Alterations of physiological cardiovascular markers in rats exposed to ozone

Epidemiology studies have shown that exposure to ambient air pollutants increase cardiovascular morbidity and mortality. Air pollution may alter ANS balance or promote systemic inflammation and oxidative stress and subsequently cause cardiovascular effects. Both blood pressure (BP), heart rate (HR) and heart rate variability (HRV) are important physiological markers for cardiovascular diseases. However, the precise mechanisms of air pollution mediated cardiac effects are still unclear. Most air pollution studies demonstrate the effects of particulate matter. Many results support that PM2.5 exposure can elevate BP, HR, and decrease HRV, but data of ozone effect are limited. Recently, more and more epidemiology studies found the association between BP and ozone. Increase ozone level will increase blood pressure both in lag and moving average model in epidemiological studies. These studies examine the effects base on the exposure greater than one day. It is not clear whether brief exposure to ozone at ambient level affects BP, HR and HRV.
Therefore, this study is designed to determine ozone effects on physiological cardiovascular markers. WKY rats were exposed to ambient air through a modified exposure system in Taipei from December, 2011 to February, 2012. Each rat was exposed to HEPA filtered air for two weeks. We measured SBP, DBP, HR, SDNN and RMSSD using radiotelemetry system. Association between hourly ozone level and physiological markers were examined using mixed effect model. We further used both single-lag model (0 day to 6 day or 0 hour to 48 hour) and moving-average model (1 day to 7 days or 1 hour to 48 hours mean) to estimate ozone daily and hourly lag or cumulative effects on physiological cardiovascular markers.
Our results found that environmentally relevant ambient level of ozone were associated with small increase both in day and hourly lag or moving average models. In day lag and moving average models, ozone significantly increased SBP and pulse pressure (PP) in current day and in cumulative models, but there was an increase in SDNN and RMSSD. In hourly lag models, ozone exposure significantly increased SBP, DBP, PP and decreased SDNN and RMSSD. The responses of SBP were observed within 5 to 8 hour in lag model, and also increased in hourly moving average models. Because rat was exposed to HEPA filtered air, we can not exclude effects of other gas pollutants such as nitrogen dioxide and carbon monoxide. Further studies of ozone cardiovascular effects on these cardiovascular markers are necessary.
Previous studies have shown the effects of air pollution greater than one day. Our findings suggest that in addition to day effects, air pollution could rapidly affect cardiovascular within hours.