To determine if asthmatic subjects (ASTH, n = 17) experience greater O3-induced pulmonary decrements than nonasthmatic subjects (NONA, n = 13), both groups were exposed for 7.6 h to both clean air and 0.16 ppm O3. Exposures consisted of seven 50-min periods of light exercise (VE = 14.2 and 15.3 l/min/m2 for ASTH and NONA, respectively), each followed by 10 min rest. A 35-min lunch period followed the third exercise. Following O3 exposure, decrements in forced expiratory volume in one second (FEV1) and FEV1 divided by forced vital capacity (FVC), corrected for air exposure, for ASTH (-19.4 +/- 3.1% and -6.2 +/- 2%, respectively) were significantly greater (p = 0.04 and 0.02) than for NONA (-9.8 +/- 1.9% and -1 +/- 1%, respectively). There was no difference (p = 0.33) for decrements in FVC between ASTH (-11.8 +/- 1.9%) and NONA (-8.8 +/- 2.1%). Nine of 17 ASTH experienced wheezing with O3, while only one experienced wheezing with air (p = 0.004); no NONA experienced wheezing. Six of 17 ASTH requested inhaled beta-agonist bronchodilator prior to and/or during O3 exposure and experienced some temporary alleviation of decrements. At end exposure, however, ASTH who were medicated had greater O3-induced decrements than those who were not medicated. ASTH who had the larger O3-induced decrements had lower baseline FEV1/FVC and lower baseline %predicted FEV1. These data indicate that in ASTH, unlike NONA, some portion of O3-induced pulmonary decrements experienced was related to bronchoconstriction, and that O3-responsiveness for ASTH depended upon baseline airway status.
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