Lung cell populations may be directly exposed to environmental airborn
e toxicants such as ozone (O-3). Since pulmonary macrophages (Mo) play
a pivotal role in host pulmonary immunocompetence, their function in
this regard may be compromised by pollutant exposure thereby giving ri
se to an increased incidence of pulmonary disease. The current in vitr
o study was designed to provide some insight into possible mechanisms
by which O-3 induces decreased host pulmonary resistance against micro
bial pathogens. Specifically, this study investigated the impact of an
acute O-3 exposure upon the ability of a cultured mouse Ms cell line
(WEHI-3) to interact with, and respond to, the major Mo-activating cyt
okine, interferon-gamma (IFN gamma). The results of this study indicat
e that WEHI-3 exposure to 1 ppm O-3 for 4 h reduced both the binding o
f, and responsivity to, IFN gamma. Among the functional parameters aff
ected by this inability to properly bind/respond to IFN gamma were: re
active oxygen intermediate production, phagocytic activity, and cellul
ar calcium ion elevation; IFN gamma-enhanced expression of surface his
tocompatibility antigens was unaffected by O-3 exposure. The reduced a
ctivity of any one of these critical Mo functions could provide a basi
s for previously-documented increases in microbial pathogen survival i
n the lungs, and overall compromise of host health following O-3 expos
ure.