To elucidate the effect of coal and diesel particulates on the susceptibility of the host to respiratory infection, CD-1-Swiss-mice were exposed for 1, 3, or 6 months to inhalation of coal dust (CD), diesel engine emissions (DEE), or a combination of both (CD/DEE), followed by initiation of influenza virus infection. Exposures were to 2mg/m3 total particulates, either singly (2mg/m3) or in combination (1mg/m3 of each). Influenza mortality was assessed, and other mice were sacrificed from 0 to 11 days after infection and assayed for virus in lung suspensions, interferon titers, and viral antibody levels. No significant differences were evident between the treatment groups after 1 month of exposure or in mortality following 3 and 6 months of exposure, but the incidence of lung consolidation in mice exposed to DEE and CD/DEE for 3 months was 96.5 and 97 percent, respectively, as compared to 61.2 percent in controls; in the 6 month group, the respective figures were twice as high as in controls. Levels of viral growth in lungs of DEE and CD/DEE treated animals were higher than in controls and were accompanied by depressed levels of interferon. Levels of influenza virus antibody were four times higher in the treated animals, especially the 6 month group, as compared to controls, but histologic studies of the lungs failed to demonstrate qualitative differences in inflammatory responses between treated and control animals, although there was evidence of different response severity relative to the particulate agent involved. After 3 and 6 months of exposure, DEE and CD/DEE animals presented evidence of focal macular collections of pigment laden macrophages. The author concludes that exposure to diesel emissions increases the severity of influenza infection, while the addition of coal dust has no significant effect.