Ozone-induced inflammation assessed in sputum and bronchial, lavage fluid from asthmatics: A new noninvasive tool in epidemiologic studies on air pollution and asthma
Jtn. Hiltermann et al., Ozone-induced inflammation assessed in sputum and bronchial, lavage fluid from asthmatics: A new noninvasive tool in epidemiologic studies on air pollution and asthma, FREE RAD B, 27(11-12), 1999, pp. 1448-1454
We investigated correlations between ozone-induced increases in inflammator
y markers in induced sputum and in bronchial lavage fluid. Sixteen voluntee
rs with intermittent asthma participated in a placebo-controlled parallel s
tudy with two exposures. Six days before and 16 h after the first exposure
to ozone (0.4 ppm during 2 h) sputum was induced with hypertonic saline. Th
is resulted in a significant increase in the sputum levels of eosinophil ca
tionic protein (ECP; 1.8-fold; p = .03), neutrophil elastase (5.0-fold; p =
.005) and the total cell number (1.6-fold; p = .02). After 4 weeks, a seco
nd exposure was randomized for air or ozone. Six days before and 16 h after
the second exposure a bronchial lavage was performed. ECP values in sputum
and in bronchial lavage fluid obtained after ozone correlated significantl
y (Rs = .79; p = .04), as did interleukin-8 (IL-8) values (Rs = .86; p = .0
1), and the percentage eosinophils (Rs = .89; p = .007). Moreover, the ozon
e-induced changes in percentage eosinophils observed in sputum and lavage f
luid were highly correlated (Rs = .93; p = .003). In conclusion, changes in
eosinophils, IL-8, and ECP markers induced by ozone and measured in sputum
reflect the inflammatory responses in the lower airways of asthmatics, and
may provide a noninvasive tool in epidemiologic studies on air pollution a
nd asthma. (C) 1999 Elsevier Science Inc.