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Effect of Same-day Sequential Exposure to Nitrogen Dioxide and Ozone on Cardiac and Ventilatory Function in Mice
Citation:
Stratford, K., R. Chesnutt, N. Kurhanewicz, N. Coates, L. Walsh, D. Terrell, A. Farraj, AND M. Hazari. Effect of Same-day Sequential Exposure to Nitrogen Dioxide and Ozone on Cardiac and Ventilatory Function in Mice. Society of Toxicology, San Diego, CA, March 22 - 26, 2015.
Impact/Purpose:
The data presented here shows that a sequential exposure to the gaseous pollutants nitrogen dioxide and then ozone causes adverse cardiac and ventilatory effects. This work addresses Agency needs with respect to determining the health effects of sequential exposure to air pollution and contributing to the risk assessment process by clarifying the synergistic/additive effects of pollutants.
Description:
This study examines the cardiac and ventilatory effects of sequential exposure to nitrogen dioxide and then ozone. The data show that mice exposed to both gases have increased arrhythmia and breathing changes not observed in the other groups. Although the mechanisms underlying air pollution-induced cardiopulmonary responses have been extensively studied, the impact one pollutant has on another is still unclear. Nitrogen dioxide (NO2) is released following combustion of hydrocarbon fuels peaking particularly in the morning of hot summer days. Ozone (O3) is produced by the reaction of ultraviolet rays from the sun on pollutants already present in the air and peaks in the afternoon. Therefore on any given summer day, individuals could be sequentially exposed to both gaseous air pollutants. We hypothesized that sequential exposure to NO2 followed by O3 on the same day would cause cardiac electrical dysfunction and ventilatory changes in mice. C57BL6 mice surgically implanted with radiotelemeters were exposed to either NO2 (0.5ppm) alone or filtered air (FA) in the morning (3hrs), removed from the exposure chambers for 2hrs and then exposed to O3 alone (0.3 ppm) or FA in the afternoon (3hrs). Electrocardiogram (ECG) and heart rate (HR) were measured continuously and ventilatory function was measured before and after each exposure in a whole-body plethysmograph. Breathing frequency (f) of mice exposed to NO2 increased during the first 5mins of the subsequent O3 exposure when compared to FA. In addition, mice exposed sequentially to NO2 then O3 experienced cardiac dysrhythmia which was not evident in other groups. Lastly, we found that a single exposure to either NO2 or O3 alone increased sensitivity to aconitine-induced arrhythmia. These studies demonstrate that sequential exposure to gaseous air pollutants causes decrements in cardiac and ventilatory function. The data suggests that prior exposure on the same day might alter, or worsen, the response during a subsequent exposure; this clearly warrants further examination, particularly for the improvement and refinement of risk assessment. (This abstract does not reflect EPA policy)