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

被引:183
作者
O'Neill, M. S.
Veves, A.
Sarnat, J. A.
Zanobetti, A.
Gold, D. R.
Economides, P. A.
Horton, E. S.
Schwartz, J.
机构
[1] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Sch Publ Hlth, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA
[3] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
[4] Emory Univ, Sch Publ Hlth, Atlanta, GA 30322 USA
[5] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA
[6] Ctr Endocrinol & Metab, Nicosia, Cyprus
[7] Joslin Diabet Ctr, Boston, MA 02215 USA
关键词
D O I
10.1136/oem.2006.030023
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
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.
引用
收藏
页码:373 / 379
页数:7
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