Inhaled particle-bound sulfate: Effects on pulmonary inflammatory responses and alveolar macrophage function

Acid sulfate-coated solid particles are a significant environmental hazard produced primarily by the combustion of fossil fuels. We have previously de scribed a system for the nascent generation of carbonaceous particles surfa ce coated with approximately 140 mu g/ m(3) acid sulfate [cpSO(4)(2-); 10 m g/m(3) carbon black (CB) and 10 ppm sulfur dioxide (SO2) at 85% relative hu midity (RH)]. The effects of inhaled cpSO(4)(2-) on pulmonary host defenses are assessed in the present work. Mice were acutely exposed (4 h) to eithe r 10 mg/m(3) CB, 10 ppm SO2 or their combination at 10% or 85% RH in a nose -only inhalation chamber. No evidence of an inflammatory response was found following any of the exposures as assessed by total cell counts and differ ential cell counts from bronchoalveolar lavage fluid. However, alveolar mac rophage Fc receptor-mediated phagocytosis decreased only following exposure to 140 mu g cpSO(4)(2-) significant suppression occurred after 24 h, maxim al suppression occurred at 3 days postexposure, and recovery to preexposure levels required 7-14 days. Intrapulmonary bactericidal activity (IBA) was also suppressed only after exposure to 140 mu g cpSO(4)(2-) suppression was maximal at I day postexposure and recovered by day 7. To assess the effect s of lower cpSO(4)(2-) concentrations, mice were repeatedly exposed to 7 mg /m(3) CB and 1 ppm SO2 at 85% RH (similar to 20 mu g/m(3) cpSO(4)(2-) for 4 h/day) for up to 6 days. A significant decrement in IBA was observed follo wing 5 and 6 days of exposure. These studies indicated that acute or repeat ed exposure to cpSO(4)(2-) could alter pulmonary host defense mechanisms.