Reduced heart rate variability, a marker of impaired cardiac autonomic function, has been linked to short-term exposure to airborne particles. This research adds to the literature by examining associations with long-term exposures to coarse particles (PM10–2.5).
Using electrocardiogram recordings from 2,780 participants (45–84 years) from three Multi-ethnic Study of Atherosclerosis sites, we assessed the standard deviation of normal to normal intervals and root-mean square differences of successive normal to normal intervals at a baseline (2000–2002) and follow-up (2010–2012) examination (mean visits/person = 1.5). Annual average concentrations of PM10–2.5 mass, copper, zinc, phosphorus, silicon, and endotoxin were estimated using site-specific spatial prediction models. We assessed associations for baseline heart rate variability and rate of change in heart rate variability over time using multivariable mixed models adjusted for time, sociodemographic, lifestyle, health, and neighborhood confounders, including copollutants.
In our primary models adjusted for demographic and lifestyle factors and site, PM10–2.5 mass was associated with 1.0% (95% confidence interval [CI]: −4.1, 2.1%) lower standard deviation of normal to normal interval levels per interquartile range of 2 μg/m3. Stronger associations, however, were observed before site adjustment and with increasing residential stability. Similar patterns were found for root-mean square differences of successive normal to normal intervals. We found little evidence for associations with other chemical species and with the rate of change in heart rate variability, though endotoxin was associated with increasing heart rate variability over time.
We found only weak evidence that long-term PM10–2.5 exposures are associated with lowered heart rate variability. Stronger associations among residentially stable individuals suggest that confirmatory studies are needed.
From the aDepartment of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI; bDivision of Public Health Sciences, Wake Forest University, Wake Forest, NC; cInstitute for Minority Health Research, University of Illinois at Chicago and Department of Preventive Medicine, Northwestern University, Chicago, IL; dDivision of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN; eDepartment of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA; fDepartment of Biostatistics, University of Washington, Seattle, WA; gDepartment of Occupational and Environmental Health, University of Iowa, Iowa City, IA; hDepartments of Medicine and Epidemiology, University of Washington, Seattle, WA; and iDepartment of Civil and Environmental Engineering, University of Washington, Seattle, WA.
Submitted 26 February 2015; accepted 28 January 2016.
Supported by supported by Grants RD833741010 and RD83169701 from the Environmental Protection Agency (EPA), Contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and Grants UL1-TR-000040 and UL1-TR-001079 from NCRR. PST was supported by National Institutes of Health Grant P30 ES005605. Although this research was supported in part by the EPA, this article has not been formally reviewed by the EPA, and the views in this document are solely those of the authors. The EPA does not endorse any products or commercial services mentioned.
The authors report no conflicts of interest.
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Correspondence: Sara Dubowsky Adar, Department of Epidemiology, University of Michigan, 1415 Washington Heights SPHII-5539, Ann Arbor, MI 48109. E-mail: email@example.com.