Document L2XodmE7qZJ9ZV0xE70rrrjd

^ f n 5 6 > T3 ' Biologic monitoring of workers ex posed to a hazardous dust must be directed to the detection of early unfavorable changes in the hope that removal from exposure will prevent the progression of disease. Since chest radiography and pulmonary function are most widely used to monitor the respiratory health of as bestos-exposed workers, it is appro priate to review the relative sensi tivity of these two methods in detecting an adverse biologic re sponse to dust exposure in this indus try. At the top of Fig 6, selected simple spirometric measurements in average percent of the standardized value are plotted by exposure group. It can be seen that after a cumulative exposure of 100 mppcf-yr there is a gradual reduction in the mean values as dust exposure increases. At the lower half of the figure, the propor tion of workers with ' irregular or rounded small opacities at the one or two category levels, is plotted for each exposure group. It is apparent that the major increase in workers at each level of radiographic change also begins to appear after a cumulative exposure of 100 mppef-yr, which again reveals a dose-response rela tionship. One must conclude from these data that in considering groups of workers with varying levels of dust exposure, radiographic evidence of small opacities within the lung fields and pulmonary functional'change are equally sensitive in detecting diffuse parenchymal abnormalities associ ated with exposure to these fibrogenic dusts. However^it. must be re membered that even in the absence of x-ray film changes, individuals may show decline in pulmonary function unexplained by other factors and pre sumably related to dust exposure. The reverse is also true, ie, radiograph ic abnormalities may appear before changes in pulmonary function. It is suggested that both methods of bio logic monitoring be used in order to detect the earliest abnormalities in the largest number of exposed work ers. In contrast to studies of mortality from malignant diseases in asbestosexposed workers, there seems to be little interaction between cigarette Standardized Value, % Fig 5.--FEV,: Distribution of standardized values. smoking and the diffuse fibrbgetiic ef fect of dust exposure in this indus try. As indicated previously, this-is demonstrated by the equallygood exposure-pdlmonary function relation ship in nonsmokers after allowance for personal smoking habits. This is not to say that cigarette smoking has not reduced pulmonary function in workers who smoke; that it has is shown by a lower position of pulmo nary function measurements, while the additional rate of decline result ing from dust exposure is similar for the smoking groups. The diffuse parenchymal and pos sible airways damage associated with asbestos dust exposure seem to be rel atively unaffected by host factors, as evidenced by the distribution of pul monary function in the lowest and highest exposure groups. In the FEV, for example, we demonstrated pri marily a shift in the group mean ob served values (downward fri'tiie'highexposure-group), rather than a significant "skewing" or "tailing" effect. Available evidence suggests that crocidolite asbestos has a greater car cinogenic effect than chrysotile.3 This suspicion has led previously to a dif ferent standard for these two fiber types in the United Kingdom. It has not been demonstrated previously that crocidolite has a more marked ef fect on the diffuse pulmonary paren chymal process. Although crocidolite exposures in the pipe-making area of one of the two plants studied were considered reasonably low, there ap pears to have been a significantly greater adverse effect on pulmonary function in workers exposed to cro cidolite than on a matched group in . 96 Arch Environ Health/Vol 30, Feb 1975 Lung Function/Weill et al ST05SS721t ployed in these two plants will deter mine if there is an excess risk of the development of neoplasms in workers employed in this industry. Fig 6 --Selected spirometric indexes of long function and prevalence of small opac ities on the chest x-ray films in relation to dust exposure. the same plant for whom no crocidolite exposure was documented. The crocidolite group has smaller lung volumes, lower FEV,, and reduced DL. This subject will be separately consid ered in the future report. Finally, threshold limit valuaaraust obviously take into consideration all demonstrated adverse health effects. This report considers only the diffuse fibrogenic effect of asbestos exposure in the asbestos cement products man ufacturing industry. However, the data from this study demonstrate not only a dose-response relationship but suggest that a threshold dust level exists in this industry-below which diffuse pulmonary fibrosis does not oc cur. While past dust levels were ex pressed in total particulate units, con version to fiber levels is desirable for evaluation of asbestos exposure. A conservative calculation using data obtained previously from simultane ous sampling with the impinger and fiber counting method, leads to a con version ratio of 2 fibers/ml for 1 ,mpppf.l: The cumulative total dust exposure level of 100 mppcf-yr would therefore be equivalent to 200 fiber/yr or an exposure to 5 fibers/ml . for a working lifetime of. 40 years. While it is hoped that this level of ex posure is "safe" in regard to the de velopment of diffuse lung changes, any such analysis must be cautiously interpreted, since follow-up of exposed workers continuing well beyond the time of their active employment may increase the incidence of radiographic and functional abnormalities. These important additional data should re sult from the longitudinal investiga tion that involves a cohort of this population. A mortality study of all workers who have ever been em Supported by a grant from the Institute of Oc cupational and Environment*] Health of the Quebec Asbestos Mining Association and a Spe cified Center of Research (SCOR) grant* Dm- sion of Lung Diseases, NHLI (HL-15092). References 1. Weill H, Waggenapack C, Bailey W, et al: Radiographic and physiologic patterns among workers engaged in manufacture of asbestos ce ment products. J Oecup Med 15248*252, 1973. 2. Meade F, Saunders MJ, Hyatt F, et aL A. tomatic measurement of lung function. La**.' 2.573-575,1965. 3. Enterline PE, Henderson V: Type of i- bestos and respiratory cancer in the asbestos in dustry. Arch Environ Health 27312-317, 1973. 4. Rossiter CE, Weill H: Ethnic differences in lung function: Evidence for proportional differ ences. Int J Epidemiol 3:55-61, 1974. 5. Paul R, Fletcher GH, A^Hison G: A com parative study between Europeans and Africans in the '*'inijig Hvastrjl of northern RhodeHa. Med p-v 5:69-74, 6. Lapp N'L. A-fjAcdia HE, Hall R, et al: Lung volume-: and flow in black and white suo jects. Yhc/'nx 29:i$-v!.681 1974. 7. Rossiter CE, Weill H: Synergism between dust exposure and smoking: An artefact in the statistical analysis of lung function? Bull Physi- opathol Retpir, to be published. 8. Williams R, Hugh-Jone* P: The stgnift- cance of lung function chaoges in asbestosis. Thorax 15:10*119, 1960. 9. Leathart GL: Clinical, bmnchographic, ra diological and physiological observations in ten cases of asbestosis. Br J Ind Med 17213-227, 1960. 10. Bader ME, Bader RA, Tierstein AS, et al: Pulmonary function and radiographic changes in 598 workers with varying duration of exposure to asbestos. J Mt. Sini6 Hotp 37A92-50& 1970. . * It RegaaGM, TaggR, Walfogd J,.^ aLThe , ; relative importance of 'clinical, ridiolo^cal and pulmonary function variables in evaluating as- bestosis and chronic obstructive airway disease . in asbestos workers. Cfcn Sci 4l5$3b!$2. V?". 12. Murphy RLH, Ciensler EA, Redding - ' et al: Low exposure to Asbestos: Gm exfch&n* ` ship pipe coverers and controls.VAreA-E* Health 25353-264, 1972. 13. Gaensier EA, Carrington CB, Cooto RE,. al: Pathological, physiological, and radiological correlations in the pneumoconioses. Ann NY Acad Sci 200374-607, 1972. 14. Muldoon BC, Tumer-Warwick M: Lung function studies in asbestos workers. Br J Dis Chest 66:121-132, 1972. 15. Jodoin G, Gibbs GW, Macklem PT, et al: Early effects ot asbestos exposure on lung func tion. Am Rev Respir &i* 104:525*535, 1971. 16. Becklake MR, Fournier-Massey G, Rossi ter CE, et al: Lung function in chrysotile as bestos mine and mill workers of Quebec. Arch Environ Health 24:401-409,1972. 17. Lynch JR, Ayer HE. Johnson DL: The in terrelationships of selected asbestos exposure in dices. Am Ind Hyy Aseoc J 31398-604, 1970. Arch Environ Health/Vol 30, Feb 1975 Lung Function/Weill et al 97 ARCH ENVIRON HEALTH V o l 3 0 , Feb 1975 pp. 88-97 4"S 0) a a rct