Document GD02vqMxn8EBVVoY4m7b8exq

ST INTERNATIONAL LABOUR OFFICE PLAINTIFF'S EXHIBIT DOW-1601 OCCUPATION AND HEALTH Encyclopaedia of Hygiene, Pathology and Social Welfare, Studied from the Point of View of Labour, Industry and Trades SUPPLEMENT This Cover contains the following Brochures: 1. Allergy and Occupation. 2. Asbestos. 3. Beryllium (Glucinium). 4. Pneumoconiosis. 5. Silicosis. For Terms of Subscription, see Page 2 of Cover GENEVA 1938 - -*3 - : ' **!?/. '" ST0852447 PREFACE The first brochure of Occupation and Health, an "Encyclopaedia of Hygiene, Pathology and Social Welfare ", prepared in collaboration with 95 scientific experts from 16 countries, was issued by the International Labour Office at the beginning of 1925. The complete series of brochures composing the Encyclopaedia, which were issued at intervals over a space of several years, was eventually published in the form of two volumes, the first appearing in 1930 and the second in 1932L In a few cases it was possible to revise the articles before their reissue in volume form, in order to take account of develop ments which had occurred in the interval following their first publication in the brochure edition. More often, however, it was impossible, owing to technical exigencies connected with printing, to do more than bring statistics up to date, and--in the case of a small number of articles only--the patho logical data. While it cannot be said that the Encyclopaedia has in any way lost its practical value by lapse of time, it must be recognised that, after an interval of about twelve years, it calls for revision and extension in the light of subse quent progress. Account must be taken of certain new processes, more especially those utilising some quite recently introduced products, which involve risks for the workers engaged in them and necessitate suitable methods of prevention. There are also certain processes and products to which only a summary reference was possible in Occupation and Health, but which since its publication have undergone such extensive development that they require more ample treatment. Again, there are conclusions based on new conceptions and fresh research, with consequent changes in occupa tional pathology, and there are results obtained by the application of certain measures of prevention or of certain legislative measures, of which it is highly important that knowledge should be disseminated. The International Labour Office therefore decided in 1935 to publish a " Supplement " to the two original volumes. Members of its Correspon dence Committee on Industrial Hygiene gave their support to the project, 1 International Labour Office: Occupation and Health. Vol. I, 999 pp'; Vol. II, 1310 pp. ST0852UU8. --2-- and promised their assistance. Various circumstances have so jar delayed the realisation of the scheme, but the Office is now happy to be able to launch the first instalment of the Supplement. The Supplement will appear in instalments of several brochures, each brochure being devoted to one complete article. A special loose-leaf binding cover will be offered to subscribers to the Supplement, in which the brochures may be arranged in alphabetical order for ease of reference, and for preservation. In compiling the two original volumes, the success of which has encouraged the Office to carry its work in this field one stage farther, the Office had the advantage of the assistance of many scientific authorities and experts on the subjects'treated. In preparing for the publication of the Supplement, it once more appealed to experts for their collaboration. The response has been no less encouraging than before, and it is largely due to the invaluable aid of these collaborators that the Office is now in a position to make this farther contribution to the diffusion of knowledge requisite for the safe guarding of the life and health of the workers. ST08524U9 ASBESTOS French: Amiante. -- German: Asbest. -- Italian: Amianio. -- Spanish: Amianio. Asbestos, although known to the an cients as a Bcientino curiosity since they were able to make a non-inflammable cloth from a substanoe believed to be of vegetable origin, had no commercial im portance until the last quarter of the nineteenth century. Then the unique fire-resisting and insulating properties of the minerafbegan to be exploited, and thereafter the expan sion of the industry has been remarkable. The multifarious uses which are found for asbestos at the present day would have amazed the pipneers of the industry. The fibrous minerals commercially known as asbestos are silicates, the silica being combined with metallic bases, mainly magnesium or iron and, to a less extent, calcium sodium or aluminium. The term is a collective name applied to a variety of silicate minerals which differ from each other in chemical composition and physical properties but resemble one another in their finely fibrous nature and the flexibility of the fibres. For practical purposes, all that goes under the name asbestos in commerce is either fibrous serpentine, or a fibrous mineral of the hornblende group, of which the most important are crocidolite, amosite and tremohte. Seipentine asbestos or chrysotile is essentially a hydrated silicate of magnesium, containing little iron and almost no calcium. The hornblende varie ties contain less magnesium and usually more calcium, aluminium and iron--cro cidolite and amosite being mainly silicates of iron. The field of utility of asbestos products has rapidly expanded and to-day is very large: new uses for asbestos are being constantly found. The mineral, the yam, or the fabric composes, or is incorporated in, a vast number of articles, ranging from matches to filter pads, from paints to roofing tiles, from nigh pressure jointing to electrodes, and from brake-linings to insulating (electric, anti-noise) and fireresisting materials in great variety. As mentioned above, varieties and grades of asbestos differ widely in their ohemical and physical qualities, and these considerations carry great weight in the choice of an appropriate grade of raw material for the purpose in view. Asbestos fibre varying in quality is of world-wide distribution, but over two-thirds of the world production of commercial fibre is derived from Canada, Rhodesia, South Afrioa, U.S.S.R. and Cyprus. About four-fifths of tne world's produc tion of asbestos is unsuitable for spuming, and it is the discovery of industrial uses for these very short Imres and the dust like waste which has been responsible for the phenomenal expansion of the industry as a whole. Extraction Hitherto asbestos has been got almost entirely by open-pit quarrying,but under ground mining will have to be resorted to in increasing extent in the future in many properties. After the mother rock containing the veins of asbestos fibre has been drilled and blasted, the loose long fibre together with adherent small pieces of rook is gathered up and sent to the cobbing shed, where, after drying, it is dressed (cobbed) by hand, freed from adherent rock, graded, screened, and then bagged ready Tor the market. This " orude ''fibre still contains a proportion of rock, dust, and short fibre useless to the spinner, whioh is removed in the preparatory processes in the factory. The broken material in the quarry after the removal of the crude fibre, where this is done, consists of rock containing the shorter fibre and still finer useful material, and barren rock. The former is sent to the mill for mechanical treatment, and the latter is dumped. All grades of fibre other than those sold in the " crude " form, are produced mecha nically in the mills. There the objeot is to extraot as much fibre out of the rock as possible, while avoiding breaking up the fibre (and thus reducing its value) by unnecessary operations. This is done by a series of orushing I.L.O.: Occupation and Health (January 1838) i ST0852450 ASBESTOS operations, at the same time opening or fluffing out the fibre and screening out the useless sand. The fibre is collected by means of air suction at each stage, graded, cleaned and bagged. The asbestos so produced is classified under an agreed defined system into " crude asbestos " and u milled asbestos". Crude asbestos consists of the hand-selec ted cross-vein material in its native or non-fibrous form. Milled asbestos consists of all grades produced by mechanical treatment of asbestos ore. These two classes are further subdivided into nine standard groups. Crude asbestos is graded into two groups (1 and 2) and milled asbestos into seven groups (3 to 9), the determining feature being length of fibre. In the case of milled fibre further classification is made by means of the standard testing machine. This machine, of standard dimensions, comprises four boxes superimposed one on the other, the bottoms of the first three boxes from above downwards being wire screens of standard dimensions and progressively finer mesh: the lowest box retains the fine material which falls through the three screens. A weighed sample of asbestos (16 ounces) having been placed in the top box, the machine is mechanically agitated in a standardised method for exaotly two minutes, and the asbestos remaining in each box is weighed. In this way the proportion of longer and shorter fibres m the sample is ascertained. The more fibre retained in the first box and the less fibre in the lowest, the higher the grade and the greater the value of the asbestos so tested. In this way the seven groups of milled fibre are further subdivided into a number of grades. Thus in group No. 3 (spinning and textile fibres), there are seven stan dard grades ranging from the specification of 8---6--1--1 (minimum) for the top grade down to specification of 0----6--2 (minimum) for the lowest grade in this group when tested in the above way. ABDestic or asbestine is a by-product from the mills in the nature of a residue containing a very low percentage of short fibre. Manufacturing Processes The asbestos, whether crude or milled, is now ready for dispatch to the factory. For textile purposes only the longer and better fibre comprised in the standard groups 1-3 (crude and spinning grades) are used. Any of these alone, or blended with each other, or blended with cotton fibre, may be spun into yam. Asbestos suitable for this purpose has to be crashed, if in the crude state, and in all cases u opened " or " flberised " before it is ready for carding. Separating (to remove iron) and sieving follow crushing, but precede opening. The subsequent carding, doubling, spin ning, and weaving processes proceed broadly as in the case of other textiles, but with essential modifications and res trictions caused by the: different physical characters of the asbestos fibre. Asbestos yarn is woven into cloth for insulation, mattress coverings, filtering material,fire curtains, fire-resisting clothing etc. Also, woven material is manufactured for belting for conveyors, brake linings and insulating tape. Asbestos millboard and paper, and asbestos cement sheets, tiles, pipes etc. are made from short fibre mixed with other materials. Asbestos may be also made up with rubber for use as jointing, with bitumens for switchboard panelling, with synthetic resins, and with paints for a variety of purposes. An important section of the industry is that engaged in the production of asbestos insulating materials. These include fiberised asbestos; "85 per cent, magnesia " (the remainder being asbestos fibre); mattresses made of asbestos cloth and filled with asbestos fibre, or " magnesia " or with other material; insulating compo sitions or plasters containing asbestos fibre and a variety of other materials, flberised asbestos stiffened into thick sheets or moulded into shaped slabs or sections, and " air cell " insulating material built up from asbestos paper. There are many other valuable uses of asbestos in manufacturing processes which need not be detailed here. Risks to Health All manipulation of asbestos fibre, by hand (as in sack filling or emptying, blending, sweeping and shovelling) or mechanically, produces dust which, if uncontrolled, is often in dangerous con centration. The inhalation of this dust over a period of time results in the develop ment of a fibrosis of the lungs, a progressive replacement of the essential active func- 2 ST085245 I asbestos tioning tissue of the lungs by inactive and useless fibrosis or scar tissue. The disease produced, asbestosis, is therefore in the same category as silicosis, which it re sembles in some respects while differing considerably in others. Since asbestos has been of commercial importance for scarcely fifty years, asbestosis is a modern disease. In contrast with silicosis we cannot trace the history of the baneful effects of the dust backwards over very many years. The first recorded case of asbestosis was that of a patient of Dr. Montague Murray who died in 1900 in the Charing Cross Hospital, London. Post-mortem examination revealed extensive diffuse pulmonary fibrosis with no evidence of pulmonary tuberculosis. The records of this case together with the pathological specimens are still preserved. This man, aged 34 at death, had worked with asbestos for some fourteen years and stated that of the ten men working in the cardroom when he commenced, he was the only survivor, all the others having died at ages round about 30. Little more was heard for a number of years concerning the effects of asbestos dust on the lungs except isolated reports in England and France of high mortality among asbestos workers, ana a note by Marchand and Riesal of the presence of unusual bodies in the lungs of an asbestos worker. This paucity of information was due to various causes. At that time the investi gation and prevention of silicosis was occupying the attention both of Govern ments and of private investigators: the use of radiography in the diagnosis of diseases of the lungs was in its infancy ; and the industry was small as regards the number of workers exposed to appreciable risk. Moreover, every new discovery emphasised the importance of silica in the free form as the predominant factor in the production of pneumonoconiosis. Thus the real and accepted importance of free as opposed to combined silica in this respect tended to obscure the possi bilities that some at least of the silicates might be equally harmful. Although, for these reasons, enquiry in 1910-11 by the Factory Department of the British Home Office both in Great Britain and in Canada failed to produce evidence of a risk from the dust sufficient to necessitate scheduling processes in the industry as dangerous, the Department decided that suppression of the dust evolved in the more dusty processes was required. From that date, therefore, in Great Britain, active measures, although inadequate by present standards, were taken to suppress dust in the more dusty processes of the industry. In 1924, however, the matter was raised 'n by the publication of a note by r E. Cooks concerning the death of an asbestos worker, the result, in his opinion, of extensive pulmonary tuberculosis, to gether with a diffuse pulmonary fibrosis which he ascribed to asbestos dust. This care was fully described by Cooke and Stuart McDonald in 1927. A few weeks later H. E. Seiler drew the attention of E. R. A. Merewether to an asbestos worker in whom he had found signs of a diffuse pulmonary fibrosis with no evi dence of tuberculosis, and further investi gation established the absence of any infective or occupational cause other than asbestos duBt. Thereupon in February 1928 a compre hensive enquiry in Great Britain waB undertaken and the results of this enquiry, which was completed in October 1928 and published in 1930, established the presence of a serious risk in the industry. In the United States and Canada the Industrial Health Service of the Metro politan Life Insurance Company carried out a similar survey between October 1929 and January 1931. Lanza, MacConnell and Fkhnel published the findings in 1935. These, together with the valuable study by Fulton, Dooley, Matthews and Houtz, published in 1935, are the only general surveys of the industry. In Italy, Lovisetto published in 1930 the results of an enquiry, and G. Mussa the results of clinical and radiological examinations. Germany possesses valuable data rela tive to asbestosis based on clinical and laboratory research. It suffices to mention the works of Baader, Gerbis (1931), Beger (1933), Beintker (1934), Alwens, Koppenh6fer (1935). etc. Essential Features of Asbestosis Asbestosis, the pulmonary fibrosis of asbestos workers, is insidious in its onset, irregular in its course, and variable in its mode of termination. It 'is helpful to visualise the disease as the slow growth of fibrous tissue (scar tissue) around the bronchioles or smaller air tubes of the lungs and between the air cells, wherever 3 ST0852452 ASBESTOS the inhaled dust comes to rest. In contrast to silicosis the former is the important site of deposit of asbestos in the lungs, as was shown by Gardner and Cummings. While new fibrous tissue is being laid down like a spider's web, that deposited earlier gradually contracts. This fibrous tissue is not only useless as a substitute for the air cells, but with continued inhalation of the causative dust, bv its invasion of new territory and consolidation of that already occupied, it gradually and literally strangles the breathing tissues of the lungs. Asbestosis is, of course, essentially a local disease and therefore it is only when the fibrosis has obliterated that reserve of lung tissue normally present, and encroached upon the remainder which iB essential for the normal functions of the individual, that symptoms apnear. Then the appearance of undue shortness of breath on any extra effort draws the worker's attention to the fact that his health is not what it should be. The other symptoms of the disease, such as cough, are equally unassuming and are readily ascribed to some common and trivial cause. From this point the progress of the disease is more rapid, since it is now encroaching on the remaining sound tissue of the lungs, already only just sufficient to maintain the worker in his ordinary daily activities. Ultimately, if no acute respiratory affection has preci pitated a fatal termination, a stage is reached when the lungs can do little more than maintain life, and the shortness of breath becomes extreme. To a great extent the outstanding features of the disease are the mechanics effects of this pervasive network of fibrous tissue induced by the retained asbestos dust. This prevents the proper aeration of the blood, becomes an increas ing obstruction to the heart's action, and, in very advanced cases, the traction on the basal masses of fibrous tissue which have consolidated with the diaphragm, pleura and pericardium, still further mechanically embarrasses an already over burdened heart. Lanza and McConnell have drawn attention to the radiological evidence of enlargement of the heart in asbestosis cases. Usually the fatal issue is determined by the onset of some acute infeotion with which the remaining undamaged lung tissue is quite unable to cope: this is commonly a low grade broncho-pneumo nia, but may be a lobar pneumonia, bronohitis, influenza, or less often, a sub acute tubercular infeotion. There is no evidence that the existence of developed asbestosis predisposes to the onset of such acute infections, but if an acute infection does supervene, the presence of the asbestosis senously impairs the chance of recovery. Intercurrent attacks of dry pleurisy, which are partially responsible for the considerable thickening of the pleura which occurs, are common, but usually only cause slight and temporary disable ment. In the absence of intercurrent infec tions the fibrosis may progress to an extreme degree; bronchiectasis, non-tubercular cavitation, and spontaneous pneu mothorax may occur. Ultimately the strain of maintaining the circulation through the partially strangled lungs becomes insupportable and general dropsy with an enlarged liver ushers in death from slow heart failure. The most important single clinical sign is that of diffuse bilateral impairment of the percussion note; this is slight in degree and associated with a slight sense of resistance. It is best elioited by very light and rapid percussion of the back of the chest from apex to base on each side. This impairment of percussion note is more marked on the right side. The auscultatory signs are variable and depend on the extent and nature of the underlying changes in the lungs, on the extent of the fibrosis with its associated pleural thicken ing, the presence of intercurrent affections, bronchiectasis, tuberculosis, and on the degree of compensatory emphysema pre sent. In the majority of cases the respiratory murmur is weakened, generally more on the right side, and often still more at the bases. Asbestosis is a dry disease during most of its course, in the absence of inter- current infections. This attribute, to gether with the diffuse distribution of the impairment of the percussion note, makes it a silent and unobtrusive disease, even more so than in the case of silicosis. The symptoms exhibited also closely resemble silicosis and may pass almost unnoticed by the subject for a considerable period, since so little inconvenience results. Be tween 50 and 60 per cent, of cases of asbestosis complain of slight cough and of undue shortness of breath on exertion, 4 S T 0 8 52453 ASBESTOS and show a duskiness or slight blueness of the lips, which contrasts with the general pallor of the face not uncommonly seen. Diagnosis In common With other forms of pneumonoconiosis the diagnosis of the disease is fraught with diffi culty; particularly is this the case in the early stages, in the late stages when associated with pulmo nary tuberculosis; and in any stage if the disease is implanted on lungs already the subject of emphysema, or if some intercurrent infection has supervened. The fibrosis, although diffuse and bilateral, may he most marked basally and on one side; less commonly the bases may be more or less emphysematous and the maximum fibrosis in the central zone of the lungs; rarely the fibrosis is most marked in the upper portion of the lungs. These factors modify the physical signs presented, as also does the pre-existent state of the chest, and of the lungs upon which the fibrosiB is implanted. Radiographic examination of the chest should never be omitted. A high level of technique is required which should be standardised. A technique which will produce an excellent film and demonstrate adequately silicotic lesions may fail to reveal the asbestos fibrosis entirely, or more often will reveal it only partially; in the latter case the radiographic picture is not only inconclusive, But most misleading. The cause of this lies in the fundamental difference between the two types of fibrosis--the discrete nodular lesions of silicosis and the close network of asbestosis. This difference is reflected in the radiographic appearances of asbestosis, which are revealed typically as a general lack of translucency in the film together with a fine pin-head mottling. This is aptly referred to by Burton Wood as "the ground-glass appearance": asso ciated with it is a shaggy appearance of the cardiac shadow. While, as is the case with silicosis, certain radiographic appearances may be looked upon as typical of the disease, frequently modi fications of, and departures from, the typical picture occur. The radiographic appearances of the developed or advanced stages of the diseases are distinctive, although as Pancoast and Pendergrass maintain, they are not specifio for that dust. Fro. l. -- Developed ssbestosls. Fio. 1 bij. -- Lung section (asbestosis). Radiograms of asbestos workers are very puzzling--more so than in the case of sihcoBis--when it comes to assessing the degree of asbestosis present, parti cularly in the earlier stageB and also in 5 ST 0852454 ASBESTOS women, owing to the shadows caBt by the breast tissue. It is of the greatest value in the diagnosis of asbestosis to possess or to have access to a collection of Fio. 2. Silicosis. absolute certainty on either physical examination or radiological examination alone; with the aid of both the pneumono- coniosis can be diagnosed with certainty if present in some degree, although not necessarily to an extent sufficient to . cause either symptoms or any disablement. In very difficult cases where gross tuberculous lesions obscure the picture, then careful investigation of the subject's expo sure to asbestos dust, particularly as to the dustiness of the process engaged in and the length of ex posure, will enable a correct decision to be reached. This latter point--careful study of the actual exposure to asbestos dust in each case--is a valuable aid in several ways, since, owing to the immobility of the asbestos fibres once they are occluded in the smaller bronchioles, it enables an estimate to be formed as to whether much or little asbestos dust is 2ed in the lungs. Whether or little dust is incarcerated in the lungs is of prime importance in coming to a correct conclusion as to the outcome in individual cases, particularly those in which the exposure has been to a dense con centration of dust for between one and two years. In such cases the radiograms will be negative since there has been no time for the fibrosis to develop, but if further radiograms are taken of these cases during the succeeding three or four years, the appearance ana development of the fibrosis can be watched. Fio. 2 fcis. -- Lung section (silicosis). radiograms of cases of asbestosis together with their clinical and industrial histories and the autopsy findings. In the light of present Knowledge, there fore, asbestosis cannot be diagnosed with Pathological Features As already mentioned, the first case of asbestosis in which pulmonary fibrosiB was noted at autopsy occurred m 1900, but the first case in which a full microscopical examination of the lung was carried out did not occur until 1927. Records of this case were published by Cooke and Hill. and McDonald. The pathological changes in the lungs may be considered under three headings: (1) The alterations which take place in the asbestos fibre after it has reached the lungs; (2) The reactions of the lung tissue; and (3) Complications and Bequelae which follow. 6 ST 0852U55 A8BI8T0S The asbestos fibre, as found in the lengths, the shortest being about the length respiratory passages of the workers, is a of a tubercle bacillus, the longest extend highly retractile, fine, elastic rod, gener- ing aoross the whole field of the micro - \ ally smooth but occasionally showing a scope. Short forms are the commoner sharp saw-like edge, and ends broken at ana naturally are more likely to penetrate varying angles. Tne fibres are of various to the deeper recesses of the lung. The 7 ST 0852456 ASBESTOS , diameter of the fibres has not yet been determined, since they appear capable of splitting longitudinally into finer and finer constituent fibres, almost indefinitely. Small bundles or sheaves are quite com mon. In the lung these fibres become coated with a colloidal yellow pigment which in the course of time becomes crenated to form irregular segments, giving the appearance of minute crustaceans. These ouriously shaped bodies were first noted by Marchand and Riesal, in Germany, as early as 1906 and, later, by Fahr and Fsioel in 1914, but the latter was unable to decide whether they were a crystalline product of haemoglobin or whether they were a direct result of dust inhalation; no further attention was called to them until 1927 when they were described by Cooke and Hill and McDonald, in Great Britain. The lastnamed suggested that they were almost certainly a product of the asbestos. Gloynb finally showed the asbestos fibre lying in'the centre of the body by dissol ving the colloidal coating with concen trated Bulphuric acid whilst under darkground illumination. These bodies have never been found in the original asbestos dust *. > Baoia (1933) has made a thorough histological and optical study of asbestos bodies. According to this author, the metallic element of the molecule of hydrated magnesium silicate Is dissolved by the acid fluids of the body, leaving a silicic acid shell. The form of the needles and their power of double refrac tion remains Intact. The asbestos body Is subse quently. formed by absorption of proteins by the needles of asbestos and subsequent coagulation In the form.of gel. The silicic acid from the shell of the asbestos needle becomes dispersed In the proteld sheath of the asbestos body and becomes gradually disintegrated. There then occurs resorption by the body fluids of the proteld mass containing the silicic acid. Oranulous bands of ferric oxide Impart to the asbestos bodies their brownish colouring. KopphnhOvkk (1935) considers that the sheath of the asbestos bodies Is not of a proteld nature and opposes Baoxa's theory as to the formation and destruction of the asbestos bodies. Sunnrus and Bronx* (1937), In a detailed study of asbestos bodies contained in the lungs of a worker who died of asbestosls, arrive at the following con clusions In regard to the mechanism of formation of the asbestos bodies. The organic substance of the latter Is composed of proteld matter. The most important element--to per cent.--of the shall of the asbestos body is Iron oxide. The inorganic part of the shell does not come from the Inhaled dust, but Is of endogenous origin, coming from the body and principally from products derived from the blood pigment. In the light of this theory, the formation of asbestos bodies u not essentially connected with the outbreak of fibrosis. A causal relation between the two processes Is perhaps doubtful In view of the fact that various authors have found these bodies In lungs of persons not suffering from asbestosls, and even In lungs free from fibrosis. On the other hand, it Is well known that the formation of asbestosls fibrosis should be connected with the presence In the lung of asbestos needles and their action on the pul monary tissue. On the basis of Interstitial localisa tion of the fibrosis at the outset and Its later extension The tissue reaction to the asbestos fibre is dependent on at least two factors: (1) The sharp, needle-like shape of the fibre which, for practical] pur poses, is indestructible, and (2) The siliceous nature of the fibre. The fibres are for the most part held up at the distal end of the respiratory bronchioles and in the alveolar ducts. Here a cellular reaction takes place con sisting of the accumulation of large pha gocytes and the production of a charac teristic cell, known as the asbestosis giant cell, which, like other foreign body giant cells, is probably not a cell but a collec tion of partially degenerated phagocytes. As the disease advances the lymphatics in the neighbourhood become blocked. Lastly fibrous tissue is formed round the affected portions of the air passages, the blood capillaries and venules, the inter lobular septa of the lung and in the pleura. The fibrosis thus produced is diffuse and readily distinguishable from the nodular fibrosis produced by free silica. Meanwhile the asbestos fibres become coated with a golden-yellow pigment which contains iron and is believed to be derived from blood proteins, to form the typical asbes tosis bodies referred to above. It is not known how long all these changes take to bring about, but Gardner and Cum mings have shown that in experimental animals small asbestosis bodies appear at the end of two months but fibrosis in the walls of the bronchioles was not noted until the end of 500 days. At the end of about two years the disease can be recognised to those parts of the lung most closely alTected by respiratory movements, there may be accepted as plausible the theory of those authors who consider mechanical Irritation and the Injuries caused by the long rigid needles as a factor In the formation of fibrosis. The distribution of the fibrosis, moreover, seems to justify the hypothesis which accords a primary Influence to respiratory movements on the migration of the large asbestos needles in the lungs. Lynch (1937) In an account of the mechanism of formation of * asbestos bodies * refers to the presence of similar bodies which he designates ` silica bodies " found In silicosis with particular mention of their occurrence In a case of typical nodular fibrosis. He states further that similar formaUons have been noted In the lungs of coal workers (Tylicotx and Dun*. Cooks) as well as In the lungs of a consider able number of subjects who died of heart failure (particularly cases of rheumatism and arterio sclerosis) without exposure to dust. The Iron content and seeming common connection with pul monary congestion and the local liberation of blood Iron raises the question as to whether the Iron of the asbestos body may not be so related at least In part, and whether congestion may at least favour produc tion of all such bodies (asbestos bodies, silica bodies, and similar formations). 8 ST0852U57 A8BSSTOS by the naked eye. It is probable that the disease takes longer than this to develop in man--at any rate to an extent sufficient to cause radiological and clinical signs. When the lungs are examined by the naked eye after death they are seen to be large and densely flbrotic, and the pleura covering them thickened with plaques of old pleurisy. Often the lung is completely adherent to the chest wall, and in advanced cases to the diaphragm with the formation of a thick and extremely dense layer of fibrous tissue. This anchoring of the lungs particularly to the diaphragm together wth the general increase of fibrous tissue in the lungs which makes them firmer than normal is the probable explanation of a curious clinical sign sometimes seen. E. R. A. Mxrkwxthxr noted that in some advanced oases the apices of the lungs may be easily seen rising in the sunken supra-clavicular areas with expiration, ana descending with inspiration. On cut surface the characteristic appear ance is that of dense, blue-black polygonal areas of asbestos, cellular debris ana pig ment, corresponding to the secondary lobules of the iung and surrounded by thick bands of inter-lobular connective tissue. Generally there is a reddened background of terminal bronchopneumo nia in the less affected portions of the lung. There are few naked eye signs of disease elsewhere. Of the complications and sequels of pulmonary asbestosis four are outstanding: (1) Purulent bronchitis; (2) Bronchopneumonia; (3) Pulmonary tuberculosis, and (4) Emphysema, with occasional rup ture of emphysematous bulls caus ing spontaneous pneumothorax. The number of cases of the latter so far described is small and it is not yet estab lished that there is any aetiologies! connection between the two diseases. The purulent bronchitis may be of long standing. The bronchopneumonia is prac tically always a late event, and recovery very rare. The pulmonary tuberculosis is chiefly of the caseous type with little or no sign of repair and the emphysema compensatory to the fibroBis. In addition to these four main complica tions may be noted two which are less common i - (1) Dilatation of the bronchial tubes resulting sometimes in what iB known clinically as dry bronchiec tasis, and (2) Carcinoma. Fio. b. -- Infra-red photomicrograph* of the aebestMla lung. Bridge and Henry have proposed that cancer, in order to be classified as of industrial origin must fulfil the following two conditions: (1) that the incidencerate in the occupation under review should exceed that in the general population to a significant extent, and (2) that in the occupation concerned there should be sufficient association of a worker with a substance proved experimentally to 9 ST 0852U58 ASBESTOS have carcinogenic properties. These two postulates cannot yet be regarded as having been fulfilled in the case of the Fio. 6. -- Lang lection stained with haemitoxylln, eosln, and Tan Oleaon, ibowing fibrous tissue surrounding aibutoi bod lea. Fio. 7. -- Section of lung, unstained, showing asbestos bodies. asbestos industry, but there is sufficient evidence to warrant careful observation in the future. The Problem of Asbestos Dust Within certain high and low limits, the concentration of asbestos dust in the air of workrooms iB the determining factor in the onset of the disease and also, within limits, concentration of dust and length of exposure determine the incidence rates in different processes in the industry. Exposure to asbestos dust for less than five years can result in the develop ment of a degree of asbestosis sufficient to oause death. Commonly, however, cases of definite asbestosis are not disco vered on examination within five years of commencing work, although a few are found. Among those worlSng who have been employed for between five and ten years in the absence of preventive measures the incidence rate is appreciable, and after ten years of such employment a steep rise in the incidence rate occurs. The incidence rates for the periods of employment 0-4 years, 5-9 years, 10-19 years, ana 20 years and over, amongst 1,512 workers examined by the British Silicosis and Asbestosis Medical Board were proportionate to the figures 1, 5.6, 30.4, 53.2. Although the incidence rate amongst those with lees than five years exposure is bo low, Buch exposure may be by no means negligible. The faot is, as suggested above, that* work in a dense concentration of asbestos dust over a comparatively short period will lead inevitably to the develop ment of a profound fibrosis, provided that the worker lives long enough for it to develop. As Gardner and Cvmminos have shown, the fibrosis takes time to appear, in fact there is a lag of some five hundred days before microscopical signs are de monstrable; it is much longer before the fibrosis matures and clinical and radio logical signs are apparent. Correlation of the facts concerning particular cases of asbestosis with those concerning the relative dustiness of the processes at which they worked leads to the conclusion that this " period of maturation " of the fibrosis is not reduced below a certain minimum period, however high the concentration of duBt in the air breathed may be. Similar considerations also show that below a certain concentration, develop ment of a disabling degree of asbestosis will not occur within the space of an average working lifetime. It appears, therefore, that a certain minimum " fibrosis-producing amount ", as it may be called, of asbestos dust must be trapped in the lungs in order to cause a disabling or serious amount of fibrosiB, and also that a certain " maturation period " must elapse before that amount of fibrosis is developed. Fatal cases of asbestosis have resulted from exposure as short as two years or 10 ST 0852459 ASBESTOS even a little less, although the fatal issue may be postponed for many years. It is important to consider What is the amount of dust which will produce this result, or conversely, what is the amount of dust which, from the practical point of view can be inhaled witn impunity. Efforts are being made, notably by American investigators (W. B. Fulton and others), to establish in terms the concentration of dust in the air whioh can be permitted with safety *. In Great Britain the problem has been approached from a different angle, that of determining what rocesses are safe rather than an exact gure for concentration of dust. E. R. A. Meriwether came to the conclusion " that in order to prevent the full develop ment of the disease among asbestos workers within the space of an average working lifetime, it is necessary to reduce the concentration of dust in the air of workrooms to a figure below that pertain ing to spinning at the time over which these cases were exposed ". Particulars of cases seem to show that with exposure to high concentrations of dust the minimum period of time which must elapse between the commencement of exposure and the production of a serious degree of asbestosis is approximately seven years--made up of the period of exposure during which the fibrosis-producing amount of dust is taken into the lungs ana the .maturation period during which the fibrosis develops--these periods, of course, overlap. This period of approximately seven years, " the asbestosis production period", as it may be called, is the minimum, and few cases mature in this period; in succes sive years, however, depending on the dustiness of the process engaged in, more cases mature. In the more dusty processes, in the absence of adequate reventive measures, the asbestosis prouction period is commonly eleven years. When aBhestosis of serious extent has matured the worker is unduly short of breath on any extra exertion, has a little oyanosis of the lips, and also a little dry oough mostly in the mornings. He finds himself disinclined to climb stairs or walk up hills, but still remains at work and usually is not anxious about the state of his health. The amount of disablement produced is surprisingly slight for a number of years. This is partly due to the character of the disease and partly to the nature of the work which, in the majority of processes in the industry in whlcn there is a risk of asbestosis, does not involve much physical exertion. Those affected may, and often do, continue at work with occasional inter missions latterly, due to exacerbations of bronohitis etc., until the condition is far advanced, although increasing inconve nience from shortness of breath iB expe rienced. Usually these casuc cease work a year or more before death, but sometimes a terminal bronchopneumonia, or other acute infection, commences while they are still at work, and there is no long period of invalidism. It is remarkable to what extent the lungs can be affected by asbestosis and yet life in a fair degree of comfort remain. Tbe reserve is, however, so slight that theaddition of any burden to the system in the form of a disturbance of health which would only slightly inconvenience a normal person, may overcome the remaining re sistance ana precipitate a fatal outcome! For these reasons and from consideration of the features present in the recorded fatal cases, the view must be accepted that the existence of even a moderate degree of asbestosis is a serious and ever present potential risk to life. Since a worker with developed asbestosis may still remain at work ana be little con cerned as to the state of his health, the question may well be asked u Is asbestosis a serious disease ? ", To this question, unfortunately, the answer is emphatically " yes ". Asbestosis and Tuberculosis i The Industrie! Hygiene Division of the National Institute of Health (united States) has examined (1937) 543 persons In asbestos textile plants. An analysis of data shows that the maximum concentra tion o( asbestos dust to which workers may be exposed without contracting asbestosis Is In the neighbourhood of 5 million particles per cubic foot and It was determined by appropriate technical measures of control that the dust concentration could be reduced to less than 2.3 million particles per cubic foot. Proof of this is now not difficult to find, as examination of data from the known fatal cases and comparison with similar data concerning fatalities from silicosis provide ample evidence. Fatalities from asbestosis and asbestosis with tuberculosis have now been reported from a number of countries. Of these the British figures are 11 ST 0852460 asbestos the most complete, since the disease has been oompensatable sinoe 1 Jane 1931. The following figures are abstracted from the Annual Report of the Chief Inspector of Factories for 1935. TABLE 1 Disease Duration or Num ber Aver age employment in yeurs of deaths at death Lon gest Shor Aver test age SUIoosls . . . 311 33.8 62.0 2.3 35.1 8Illcols with tuberculosis . 3S1 52.4 67.0 2.0 31.7 Asbestosis . . -Asbestosis with tuberculosis . 62 *1.9 27.0 1.5 12.4 30 37.1 29.0 0.S 9.5 Table 1 gives particulars of 702 deaths from silicosis or silicosis with tuberculosis and of 82 Trom asbestosis or asbeBtosis table 2 It will be observed that: (1) The average duration of employ ment in the asbestos industry suf ficient to cause a fatal degree of asbestosis was 12.4 years as com pared with 35.1 years for all cases of silicosis. The actual average length of exposure to asbestos dust was, however, still less. (2) The shortest length of exposure to asbestos dust which ultimately caused death from fibrosis of the lungs was 1.5 yean. (3) Asbestosis is comparable with the most serious silicosis risks with respect to length of exposure which will cause a fatal degree of fibrosiB. (4) Although the numben in the as bestosis group are small it will be noted that m 36.6 per cent, the disease was accompanied by tuber culosis, while in the silicosis group 55.7 per oent. were accompanied by tuberculosis, suggesting a less close association between asbestosis and tuberculosis than is the case with silicosis and tuberculosis. Disease Duration Num ber of deaths Aver se tge at death of employment In years Lon Shor Aver gest test age Pottery : Silicosis. . . 159 58.0 82.0 2.8 39.2 Silicosis wltb tuberculosis. 164 54.1 07.0 5.0 36.4 Sandstone: Silicosis. . . 78 58.5 57.0 9.0 38.3 SUIoosls wltb tuberculosis. Grinding or me 68 53.9 53.0 10.0 35.3 tals: Silicosis. . . SUlcosls wltb 26 56.1 56.0 18.0 34.3 tuberculosis. Sandblasting: 73 52.1 52.0 2.8 31.5 8illcosls. . . SUIoosls wltb 15 44.5 20.0 4.0 10.7 tuberculosis. 36 44.4 20.0 2.0 8.4 Manufacture of scouring pow ders: Silicosis . . . Silicosis wltb 8 34.7 37.0 2.3 9.2 tuberculosis. Miscellaneous: 2 33.5 10.8 2.0 6.4 SUlcosls . . . Silicosis wltb 25 53.3 45.0 6.0 22.5 tuberculosis. 28 49.9 50.0 9.0 25.6 with tuberculosis. In table 2 the cases of silicosis and of silicosis with tuberculosis are distributed according to the industries concerned. Further confirmation is found in the after history of the 95 cases of asbeBtosis and the 5 cases of asbestosis with tuber culosis found by E. R. A. Merewkther in his original enquiry in 1928. Of these 100 cases, although a number have mi grated from the industry and have been lost sight of, 23 are known to have died, 12 from asbestosis, 9 from asbestosis with tuberculosis, and 2 from other conditions in both of whom a considerable degree of asbestosis was found on autopsy. Of the remainder a number are partially or wholly disabled on account of the disease. As mentioned previously, the risk to life associated with asbestosis is a complex one. Primarily the fibrosis and the re sulting mechanical embarrassment of the pulmonary circulation develop in step with each other. The supervention in an indi vidual with asbestosis, therefore, of any disease which adds to this strain brings with it a greater risk to life than would be the case in a normal person. Amongst such diseases, infections of the respiratory tract, and especially bronchopneumonia and tuberculosis, hold first place. The risk .from tuberculosis requires special consideration because of its ac cepted importance in asbestosis as in silicosis ana because of its infective nature. 12 ST085246 I asbestos The interaction of asbestosis and tuber culous is of moment in determining both the real importance of asbestosis as an industrial risk and also the scope and pro bable effectiveness of projected preventive measures. There are a number of aspects to this relationship which have to be clearly defined ana as yet the data are insufficient. Gardner and Cummings, as a result of their experimental work on guinea-pigs, have established a point of the greatest importance, namely, that a primary tuber culous infection is influenced only to a limited degree by inhaled asbestos and that the tendency to healing by fibrosis is marked. They emphasised the contrast in this respeot between the effect of asbestos and of free silica, with which the tendency was overwhelmingly towards the produc tion of generalised chronic tuberculosis of the lungs and viscera. These same workers found in another group of experiments where the tuber culous infection was implanted on to an existing asbestos fibrosis that the stimu lating effect on the tuberculous infection was more marked than when the infection and inhalation of asbestos were instituted simultaneously, but the ultimate outcome had not yet been observed. They also stated that the combined action of asbestos dust and tubercle bacilli in the lung pro duced more fibrosis than did either agent acting independently. In a subsequent paper, Burton Wood and Gloyne reviewed a series of 100 cases of asbestosis which had been under their observation. In this group they found 30 cases with pulmonary tuberculosis, 21 being active and 9 obsolescent. They pointed out that the group with obsoles cent tuberculosis emphasises the fact that obsolescent tuberculosis in the human is not necessarily reactivated by asbestosis. In the series of deaths analysed above it was noted that asbestosis was asso ciated with tuberculosis in a much lower percentage than was the case with Bilicosis. J. Rush Shull in an analysis of 71 cases of asbestosis notes the presence of tuber culosis in 10, one of which showed a healed miliary tuberculosis. Although it is not possible yet to answer categorically (1) Does the inhalation of asbestos (a) antecedently, (b) coincidently, (c) subsequently to a tuberculous infection favour the development of the tuberculous process or not, and (2) What is the effect of the presence of (a) a slight, (b) a moderate, (c) an advanoed degree of asbestosis on (i) the implantation, (ii) the develop ment of a tuberculous infection, these observations suggest that whatever the added risk to asbestos workers from pulmonary tuberculosis may be (and there appears to be some), it is less than that associated with silicosis. It is worth re cording that in two oases signs of both silicosis and asbestosis have neen found at autopsy, in one of which there was also pulmonary tuberculosis. Preventive Measures The risk from asbestosis in the asbestos industry is no less grave than the moBt serious risks from smcosis in the silicosis producing industries. The preventive mea sures necessary, therefore, will be exten sive and stringent. The essential is dust suppression in all processes to a safe level, which level may be determined by refer ence to a definite concentration of dust in the air of the workrooms or by reference to the amount of dust produced in a pro cess which has been shown to be safe. There are advantages and disadvantages associated with eaoh of these standards, but space does not permit of their discus sion here. In Great Britain the second of these alternative methods was adopted. A Joint Committee of representatives of the Faotory Department of the Home Office and of the Asbestos Textile Manu facturers agreed on a practical standard based on Merewether's suggestion as to the relationship between the safe level of dust concentration and that evolved in spinning processes. This Committee concluded on the evidence then available that u For practical purposes, the conditions arising from flyer spinning1 ci arried on without exhaust under good general conditions may, it seems to the Committee, be taken as the " dust datum "... If, therefore, a particular process appears to give rise to dust in excess of that associated with such flyer spinning, the Committee regard the need for preventive measures as established." i The dust production In ring spinning is above the sale level and the Regulations retjulre the pro vision ol local exhaust ventilation to the process. 13 ST0852U62 ASBESTOS In Maroh 1932 a comprehensive Code of Regulations designed to suppress the dust produced in all processes to at least the level of that " arising from flyer spinning carried on without exhaust under good general conditions " came into force. These Regulations apply the following principles to achieve this standard: (1) Ap plication of efficient localised exhaust ven tilation at dust producing points. (2) Sub stitution of enclosed mechanical methods for hand conveyance and for dusty hand work generally. (3) Effective enclosure of dust-producing machines and plant. (4) Substitution of wet methods for dry. (5) Elimination of certain dust-produoing appliances. (6) Effectual separation of processes to prevent unnecessary exposure to dust. (7) Use of saoks o{ close texture for interna] work in the factory, and cleaning of them by machinery. (8) Efficient cleaning system. (9) Precau tions to prevent dust from asbestos in storage chambers or bins entering the workrooms. (10) Regular examination and testing of ventilating plant; dust settling and filtering apparatus not to be allowed in workrooms. (11) Breathing apparatus of approved type to be provided for per sons employed m certain operations. The Regulations aleo prohibit the employment of young persons under the age of 18 in the most dusty processes. In order to achieve the object of the Regulations problems of ventilating en gineering of the utmost difficulty had to be solved, particularly on the textile side of the industry, where the application of local exhaust ventilation ana other me thods of dust suppression of a high stan dard to operations in which the necessity for it had never been envisaged before, was required. Other preventive measures in force in Great Britain include the control of the disease by periodical medical examination of the workers, by which those unfitted by health reasons are prevented from entering the industry ana cases of asbestosis and of pulmonary tuberculosis are detected at the earliest possible moment. A practical maxim of the greatest value is that every translation of fiberised asbestos in the factory produces dust which, if not controlled, is dangerous. for asbestosis and asbestosis accompanied by tuberculosis for all workmen employed at any time on or after May 1931 In any process specified in a comprehensive schedule. In Germany the Order of 16 December 1986, and in Danzig, the Order of 11 March 1937, grant compensation for terious asbestosis affecting workers coming within accident insurance legislation. In the United States the Law of 26 March 1935 passed in North Carolina provides for compensation of asbes tosis in a certain number of industries K The problem of compensation for asbestosis was considered by the Correspondence Com mittee on Industrial Hygiene of the Inter national Labour Office which, at its last meeting in October 1935, decided to recom mend to the Governing Body the following formula for inscription in the international schedule: "Asbestosis, with or without pulmonary tuberculosis, provided that asbes tosis is an essential factor in causing the resultant incapacity or death " when occurring amongst workers engaged in "industries or processes recognised under national law or regulations as involving exposure to the risk of asbestosis ". The Committee made the further recommendation that " it is advisable to recommend that those countries which so far are without adequate knowledge of the question should cany out in the near future the requisite enquiries and research for determining the extent of the occupational risk involved." Bibliography Beger in Virchow's Archie, Vol. 290, 1933, pp. 280-353. Cooks, W. E. Brit. Med. J., 26 July 1924, p. 147, and 3 Dec. 1937, p. 1024. Fulton W. B.p Dooley A., Matthews J. and Houtz R. L. Dept, of Labour, Pennsyl vania. Special Bulletins, No. 37,1 Oct. 1934 and No. 42, 20 Sept. 1935. Gloyne S. R., in Tubercle, 1929, p. 404; Lancet, 1932, Vol. 1, 1351; Tubercle, 1933, p. 208, 445, 483, 550; 1935, p. 5. Home Office: Report on Conference between Employers and Inspectors concerning Meth ods for suppressing Dust in Asbestos Textile Factories. H.M. Stat. Off. London, 1931. KoppenhOfer in Arch. f. Gew. Path. u. Gew.Hyg. Vol. VI, 1935, No. 1, pp. 38-63. Berlin. Lanza A. J., Macconnell W. J. and Fbhnel J. W. U.S.A. Publ. Health Rep. 4 Jan. 1935. Compensation for Asbestosis Great Britain was the first country to pass special legislation relative to compensation i Among the States which accord compensation lor asbestosis hr blanket coverage, there are some In which the general coverage Law contains special ?revisions concerning asbestosis: Illinois (Law of S March 1930), Indiana (Law of 6 March 1937), Pennsylvania (Law of 1937). 14 ST0852463 ASBESTOS Lynch, K. M. in Journ. Amer. Msd. Assoc., 11 Dec. 1937, pp. 1974-78, Chicago. McDonald S. Brit. Med. J., 3 Dec. 1937, p. 1025. McPhiitiks S. B. /. of Ind. Hyg. and Tox. April 1936, p. 229. Boston. - Msriwethir E. R. A. " The Occurrence of Pulmonary Fibrosis and Other Pulmonary Affections of Asbestos Workers." Jown. of Ind. Byg. May 1930, p. 198 and June 1930, p. 239. ------ " Memorandum on Tuberculosis ". Tu bercle, Noy. 1933, p. 69; Dec. 1933, p. 109. Jan. 1984, p. 152. ------ and Price C. W. Report on the Effect* of Atbettos Dust on the Lung* and Dutt Suppression in the Asbestos Industry. H. MStat. Off., London, 1930. 8hull J. R. Radiology, Sept. 1936, p. 279, Syracuse, U.S.A. Sundius N. and Bygdin A. in Arch. f. Gcw.-Path. u. Geto.-Hyg. Vol. VIII, 1937, No. 1, pp. 26-70. Berlin. Figs. 1 bis and 2 are taken from lung sections stained by E. H. Sarsons, of Bir mingham University, with his modification of Mallory's method. Figs. 8 to 7 are taken from various publica tions by S. Roodhouse Gloyne. Dr. 8. R. Gloyne (London) and Dr. E. B. A. Merewether (Birmingham). 15