Cited by 914Occupational and environmental lung diseasesAir Quality and Health ImpactsAntioxidant Activity and Oxidative Stress

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Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

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Valavanidis, Athanasios, Vlachogianni, Thomais, Fiotakis, Konstantinos, Loridas, Spyridon·2013·International Journal of Environmental Research and Public Health

DOI 10.3390/ijerph10093886PMC PMC3799517

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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.

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Additional file 2 of Identification of molecular subgroups and establishment of risk model based on the response to oxidative stress to predict overall survival of patients with lung adenocarcinoma
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Additional file 3 of Identification of molecular subgroups and establishment of risk model based on the response to oxidative stress to predict overall survival of patients with lung adenocarcinoma
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Additional file 5 of Oxidative stress genes in patients with esophageal squamous cell carcinoma: construction of a novel prognostic signature and characterization of tumor microenvironment infiltration
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Additional file 2 of Oxidative stress genes in patients with esophageal squamous cell carcinoma: construction of a novel prognostic signature and characterization of tumor microenvironment infiltration
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Additional file 8 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 4 of Oxidative stress genes in patients with esophageal squamous cell carcinoma: construction of a novel prognostic signature and characterization of tumor microenvironment infiltration
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Additional file 6 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 2 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 4 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 7 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 3 of Oxidative stress genes in patients with esophageal squamous cell carcinoma: construction of a novel prognostic signature and characterization of tumor microenvironment infiltration
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Additional file 3 of Alcohol and e-cigarette damage alveolar-epithelial barrier by activation of P2X7r and provoke brain endothelial injury via extracellular vesicles
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Additional file 2 of Alcohol and e-cigarette damage alveolar-epithelial barrier by activation of P2X7r and provoke brain endothelial injury via extracellular vesicles
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Additional file 1 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 3 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Additional file 6 of Oxidative stress genes in patients with esophageal squamous cell carcinoma: construction of a novel prognostic signature and characterization of tumor microenvironment infiltration
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Additional file 5 of Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies
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Authors: Valavanidis, A., Vlachogianni, T., Fiotakis, K., & Loridas, S.
Affiliations: National and Kapodistrian University of Athens (GR)
Corresponding author: Valavanidis, Athanasios
ORCID: Valavanidis, Athanasios
Vlachogianni, Thomais
Venue: International Journal of Environmental Research and Public Health
Publisher: MDPI AG
Published: 2013-08-27
Volume: 10
Issue: 9
Pages: 3886-3907
ISSN: 1660-4601 (ISSN-L)
DOI: 10.3390/ijerph10093886
PMC: PMC3799517
OpenAlex: W2036942985
Cited by: 910
References: 180
Citations by year: 2026: 52 · 2025: 82 · 2024: 132 · 2023: 103 · 2022: 112 · 2021: 87 · 2020: 67 · 2019: 78 · 2018: 51 · 2017: 46 · 2016: 48 · 2015: 33 · 2014: 16 · 2013: 2
FWCI: 5.15
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (vor)
Locations: International Journal of Environmental Research and Public Health (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
RePEc: Research Papers in Economics (submittedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords: pulmonary oxidative stress, reactive oxygen species, reactive nitrogen species, lung inflammation, lung carcinogenesis, respirable particles, fibrous dust, asbestos fibers, quartz, ozone, diesel soot, tobacco smoke, oxidative DNA damage, telomere shortening, macrophage activation, transcription factors, air pollution, occupational exposure
MeSH terms: Air Pollutants, Animals, DNA Damage, Humans, Lung, Lung Neoplasms, Ozone, Pneumonia, Reactive Oxygen Species, Oxidative Stress, Particulate Matter

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Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

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