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Cited by 107Air Quality and Health ImpactsAsthma and respiratory diseasesIndoor Air Quality and Microbial Exposure

Effects of 0.2 ppm ozone on biomarkers of inflammation in bronchoalveolar lavage fluid and bronchial mucosa of healthy subjects

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Krishna, MT, Madden, J, Teran, LM, Biscione, GL, Lau, LC, Withers, NJ, Sandstrom, T, Mudway, I +4 more·1998·European Respiratory Journal
DOI 10.1183/09031936.98.11061294
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Abstract

Short-term exposure to ozone at peak ambient levels induces neutrophil influx and impairs lung function in healthy humans. In order to investigate the mechanisms contributing to neutrophil recruitment and to examine the role of T-cells in the acute inflammatory response, we exposed 12 healthy humans to 0.2 parts per million (ppm) of ozone and filtered air on two separate occasions for 2 h with intermittent periods of rest and exercise (minute ventilation = 30 L x min(-1)). Fibreoptic bronchoscopy was performed 6 h after the end of exposures. Total protein, tryptase, histamine, myeloperoxidase, interleukin (IL)-8 and growth-related oncogene-alpha (Gro-alpha) were measured and total and differential cell counts were performed in bronchoalveolar lavage (BAL) fluid. Flow cytometry was performed on BAL cells to study total T-cells, T-cell receptors (alphabeta and gammadelta), T-cell subsets (CD4+ and CD8+ cells) and activated T-cell subsets (CD25+). Using immunohistochemistry, neutrophils, mast cells, total T-cell numbers, T-cell subsets, CD25+ T-cells and leukocyte endothelial adhesion molecules including P-selectin, E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 were quantified in the bronchial biopsies. Paired samples were available from nine subjects. Following ozone exposure there was a threefold increase in the proportion of polymorphonuclear neutrophils (PMNs) (p=0.07) and epithelial cells (p=0.05) in BAL fluid. This was accompanied by increased concentrations of IL-8 (p=0.01), Gro-alpha (p=0.05) and total protein (p=0.058). A significant positive correlation was demonstrated between the two chemokines and proportion of PMNs in BAL fluid. After ozone exposure there was a significant decrease in the CD4/CD8 ratio (p=0.05) and the proportion of activated CD4+ (p=0.01) and CD8+ T-cells (p=0.04). However, no significant changes were demonstrable in any of the inflammatory markers studied in the biopsies. Short-term exposure of healthy humans to 0.2 ppm ozone induced a neutrophil influx in peripheral airways at 6 h post exposure, but no apparent inflammatory response in proximal airways. This response seems to be mediated at least in part by interleukin-8 and growth-related oncogene-alpha.

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  • Ozone-induced neutrophil influx in human peripheral airways was partly mediated by IL-8.

    “Krishna et al. further confirmed that ozone-induced neutrophil influx in human peripheral airways was partly mediated by IL-8 (38).”

    From Ozone pollution: A Major health hazard worldwide (2019) · cites this paper as [38]

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Research works printed but not linked: 4

  1. Montefort S, Gratziou C, Goulding D, et al. Bronchial biopsy evidence for leucocyte infiltration and upregula- tion of leucocyte-endothelial adhesion molecules 6 hours after local allergen challenge of sensitised asthmatic air- ways. J Clin Invest 1994; 93: 1411-1421.
  2. Bleavins MR, Sargent NE, Dziedzic D. Effect of cyclo- sporin A on ozone induced pulmonary lesion formation: pharmacological elimination of T-lymphocyte regulatory response. Arch Environ Contam Toxicol 1995; 28: 240- 247.
  3. Britten KM, Howarth PH, Roche WR. Immunohisto- chemistry on resin sections: a comparison of resin em- bedding techniques on small mucosal biopsies. Biotech Histochem 1993; 68: 271-280.
  4. Aris R, Ferrando R, Chen LC, Christian D, Balmes JR. Increased ICAM expression on human bronchial epithe- lium after acute exposure to ozone. Am J Respir Crit Care Med 1995; 151: A26.

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Authors
Krishna, M., Madden, J., Teran, L., Biscione, G., Lau, L., Withers, N., Sandstrom, T., Mudway, I., Kelly, F., Walls, A., Frew, A., & Holgate, S.
Affiliations
Southampton General Hospital (GB)
ORCID
Venue
European Respiratory Journal
Publisher
European Respiratory Society (ERS)
Published
1998-06-01
Volume
11
Issue
6
Pages
1294-1300
ISSN
  • 0903-1936 (ISSN-L)
  • 1399-3003
DOI
10.1183/09031936.98.11061294
OpenAlex
W2105407937
Cited by
107
References
27
Citations by year
2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 4
FWCI
4.54
Type
journal article
Language
en
Open access
Locations
  • European Respiratory Journal (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • British Lung Foundation
  • Medical Research Council
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
Keywords
ozone exposure, air pollution health effects, neutrophil recruitment, bronchoalveolar lavage fluid, bronchial mucosa, T cell subsets, CD4/CD8 ratio, interleukin-8, growth-related oncogene alpha, chemokines, leukocyte adhesion molecules, P-selectin, E-selectin, ICAM-1, VCAM-1, mast cells, myeloperoxidase, tryptase, histamine, healthy volunteers
MeSH terms
Adult, Bronchi, Bronchoalveolar Lavage Fluid, Cell Count, Double-Blind Method, Female, Flow Cytometry, Histamine, Humans, Immunohistochemistry, Male, Mucous Membrane, Peroxidase, Neutrophils, Oxidants, Photochemical, Ozone, Serine Endopeptidases, Receptors, Interleukin-2, Oncogene Proteins, Cell Adhesion Molecules, T-Lymphocyte Subsets, Interleukin-8, Cross-Over Studies, Inflammation Mediators, Tryptases, Chymases

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