Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4469812 | Environmental Research | 2013 | 8 Pages |
BackgroundOxidative 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.MethodsA 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.ResultsHigher 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.ConclusionsThese 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.
► We assess the association between traffic emissions and oxidative stress biomarkers. ► Higher traffic emissions were associated with decreased glutathione and elevated glutathione peroxidase. ► Stronger associations were suggested among women without tobacco smoke exposure. ► Associations were also stronger for measurements made in warmer months.