Non-malignant asbestos-related diseases in Brazilian asbestos-cement workers.

BACKGROUND: Production of asbestos-cement products in Brazil started in the 1940s, peaked in the 60-70s and is still an active industry. This study was designed to assess the non-malignant effects of asbestos exposure in the asbestos-cement industry in Brazil. METHODS: A group of 828 former asbestos-cement workers enrolled in a cross-sectional and cohort study of respiratory morbidity, submitted to a detailed occupational history, respiratory symptoms questionnaire, spirometry, PA chest x-ray, and high resolution computed chest tomography (HRCT). Asbestos exposure was assessed by years of exposure, cumulative exposure (a semi-quantitative method), and latency time from first exposure. Asbestosis and pleural thickening were assessed according to HRCT criteria. RESULTS: Asbestosis was present in 74 (8.9%) and pleural thickening in 246 (29.7%). Using the HRCT as the "best available evidence", it was shown that were more false negatives than false positives in the x-ray readings for parenchymal (21.6% false negatives, 4.2% false positives) and pleural (26.0% false negatives, 14.4% false positives) diseases due to asbestos. Latency time from first exposure was the best predictor for both asbestosis and pleural thickening. Subjects in the higher exposure groups presented lower levels of lung function. Obstructive defects were significantly related to smoking, shortness of breath, body mass index, and age, whereas restrictive defects were related to asbestosis, shortness of breath, and latency time. Chronic bronchitis increased with latency time in the three smoking groups and was significantly related to pleural thickening (OR 1.56 (1.00-2.42)). Shortness of breath was significantly associated with body mass index and pleural thickening (OR 1.30 (1.24-2.09)). CONCLUSIONS: Pleural thickening and asbestosis showed a significant association with latency time and exposure. FVC and FEV(1) decreased across increasing profusion with an added effect of pleural thickening. There was a significant and independent effect of exposure on lower levels of FVC and FEV(1). Obstructive defects were mainly related to smoking and restriction to asbestosis. Dust exposure and smoking were synergistic in increasing chronic bronchitis and shortness of breath report. Shortness of breath report was also related to pleural thickening and higher body mass index.

Asbestos-Related Pleural Thickening is Independently Associated With Lower Levels of Lung Function and with Shortness of Breath.

This study investigated the relative contribution of asbestos-related pleural thickening (PT) to lung function indices and to respiratory symptoms. A group of 828 former asbestos cement workers enrolled in a cross-sectional and cohort study of respiratory morbidity and submitted to a detailed occupational history, respiratory symptoms questionnaire, spirometry, postero-anterior chest x-ray, and high-resolution computed chest tomography (HRCT). Asbestos exposure was assessed by years of exposure (a semi-quantitative method), cumulative exposure, and latency time from first exposure. Smoking was assessed in pack-years. PT and asbestosis were assessed according to HRCT criteria. Statistical analysis included descriptive analysis, univariate and multivariate analysis of variance for comparisons of factors related to PT, stepwise multiple regression analysis for continuous dependent variables, and logistic regression analysis for dichotomous dependent variables. Mean age was 51.4 (SD 10.5) years, mean years of exposure 12.4 (SD 8.8), mean cumulative exposure 79.9 (SD 68.5), and mean latency time 25.2 yr (SD 10.4). Of the 828, 238 (28.7%) were smokers, 288 (34.8%) former smokers, and 302 (36.2%) nonsmokers. PT was present in 246 (29.7%) and asbestosis in 74 (8.9%); 97 (11.9%) had shortness of breath of Grade III or more. PT subjects had lower height-adjusted forced vital capacity (FVC) and forced expiratory volume in I s (FEV1) and lower FEV1/FVC% (p < .00001 for all). Variables significantly related to PT were age (p < .000 1), years of exposure (p < .0000 1), cumulative exposure (p < .00001), latency time (p < .00001), pack-years (p < .0000 1), and asbestosis (p < .00 1). In a multiple stepwise regression model, after controlling for confounders, height adjusted FEV1 and FVC were in versely and significantly associated with PT, mainly when associated with asbestosis. A logistic regression model with shortness of brea th as the dependent va riable, con trolled for confounders, showed that PT was significa ntly associated with the symptom, even without asbestosis. In conclusion, PT is independently associated with lower va lues of FEV1 and FVC. PT is also independently associated with an increased risk of shortn ess of breath report. PT should be considered as a disease for clinical follow up and for compensa tion claims.