Ozone exposure causes acute decrements in pulmonary function, increases air
way responsiveness, and changes the breathing pattern. We examined these re
sponses in 19 ozone-responsive(Delta FEV1 > 5%) young females exposed to bo
th air and 0.35 ppm ozone. The randomized 75-min exposures included two 30-
min exercise periods at V-E approximate to 40 L/min. Responses were measure
d before, during and after exposure and at 18 and 42 h postexposure. FVC, F
EV1, and FIV0.5 decreased (p < .01) immediately postexposure by 13.2%, 19.9
%, and 20.8%, respectively, and the airway responsiveness was significantly
increased. Raw increased (p < .05), while TGV remained essentially unchang
ed. At 78 h postexposure, the airways were still hyperresponsive and FEV1 a
nd FIV0.5 were still 5% below the preexposure levels. There were no residua
l effects in any of the variables at 42 h postexposure. During exercise in
ozone the tidal Volume was decreased (-14%) and respiratory frequency incre
ased (+15%). The changes in airway responsiveness were not related to chang
es in spirometric measurements. We found no significant differences between
postair and postozone mouth occlusion pressure (Pm-0.1) and the hypercapni
c response to CO2 rebreathing. We conclude that ozone induced typical acute
changes in airway responsiveness and that ventilatory (exercise), spiromet
ric (inspiratory and expiratory), and plethysmographic pulmonary function m
ay show some residual effects for up to 18 h after exposure. The ozone-indu
ced alteration in breathing pattern during exercise does not appear to be r
elated to a change in ventilatory drive.