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Interactions of environmentally relevant polyethylene terephthalate (PET) micro-nanoplastics with toxic elements and organic co-pollutants: Chemical corona formation and impact on toxicity and bioavailability during gastrointestinal co-ingestion
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Tiny plastic particles from bottles and packaging (PET microplastics) can act like magnets, picking up toxic metals (arsenic, lead) and chemicals (like PFOS "forever chemicals") from their surroundings and carrying them into your gut. In lab tests using a model of the human intestine, these plastic-chemical combos didn't kill cells outright, but they increased stress inside cells and helped the toxic substances slip through the gut lining more easily by weakening the "seals" between intestinal cells. This suggests that eating microplastics alongside common pollutants might make those pollutants more harmful by helping your
The ability of environmental pollutants (EPs) to interact with and form chemical coronas on micro-nanoplastics (MNPs) raises significant concerns about potential toxicological effects in biological systems. Here, we investigated the formation of chemical coronas of toxic elements (Arsenic-As, Lead-Pb, and Chromium-Cr) and organic pollutants (PFOS and boscalid), on polyethylene terephthalate (PET) PM 10 MNPs generated by simulating a key scenario of the degradation lifecycle of plastics: cryomilling (mimics fragmentation process) followed by 21-day UV photo-oxidation (aged MNPs). Additionally, a small intestinal epithelium (SIE) model, coupled with three-phase simulated gastrointestinal digestion, was employed to evaluate the fate of EP coronas across the gastrointestinal tract (GIT) and the toxicity and bioavailability of MNPs and EPs. PET MNPs sorbed substantial amounts of toxic elements and organic pollutants in water (fasting food model). However, EP fate across the GIT during digestion was EP-specific, with toxic elements (As and Pb) generally being desorbed across GIT to a significantly greater extent than organic pollutants. PET MNPs and EPs alone, and their co-ingested mixture (PET MNPs+EPs), were not cytotoxic, but PET MNPs+EPs increased the intracellular oxidative stress in the SIE. More importantly, the presence of PET MNPs increased the translocation of most EPs (As, Pb, PFOS, and boscalid) in the SIE, while the presence of EPs had no effect on uptake and translocation of co-ingested PET MNPs. The enhanced bioavailability of EPs promoted by PET MNPs was associated with downregulation of cell junction genes, indicating modulation of epithelial barrier-associated pathways at the molecular level. The study highlights potential public health concerns arising from co-ingestion of EPs and MNPs, including the formation of EP chemical coronas on MNPs and their influence on EP bioavailability.
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This study tested what happens when human intestinal cells are exposed to PET microplastics combined with PFOA, a persistent chemical pollutant often called a forever chemical. The combination was more toxic than either substance alone, causing greater cell damage and weakening the intestinal barrier that normally keeps harmful substances out of the bloodstream. The findings suggest that microplastics carrying adsorbed pollutants like PFOA could pose greater risks to gut health than microplastics by themselves.
Polyethylene terephthalate and polypropylene nanoplastics toxicity in vitro: Comparative analysis of paraquat adsorption and cytotoxicity
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Tiny plastic particles from common products (like water bottles, made of PET plastic) can act like sponges for toxic chemicals, including the weed-killer paraquat, and carry them into our cells. In lab tests, these PET nanoplastics soaked up more paraquat and caused more cell damage than another common plastic type (PP), and the combination of plastic plus pesticide was more harmful than either alone. This suggests that plastic pollution in our environment may make certain toxic chemicals more dangerous by acting as delivery vehicles into our bodies, an interaction that's rarely considered in current health and safety assessments.
Trojan horse in the intestine: A review on the biotoxicity of microplastics combined environmental contaminants
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This review examines how microplastics act as 'Trojan horses' by carrying other environmental contaminants such as heavy metals, persistent organic pollutants, and pathogens into the intestinal system. Researchers analyzed the mechanisms by which microplastics adsorb and release these co-contaminants and how the combinations affect the gut barrier. The study highlights that the interactive toxicity of microplastics with other pollutants may be more harmful than either pollutant alone, particularly to intestinal health.
Weathered microplastics reshape gastrointestinal responses to per- and polyfluoroalkyl substances during co-exposure
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Researchers studied how weathered plastic particles and PFAS chemicals (often called "forever chemicals") affect human intestinal cells and mice when combined. Combined exposure reduced some immediate cell damage but worsened others, including mitochondrial problems, intestinal inflammation, and changes to gut bacteria and gene activity, showing that plastics reshape rather than simply increase or decrease PFAS effects.
Adsorption of copper, nickel and tributyltin ions on microplastics and combined toxicity on in vitro intestinal epithelium
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Tiny plastic particles in our environment can act like magnets for toxic metals (copper and nickel) and a harmful chemical once used in boat paint (tributyltin), soaking them up and potentially carrying them into our bodies. When researchers tested how these plastic-metal combos affect cells lining the gut, the first barrier these particles would hit after we eat or drink them, they found signs of added toxicity, suggesting microplastics might make these pollutants more harmful than they'd be on their own. This matters because it hints that the health risks of microplastics may partly come from what they're carrying, not just the plastic itself.
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