The effect of oxidant exposure on the immediate airway response to immunologic challenge is controversial. We investigated the response of canine peripheral airways to antigen aerosol, 1–3 h and 24 h after a 5‐min exposure to 1 ppm ozone. In dogs that were natively sensitive toAscaris suumantigen, resistance to flow through the collateral system (Rcs) was measured using the wedged bronchoscope technique. In eight dogs, four sublobar segments of each lung were wedged: two were exposed to ozone for 5 min and two (control) received air with 5% CO2. Ozone caused a mean (±SE) increase inRcsof 75 ± 15%, which returned to baseline after 1–3 h. The increase inRcselicited by subsequent administration of antigen aerosol (25 μl, 0.27 mg protein/ml) to the ozone‐exposed segments (312.0 ± 70.6%) was attenuated by 22% compared to controls (398.9 ± 83.0% p < .05). In another series of experiments (n = 5), segments were exposed to ozone or air and challenged with antigen 24 h later and a significant attenuation (38%) of the antigen‐induced increase inRcswas detected compared to controls (178.5 ± 57.9 vs. 289.0 ± 62.2; p < .05). Cellular influx of polymorphonuclear leukocytes (PMNs) was not detected by bronchoalveolar lavage (BAL) 1–3 h after ozone, but was found after24 h (19.8 vs. 4.7% p < .01). A significant increase in PMNs was detected in exposed subepithelial tissues 1–3 h after ozone compared to unexposed tissues. Tissue PMNs were not significantly different from unexposed tissues after 24 h, but a shift toward degranulation of mast cells was detected in ozone‐exposed tissues at this time. These data suggest that theRCSresponse to antigen is attenuated 1–3 h and 24 h after acute (5 min) exposure to 1 ppm ozone, and this effect occurs independently of PMNs in the airways.