Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms

Our plain-English summary of Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms, by A. Valavanidis, T. Vlachogianni, K. Fiotakis, et al (International Journal of Environmental Research and Public Health, 2013).

The study

• Authors: A. Valavanidis, T. Vlachogianni, K. Fiotakis, S. Loridas
• Journal: International Journal of Environmental Research and Public Health
• Published: 2013;10(9):3886-907
• Type of article: Review
• Cited by: 554 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM₁₀ and PM₂.₅) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.

In plain English

This article was a narrative review, not a new study. The authors, from the Department of Chemistry at the University of Athens, summarised published research on how reactive oxygen species (oxygen-containing molecules the body needs at normal levels but that can damage cells in excess) and oxidative stress in the lungs may lead to inflammation and lung cancer. The agents covered were inhalable particulate matter from air pollution, quartz, metal powders, mineral fibres including asbestos, ozone, engine soot and tobacco smoke. Asbestos was mentioned only briefly. The review did not discuss particular asbestos fiber types, mesothelioma or asbestosis. It described proposed mechanisms: DNA damage from oxidation, inflammation driven by immune cells, telomere shortening, and activation of transcription factors. Among experiments reporting combined effects, it listed work on mineral fibres together with tobacco smoke. The article did not say how the studies were chosen. The authors concluded that the evidence supports a link between oxidative stress and increased malignant respiratory disease, and that inhalable particles, mineral fibres, dusts, cigarette smoke and ozone have a role in generating these reactive species.

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 literature (no search method or number of studies reported)
• Who was studied: No study population; the article reviewed published experimental, clinical and epidemiological literature on the lungs
• Exposure: Inhalable quartz, metal powders, mineral asbestos fibers, ozone, gasoline and diesel engine soot, tobacco smoke, and ambient air pollution particles (PM10 and PM2.5); no specific asbestos fiber types or doses discussed
• Main results:
  • The review described reactive oxygen species as necessary for normal cell processes at low concentrations but hazardous at higher concentrations, when they can cause oxidative damage to cell components
  • Among experimental studies reporting combined (synergistic) increases in reactive oxygen species generation, the review listed a study of mineral fibres together with tobacco smoke
  • The review described several transcription factors linked to cancer mechanisms and stated that most of them are activated by particulate matter, tobacco smoke and mineral fibers that generate reactive oxygen species
• The authors' conclusion: The authors concluded that their review highlights the role of inhalable particulate matter, mineral fibres, dusts, cigarette smoke and ozone in generating reactive oxygen and nitrogen species. They also concluded that evidence supports a correlation between oxidative stress and increased incidence of malignant respiratory diseases.

Topics

Medical terms in this study, explained in our Lexicon: Oxidative Stress, Inflammation, Carcinogenesis, Reactive Oxygen Species (ROS), Lung Cancer, Respirable Fiber, Synergistic Effect, Carcinogenic.

Related studies

• 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)
• Mobilization of iron from urban particulates leads to generation of reactive oxygen species in vitro and induction of ferritin synthesis in human lung epithelial cells — K.R. Smith, A.E. Aust (1997)
• Interactions of exogenous or evoked agents and particles: the role of reactive oxygen species — A. Churg (2003)
• Mitochondria-derived reactive intermediate species mediate asbestos-induced genotoxicity and oxidative stress-responsive signaling pathways — S.X. Huang, M.A. Partridge, et al. (2012)
• Oxidative and cytotoxic stress induced by inorganic granular and fibrous particles — S. Helmig, D. Walter, et al. (2018)
• Carbon nanotubes induce inflammation but decrease the production of reactive oxygen species in lung — D. Crouzier, S. Follot, et al. (2010)

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