Environmental health perspectives · 2010
Particulate air pollution, metabolic syndrome, and heart rate variability: the multi-ethnic study of atherosclerosis (MESA).
СтатьяПоддержка NIH: внешняя программаПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Park Sung Kyun, Auchincloss Amy H, O'Neill Marie S, Prineas Ronald, Correa Juan C, Keeler Jerry, Barr R Graham, Kaufman Joel D, Diez Roux Ana V
Аннотация
BACKGROUND: Cardiac autonomic dysfunction has been suggested as a possible biologic pathway for the association between fine particulate matter ≤ 2.5 µm 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 µg/m3) 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.
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 µg/m3) 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.