Relationship between acute ozone responsiveness and chronic loss of lung function in residents of a high-ozone community.

We hypothesized that acute respiratory responsiveness to ozone predicts chronic lung injury from repeated exposure to ozone-containing air pollution. We tested this hypothesis in 164 middle-aged nonsmoking residents of an ozone-polluted community who underwent lung-function measurements during 1986 and 1987 (i.e., time 3). The time-3 study was a follow up of more comprehensive studies conducted in 1977-1978 (time 1) and in 1982-1983 (time 2). In contrast to the apparent rapid (i.e., approximately 60 ml/y) decline in lung-function measurements between times 1 and 2, our subjects showed little change in forced vital capacity (FVC) or forced expired volume in 1 s (FEV1.0) between times 2 and 3, and they experienced a normal decline between times 1 and 3. A subgroup (n = 45) underwent 2-h laboratory ozone exposures to 0.4 ppm ozone, accompanied by intermittent exercise, and they experienced mild acute reductions in FEV1.0 and FVC, but there was little change in bronchial responsiveness to methacholine. Individual acute responses to laboratory ozone were not correlated with individual long-term changes between times 1 and 3. In summary, the results did not support our initial hypothesis, and they did not confirm rapid function decline in nonsmokers chronically exposed to ozone-containing air pollution.