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Insights to cellular and molecular impacts of micro/nanoplastics and their additives for carcinogenic risks
Summary
Tiny plastic particles that build up in our bodies from everyday plastic use may do more than just sit there, this review pulls together existing research suggesting they could damage cells in ways linked to cancer development, including in the brain, lungs, colon, and breast. The proposed mechanisms include causing cell stress, damaging DNA, and triggering ongoing inflammation, all of which are known contributors to tumor growth. While this is a summary of early, still-developing science rather than definitive proof that plastics cause cancer, it highlights a real concern worth watching as researchers work to understand exactly how much risk our growing plastic expos
The widespread use of plastics in daily life has led to the pervasive accumulation of microplastics and nanoplastics (M/N-Ps) in the environment. Their improper disposal and non-biodegradability have raised significant biomedical and ecological concerns. Recent evidence indicates that M/N-P exposure may be associated with the development and progression of various carcinogenic effects leading to cancers. However, despite growing evidence of M/N-Ps bioaccumulation in human tissues, a unified mechanistic framework linking M/N-Ps exposure to direct tumor progression across multiple cancer types remains absent from the literature. This review provides a comprehensive exploration of the cellular and biomolecular interactions between M/N-Ps, their additives, and human cells, detailing their detrimental effects. It further elucidates the hypothesized role of M/N-P exposure in cancer progression by investigating its proposed link to specific cancer types, including brain, oral, colorectal, lung, leukemia, prostate, ovarian, gastric, pancreatic, and breast cancer. The mechanistic pathways discussed include oxidative stress, DNA damage, chronic inflammation, and dysregulated cell signaling. Critically, this review advances beyond cataloguing inflammatory and oxidative effects to synthesize the evidence linking M/N-Ps to mechanisms of tumor cell proliferation and invasion. Additionally, the review highlights future research perspectives, addressing the need for in-depth mechanistic studies, improved detection methods, and regulatory policies. The mechanistic synthesis presented here offers researchers, clinicians, and policymakers a structured framework for understanding M/N-P induced oncogenesis, addressing a critical research gap in translating environmental plastic exposure data into organ-specific cancer risk assessment and therapeutic strategy.