4.5 Article

Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility

Journal

OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
Volume 64, Issue 6, Pages 373-379

Publisher

BMJ PUBLISHING GROUP
DOI: 10.1136/oem.2006.030023

Keywords

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Funding

  1. NCRR NIH HHS [M01 RR001032, RR 01032] Funding Source: Medline
  2. NIDDK NIH HHS [2P30-DK-36836] Funding Source: Medline
  3. NIEHS NIH HHS [ES00002, T32 ES007069, P30 ES000002, P01 ES009825, 2 T32 ES07069-24] Funding Source: Medline

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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.

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