Earlier, we found that acute ozone (O3) exposure caused, along with inflammation, greater, more protracted changes in small airway function (isovolumetric V max at intermediate to low lung volumes) than in FVC or FEV1. To test if this distinction prevailed with repetitive O3 exposure, we exposed eight healthy adults on four consecutive days alternatively to filtered air (FA) and O3 (0.25 ppm x 2 h). Isovolumetric FEF25-75, Vmax50, and Vmax75, were grouped into a single value representing small airway function (SAW(grp)); respiratory frequency (f) and tidal volume (VT) were monitored during exercise. On Day 5, peripheral airway resistance (Rp) was measured followed by lavage. All daily spirometric and ventilatory changes declined in magnitude (adapted) after one or more days of O3 exposure. In addition, SAW(grp), f, and VT showed persistent changes beginning with Day 2, denoted either by depression of the preexposure baseline (SAW(grp)) or exaggerated tachypnea during exercise. O3-induced neutrophilia (p = 0.04) was present in lavage fluid. The possible relationship between these persistent changes in small airway function, measured in days, and the likelihood of cumulative injury in the same region if exposure is long term, is unknown.