Am. J. Respir. Crit. Care Med., Volume 156, Number 3, September 1997, 728-736

Airway Inflammation in Smokers and Nonsmokers with Varying Responsiveness to Ozone

ALFONSO TORRES, MARK J. UTELL, PAUL E. MOROW, KAREN Z. VOTER, JOHN C. WHITIN, CHRISTOPHER COX, R. JOHN LOONEY, DONNA M. SPEERS, YING TSAI, and MARK W. FRAMPTON

Departments of Medicine, Environmental Medicine, Pediatrics, and Biostatistics, University of Rochester School of Medicine, Rochester, New York

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 non-responders, 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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