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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.
The widespread use of plastics has revolutionized material science but also led to significant environmental concerns, particularly with the rise of microplastics (MPs). This chapter explores the emergence of MPs as an oncological risk factor. We detail the sources and types of MPs, human exposure routes, and their systemic effects on human health. Particular attention is given to their role in promoting carcinogenesis across various organs, including the lungs, brain, reproductive system, skin, gastrointestinal tract, and kidneys. Mechanistic insights into how MPs trigger oxidative stress, DNA damage, and hormonal disruption are discussed. The chapter also explores emerging therapeutic strategies, including pharmacological, repurposed therapies, pathway-targeted, and immunological interventions, highlighting the urgent need for interdisciplinary approaches to mitigate MPs-induced carcinogenicity.
More Papers Like This
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.
Micro(nano)plastics pollution and human health: How plastics can induce carcinogenesis to humans?
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This review examines how microplastics and nanoplastics enter the human body through food, water, and air, and how they may contribute to cancer development. Common plastic types like polystyrene and PVC, along with toxic chemicals they carry such as PAHs and PCBs, have been linked to DNA damage, oxidative stress, and inflammation, all of which can promote cancer. The paper highlights that while the evidence is growing, more research is needed to understand the full cancer risk from chronic microplastic exposure.
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.
Microplastic-induced carcinogenesis: Molecular mechanisms, cellular interactions, and toxicological implications
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Tiny plastic particles that we breathe, eat, and touch every day are now showing up in our blood, lungs, and other organs, and this review of existing research explains how they might contribute to cancer. Microplastics can trigger cell damage, inflammation, and disrupted signaling in ways linked to tumor growth, and they can also act like tiny rafts that ferry other harmful chemicals and toxins deeper into our bodies. While scientists haven't proven microplastics directly cause cancer in humans yet, the mounting evidence is a strong signal that reducing plastic exposure and pushing for more research should be a public health pri
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.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.