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Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility
  1. M S O’Neill1,
  2. A Veves2,
  3. J A Sarnat3,
  4. A Zanobetti4,
  5. D R Gold4,
  6. P A Economides5,
  7. E S Horton6,
  8. J Schwartz4
  1. 1Departments of Epidemiology and Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA
  2. 2Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  3. 3Emory University School of Public Health, Atlanta, Georgia, USA
  4. 4Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
  5. 5Center for Endocrinology and Metabolism, Nicosia, Cyprus
  6. 6Joslin Diabetes Center, Boston, Massachusetts, USA
  1. Correspondence to:
 Dr M S O’Neill
 University of Michigan School of Public Health, 6631 SPH Tower, 109 South Observatory, Ann Arbor, MI 48109, USA; marieo{at}


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.

Aim: 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 PM2.5, 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.

  • AT, apparent temperature
  • BC, black carbon
  • BMI, body mass index
  • HbAlc, glycosylated haemoglobin
  • ICAM-1, intercellular adhesion molecule 1
  • PM2.5, particles <2.5 μm in aerodynamic diameter, known as fine particles
  • PM10, particles <10 μm in aerodynamic diameter
  • SO42−, sulphate
  • VCAM-1, vascular cell adhesion molecule 1
  • vWF, von Willebrand factor

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  • Published Online First 19 December 2006

  • Competing interests: None.