title: Ambient PM2.5 exposure up-regulates the expression of costimulatory receptors on circulating monocytes in diabetic individuals.
abstract: BACKGROUND
  Exposure of humans to air pollutants such as ozone and particulate matter (PM) may result in airway and systemic inflammation and altered immune function. One putative mechanism may be through modification of cell-surface costimulatory molecules.
  
  
  OBJECTIVE
  We examined whether changes in expression of costimulatory molecules on circulating cells are associated with ambient levels of fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] in a susceptible population of diabetic individuals.
  
  
  METHODS
  Twenty subjects were studied for 4 consecutive days. Daily measurements of PM2.5 and meteorologic data were acquired on the rooftop of the exam site. Circulating cell-surface markers that mediate innate immune and inflammatory responses were assessed by flow cytometry on each day. Sensitivity analysis was conducted on glutathione S-transferase M1 (GSTM1) genotype, body mass index, and glycosylated hemoglobin A1c (HbA1c) levels to determine their role as effect modifiers. Data were analyzed using random effects models adjusting for season, weekday, and meteorology.
  
  
  RESULTS
  We found significantly increased monocyte expression (mean fluorescent intensity) of CD80, CD40, CD86, HLA-DR, and CD23 per 10-μg/m3 increase in PM2.5 at 2- to 4-day lag times after exposure. These findings were significantly higher in obese individuals, in individuals with HbA1c > 7%, and in participants who were GSTM1 null.
  
  
  CONCLUSIONS
  Exposure to PM2.5 can enhance antigen-presenting cell phenotypes on circulating cells, which may have consequences in the development of allergic or autoimmune diseases. These effects are amplified in diabetic individuals with characteristics that are associated with insulin resistance or with oxidative stress.
authors.affiliation: Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Schneider
authors.forename: Neil E
authors.initials: NE
authors.lastname: Alexis
authors.forename: David
authors.initials: D
authors.lastname: Diaz-Sanchez
authors.forename: Lucas M
authors.initials: LM
authors.lastname: Neas
authors.forename: Shirley
authors.initials: S
authors.lastname: Harder
authors.forename: Margaret C
authors.initials: MC
authors.lastname: Herbst
authors.forename: Wayne E
authors.initials: WE
authors.lastname: Cascio
authors.forename: John B
authors.initials: JB
authors.lastname: Buse
authors.forename: Annette
authors.initials: A
authors.lastname: Peters
authors.forename: Robert B
authors.initials: RB
authors.lastname: Devlin
mesh_terms: D000368:Aged; D017951:Antigen Presentation / Q000187:drug effects*; D000938:Antigen-Presenting Cells / Q000187:drug effects / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology* / Q000503:physiopathology*; D004781:Environmental Exposure; D005260:Female; D005982:Glutathione Transferase / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D052638:Particulate Matter / Q000633:toxicity*; D012621:Seasons; D015854:Up-Regulation / Q000187:drug effects; D014887:Weather
chemical_list: D015703:Antigens, CD; D005982:Glutathione Transferase; D006442:Glycated Hemoglobin; D052638:Particulate Matter; C517652:hemoglobin A1c protein, human