Background The 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. Methods We 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. Results After 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). Conclusions These 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.

The immediate effect within minutes to hours of personal exposure to ambient fine particulate matter (PM2.5) on cardiac autonomic function is limited, particularly at night. Our study aimed to assess the lagged association between personal exposure to PM2.5 and nocturnal heart rate variability (HRV). Repeated measures panel study among 21 community adults recruited from a local health clinic during the period of March 1, 2004 to August 31, 2004, in Boston, Massachusetts, in the United States. Ambulatory electrocardiogram (ECG) and continuous monitoring of personal exposure to PM2.5 and were measured for up to two consecutive days. We calculated 5-min time-specific average PM2.5 exposure for each participant. Mixed effects models were fit for 5-min standard deviation of normal-to-normal intervals (SDNN) and 5-min heart rate (HR) in relation to 5-min PM2.5 exposure lagged in 5-min intervals up to 4 hours. We found an 8.4% decrease in nocturnal SDNN (95% CI: −11.3% to −5.5%) and a 1.9% increase in nighttime HR (95% CI: 1.1% to 2.7%) for an interquartile range (IQR) increase in PM2.5 (13.6 µg/m3), after adjusting for confounders. Significant decreases in nocturnal SDNN associated with PM2.5 exposure occurred within 2.5 hours. The largest decrease in nocturnal SDNN of −12.8% (95% CI: −16.4 to −9.1%) that was associated with PM2.5 exposure was found with a lag of 25 minutes. Rapid changes in nocturnal HRV associated with personal PM2.5 exposure occurred within the previous 2.5 hours, with the largest effects at 25 minutes, suggesting immediate cardiac autonomic effects of fine particulate exposure.

No abstract

Objective-To investigate the association between PM 2.5 and urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) in hypertensive and non-hypertensive individuals.Methods-Twelve hypertensives and nine non-hypertensives were monitored during a 36-hour period using a repeated-measures panel study design. Personal exposure to PM 2.5 was assessed using a real-time continuous monitor. Spot urine samples collected at 12-hour intervals were analyzed for 8-OHdG.Results-Exposure to PM 2.5 was associated with a decrease in 8-OHdG in hypertensives compared to an increase in non-hypertensives, after adjusting for age, gender, smoking status, and time of day.Conclusions-Results suggest modification of the association between PM 2.5 exposure and urinary 8-OHdG by hypertension status. Antioxidant activity present in antihypertensive medications may play a role or PM 2.5 exposure may reduce the capacity to repair DNA damage in hypertensives. These results should be confirmed with further investigation.