Effects of Personal Exposure to Ambient Fine Particulate Matter on Acute Change in Nocturnal Heart Rate Variability in Subjects Without Overt Heart Disease

Abstract

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. 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 and continuous monitoring of personal exposure to PM2.5 and were measured for up to 2 consecutive days. We calculated 5-minute time-specific average PM2.5 exposure for each participant. Mixed-effects models were fit for 5-minute SD of normal-to-normal intervals (SDNN) and 5-minute heart rate in relation to 5-minute PM2.5 exposure lagged in 5-minute intervals up to 4 hours. We found an 8.4% decrease in nocturnal SDNN (95% confidence interval [CI] -11.3% to -5.5%) and a 1.9% increase in nighttime heart rate (95% CI 1.1% to 2.7%) for an interquartile range increase in PM2.5 (13.6 μg/m(3)), 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 heart rate variability 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.

Figure 1

Overview of study design and measurements

Figure 2

Adjusted percent changes and 95% CIs in nocturnal SDNN and nocturnal HR for an IQR increase in PM_2.5 (13.6 µg/m³). Models were adjusted for age, gender, smoking status, use of statin, use of NSAIDs, use of hypertension medication (beta blocker, calcium channel blocker or ACE inhibitors/angiotensin receptor blockers), and use of aspirin. Circle black/white symbols indicate the effect estimate.

Figure 2

Adjusted percent changes and 95% CIs in nocturnal SDNN and nocturnal HR for an IQR increase in PM_2.5 (13.6 µg/m³). Models were adjusted for age, gender, smoking status, use of statin, use of NSAIDs, use of hypertension medication (beta blocker, calcium channel blocker or ACE inhibitors/angiotensin receptor blockers), and use of aspirin. Circle black/white symbols indicate the effect estimate.