title: Exposure to traffic emissions: associations with biomarkers of antioxidant status and oxidative damage.
abstract: BACKGROUND
  Oxidative stress has been implicated as a possible mechanism for adverse health effects associated with traffic emissions. We examined the association of an estimate of traffic emissions with blood biomarkers of antioxidant capacity (glutathione, glutathione peroxidase, trolox-equivalent antioxidant capacity) and oxidative damage (thiobarbituric acid-reactive substances (TBARS)) among 1810 healthy women, randomly selected from Erie and Niagara Counties in Western New York.
  
  
  METHODS
  A geographic traffic emission and meteorological dispersion model was used to estimate annual polycyclic aromatic hydrocarbon (PAH) exposure from traffic emissions for each woman based on her residence at the time of study. Associations of traffic-related PAH exposure with measures of oxidative stress and antioxidant capacity were examined in multiple regression analyses with adjustment for potential confounders.
  
  
  RESULTS
  Higher traffic-related PAH exposure was associated with decreased glutathione and increased glutathione peroxidase. Stronger associations between traffic-related PAH exposure and levels of glutathione and glutathione peroxidase were suggested among nonsmoking women without secondhand smoke exposure, especially among premenopausal nonsmoking women. Associations were also stronger for measurements made in warmer months.
  
  
  CONCLUSIONS
  These findings suggest that PAHs or other components of traffic emissions may impact anti-oxidative capacity among healthy women, particularly premenopausal non-smokers without secondhand smoke exposure.
authors.affiliation: Department of Social and Preventive Medicine, University at Buffalo, Buffalo, NY, USA. yanlili@buffalo.edu
authors.forename: Yanli
authors.initials: Y
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Nie
authors.forename: Jan
authors.initials: J
authors.lastname: Beyea
authors.forename: Carole B
authors.initials: CB
authors.lastname: Rudra
authors.forename: Richard W
authors.initials: RW
authors.lastname: Browne
authors.forename: Matthew R
authors.initials: MR
authors.lastname: Bonner
authors.forename: Lina
authors.initials: L
authors.lastname: Mu
authors.forename: Maurizio
authors.initials: M
authors.lastname: Trevisan
authors.forename: Jo L
authors.initials: JL
authors.lastname: Freudenheim
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000032:analysis*; D015415:Biomarkers / Q000097:blood*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D008685:Meteorological Concepts; D008875:Middle Aged; D009518:New York; D018384:Oxidative Stress / Q000187:drug effects*; D011084:Polycyclic Aromatic Hydrocarbons / Q000032:analysis / Q000633:toxicity*; D017697:Premenopause; D012044:Regression Analysis; D012907:Smoking; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014028:Tobacco Smoke Pollution / Q000009:adverse effects; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D011084:Polycyclic Aromatic Hydrocarbons; D017392:Thiobarbituric Acid Reactive Substances; D014028:Tobacco Smoke Pollution; D001335:Vehicle Emissions; D005979:Glutathione Peroxidase; D005978:Glutathione