Document Detail

Ozone exposure and the production of reactive oxygen species by bronchoalveolar cells in humans.
MedLine Citation:
PMID:  11445887     Owner:  NLM     Status:  MEDLINE    
Exposure to ozone injures respiratory epithelium, and the mechanisms may involve the generation of reactive oxygen species (ROS). This study tested the hypothesis that ozone exposure increases the airway burden of ROS to a greater degree in smokers than nonsmokers, and that this effect is independent of ozone-induced changes in spirometry. Healthy subjects were selected as either responders (decrement in FEV1 > 15%) or nonresponders (decrement in FEV1 < 5%) to ozone; each underwent 2 exposures to ozone and 1 to air, with bronchoalveolar lavage (BAL) performed 30 min (early) and 18 h (late) after exposure. Release of superoxide anion (O2(-)) was used as a measure of ROS release by all BAL cells, and flow cytometry was used to detect ROS production in alveolar macrophages (AM) only. Recovery of AM was approximately threefold greater in smokers than nonsmokers. Unstimulated, but not stimulated, cells obtained by BAL from smokers released approximately twofold greater amounts of O2(-) than cells from nonsmokers, both early and late after ozone exposure (p =.012 and p =.046, respectively). Stimulated, but not unstimulated, ROS generation by AM from smokers increased following ozone exposure, but the ozone effect was not significant. ROS production by AM decreased in nonsmokers (air vs. ozone late, p =.014). Total protein, albumin, and immunoglobulin M (IgM) increased in BAL fluid, consistent with an increase in epithelial permeability. In addition, the concentration of alpha2-macroglobulin increased approximately threefold 18 h after exposure in nonsmokers (p <.001). No relationship was found between measures of ROS production and lung function responsiveness to ozone. These studies suggest the airways of smokers experience a greater burden of ROS than those of nonsmokers following ozone exposure.
K Z Voter; J C Whitin; A Torres; P E Morrow; C Cox; Y Tsai; M J Utell; M W Frampton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Inhalation toxicology     Volume:  13     ISSN:  0895-8378     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-07-10     Completed Date:  2001-08-02     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  465-83     Citation Subset:  IM    
Departments of Medicine, Pediatrics, Environmental Medicine, and Biostatistics, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave., Box 692, Rochester, NY 14642-8692, USA.
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MeSH Terms
Administration, Inhalation
Albumins / analysis
Bronchoalveolar Lavage Fluid / chemistry,  cytology
Flow Cytometry
Fluorescent Antibody Technique
Immunoglobulin M / analysis
Macrophages, Alveolar / cytology,  drug effects*,  metabolism
Ozone / adverse effects*
Proteins / analysis
Reactive Oxygen Species / metabolism*
Smoking / adverse effects*
Superoxides / metabolism
alpha-Macroglobulins / analysis
Grant Support
Reg. No./Substance:
0/Albumins; 0/Immunoglobulin M; 0/Proteins; 0/Reactive Oxygen Species; 0/alpha-Macroglobulins; 10028-15-6/Ozone; 11062-77-4/Superoxides

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