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Air pollution and inflammation in type 2 diabetes: A mechanism for susceptibility
  1. Marie S. O'Neill (marieo{at}
  1. University of Michigan, United States
    1. Aristidis Veves (aveves{at}
    1. Beth Israel Deaconess Medical Center, United States
      1. Jeremy A. Sarnat (jsarnat{at}
      1. Emory University, United States
        1. Antonella Zanobetti (azanobet{at}
        1. Harvard University, United States
          1. Diane R. Gold (redrg{at}
          1. Harvard University, United States
            1. Panayiotis A. Economides (peconomi{at}
            1. Center for Endocrinology and Metabolism, Nicosia, Cyprus
              1. Edward Horton (edward.hortin{at}
              1. Joslin Diabetes Center, United States
                1. Joel Schwartz (jschwrtz{at}
                1. Harvard School of Public Health, United States


                  Objectives: 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. We examined 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 sulfates (SO4 2-)) were measured approximately 500 meters from the patient exam 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, HbA1c, cholesterol, smoking history, and body mass index (BMI) 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.

                  • air pollution
                  • diabetes mellitus
                  • inflammation

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