Effect of diesel exhaust inhalation on antioxidant and oxidative stress responses in adults with metabolic syndrome.
BACKGROUND
Traffic-related air pollution is associated with cardiovascular morbidity and mortality. Although the biological mechanisms are not well understood, oxidative stress may be a primary pathway. Subpopulations, such as individuals with metabolic syndrome (MeS), may be at increased risk of adverse effects associated with air pollution. Our aim was to assess the relationship between exposure to diesel exhaust (DE) and indicators of systemic antioxidant and oxidative responses in adults with MeS. We hypothesized that DE exposure would result in greater oxidative stress and antioxidant responses compared with filtered air (FA).


METHODS
Ten adult subjects with MeS were exposed on separate days for two hours to FA or DE (at 200microg/m3), in a double blind, crossover experiment. Urinary 8-isoPGF2alpha (F2-isoprostanes), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were assessed as markers of oxidative stress at 3 hrs and 22 hrs, respectively, after exposure initiation. To assess the short-term antioxidant response we analyzed plasma ascorbic acid (AA) 90 minutes after exposure initiation. All outcomes were compared to pre-exposure levels, and mean changes were compared between FA and DE exposures.


RESULTS
Mean changes in urinary F2-isoprostanes (ng/mg creatinine), (-0.05 [95% CI = -0.29, 0.15]), and 8-OHdG (microg/g creatinine) (-0.09 [-0.13, 0.31]), were not statistically significant. Mean changes in plasma AA (mg/dl) were also not significant (-0.02 [-0.78, 0.04]).


CONCLUSIONS
In this carefully controlled experiment, we did not detect significant changes in oxidative stress or systemic antioxidant responses in subjects with MeS exposed to 200microg/m3 DE.
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, 98195, USA. drjnd@u.washington.edu
Jason
J
Allen
Carol A
CA
Trenga
Alon
A
Peretz
Jeffrey H
JH
Sullivan
Christopher C
CC
Carlsten
Joel D
JD
Kaufman
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers / Q000097:blood / Q000652:urine; D003404:Creatinine / Q000097:blood / Q000652:urine; D018592:Cross-Over Studies; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D004311:Double-Blind Method; D028441:F2-Isoprostanes / Q000652:urine; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019570:Inhalation Exposure / Q000009:adverse effects*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000378:metabolism* / Q000652:urine; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D001335:Vehicle Emissions / Q000506:poisoning*; D055815:Young Adult
D000975:Antioxidants; D015415:Biomarkers; D028441:F2-Isoprostanes; D001335:Vehicle Emissions; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003404:Creatinine; D003849:Deoxyguanosine; D001205:Ascorbic Acid