Research Projects

Atmospheric concentrations of ozone, nitrogen dioxide, carbon monoxide, etc., considerably above ambient have been shown to represent a significant health hazard (l-5). Unfortunately, at the present time we do not have a laboratory test system to assess the biological significance of ambient concentrations of these pollutants. This inability to demonstrate biological consequences with relevant pollutant exposures necessitates that air pollution control standards be arbitrary and insufficiently objective. Recent studies in our laboratory (funded by the Clean Air for California Program Project S-5) have demonstrated in mice and rats that ozone exposure significantly impairs intrapulmonary bactericidal function (6-8). These experiments showed a concentration dependent inhibition in murine ability to kill inhaled bacteria following exposures of four hours or more to ozone concentrations of 0.62 ppm and greater.

Previous investigations have shown that intrapulmonary bactericidal activity is due to phagocytosis by pulmonary macrophages and that this cell system is the primary host defense against inhaled bacteria (9). Since the anatomic position of the pulmonary macrophage virtually obligates intimate exposure to any inhaled pollutant, this key element in defense might well suffer when any potentially toxic substance is inhaled. Therefore, although the mechanisms responsible for much pollutant induced impairments in pulmonary function are not well understood, it is likely that abnormalities in bactericidal function will occur and correlate with increasing concentrations of the pollutant.