期刊
ENVIRONMENTAL HEALTH PERSPECTIVES
卷 118, 期 10, 页码 1406-1411出版社
US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.0901778
关键词
air pollution; autonomic nervous system; heart rate variability; metabolic syndrome; PM2.5
资金
- National Institute of Environmental Health Sciences [K01-ES016587-01A1]
- U.S. Environmental Protection Agency [R830543, RD831697]
- National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95165, N01-HC-95169]
BACKGROUND: Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter <= 2.5 mu m in diameter (PM2.5) and cardiovascular disease (CVD). We examined the associations of PM2.5 with heart rate variability, a marker of autonomic function, and whether metabolic syndrome (MetS) modified these associations. METHODS: We used data from the Multi-Ethnic Study of Atherosclerosis to measure the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive differences (rMSSD) of 5,465 participants 45-84 years old who were free of CVD at the baseline examination (2000-2002). Data from the U. S. regulatory monitor network were used to estimate ambient PM2.5 concentrations at the participants' residences. MetS was defined as having three or more of the following criteria: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein cholesterol, high blood pressure, and high fasting glucose. RESULTS: After controlling for confounders, we found that an interquartile range (IQR) increase in 2-day average PM2.5 (10.2 mu g/m(3)) was associated with a 2.1% decrease in rMSSD [95% confidence interval (CI), -4.2 to 0.0] and nonsignificantly associated with a 1.8% decrease in SDNN (95% CI, -3.7 to 0.1). Associations were stronger among individuals with MetS than among those without MetS: an IQR elevation in 2-day PM2.5 was associated with a 6.2% decrease in rMSSD (95% CI, -9.4 to -2.9) among participants with MetS, whereas almost no change was found among participants without MetS (p-interaction = 0.005). Similar effect modification was observed in SDNN (p-interaction = 0.011). CONCLUSION: These findings suggest that autonomic dysfunction may be a mechanism through which PM exposure affects cardiovascular risk, especially among persons with MetS.
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