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Air pollution, obesity, genes and cellular adhesion molecules
  1. Jaime Madrigano1,2,
  2. Andrea Baccarelli3,
  3. Robert O Wright2,4,
  4. Helen Suh2,
  5. David Sparrow5,
  6. Pantel S Vokonas5,
  7. Joel Schwartz1,2,4
  1. 1Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
  2. 2Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
  3. 3Center of Molecular and Genetic Epidemiology, IRCCS Maggiore Policlinico Hospital Foundation and Department of Environmental and Occupational Health, University of Milan, Milan, Italy
  4. 4Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, USA
  5. 5VA Normative Ageing Study, VA Boston, Department of Medicine, Boston University School of Medicine, Boston, USA
  1. Correspondence to Jaime Madrigano, Exposure, Epidemiology and Risk Program, Harvard School of Public Health, Landmark Center West, Suite 415, 401 Park Drive, Boston, Massachusetts 02215, USA; jmadriga{at}


Objectives Particulate matter has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete. We examined the association between particulate matter and cell adhesion molecules. We also investigated the modifying effect of genotype and phenotype variation to gain insight into the relevant biological pathways for this association.

Methods We used mixed regression models to examine the association of PM2.5 (particulate matter ≤2.5 μm in diameter) and black carbon with serum concentrations of soluble intercellular adhesion molecule (sICAM-1) and soluble vascular cell adhesion molecule (sVCAM-1), markers of endothelial function and inflammation, in a longitudinal study of 809 participants in the Normative Ageing Study (1819 total observations). We also examined whether this association was modified by genotype, obesity or diabetes status. Genes selected for analyses were either related to oxidative stress, endothelial function, lipid metabolism or metal processing.

Results Black carbon during the 2 days prior to blood draw was significantly associated with increased sVCAM-1 (4.5% increase per 1 μg/m3, 95% CI 1.1 to 8.0). Neither pollutant was associated with sICAM-1. Larger effects of black carbon on sVCAM were seen in subjects with obesity (p=0.007) and who were GSTM1 null (p=0.02).

Conclusions Black carbon is associated with markers of endothelial function and inflammation. Genes related to oxidative defence may modify this association.

  • Air pollution
  • epidemiology
  • genetic susceptibility
  • particulates

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  • Funding This study was funded by the National Institutes of Health, the US Environmental Protection Agency and the US Department of Veterans Affairs.

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the Harvard School of Public Health Institutional Review Board, Boston, MA, the Partners Healthcare Human Research Committee, Boston MA and the Veterans Administration Hospitals Institutional Review Board.

  • Provenance and peer review Not commissioned; externally peer reviewed.