Statistically significant changes (P less than .05) were observed in erythrocytes (RBC) and sera of young adult human males following a single short-term exposure to 0.50 ppm ozone (O3) for 2 3/4 hours. The RBC membrane fragility, glucose-6-phosphate dehydrogenase (G-6-PDH) and lactate dehydrogenase (LDH) enzyme activities were increased, while RBC acetylcholinesterase (AcChase) activity and reduced glutathione (GSH) levels were decreased. The RBC glutathione reductase (GSSRase) activities were not significantly altered. Serum GSSRase activity, however, was significantly decreased while serum vitamin E, and lipid peroxidation levels were significantly increased. These alterations tend to disappear gradually, but were still detectable two weeks following exposure.

Comparison of published reports on physiological effects of exposure to ozone (O3) suggests that Canadians are more reactive than southern Californians. Responses of subjects and experimental methods were compared in a cooperative investigation of this apparent difference in reactivity. Four Canadians and four Californians were exposed to 0.37 ppm O3 in purified air at 21 degrees C and 50% relative humidity for 2 hours with intermittent light exercise. Exposures to purified air alone served as controls. Responses of subjects were similar to those observed previously: Canadians on the average showed greater clinical and physiological reactivity to exposure than did Californians, who were no more than minimally reactive. Canadians also showed larger increases in erythrocyte fragility following exposure. No methodological differences sufficient to explain different results of previous studies were found. Although other possible explanations have not been ruled out entirely, adaptation of southern Californians to chronic ambient O3 exposure is a rational hypothesis to explain these results.

Because of the possible threat to public health posed by photochemical air pollution, a need exists for experimental studies of short-term respiratory effects of air pollutant exposure in humans. Such studies require rigorous control and comprehensive documentation of the experimental air environment and exposure conditions to ensure that results are both reliable and relevant to public health questions. In addition to biochemical, behavioral, and clinical evaluations, comprehensive pulmonary testing is required to assure that effects at different levels of the respiratory tract are detected. An experimental design based on these principles is described. Studies using this design have shown a wide range of sensitivity to the pollutant ozone and important adverse health effects in sensitive individuals under exposure conditions similar to those experienced during ambient pollution episodes.

Vitamin E deficiency in rats is associated with a greater susceptibility to lethal levels of ozone. Exposure of rats to sublethal ozone concentrations produces an accelerated decline in serum vitamin E levels. These findings are consistent with the possibility that lipid peroxidation is a mechanism of ozone toxicity.