Abstract
Ambient levels of particulate matter have been linked to cardiovascular disease. The mechanisms mediating these associations are poorly understood. One candidate mechanism is inflammation. Using data from the Multi-Ethnic Study of Atherosclerosis (2000-2002), the authors investigated the relation between exposure to particulate matter of less than or equal to 2.5 μm in diameter (PM2.5) and C-reactive protei1n concentration in 5,634 persons aged 45-84 years who were free of cardiovascular disease. Data from US Environmental Protection Agency monitors were used to estimate PM2.5 exposures for the prior day, prior 2 days, prior week, prior 30 days, and prior 60 days. Only the 30-day and 60-day mean exposures showed a weak positive association with C-reactive protein, and confidence intervals were wide: relative increases in C-reactive protein per 10 μg/m3 of PM2.5 adjusted for person-level covariates were 3% (95% confidence interval (CI): -2, 10) for a 30-day mean and 4% (95% CI: -3, 11.0) for a 60-day mean. The means of 7-day, 30-day, and 60-day exposures were weakly, positively, and nonsignificantly associated with the odds of C-reactive protein of greater than or equal to 3 mg/liter: adjusted odds ratios were 1.05 (95% CI: 0.96, 1.15), 1.12 (95% CI: 0.98, 1.29), and 1.12 (95% CI: 0.96, 1.32), respectively. Slightly stronger associations were observed in persons without other risk factors for elevated C-reactive protein, but this heterogeneity was not statistically significant. The authors' results are not compatible with strong effects of particulate matter exposures on population levels of C-reactive protein.
Original language | English (US) |
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Pages (from-to) | 437-448 |
Number of pages | 12 |
Journal | American journal of epidemiology |
Volume | 164 |
Issue number | 5 |
DOIs | |
State | Published - Sep 2006 |
Bibliographical note
Funding Information:MESA is supported by contracts N01-HC-95159 through N01-HC-95165 and by contract N01-HC-95169 from the National Heart, Lung, and Blood Institute. This work was supported by grant R830543 (A. D. R.) from the Environmental Protection Agency.
Keywords
- Air pollutants
- Cardiovascular diseases
- Environmental
- Inflammation