Abstract 9390: Rapid Effects of Personal-Level Ambient Fine Particulate Matter Exposure on Arterial Hemodynamics and Vascular Function during the Same Day
Background: Ambient fine particulate matter < 2.5 μm (PM2.5) levels are associated with alterations in arterial hemodynamics and vascular function one or more days later. However, the characteristics of the same-day rapid exposure-response relationships within hours of exposures remain unclear.
Objectives and Methods: We aimed to explore the effects of personal PM2.5 exposures within the preceding 24 hours on blood pressure (BP), heart rate (HR), brachial artery diameter (BAD), endothelial function (flow-mediated dilatation (FMD)) and nitroglycerin-mediated dilatation (NMD). Fifty-one non-smoking general population subjects living in Wayne County Michigan, who were participating in the Detroit Exposure and Aerosol Research Study conducted by the Environmental Protection Agency, had up to 5 consecutive days of 24-hour personal PM2.5 monitoring and daily cardiovascular (CV) measurements performed in their households during summer and/or winter periods. The associations between integrated hour-long total personal PM2.5 exposure (TPE) levels (continuous nephelometry among protocol compliant subjects with low or no secondhand tobacco smoke (SHS) exposures) with the CV outcomes were assessed over a 24-hour period by linear mixed-models.
Results: The alterations in HR, BAD, and FMD that were significantly associated with TPE during the preceding 24 hours occurred in a consistent biological manner. Higher TPE levels (per 10 μg/m3) during several periods within the first 11 hours were related to increases in HR (+0.38 to +0.78 beats/min, p values<0.05). TPE 2 hours earlier was also associated with a significant increase in BAD (+0.018 mm, p=0.035) and a reduction in FMD (−0.26 p=0.048). There were no consistent associations with BP or NMD.
Conclusions: Brief hour-long elevations in ambient TPE levels encountered during routine daily activity in the absence of SHS were associated with small increases in HR and trends toward conduit arterial vasodilatation and endothelial dysfunction within only hours of exposure. These responses are most consistent with acute PM2.5-induced autonomic imbalance favoring sympathetic activity and could potentially contribute to a rapid increase in CV risk among susceptible individuals.
- © 2010 by American Heart Association, Inc.