Role of oxidants in interstitial lung diseases: pneumoconioses, constrictive bronchiolitis, and chronic tropical pulmonary eosinophilia

Our plain-English summary of Role of oxidants in interstitial lung diseases: pneumoconioses, constrictive bronchiolitis, and chronic tropical pulmonary eosinophilia, by W.N. Rom (Mediators of Inflammation, 2011).

The study

• Author: W.N. Rom
• Journal: Mediators of Inflammation
• Published: 2011;2011:407657
• Type of article: Review
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Oxidants such as superoxide anion, hydrogen peroxide, and myeloperoxidase from activated inflammatory cells in the lower respiratory tract contribute to inflammation and injury. Etiologic agents include inorganic particulates such as asbestos, silica, or coal mine dust or mixtures of inorganic dust and combustion materials found in World Trade Center dust and smoke. These etiologic agents are phagocytosed by alveolar macrophages or bronchial epithelial cells and release chemotactic factors that recruit inflammatory cells to the lung. Chemotactic factors attract and activate neutrophils, eosinophils, mast cells, and lymphocytes and further activate macrophages to release more oxidants. Inorganic dusts target alveolar macrophages, World Trade Center dust targets bronchial epithelial cells, and eosinophils characterize tropical pulmonary eosinophilia (TPE) caused by filarial organisms. The technique of bronchoalveolar lavage in humans has recovered alveolar macrophages (AMs) in dust diseases and eosinophils in TPE that release increased amounts of oxidants in vitro. Interestingly, TPE has massively increased eosinophils in the acute form and after treatment can still have ongoing eosinophilic inflammation. A course of prednisone for one week can reduce the oxidant burden and attendant inflammation and may be a strategy to prevent chronic TPE and interstitial lung disease.

In plain English

This was a single-author review of how oxidants, such as superoxide anion and hydrogen peroxide released by activated inflammatory cells, contribute to lung inflammation and injury. It covered three areas: dust diseases (pneumoconioses) caused by coal, silica or asbestos; dust from the World Trade Center collapse, which contained asbestos insulation among other materials; and tropical pulmonary eosinophilia, caused by an immune reaction to filarial parasites. The review described earlier studies in which lung-wash (bronchoalveolar lavage) cells from patients with coal workers' pneumoconiosis, asbestosis and silicosis released increased levels of these oxidants and of fibronectin. It described one firefighter exposed to World Trade Center dust whose lavage contained 70% eosinophils and who was diagnosed with acute eosinophilic pneumonia. For tropical pulmonary eosinophilia, it reported a one-week prednisone course, given after earlier diethylcarbamazine treatment, that 12 people completed. Superoxide anion release declined in 10 of 12 subjects and hydrogen peroxide release in 9 of 11. The author concluded that a week of prednisone can reduce the oxidant burden and may be a strategy to prevent chronic tropical pulmonary eosinophilia and interstitial lung disease.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Review article (narrative review by a single author, drawing largely on earlier studies)
• Who was studied: No study population of its own. The review discussed workers with occupational coal, silica or asbestos exposure, people exposed to World Trade Center dust (firefighters, rescue and clean-up workers, residents), and people with tropical pulmonary eosinophilia studied in India.
• Exposure: Inorganic dusts (asbestos, silica, coal mine dust). World Trade Center dust containing gypsum, plastics, cement, fibrous glass, asbestos insulation and metals, plus smoke. Filarial parasites (Wuchereria bancrofti and Brugia malayi) in tropical pulmonary eosinophilia.
• Main results:
  • From earlier studies cited in the review: freshly recovered bronchoalveolar lavage cells from patients with coal workers' pneumoconiosis, asbestosis and silicosis released increased levels of superoxide anion and hydrogen peroxide.
  • From earlier studies cited in the review: in these dust-exposed patients, higher oxidant levels were noted in those with respiratory impairment compared with normal nonsmoking volunteers.
  • From earlier studies cited in the review: lavage cell supernatants from dust-exposed patients showed increased fibronectin compared with nonsmoking controls, along with increased growth factors and cytokines.
  • In one firefighter admitted two weeks after the World Trade Center collapse, lavage showed 70% eosinophils and acute eosinophilic pneumonia was diagnosed.
  • In twenty people with chronic tropical pulmonary eosinophilia (6 smokers, 14 nonsmokers), lavage cells showed a significant spontaneous increase in superoxide anion and hydrogen peroxide release compared with six normal nonsmokers, a mean of 8 months after diethylcarbamazine therapy.
  • The one-week oral prednisone course was given to people with tropical pulmonary eosinophilia who had already been treated with diethylcarbamazine.
  • After about one week of oral prednisone in these people with tropical pulmonary eosinophilia, 12 completed the trial. The percentage of lavage eosinophils declined or stayed the same in all of them.
  • In the same prednisone trial, superoxide anion release declined in 10 of 12 subjects and hydrogen peroxide release declined in 9 of 11 subjects.
• The authors' conclusion: The author concluded that a one-week course of prednisone can reduce the oxidant burden and attendant inflammation and may be a strategy to prevent chronic tropical pulmonary eosinophilia and interstitial lung disease. The author also stated that oxidants trigger macrophage activation upon phagocytosis of inorganic dust particles.

Topics

Medical terms in this study, explained in our Lexicon: Interstitial Lung Disease, Superoxide, Inflammation, Alveolar Macrophage, Macrophage, Bronchoalveolar Lavage (BAL), Eosinophilic.

Related studies

• Characterization of the lower respiratory tract inflammation of nonsmoking individuals with interstitial lung disease associated with chronic inhalation of inorganic dusts — W.N. Rom, P.B. Bitterman, et al. (1987)
• Interstitial Lung Diseases in Developing Countries — P. Rivera-Ortega, M. Molina-Molina (2019)
• Modulation of mitochondrial gene expression in pulmonary epithelial cells exposed to oxidants — Y.M. Janssen, K.E. Driscoll, et al. (1998)
• Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases — A. Shukla, M. Gulumian, et al. (2003)
• The evidence of benefits of exercise training in interstitial lung disease: a randomised controlled trial — L.M. Dowman, C.F. McDonald, et al. (2017)
• Peribronchiolar metaplasia: a common histologic lesion in diffuse lung disease and a rare cause of interstitial lung disease: clinicopathologic features of 15 cases — J. Fukuoka, T.J. Franks, et al. (2005)

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