Ambient ozone concentrations induce airway hyperresponsiveness in some ratstrains

Ozone is known to induce airway hyperresponsiveness (AHR) in humans and ani mals. Previous studies in animals used high exposure levels and reported in consistent results. The aim of this study was to investigate the effect of a single low-level ozone exposure on different inbred rat strains. Nine rat strains were exposed to 0.05 parts per million (ppm) for 4 h and a irway responsiveness to intravenous 5-hydroxytryptamine (HT) examined. Bron choalveolar lavage fluid (BALF) was examined for the presence of inflammato ry cells and markers. Lewis, BDII and Long-Evans rats developed AHR 90 min after ozone exposure, whereas Wistar, Sprague-Dawley, Fisher 344, Brown-Norway, BDE and DA rats d id not. Baseline airway responsiveness to 5-HT differed significantly betwe en rat strains, but did not correlate,vith the presence or absence of ozone -induced AHR. No inflammatory cell influx was found in BALF of any rat stra in. In Long-Evans rats, AHR lasted up to 12 h after ozone exposure despite the absence of an inflammatory cell influx or increase in lactate dehydroge nase, alkaline phosphatase or total protein in BALF. In conclusion, exposure to an ambient concentration of ozone induced airway hyperresponsiveness without airway inflammation in some highly inbred rat strains. Genetic factors are likely to account for the observed variability in sensitivity of the airways to ozone.