Alveolar macrophages lie on the air side of the alveolar-capillary barrier of the lung. They originate from circulating monocytes and are an important first-line host defense against inhaled microorganisms. In monocytes and macrophages, phagocytosis is associated with an increase in O2 consumption and superoxide anion (O2-) generation, that is, "the respiratory burst". O2- is the precursor of highly reactive, oxygen-derived free radicals that are used to kill potential pathogens. Although it is well known that airborne particulate matter inhibits the phagocytic activity of alveolar macrophages, very little is known about the effect of airborne particulate extracts on the respiratory burst. In this study, monocytes isolated from the peripheral blood were incubated for 2 hr at 37 degrees C with increasing concentrations of particulate extract and then stimulated for 30 min with phorbol 12-myristate 13 acetate (PMA) or with Zymosan. The released O2- was measured by the superoxide dismutase inhibitable reduction of cytochrome C. The results cleary showed that, at a particulate concentration of 0.17 mg/mL, the production of O2- was reduced to 22% and 40% of the control values when the cells were stimulated with PMA and Zymosan, respectively. Concomitantly, there was a release of LDH in the supernatant (50% of the total), indicating that a large proportion of cells were damaged by the treatment with the environmental pollutants, and some cytosolic components were released from the cells. Giemsa staining of the treated monocytes revealed the presence of many cells with a dispersed cytosol; the nucleus, although not destroyed, had a different shape. It was suggested that the airborne particulate matter has a toxic effect that induces the disintegration of the plasma membrane. Cytosolic factors (proteins and coenzymes) necessary for O2- production leak from the cells and superoxide generation is therefore reduced. It remains to be determined whether this phenomenon also occurs in vivo.