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Cross-Organ Toxicity and Metabolic Responses to Food Chain-Transferred Nanoplastics: Mechanistic Insights from a Multiomics Perspective

ACS Nano 2026 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Yutian Shi, Yuheng Li, Yuewen Han, Guoming Sun, Huayang Sun, Yijing Wang, Xinrui Nan, Ruixuan Qu, Ning Zhang, Xin Zhao, Baoqin Liu

Summary

Scientists tracked tiny plastic particles as they moved up the food chain—from plastic to worms to mice—and found the plastics built up throughout the body, affecting the heart and disrupting how the body processes fat and manages inflammation. The liver seemed to act as a control center, spreading these effects to other organs. This matters because it shows plastic pollution could pose real risks to our health through the food we eat, not just where the plastic ends up in the environment—though more research is needed to know what this means for long-term human health.

Polymers
Models

Against the backdrop of escalating global plastic pollution, there is an urgent need to elucidate the systemic health risks posed by nanoplastics (NPs) as emerging environmental contaminants that enter higher organisms through the food chain. This study employed a three-level trophic transfer model, examining the pathway from polystyrene nanoparticles to Tenebrio molitor larvae and subsequently to mice, offering a comprehensive elucidation of the mechanisms behind the multiorgan toxicity associated with food chain-transferred nanoplastics (FCT-NPs). Our results demonstrated extensive accumulation of FCT-NPs across multiple organs via systemic circulation. Integrative multiorgan omics analysis revealed that FCT-NPs primarily induced two major categories of multiorgan comorbidities: cardiovascular diseases and metabolic disorders, with the liver identified as a central metabolic hub that potentially regulates other organs through bile acid-mediated metabolic crosstalk. Mechanistically, dysregulation of key genes, such as MTOR and FN1, activated Wnt and TGF-β signaling pathways, which in turn promoted organ fibrosis. Additionally, aberrant expression of critical regulators─including CAT, LPL, NQO1, and APOE ─was found to drive oxidative stress and disrupt lipid metabolism. These findings provide crucial scientific evidence for FCT-NPs risk assessment and underscore the imperative for enhanced plastic pollution control and further investigation into long-term exposure effects.

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