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A comprehensive examination of the impact of environmental pollution on lung cancer: A review
Summary
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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