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Dietary coexposure to micro- and nano-plastics and metabolism-disrupting chemicals: Combined hepatotoxicity — insights from mammalian and cellular models
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Tiny plastic particles from our food can act like tiny taxis for other harmful chemicals, including forever chemicals, BPA, and heavy metals, carrying them deeper into our bodies, and this review of animal and lab-cell studies found that these combos usually cause *more* liver damage together than either would alone. This matters because most safety testing looks at one chemical at a time, so real-world exposure to these mixtures through everyday food may be riskier to liver health than current research accounts for.
Micro- and nano-plastics (MNPs), omnipresent in the environment, can act as carriers of metabolism-disrupting chemicals (MDCs) and can enter the human body through the food web, thereby increasing coexposure risk. Although the combined hepatotoxicity has been reported, the underlying mechanism has not yet been well understood. Given the limited evidence from the human aspect, this review is mainly based on the evidence from mammalian and in vitro studies. We reviewed articles published in PubMed, Web of science and Scopus related to this topic (singular hepatotoxicity, interaction, and combined toxicity) and conducted a classified summary analysis. Our analysis summarized that the interactions between MNPs and the four main types of MDCs (per- and polyfluoroalkyl substances, bisphenol A, phthalates, and heavy metals), especially in the gastrointestinal environment, are regulated by factors such as pH, the biomolecular corona, and physiological state. Current research indicates that the combined liver toxicity of MNPs and MDCs is primarily synergistic under most tested conditions, with antagonistic effects observed only in a few specific circumstances (such as protein corona formation and high concentration of polystyrene microplastics). Mechanistically, coexposure induces multilevel perturbations, from initial physicochemical interactions such as carrier effects and corona formation to cellular dysfunction, and further to systemic effects mediated by the gut-liver axis. We distinguish the differences in the contaminant interactions and transport mechanisms of microplastics and nanoplastics, and explore the regulatory conditions for the combined effects. Finally, we analyze environmental realism and research limitations, proposing future directions for subsequent research on the impacts of dietary coexposure on the environment and human health.
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Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice
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Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
Synergistic Toxicity of Combined Exposure to Acrylamide and Polystyrene Nanoplastics on the Gut–Liver Axis in Mice
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Researchers exposed mice to a combination of acrylamide, a common food processing byproduct, and polystyrene nanoplastics through drinking water and found that the combined exposure caused more severe gut and liver damage than either substance alone. The co-exposure disrupted gut barrier integrity, altered gut bacteria composition, and caused widespread metabolic changes. The study suggests that the interaction between nanoplastics and other food contaminants may amplify health risks beyond what each poses individually.
Combined toxicity of co-exposure to polystyrene nanoplastics and arsenic on the gut-liver axis in mice.
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Mice exposed to both nanoplastics and arsenic together, common pollutants that can show up in food and water, suffered worse gut and liver damage than expected, including a weakened gut barrier, disrupted gut bacteria, and increased inflammation. This suggests that real-world exposure to multiple pollutants at once may pose greater health risks than studying each one alone would predict.
Combined toxicity of polystyrene microplastics and perfluorobutane sulfonate on mouse liver: Impact on lipid metabolism and gut-liver axis disruption
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This study examined what happens when mice are exposed to both polystyrene microplastics and PFBS (a type of "forever chemical") at the same time. The combination caused significantly worse liver damage than either pollutant alone, disrupting fat metabolism and triggering gut bacteria imbalances that further harmed the liver through the gut-liver connection. These findings are concerning because microplastics can absorb PFAS chemicals in the environment, meaning people may often be exposed to both together.
Toxicity of polyethylene terephthalate microplastics and dimethyl phthalate in male Sprague-Dawley rats: Insights into oxidative stress, DNA damage, and histopathological impacts
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Researchers exposed male rats to polyethylene terephthalate microplastics and dimethyl phthalate, a common plasticizer, both individually and in combination over 28 days. The co-exposure group showed significantly elevated markers of oxidative DNA damage, severe liver tissue degeneration, and liver enlargement compared to controls. The study highlights the potential for synergistic health effects when microplastics and their associated chemical additives are encountered together.
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