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July 1971

Antioxidants vs Lung Disease

Author Affiliations

Richland, Wash

From the Biology Department, Pacific Northwest Laboratories, Battelle Memorial Institute, Richland, Wash. Dr. Menzel is now with Ross Laboratories, Columbus, Ohio.

Arch Intern Med. 1971;128(1):88-93. doi:10.1001/archinte.1971.00310190092011

Oxidation of fatty acid methyl esters was markedly increased by trace quantities (1.5 ppm) of nitrogen dioxide or ozone. Nitrogen dioxide-catalyzed oxidation occurred through conventional peroxidation mechanisms. Ozone reacted in thin films by directly attacking the double bond. Phenolic antioxidants retarded NO2—but not O3—oxidation. In aqueous media, O3-oxidation occurred by direct attack and peroxidation; NO2-oxidation by conventional peroxidation. Both were retarded by phenolic antioxidants. Exposure of rats to 10 ppm NO2 for four weeks resulted in reduction of polyunsaturated fatty acids in the vitamin E-depleted group. Exposure to 1.0 ppm ozone resulted in death from pulmonary edema of all animals within 22 days. Lethal time for 50% of the population (LT50) was 8.2 days for vitamin E-depleted animals, and 18.5 days for those receiving vitamin E. Vitamin E appears to protect against the biological effects of photochemical air pollutants.