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Comparative dose-response assessment of various combustion source particles to indcue acute lung-injury and exacerbate atherosclerosis in ApoE-Mice
Citation:
DREHER, K. L., R. J. SNYDER, N. Haykai, AND H. Floyd. Comparative dose-response assessment of various combustion source particles to indcue acute lung-injury and exacerbate atherosclerosis in ApoE-Mice. Presented at American Association for Aerosol Research 2010 Conference, San Diego, CA, May 22 - 26, 2010.
Impact/Purpose:
Studies have demonstrated the ability of air particulate pollution to exacerbate atherosclerosis. Research has yet to determine the contribution of specific sources and particle physicochemical properties responsible for this health effect. ApoE-I-mice were employed in a subchronic dose-response exposure design to examine the effect of specific combustion source particles (diesel coal, oil and volcanic ash) had on atherosclerosis in conjunction with their ability to induced acute lung inflammation and inherent reactivity. Results indicated exposure to combustion source particles exacerbates atherosclerosis in a manner independent of both their ability to induce acute lung inflammation, particle reactivity or dietary fat.
Description:
Exposure to concentrated ambient particles (CAPs) has been shown to increase arterial plaque area and size in atherosclerosis susceptible mice. CAPs are a complex aerosol mixture consisting of wind-blown dust. emissions from the combustion of fossil fuels, and secondary transformation products. Research has yet to determine the contribution of specific sources and specific particle physicochemical properties to CAPs-induced exacerbation of cardiovascular disease (CVD). Experiments were initiated to assess the effect of specific combustion source particles on CVD in comparison with their ability to induced acute lung inflammation and inherent reactivity. Studies examined the ability of equivalent amounts of diesel exhaust particles (DEP), coal fly ash (CFA), residual oil fly ash (ROFA), and Mt. St. Helen's [MSH) volcanic ash to affect plaque area following pulmonary exposure by pharyngeal aspiration (5, 10,23 ug/mouse/week) of ApoE-Imice fed high fat or normal chow diets (23 ug/mouse/week) for 3 months. Acute pulmonary inflammation of each particle was assessed by bronchoalveolar lavage 24 hr following ApoE exposure to 10 or 23 ug/mouse. Inherent particle reactivity was assessed by the thiobarbituric acid substance assay (TSARS). Quantitative analysis of plaques demonstrated a significant increase in plaque area within all exposure\dose groups fed normal chow compared to saline exposed controls. No difference versus controls was observed in any of the exposure\dose groups fed the high fat chow. No hierarchy in the ability to increase plaque area was observed among the different combustion particles. ROFA, DEP, and MSH particles displayed differential TBARS activity and acute pulmonary inflammation at 24h post-exposure, which did not correlate with their ability to increase plaque size. These resultsindicate that exposure to combustion source particles exacerbates atherosclerosis in the ApoE/-model in a manner independent of both their ability to induce pulmonary inflammation, inherent particle reactivity and dietary fat intake. (This abstract does not necessarily reflect EPA policy)