Document zdRMmkD7o5EjeJ5Y0V9XBNeEz

FILE NAME: Eagle-Picher (EP) DATE: 1938 DOC#: EP008 DOCUMENT DESCRIPTION: Book Excerpt - Occupation and Health - Asbestos s oH i f ] 40 , ; OCCUPATION AND HEALTH. j . . .Encyclopaedia of H ygiene, P athology and Social W elfare \ - ------ SUPPLEMENT i I Several years have elapsed since the International Labour Olficc published its twn-v.dum<-( Encyclopaedia of Iiulustrial Hygiene (see page \ of this cover), a work which has won whhvprc.i.ij recognition as a standard book of rcfcrcnco on the health hazards of industrial and business life j In the meantime, new discoveries have been made, new processes adopted, and safeguards and remedies applied. j It has therefore become necessary to bring the Encyclopaedia into lino with advam-it^ knowledge and practice. To meet this need, the International Labour Otlicc has decided to publish a Supplement containing such additions and revisions ns arc required to keep the original work abn ust j present-day progress. 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Goddard Limited, 255A, George Street, Sydney. * Australian League of Nations Union (X.S.W. Branch), Savings Bank Building, 14-20 CnsUereagh Street, Sydney. Canada: League of Nations Society (Canada), 124, Wellington Street, Ottawa. Ch i n a : Mr. Ilai-Fong Cheng, 754, Bubbling Well Road, Shanghai; or Commercial Press Limited, 211, Ilonan Road, Shanghai. Great Britain: Brandi Ollice, International Labour Office, 12, Victoria Street, London, S-UM. I ndia: International Labour Ofiico (Indian Branch), .Yew Delhi. I reland: I Messrs. Eason and Sons Limited, 40 and 41.1 Lower O'Connell Street, Dublin. J apan: ! Brandi Oilire, International Labour Office, Sliisei Kuikau Building, Ilibiya Park, Kojimacliiku, Tokyo. Maru7.cn Company Limited (Muruzcti Ivabushiki-Kaisha), G, Nibonbashi, ToroSancbome, Tokyo. N ew Zealand: The Labour Book Room, 126, Vivian Street, Wellington. U nited States: Branch Office, International Labour Office, 734, Jackson Place, Washington, D.C. ASBESTOS French: Amiante. -- German: Asbest. -- Italian: Amianto. -- Spanish: Amianto. rt rtr^frs1m v.'f r r v fXprm v tS^ e X JS>Ht^9KT^`!rf Asbestos, although known to the an chemical and physical qualities, and these cients as a scientific curiosity since they considerations carry great weight in the were able to make a non-inflammable choice of an appropriate grade of raw cloth from a substance believed to be of material for the purpose in view. Asbestos vegetable origin, had no commercial im fibre varying in quality is of world-wide portance until the last quarter of the distribution, but over two-thirds of the nineteenth century. world production of commercial fibre is Then the unique fire-resisting and derived from Canada, Rhodesia, South insulating properties of the mineral began Africa, U.S.S.R. and Cyprus. to be exploited, and thereafter the expan About four-fifths of the world's produc sion of the industry has been remarkable. tion of asbestos is unsuitable for spinning, Tlic multifarious uses which are found for and it is the discovery of industrial uses asbestos at the present day would have for these very short fibres and the dust amazed the pioneers of the industry. like waste which has been responsible The fibrous minerals commercially for the phenomenal expansion of the known as asbestos are silicates, the silica industry as a whole. being combined with metallic bases, mainly magnesium or iron and, to a less extent , calcium sodium or aluminium. The E xtraction term is a collective name applied l \ a . Hitherto asbestos has been got almost variety <: ii<1 miner?! n differ entirely by open-pit quarrying, but under from ea* i. i h* i* in -tiuin ! rompo.-ilion ground mining will have to be resorted to and physic.it p.-'ipertios but inhlo one in increasing extent in the future in many another in their finely fibrous nature and properties. the flexibility of the fibres. After the mother rock containing the For practical purposes, all that goes veins of asbestos fibre has been drilled and under the name asbestos in commerce is blasted, the loose long fibre together with either fibrous serpentine, or a librous adherent small pieces of rock is gathered mineral of the hornblende group, of which tip and sent to the cobbing shed, where, the most important are crocidolite, amosite after drying, it is dressed (cobbed) by and tremolite. Serpentine asbestos or hand, freed from adherent rock, graded, chrysolite is essentially a hydrated silicate screened, and then bagged ready for the of magnesium, containing little iron and market. This " crude " fibre still contains almost no calcium. The hornblende varie a proportion of rock, dust, and short libre ties contain less magnesium and usually useless to the spinner, which is removed more calcium, aluminium and iron--cro in the preparatory processes in the factory. cidolite and amosite being mainly silicates The broken material in the quarry after \ of iron. the removal of the crude fibre, where this The field of utility of asbestos products is done, consists of rock containing the has rapidly expanded and to-day is very shorter fibre and still finer useful material, ` large: new uses for asbestos are being and barren rock. The former is sent to the constantly found. The mineral, the yarn, mill for mechanical treatment, and the f or the fabric composes, or is incorporated latter is dumped. 5 in, a vast number of articles, ranging from All grades of fibre other than those sold matches to filter pads, from paints to in the " crude " form, are produced mecha roofing tiles, from nigh pressure jointing nically in the mills. There the object to electrodes, and from brake-linings to is to extract as much fibre out of the rock insulating (electric, anti-noise) and fire- as possible, while avoiding breaking up resisting materials in great variety. the fibre (and thus reducing its value) by As mentioned above, varieties and unnecessary operations. grades of asbestos differ widely in their This is done by a series of crushing L I.L.O.: Occupation and Health (January 1938) asdI stos operations, at the same time opening 01 nulling out the fibre and screening out th< useless sand. The fibre is collected bj 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 " milled asbestos" '-rude asbestos consists of the hand-selec ted cross-vein material in its native or non-librous 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 liner mesh: the lowest box retains the fine material which falls through the ihree screens. A weighed sample of asbestos (It. ounces) having been placed in the top box, the machine is mechanically agitated in a standardised method for exactly two minutes, and the asbestos remaining in each box is weighed. In this wav 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 ashes!..s so tested. In this way the seven groups of mill.' fibre are further subdivided into a numbe of grades, l hus in group Mo. 3 (spinnin and textile fibres), there are seven stan dard grades ranging from the speciiicatioi of 8---6-- 1-- 1 (minimum) for the top grad. down to specification of 0--8--6__! (minimum) for the lowest grade in thii group when tested in the above way. Asoestic or asbestine is a by-produci from the mills in the nature of a residui containing a very low percentage of short fibre. ` Manufacturing P rocesses 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 a r e 'u s e d ^ ^CrU<*e an<* spinn*ng grades) Any of these alone, or blended with each other, or blended with cotton fibre may be spun into yarn. ' Asbestos suitable for this purpose lias to be crushed, if in the crude state, and in all cases " opened " or " fiberised - before it is ready for carding. Separating (to remove iron) and sieving follow crushing, but precede opening. * The subsequent carding, doubling, spinmng, and weaving processes proceed broadly as m 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-resistingclothing 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 ns 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 fiber ised asbestos; " 85 per cent, magnesia " (the remainder being asbestos fibre): mattresses made of asbestos cloth and filled with ashes for. fibre, or " magnesia " or with other rr.o, ml: insulating compo- or I'h.:-.-; containing asbestos . and a >;::>% of other materials, fiberised 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 m 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- ; ') ..III ! .IS i II TI' tu 'lili. IllimI 'S. |.ll tur ill" ing red tlgS ad te. tli Iso `f. a". tor i, is ios ,.*r!, i .nd i.i " .po . -*: lilis. ft ? : .as. Ililt k <ll iich by vi ai:, . i or i, if fon - dust elopssive i'unc- 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, amt a note 1-v M.wioiia..ii ami Hie -* ` Hu* |>resi*iK! ,, -.nil bodies in the id an n-'ivates \k -:r. This .unity of informal ion 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 ASBESTOS 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 again by the publication of a note by W. E. Cooke 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 case was fully described by Cooke and Stuart McDonald in 1927. A few weeks later H. E. Seiler drew the attention of E. R. A. Merewetiier 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 dust. Thereupon in February 1928 a compre hensive enquiry in Great Britain was 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 192!' and January 1931. Lanza, MacConneli. and Feiinei. published the findings in 1935. These, together with the valuable study by Fulton, Dooley, Mattiiews and IIoutz, published in 1935, are the only general surveys of the industry. In Italy, I.ovisetto published in 1930 the results of an enquiry, and G. Missy 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, Gemms (1931), Beger (1933), Bei.ntker (1934), Alwe.ns. Koppeniiofer (1935), etc. Essential F eatures 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 L<> visualise the disease as the slow; growth of fibrous tissue (scar tissue) around the bronchioles or smaller uir tubes of the lungs and between the air cells, wherever ASBESTOS * the inhaled dust comes to rest. In contrast to silicosis the former is the important site of deposit of asbestos in the Iiinys, 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 \ substitute for the air cells, but with continued inhalation of the causative dust, by 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, essontiallv local disease and therefore it is in!, when the fibrosis has obliterated that reserve of lung tissue normally present, and encroached upon the remainder which is essential for the normal functions of the individual, that symptoms appear. 1 hen 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. hrom 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 suflicient 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 arc the mechanical 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 librous 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 infection with which the remaining undamaged lung tissue is quite unabie to cope: this is commonly a low grade broncho-pneumo nia, but may be a lobar pneumonia, bronchitis, influenza, or less often, a sub acute tubercular infection. 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 seriously impairs the chance of recovery. ' Intercurrent attacks of dry pleurisy, which are partially responsible for the considerable lim-kcning of the pleura which occur. mmon, but usually only cause s!i_-: I temporary disable- ;->it. ' * In the absem i of intercurrcnt infec tions the fibrosis may progress to an extreme degree; bronchiectasis, non-tuber cular 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 elicited 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. and show duskiness or slight ltim-ncssof 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 be 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 fibrosis 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, hut 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 asbes tosis. 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 u.vanced ASBESTOS stag,,es of the diseases are distinctive, although as Pancoast and P endergrass maintain, they are not specific for that dust. -''. '--vis.';-1 KlO. 1. -- Dc'\ Hoped asbeHosis. Fio. 1 Sit. -- Lung section (asbestosis). Radiograms of asbestos workers are very puzzling--more so than in the case of siliin^i when it comes to assessing the <! f asbestosis present, parti cularly m f earlier stages and also in 5 ASBESTOS women, owing to the shadows cast 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 absolute certainty on either physical examination or radiological examination alone; with the aid of both the pneumonoconiosis can be diagnosed with certainty if present in some degree, although l.vs -v . y not necessarily to an extent sufficient . * ..'j to cause either symptoms or any i A-JiSi** - disablement. In very difficult cases `n r^b^-:*. V: where gross tuberculous lesions -Cft. V? 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 trapped in the lungs. Whether much 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, *. -ft rs^rc^* w ; '; i? particularly those in which the : exposure has been to a dense con - - centration of dust for between one Km. .siliowMs. 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 arc taken of these cases during the succeeding three or four years, the appearance and development of the fibrosis can be watched. Km. bu. -- Luiig 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 P athological F e a t ir e s As already mentioned, the first case of asbestosis in which pulmonary fibrosis 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 Co o k e and H il l . and M cD o n a l d . 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 sequelae which follow. The asbestos fibre, as found in the respiratory passages of the workers, is a highly refractile, line, elastic rod, gener- ASBESTOS lengths, the shortest being about the length of a tubercle bacillus, the longest extend ing across the whole field of the micro- ally smooth but occasionally showing a sharp saw-like edge, and ends broken at varying angles. The fibres are of various scope. Short forms are the commoner and naturally are more likely to penetrate to the deeper recesses of the lung. The `a X ! tCD'CiM tfc .i4 / 3/! frf*tC:U*N j j UDlCtNE : / 1 * VNOUVN i\i . J UtXCINS !' JfNOUTN j*OIC*N r; 'v !/ 1 TNOI1VN EOiciNe 7N0UVN EOlCINt * V ASBESTOS diameter of the fibres has not yet been determined, since they appear capable of splitting longitudinally into liner and finer constituent fibres, almost indefinitely. Small bundles or sheaves are quite com mon. In the lung these fibres become 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 coated with a colloidal yellow pigment which in the course of time becomes (2) The siliceous nature of the fibre. crenatcd to iorm irregular segments, giving The fibres are for the most part held the appearance of minute crustaceans. up at the distal end of the respiratory These curiously shaped bodies were first bronchioles and in the alveolar ducts. noted by M a h ciia n d and H ie s a l , in Here a cellular reaction takes place con t Germany, as early as 1906 and, later, by sisting of the accumulation of large pha F a u r and F e ig e l in 1914, but the latter gocytes and the production of a charac ft was unable to decide whether they were teristic cell, known as the asbestosis giant If; a crystalline product of haemoglobin or cell, which, like other foreign body giant whether they were a direct result of dust cells, is probably not a cell but a*collec inhalation; no further attention was tion of partially degenerated phagocytes. t r, called to them until 1927 when they were As the disease advances the lymphatics described by Co o k e and H il l and in the neighbi'iiiliiuid become blocked. l Mc D o n a l d , in Great liritain. The last ! ally fibrous t--t.- is formed round the named suggested that they were ala a.! ilT-'. **ii p->rti" - Mi.> air passages, the h certainly a product of the nsbed* ' i.i capioii.' . i mules, the inter t . G lo y n e finally showed the a s b e sto s fibre i .J a r septa oi l!.< lung and in the pleura. n r- lying in the centre of the body by dissol The fibrosis thus produced is diffuse and ving the colloidal coating with "concen readily distinguishable from the nodular fi . trated sulphuric acid whilst under dark- fibrosis produced by free silica. Meanwhile ground illumination. These bodies have the asbestos fibres become coated with a never been found in the original asbestos golden-yellow pigment which contains dust *. iron and is believed to be derived from blood proteinsi to form the typical asbes > Begkji (1933) has made a thorough histological tosis bodies referred to above. It is not and optical study of asbestos bodies. According to this author, the metallic element ut the molecule of known how long all these changes take hydrated magnesium silicate is dissolved by the acid to bring about, but G a r d n e r and C um fluids of the body, leaving a silicic arid shell. The form of the needles and their power or double refrac m ings have shown that in experimental tion remains intact. The asbestos body is subse animals small asbestosis bodies appear quently formed by absorption of proteins by the needles of asbestos and subsequent coagulation In at the end of two months but fibrosis m the lhe form of gel. The silicic acid from the shell of walls of the bronchioles was not noted until the asbestos needle becomes dispersed in the protcid shcalh of the asbestos body and becomes gradually the end of 500 days. At the end of about disintegrated. There then occurs resorption by the two years the disease can be recognised body fluids of the protcid mass containing the silicic acid. Urantiious bands of ferric oxide impart to the asbestos bodies their brownish colouring. Kon-km iOfeh (1935) considers th a t the sheath to those parts of the lung most closely affected by of the astiest os bodies is not of a proteid nature and respiratory movements, there may be accepted as opposes Bkgek's theory as to the formation and destruction of the asbestos bodies. plausible the theory of those authors who consider mechanical irritation and the Injuries caused by the i-ii .Si'notes and Btodek (1937), in a detailed study long rigid needles as a factor in the formation of of asbestos bodies contained In the lungs of a worker llbrosis. The distribution of the fibrosis, moreover, who died of asbestosis. arrive at the following con seems to justify the hypothesis which accords a clusions in regard to the mechanism of formation of primary influence to respiratory movements on the the asbestos bodies. The organic substance of the migration of the large aabestos needles in the lungs. latter is composed of protcid matter. The most L rncx (1937) In an account of the mechanism of Important element--(0 per cent.--of the theU of formation of * asbestos bodies * refers to the presence the asbestos body la Iron oxide. The Inorganic part of similar bodies which he designates * silica bodies ' of the shell docs not come from the Inhaled dust, but found in silicosis with particular mention of their Is of endogenous origin, comlug from the body and occurrence In a case of typical nodular fibrosis. He * principally from products derived from the blood pigment. In the light of this theory, the formation states further that similar formations have been noted in the lungs of coal workers (Ttlccotx and Is of asbestos bodies Is not esseutlally connected with Doim, Cooks) as well as In the lungs of a consider the outbreak of fibrosis. A causal relation between ab le number of subjects who died of heart failure the two processes Is perhaps doubtful In view of the (particularly cases of rheumatism and arterio fact that various authors have found these bodies sclerosis) without exposure to dust. The iron in lungs of persons not suffering from asbestosis, and content and seeming common connection with pul even in lungs free from fibrosis. On the other hand, monary congestion and the local liberation of blood it Is well known that the formation of asbestosis Iron raises the question as to whether the iron of the llbrosis should be connected with the presence in the asbestos body may not be so related at least in part, lung of asbestos needles and their action on the pul and whether congestion may at least favour produc monary tissue. On the basis of interstitial localisa tion of all such bodies (asbestos bodies, silica bodies, k tion of the Qbrosis at the outset and its later extension and similar formations). 8 ii.- -- - qr-- ASBESTOS r by the naked eye. It is probable that the The number of cases of the latter so far disease takes longer than this to develop described is small and it is not yet estab in man--at any rate to an extent sufficient lished that there is any aetiological to* cause radiological and clinical signs. connection between the two diseases. When the lungs are examined by the naked eye after death they are seen to be T large and densely fibrotic, and the pleura covering them thickened with plaques of old pleurisy. Often the lung is completely 'i*- 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 with the gen-":! * 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. Mere- w e t h e r noted that in some advanced cases 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 and pig ment, corresponding to the secondary lobules of the lung 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 sequela: of pulmonary asbestosis four are outstanding: (1) Purulent bronchitis; (2) Bronchopneumonia; (3) Pulmonary tuberculosis, and (4) Emphysema, with occasional rup ture of emphysematous bull caus ing spontaneous pneumothorax. 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 tnc emphysema compensatory to the fibrosis. In addition to these four main complica tions may be noted two which are less common: (1) Dilatation of the bronchial tubes resulting sometimes in what is known clinically as dry bronchiec tasis, and (2) Carcinoma. F ig. 5. -- Infra-red photumicroirraplis of the ashrstnsis lone. Bridge and IIexry have proposed that cancer, in order to he 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 ! ii `V. * fc : s i ASBESTOS h&ve carcinogenic properties. These two postulates cannot yet lie regarded as I having been fullilled in Iho case of the of exposure determine the incidence rates m 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 cause death. Commonly, however, cases of definite asbestosis are not disco vered on examination within five years of commencing work, although a few are round. Among those working who have been employed for between five and ten yeara in the absence of preventive measures the incidence rate is appreciable, and after ten years of such employment a steep rise m the incidence rate occurs. The incidence rates for the periods of employment 0-4 years, 5-9 years, 10-19 years, and 2 years and over, amongst 1,512 workers examined .ihe. ritls,h Silicosis and Asbestosis Medical Board were proportionate to the figures 1, 5.6, 30.4, 53.2. Although the incidence rate amungst those with less than five years exposure is "" k ? ' ' ' H o n stainril wiili liurmatoxylln cosmr anil van Oirsmi, sliowim; lllirmis tissue ' surroiimlin asli<si.,s |.,,,Hcs. so low such exposure may be by no means negligible. The fact 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 I develop. AsG vr i>x e u an d C i m m in o s have shown, the fibrosis takes time to appear, m 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 Ihe facts couch niir.- particular cases of asbestosis will -use concerning the diisiii,.: ,,. processes at which ' worked .... ie conclusion that tin* period of inului ution n of the fibrosis is not reduced below a certain minimum period, however high the concentration of dust in the air breathed may be. Similar considerations also show that I Fio. 7. -- Section of lung, unstained, showing asbestos bodh-s. asbestos industry, but there is sufiieioH evidence to warrant, careful observation in the future. below a certain concentration, develop ment of a disa Mia degree of asbestosis will net occur iaiii the space of an / ' rage workii:_- d . iune. it appears, therefore, that a certain minimum " fibrosis-producing amount " The P r o b l e m o f A s b e s t o s Dust as it may be called, of asbestos dust must be trapped in the lungs in order to cause Within certain high and low limit, the concentration of asbestos dust in the air of workrooms is the determining factor in the onset of the disease and also, within limits, concentration of dust and length a disabling or serious amount of fibrosis, and also that a certain " maturation must elapse before that amount of fibrosis is developed. Fatal cases of asoestosis have resulted from exposure as short as two years or 10 ASBESTOS | even a little less, although the fatal issue cyanosis of the lips, and also a little dry | may be postponed for many years. cough mostly in the mornings. He finds It is important to consider what is the himself disinclined to climb stairs or walk amount of dust which will produce this up hills, but still remains at work and result, or conversely, what is the amount usually is not anxious about the state of of dust which, from the practical point of his health. (view can be inhaled with impunity. Efforts are being made, notably by American investigators (W. B. F ulton and others), to establish in terms the concentration of dust in the air which, 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 figurc for concentration of dust. E. R. A. Merewetiier 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 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 which 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 bronchitis etc., until the condition is far' advanced, although increasing inconve nience from shortness of breath is expe rienced. working lifetime, it is necessary to reduce Ithe 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 Usually these cases 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. with exposure to high concentrations of dust the minimum period of time which must elaiw.- between the ei-nmencciucnt ofexpe-i; n.i the prodn ii serious degree <!'. l- -ii*si< is api -oxiniai'. ly seven years--lua-e ut> id the perhu! <! exposure during whali the librosis-pruducing amount of dust is taken into the lungs and the maturation period during which the fibrosis develops--these periods, of course, overlap. This period of approximately seven years, " the ashestosis 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 preventive measures, the asbestosis pro duction period is commonly eleven years. When asbestosis of serious extent has It is remarkable to what extent the lungs can be affected by asbestosis and yet life in a fair degree of comfort remain. The reserve is, however, so slight that the addition of any burden to tbie system in the form of a disturbance of health which would only slightly inconvenience a normal person, may overcome the remaining re sistance and precipitate a fatal outcome. For these reasons and from consideration of the features present in the recorded fatal cases, the view must bo 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 " Is asbestosis a serious disease ? ". To this question, unfortunately, the answer is emphatically matured the worker is unduly short of breath on any extra exertion, has a little A sbestosis ash T uberculosis i The Industrial Hygiene Division of the National Institute of Health (United States) has examined (193?) 543 persons in asbestos textile plants. An analysis of data shows that the maximum concentra tion of asbestos dust to which workers may be exposed without contractintf 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 rould he reduced to less than .5 million particles ler 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 Hie British figures are. 11 \ ASBESTOS *lhe moat complete, since the disease has been compensatable since 1 June 1931. The following figures arc abstracted from the Annual Report of the Chief Inspector of Factories for 1935. TABLE 1 Disease Num ber of deaths Aver age at death Duration or employment in years Lon- Shor Aver Kcst test age Silicosis , , . 311 55.8 62.0 2.3 35.1 Silicosis with tuberculosis . 391 52.4 67.0 2.0 31.7 Asbestosis . . Asbestosis with tuberculosis . 52 41.9 27.0 1.5 12.4 30 37.1 29.0 0.8 9.5 Table 1 gives particulars of 702 deaths from silicosis or silicosis with tuberculosis and of 82 from asbestosis or asbestosis 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- j pared with 35.1 years for all cases \ of silicosis. The actual average 1 length of exposure to asbestos dust was, however, still less. (2) The shortest length of exposure to ( asbestos dust which ultimatelv S caused death from fibrosis of the ( lungs was 1.5 years. [ (3) Asbestosis is comparable with the ) most serious silicosis risks with I respect to length of exposure which i will cause a fatal degree of fibrosis, t (4) Although the numbers in the as bestosis group are small it will be noted that in 36.6 per cent, the disease was accompanied by tuber culosis, while in the silicosis group 55.7percent, were accompanied by tuberculosis, suggesting a less close association between asbestosis and tuberculosis than is the case with silicosis and tuberculosis. Disease I'o t l r r y ; Silit'HHlS . . , Silicosis Willi tuliercnlnsis. Sandstone: ' Sflirosis. . . Silicosis with tuberculosis . (iriiuiinKof metats: Silicosis . . . Silicosis with liihcrriilnsis. SandM.istliitf: Silicosis . . . Silicosis with tuberculosis. Manufacture of scourim; pow ders: Silicosis . . . Silicosis willi tuberculosis. Miscellaneous: Silicosis . . . Silicosis with tuberculosis. her of deaths t.Vj Hi 4 78 88 26 IS ms 8 n 25 28 Duration Aver- of employment ar In years at lealii ! ifi -t ! i i j Vv-'f- 5.8.0 54.1 7.0 ** H 5.0 3*). 4 56.5 57.ft 9.(1 38.3 5:1. 10.0 35.3 56.1 5'.0 18.0 34.3 52.1 52.ll 31.5 44.5 2U.0 4.0 10.7 45.4 20.1 2.0 S.4 3-4.7 17.0 3.1.5 10.8 5.1.3 45.0 49.9 50.0 2.3 9_* 2.0 6.4 6.0 `2.5 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 asbestosis and the 5 ea-i.., of asbestosis with tuber I '".ilosis foim.i : \ K. R. A. MEnEWETiiEn in ins original o ;i!i:y 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 ASBESTOS In March 1932 a comprehensive Code of Regulations designed to suppress the dust produced in all processes to at least the level ol 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-producing appliances. (6) Effectual separation of processes to prevent unnecessary exposure to dust. (7) Use of sacks of close texture for internal work in the factory, and cleaning of them by machinery. (8) Eflicicnt cleaning system. (9) Precau tions to prevent dust from asbestos in storage chambers or bins entering the workrooms. (19) Regular examination and testing of ventilating plant; dust settling and filtering apparatus not to he allowed in workrooms. (11) Breathing apparatus of approved type to be provided tor per sons employed in certain operations. The Regulations also prohibit the employment of young persons under the age of 18 in the most dusty processes. In order to achieve the objected 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 and 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 m 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 asbes- tosis and of pulmonary tuberculosis are detected at the earliest possible moment. 1A practical maxim of the greatest value is that every translation of fiberised asbestos in the factory produces dust which, if not controlled, is dangerous. Co m pen sa tio n fo b A sbesto sis , Great Britain was the first country to pass \ special legislation relative to compensation for asbestosis and asbestosis accompanied bv 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 1936, and in Danzig, the Order of 11 March 1937, grunt compensation for serious asbestosis life-li.ig worker; ?;!ing within accident iov)mice Icgislnli ; n the United States in. ! . w of 26 Man-L 1935 passed in North Carolina provides for compensation of asbes tosis in a certain number of industriesl. 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 carry out in the near future Uie requisite enquiries and research for determining the extent of the occupational risk involved." Bibliography B cgcr in Virchow's Archie, Vol. 290, 1933, pp. 280-353. Cooke, W. E. Brit. Med. / . , 26 July 1921, p. 147, and 3 Dec. 1937, p. 1024. - F ulton W. B., Dooley A., Matthews J. and Houtz R. L. Dept, of Labour, Pennsyl vania. Speciol Bulletins, No. 37,1 Oct. 193-* 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, K o ppe n iio fer in Arch. f. Gew. Path. it. Gcw.Hyg. Vol. VI, 1935, No. 1, pp. 38-63. Lana A. J.. Macconnell W. J. and F ehnel J. \V. U.S.A. Publ. Health Rep. 4 Jan. 1935.' ' i Among the States which accord compensation for asbestosis by blanket coverage, there are some In which the general coverage Law contains special provisions concerning asbestosis: Illinois (Law nf 16 March 1936), Indiana (Law of 6 March I93<>. Pennsylvania (Law of 1937). Lynch, K. M. in Journ. Amer. Med. A ttoe., 11 Dec. 1937, pp. 1974-78, Chicago. McDonald S. Bril. Med. J ., 3 Dec. 1937, p! 1025. McP heeters 3. B. J. of Jnd. Hyg. and Tox. April 1936, p. 229. Boston. Mer ew eth er E. R. A. " The Occurrence of Pulmonary Fibrosis and Other Pulmonary Affections of Asbestos Workers." Journ. of Jnd. Hyg. May 1930, p. 198 and June 1930, p. 239. ------ " Memorandum on Tuberculosis T u bereU, Nov. 1933, p. 69; Dec. 1933, p. 109. Jan. 1934, p. 152. ------ and P rice C. W. Report on the Effects of Asbestos Dust on the Lungs and Dust ASBESTOS ' Suppression in the Asbestos Industry. H. MStat. Off., Ixmdon, 1930. Shull J. R. Radiology, Sept. 1936, p. 279, Syracuse, U.S.A. Sundius N. and Bycden A. in Arch. f. Gew.-Path. u. Gew.-lyg. Vol. V III, 1937, No. 1, pp. 26-70. Berlin. Figs. 1 bis and 2 bis are taken from lung sections stained by E. H. Sarsons, of Bir mingham University, with his modification of Mallory's method. Figs. 3 to 7 are taken from various publica tions by S. Roodhouse Gloyne. Dr. S. R. Gloyne (London) and Dr. E. R. A. Merewether (Birmingham). 15