UC Irvine

Proliferation of atherosclerotic lesions has been linked to environmental exposures to ambient particulate matter (PM) in susceptible mouse models and could be one factor in the epidemiological link between air pollution and increased cardiovascular mortality. However, less is known about the progression of atherosclerosis following exposure to ozone or a mixture of ozone and PM. Both ozone and PM exposure can cause free radical formation that can lead to cellular damage and stimulation of inflammatory processes in the vasculature. One of the consequences of inflammation in the vasculature is proliferation of smooth muscle cells (SMCs). The purpose of this research was to investigate if concentrated ambient particles (CAPs) with or without ozone exposure leads to smooth muscle proliferation in blood vasculature of mice predisposed to developing atherosclerosis. ApoE -/- 12-week-old mice (~15/group) were exposed to CAPs (10x Irvine, CA ambient levels), 200 ppb ozone, or a mixture of CAPs and ozone, for five hours a day for four days a week. A control group was exposed during the same period to clean, filtered air. The specific vessel examined was the brachiocephalic artery. The smooth muscle present on tissue sections of these vessels were visualized by using an anti-alpha smooth muscle actin (SMA) antibody and streptavidin-biotin for detection. The smooth muscle actin stained areas within each arterial tissue were calculated using Microsoft Paint, Image J, Photoshop, and MATLAB. Results suggested that there was less smooth muscle area in the groups exposed to ozone. These findings were not statistically significant at the p < 0.05 level.