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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
Open accessAbstract
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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“This is particularly true for cancers of the skin and lung, as both organs are directly exposed to additional sources of environmental ROS which contribute to cancer initiation and aggravation [158,159].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [159]
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“Polycyclic aromatic hydrocarbons may be metabolically activated to generate reactive oxygen species (ROS) that can react to form bulky DNA adducts or strand breaks on cellular DNA.[7]”
From Bad air gets under your skin (2017) · cites this paper as [7]
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Prasad, K. N. (2015) · Journal of the American College of Nutrition · doi:10.1080/07315724.2014.1003419 · Cited by 25
Synergistic inflammatory effect of PM10 with mycotoxin deoxynivalenol on human lung epithelial cells
Capasso, L., Longhin, E., Caloni, F., Camatini, M., & Gualtieri, M. (2015) · Toxicon · doi:10.1016/j.toxicon.2015.08.008 · Cited by 25
Zhang, R., Lai, L., Dong, X., He, J., You, D., Chen, C., Lin, L., Zhu, Y., Huang, H., Shen, S., et al. (2019) · Molecular Oncology · doi:10.1002/1878-0261.12482 · Cited by 26
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Therapeutic role of flavonoids in lung inflammatory disorders
Beigh, S., Rehman, M. U., Khan, A., Patil, B. R., Makeen, H. A., Rasool, S., Rashid, S., Arafah, A. M., & Kamal, M. A. (2022) · Phytomedicine Plus · doi:10.1016/j.phyplu.2022.100221 · Cited by 26
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Graphite particles induce ROS formation in cell free systems and human cells
Zerbi, G., Barbon, A., Bengalli, R. D., Lucotti, A., Catelani, T., Tampieri, F., Gualtieri, M., D’Arienzo, M., Morazzoni, F., & Camatini, M. (2017) · Nanoscale · doi:10.1039/c7nr02540h · Cited by 24
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Metadata
- Authors
- Valavanidis, A., Vlachogianni, T., Fiotakis, K., & Loridas, S.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Corresponding author
- Valavanidis, Athanasios
- 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)
- 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
- 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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