Short-term exposure to air pollution may affect ventricular repolarization, but there is limited information on how long-term exposures might affect the surface ventricular electrocardiographic (ECG) abnormalities associated with cardiovascular events. We carried out a study to determine whether long-term air pollution exposure is associated with abnormalities of ventricular repolarization and conduction in adults without known cardiovascular disease.
A total of 4783 participants free of clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis underwent 12-lead ECG examinations, cardiac-computed tomography, and calcium scoring, as well as estimation of air pollution exposure using a finely resolved spatiotemporal model to determine long-term average individual exposure to fine particulate matter (PM2.5) and proximity to major roadways. We assessed ventricular electrical abnormalities including presence of QT prolongation (Rautaharju QTrr criteria) and intraventricular conduction delay (QRS duration >120 milliseconds). We used logistic regression to determine the adjusted relationship between air pollution exposures and ECG abnormalities.
A 10-μg/m3 increase in estimated residential PM2.5 was associated with an increased odds of prevalent QT prolongation (adjusted odds ratio [OR] = 1.6 [95% confidence interval (CI) = 1.2–2.2]) and intraventricular conduction delay (1.7 [1.0–2.6]), independent of coronary-artery calcium score. Living near major roadways was not associated with ventricular electrical abnormalities. No evidence of effect modification by traditional risk factors or study site was observed.
This study demonstrates an association between long-term exposure to air pollution and ventricular repolarization and conduction abnormalities in adults without clinical cardiovascular disease, independent of subclinical coronary arterial calcification.
SUPPLEMENTAL DIGITAL CONTENT IS AVAILABLE IN THE TEXT.
From the Departments of aMedicine, bDepartment of Environmental & Occupational Health Sciences, and cDepartment of Biostatistics, University of Washington, Seattle, WA; dDivision of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC; eDivision of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA; fDepartment of Epidemiology, University of Washington, Seattle, WA; and gDepartment of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI.
Submitted 16 February 2011; accepted 17 May 2011; posted 14 September 2011.
Supported by National Heart, Lung, and Blood Institute contracts N01-HC-95159 through N01-HC-95165 and N01-HC-95169; U.S. Environmental Protection Agency STAR Grant RD831697; National Institute of Environmental Health Sciences grant K24ES013195 (to J.D.K.); and National Institute of Environmental Health Sciences grant K23ES019575 (to V.C.V.)
Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com).
Correspondence: Victor C. Van Hee, Department of Environmental and Occupational Health Sciences, University of Washington, Box 359739, Seattle, WA 98104. E-mail: firstname.lastname@example.org.