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Abstract
It has been repeatedly observed that ozone (O3) re-exposure within 24 h elicits enhanced pulmonary function responses. However, there are only limited observations concerning re-exposure to O3 at intervals between 24 h and several days. The present study was designed to assess the effects of re-exposure to 0.35 ppm O3 at intervals of 24, 48, 72, and 120 h. Forty young adult male subjects were assigned randomly to one of four groups in ascending order of time to re-exposure (groups 1–4). Each exercised on a bicycle ergometer for 60 min at a workload that elicited a mean ventilation of 60 l/min on three occasions: protocol 1 (P1), filtered air (FA); protocol 2 (P2), 0.35 ppm O3; and protocol 3 (P3), 0.35 ppm O3. In addition to standard pulmonary function measures, specific airway resistance (SRaw); exercise ventilatory pattern, i.e., respiratory frequency (fR) and tidal volume (VT); and subjective symptoms (SS) were assessed. Statistical analysis revealed significant differences (p < .05) for all groups between the FA (P1) responses and those for the two O3 exposures (P2, P3) for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), SRaw, fR, VT, and SS. When the two O3 exposures (P2 and P3) were compared, only group 1 (24 h) responses were statistically significant upon re-exposure: FEV1.0, −16.1 vs. −30.4% (p < .003); SRaw, 20.5 vs. 34.5% (p < .05); fR, 44.2 vs. 65.3% (p < .001); and SS (p < .015). Analysis of O3 re-exposure data for group 2 (48 h) indicated a trend toward significantly enhanced responsiveness: FEV1.0, −14.4 vs. −20.6% (p < .12); SRaw, 13.4 vs. 23.7% (p < .10); fR, 40.4 vs. 53.2% (p < .10); VT, −24.2 vs. −31.7% (p <.10); and SS (p > .10). Statistical analyses for groups 3–4 (72–120 h intervening) revealed no significant differences upon re-exposure to O3. Our observations demonstrated that, for the total O3 inhaled dose used in this study, the enhanced pulmonary function responsiveness noted upon re-exposure to O3 within 24 h may persist for up to 48 h in some subjects, but is absent 72 h after initial O3 exposure.