2 | 1 | 6 | 3 | 6 | 2 | 14 | 3 | 1 | 1 | 8 | 2 | 8 | 5 | 5 | 4 | 7 | 1 | |||||
My own experience does not lead me to expect much in elucidation of industrial diseases from the Sick Insurance Societies. In Austria they make a statistical return as to the causation of illness to the central authorities. I have myself—in my capacity as an official of the State Central Board—examined these in order to try and gain knowledge of the extent of industrial disease in Bohemia. In spite of the returns drawn up by the district surgeon who visits the factories in question, it was impossible for me to obtain a complete picture of the extent of industrial sickness. The reports only give valuable data on which to base action in particular cases, and from this standpoint I do not under-estimate their value. But so far as the expressed wish of the International Association is concerned they appear to fulfil it, inasmuch as for specially dangerous trades special reports are issued, the Austrian law for sick insurance requiring such industries to institute separate sick insurance funds with separate statistics. Hence, under present conditions, I do not see how the duty of notification will be effective. There remains the endeavour to secure insurance and the right to claim compensation for industrial disease in the same way as is provided for accidents. This point was fully discussed at the eighth International Congress for Workmen’s Insurance held in Rome in 1908. There is no valid ground for granting compensation only for sudden disturbance of health arising in the course of employment by accident or acute poisoning, and withholding it in the case of gradual disturbance of health caused equally by the trade, as the effects of such chronic indisposition weigh often no less heavily on the sufferer. Inclusion of industrial disease in the same category as accident insurance, as indeed has been done in France, Switzerland and Great Britain, has, apart from the fact that it is dictated by fairness and humanity, the advantage of removing existing hardship and of solving doubtful cases. Correct statistics, further, would thus be obtainable for the first time, and the employer by insurance would be freed from the legal proceedings now frequently brought against him for injury due to chronic industrial poisoning. And it seems the more right and just course to institute a general scheme of insurance against industrial disease than to have recourse to an Employer’s Liability Act in this or that case, particularly as the question often arises in regard to a disease which develops gradually—In whose employment was the disease contracted?
Clearly in such a scheme of insurance against both accident and industrial disease only specific industrial diseases would be included, i.e. diseases in which the connection with the industry can be clearly established as due to causes inherent in the industry, and traceable to definite materials used. Such diseases as tuberculosis and the effects of dust inhalation (bronchitis, &c.), which as industrial diseases occur only too often, cannot be called specific, because they arise outside the industry and make decision impossible as to whether or not in a particular case the disease owed its origin to the occupation. In order to determine what should be regarded as specific industrial poisons it was deemed necessary to draw up a schedule. For one such list Sommerfeld (in collaboration with Oliver and Putzeys) is responsible, Carozzi of Milan for a second, and Fischer[F] for a third, published in 1910. Those by Sommerfeld and Fischer are constructed in similar fashion—enumeration of (1) the poisonous substance, (2) the industries in which it is made or used, (3) the channel of absorption, and (4) the symptoms produced. Sommerfeld enumerates the poisons in alphabetical order, noting against each the requisite preventive measures, while Fischer adopts a chemical classification, confining himself to general introductory remarks as to prevention.
Sommerfeld proposes to limit notification to poisoning sharply defined as to the symptoms set up, such as lead, phosphorus, mercury, arsenic, chromium, carbonic oxide, aniline, benzene, nitrobenzene, carbon bisulphide, and nitrous fumes. This simplifies the obligation to notify, but does not dissipate the fears expressed above as to the difficulty, because in the present development of the chemical industries new substances involving new danger to the persons handling them are constantly being discovered, and thus there can be no finality as to which industrial poisonings should entitle to compensation. And if recourse were had from time to time to additions of new substances to the schedule, reliance would have to be placed on experience with regard to each substance added, and thus the actual individual who had suffered would not benefit. Fischer, indeed, acknowledges that any schedule must be incomplete, and emphasises the fact that continual additions would be necessary; otherwise it would be better to refrain altogether from publication of a list. Such lists may be valuable guides, but no sure foundation for insurance legislation. The only possible way to do this is to give as far as possible a correct definition of the industrial diseases entitling to compensation and, in isolated cases, to leave the decision to the expert opinion of competent judges.
Extension of workmen’s insurance to cover chronic industrial poisoning is, however, most desirable in the interest of employers and employed, and also of science. The German accident insurance legislation is especially suited to do this, since the trade organisations direct their attention not only to the prevention of accidents but of industrial diseases also.