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
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.