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Micro/Nanoplastics and Lithium Iron Phosphate at Environmentally Relevant Dose Triggers Hepatic Fibrosis: Unseen Risks of Global Renewable Energy
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Researchers found that environmentally relevant co-exposure to PVC-derived micro/nanoplastics and lithium iron phosphate — a material released by expanding battery manufacturing — synergistically damaged the liver in mice via a gut-liver axis mechanism, disrupting gut microbial balance, depleting short-chain fatty acids, and activating fibrogenic signaling pathways that together drove hepatic fibrosis at levels neither pollutant caused alone.
The rapid expansion of the global renewable energy industry has led to increasing environmental release of LiFePO₄ (LFP) and polyvinyl chloride-derived micro/nanoplastics (PVC), yet their combined impacts remain largely unexplored. Here, we demonstrate that chronic co-exposure to environmentally relevant levels of PVC and LFP exerts synergistic hepatotoxicity through a gut-liver axis. Multi-omics integration reveals that co-exposure disrupts intestinal microbial homeostasis, depletes short-chain fatty acids, barrier integrity, and elevates plasma lipopolysaccharide (LPS) and pro-inflammatory cytokines. This gut barrier disruption permits portal translocation of LPS, PVC, and iron, initiating a hepatic inflammatory cascade. Concurrently, PVC and iron enrichment in both the intestine and liver, and lithium depletion in the liver under co-exposure exacerbate oxidative stress. Transcriptomic profiling identifies activation of the p38-cPLA₂-arachidonic acid axis and TGF-β/α-SMA signaling, linking metabolic inflammation to extracellular matrix remodeling and fibrosis. In vitro assays further confirm that co-exposures induce synergistic cytotoxicity and upregulate fibrogenic proteins. Collectively, these findings provide the first mechanistic evidence that co-exposure enhances hepatic fibrosis. This study not only underscores the overlooked health risks posed by composite pollution from renewable energy systems but also highlights the urgent need for sustainable material management and toxicity-informed design in the clean energy transition.
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Ferroptosis and hepatic fibrosis induced by cooperative exposure to polylactic acid nanoplastics and copper: Emphasis on gut microbiota dysbiosis
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Researchers investigated the combined hepatotoxicity of polylactic acid nanoplastics and copper in mice, focusing on the gut-liver axis. The study found that co-exposure caused synergistic liver damage through ferroptosis, characterized by disrupted glutathione and iron homeostasis, along with gut microbiota dysbiosis and hepatic fibrosis more severe than either pollutant alone.
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.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
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This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Microplastics, nanoplastics and liver disease: an emerging health concern?
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Researchers reviewed emerging evidence that microplastics and nanoplastics accumulate in human liver tissue at increasing concentrations over the past decade, trigger oxidative stress, fibrogenesis, and inflammation in cell and animal models, and may carry microbial pathogens and endocrine-disrupting chemicals, introducing the concept of plastic-induced liver injury as a new focus for environmental hepatology.
The mechanistic nexus between microplastics and chronic liver disease: A review of current evidence
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Researchers reviewed the mechanisms by which microplastics accumulate in liver tissue and worsen chronic liver disease, finding that MPs activate cell death pathways, trigger oxidative stress and inflammation, promote fibrosis, and disrupt metabolic and microbial regulation — and can amplify damage from co-occurring hepatotoxic substances.
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