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Long‑term exposure of polyethylene nanoplastics promotes colorectal tumorigenesis
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Researchers exposed mice to polyethylene nanoplastics over 66 days and found significantly more colon tumors and heavier tumor burdens compared to controls, with nanoplastics alone triggering colorectal polyps, suggesting these particles promote tumor initiation by disrupting mitochondrial structure and amplifying chronic intestinal inflammation.
Nanoplastics are emerging contaminants which can induce intestinal inflammation and dysfunction, yet their possible influence on colorectal tumorigenesis remains unclear. Here, six‑week‑old male mice were exposed to 125 mg/L 80 nm polyethylene nanoplastics, polyethylene nanoplastic/azoxymethane, polyethylene nanoplastics/azoxymethane/dextran sulfate sodium, and controls for 66 days. We assessed intestinal symptoms, colorectal tumorigenesis, and pathological, ultrastructural and molecular changes. Results show more colon tumors, of 18.3 versus 13.5, and heavier tumor burdens, of 113.1 versus 67.7 mm2 in the mice treated with nanoplastics/azoxymethane/dextran sulfate sodium. Similarly, there were more colon tumors, of 6.0 versus 2.2, and heavier tumor burdens, of 26.0 versus 7.0 mm2 in mice treated with nanoplastics/azoxymethane. Mice treated with nanoplastics alone developed colorectal neoplasms, of 2.9, with tumor burdens of 10.6 mm2 and a pathology of polyp. Exposure to nanoplastics promoted tumor‑associated macrophages infiltration; disrupted microvilli, intercellular junctions, and the mitochondrial structures of colonic epithelium; and activated inflammation‑associated signaling pathways. Overall, the exposure to polyethylene nanoplastics facilitates the initiation and promotion of colorectal tumorigenesis, possibly by affecting mitochondrial structure and aggravating chronic colitis.
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Researchers examined the potential role of micro- and nanoplastics in cancer development, reviewing mechanistic evidence for how these ubiquitous particles may disrupt cellular processes and promote tumor-associated pathways. The paper calls for greater scientific and regulatory attention to the oncological risks of chronic low-level plastic particle exposure.
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