Abstract

Airborne particles Jess than 10 μsm in mass median aerodynamic diameter are associated with adverse effects on human health including chronic lung diseases and mortality, but the mechanisms by which these particles might cause or aggravate diseases are not specifically known. PM-10 represents a complex mixture, both in terms of size and chemical composition, and it contains both aqueous-media soluble and insoluble particles. Furthermore, the ambient aerosol composition varies markedly in different locations and at different times in the same location. To test the effects of PM-10 on pulmonary defenses in relation to specific cell targets, barrier-reared Sprague-Dawley rats were exposed to purified air, to two important constituents of the fine-particle 2.5 μm MMAD) fraction of PM-10. Exposures were 4 h/day, 4 dayslwk for 8 wk. Macrophage-dependent lung defense functions were significantly depressed by NOf, SO42-, and the high-concentration road dust exposures, compared to purified air controls. Lung permeability, as determined from measurements of albumin concentrations in bronchoalveolar lavage fluid, was significantly greater in rats exposed to high concentrations of road dust and NO3-, but not to SO42-, when compared to air-exposed controls. Quantitative histopathologic analyses, which included measurements of alveolar nuclear density, alveolar chord length, alveolar septal thickness, and alveolar cross sectional area, showed moderate to substantial changes. In general, the severity of the responses was in the order of SO42-NO3-road dust. The findings are consistent with those of epidemiological studies. This study also supports the hypothesis that the fine fraction of PM-10 is more toxic than the coarse fraction. © 1995 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.