Background Higher ambient fine particulate matter (PM2.5) levels can be associated with increased blood pressure and vascular dysfunction.
Objectives To determine the differential effects on blood pressure and vascular function of daily changes in community ambient- versus personal-level PM2.5 measurements.
Methods Cardiovascular outcomes included vascular tone and function and blood pressure measured in 65 non-smoking subjects. PM2.5 exposure metrics included 24 h integrated personal- (by vest monitors) and community-based ambient levels measured for up to 5 consecutive days (357 observations). Associations between community- and personal-level PM2.5 exposures with alterations in cardiovascular outcomes were assessed by linear mixed models.
Results Mean daily personal and community measures of PM2.5 were 21.9±24.8 and 15.4±7.5 μg/m3, respectively. Community PM2.5 levels were not associated with cardiovascular outcomes. However, a 10 μg/m3 increase in total personal-level PM2.5 exposure (TPE) was associated with systolic blood pressure elevation (+1.41 mm Hg; lag day 1, p<0.001) and trends towards vasoconstriction in subsets of individuals (0.08 mm; lag day 2 among subjects with low secondhand smoke exposure, p=0.07). TPE and secondhand smoke were associated with elevated systolic blood pressure on lag day 1. Flow-mediated dilatation was not associated with any exposure.
Conclusions Exposure to higher personal-level PM2.5 during routine daily activity measured with low-bias and minimally-confounded personal monitors was associated with modest increases in systolic blood pressure and trends towards arterial vasoconstriction. Comparable elevations in community PM2.5 levels were not related to these outcomes, suggesting that specific components within personal and background ambient PM2.5 may elicit differing cardiovascular responses.
- Blood vessels
- endothelial function
- air pollution
- biological monitoring
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Funding The US EPA through its Office of Research and Development partially funded and conducted the research under contract 68-D-00-012 (RTI International), EP-D-04-068 (Battelle Columbus Laboratory), 68-D-00-206 and EP-05-D-065 (Alion Science and Technology). It has not been subjected to Agency review and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. This study was also supported by the Electric Power Research Institute (contract EP-P15887/C7915) and by a National Institutes of Health General Clinical Research Center Grant (M01-RR000042).
Competing interests None.
Ethics approval This study was conducted with the approval of the University of Michigan.
Provenance and peer review Not commissioned; externally peer reviewed.
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