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A comprehensive examination of the impact of environmental pollution on lung cancer: A review
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This review examined how environmental pollutants, including fine particulate matter, heavy metals, and microplastics, contribute to lung cancer risk through various biological pathways. Researchers found that these pollutants can trigger inflammation, DNA damage, and disruption of cellular signaling that promotes tumor growth. The study emphasizes that understanding these mechanisms is essential for developing better prevention strategies against pollution-related lung cancer.
Environmental pollutants play a significant role in increasing the susceptibility to lung cancer by triggering various biological mechanisms that lead to lung injury and tumorigenesis. Excessive PM2.5 exposure contributes to the overall burden of lung cancer via Wnt/β-catenin, Reactive oxygen species-DNA methyltransferases (ROS-DNMT), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/Akt), Janus kinase/signal transducers and activators of transcription (JAK/STAT) signalling pathways. The primary mechanisms by which NO contributes to the occurrence and development of pulmonary neoplasm revolve around the production and regulation of ROS. Occupational exposure and ecosystem pollution to hazardous substances, including microplastics, pesticides, asbestos, cadmium, and nickel, are the well-established risk factors for the development of lung cancer via DNA damage, oxidative stress, and inflammation pathways. This review emphasizes the importance of effective prevention strategies for lung cancer by reducing environmental pollution levels.
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Exposure to environmental xenobiotics and lung tissue function: A comprehensive review on biological mechanisms and pathways
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This comprehensive review examines how environmental pollutants including microplastics, heavy metals, and volatile organic compounds damage lung tissue through mechanisms like oxidative stress, inflammation, and disruption of cellular barriers. The study suggests these pollutants contribute to chronic respiratory diseases and highlights how they can also cause epigenetic changes that may affect future generations.
Molecular mechanisms of air pollution–induced carcinogenesis and the emerging role of microplastics
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This review examined the molecular mechanisms by which air pollution components — including fine particulate matter, microplastics, volatile organic compounds, and heavy metals — contribute to cancer development. The authors identify microplastics as an emerging air pollution carcinogen that can carry and deliver chemical carcinogens into lung tissue.
Microplastics Exposure Impact on Lung Cancer—Literature Review
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This review examines the relationship between micro- and nanoplastic exposure and lung cancer development, summarizing evidence that these particles can enter the respiratory system through inhaled air, contaminated food, and other pathways. Researchers found that microplastics may promote inflammatory and oxidative processes in lung tissue that are associated with cancer progression. The study suggests that chronic microplastic exposure warrants consideration as a potential contributing factor in lung cancer research.
Microplastics and Cancer: A Comprehensive Review of Their Impact on Tumor Progression and Mechanisms of Carcinogenesis
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This comprehensive review examines the growing body of evidence linking microplastic exposure to various types of cancer, including colorectal, lung, liver, and breast cancers. Researchers found that microplastics and nanoplastics may promote tumor progression through mechanisms including oxidative stress, chronic inflammation, and disruption of cellular signaling pathways. While the evidence is still emerging, the study highlights the need for further research into the potential cancer-related risks of widespread microplastic exposure.
Plastic Pollution and Cancer
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Researchers reviewed the mechanisms by which microplastics may contribute to cancer risk across multiple organ systems, summarizing how oxidative stress, DNA damage, and hormonal disruption drive carcinogenesis in the lungs, brain, gastrointestinal tract, and reproductive system, and surveying emerging pharmacological and immunological strategies to counter these effects.
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