Abstract 6213: Adverse Cardiovascular Responses to Alterations in Daily Levels of Personal and Ambient Fine Particulate Matter Air Pollution
Exposure to fine particulate matter <2.5 μm (PM2.5) air pollution is associated with an increased risk for cardiovascular (CV) events. Studies of high concentrations of PM2.5 suggest that vascular endothelial dysfunction and an acute pro-hypertensive response may explain this relationship. However, whether daily changes in PM2.5 at ambient levels are capable of triggering these CV reactions and if there are differential responses to PM of ambient origin versus non-ambient origin remain to be elucidated. The CV study of the Detroit Exposure and Aerosol Research Study linked ambient PM2.5 to changes in endothelial function, determined by brachial flow mediated dilatation (FMD) at the subject’s residence, and blood pressure (BP) in 65 non-smoking subjects (age 45 ± 16 years). PM2.5 exposures were measured by the collection of daily 24-hour integrated personal (subjects wearing vests) and community-based ambient levels for five consecutive days during the summer and the following winter. Each subject could have up to 10 repeated measurement days for both PM2.5 and the CV outcomes. Associations were investigated by a mixed model adjusting for age, gender, race, and outdoor temperature. Mean BP and FMD were 130 ± 20/77 ± 11 mm Hg and 4.6 ± 9.9%, respectively. Mean personal and community-based measures of PM2.5 mass were 22 ± 25 μg/m3 and 15 ± 8 μg/m3, respectively. A 10 μg/m3 increase in the prior day personal exposure level of PM2.5 was associated with an elevation in systolic BP of 1.6 mm Hg (p<0.01) in subjects wearing their vests with at least 60% compliance. There were no significant associations with FMD. On the other hand, a 10 μg/m3 increase in the prior day ambient PM2.5 level was associated with a reduction in FMD of 0.82% (p<0.1). Personal PM2.5 mass concentrations influenced by both ambient and non-ambient sources were linked to a higher systolic BP; whereas community-based ambient PM2.5 mass concentrations were observed to impair endothelial function. Both adverse CV responses may be key mechanisms whereby present-day ambient fine particle levels can trigger acute CV events. These findings also suggest that the sources and characteristics of air pollutants may be important determinants of the health responses.