Research Program Area: Health & Exposure
We tested the hypothesis that persons with acute respiratory responsiveness to ozone (OS) are at high risk of chronic lung injury from repeated exposure to oxidant air pollution. Nonsmoking, chronically oxidant-exposed adult residents (n - 164) of Glendora, California underwent lung function measurements in the field during 1986-87 (time 3) as a follow up of larger-scale field studies in 1977-78 (time 1) and 1982-83 (time 2). Although these 164 subjects showed a large annual decrease in forced expired volume in one second (FEV,) between time 1 and time 2; they did not show continued decline in lung function between time 2 and time 3. Forty-five members of the time 3 group were studied in the laboratory in 1989 (time 4) and showed statistically significant but mild acute reductions in FEV1 and forced vital capacity (FVC) during two-hour controlled chamber exposures to 0.4 ppm ozone (O3), in comparison with exposures to clean air. Post-exposure bronchial responsiveness to inhaled methacholine was not statistically significantly different between O3 and clean air exposures at time 4. Lung function (FEV1, and FVC) responses to acute O3 exposures at time 4 correlated poorly with longer-term FEV1 or FVC changes (possibly influenced by chronic ambient oxidant exposure), as measured over the previous time intervals (times l-3). These results do not support the hypothesis that acute lung function responses to ozone exposure can predict chronic effects in typical middle-aged nonsmokers residing in oxidant-polluted communities, or that such people experience unusually rapid long-term lung function decline.
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