The process of infection has been defined as an interaction of a host, a microbe, and the environment. In the natural environment, healthy individuals exist in equilibrium with potentially pathogenic microorganisms. Using this concept, an animal-model system was developed to study the effects of pollutants that can affect this equilibrium and result in acute pulmonary disease. Increase of mortality from exposure to several pathogenic organisms has been reported for a variety of animal species after exposure to ozone, nitrogen dioxide, and a variety of trace metals. There are a number of possible mechanisms by which the lung can become more vulnerable to microorganisms. These include (1) reduction in deposition or retention of bacteria, (2) slowing of physical removal of bacterial cells by the mucociliary mechanisms, (3) dysfunction of the alveolar macrophages, (4) alteration of the acellular lining material (surfactant) of the deep lung, (5) the presence of edema fluid or inflammatory exudate in the airway, and (6) pulmonary immunosuppression. The influence of environmental pollutants on each of these factors is discussed.