Ambient Particulate Air Pollution, Heart Rate Variability, and Blood Markers of Inflammation in a Panel of Elderly Subjects

Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. I...

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Published inEnvironmental health perspectives Vol. 112; no. 3; pp. 339 - 345
Main Authors Pope, C. Arden, Hansen, Matthew L., Long, Russell W., Nielsen, Karen R., Eatough, Norman L., Wilson, William E., Eatough, Delbert J.
Format Journal Article
LanguageEnglish
Published United States National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare 01.03.2004
National Institute of Environmental Health Sciences
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Summary:Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter ≤ 2.5 μm ( PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100-μ g/ m3increase in PM2.5was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 11)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = 0.17)-mg/dL increase in CRP. The PM2.5- HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM2.5was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM2.5; however, the small statistically significant associations that were observed suggest that exposure to PM2.5may be one of multiple factors that influence HRV and CRP.
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ISSN:0091-6765
1552-9924
DOI:10.1289/ehp.6588