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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.
The global prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has reached epidemic proportions, creating a substantial healthcare burden. While traditionally attributed to caloric excess and sedentary lifestyles, the incomplete explanation provided by these factors alone has spurred the investigation of novel etiological agents. There is now compelling evidence that chronic, low-dose exposure to environmental endocrine-disrupting chemicals (EDCs) is a significant and underappreciated risk factor driving MASLD pathogenesis. This review synthesizes the current human epidemiological and mechanistic evidence, focusing on the last five years, to elucidate the role of both established EDCs (e.g., phthalates, bisphenols, PFAS, organochlorine pesticides) and emerging contaminants, notably micro- and nanoplastics (MNPs). We detail how these pervasive pollutants promote hepatic steatosis, inflammation, and fibrosis by disrupting nuclear receptor signaling (e.g., PPARγ), inducing gut dysbiosis and barrier dysfunction, causing mitochondrial and lysosomal impairment, and reprogramming lipid metabolism. The review highlights that MNPs, in particular, represent a frontier in environmental hepatotoxicity, with recent data revealing their ability to bioaccumulate and exacerbate metabolic insults through novel mechanisms. By integrating evidence from population studies and experimental models, this review underscores the necessity of incorporating the "exposome" into the MASLD etiological framework. It concludes that mitigating this public health challenge requires concerted efforts in advancing research on chemical mixtures and critical exposure windows, alongside implementing policies aimed at reducing environmental exposure.
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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.
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