Air Pollution, Obesity, Genes, and Cellular Adhesion Molecules
- Jaime Madrigano1,*,
- Andrea Baccarelli2,
- Robert Wright3,
- Helen Suh1,
- David Sparrow4,
- Pantel Vokonas4,
- Joel Schwartz1
- 1 Harvard School of Public Health, United States;
- 2 Dept. Environmental and Occupational Health, Univ. Milan, Italy;
- 3 Harvard University, United States;
- 4 Veterans Affairs Boston Healthcare System, United States
- Correspondence to: Jaime Madrigano, Epidemiology; Environmental Health, Harvard School of Public Health, 677 Huntington Avenue, Boston, 02115, United States; jmadriga{at}hsph.harvard.edu
- Received 8 February 2009
- Accepted 5 October 2009
- Published Online First 2 November 2009
Abstract
Objectives: Particulate matter (PM) has been associated with acute cardiovascular outcomes, but our understanding of the mechanism is incomplete. We examined the association between PM 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 and black carbon (BC) 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 Aging 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: BC during the 2 days prior to blood draw was significantly associated with increased sVCAM-1 (4.5% increase per 1µg/m3 95% CI 1.1, 8.0). Neither pollutant was associated with sICAM-1. Larger effects of BC on sVCAM were seen in subjects with obesity (p=0.007) and who were GSTM1 null (p=0.02).
Conclusions: BC is associated with markers of endothelial function and inflammation. Genes related to oxidative defense may modify this association.
