Oxidative stress, inflammation, and pulmonary function assessment in rats exposed to laboratory-generated pollutant mixtures.

Oxidative stress may mediate adverse health effects of many inhaled pollutants. Cardiopulmonary responses of Sprague-Dawley rats to inhalation of whole or filtered gasoline engine exhaust (GEE, FGEE); simulated downwind coal emission atmospheres (SDCAs) from two types of coal, each tested at two concentrations; and two concentrations of re-aerosolized paved road dust (RD) were evaluated. In situ chemiluminescence and thiobarbituric acid-reactive substances (TBARS) were used to evaluate oxidative reactions in the lungs, heart, and liver immediately following exposures. Pulmonary inflammatory responses were measured by bronchoalveolar lavage (BAL) cell counts. Respiratory function parameters during exposure were measured by plethysmography. Only GEE significantly enhanced in situ chemiluminescence (all three organs), but only exposure to the high RD concentration increased TBARS (hearts only). There was a weak trend toward increased macrophages recovered in lavage fluid from both SDCAs, and macrophages were significantly elevated by both FGEE and the lower concentration of RD. Respiratory function effects were small, though the effects of the Central Appalachian low-sulfur SDCA on enhanced pause and the effects of the Powder River Basin SCDA on tidal volume were significant. The discordance between the oxidative stress indicators may relate to the use of a single time point in the context of dynamic changes in compensatory mechanisms. These results further suggest that inflammatory responses measured by BAL cellularity may not always correlate with oxidative stress. Overall, the toxicological effects from exposure to these pollutant mixtures were subtle, but the results show differences in the effects of atmospheres having different physical/chemical characteristics.