Acute exposure to traffic-related air pollution alters antioxidant status in healthy adults.

BACKGROUND

Exposure to traffic-related air pollution is associated with an increased risk of cardiovascular and respiratory disease. Evidence suggests that inhaled pollutants precipitate these effects via multiple pathways involving oxidative stress.

OBJECTIVE

Postulating that a decrease in circulating antioxidant levels reflect an oxidative response, we investigated the effect of inhaled diesel exhaust (DE) on the ratio of reduced to oxidized glutathione (GSH/GSSG) in healthy adults, and whether pre-exposure antioxidant supplementation blunted this response. We also examined exposure-related changes in antioxidant/stress response leukocyte gene expression (GCLc, HMOX-1, IL-6, TGFβ) and plasma IL-6 levels.

METHODS

Nineteen nonsmoking adults participated in a double-blind, randomized, four-way crossover study. Each subject completed 120-min exposures to filtered air and DE (200 μg/m), with and without antioxidant pretreatment. Antioxidant comprised 1000 mg ascorbate for 7 days and 1200 mg N-acetylcysteine 1 day prior to exposure, with 1000 mg and 600 mg, respectively, administered 2 h prior to exposure. Whole blood glutathione was measured pre- and post-exposure; plasma IL-6 and mRNA expression were quantified pre, during and post exposure.

RESULTS

Diesel exhaust exposure was associated with significantly decreased GSH/GSSG (p = 0.001) and a 4-fold increase in IL-6 mRNA (p = 0.01) post exposure. Antioxidant pretreatment did not significantly mediate the effect of DE exposure on GSH/GSSG, though appeared to decrease the effect of exposure on IL-6 mRNA expression.

CONCLUSIONS

Acute DE inhalation induced detectable oxidative effects in healthy adults, which were not significantly attenuated by the selected antioxidant pre-treatment. This finding supports the premise that oxidative stress is one mechanism underlying the adverse effects of traffic-related air pollution.

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