In Southern California coastal regions, morning fog is often acidified by the presence of nitric acid (HNO3). Peak exposure to ozone (O3) usually occurs in the afternoon and evening, after the fog has dissipated. To determine whether fog containing HNO3 might enhance pulmonary responses to O3, we studied a group of healthy, athletic subjects selected for lung function sensitivity to O3. On 3 separate days, the subjects exercised for 2 h in atmospheres containing HNO3 fog (0.5 mg/ml), H2O fog, or clean, filtered air. After a 1-h break, they exercised for an additional 3 h in an atmosphere containing 0.20 ppm O3. Surprisingly, the mean O3-induced decrements in FEV1 and FVC were smaller after exercise in each fog-containing atmosphere than they were after exercise in clean, filtered air. The mean (± SEM) O3-induced decrements in FEV1 were 26.4 ± 5.3% after air, 17.1 ± 3.7% after H2O fog, and 18.0 ± 4.3% after HNO3 fog, and in FVC they were 19.9 ± 4.7% after air, 13.6 ± 2.8% after H2O fog, and 13.6 ± 4.2% after HNO3 fog. Although the O3-sensitive subjects studied were selected from a healthy group of volunteers solely on the basis of sensitivity to O3, as a group they were significantly more responsive to methacholine than was a group of subjects previously studied in our laboratory, and were also significantly more responsive to methacholine than was a group of similarly recruited subjects found not to be sensitive to O3 (mean ± SEM PC100 of 2.95 ± 0.80 mg/ml for the O3-sensitive subjects and 18.67 ± 4.54 mg/ml for the nonsensitive subjects, p < 0.005). These results indicate that prior exposure to HNO3 or H2O fog does not potentiate, but may attenuate, O3-induced decrements in pulmonary function. In addition, our finding of increased methacholine responsiveness in O3-sensitive subjects suggests that airway hyperresponsiveness may be a risk factor for O3 sensitivity even among healthy, asymptomatic athletes.
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Christian et al. (1991) studied this question.