title: Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility.
abstract: BACKGROUND
  Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction-processes in which cell adhesion molecules and inflammatory markers play important roles.
  
  
  OBJECTIVE
  To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes.
  
  
  METHODS
  Daily average ambient levels of air pollution (fine particles (PM2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM-1, VCAM-1 and vWF. Linear regressions were fit to plasma levels of ICAM-1, VCAM-1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors.
  
  
  RESULTS
  Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM(2.5), BC and VCAM-1 were particularly strong.
  
  
  CONCLUSIONS
  These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution-associated cardiovascular events among those with diabetes.
authors.affiliation: Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan 48109, USA. marieo@umich.edu
authors.forename: M S
authors.initials: MS
authors.lastname: O'Neill
authors.forename: A
authors.initials: A
authors.lastname: Veves
authors.forename: J A
authors.initials: JA
authors.lastname: Sarnat
authors.forename: A
authors.initials: A
authors.lastname: Zanobetti
authors.forename: D R
authors.initials: DR
authors.lastname: Gold
authors.forename: P A
authors.initials: PA
authors.lastname: Economides
authors.forename: E S
authors.initials: ES
authors.lastname: Horton
authors.forename: J
authors.initials: J
authors.lastname: Schwartz
mesh_terms: D000328:Adult; D001900:Boston / Q000453:epidemiology; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology; D003925:Diabetic Angiopathies / Q000097:blood* / Q000139:chemically induced / Q000453:epidemiology; D004198:Disease Susceptibility / Q000097:blood / Q000139:chemically induced; D004781:Environmental Exposure / Q000009:adverse effects / Q000032:analysis; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D052638:Particulate Matter / Q000633:toxicity*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014657:Vasculitis / Q000097:blood / Q000139:chemically induced* / Q000453:epidemiology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D052638:Particulate Matter; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1