Abstract
BackgroundExposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; however, most studies have focused on fine particulate matter (PM2.5) exposure and CVD. Coarse particulate matter (PM10–2.5) exposure has not been extensively studied, particularly for long-term exposure, and the biological mechanisms remain uncertain.MethodsWe examined the association between ambient concentrations of PM10–2.5 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 PM10–2.5, as well as co-pollutants. Linear mixed-effects regression models were used to describe the association between PM10–2.5 exposure and markers, including demographic, health and other covariates.ResultsEach interquartile (4 μg/m3) increase in one-year PM10–2.5 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 PM10–2.5 and PAI-1 remained unchanged with adjustment for PM2.5, ozone, nitrogen dioxide, and carbon monoxide.ConclusionsLong-term PM10–2.5 exposure may be associated with changes in coagulation independently from PM2.5, and thus, contribute to CVD risk in midlife women.
Highlights
Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; most studies have focused on fine particulate matter (PM2.5) exposure and CVD
The authors further identified that endotoxin and copper in PM10–2.5 contributed most to inflammation and coagulation effects, respectively, which were robust to the adjustment for PM2.5
Our findings suggest that the associations between plasminogen activator inhibitor-1 (PAI-1) and one-year PM10–2.5 exposure appeared strong in some subgroups, including women with a body mass index (BMI) < 25, women who were peri-menopausal, women with equivalent or less than a high school education, and women who reported low alcohol consumption
Summary
Exposure to particulate matter air pollution has been associated with cardiovascular disease (CVD) morbidity and mortality; most studies have focused on fine particulate matter (PM2.5) exposure and CVD. Cardiovascular disease (CVD) is the leading cause of death for men and women in the US [1] Risk factors such as sex, age, increased blood pressure, high cholesterol, and smoking, only account for approximately 50% of cardiac events [2]. Evidence suggests that exposure to particulate matter air pollution is associated with cardiovascular morbidity and mortality, potentially through its ability to increase inflammation and coagulation [3]. Most available research has been focused on the health impacts of PM2.5 exposure; potential health effects from exposure to coarse particulate matter with an aerodynamic diameter between 2.5 and 10 μm (PM10–2.5 or coarse particles) might differ from exposure to PM2.5 due to the components, sources, and size. Our understanding of the health impacts from PM10–2.5 exposure is limited, and no specific regulatory standards exist for PM10–2.5 [4]
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