Document v6zp2bMJqnn5qegYVg9w4ye68

American Journal of Industrial Medicine 19:161-169 (1991) Chrysotile Asbestos and Health in Zimbabwe: I. Analysis of Miners and Millers Compensated for Asbestos-Related Diseases Since Independence (1980) Mark R. Cullen, md, and Rabelan S. Baloyi, PhD Data on the health effects caused by locally mined chrysotile asbestos in Zimbabwe have been very limited. The prevailing local view has been that risk is minimal. In this report we critically reassess the cases of 51 individuals with asbestos exposure who have been compensated by the Central Pneumoconiosis Bureau since independence in 1980. Re sults demonstrate that the major health risks of exposure reported elsewhere--morbid asbestosis, nonmalignant pleural disease, malignant mesothelioma, and lung cancer--all occur in Zimbabwe, at least among workers in the asbestos mines and mills. It is concluded that further investigation and control measures in the industry are warranted. Key words: asbestosis, pleural disease, mesothelioma, lung cancer, chrysotile miners, chrysotile millers INTRODUCTION As one of the world's major suppliers of chrysotile asbestos and producer of several important asbestos products, Zimbabwe has a sizeable population exposed to the mineral, occupationally and environmentally. Currently, some 7,000 men are engaged in mining and milling of the major ore bodies in the Midlands, with another 3,000-4,000 engaged in the manufacture of asbestos construction materials (cement, asphalt, tiles) and automotive products (brakes, gaskets, clutches). An undetermined number of people are further exposed in the use, repair, and disposal of these ma terials. Some 40,000-45,000 people live within a few kilometers of the mills and mines; a large portion of the population lives and works in buildings made from asbestos materials. Despite these exposures, some of which have been ongoing for decades (the mines opening about 1910), there is general optimism among local observers that Yale New Haven Occupational Medicine Program, Yale University School of Medicine, New Haven, Connecticut (M.R.C.). Department of Occupational Health, Safety and Workers' Compensation, Ministry of Labour, Manpower Planning and Social Welfare, Harare, Zimbabwe (R.S.B.). Address reprint requests to Dr. Mark R. Cullen, Yale University School of Medicine, Occupational Medicine Program, 333 Cedar Street, New Haven, CT 06511. Accepted for publication June 20, 1990. 1991 Wiley-Liss, Inc. 162 Cullen and Baloyi health effects have been limited and a suggestion that the product itself--a hugely important export commodity--may be safer than amphibole or even chrysotile as bestos mined and processed elsewhere in the world. Although some of this impression may result from perhaps premature acceptance of some published opinions from Europe and North America regarding the lesser toxicities of chrysotile generally [Cullen, 1987], at least some opinion has been founded in observation, or rather lack of observations of anticipated sequelae, e.g., asbestosis, lung cancer, or mesothe lioma. Four papers have been published on the subject. Gelfand and Morton [1969] reviewed the asbestos-associated cases certified by the Pneumoconiosis Bureau be tween 1963 and 1967. Only 37 cases met international criteria for asbestosis, once cases of apparent silicosis or tuberculosis were excluded. The authors, without critical analysis of their data source, extrapolate from the results quantitative evidence of a very low rate of asbestosis given the total numbers apparently at risk. In 1977, Walker, a mine physician, described the absence of even a single case of malignant mesothelioma either in his personal experience or, to his knowledge, anywhere in the country. He also commented on the rarity of asbestosis and asbestosrelated pleural disease in the mining populations he had cared for but did not provide quantitative information. Two years later, Mostert and Meintjes [1979] reported six cases of railwaymen who had developed asbestosis (four cases) and mesothelioma (two cases). Their careful review of exposures, however, clearly documented that each man had had some exposures to nonlocally mined amphibole fibers; indeed, each had worked during the time when crocidolite asbestos was being imported and used by the rail roads. In a note published in 1983, Mossup commented again on the rarity of asbestosrelated diseases in his experience, claiming further that few cases were being iden tified by the Pneumoconiosis Bureau despite expansion of its role. He presented, as well, results of a proportional cancer mortality analysis of asbestos miners done using the cancer registry of the Mpilo Central Hospital, which draws referrals from the mine area. These data show that only 12% of all cancers registered among asbestosexposed workers were primary bronchogenic, a rate similar to other occupational groups; this would suggest the absence of an asbestos effect, which would be ex pected to elevate the proportion of lung cancers as well as the total incidence of cancer cases (which could not be assessed by this method). In an as yet unpublished study, Armstrong and Elmes [1985] performed a cross-sectional survey of all active asbestos cement plant workers and a sample of asbestos mine and mill workers with more than 10 years of exposure. Among cement workers, for whom measured and extrapolated exposure levels were available, a clear dose-response of asbestos fiber on forced vital capacity and radiographic changes was demonstrated, consistent with previous studies of the cement industry in other coun tries. At the mines and mills, parenchymal radiographic abnormalities (ILO grade 1/0 or greater) were noted in 20% (mines) and 26% (mills), although the representative ness of the sample was not verified. As well, no dose-response could be shown on lung function using a surrogate index of exposure, years of exposure. No actual or reconstructed air levels were available at that time for the analysis. Given these very limited data sources, it was the aim of the present investigators to gain a clearer picture of the risks in the various exposure settings for malignant and 164 Cullen and Baloyi the X-rays, demographic data, medical and occupational histories, and laboratory reports. The basis for best-evidence diagnoses and vital status when known was also recorded. Final analysis was limited to cases meeting the following criteria. 1) Best evidence diagnosis was of an asbestos-related disease (asbestosis, benign pleural disease, lung cancer, or malignant mesothelioma); 2) Exposure to asbestos occurred exclusively at a Zimbabwe asbestos mine or mill, since general knowledge of expo sures to the total workforce is available and because universal X-rays have been performed during the period of interest. RESULTS Among the approximately 300 men certified by the Bureau as having occupational lung disease since 1980, 54 were identified as having worked at some time at an asbestos mining or manufacturing facility. Complete Bureau records and X-ray files were available on 51 of these men, who thus formed the study population. An attempt was made first to assign a clinical-radiologic diagnosis in each case, based on the records. In most cases, this was accomplished by radiographic inter pretation coupled with review of reports of physical examination and sputum smears and culture for acid-fast bacteria. This strategy was necessary because, in the majority of cases, no detailed clinical evaluation, e.g., functional studies, bronchoscopy, biopsy, etc., had ever been conducted and patients were dispersed geographically. Even among the 17 confirmed to have died, only five had received postmortem examinations, but two others had had premortem lung biopsies. Notably, biopsy or autopsy results were the initial basis for compensation in six of these seven cases; only one man in the series had been certified for compensation on clinical grounds and subsequently had histologic (postmortem) confirmation of diagnosis. Using this classification strategy, diagnoses were as follows: Ten cases had tuberculosis, smear- and culture-proven in six, suspected and treated clinically in the other four. In none of these cases could underlying pneumoconiosis be established. Eight cases met radiographic criteria for silicosis (i.e., symmetric small rounded opacities), simple in two and complicated in six. Among the latter, two were dem onstrated to have superimposed pulmonary tuberculosis by culture or biopsy; the remainder had typical features of progressive massive fibrosis. Interestingly, in five cases, no exposure to dust other than asbestos mining or milling could be docu mented. Six cases appeared not to have diseases primarily associated with dust or fiber exposures. One had chronic obstructive pulmonary disease demonstrated functionally and radiographically. A second had autopsy-documented adenocarcinoma of the pros tate. Two had focal infiltrates most consistent with infectious pneumonitis. One had clinically recognized congestive cardiac failure. The last had a diffuse, symmetric profusion of thick irregular opacities (ILO U/U) associated with hilar and paratracheal node enlargement, most consistent with some granulomatous lung disease, likely sarcoidosis; insufficient data were available for better classification. This left 27 men with findings consistent with one or more of the asbestosassociated diseases. Detailed clinical and occupational data on these workers appears in Table I. The findings can be summarized as follows:  sbestosi probabl te rm in t 'Sites: I, 2, active asbestos mines/mills, 3 -5 , closed asbestos mines/mills. oc v*r oo O' V -2 T2 *9 "3 eco I v-> --T> O^LN. O--' 00 CQ co <3 ii .5 e ^O _f*T u - = 32 -2 n" -1 u c r- 2 CJ * oc u .* > <3< < u J* * 41 30 CCO s o Vc c i o 00 ON T >N a- II - A "co H JO I 8 "ovir v 41 9 M ,2 >i a 2 XS VI --CO J8 - u o iJO to 1v5i < NOOO O' c3 5 <N ovi 15 V) < NO 00 O' 5 O' f*1 "O o c E| o E 1) 3 V) 83 . o Z z8 O Z r- f*1 NO 30 ON 30 O' e OO O' O TO > *oe c 41 41 >> u > dS < D a < < < << < u JoO 4s1 s cn -- * o 41 TO .c 5 c/1 CO J s. o n-- o co 8. o S cq Q NO fS 00 kn O' ON O' O' O' T 7 i ON T-- T m T NO iI NO o rl a vl --T - aa. ps -- ^ a o js os a. co -- 0 e X _ s5 J* U o I 3 eu o S 18 V) Vl a 's Vl 'vOi `vo5 S 2 O trt Vl to 3 VI 1V5) 1V5l a 1V5l <<<< a a NO ON s sm O 5-= sOO O Ja-J vzJi O' Tf D2 M_ (w4 ^3 *i Vl o r ^3 S? vi -- 41 c .2 C?5J jig- "c^ o *2 u "SZ Vl <2 41 JW ~-- ^Oco" ^o rOo 2 .9 32 x Sw CO X 41 c a 2 *3 PS a cO _ V2 ~ eo ?S Ji jo 2-- a^ xS >co1 --a 2 *o V2 . ,25 01 X ,, Ba X _ != o = O' a= c0 --3 0 "7 v " 1 IVl 32 J= J2 JD c J2 e o. v> VoI --^ Vyl O- Q. CO Uu JU CO o 1 o <0 O o cCO "2 a 38 Vl O to Vl eccoop *3 TM> <EU wa *-4a> | 00 t> =3 S Vl '3o Vl | VI "O3 to 1V5l *V01 Vl 1 vi" *> -= * oV&E>l e i 5 "35 a 1 Vl a =3 S2 H Vl VOl Vl 1V5l < s<<<< << < aaa iss mO i .5 ^ O' O' 5 ** O' O' 1 9 Da o--n r5n D- -- <N O' -- O' -- <N vCNr no rC-S Health Effects of Zimbabwean Asbestos 169 Mossup RT (1983): Asbestos hazards in Zimbabwe. Central African J Med 29:117-118. Mostert C, Meintjes R (1979): Asbestosis and mesothelioma on the Rhodesia railways. Central African J Med 25:72-74. Musch DC, Higgins ITT, Landus JR (1985): Some factors influencing interobserver variation in classi fying simple pneumoconiosis. Br J Ind Med 42:346-349. Walker N (1977): Mesothelioma in Rhodesia's asbestos mines. Rhodesian J Occup Health 4:1-3.