ArticleJournal of occupational medicine and toxicology (London, England)2006
Analysis of airway secretions in a model of sulfur dioxide induced chronic obstructive pulmonary disease (COPD).
Article in Journal of occupational medicine and toxicology (London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cardiorespiratory health effects of gaseous ambient air pollution exposure in low and middle income countries: a systematic review and meta-analysis.Environmental health : a global access science source · 2018Pooled it
- Toxic Effects of Sulfur Dioxide: A Review.Toxics · 2026Review
- Research Progress on Animal Models of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026Review
- Pulmonary Emphysema: Current Understanding of Disease Pathogenesis and Therapeutic Approaches.Biomedicines · 2025Review
- New Insights into the Role of NLRP3 Inflammasome in Pathogenesis and Treatment of Chronic Obstructive Pulmonary Disease.Journal of inflammation research · 2021Review
- Differential lung inflammation and injury with tobacco smoke exposure in Wistar Kyoto and spontaneously hypertensive rats.Inhalation toxicology · 2020Article
- A Novel Murine Chronic Obstructive Pulmonary Disease Model and the Pathogenic Role of MicroRNA-21.Frontiers in physiology · 2018Article
- The Relationship between Airway Inflammation and Exacerbation in Chronic Obstructive Pulmonary Disease.Tuberculosis and respiratory diseases · 2017Review
- Radiomics-based differentiation of lung disease models generated by polluted air based on X-ray computed tomography data.BMC medical imaging · 2016Article
- Comparison between cigarette smoke-induced emphysema and cigarette smoke extract-induced emphysema.Tobacco induced diseases · 2015Article
- Environmental risk factors for Pneumocystis pneumonia hospitalizations in HIV patients.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2013Article
- The effects of sleep hypoxia on coagulant factors and hepatic inflammation in emphysematous rats.PloS one · 2010Article
- Shift work and pathological conditions.Journal of occupational medicine and toxicology (London, England) · 2006Article
- The toxicity of cadmium and resulting hazards for human health.Journal of occupational medicine and toxicology (London, England) · 2006Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypersecretion and chronic phlegm are major symptoms of chronic obstructive pulmonary disease (COPD) but animal models of COPD with a defined functional hypersecretion have not been established so far. To identify an animal model of combined morphological signs of airway inflammation and functional hypersecretion, rats were continuously exposed to different levels of sulfur dioxide (SO2, 5 ppm, 10 ppm, 20 ppm, 40 ppm, 80 ppm) for 3 (short-term) or 20-25 (long-term) days. Histology revealed a dose-dependent increase in edema formation and inflammatory cell infiltration in short-term-exposed animals. The submucosal edema was replaced by fibrosis after long-term-exposure. The basal secretory activity was only significantly increased in the 20 ppm group. Also, stimulated secretion was significantly increased only after exposure to 20 ppm. BrdU-assays and AgNOR-analysis demonstrated cellular metaplasia and glandular hypertrophy rather than hyperplasia as the underlying morphological correlate of the hypersecretion. In summary, SO2-exposure can lead to characteristic airway remodeling and changes in mucus secretion in rats. As only long-term exposure to 20 ppm leads to a combination of hypersecretion and airway inflammation, only this mode of exposure should be used to mimic human COPD. Concentrations less or higher than 20 ppm or short term exposure do not induce the respiratory symptom of hypersecretion. The present model may be used to characterize the effects of new compounds on mucus secretion in the background of experimental COPD.
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Registered trials
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