EFFECTS OF LOW-LEVEL OZONE EXPOSURE ON REACTIVITY AND CONDUCTANCE IN GUINEA-PIG AIRWAYS

Citation
A. Johnson et al., EFFECTS OF LOW-LEVEL OZONE EXPOSURE ON REACTIVITY AND CONDUCTANCE IN GUINEA-PIG AIRWAYS, Inhalation toxicology, 10(2), 1998, pp. 155-172
Citations number
37
Categorie Soggetti
Toxicology
Journal title
ISSN journal
08958378
Volume
10
Issue
2
Year of publication
1998
Pages
155 - 172
Database
ISI
SICI code
0895-8378(1998)10:2<155:EOLOEO>2.0.ZU;2-G
Abstract
Previous studies have shown airway hyperreactivity in guinea pigs indu ced by ozone concentrations from 1 to 4 ppm for periods of up to 4 h. Ambient ozone levels only rarely exceed 0.2 ppm in megacities such as Mexico City and normally lie below 0.1 ppm. Here we investigate the ef fects of an ozone concentration of between 0.3 and 0.45 ppm upon airwa y function and inflammatory cell influx in guinea pigs. Airway functio n was monitored in conscious guinea pigs over a 24-h time course follo wing a 2-h ozone exposure. A significant bronchoconstriction was seen as a decrease in specific airway conductance (sG(aw)) at 0.25, 0.5, an d 4 h postozone, with a recovery to basal values after 7 h, which last ed for the following 17 h. Airway reactivity to methacholine and 5-hyd roxytryptamine (5-HT), both iv and inhaled, was assessed in anesthetiz ed guinea pigs between 2 and 3 h after an ozone exposure of the consci ous animal. A clear ozone-induced airway hyperreactivity was observed as a leftward shift of the dose-response curve for both methacholine a nd 5-HT compared with air-exposed controls. Guinea pigs that were sens itized with ovalbumin, however, did not reveal ozone-induced airway hy perreactivity to methacholine and the hyperreactivity to 5-HT was redu ced. This was attributed to an interaction between ozone and the sensi tization process, as sensitization per se did not affect airway reacti vity. The airway hyperreactivity appeared to be mediated by the vagus nerves, as vagotomized, unsensitized, anesthetized guinea pigs failed to exhibit ozone-induced airway hyperreactivity to either spasmogen. A irways inflammation was apparent from bronchoalveolar lavage of ozone- exposed animals, which revealed a significant influx of inflammatory c ells, in particular eosinophils, compared to air-exposed controls. Wet -dry lung weight measurements, however, did not reveal significant ede ma and/or secretions in the airways of sensitized or unsensitized anim als after ozone exposure.