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, Konstantinos Fiotakis, Spyridon Loridas. International Journal of Environmental Research and Public Health, 2013

820 citations recorded by the source corpus.

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.

Subfields: Global and Planetary Change, Health, Toxicology and Mutagenesis

View Paper: https://www.semanticscholar.org/paper/8d882fa3811b716dc84cadba9ff8efc36037f36b

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Citations in the corpus

Oxidative stress, free radicals and antioxidants: potential crosstalk in the pathophysiology of human diseases (2023, background): “This condition is related to significant DNA damage and genomic instability, leading to neoplastic progression and initiation (Valavanidis et al., 2013).”
Airborne microplastics: Consequences to human health? (2018, neutral): “…detection by the immune system and pro-inflammatory mediators promoting angiogenesis and mitogenesis, favoring the formation and progression of malignant cells (Chang, 2010; Churg and Brauer, 2000; Donaldson et al., 2002; Donaldson and Tran, 2002; Schwarze et al., 2006; Valavanidis et al., 2013).”
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives (2022, background): “OS induces lesions in DNA, which reveals that ROS-induced OS could lead to gene and chromosome mutations through DNA double-strand breaks (DSBs) [91,92].”
Oxidative Stress: Harms and Benefits for Human Health (2017, background): “It is worth to note that Valavanidis and colleagues [28] have already proposed 8-OHdG levels in a tissue as biomarker of oxidative stress.”
Effects of air pollution on human health and practical measures for prevention in Iran (2016, neutral): “[72‐77] Asthma is a respiratory disease which may be developed as a result of exposure to air toxicants.”