EXPOSURE-RESPONSE ANALYSIS OF RISK OF RESPIRATORY-DISEASE ASSOCIATED WITH OCCUPATIONAL EXPOSURE TO CHRYSOTILE ASBESTOS

Citation
L. Stayner et al., EXPOSURE-RESPONSE ANALYSIS OF RISK OF RESPIRATORY-DISEASE ASSOCIATED WITH OCCUPATIONAL EXPOSURE TO CHRYSOTILE ASBESTOS, Occupational and environmental medicine, 54(9), 1997, pp. 646-652
Citations number
27
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
13510711
Volume
54
Issue
9
Year of publication
1997
Pages
646 - 652
Database
ISI
SICI code
1351-0711(1997)54:9<646:EAOROR>2.0.ZU;2-5
Abstract
Objectives-To evaluate alternative models and estimate risk of mortali ty from lung cancer and asbestosis after occupational exposure to chry sotile asbestos.Methods-Data were used from a recent update of a cohor t mortality study of workers in a South Carolina textile factory. Alte rnative exposure-response models were evaluated with Poisson regressio n. A model designed to evaluate evidence of a threshold response was a lso fitted. Lifetime risks of lung cancer and asbestosis were estimate d with an actuarial approach that accounts for competing causes of dea th. Results-A highly significant exposure-response relation was found for both lung cancer and asbestosis. The exposure-response relation fo r lung cancer seemed to be linear on a multiplicative scale, which is consistent with previous analyses of lung cancer and exposure to asbes tos. In contrast, the exposure-response relation for asbestosis seemed to be nonlinear on a multiplicative scale in this analysis. There was no significant evidence for a threshold in models of either the lung cancer or asbestosis, The excess lifetime risk for white men exposed f or 45 years at the recently revised OSHA standard of 0.1 fibre/ml was predicted to be about 5/1000 for lung cancer, and 2/1000 for asbestosi s. Conclusions-This study confirms the findings from previous investig ations of a strong exposure-response relation between exposure to chry sotile asbestos and mortality from lung cancer, and asbestosis. The ri sk estimates for lung cancer derived from this analysis are higher tha n those derived from other populations exposed to chrysotile asbestos. Possible reasons for this discrepancy are discussed.