Long-distance transportation and improper storage unavoidably lead to the leaching, retention, and aging of bottle-sourced poly(ethylene terephthalate) (PET) microplastics (MPs) in bottled water, posing an exposure risk to public health. Using a zebrafish model, we discovered that chronic exposure (80 days) to thermally aged bottle-derived PET MPs (retained for 7 days at 60 °C) at realistic concentrations (10 and 100 μg/L) caused substantial hepatic histopathological damage and steatosis, whereas pristine PET MPs stored at 25 °C did not. Integrative analyses suggested that thermal aging induced PET fragmentation, surface roughening, and enhancement of bioadhesion, intensifying gut MP retention (maximally 6.524 μg/g tissues), barrier integrity damage, and microbiota dysbiosis. Biochemical analyses, transcriptomics, and blocking experiments validated that intestinal homeostasis disruption stimulated lipopolysaccharide oversecretion and induced intestinal inflammation through activating the LPS/TLR4/NF-kB pathway, which further contributed to systemic and hepatic inflammations, insulin resistance, and de novo lipogenesis, culminating in steatosis. Intervention with Lactobacillus rhamnosus and sodium butyrate reduced MP-driven hepatic steatosis by restoring gut microbiota and barrier functions. Our findings clarified the mechanisms by which thermally aged PET exacerbated progression to steatosis through the gut-liver axis and proposed the intestine-targeted mitigation strategies against hepatic disorders, advocating concerns on long-term exposure risks of bottle-derived MPs under improper storage conditions.
Zhang et al. (2026) studied this question.