Citation:

Farraj, A., F. Malik, N. Coates, L. Walsh, D. Winsett, D. Terrell, L. Thompson, AND M. Hazari. Morning NO2 Exposure Sensitizes Hypertensive Rats to the Cardiovascular Effects of O3 Exposure in the Afternoon. Society of Toxicology, San Diego, CA, March 22 - 26, 2015.

Impact/Purpose:

These findings demonstrate that some of the cardiovascular health effects of air pollution may stem from sequential exposure to peak concentrations of pollutants that may occur over the course of a day. This may help elucidate the mechanisms behind adverse cardiovascular outcomes resulting from exposure to air pollution.

Description:

Although ambient air sheds vary in composition, specific pollutants typically peak at predictable times throughout the course of a day. For example, in urban environments, peak nitrogen dioxide (NO2) and particulate matter levels coincide with rush hour traffic in the morning and afternoon, while peak levels of ozone (O3), a photochemical reaction product, occur in the afternoon. Given the possibility that exposure to a single pollutant may sensitize an individual to the effects of a second pollutant, we hypothesized that pre-exposure to NO2 in the morning will exaggerate the cardiovascular effects of O3 exposure in the afternoon in rats. Rats were divided into the following groups that were each exposed for 3 hours in the morning (m) and 3 hours in the afternoon (a) on the same day: 1) m-Air/a-Air, 2) m-Air/a-O3 (0.3 ppm), 3) m-NO2 (0.5 ppm)/a-Air, and 4) m-NO2/a-O3. Rats were monitored for heart rate (HR), blood pressure, electrocardiogram (ECG), and heart rate variability (HRV), an indicator of autonomic tone. Sensitivity to arrhythmia was measured in a separate cohort as the threshold dose of aconitine required to elicit cardiac arrhythmia. Only m-NO2/a-O3 caused several ECG changes including decreased HR and increased PR, QRS and QTcF intervals. In addition, only m-NO2/a-O3 exposure decreased systolic and diastolic blood pressures and core body temperature, and increased QA interval, suggesting decreased cardiac contractility. Exposure to m-Air/a-O3, m-NO2/a-O3, and m-NO2/a-Air each caused greater sensitivity to aconitine-induced ventricular premature beats and tachycardia relative to m-Air/a-Air. HRV and lung/systemic toxicity data will also be presented. These data indicate that priming effects from short term sequential exposure to air pollution components may underlie some adverse cardiovascular health outcomes (This abstract does not reflect EPA policy).

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