• Airway hyperresponsiveness;
  • airway inflammation;
  • extravasation;
  • 5-hydroxytryptamine;
  • ozone;
  • rat


Ozone is known to induce airway hyperresponsiveness (AHR) in humans and animals. Previous studies in animals used high exposure levels and reported inconsistent 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 airway responsiveness to intravenous 5-hydroxytryptamine (HT) examined. Bronchoalveolar lavage fluid (BALF) was examined for the presence of inflammatory 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 did not. Baseline airway responsiveness to 5-HT differed significantly between rat strains, but did not correlate with the presence or absence of ozone-induced AHR. No inflammatory cell influx was found in BALF of any rat strain. 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 dehydrogenase, 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.

Eur Respir J 1999; 14: 125–131.