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IJE Advance Access originally published online on July 14, 2006
International Journal of Epidemiology 2006 35(5):1347-1354; doi:10.1093/ije/dyl132
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2006; all rights reserved.

Article

Inflammatory markers and particulate air pollution: characterizing the pathway to disease

Ariana Zeka1,*, James R Sullivan1, Pantel S Vokonas2, David Sparrow2 and Joel Schwartz1

1 Exposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
2 VA Normative Aging Study, VA Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA, USA

* Corresponding author. Exposure, Epidemiology, and Risk Program, Department of Environmental Health, Harvard School of Public Health, 401 Park Drive, Suite 415 W, PO Box 15677, Boston, MA 02115, USA. E-mail: azeka{at}hsph.harvard.edu

Background Increased concentrations of particles in air have been related to changes in inflammatory markers that in turn are hypothesized in mediating the particle effects on cardiovascular disease. The present work examined this association in an elderly cohort in the Greater Boston area and addresses the relative role of particles from different sources.

Methods The study included 710 subjects, active members of the VA Normative Aging Study cohort with measurements of blood markers. Concentrations of particle number (PN), black carbon (BC), fine particulate matter (PM2.5), and sulphates were measured at a central site near the examination site.

Results Positive associations were found between traffic-related particles (PN and BC) and inflammatory markers, but only suggestive associations were found with exposures to PM2.5 and sulphates. The particle effect on the inflammatory markers was greater among subjects older than 78 years and among obese. A suggestion for a greater effect of particles on inflammatory markers among GSTM1-null subjects and non-users of statin drugs was also seen.

Conclusions The findings of the study support the hypothesis that particles can induce cardiovascular disease through inflammatory pathways, suggestive of a greater toxicity of traffic-related particles.

Keywords Air pollution, C-reactive protein, blood sedimentation, fibrinogen, inflammation, sulphates, white blood cells

Accepted 23 May 2006


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