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Co-exposure to ultrafine particulate matter and ozone causes electrocardiogram changes indicative of increased arrhythmia risk in mice
Kurhanewicz, N., R. McIntosh-Kastrinsky, L. Walsh, A. Farraj, AND M. Hazari. Co-exposure to ultrafine particulate matter and ozone causes electrocardiogram changes indicative of increased arrhythmia risk in mice. Presented at Society of Toxicology, March 10 - 14, 2013.
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.
Numerous studies have shown a relationship between acute air pollution exposure and increased risk for cardiovascular morbidity and mortality. Due to the inherent complexity of air pollution, recent studies have focused on co-exposures to better understand potential interactions. 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. We hypothesized that ozone co-exposure would enhance the acute effects of particles, particularly UFP. Conscious unrestrained C57BL/6 mice implanted with radiotelemeters 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 (4hrs); separate groups were exposed to either filtered air or O3 only. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Control animals experienced a decrease in HR during exposure. In relation, neither PM2.5 nor UFP alone caused any change, however with O3 co-exposure, HR remained transiently elevated above control levels. Exposure to UFP+O3 caused decreased PR-interval, transient increase in QRS, and increased QTc. PM2.5 alone caused QRS to decrease and O3 alone caused a decrease in QRS interval and QTc. There were no other significant differences in the ECG of any groups. Lastly, only animals exposed to UFP+O3 had an increase in the number of non-conductive P-waves; there were no differences in other arrhythmia counts. These data suggest that ozone co-expoure might worsen the stress response to PM, especially UFP, and cause repolarization heterogeneity in the heart, which would increase the risk of arrhythmogenesis. As such, this indicates that the cardiovascular effects of particle and gas co-exposures are not easily characterized, potentially increasing the complexity of risk assessment.