Activated alveolar macrophages (AMs) secrete interleukine (IL)-1 beta, IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta (TGF-beta), whose inflammatory and fibroblast-activating characteristics may play a role in the maintenance of pulmonary inflammatory processes and subsequent fibrosis. Human AMs were transferred to a gas cylinder and exposed to NO2 in concentrations ranging from 0.1 to 0.5 ppm in synthetic air for 30 min at 37 degree C. AMs were fixed on a polycarbonate membrane and placed on culture medium. A culture was established, with the exposed AM (nonstimulated or stimulated with 1 microgram/ml lipopolysaccharide [LPS]), and the remaining cells were used to determine the cytokines. IL-1 beta, IL-6, and IL-8 were quantified by commercial enzyme-linked immunosorbent assay kits (ELISA kits). TNF-alpha was determined with a "sandwich" ELISA, using the biotin-streptavidin system. NO2 exposure of nonstimulated AM did not result in changes in IL-1 beta, IL-6, TNF-alpha, and TGF-beta release, compared to the situation with control experiments. Exposure for 30 min to NO2 induced a significant decrease of LPS-stimulated IL-1 Beta, IL-6, IL-8, and TNF-alpha (p < .05). The release of TGF-beta was not significantly affected by NO2 exposure. Cytotoxicity of AM was checked by trypan blue exclusion, with values ranging from 1.3 to 3.0%. NO2 exposure of LPS-stimulated AM resulted in a functional impairment of AM after NO2 exposure regarding IL-1 beta, IL-6, IL-8, and TNF-alpha. Neither the spontaneous nor the stimulated release of TGF-beta were influenced by NO2.