Oxidative stress and systemic inflammation as modifiers of cardiac autonomic responses to particulate air pollution

BackgroundThe role of oxidative stress and systemic inflammation on the association between personal exposures to ambient fine particulate matter ≤ 2.5 μm in diameter (PM2.5) and cardiac autonomic dysfunction, indicated by reduction in heart rate variability (HRV), has not been examined.MethodsWe performed a repeated measures study on community adults in a densely populated inner city neighborhood in Boston, Massachusetts. Continuous ambulatory electrocardiogram (ECG) monitoring and personal exposure to PM2.5 were measured for up to two consecutive days. Peripheral blood and spot urine samples were collected at 12-hour intervals for the measurements of markers of inflammation including C-reactive protein (CRP), fibrinogen, white blood cell (WBC) and platelet counts as well as for the analysis of urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage.ResultsAfter adjusting for confounders, we found a pronounced decrease in nighttime standard deviation of normal-to normal intervals (SDNN): an interquartile range (IQR) increase in PM2.5 (13.6 μg/m3) was associated with an 8.4% decrease in SDNN (95% CI: − 11.3 to − 5.5). Compared with the lower eightieth percentile, significantly greater PM2.5 associated nighttime SDNN reductions were observed among subjects in the upper twentieth percentile of 8-OHdG by − 25.3%, CRP by − 24.9%, fibrinogen by − 28.7%, WBC by − 23.4%, and platelet counts by − 24.0% (all P < 0.0001; all Pinteraction < 0.01).ConclusionsThese data suggest that oxidative stress and systemic inflammation exacerbate the adverse effects of PM2.5 on the cardiac autonomic function even at ambient levels of exposure.