Abstract
BACKGROUND: Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM(2.5)) exposure and CVD. Coarse particulate matter (PM(10-2.5)) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain. METHODS: We examined the association between ambient concentrations of PM(10-2.5) and inflammatory and hemostatic makers that have been linked to CVD. Annual questionnaire and clinical data were obtained from 1694 women (≥ 55 years old in 1999) enrolled in the longitudinal Study of Women's Health Across the Nation (SWAN) at six study sites from 1999 to 2004. Residential locations and the USEPA air monitoring network measurements were used to assign exposure to one-year PM(10-2.5), as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM(10-2.5) exposure and markers, including demographic, health and other covariates. RESULTS: Each interquartile (4 μg/m(3)) increase in one-year PM(10-2.5) exposure was associated with a 5.5% (95% confidence interval [CI]: 1.8, 9.4%) increase in levels of plasminogen activator inhibitor-1 (PAI-1) and 4.1% (95% CI: - 0.1, 8.6%) increase in high-sensitivity C-creative Protein (hs-CRP). Stratified analyses suggested that the association with PAI-1 was particularly strong in some subgroups, including women who were peri-menopausal, were less educated, had a body mass index lower than 25, and reported low alcohol consumption. The association between PM(10-2.5) and PAI-1 remained unchanged with adjustment for PM(2.5), ozone, nitrogen dioxide, and carbon monoxide. CONCLUSIONS: Long-term PM(10-2.5) exposure may be associated with changes in coagulation independently from PM(2.5), and thus, contribute to CVD risk in midlife women.