The role of oxygen free radicals in occupational and environmental lung diseases

Our plain-English summary of The role of oxygen free radicals in occupational and environmental lung diseases, by V. Vallyathan, X. Shi (Environmental Health Perspectives, 1997).

The study

• Authors: V. Vallyathan, X. Shi
• Journal: Environmental Health Perspectives
• Published: 1997;105 Suppl 1(Suppl 1):165-77
• Type of article: Review
• Cited by: 127 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. The pulmonary system is particularly vulnerable to ROS-induced injury because of its continuous exposure to toxic pollutants from a wide variety of sources in the ambient air. Additionally, lungs are exposed systemically to ROS generated from xenobiotic compounds and endogenous sources. This review describes the sources of endogenous and exogenous ROS generation in the lung. Special emphasis is given to major sources of ROS in occupational and environmental exposures to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. ROS-induced lung injury at different target levels may contribute to similar patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events. Understanding the interactions of these intricate mechanistic events is important in the prevention and amelioration of lung injury that results from acute and chronic exposures to toxins in ambient air.

In plain English

This article was a review, not a new study. The authors, from the National Institute for Occupational Safety and Health, described how reactive oxygen species (ROS), oxygen free radicals and related molecules, form in the lung. They covered asbestos, crystalline silica, coal, diesel, chromium, bleomycin, herbicides, nitric oxide, ozone, radiation and cigarette smoke. On asbestos, the review stated that iron in the fibers can promote ROS formation when lung cells engulf them. It gave approximate iron contents of amosite 34%, crocidolite 18%, tremolite 4% and chrysotile 1 to 2%. It summarized earlier laboratory studies by other researchers. In one, amosite, crocidolite and chrysotile catalyzed the generation of hydroxyl radicals from hydrogen peroxide, with the strongest signal from amosite. In another, which used a cell-free fat mixture rather than living cells, chrysotile caused the least lipid peroxidation (damage to fats). A third found that crocidolite and cigarette smoke acted synergistically, increasing strand breaks in isolated DNA. The authors concluded that ROS are increasingly recognized as mediators of early cell injury in lung diseases. They set antioxidant defenses aside as reviewed elsewhere and mentioned some only briefly.

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: Narrative review of published research (mainly laboratory, cell and animal studies)
• Who was studied: No study population; the authors reviewed published literature on free radical generation and lung injury
• Exposure: Occupational and environmental agents: asbestos (chrysotile, amosite, crocidolite, tremolite), crystalline silica, coal mine dust, diesel emissions, chromium, bleomycin, herbicides (paraquat, diquat), nitric oxide, ozone, radiation and cigarette smoke
• Main results:
  • The review stated that iron in asbestos fibers can promote ROS generation when the fibers are engulfed by cells (phagocytosis)
  • The review gave approximate iron contents: amphiboles (amosite about 34%, crocidolite about 18%, tremolite about 4%) contain more iron than the serpentine chrysotile (about 1 to 2%)
  • Citing Weitzman and Graceffa, the review reported that amosite, crocidolite and chrysotile asbestos catalyzed hydroxyl radical generation from hydrogen peroxide. The signal was stronger from amosite than from crocidolite and chrysotile.
  • Citing Weitzman and Weitberg, the review reported results from a cell-free phospholipid emulsion. Amosite and crocidolite caused significant lipid peroxidation, while chrysotile, which contains the least iron, caused the least.
  • Citing Jackson et al., the review reported that crocidolite asbestos and cigarette smoke synergistically increased DNA strand breaks in isolated DNA
  • The review stated that engulfing asbestos increases the release of superoxide from alveolar macrophages and neutrophils
• The authors' conclusion: The authors concluded that ROS are frequently associated with many lung diseases and are increasingly recognized as mediators of early cell injury in lung diseases
• Limitations the authors state:
  • The authors called antioxidant defenses important in disease processes but said they would not discuss them because the subject had been reviewed elsewhere. Some antioxidants are still mentioned briefly in the text.
  • The authors noted that the mechanisms causing the different asbestos-associated diseases remain speculative

Topics

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS), Environmental Exposure, Crystalline, Cytokine.

Related studies

• Oxygen radicals and asbestos-mediated disease — T.R. Quinlan, J.P. Marsh, et al. (1994)
• Tobacco smoke: involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles — A. Valavanidis, T. Vlachogianni, et al. (2009)
• The role of free radicals in asbestos-induced diseases — D.W. Kamp, P. Graceffa, et al. (1992)
• Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases — P.W. Nyberg, S.A. Nordman, et al. (1994)
• Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease — B.T. Mossman, J.P. Marsh (1989)
• Interactions of exogenous or evoked agents and particles: the role of reactive oxygen species — A. Churg (2003)

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