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FILE NAME: Z//E DATE: DOC#: /E DOCUMENT DESCRIPTION::ZWZZtZ Z INDIAN JOURNAL OF OCCUPATIONAL HEALTH, -1-9-8-3-(-A--p-ri-l-)-; --X-X-V--I(-4-)-: --3-0-5---3-1-3-. -------- "PATTERN OF ASBESTOS WORKERS IN BOMBAY"* S. P. SHAH, S.R. KAMAT, & A. A. MAHASHUR** SUMMARY: ed VC and diffusing capacity may pre- A study of 28 _workers. ex~os_ed ' lO cede ch:mges i.n the chest roentogenogram or are seen with equivocal radio- asbestos, and reporting to thts um~ is p~e lo!!i:::al changes. sented. They were thoroughly mvest1- ~ .!!ated with radiographs,, lung function An over-all diaroosil,; of asbestosis is a~d arteri3:1 blocd gases at ~est and based upon: physical signs of pulrno~fter ex~rc1se to detect established ca~- ~ary fibrosis..ra.diological ab~ormali/"i1eard ~."l 15 (46%) workers). In ties and r:stnct1ve changes m lung f~s4es of asbestosis. subjects there Basal rales were obvious ~bwnoerr- malities en radiographs suggestive of asbf:stcsis. Radiologit::ally the small re- ticu1oncdular opacities in lower and middle zones were commonly found. In 5 workers there was evidence of fsutn~cntdiaodns.criteWriait,hs-1sl0i.CTwhet modification of used the fol- lowin(T evidence for the di.acrnosis of 0 asbesw3is : (1) Adequate hi.story of exposure to asbestos fibre at work. obstru:::tbn but in most cases restric- (2) Clini::al presentation of breath- ti vc functional defect was seen. Arte- lessness. cough, clubbing and fine rid oxygen desaturation on exercise rales on ausculation. occured in 8 (35%) workers. (3) Radiologi.::al evidence of pleural INTRODUCTION : plaques, calcification or reticulo- nodular shadows suggestive of in- Alongwith wider l\lse in industries, terstitial fibrosis. world consumption of asbestos is es- (4) Restrictive functional disability and calating; so also the awareness of health hazards due to asbestos exposure has arterial blood gases alteration at rest or on exercise testing. come significant i,n past 30 years. Tho- U!Zh a typical advanced asbestosis is We could not use D co as a test due diagnosed without difficulty, on the to technical reasons as also lung r.asis of clini:al findings, radiological biopsy t 1 as unnecessary for confirm- abnormalities and rest;ktive charges in ing the di,3.gnosis of asbestosis. De- pulnionary function, but the industrial monstration of asbestos bodies in spu- r.hysician should be concerned with tum was also not included in criteria diarrnosin!Z, an early asbestosis. Leath- as it does not usually prove asbesto11'1 ' has- Sll!!<!ested that the earliest ~is. 10.12 sfi.nendci~ngofinbasaasbl ecsrteopsiistatmioanys. bWe htilhee opthree-r MATERIAL & METHODS: ,-;orkers 2-4 have fr"Jnd that abnorrnali- From suspected exposed workers, ti~s in lung fun:tion parti:ularly reduc- 28 were studied fully to evaluate for "'*Presented during 31st Annual Conventi:::m March '83. Work sponsored by K:la:hand Re.:;ear:::h Endowment IAOH Bombay Bran:h. Dcpatment of Ch~st Mcdi:ine Seth G. S. Medical College & K.E.M. Hcsp;~nl. Parcl. Bombay-tf.()O 012. 305 6318 10 11 12 l 3 71 88 306 INDIAN JOURNAL OF ahnormaliti.zs associated with asbesto~s. They had been working in _different factories in the city. The mvestil!ations consbted of full radiograph. clini::al examination, ~ung function and blood gas s_tudies. Chest. exam~nati~n, particularly mcluded lookmg tor fme basal rales and presence of finger clubbing. Spirometry was done on Stead-Well's spiromcter before and after a bronchodilator aerosol. All lung functions have been expressed as per- centage of predicted values as per .In- dian norms. u As per standard cnte- ria normal functions were with.i.n 20% of predicted values, mild disability between 60-80% moderate between 40-5'0% and seveire disabiEty less than 40c;;,. In all subjects blood gas studies before and after exercise (as an alternative to Dco studies) was done on the same day. RESULTS: All 28 workers were males with a OCCUPATIONAL HEALIB . ..'. mean age of 36 years (Table No. 1). Table 1 : Age Distribution exposed workers. Age in Years 21-30 31-40 41-50 51-60 Mean Age : 46 Years. of asbestos 4 (14%) 17 (63o/) 6 (20%) 1 ( 3%) Of these 20 (71 % ) were smokers, including 3 heavy (2Q+ /day) smokers. These belonged to differe.nt departments like winding, spinning. polishing etc. with a mean exposure to as- bestos fibre of 12.9 years. Of thes1 20 (72%) had been exposed for over 10 years. While mean latent period before any clinical symptom:; was 11.9 years but 6 (20%) manifested after an c:xposure of over 15 years. (Table 2). Table 2: Duration of exposure to asbestos and time lag before of symptoms. development Yrs. of exposure No. of patients Period No. of patients 1-5 6-10 11-15 16-20 1 (3%) 7 (25%) 14 (47%) 7 (25%) Mean - 12.9 years Breathlessness on exertion was a prominant symptom in 26 workers (93 % ). Dull aching chest pain and feeling of tightness in chest was commoner in workers with pleural or ctdvanced !'.'Jlmonary involvement. Unusually 22 (79%) workers also compla;!1ed of anorexia, weakness and weight loss (Table No. 3). 1-5 6-10 11-15 16-20 5 (18%) 8 (29%) 9 (33%) 6 (20%) Mean - 11.9 Years Table 3 : Clinical symptoms in 28 asbestos workers. 1. Breathlessness 2. Anorexia, Wt. Loss Weakness etc. 3. Chest pain 4. Cough 26(93 <'>'.,) 22(79%) 16(57%) 15(46%) Mean duration of symptoms 2.73 Yrs. PATIERN OF ASBEST0$ WORKERS IN BOMBAY 307 Finger clubbing (gr. I-II) was seen in 7 workers (25% ). The presence of tine rales was common in subjects present where'in the radiograph showed small reticulo-nodular deposits or honey combing. Radiological evidence suggesting asbestosis was seen in 24 patients (Table No. 4). Mainly there were bi.- Table 4: Radiological patterns in asbestos workers Pleural involvement only Parenchymal involvement Pleural & Parenchymal Normal Nonspecific 2 (7%) only 9 (32%) " 13 (47%) 2 ( 7%) 2 ( 7%) lateral fine reti::ulo-nodular deposits in lower and mid zones (79%) (Fig. 1 & 2). Pleural involvement :~as seen in 15 (54%). It was more common on the lateral parietal layer than on diaphragmatic layer (Fig. 3). One worker presented with circular mass on left lateral wall in upper zone wi.tll pleural involvement on right side thought to be malignant. However this had not changed over 4 years as compared with earlier X-rays : later we aspirated pus by direct puncture from this mass (Fig. 4). Low FEV 1 was seen in 5 workers (17% ); while VC% of predicted was abnormal in 15(53%) workers, suggest;,ng that restrictive ventilatory defect is more easily judged by FVC Small 'bead-like' and fine linear opocitie1 in tarlp as~sto1ts. ' ' ... ~<:::\~.:+ ,/< ~>:~~ ~. ,.. ~< Smalt nodular and linear opacities, mare in both lower zones than mid zone. Note the shaggy heart borders. ', ~... ~ r' . , , ., ' Bilateral e xten.<ive pleural thieken in~ with ra/rif;rrrti()ll. I PATTERN OF ASBES'I OS WORKERS lN BOMBAY 30') Cicular rounded opacity on left lateral wall. (fable No. 5). This was probably commens.urate to the degree of pleural involvement (Table No. 6) 5 workers refused arterial blood gas study. Mean pO 1 at rest was 86 mm of Hg while was mean paCO 2 was suggesting mild hyn3~6r.v8enmtimlatioonf Hg at rest. Mean Sa0. 2 96% at rest while it decreased to 95% on exercise (Table No. 6J. S~gnificant arterial oxy:- gen desaturation on exercise c::cured in 8(35o/c) workers. Murray reported the first case of pul- monary asbestos is in 1907. In 1930, asbestosis was recognised as an indus- trial disease and preventive measures were taken. . d 1s th all d l It IS reporte at usu y a e. ay of several decades occurs between first ~xpos.:ire an~ onset ?f symptoms an.d m no study m man, It has been possi ble to rneasur~ the dose. In our study mean lag p.;:nod was 11.9 years. DISCUSSION : The study narrates our experience and may not reflect on the relative incidence of asbestosj,c; in Bomba\'. The hacards due to exposure of asbestosis were first recognised in Ftirop~ 14 at the b~ginning of the '.?.'Jth :cntury. Thou2h we have not agsessed the role of -~making in our study. this has been established hy others. '' Asbestos inhalation also produces pulmonary fibnsis. 11- 18 While a hi!lh prevalence of fibrosis is ~cen in smoking asbestos workers hut it is uncertain whether the two hav:: ~m additive effect. e \ Table S : Spirometric indices in asbestos workers FEV 1 % % FVC VC Obs. % VC Pred. Mean L40 L60 740 1(3%) 4(14%) 4(14%) FEV.1 %- 86.27% FVC L80 Normal 760 4(14%) 23(83%) 7(25%) 13(47%) VCObs% 76.82% VC Pred. Table 6 : SummacyJ of radiographic and functional changes. Sr. No. Radiology PFT 0 R Pa02 in mm of Hg SaOz Rest Exer. On Exer. 1. A.BN \.iJ ABN(Mod) 76 2. ABN (1) N ABN(Mod) 91 3. ABN(2) N N 106 t 4. ABN (3) N ABN (Mild) 78 5. ABN (2) N N 102 6. :":' ABN (2) N ABN (Mild) 100 7. AJ:Sl'l\1'1~) N N 84 8. ABN (2) N ABN(Mod) 9. l. N N N 112 . 10. ABN (2)' N ABN (Mild) 92 11. ABN (3) N ABN (S) 70 12. ABN (3) N ABN (Mild) 81.5 i 13. ABN (3) N ABN (Severe) 56 - 14. ABN (3} N ABN (Severe) 102 i 15. ABN (3) N N 83 16. ABN (3) N ABN (Severe) 66 17. ABN(2) N N 18. .. ABN (2) N N 99 19. ABN (3)ABN (Mild) N 20. ABN (3' N N 100 21. ABN (2) ABN (Mod)ABN (Mod) 64 22. ABN (2) ABN (Mild) N 23. ABN (3)ABN (Mild) N 76 24. N N N 25. ABN (3) N ABN (Mild) 71 - . 26. ABN {3) N ABN <Mild) 90 .... 27. ABN (3)ABN <Mod)ABN (Mild)-100 28. ABN (NS) N N 88 81 NC 93 101 94 97 NC 106 NC 112 t 111 NC 95 NC 51.5 87 60 62 88 43.5 100 NC 97 NC 65 NC 73 ..I. 83 t 81 l "., NC 98 l 0-0bstructive R-Restrictive .NC-No change ABN Abnormal ! 1-Pleural involvement 2-Parenchymal involvement 3-Pleural + Parenchymal involvement N-Normal NS-Non-specific Sao,~ L + 0.5% Sa02- L - 0.5% NC 0.5% PATTERN OF ASBESTOS WORKERS IN BOMBAY 311 There is high risk of developing lung cancer in asbestos workers who arc smokers. In a study by Selikoff '' the combination of asbestos exposure and cigarettes increased the risk 90 times as compared with control group. Relati.ve contribution of cigareae smoking to malignancy is not assessed in our study as the exposure period is short. Oinical features of asbestosis are not pathognomonic. Breathlessness on exertion was the predominant symptom in our study. Breathlessness is seen first after heavy work and then with smaller exertion as the disease progresses. As reported by Parkes " , the degree of breathlessness does not correlate well with abnormal physical signs in the lung and radiographic appearances. Other surprising feature was presence of generalised symptoms like anorexia, weight loss and weakness in 22 workers (79% ). This perhaps related to chronic tiredness and mild dyspnoea. In majority of cases only a small quantity of sputum was complained. Chest tightness was common in patient with advanced disease probably due to stiffness of lung while chest pain was present with involvement of pleura. Fine crepitations are the earliest and most constant physical sign as reported earlier. 7 20 They were first detected either at the bases after a deep inspirati1on. As the fibrosis progress they become more numerous and widespread. An important feature of this i-.; that they are persistent and not altered by coughing, .as is often with other lung diseases. The difficulties in the diagnosis of early radiological changes of asb~s tosis has been emphasized repeatedly by Pender~ras since 19~8. so it is not fo'Jrprising to find a difference of ooinion in radiological dia.~csis. Radio- graphic abnormalities like bilateral small irregular linear opacities predominant in the lower lung fields, are suggestive of interestit!al fibrosis 22, l3 The early bilateral changes are grst seen in costophrenic angles in different torms of increased basal vascular markings; these may be thickened particularly at branchings with small rounded bead like opacities along the path of finer markingsj and a horizontal pattern resembling kerley's B lines. :1.J.2 In more advanced cases a honey combing pattern is common either due to fibrosis or superimposition effect of different radiodensities. When fibrosis is severe, the outlines of the diaphragm and heart shado:>w may become blurred and shaggy (Fig. 2). Rounded opacities similar to silicosis are occasionally seen probably due to free silica present in asbestos cement dust. 2s But larger opacities resembling those of Caplan's syndrome and progressive massive fibrosis are unusual, with 1lS bestosis. According to Yazicogl'll ct al, 26 the first obvious sign si~ 'i's the de- velopment of geographic calcified plaques in the pleura, radiographic chan~es of p,u.lmonary fibrosis develop later. As suggested by. Gibbs. 27 the changei> in pulmonary mechanics were considered to be early because they occured in workers who had no radiological evidence of disease or definite changes in other measurements of lung function. The characteristic abnormalities reported include pro~essive reduction in VC, TLC and in diffusing capacitv, increased static recoil pressure, decreased lung compliance and decreased VC% predicted, without airways obstruction. The restrictive lung lesion in asbestosis with decreased inspiratory capacitv and decreased lung volume is probably caused both by pleural adhesion and plaques and bv shrinkage due to pulmonary fibrosis. 21 312 INDIAN JOURNAL OF CCCUPATIONAL HEALTH Airways obstruction was not considered a feature of asbestosis. 4 Though recent reports 29 express the view that obstruction especially of small air:ways 5. Mcvittie J.C. (1965), Asbestos in Great Britain. Annals of the New York academy of scie.nce 132:128138. is not uncommon. It is widely known ...,... that the main functional defect in asbestosis is reduced diffusing capacity of the lungs, this was in- ferred from occurence of arterial oxygen desaturation especially after exer- 6. Berry G.,. Gilson J.C. et al (1979), Asbestosis a study of dose-response relationship in an asbestos textile factory. Brit. Jr. of Indus- trial Med. 36:98-112. cises as in our suudy too. 7. Murphy R.L.H., Gaensier S.A. ACKNOWLEDGEMENTS: ThiS study received financial sup- port from Nandlal Kilachand endow- (1978), Diagnosis of asbestosis -observation from a longitudinal survey of shipyard pipe coverers. The Am. Jr. of Med. 65:488-498. ment under the auspices of Indian Association of Occupational Health for wJ:iich -we are extremely grateful and indebted to them. We also thank Dr. C. K. Deshpande, Dean for per_mitting this study. Most subjects were seen through kind reference of Insurance doctors particularly Dr. H. S. Bharati and Dr. P. K. Rane. In doinl? lung function help rendered by Smt. S~ S: Athawale is ackn~wledged. REFERENCES : 8. Faysal M.H., Gerald Nash et al (1977), The significance of asbestos expm:ure in the diagnosis of mesothelioma - A 28 vears exposure from a major urban hos pital Am. R.ev. of Resp. Dis. i L.5: 761-767. 9. Epler G.R., Carrington C.B. et al (1978), Crackles (Rales) in the interstitial pulmonary disease Chest 73:333-339. 1. Leathart G.L. (1968), Pulmonary function test in asbestos workers. Trans. Soc. Occup. Med. 18 10. Parkes R. W. (1977), Asb~sto!': re- lated disorders Brit. Jr. Dis. Chest 67:261-300. 49-53. 2~ Hans Weill, Morton (1975), Lung iiunction M. et al consequ- 11. Scott J.K., Hunt R.C. (1975) The diagnosis of asbestosis. Brit. Jr. Dis. Chest 69:51-56. ences of dust exposure in asbestos cement manufacturing plants. Archieves of Environmental Heal h. 30:88-97. 3; Becklake M.R.. G~ McDonald et al (1970); Lung function in relation . to chest radiographic change.; in Quebec asbestos workers. Bull. Physiol. Path. Resp. 6:637. 12. Becklake M.R. (1976), Asbestos related disease of the lung and ,other organs. Am. Rev. Resp. Dis. 114: 187-227.. 13. S.R. Kamat; B.S. Sarma, C. Ven- katraman et al (1977), Indian norms for pulmonary function observed values prediction equation and intercorrelations. The Jr. oi ~. Willi.'lIIl R .. Hugh-Jone; P. (1960), . . Th"e .. significance of lung fUiction the association of physicians of India 25:531-540. changes in asbestosis Thorax 15: 14. Const::mtindis K. (19.77), Asbes- 109-119. tos exposure -: its related dis- ': ; t ~ . PATTERN OF ASBESTOS WORKERS IN BO:MBAY 313 orders. Brit. Jr. of Clinical practise 31:89-101. 15. Editorial (1981), Asbestos and public health. Thorax 36:241 244. 16. Weiss W. (1969), Cigarette smoking and diffuse pulmonary fibrosis: Am. Rev. Resp. Dis. 99: 23. Roger William, P. Hugh Jones (1960), The radiological diagnosis of asbestosis, Thorax 15 103-108. 24. Fletcher D.E., Edge J.R. (1970), The -early radiological changes in pulmonary and pleural asbestosis. Clini. Radiol. 25:355. 67-77. 17. Wright G.W. (1969), Asbestos and health in 1969 Am. Rev. Resp. Dis. 100: 467-479. 25. Ostrolenk. D., Nice C.M. (1968), Asbestosis and nodular lesion of the Lung. Brit. Jr. of Dis. Chest 54:266. 18. Weiss William (1971), Cigarette smoking, asbestosis and pulmo- nary fibrosis Am. Rev. Resp. Dis. 104:223_227. 26. Yazicioglu S., R. Ilcayto et al (1980), Pleural calcification, pleural mesothelioma and bronchial cancers caused by tremolitc dust, 19. Selikofi I.J., Echyler et al (1968), Thorax 35:564-569. Asbestos exposure, smoking and 27. Gibbs G.W., Jodoin G. et al Neoplasia. The Jr. of Am. Med. (1971), Early effect of asbestos Association 204:106-112. exposure in hmg function 20. Nath A.R., Capel L.H. (1974), Am. Rev. Resp. Dis. 104:525- Crackles -- early and late, Tho- 533. rax 29:223-227. 28. Brian E.H. and William R. (1961), 21. Chem et al (1973), Asbestos workers in Singapore. Arch. Environ. Pathology of asbestosis with re- ference to lung function Thorax Health 26:290-293. 17:261-28-1. 22. Soutar C.A., Simon G.. Turnes Warwick M. et al (i974), The~ 29. Muldoon B.C., Warwick M.T. radiology of asbestos induced di- (1972), Lung function studies in sease of the lungs. Brit. Jr. of asbestos workers. Brit. Jr. Dis. diseases of the Chest 65:235-252. Chest 60:"121.