We evaluated the effect of chronic tobacco smoke exposure on the function of the alveolar macrophage (AM) in mice. Tumor necrosis factor-α production of the AM triggered by lipopolysaccharides was smaller in smoke-exposed mice as compared to control mice but did not reach statistical significance (27.3 ± 4.0 vs. 34.8 ± 4.9 U/ml). The percentage of AM which did not phago-cytize latex particles in the smoke-exposed mice was significantly larger than that in control mice (33.9 ± 2.3 vs. 20.8 ± 2.1%; p < 0.05). la antigen expression of the AM was significantly larger in smoke-exposed mice (cytotoxicity index: 0.180 ± 0.033 vs. 0.038 ± 0.0118; p < O.Ol). The asialo-GMl antigen expression was similar in both groups (0.949 ± 0.007 vs. 0.961 ± 0.011). Although the precise mechanisms of these functional changes of the AM by tobacco smoke exposure are not clear, they may have some immunological effects on the alveolar space.