Document jBQdB1GqYkadZ18DrLwm03MdQ

FILE NAME: Asbestos in India (IND) DATE: 1982 DOC#: IND014 DOCUMENT DESCRIPTION: Journal Article - The Asbestos Connection THE CONNECTION .,-Jk-farieties -- the,soft and coiled st\ . ^pontine variety occurring as chrysoii* f fibres, and thd straight amphibole'1 - vjjj-icty occurring as amosite. cio- -. <^ l* " `C!dolite, anthophyllite, trem olite. actinolite, etc. Ninety per cent ot the 6 million tonnes of asbestos mined in the world is chrysotile and about 7 per cent crocidolite. The Asescroaudsodsisisebaeseinsg. iSntcurdeiaessinsghloywlinskoemdewwitohrkaenrusminbtehreof asbestos industry in India are suffering from asbestosis physical properties of the f bres play a role in causing diseases, as we shall see later. For instance, the soft and the e uled variety causes asbestosis while the harsh and the stii! varieties can penetrate the lungs and reach I i s unique characteristics use strength, wear-resistance .in,! t!e x i b i 111y have found _-~_,U's useful in over three commercial and industrial _rr but it has one serious - ..> -acs--it can cause severe health .-.cards, inhalation of asbestos and its diversion in the lungs can lead to ..ocmosis (a lung disease), lung can- cr and cancers of the membranes lin- the lungs and the abdomen rmexcthelionfa of the pleura and the peritoneum). ` The Factories Act, 1948, stipulates stringent preventive control measures atu. Aasbestos exposure, protective e q u,, meni for workers and their periodical examination. Because of the serious nature of asbestosis, it has been made a notifiable disease under section 89 of the Factories Act, and also a compensable disease under the W orkmen's C om pensation Act. Though there are no Indian stan dards" international standards set limits to asbestos exposure to work ers. ranging from two fibres per cubic centimetre"(2 million fibres per cubic metre) to 0.2 fibre per cc for different \aneties of asbestos fibres. But the Asbestos Working Group in the US reported in 1980 that there is no safe exposure limit for asbestos, that all com m ercial and several n on commercial forms of asbestos cause disease and recommended a new stan- daidot'O 1 fibre per cc as a maximum woi ' ce exposure limit. This is the sma z quantity that can be mea- suied b\ techniques currently avail- uhie ' Despite this awareness and the statutory provisions, workers in India ire still exposed to much higher levels ot asbestos, and some suffer from asbestosis as revealed by studies, car ped out so far. In a study done m an asbestos cement factory last year in .his author and Dr. V P. Gupta of the ( entral Labour Institute, Bom bay . we lound that 6.5 per cent ot the DO workers examined suffered from asbesioMS, environmental measure ments showed asbestos concentra tion, atinre the threshold levels in two sections within the factors And in April this year, Drs S P Shah and S R Kamat, of the Department ol Chest Medicine, G. S. Medical Col lege and K. E. M. Hospital, Bombay, reported 24 cases of asbestosis at a conference on occupational health. No case of cancer -due to asbestos has, however, been notified yet. This can be due to the fact that asbestos workers are not followed-up after they retire and occupational histories of cancer patients are not recorded. In cross-sectional studies of workers, it will be difficult to find a person who is still working while suffering from lung cancer or mesothelioma of pleura. The asbestos industry in India em ploys about 7,000 workers in 19 units spread in Andhra Pradesh, Gujarat, Haryana, Maharashtra and Tamil Nadu. Much of the asbestos used here is imported, andonly a small quantity, about 20,000 tonnes, is mined in Andhra Pradesh, Bihar and Rajas than. Various studies and reports in the press have recently highlighted asbestos health risks, and this has caused an increased awareness among the management and workers, result ing in improved working conditions But only a continuous follow-up will indicate whether the hazards are suffi ciently controlled or not. Unlike in most other cases of occu pational diseases, asbestosis has no cure and continues even if the afflicted worker is removed from the source of exposure ; even if conditions are better in a factory today, the his tory of past exposure becomes a key factor, since asbestosis develops slow ly and appears after 15 to 35 years As for mesothelioma, even a short expo sure can cause it, and it is difficult to prevent. All this has prompted a ban on the use of asbestos and a search foi substitutes in some countries It is also statutory in western countries to use a warning label on asbestos pioducts A sbestos and Its uses A naturally occurmg m incial, consisting mainly of silicates in the fibrous form, asbestos derives its name from a Greek word meaning " unquenchable , it comes m two the pleura to cause mesothelioma of the pleura. The mineral fibres are processed or mixed into various products -- tioor tilings, gaskets and packings building materials as asbestos ce- msfiT sheets, friction products like brake and clutch linings, paints, coating and sealants, asbestos rein forced" plastics for electric motor components, asbestos cement pipes for chemical process pipings, water supply pipes and electric wire con duits. asbestos textiles for heat and fir e -p r o te c tiv e clo th in g and draperies, asbestos paper for bever age filters, gas vapour ducts for corrosive compounds, electric wire insulation, etc. Nearly 80 per cent of the production in India goes to make asbestos cement. In several of these processes, asbes tos fibres and dust are released and inhaled by workers Particularly dusty arc mixing of fibres, dismantling of old lagging, spraying asbestos fibres on walls and ceilings, carding, weav ing and spinning of fibres, twisting asbestos around welding rods, use of asbestos for rope, either dry or w et. to grout expansion gaps between refrac tory bricks in furnaces and kilns and clearing and maintenance of exhaust ventilation ducts and disposal units The risk of getting asbestosis is the highest in the textile manufacturing and insulation processes where the fibres are finely divided ind is the least in asbestos mining where air borne fibres are very few. it has been estim ated that asbestos insulation yvorkers are eight times mure likely to develop lung cancer than the general population; for smokers, the risk is ninety-two times higher. The size and type of the iibres and how they are dispersed ate important in causing the hazards. Harsh and straight fibres are more likely to reach the periphery ol the lungs anc; thv plcura; crocidolite. yytuch is a straight fibre, is more likely to cause mesothe lioma than other fib re, Soft md coiled fibres, like chi .-sotile md anthophyllite, aie probably mvoived m ore in asbestosis Fibrc^ 'Onger than 200 micrometres and wider than a 5< it n< i To ii -Vi I i ; , :98d 43 micrometres are intercepted in the nose and cleared by the cilia. The de creasing diameter of the pheripheral airways" in the respiratory tract also helps "block the larger fibres. Disper >. hi is another important factor; wide lispersion allows dust particles to penetrate deeper into the respiratory system and m this way the manufac ture of asbestos textiles, where fibres are widely dispersed, is more danger ous That asbestosis is a serious afflic tion among asbestos textile workers was established beyond doubt by the 1430s (the first case was reported in the UK m 1900). In asbestosis, the inhaled fibres damage tlie airsacs in 'ho lungs. This impairs the process of as exchange between the oxygen in the inhaled'air and the carbon dioxide in the blood, and turns the elastic tis sue between the airsacs into rigid col lagenous tissue which is termed pul monary interstitial fibrosis (Fig. 1). Consequently, the lung function is restricted; the person feels increasing ly breathless on exertion and finally disabled to varying degrees. A nd once the disease sets in, it progresses even after the worker is prevented from further exposure to asbestos, and there is no specific treatment. Asbes tosis, however, occurs only in occupa tional asbestos workers, and depends mainly on cumulative exposure to asbestos dust. Smoking increases the risk. How is asbestosis diagnosed? This is based on the history of exposure to asbestos and symptoms of breathless ness on exertion, end inspiratory crackles (crackling sound heard at the end of the inspiratory phase of the breath sound because of the forced opening of the smaller airways which are closed during inspiration due to interstitial fibrosis), reduction of lung function such as transfer factor and \ita! capacity, finger-clubbing or the Area of lymphatic vessels rritation '(iron-cot hemoglo! alveolar asbestos denses or coating o its cytup cell wall i tos bodie mechanis using a~$ sputum appear g< dumb-be Jn eni Fig. 2. Asbestos bodies appear as elongated, golden brown structures, 20 I- 1/ micrometres long and 3 to 5 micrometres wide, with dumb-bell-shaped ends thickening of the nail beds (which can occur in a variety of respiratory, car diovascular and other diseases, or may even be hereditary and not speci fic to asbestosis) and radiological find ings of parenchymal fibrosis. Accord ing to the Pneumoconioses Medical Board, UK. a worker who has been exposed to asbestos and shows any twit of the above symptoms and disability is certified to suffer from asbestosis and one with the symptoms but with out disability as "possible asbestosis" Using this criteria. w'C conducted a study, selecting 320 workers at ran dom out of the 960 employees in an asbestos factory in the middle of 1981 < J h e workers were subjected to thorough medical examination, includ ing lung function tests and chest X-ray full-size\The results revealed that 20 workersssuffered from asbestosis, and showed "restrictive-type" reduced lung function. The workers were ex posed to both crocidohte (blue fibre) and .chrysotile fibres, and fibre con centrations were highei than the per missible levels in the fib.e grinding and loading, and pipe-finishing de partments But the 20 woi keis suffer ing from asbestosis were scattered in all departments. This a as probably due to high exposure m the past (for which there was no tecord) in all de partments and infeidepartmental mixing of workers^Dust control mea sures in the factorvShad been mtro- duced only two yearn before tl udy while the afflicted workers hau been exposed foi an average >n 12 years. And ioi the same length ot exposure, asbestosis incidence was highei in smokers than in non-smokers Mea sures to control expo;ure in (he two ciepai tments and effective/medicai monitoring of all employees were sug )T0SlC'.I UIAtJ tIJh!e^ mUIUaMnCaJtCtAe.'iii'. iity\ There is a point to remcm.bct A person who inhale- asbestos li `u-s may show asbestos beidle:s m the bpib turn, and the presence uf 'heve nouhes in the sputum is gerici ail;, nustaki.' to indicate asbesioso Hi! > u Thu, 'O Asbestos fibres, on rcaching the air sue. causes h tm oh >is tie:au^t jf sBtxa :he rettili aom. The is rmstrT sure, anc than non are at m tubercuk are at hi cancer. c- tr-c ch < by the c asbestos, health h; Merewet on a stui recording dies con cancer dc cancers, mon in tl unlike a related. > been obsi group A risk. Mesotl peritoneu occuring and is sol posure. E nv ' ca 40 , Mrs. smoking cancer ha tives of , been exp clothes c. tions ne mine- ar non-occe ^ 'his part! regulator mamtena product1 clothes a that the wprk clot k j'hougi irom ash / /rritation. This liberates hemosiderin /(iron -con tain ing component in the hemoglobin) which is taken up by the alveolar macrophage along with the asbestos fibre. The macrophage con denses on the asbestos fibre to give it a coating of hemosiderin and protein of its cytoplasm, and the macrophage cell wall ruptures, giving rise to asbes tos bodies This is basically a defence mechanism. Under light microscopy, using a wet smear from a centrifuged sputum specimen, asbestos bodies appear golden yellow, rectilinear and dumb-bell shaped at the ends (Fig. 2). In general, asbestosis appears 15 to 35 years after first exposure to asbes tos, and the occurrence is time-and dose-related: this means that the dis ease showing up today is not necessarily the result o f present-day work condi dons. The risk ot contracting asbestosis is minimal below a certain expo sure, and smokers carry a higher risk than non-smokers". Asbestos workers are at no excess risk of contracting tuberculosis, but asbestosis patients are at high risk of developing lung cancer. keeping the exposure to asbestos within the prescribed threshold limit, mesothelioma of pleura and peri toneum is difficult to prevent. Mea sures are, therefore, being adopted in other countries to find harmless sub stitutes for asbestos. Besides, these countries have also made it statutory to use warning labels on all products containing asbestoD How exactly asbestos causes these disease is not still clearly known. One of the theories put forth earlier incri minated the fibrous nature of asbestos because fibres smaller than 5 mic rometres in length or finely powdered asbestos caused negligible effect. But considering there are other fibres, in cluding man-made fibres, which do not pose a similar threat, asbestos hazards were attributed to it^ibrous nature and the chemical properties -- pling^m e of 15 minutes, mainly to prevent mesothelioma). In 197b. this was recommended to be reduced to 0.1 fibre per cc with a peak concentra tion not exceeding 0.5 fibre per cc. in 1980, following the Asbestos Work ing Group's (established by the niosh and the Occupational Safety and Health Association, O SHA, USA i finding that there was indeed no sate exposure limit, OSHA promulgated a maximum workplace exposure limit o f 0.1 fibre per cc. Debates are also going on among the European coun fries about muejj reduced and strin gent standards .^Meanwhile, occupa tional health and environmental agencies have proposed a ban on all non-essential uses of asbestos^ To prevent asb estos health hazards, the simple and most effective way is to eliminate asbestos by using 'ar>c<?'-C8(.'S''n~ C h p m , r n l $ by N Irvin g S e ' cted to , includ;st X-ray 1 that 20 tsis, and reduced vere exle fibre) ure conthe pergrinding ting de s suffertered in irobably last (for n all detmental ro! mea n mtro- \ -idy ao oeen 2 years, cposure. igher in 's. Meahe two medical /ere sug- ler here, os fibres the spu.e bodies taken to not so C r ^r-causing capacity V.xUch concern is now being caused by the cancer-inducing capacity of asbestos. Lung cancer as an asbestos health hazard was first reported by Merewether in the UK in 1947 based on a study of 235 death certificates recording asbestosis. Later, other stu dies confirmed this. Asbestos lung cancer does not differ from other lung cancers, except that it is more com mon in the lower lobes. And though, unlike asbestosis. it is not doserelated, significantly greater risk has been observed in the highest exposure group. Again smokers run a higher risk. Mesothelioma of pleura and the peritoneum is a rare form o f cancer ocquring in the general population, and is solely attributed to asbestos ex posure E ves an exposure as short as a mv C clT, CiSwirc" c . i *> C s i i i C c i d i t c r --U t o ars A : : in umcr cases. cancer has been, reported among rela tives oi asbestos workers, who had been exposed to asbestos from woik clothes carried home, among popula tions near asbestos factories and mines and among people who had non-oecupational asbestos exposuic. /fh is particularly cresses the need foi regulating asbestos waste disposal, maintenance and repair of asbestos produces and provision of work clothes and lockers in factories so that the workers do not go home in .1 /Ar V' 1. . . "N A labourer's hut made almost entirely from asbestos scraps fibre dissolution in biological fluids and liberation of toxic elements like magnesium, nickel and chromium.^ Threshold limit value As fresh evidence accumulated ab- ut me harmrui effects, particularly of -.c-'-i-ihelioma, the asbestos exposure . -- been continuously revised. Cumulative asbestos exposure is ex pressed as fibre/years per cc and is obtained by multiplying the average concentration of fibres during work hours and the length in years of a worker's exposure. It was earlier found that less than one per cent of the w'orkers developed asbestosis at an exposure of 100 fibre/years per cc. Based on this, the National Institute of Occupational Safety and Health f n io s h ) , U SA , had suggested a threshold limit value for exposure of two fihres ner cc and a neak concen- other harmless fibres. A good deal of research is going on elsewhere to find these substitutes. And one such is polypropylene wire mesh which can be used in place of asbestos for rein forcing cement. Because of its wide varSit" of .uses, asfeesios e ^ n o ' however, be easily eliminated. Till such time as asbestos is in use. all mea sures must be taken to prevent harm to workers, their families and those who use asbestos products. Within the factory, therefore workers must be first educated about the health hazards and correct woik practices^The factory must maintam good house-keeping, general venhl., tion and local exhaust ventilation fibres should be mixed in a wet condi tion and floors swept and sc nibbed with wet mops to keep airborne fibre concentrations within prescribed limits, workplaces should be morn- Monitoring airborne asbestos fibres The casual conj^iori t^&een the, inhalation of asbjtstbjfibfes |nd the production lung fibrosis or ^beistbsisf^^ichml^arcino- ma and mesotheliotri^ is now fully established. Though the increased mor tality from the incidence of lung cancer has been linked withoccupational expo sure to asbestos, the association be tween general airborne exposures and increased lung cancer mortality has npt yet been established. This is primarily because of the low leyel exposure to asbestos, especially when other known and suspected carcinogens are present in the atmosphere. The problem is compounded by the lack of a reliable method for the quantitative analysis of airborne asfisstosSfcreiwhen they are present is much Jpwetyconcentrations than other particles. The method now recommended is applicable for occupa tional setfingsand depends on visual discrimination of fibres*h thepresence of a background of nori-fibrous parti cles. . The membrane ^ e ij. jn which greater than'| |iic^i^^s-'in-len^it*are: - counted w as/p ^ b fysf^ t used^y the; British *Safety - (BOHS) in th^s^dyln a s b e s t o s tactile factory. It ^ rripw^greext that asbestos fibres are the etiological oontaminant of concern; hence the currently recom mended safe air.'||ricehtrations and sampling procedures art defined in terms of fibre concentration and not otherwise. Panicles with the following geometric dimensions are called as fibres: length greater than 5 mic rometres, diameter less than 3 mic rometres, and a length-to-diameter ratio greater than 3:1. Only such fibres collected on the membrane filter are counted at 400 to 450 times magnifica tion (4 mm objective) with phase con trast illumination. The main disadvantage of this method is that it does not differentiate asbestos from other fibres. Airborne fibres smaller than 5 micrometres in length may also be present in the environment arid will be%awn on the membrane filter: however, these can not to be counted using the currently recommended membrane filter techni que with phase contrast microscopy. Electron microscopy can be used for identification and evaluation of such fibres. The use of this technique may not be practical for routine air monitor-. ing and the results cannot be directly compared to the current permissible limits. Besides, the significance of such small fibres s nor yet definitely b e e s . There is a general consensus in g nic nature o f asbestos' fibre. Neverthe less, dw workii^ group of the Intema- tionalAgency for Research on Cancer in 19T7 concluded that fibres greater than S mirpmetres in length ape more ^ct|&||>^^ucirig tumours, thus the ; danp^r^f fh fibre,. Its' length and inorphoiqgy .are the important para meters in the etiology of lung diseases associated with exposure to* asbestos fibres. . .* .VC; ' : The setting of various standard for asbestos for the protection of workers' health was based on this theory and the concept that exposure up to certain levels can be tolerated wjthout undue risks. In 1980, both the US National Institute of Occupational Safety and Health ,<niosh) and the Occupational Safety and Health Administration (OSHA) concluded that: (1) there is no safe exposure limit for asbestos; (2) all com m ercial and several non commercial forms of asbestos cause disease; (3) a new standard of 0.1 fibre per cc should be used as a maximum workplace exposure limit; and (4) optic- al phase contrast microscopy is the most reliable and economi&Jy . feasible method for determining airbbrfie levels of asbestos, with the lowest' reliable detection bmit of 0.1 fibre per cc. Various'tedonques have been sug gested for evaluation of airborne asbes tos fibres while the airborne samples are collected on a membrane filter and counted with the aid of phase contrast microscopy The current standardised membrane filter methods of tibre- counting developed bv the boms, Niostt. the American Conference ot Governmental Industrial Hygienists and the Asbestos International A sso ciation (A1A) are more or less similar. Aas method can be used. The \ i \ method is. however, used as a reteieace so that results from different cotmmes can be compared. Other methods which have been used for identifying and characterising the fibres are: infrared spectroscopy, pola rised fight microscopy and X-ray dif fraction analysis. The methods cannot be used for evaluation of airborne asbestos fibres. The membrane filter method, though considered to be still the standard technique for monitoring asbestos in the occupational environ ment, is time-consuming and tei ), besides open, to considerable ex perimental error and arbitrariness in the number of fibres counted. Hence there is a need for evaluating asbestos expo sure by a faster and more feasible technique. One instrument which is capable of giving rapid fibrous concen trations in the air is the Fibrous Aerosol Monitor, Model FAM-1 . developed by the GCA Corporation, USA, under contract to NIOSH. The instrument has been evaluated against the nioshapproved membrane filter sampling technique and the results have shown a strong correlation. The instrument is now available in the market. S. CHAKRAVORTi Mr. Chakravorti is Deputy Director (Che mical), Central Labour Institute, Bombay. check if the control measures are adequate or not. Workers' health should be moni tored through an effective industrial health programme. This programme should include sputum examination for exfoliated malignant cells, lung function tests and full-size chest Xrays. This will help in early diagnosis of asbestosis and lung cancer and in form about the adequacy of the safety measures used. Smokers should be discouraged from working in asbestos factories, and a "quit smoking prog ramme" should persuade smoking workers to give up smoking. Workers' condition should also be followed up after they are discharged from work on medical grounds or on retirement. It is also important to protect a work er's job even after he is paid any com pensation for asbestosis or lung can cer due to asbestos. And all workers should be provided'with work uni form s and lockers, and proper arrangements for washing and bath so that they do not expose their family members to asbestos. To protect the population in the vicinity of a factory, it is essential to pack and dispose the wastes carefully. Other countries use highly trained personnel for this job. All asbestoscontaining products should carry a warning label so that users, like gar age workers who repair brake Jngs or ship breakers (asbestos is used for insulation in ships), take adequate precaution and use protective device while handling asbestos Dr Kumar was till re cently Deputy Director (Medical), at the Central Labour Institute, Bom bay. Earlier, he was a medical officer at Coal India Ltd. After graduat / mg in medicine from Bangalore University, Dr Kumar specialised in industrial riealtn at the All-India Institute of Public Health Calcutta. He is now an industrial physician at the Ciba-Geigy of India, Ltd, Bombay. 46 St i, - <; Toimi Jt to 1982 A