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Disruption of the programmed cell death nexus: potential roles of microplastics and nanoplastics in tumorigenesis
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This review summarizes existing research on how microplastics and nanoplastics, now found in air, water, food and the human body, may contribute to cancer. It describes possible ways these particles disrupt normal cell death processes and carry other chemicals into cells, and notes major gaps that future studies would need to address.
As global plastic pollution continues to intensify, microplastics and nanoplastics (MPs/NPs) have become widely distributed in air, water, the food chain, and even the human body, constituting a novel environmental exposure that is difficult to avoid. Although there is still insufficient evidence to classify MPs/NPs as established human carcinogens, a growing body of research suggests that they may participate in tumor initiation and progression through multiple pathways, including the intrinsic toxicity of the particles themselves, pollutant carrier effects, and microenvironmental remodeling. MPs/NPs can not only enter the human body through ingestion and inhalation and achieve multi-organ distribution, but can also serve as delivery platforms for polycyclic aromatic hydrocarbons, heavy metals, and plastic additives, thereby producing a “Trojan horse” effect that amplifies the toxicity of combined exposures. This review summarizes current progress in research linking MPs/NPs to cancer, with a particular focus on their role in disrupting the cell death network. Through shared upstream events such as oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, and inflammasome activation, MPs/NPs may disturb the dynamic balance among apoptosis, ferroptosis, pyroptosis, necroptosis, and cuproptosis, as well as autophagy-related stress responses, thereby exerting effects during tumor initiation, tumor microenvironment formation, tumor progression, and therapeutic resistance. We therefore present the cell death network as a hypothesis framework, and identify major methodological limitations. Future studies integrating standardized exposure assessment, systems biology, and prospective research are needed to further elucidate the key mechanisms through which MPs/NPs promote tumorigenesis via perturbation of the cell death network and to provide a theoretical basis for related health risk assessment and intervention strategies.
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This review examines emerging evidence that microplastics and nanoplastics may contribute to cancer-related processes by crossing biological barriers and accumulating in tissues. The study highlights that these particles can cause oxidative stress, inflammation, DNA damage, and barrier dysfunction at the cellular level, and may promote tumor-supporting processes including angiogenesis and immune evasion.
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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.
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.
Do microplastics (MPs) and nanoplastics (NPs) directly contribute to human carcinogenesis?
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This review examines whether microplastics and nanoplastics could directly contribute to cancer development in humans. Evidence from lab and animal studies shows these particles can cause DNA damage, chronic inflammation, oxidative stress, and disrupt important cancer-related signaling pathways. While a direct causal link to human cancer has not been proven yet, the review argues that microplastics should be considered potential cancer-promoting agents that warrant urgent further research.
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