TY - JOUR
T1 - Airway inflammation in smokers and nonsmokers with varying responsiveness to ozone
AU - Torres, Alfonso
AU - Utell, Mark J.
AU - Morow, Paul E.
AU - Voter, Karen Z.
AU - Whitin, John C.
AU - Cox, Christopher
AU - Looney, R. John
AU - Speers, Donna M.
AU - Tsai, Ying
AU - Frampton, Mark W.
PY - 1997
Y1 - 1997
N2 - Exposure to ozone causes symptoms, changes in lung function, and airway inflammation. We studied whether individuals who differ in lung-function responsiveness to ozone, or in smoking status, also differ in susceptibility to airway inflammation. Healthy subjects were selected on the basis of responsiveness to a classifying exposure to 0.22 ppm ozone for 4 h with exercise (responders, with a decrease in FEV1 > 15%; and nonresponders, with a decrease in FEV1 < 5%). Three groups were studied: nonsmoker-nonresponders (n = 12), nonsmoker-responders (n = 13), and smokers (n = 13, 11 nonresponders and two responders). Each subject underwent two exposures to ozone and one to air, separated by at least 3 wk; bronchoalveolar and nasal lavages were performed on three occasions: immediately (early) and 18 h (late) after ozone exposure, and either early or late after air exposure. Recovery of polymorphonuclear leukocytes (PMN) increased progressively in all groups, and by up to 6-fold late after ozone exposure. Interleukin-6 (IL-6) and IL-8 increased early (by up to 10-fold and up to 2-fold, respectively), and correlated with the late increase in PMN. Lymphocytes, mast cells, and eosinophils also increased late after exposure. We conclude that ozone- induced airway inflammation is independent of smoking status or airway responsiveness to ozone.
AB - Exposure to ozone causes symptoms, changes in lung function, and airway inflammation. We studied whether individuals who differ in lung-function responsiveness to ozone, or in smoking status, also differ in susceptibility to airway inflammation. Healthy subjects were selected on the basis of responsiveness to a classifying exposure to 0.22 ppm ozone for 4 h with exercise (responders, with a decrease in FEV1 > 15%; and nonresponders, with a decrease in FEV1 < 5%). Three groups were studied: nonsmoker-nonresponders (n = 12), nonsmoker-responders (n = 13), and smokers (n = 13, 11 nonresponders and two responders). Each subject underwent two exposures to ozone and one to air, separated by at least 3 wk; bronchoalveolar and nasal lavages were performed on three occasions: immediately (early) and 18 h (late) after ozone exposure, and either early or late after air exposure. Recovery of polymorphonuclear leukocytes (PMN) increased progressively in all groups, and by up to 6-fold late after ozone exposure. Interleukin-6 (IL-6) and IL-8 increased early (by up to 10-fold and up to 2-fold, respectively), and correlated with the late increase in PMN. Lymphocytes, mast cells, and eosinophils also increased late after exposure. We conclude that ozone- induced airway inflammation is independent of smoking status or airway responsiveness to ozone.
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U2 - 10.1164/ajrccm.156.3.9601054
DO - 10.1164/ajrccm.156.3.9601054
M3 - Article
C2 - 9309986
AN - SCOPUS:9844240490
SN - 1073-449X
VL - 156
SP - 728
EP - 736
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 3 I
ER -