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

@article{citeulike:2998723, 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. 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 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.}, address = {Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan 48109, USA. marieo@umich.edu}, author = {O'Neill, M. S. and Veves, A. and Sarnat, J. A. and Zanobetti, A. and Gold, D. R. and Economides, P. A. and Horton, E. S. and Schwartz, J.}, citeulike-article-id = {2998723}, citeulike-linkout-0 = {http://dx.doi.org/10.1136/oem.2006.030023}, citeulike-linkout-1 = {http://oem.bmj.com/cgi/content/abstract/64/6/373}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/17182639}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=17182639}, doi = {10.1136/oem.2006.030023}, issn = {1470-7926}, journal = {Occupational and environmental medicine}, keywords = {air-pollution, inflammation}, month = {June}, number = {6}, pages = {373--379}, posted-at = {2009-04-02 03:15:13}, priority = {2}, title = {Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility.}, url = {http://dx.doi.org/10.1136/oem.2006.030023}, volume = {64}, year = {2007} }

TY - JOUR ID - citeulike:2998723 L3 - citeulike-article-id:2998723 N2 - 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 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. IS - 6 JF - Occupational and environmental medicine SN - 1470-7926 AD - Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan 48109, USA. marieo@umich.edu EP - 379 TI - Air pollution and inflammation in type 2 diabetes: a mechanism for susceptibility. VL - 64 SP - 373 KW - air-pollution KW - inflammation AU - O'Neill, MS AU - Veves, A AU - Sarnat, JA AU - Zanobetti, A AU - Gold, DR AU - Economides, PA AU - Horton, ES AU - Schwartz, J PY - 2007/06// UR - http://dx.doi.org/10.1136/oem.2006.030023 ER -