Ozone-induced inflammation in the lower airways of human subjects
Abstract
Abstract Although ozone (O3) has been shown to induce inflammation in the lungs of animals, very little is known about its inflammatory effects on humans. In this study, 11 healthy nonsmoking men, 18 to 35 yr of age (mean, 25.4 ± 3.5), were exposed once to 0.4 ppm O3 and once to filtered air for 2 h with intermittent exercise. Eighteen hours later, bronchoalveolar lavage (BAL) was performed and the cells and fluid were analyzed for various indicators of inflammation. There was an 8.2-fold increase in the percentage of polymorphonuclear leukocytes (PMN) in the total cell population, and a small but significant decrease in the percentage of macrophages after exposure to O3. Immunoreactive neutrophil elastase often associated with inflammation and lung damage increased by 3.8-fold in the fluid while its activity increased 20.6-fold in the lavaged cells. A 2-fold increase in the levels of protein, albumin, and IgG suggested increased vascular permeability of the lung. Several biochemical markers that could act as chemotactic or regulatory factors in an inflammatory response were examined in the BAL fluid (BALF). The level of complement fragment C3α was increased by 1.7-fold. The chemotactic leukotriene B4 was unchanged while prostaglandin E2 increased 2-fold. In contrast, three enzyme systems of phagocytes with potentially damaging effects on tissues and microbes, namely, NADPH-oxidase and the lysosomal enzymes acid phosphatase and β-glucuronidase, were increased neither in the lavaged fluid nor cells. In addition, the amounts of f ibrogenic-related molecules were assessed in BALF. Fibronectin was elevated 6.4-fold while tissue factor and factor VII, two initiating proteins of the extrinsic coagulation pathway, increased by 2.1- and 1.8-fold, respectively. Urokinase plasminogen activator (U-PA), a neutral protease with fibrinolytic activity, increased by 3.6-fold. The findings show that an acute exposure to 0.4 ppm O3 results in increased levels of inflammatory cells and soluble factors potentially capable of producing damage in the lower airways of humans.
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An acute exposure to ozone (0.4 ppm for 2 h) resulted in 8.2-fold increase of polymorphonuclear leukocytes in bronchial alveolar lavage fluid and enhanced level of inflammatory mediators in the lower airways of humans.
“A seminal work by Koren et al. demonstrated that an acute exposure to ozone (0.4 ppm for 2 h) resulted in 8.2-fold increase of polymorphonuclear leukocytes (PMN) in bronchial alveolar lavage (BAL) fluid and enhanced level of inflammatory mediators in the lower airways of humans (37).”
From Ozone pollution: A Major health hazard worldwide (2019) · cites this paper as [37]
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- Authors
- Koren, H. S., Devlin, R. B., Graham, D. E., Mann, R., McGee, M. P., Horstman, D. H., Kozumbo, W. J., Becker, S., House, D. E., McDonnell, W. F., & Bromberg, P. A.
- Affiliations
- Environmental Protection Agency (US)
- Venue
- American Review of Respiratory Disease
- Publisher
- Oxford University Press (OUP)
- Published
- 1989-02-01
- Volume
- 139
- Issue
- 2
- Pages
- 407-415
- ISSN
- 0003-0805 (ISSN-L)
- OpenAlex
- W2018419112
- Cited by
- 499
- References
- 43
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 7 · 2019: 7 · 2018: 4 · 2017: 9 · 2016: 6 · 2015: 7 · 2014: 6 · 2013: 9 · 2012: 16
- FWCI
- 24.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Review of Respiratory Disease (publishedVersion)
- PubMed (publishedVersion)
- 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, air pollution, airway inflammation, lower respiratory tract, bronchoalveolar lavage, neutrophil elastase, polymorphonuclear leukocytes, leukotriene B4, prostaglandin E2, fibronectin, tissue factor, urokinase, vascular permeability, acute ozone exposure
- MeSH terms
- Acute Disease, Adolescent, Adult, Bronchoalveolar Lavage Fluid, Bronchoscopy, Humans, Lung, Male, Ozone, Pneumonia, Time Factors, Biomarkers
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