Recent exposure to particulate matter and C-reactive protein concentration in the multi-ethnic study of atherosclerosis

Ana V Diez Roux, A. H. Auchincloss, B. Astor, R. G. Barr, M. Cushman, T. Dvonch, D. R. Jacobs, J. Kaufman, X. Lin, P. Samson

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53 Scopus citations


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 languageEnglish (US)
Pages (from-to)437-448
Number of pages12
JournalAmerican journal of epidemiology
Issue number5
StatePublished - 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.


  • Air pollutants
  • Cardiovascular diseases
  • Environmental
  • Inflammation


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