Occupational and environmental medicine · 2012
Longitudinal decline in lung function in former asbestos exposed workers.
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Algranti Eduardo, Mendonça Elizabete Medina Coeli, Hnizdo Eva, De Capitani Eduardo Mello, Freitas Jefferson Benedito Pires, Raile Vilton, Bussacos Marco A
Аннотация
BACKGROUND: This study was designed to assess the effect of asbestos exposure on longitudinal lung function decline.
METHODS: A group of 502 former asbestos-cement workers with at least two spirometry tests 4 years apart. Repeated evaluations included respiratory symptoms questionnaire, spirometry and chest imaging. Asbestos exposure was ascertained as years of exposure, an index of cumulative exposure and latency time. The mixed effects model was used to evaluate the effect of exposure on the level and rate of change in forced expiratory volume in 1 s (FEV(1)) and forced vital capacity (FVC).
RESULTS: Mean age at entry was 51 (SD 9.9) years, mean latency time 25.6 (SD 10.0) years, mean follow-up time 9.1 (SD 2.8) years and mean number of spirometry tests 3.5. The FEV(1) level was significantly related to pack-years of smoking at entry and during the follow-up, the index of cumulative asbestos exposure at entry, and the presence of asbestosis at follow-up. The FVC level was significantly related to pack-years of smoking during the follow-up, cumulative asbestos exposure at entry, asbestosis and pleural thickening at follow-up, and body mass index at entry. Asbestos exposure was not associated with increasing rates of FEV(1) and FVC decline. However, FEV(1) regression slopes with age, estimated by terciles of cumulative exposure, showed significant differences. Combined effects of smoking and exposure conferred further acceleration in lung function decline.
CONCLUSIONS: Occupational exposure in asbestos-cement industry was a risk factor for increased lung function decline. The effect seems to be mostly concentrated during the working period. Smoking and exposure had synergic effects.
METHODS: A group of 502 former asbestos-cement workers with at least two spirometry tests 4 years apart. Repeated evaluations included respiratory symptoms questionnaire, spirometry and chest imaging. Asbestos exposure was ascertained as years of exposure, an index of cumulative exposure and latency time. The mixed effects model was used to evaluate the effect of exposure on the level and rate of change in forced expiratory volume in 1 s (FEV(1)) and forced vital capacity (FVC).
RESULTS: Mean age at entry was 51 (SD 9.9) years, mean latency time 25.6 (SD 10.0) years, mean follow-up time 9.1 (SD 2.8) years and mean number of spirometry tests 3.5. The FEV(1) level was significantly related to pack-years of smoking at entry and during the follow-up, the index of cumulative asbestos exposure at entry, and the presence of asbestosis at follow-up. The FVC level was significantly related to pack-years of smoking during the follow-up, cumulative asbestos exposure at entry, asbestosis and pleural thickening at follow-up, and body mass index at entry. Asbestos exposure was not associated with increasing rates of FEV(1) and FVC decline. However, FEV(1) regression slopes with age, estimated by terciles of cumulative exposure, showed significant differences. Combined effects of smoking and exposure conferred further acceleration in lung function decline.
CONCLUSIONS: Occupational exposure in asbestos-cement industry was a risk factor for increased lung function decline. The effect seems to be mostly concentrated during the working period. Smoking and exposure had synergic effects.