title: Medium-term exposure to traffic-related air pollution and markers of inflammation and endothelial function.
abstract: BACKGROUND
  Exposure to traffic-related air pollution (TRAP) contributes to increased cardiovascular risk. Land-use regression models can improve exposure assessment for TRAP.
  
  
  OBJECTIVE
  We examined the association between medium-term concentrations of black carbon (BC) estimated by land-use regression and levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), both markers of inflammatory and endothelial response.
  
  
  METHODS
  We studied 642 elderly men participating in the Veterans Administration (VA) Normative Aging Study with repeated measurements of sICAM-1 and sVCAM-1 during 1999-2008. Daily estimates of BC exposure at each geocoded participant address were derived using a validated spatiotemporal model and averaged to form 4-, 8-, and 12-week exposures. We used linear mixed models to estimate associations, controlling for confounders. We examined effect modification by statin use, obesity, and diabetes.
  
  
  RESULTS
  We found statistically significant positive associations between BC and sICAM-1 for averages of 4, 8, and 12 weeks. An interquartile-range increase in 8-week BC exposure (0.30 μg/m3) was associated with a 1.58% increase in sICAM-1 (95% confidence interval, 0.18-3.00%). Overall associations between sVCAM-1 and BC exposures were suggestive but not statistically significant. We found a significant interaction with diabetes-where diabetics were more susceptible to the effect of BC-for both sICAM-1 and sVCAM-1. We also observed an interaction with statin use, which was statistically significant for sVCAM-1 and suggestive for sICAM-1. We found no evidence of an interaction with obesity.
  
  
  CONCLUSIONS
  Our results suggest that medium-term exposure to TRAP may induce an increased inflammatory/endothelial response, especially among diabetics and those not using statins.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02215, USA. salexeeff@fas.harvard.edu
authors.forename: Stacey E
authors.initials: SE
authors.lastname: Alexeeff
authors.forename: Brent A
authors.initials: BA
authors.lastname: Coull
authors.forename: Alexandros
authors.initials: A
authors.lastname: Gryparis
authors.forename: Helen
authors.initials: H
authors.lastname: Suh
authors.forename: David
authors.initials: D
authors.lastname: Sparrow
authors.forename: Pantel S
authors.initials: PS
authors.lastname: Vokonas
authors.forename: Joel
authors.initials: J
authors.lastname: Schwartz
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000032:analysis* / Q000633:toxicity; D001900:Boston / Q000453:epidemiology; D004727:Endothelium / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D053260:Soot / Q000032:analysis* / Q000633:toxicity; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D001335:Vehicle Emissions / Q000032:analysis* / Q000633:toxicity
chemical_list: D000393:Air Pollutants; D053260:Soot; D019010:Vascular Cell Adhesion Molecule-1; D001335:Vehicle Emissions; D018799:Intercellular Adhesion Molecule-1