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Bisphenols exposure and non-alcoholic fatty liver disease: from environmental trigger to molecular pathogenesis
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This review synthesizes epidemiological and mechanistic evidence linking bisphenol A and its substitutes (BPS, BPF) to non-alcoholic fatty liver disease, showing that these plasticizer chemicals disrupt hepatic fat metabolism, impair insulin signaling, activate inflammatory pathways, and interact synergistically with high-fat diets and other plasticizers to drive liver disease progression.
Bisphenols (BPs), including bisphenol A (BPA) and its substitutes (BPS, BPF), are ubiquitous environmental contaminants with emerging links to metabolic disorders. This review synthesizes current evidence on the role of BP exposure in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), a global health crisis affecting 25% of adults worldwide. Epidemiological studies reveal significant positive associations between urinary/serum BP levels and NAFLD risk, particularly in males, with maternal exposure correlating to transgenerational metabolic dysfunction. Mechanistically, BPs disrupt hepatic lipid homeostasis by activating PPAR-γ and suppressing fatty acid oxidation while concurrently inducing insulin resistance via impaired IRS-1/PI3K/Akt signaling. Oxidative stress, NLRP3 inflammasome activation, and gut-liver axis perturbations further exacerbate steatosis and inflammation. Co-exposure with phthalates or high-fat diets amplifies hepatotoxicity, highlighting synergistic environmental risks. Critically, developmental and sex-specific susceptibility underscores the need for tailored interventions. We propose preventive strategies to mitigate NAFLD progression, including BP avoidance and policy reforms. This work bridges gaps between environmental epidemiology and molecular toxicology, emphasizing BPs as modifiable drivers of metabolic liver disease.
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Overview of the hazardous impacts of metabolism-disrupting chemicals on the progression of fatty liver diseases.
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This review examined how metabolism-disrupting chemicals (MDCs)—including bisphenol A and phthalates from plastics—promote the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD). MDC exposure was found to impair liver lipid homeostasis and contribute to the global rise in fatty liver disease.
Exploring the Classic and Novel Pathogenetic Insights of Plastic Exposure in the Genesis and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
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This review examined how micro/nanoplastic (MNP) exposure contributes to the genesis and progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), the predominant liver disease in industrialized countries. Oral MNP exposure impacts the gut-liver axis, promotes steatosis through metabolic dysfunction and inflammation, and plastic additives like BPA act as exogenous factors that may trigger trained immunity pathways worsening MASLD.
The nexus of environmental endocrine-disrupting chemical exposure and metabolic dysfunction-associated steatotic liver disease: An emerging public health challenge
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This review examines evidence that chronic low-dose exposure to endocrine-disrupting chemicals, including micro- and nanoplastics, may be an underappreciated factor driving the global rise of metabolic liver disease. Researchers found that these pollutants can promote liver fat accumulation, inflammation, and scarring by disrupting hormone signaling, gut health, and mitochondrial function. The study suggests that environmental chemical exposures should be considered alongside diet and lifestyle when assessing liver disease risk.
Nanoplastics disrupt hepatic lipid metabolism via the inhibition of PPARγ: a study based on digestive system exposure
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Using data from a large U.S. health survey, researchers linked bottled water consumption (a known source of nanoplastic exposure) to higher rates of nonalcoholic fatty liver disease. In mouse experiments, nanoplastics disrupted fat metabolism in the liver by blocking a key protein called PPARgamma. This suggests that nanoplastics entering the body through everyday drinking water could contribute to liver disease by interfering with how the liver processes fats.
Plastic compounds and liver diseases: Whether bisphenol A is the only culprit
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This review looks at how plastic-derived chemicals beyond just bisphenol A (BPA) can damage the liver, particularly by contributing to non-alcoholic fatty liver disease (NAFLD). The authors find that microplastics, nanoplastics, and various bisphenol alternatives all show links to liver problems, suggesting that the full range of plastic pollutants -- not just BPA -- may pose a greater threat to liver health than previously understood.
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