title: Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function.
abstract: BACKGROUND
  Epidemiological studies suggest that people with diabetes are vulnerable to cardiovascular health effects associated with exposure to particle air pollution. Endothelial and vascular function is impaired in diabetes and may be related to increased cardiovascular risk. We examined whether endothelium-dependent and -independent vascular reactivity was associated with particle exposure in individuals with and without diabetes.
  
  
  RESULTS
  Study subjects were 270 greater-Boston residents. We measured 24-hour average ambient levels of air pollution (fine particles [PM2.5], particle number, black carbon, and sulfates [SO4(2-)]) approximately 500 m from the patient examination site. Pollutant concentrations were evaluated for associations with vascular reactivity. Linear regressions were fit to the percent change in brachial artery diameter (flow mediated and nitroglycerin mediated), with the particulate pollutant index, apparent temperature, season, age, race, sex, smoking history, and body mass index as predictors. Models were fit to all subjects and then stratified by diagnosed diabetes versus at risk for diabetes. Six-day moving averages of all 4 particle metrics were associated with decreased vascular reactivity among patients with diabetes but not those at risk. Interquartile range increases in SO4(2-) were associated with decreased flow-mediated (-10.7%; 95% CI, -17.3 to -3.5) and nitroglycerin-mediated (-5.4%; 95% CI, -10.5 to -0.1) vascular reactivity among those with diabetes. Black carbon increases were associated with decreased flow-mediated vascular reactivity (-12.6%; 95% CI, -21.7 to -2.4), and PM2.5 was associated with nitroglycerin-mediated reactivity (-7.6%; 95% CI, -12.8 to -2.1). Effects were stronger in type II than type I diabetes.
  
  
  CONCLUSIONS
  Diabetes confers vulnerability to particles associated with coal-burning power plants and traffic.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, Mass, USA. marieo@umich.edu
authors.forename: Marie S
authors.initials: MS
authors.lastname: O'Neill
authors.forename: Aristidis
authors.initials: A
authors.lastname: Veves
authors.forename: Antonella
authors.initials: A
authors.lastname: Zanobetti
authors.forename: Jeremy A
authors.initials: JA
authors.lastname: Sarnat
authors.forename: Diane R
authors.initials: DR
authors.lastname: Gold
authors.forename: Panayiotis A
authors.initials: PA
authors.lastname: Economides
authors.forename: Edward S
authors.initials: ES
authors.lastname: Horton
authors.forename: Joel
authors.initials: J
authors.lastname: Schwartz
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000397:Air Pollution / Q000009:adverse effects* / Q000032:analysis; D001808:Blood Vessels / Q000503:physiopathology*; D001900:Boston / Q000453:epidemiology; D002244:Carbon / Q000032:analysis; D002986:Clinical Trials as Topic; D003920:Diabetes Mellitus / Q000453:epidemiology / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000453:epidemiology / Q000209:etiology*; D004198:Disease Susceptibility; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010316:Particle Size; D012307:Risk Factors; D013431:Sulfates / Q000032:analysis; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D013431:Sulfates; D002244:Carbon