4.7 Article

Endothelial Dysfunction: Associations with Exposure to Ambient Fine Particles in Diabetic Individuals

Journal

ENVIRONMENTAL HEALTH PERSPECTIVES
Volume 116, Issue 12, Pages 1666-1674

Publisher

US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
DOI: 10.1289/ehp.11666

Keywords

air pollution; diabetes; endothelial dysfunction; environmental epidemiology; particulate matter

Funding

  1. U.S. Environmental Protection Agency (EPA) [CR83346301]
  2. Division of Research Resources [RR00046]
  3. U.S. National Institutes of Health
  4. Helmholtz Zentrum Munchen-German Research Center for Environmental Health
  5. Rochester Particle Center [RD832415]
  6. U.S. Environmental Protection Agency
  7. University of North Carolina at Chapel Hill

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BACKGROUND: Exposure to fine airborne particulate matter [<= 2.5 mu m in aerodynamic diameter (PM2.5)] has been associated with cardiovascular and hematologic effects, especially in older people with cardiovascular disease. Some epidemiologic studies suggest that adults with diabetes also may be a particularly susceptible population. OBJECTIVES: The purpose of this study was to analyze the short-term effects of ambient PM2.5 on markers of endothelial function in diabetic volunteers. METHODS: We conducted a prospective panel study in 22 people with type 2 diabetes mellitus in Chapel Hill, North Carolina (USA), from November 2004 to December 2005. We acquired daily measurements of PM2.5 and meteorologic data at central monitoring sites. On 4 consecutive days, we measured endothelial function by brachial artery ultrasound in all participants and by pulsewave measurements in a subgroup. Data were analyzed using additive mixed models with a random participant effect and adjusted for season, day of the week, and meteorology. RESULTS: Flow-mediated dilatation decreased in association with PM2.5 during the first 24 hr, whereas small-artery elasticity index decreased with a delay of 1 and 3 days. These PM2.5-associated decrements in endothelial function were greater among participants with a high body mass index, high glycosylated hemoglobin Ale, low adiponectin, or the null polymorphism of glutathione S-transferase M1. However, high levels of myeloperoxidase on the examination day led to strongest effects on endothelial dysfunction. CONCLUSIONS: These data demonstrate that PM2.5 exposure may cause immediate endothelial dysfunction. Clinical characteristics associated with insulin resistance were associated with enhanced effects of PM on endothelial function. In addition, participants with greater oxidative potential seem to be more susceptible.

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