title: Airway inflammation in smokers and nonsmokers with varying responsiveness to ozone.
abstract: 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.
authors.affiliation: Department of Medicine, University of Rochester School of Medicine, New York 14642-8692, USA.
authors.forename: A
authors.initials: A
authors.lastname: Torres
authors.forename: M J
authors.initials: MJ
authors.lastname: Utell
authors.forename: P E
authors.initials: PE
authors.lastname: Morow
authors.forename: K Z
authors.initials: KZ
authors.lastname: Voter
authors.forename: J C
authors.initials: JC
authors.lastname: Whitin
authors.forename: C
authors.initials: C
authors.lastname: Cox
authors.forename: R J
authors.initials: RJ
authors.lastname: Looney
authors.forename: D M
authors.initials: DM
authors.lastname: Speers
authors.forename: Y
authors.initials: Y
authors.lastname: Tsai
authors.forename: M W
authors.initials: MW
authors.lastname: Frampton
mesh_terms: D000293:Adolescent; D000328:Adult; D016535:Bronchial Hyperreactivity / Q000139:chemically induced* / Q000276:immunology* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004198:Disease Susceptibility; D005260:Female; D005541:Forced Expiratory Volume / Q000187:drug effects; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D009504:Neutrophils; D010083:Oxidants, Photochemical / Q000633:toxicity*; D010126:Ozone / Q000633:toxicity*; D012907:Smoking / Q000009:adverse effects*
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D010083:Oxidants, Photochemical; D010126:Ozone