Pulmonary macrophages are an important component of immune defense against inhaled foreign particles and microorganisms. In humans and other mammals, exposure to moderate amounts of ozone (O3) can inhibit functional capacities of alveolar macrophages. In many wilderness areas downwind of urban centers, ozone levels frequently exceed national standards. We report results of 4-h inhalation exposures to 0.8 parts per million O3 on pulmonary macrophage viability and phagocytosis capacity in marine toads, Bufo marinus. At 1 and 24 h after ozone exposure, macrophages had reduced in vitro capacity to phagocytize fluorescent polystyrene microspheres. By 48 h postexposure, there were no differences in these macrophage functions between ozone- and air-exposed toads. Macrophage yield did not differ among exposure groups nor did exposure to elevated temperatures (30 degrees C) for up to 48 h affect recovery of macrophages. However, compared with the millions of macrophages per milliliter recovered in mammals by similar procedures, pulmonary macrophage yield was typically in the range of 50 to 200 x 10(3) per milliliter extracted fluid. These results are the first to report effects of an air pollutant on amphibian immune system function and suggest a possible role of oxidant air pollutants in regional declines of amphibian populations.