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Air Pollution and Markers of Coagulation, Inflammation, and Endothelial Function: Associations and Epigene-environment Interactions in an Elderly Cohort

Bind, Marie-Abelea; Baccarelli, Andreaa; Zanobetti, Antonellaa; Tarantini, Letiziab; Suh, Helena; Vokonas, Pantelc; Schwartz, Joela

doi: 10.1097/EDE.0b013e31824523f0
Air Pollution

Background: Previous studies suggest that air pollution is related to thrombosis, inflammation, and endothelial dysfunction. Mechanisms and sources of susceptibility are still unclear. One possibility is that these associations can be modified by DNA methylation states.

Methods: We conducted a cohort study with repeated measurements of fibrinogen, C-reactive protein, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in 704 elderly men participating in the Veterans Administration Normative Aging Study (2000–2009). We investigated short- and intermediate-term air pollution effects on these blood markers, and epigene-environment interactions by DNA methylation of Alu, LINE-1, tissue factor (F3), Toll-like receptor 2 (TLR-2), and ICAM-1.

Results: We found effects of particle number, black carbon, nitrogen dioxide (NO2), and carbon monoxide (CO) on fibrinogen. Ozone was a predictor of C-reactive protein and ICAM-1. Particle number, black carbon, NO2, CO, PM2.5, and sulfates were associated with ICAM-1 and VCAM-1. An interquartile range increase in 24-hour exposure for NO2 was associated with a 1.7% (95% confidence interval = 0.2%–3.3%) increase in fibrinogen for ozone; a 10.8% (2.2%–20.0%) increase in C-reactive protein for particle number; a 5.9% (3.6%–8.3%) increase in ICAM-1; and for PM2.5, a 3.7% (1.7%–5.8%) increase in VCAM-1. The air pollution effect was stronger among subjects having higher Alu, lower LINE-1, tissue factor, or TLR-2 methylation status.

Conclusion: We observed associations of traffic-related pollutants on fibrinogen, and both traffic and secondary particles on C-reactive protein, ICAM-1, and VCAM-1. There was effect modification by DNA methylation status, indicating that epigenetic states can convey susceptibility to air pollution.

Supplemental Digital Content is available in the text.

From the aExposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA; bCenter of Molecular and Genetic Epidemiology, IRCCS Ca' Granda Ospedale Maggiore Policlinico Foundation & Department of Environmental and Occupational Health, University of Milan, Milan, Italy; cVA Normative Aging Study, VA Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA.

Submitted 10 September 2010; accepted 25 October 2011; posted online 11 January 2012.

Supported by the U.S. Environmental Protection Agency grants EPA R827353 and R832416; National Institute of Environmental Health Sciences (NIEHS) grants RO1-ES015172, 2RO1-ES015172, ES014663, ES00002, PO1_ES008925 and Clean Air Act (CLARC) grant RD-83479701. The VA Normative Aging Study is supported by the Cooperative Studies Program/Epidemiology Research and Information Center of the U.S. Department of Veterans Affairs and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston, Massachusetts. The authors reported no other financial interests related to this research.

Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com). This content is not peer-reviewed or copy-edited; it is the sole responsibility of the author.

Correspondence: Marie-Abele Bind, Department of Environmental Health, Exposure, Epidemiology, and Risk Program, 401 Park Drive, Landmark Center, Suite 415, Boston, MA 02115. E-mail: mbind@hsph.harvard.edu.

© 2012 Lippincott Williams & Wilkins, Inc.