Exposure to 1 ppm ozone attenuates the immediate antigenic response of canine peripheral airways

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Abstract
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 to Ascaris suum antigen, resistance to flow through the collateral system (R cs ) 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 in R cs of 75 ± 15%, which returned to baseline after 1–3 h. The increase in R cs elicited 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 in R cs was 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 the R CS response 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.