Studies have reported associations between long-term air pollution exposures and cardiovascular mortality. The biological mechanisms connecting them remain uncertain.
We examined associations of fine particles (PM2.5) and ozone with serum markers of cardiovascular disease risk in a cohort of midlife women. We obtained information from women enrolled at six sites in the multi-ethnic, longitudinal Study of Women’s Health Across the Nation, including repeated measurements of high-sensitivity C-reactive protein, fibrinogen, tissue-type plasminogen activator antigen, plasminogen activator inhibitor type 1, and factor VIIc (factor VII coagulant activity). We obtained residence-proximate PM2.5 and ozone monitoring data for a maximum five annual visits, calculating prior year, 6-month, 1-month, and 1-day exposures and their relations to serum markers using longitudinal mixed models.
For the 2,086 women studied from 1999 to 2004, PM2.5 exposures were associated with all blood markers except factor VIIc after adjusting for age, race/ethnicity, education, site, body mass index, smoking, and recent alcohol use. Adjusted associations were strongest for prior year exposures for high-sensitivity C-reactive protein (21% increase per 10 μg/m3 PM2.5, 95% confidence interval [CI]: 6.6, 37), tissue-type plasminogen activator antigen (8.6%, 95% CI: 1.8, 16), and plasminogen activator inhibitor (35%, 95% CI: 19, 53). An association was also observed between year prior ozone exposure and factor VIIc (5.7% increase per 10 ppb ozone, 95% CI: 2.9, 8.5).
Our findings suggest that prior year exposures to PM2.5 and ozone are associated with adverse effects on inflammatory and hemostatic pathways for cardiovascular outcomes in midlife women.
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From the aOffice of Environmental Health Hazard Assessment, California Environmental Protection Agency, Oakland, CA; bDepartment of Public Health Sciences, University of California Davis School of Medicine, Davis, CA; cKaiser Permanente Division of Research, Oakland, CA; dDepartment of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA; eDepartment of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA; fDepartment of Medicine, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA; gRush University Medical Center, Chicago, IL; hSchool of Public Health, University of Michigan, Ann Arbor, MI; iSaul R. Korey Department of Neurology, and Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY; and jDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Hospital and Health Systems, Ann Arbor, MI.
Submitted 11 April 2014; accepted 20 November 2015.
The authors report no conflicts of interest.
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Correspondence: Rachel Broadwin, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, 1515 Clay Street, 16th Floor, Oakland, CA 94612. E-mail: firstname.lastname@example.org.