PULMONARY BIOCHEMICAL ALTERATIONS RESULTING FROM OZONE EXPOSURE

Metabolic response of lung tissue to ozone was studied in rats and monkeys after exposure of animals to various levels of ozone (0·1–0·8 ppm) for 1–30 days. In rats, 0–8 ppm ozone exposure resulted in a 40–50% augmentation of oxygen utilization in lung homogenate in the presence of an added substrate (e.g. succinate or 2-oxoglutarate). Activities of marker enzymes, viz. mitochondrial succinate-cytochrome c reductase; microsomal NADPH-cytochrome c reductase and cytosolic glucose-6-phosphate dehydrogenase, increased maximally (40–70% over control) after 3–4 days of exposure, and remained elevated throughout the 0·8 ppm ozone exposure for 30 days. In monkeys, the observations were the same except that the magnitude of biochemical changes was relatively smaller. Exposure of animals to lower levels of ozone resulted in proportionately smaller biochemical changes in the lung, and ozone effects were detectable up to the 0·2 ppm level. While 0·1 ppm ozone exposure was ineffective, dietary deficiency of vitamin E, a natural antioxidant, increased the sensitivity of rat lungs to this concentration of ozone. The results suggest that low-level ozone exposures may cause metabolic alterations in the lung, and that dietary supplementation of vitamin E may offer protection against oxidant stress.