chambers for 5 days at 100 or 250 mg m~ 3 . Following the exposure period, cells and fluids from sham and silica-exposed animals were recovered by bronchoalveolar lavage (BAL). Granulocytes, as well as lactate dehydrogenase (LDH), N-acetylglucomsaminidase (NAG) and protein values were measured in BAL fluids at several postexposure time periods. In addition, the lungs of exposed mice were processed for BrdU pulmonary cell labeling, histopathological and morphometric analysis. The results showed that a 5 day exposure to silica produced a sustained, but low-level inflammatory response, measured up through 6 months postexposure in the lungs of black and beige mice. Cell labelling of terminal airway and lung parenchymal cells in beige and black mice were enhanced over corresponding unexposed controls. The results demonstrated minor differences in the pulmonary inflammatory or cell proliferative responses between the two strains of silicaexposed mice. Preliminary morphometric analysis of pulmonary lesions among silica-exposed beige and black mice did not show a dose response relationship, however, the lesions were similar in nature and in distribution at 6 months postexposure. In general, the mice demonstrated a mild response to silica exposure when compared to the two strains of rats. We had expected to observe a reduced pulmonary response to inhaled silica particles in the neutrophil-defective beige mouse relative to the normal C57 black mouse. However, the species effect (i.e. reduced responsiveness in mice) seemed to take precedence over the differences in response among the two strains. Although it has been reported by others that exposure to silica may cause pulmonary fibrosis in mice, our results following acute exposures indicate that the two strains of mice tested here are much less responsive to the toxic effects of silica when compared to exposed rats.
