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Antioxidants vs Lung Disease

Jeffery N. Roehm, PhD; John G. Hadley; Daniel B. Menzel, PhD
Arch Intern Med. 1971;128(1):88-93. doi:10.1001/archinte.1971.00310190092011.
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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.


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