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Particulate Air Pollution Exposure and C-reactive Protein During Early Pregnancy

Lee, Pei-Chena; Talbott, Evelyn O.a; Roberts, James M.a,b; Catov, Janet M.a,b; Sharma, Ravi K.c; Ritz, Beated

doi: 10.1097/EDE.0b013e31821c6c58
Air Pollution: Original Article

Background: It is not well understood how air pollution leads to adverse pregnancy outcomes. One pathway may be through C-reactive protein, a biomarker of systemic inflammation that has been reported to increase the risk of preterm delivery. We examined whether air pollution influences serum concentrations of C-reactive protein in early pregnancy.

Methods: We studied 1696 pregnant women in Allegheny County, PA, from 1997 through 2001. C-reactive protein concentrations were assayed in blood collected before the 22nd week of gestation. We estimated levels of particles of less than 10 μm (PM10) and less than 2.5 μm diameter (PM2.5), carbon monoxide, nitrogen dioxide, sulfur dioxide, and ozone at the maternal zip code using Kriging interpolation for measurements obtained from ambient stations. Associations between air pollution and high C-reactive protein concentrations (≥8 ng/mL) were evaluated using logistic regression.

Results: Among nonsmokers, an observed 9.2 μg/m3 increase in PM10 (averaged over 28 days prior to the blood sample) was associated with an odds ratios of 1.41 for high C-reactive protein concentrations (95% confidence interval = 0.99–2.00). Similarly, a 4.6 μg/m3 increase in PM2.5 was associated with an odds ratio of 1.47 (1.05–2.06). The odds ratio was 1.49 (0.75–2.96) per 7.9 ppb increase in ozone during summer. There were no associations in smokers or for other air pollutants, and there was no evidence for effect-measure modification by obesity.

Conclusions: PM10, PM2.5, and ozone exposures were associated with increased C-reactive protein concentrations in early pregnancy, suggesting that these air pollutants contribute to inflammation and thereby possibly to adverse pregnancy outcomes.


From the aDepartment of Epidemiology, Graduate School of Public Health, bDepartment of Obstetrics and Gynecology, School of Medicine, and cDepartment of Behavioral and Community Health Sciences, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; and dDepartment of Epidemiology, School of Public Health, University of California at Los Angeles, CA.

Submitted 17 August 2010; accepted 17 January 2011; posted 22 April 2011.

Supported by the Department of Epidemiology, University of Pittsburgh.

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Correspondence: Pei-Chen Lee, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, 507 Parran Hall 130 DeSoto St, Pittsburgh, PA 15261. E-mail:

© 2011 Lippincott Williams & Wilkins, Inc.