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ASSESSMENT OF TOXICITY OF OIL COMBUSTION EMISSION EXPOSURE IN NORMAL AND HYPERTENSIVE RATS
Citation:
Gilmour, M I., U P. Kodavanti, K L. Dreher, M. J. Daniels, M. Schladweiler, Q T. Krantz, W P. Linak, C A. Miller, AND D L. Costa. ASSESSMENT OF TOXICITY OF OIL COMBUSTION EMISSION EXPOSURE IN NORMAL AND HYPERTENSIVE RATS. Presented at Society of Toxicology, Baltimore, MD, March 21-25, 2004.
Description:
It has been suggested that the increased morbidity and mortality associated with exposure to airborne particulates (PM) is related to materials derived from combustion sources such as gasoline, diesel, oil, wood and coal. In these studies heavy oil # 5 was burned in a residual oil combustor previously shown to produce approximately 150 mg/m3 of PM. The particles were then passed through a 2.2 m cyclone and diluted with clean ambient air. The resulting PM was then directed to a Hinners animal exposure chamber equipped for continuous monitoring of O2, CO, CO2, NOx, SO2, as well as total particle concentrations. Mean PM 2.5 concentrations ranged between 2 and 3 mg/m-3 with SO2 denuded to 2-3 ppm and 20-30 ppm NOx. Sprague Dawley and spontaneously hypertensive (SHR) rats were exposed to the combustion atmosphere for 4 hrs for one or three days and immediately and 20 hr later assessed for changes in systemic and pulmonary markers of injury and inflammation. Exposure to the emission atmosphere caused an increase in neutrophils and BAL lysozyme in both rat strains, but no significant changes in other markers of lung injury such as protein and LDH. Increased vanadium levels detected in the plasma of CEAS-exposed Sprague Dawley rats were associated with an elevated platelet count and decreased white blood cell numbers. Analysis of systemic biomarkers in SHR rats is in process. We conclude that these acute exposures resulted in modest levels of pulmonary inflammation, and that the biological effects may be more prominent in the systemic circulation. Future studies will determine the relative contribution of gases versus particles on these responses, and will test whether animals with cardiopulmonary disease are further compromised by such exposures. (This abstract does not necessarily reflect EPA policy.)