We hypothesized that exposure of:healthy humans to ozone causes both ozonat
ion and peroxidation of lipids in lung epithelial lining fluid. Twelve smok
ers and 15 nonsmokers (eight lung function "responders" and seven "nonrespo
nders") were exposed once to air and twice to 0.22 ppm ozone For 4 h with e
xercise in an environmental chamber, with each exposure separated by at lea
st 3 wk. Bronchoalveolar ravage (BAL) was performed immediately after one o
zone exposure and 18 h after the other ozone exposure. BAL fluid was analyz
ed for the aldehyde products of ozonation and lipid peroxidation, nonanal (
C9) and hexanal (C6), as well as total protein, albumin, and immunoglobulin
NI as markers of changes In epithelial permeability. Ozone exposure result
ed in a significant early increase in C9 (p = 0.0001), with no statisticall
y significant relationship between increases in C9 and lung function change
s, airway inflammation, or changes in epithelial permeability. increases in
C6 levels were not statistically significant (p = 0.16). Both CB and C6 le
vels returned to baseline by 18 h after exposure. These studies confirm tha
t exposure to ozone with exercise, at concentrations relevant to urban outd
oor air, results in ozonation of lipids in the airway epithelial lining flu
id of humans.