Am. J. Respir. Crit. Care Med., Volume 164, Number 5, September 2001, 819-825

Effect of Antioxidant Supplementation on Ozone-Induced Lung Injury in Human Subjects

JAMES M. SAMET, GARY E. HATCH, DONALD HORSTMAN, SUSAN STECK-SCOTT, LENORE ARAB, PHILIP A. BROMBERG, MARK LEVINE, WILLIAM F. MCDONNELL, and ROBERT B. DEVLIN

Human Studies and Experimental Toxicology Divisions, National Health and Environmental Effects Research Laboratory, Research Triangle Park, and Department of Nutrition and Center for Environmental Medicine and Lung Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland

To determine whether antioxidants can influence human susceptibility to ozone (O₃)-induced changes in lung function and airway inflammation, we placed 31 healthy nonsmoking adults (18 to 35 yr old) on a diet low in ascorbate for 3 wk. At 1 wk, subjects were exposed to filtered air for 2 h while exercising (20 L/min/m²), and then underwent bronchoalveolar lavage (BAL) and were randomly assigned to receive either a placebo or 250 mg of vitamin C, 50 IU of -tocopherol, and 12 oz of vegetable cocktail daily for 2 wk. Subjects were then exposed to 0.4 ppm O₃ for 2 h and underwent a second BAL. On the day of the O₃ exposure, supplemented subjects were found to have significantly increased levels of plasma ascorbate, tocopherols, and carotenoids as compared with those of the placebo group. Pulmonary function testing showed that O₃-induced reductions in FEV₁ and FVC were 30% and 24% smaller, respectively, in the supplemented cohort. In contrast, the inflammatory response to O₃ inhalation, as represented by the percent neutrophils and the concentration of interleukin-6 recovered in the BAL fluid at 1 h after O₃ exposure was not different for the two groups. These data suggest that dietary antioxidants protect against O₃-induced pulmonary function decrements in humans.

Keywords: antioxidants; ozone; human; inflammation

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