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Ozone co-exposure modifies cardiac function responses to fine and ultrafine particulate matter in mice
Citation:
McIntosh-Kastrinsky, R., H. Tong, N. Kurhanewicz, L. Walsh, A. Farraj, AND M. Hazari. Ozone co-exposure modifies cardiac function responses to fine and ultrafine particulate matter in mice. Presented at Society of Toxicology, March 10 - 14, 2013.
Impact/Purpose:
The purpose of this study was to determine the cardiac effects of concentrated ambient particles (CAPs) and ozone co-exposure in mice. This work fulfills Agency goals because it examines the detrimental health effects of air pollution and will add data which could be used for risk assessment.
Description:
There is growing evidence from epidemiological studies that show acute exposure to particulate matter (PM) increases the risk of cardiovascular morbidity and mortality. Although the data supporting these findings are increasingly more convincing, the immediate impact of PM inhalation on cardiac function needs to be further clarified; this is particularly true of multipollutant exposures. Thus, this study was designed to evaluate the cardiac effects of concentrated ambient fine (PM2.5) and ultrafine (UFP) particles with and without ozone (O3) co-exposure. Based on previous findings, we hypothesized that UFP would cause the greatest decrement in cardiac function and that O3 co-exposure would worsen the response. Mice were exposed by whole-body inhalation to either 250 g/m3 PM2.5 or 100 g/m3 UFP with or without 0.3 ppm O3; separate groups were exposed to either filtered air or O3 only. Twenty-four hours after exposure, cardiac function was assessed using a Langendorff cardiac perfusion preparation. Coronary flow, left ventricular developed pressure (LVDP) and contractility were measured before and after cardiac ischemia/reperfusion (I/R) injury. PM2.5 or O3 alone, or co-exposure to UFP+O3 caused a significant decrease in baseline LVDP and contractility. Interestingly, UFP alone or PM2.5+O3 did not cause significant decrements in cardiac function when compared to controls, nor were there significant differences in recovery LVDP or contractility between any group after I/R injury. These data suggest that the cardiac effects of PM inhalation are dependent on particle size and that O3 interacts with PM2.5 and UFP differently, resulting in varied cardiac impacts. Thus, these findings indicate that the cardiovascular effects of particle and gas co-exposures are not simply additive or generalizable, which increases the complexity of risk assessment.