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Microplastics and Nanoplastics as Emerging Contributors to Carcinogenesis: Mechanisms, Organ-Specific Risks, and Therapeutic Opportunities
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Researchers review how microplastics and nanoplastics enter human tissues via ingestion, inhalation, and skin contact and may promote cancer through chronic inflammation, oxidative stress, genotoxicity, and endocrine disruption from plastic additives, highlighting particular organ-level vulnerabilities in the gut, liver, and lungs.
Microplastics and nanoplastics (MNPs) are increasingly recognized as ubiquitous environmental contaminants present in air, water, food, and human tissues. Chronic exposure may occur through ingestion, inhalation, and dermal routes, with emerging evidence suggesting biologically relevant accumulation in multiple organ systems. A growing body of literature supports plausible links between MNP exposure and carcinogenesis through overlapping mechanisms including chronic inflammation, oxidative stress, endocrine disruption from plastic-associated chemicals, genotoxicity, and altered cellular signaling. This perspective reviews key mechanistic pathways, highlights organ-specific vulnerabilities in the gastrointestinal tract, liver, and lungs, and outlines interaction-mediated therapeutic concepts as proactive countermeasures. Improved exposure assessment, standardized biomonitoring, and translational mitigation strategies are needed to better define and address cancer-relevant risks in an increasingly plastic-contaminated world.
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Microplastics and Nanoplastics as Emerging Contributors to Carcinogenesis: Mechanisms, Organ-Specific Risks, and Therapeutic Opportunities
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Researchers reviewed plausible mechanistic links between micro- and nanoplastic exposure and cancer risk, including chronic inflammation, oxidative stress, endocrine disruption from plasticizers, and genotoxicity, with particular organ-level vulnerabilities in the gastrointestinal tract, liver, and lungs, and outlined interaction-based therapeutic concepts as early countermeasures.
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.
From Exposure to Oncogenesis: the Role of Microplastics and Associated Pollutants in Cancer - a Literature Review
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This literature review examined the growing evidence linking microplastic exposure to cancer development. Microplastics have been found in human lung, liver, and colon tissue, and research suggests they may promote cancer through chronic inflammation, oxidative stress, and by carrying known carcinogens like heavy metals and persistent organic pollutants into the body.
Microplastics as emerging carcinogens: from environmental pollutants to oncogenic drivers
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This review examines growing evidence that microplastics and nanoplastics may play a role in cancer development, with these particles found in human tumor tissues from the lungs, colon, stomach, breast, and other organs. The particles appear to promote cancer through chronic inflammation, oxidative stress, DNA damage, and disruption of key cancer-related signaling pathways. While direct proof of causation in humans is still lacking, the accumulating evidence from lab studies, animal experiments, and human tissue analysis suggests microplastics deserve serious attention as potential contributors to cancer risk.
The hidden threat: Microplastics and cancer biology
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This review synthesizes current research on the potential links between micro- and nanoplastic exposure and cancer biology, examining how these particles may contribute to tumor development in organs including the gut, lungs, skin, liver, kidney, and brain. The study suggests that chronic exposure to plastic particles can trigger molecular changes such as oxidative stress, inflammation, and DNA damage that are associated with cancer initiation, though clear causal evidence in humans is still lacking.
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