Citation:

Farraj, A., F. Malik, N. Coates, L. Walsh, D. Winsett, D. Terrell, L. Thompson, W. Cascio, AND M. Hazari. Morning NO2 Exposure Sensitizes Hypertensive Rats to the Cardiovascular Effects of Same Day O3 Exposure in the Afternoon. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, 28(4):170-179, (2016).

Impact/Purpose:

Given that ambient air sheds contain complex mixtures of air pollutants, there is a pressing need to determine the potential for exposure co-pollutants to have interactive health effects. This need is a research focus outlined in Task 045 of ACE’s current research action plan. One type of interactive effect may stem from the priming effects of an exposure to an air pollutant that modifies an organism such that secondary exposure to the same or different pollutant causes greater than additive responses. The current study illustrates for the first time the priming effects of prior nitrogen dioxide inhalation on the cardiovascular responses to same day inhaled ozone exposure, and provides suggestive evidence for a mechanism of action involving the autonomic nervous system. These findings point to a phenomenon that may account for adverse health effects at lower exposure concentrations. Awareness of the potential for such interactive effects as part of larger multi-pollutant approach to air pollution health assessment may strengthen single pollutant standard determinations.

Description:

Within urban air sheds specific ambient air pollutants typically peak at predictable times throughout the day. For example, in environments dominated by mobile sources, peak nitrogen dioxide (NO2) and particulate matter levels coincide with morning and afternoon rush hours , while peak levels of ozone (O3), a photochemical reaction product, occur in the afternoon. Given the possibility that exposure to a single pollutant might sensitize the cardiopulmonary system to the effects of a subsequent exposure to a second pollutant, we hypothesized that a morning exposure to NO2 will exaggerate the cardiovascular effects of an afternoon O3 exposure in rats. Rats were divided into four 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. Implanted telemetry devices recorded and transmitted blood pressure, electrocardiographic (ECG) and body temperature data. Electrocardiographic data was post-processed to calculate heart rate (HR), electrocardiographic intervals (PR intervals and QT interval corrected for heart rate) and heart rate variability (HRV), an indicator of autonomic tone; and the QA interval, an index of cardiac contractility. Sensitivity to arrhythmia was measured in a separate cohort as the threshold dose of aconitine required to elicit cardiac arrhythmia. Only sequential exposure to NO2 in the morning and O3 in the afternoon (m-NO2/a-O3) caused significant changes in electrophysiological, mechanical and autonomic parameters. These included decreased HR, and increased PR, and QTc intervals and increased HRV consistent with increased parasympathetic tone. In addition, only m-NO2/a-O3 exposure decreased systolic and diastolic blood pressures and core body temperature, and increased pulse pressure and QA interval, suggesting decreased cardiac contractility. These data show that transient sequential exposures to inhaled NO2 and O3 on the same day induces significant changes in physiological systems that were not measured with each pollutant alone. The findings indicate that the initial exposure to NO2 produced a priming effect that causes an enhanced response to a subsequent exposure to O3. While the mechanism of the priming effect is not known, the observation of this phenomenon could provide insight into the epidemiological observations of cardiovascular morbidity and mortality associated with exposures to low concentrations of O3.

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