Workers exposed to asbestos fibers are known to be at increased risk of metaplastic airway disease and carcinoma. Although the risk of developing these diseases is increased markedly by asbestos exposure, the incidence of disease in the entire population is fairly low, approximately 1 case of cancer per 100 man-years of observation. This suggests that important host factors modulate the appearance of disease in subjects with similar risk factors. We have developed a number of sensitive biochemical markers, indicative of bronchial mucosal injury and metaplasia, which are manifest in a subpopulation of young smokers without asbestos exposure. We propose to utilize bronchoalveolar lavage to recover a homogeneous sample of bronchial and alveolar proteins for analysis from 100 subjects with known asbestos exposure. Subjects will be stratified by exposure history, radiographic and physiologic evidence of lung parenchymal fibrosis, smoking history and retinoid ingestion. We will compare these patients to smoking and non-smoking volunteers and cancer patients and analyze these data to determine whether analysis of bronchial proteins can indicate a subpopulation with early biochemical evidence of lung disease and whether retinoid ingestion is a factor which influences markers of airway injury and metaplasia.
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