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Ingested microplastics pose a potentially serious risk to the gastrointestinal microenvironment
Summary
This review argues that ingested microplastics pose a serious potential risk to the gastrointestinal microenvironment by disrupting the gut microbiome, irritating the intestinal lining, and potentially carrying toxic additives and adsorbed chemicals into the digestive tract. Given that human microplastic ingestion is now unavoidable, the authors call for urgent research into gastrointestinal health effects.
Abstract BACKGROUND Plastic pollution has increased exponentially over the past 70 years. Slow breakdown of plastic materials primarily leads to smaller and smaller microplastic particles (MP), but not actual degradation of the material. We now face extensive MP contamination of our food and water sources, raising ecological and public health concerns. MP ingestion by humans is now an inevitable consequence of global plastic pollution, and we are only now becoming aware of this burgeoning crisis. Given this crisis, there is also an important gap in knowledge regarding how MP affect the major direct organ of contact, the gastrointestinal tract. We provide compelling evidence that MP affect both intestinal epithelium and macrophages. DESIGN We utilized human colonic organoids and colonic cell lines to examine the effects of MP on intestinal permeability and wound healing. Additionally, we examined the effects of microplastics on macrophage function and metabolism. Lastly, we examined the in vivo response to microplastics in animal models. RESULTS Regarding the intestinal barrier, we show MP impede wound healing and affects intestinal permeability. In macrophages, phagocytosis of MP leads to the upregulation of costimulatory molecules and induces metabolic shift towards glycolysis. In vivo MP ingestion affects the weight and microbiota composition of mice. CONCLUSION In summary, our findings indicate MP ingestion may pose a serious human health hazard by disrupting both intestinal epithelial barrier and macrophage function subsequently causing intestinal permeability, dysbiosis, and an inflammatory state that could lead to intestinal and systemic inflammation.
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