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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
Summary
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.