Many epidemiologic studies have shown excessive respiratory disease morbidity in areas of high atmospheric pollution. This study was designed to develop and characterize an animal model and investigate the possible interactive effects of infection and particulate air pollutants using small laboratory animals. Models of human parainfluenza virus type 3 disease were established by aerosol inoculation of hamsters and cotton rats. The temporal course of the following were examined: lung virus titers; pulmonary histopathology; alveolar macrophage function; changes in pulmonary mechanics; serum antibody development and upper respiratory tract histopathology. Animals were exposed acutely (2 hours) to ammonium nitrate or lead oxide respirable aerosols before or following viral inoculation. Exposures ranging from 59-66 mg/cu. m. but not 0.76 mg/cu. m. of the nitrate resulted in a one-day extension of viral replication and concommitant retardation of peribronchial lymphocytic infiltration. Lead oxide exposures at levels greater than 2,350 micrograms/cu. m. increased lung virus titers and serum antibody titers. The models developed in these studies may be useful for future work on chronic exposure to the same or other pollutants and on the pathogenesis of virus/pollutant interactions.