Faculty Bibliography

A disordered immunologic activity has been observed in humans and animal models of asbestosis and silicosis. To characterize the lung immunologic response following long-term occupational exposure to asbestos, bronchoalveolar lavage (BAL) was performed on 28 nonsmoking individuals. Increased BAL lymphocytes were observed in one third. Lung lymphocytes were predominantly of the CD4+ helper-inducer subtype with increased CD4+/CD8+ ratio and increased surface expression of DR antigen consistent with the activation phenotype. Histologic evaluation of lung tissue from two individuals with lymphocytic-macrophage alveolitis and asbestos exposure revealed an infiltration of alveolar walls with chronic inflammatory mononuclear cells (lymphocytes). Interferon gamma was spontaneously released by BAL cells from 19 (76 percent) of 25 of the individuals with asbestos exposure and only one of ten normal controls. The release of interferon gamma by BAL cells could be further stimulated with concanavalin A and suppressed by cyclosporine. Although asbestosis is characterized by a predominant alveolar macrophage alveolitis, there is a subgroup with lymphocytic alveolitis and activated lymphocytes participating in the inflammatory response, especially in those without respiratory impairment early in the course of the disease process

Long-term asbestos workers who insulate pipes and boilers may develop interstitial lung disease associated with loss of lung function. To quantitate annual loss of lung function, 77 individuals with chest X-rays greater than or equal to 1/0 ILO category who were life-long non-smokers or ex-smokers for greater than 5 years were evaluated. Study parameters included pulmonary function tests and bronchoalveolar lavage for a mean of 3 visits over 30 +/- 2 months. The study participants were 56 +/- 1 years old and had 31 +/- 1 years' occupational exposure to asbestos. At the first visit, multiple regression analysis revealed significant associations between rales or radiographic opacities and VC, FEV1, and total lung capacity; significant associations were also found between neutrophils/ml lavage fluid with FEV1 and diffusing capacity (all p less than 0.05). Annual declines for the asbestos-exposed were VC -92 +/- 28 ml/yr and FEV1 -66 +/- 21 ml/yr. Declines in VC and FEV1 were less in those with reduced lung function at the initial visit. There were no significant associations between any of the annual declines and cells recovered by bronchoalveolar lavage. Compared to other asbestos-exposed cohorts followed longitudinally, asbestos insulators with radiographs greater than or equal to 1/0 and exposure greater than or equal to 20 years have larger rates of FVC and FEV1 decline for both non-smokers and ex-smokers