Citation:

Philips, K., K. Stratford, L. Walsh, M. Khan, L. Thompson, W. Oshiro, G. Hudson, D. Herr, A. Farraj, AND M. Hazari. The Effect of Intermittent Noise Stress on Ozone-Induced Cardiovascular Dysfunction in Wistar-Kyoto Rats. Society of Toxicology Annual Meeting, Baltimore, Maryland, March 12 - 16, 2017.

Impact/Purpose:

This work helps disentangle the complexity of ambient air sheds, which in addition to having variable air pollution mixtures, have co-located stressors such as noise pollution, particularly in urban environments. The elicitation of greater than additive effects with air pollution and noise provides evidence for synergism and thus may be a biologically plausible mechanism driving some of the epidemiological evidence linking exposure to air pollution to increased cardiovascular morbidity and mortality.

Description:

Previous studies have established that acute exposure to air pollution increases the risk of cardiovascular dysfunction. Intrinsic factors are likely the most important determinants of how the body responds to an exposure. But data also suggests that non-environmental stressors like noise, which is a common urban public health problem, can modify and indeed worsen the response. Noise can cause obvious psychological disturbances typical of non-specific stress, but also changes that can increase the number of cardiovascular disease related mortalities. Therefore, we hypothesized that short-term exposure to noise would worsen the cardiovascular response to ozone. Male Wistar-Kyoto rats were implanted with radiotelemeters for the measurement of heart rate (HR), blood pressure (BP) and electrocardiogram (ECG) and exposed to intermittent noise (85-90 dB) for one week after which they were exposed to either ozone (0.8 ppm) or filtered air. Left ventricular functional responses to dobutamine were measured using a Millar probe as well as arrhythmic sensitivity to aconitine in a separate set of untelemetered rats 24 hours after exposure. HR and BP decreased in all telemetered animals during ozone exposure; noise caused BP and HR to increase. Baseline left ventricular pressure (LVP) was significantly higher in animals exposed to both noise and ozone when compared to no noise; furthermore those animals had the least amount of change in LVP, dP/dT max and min with increasing doses of dobutamine. These animals also had a higher arrhythmic sensitivity to aconitine. In conclusion, these results suggest that noise alters the cardiovascular response to ozone exposure. Thus, non-environmental stressors may be playing an important role in modifying the response to air pollution and may in fact increase the risk in people with underlying cardiovascular disease. (This abstract does not reflect USEPA policy)

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