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A single oral exposure to polyethylene terephthalate microplastics causes mild metabolic and gastrointestinal disruption: dose and sex determinants

Drug and Chemical Toxicology 2026 Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ashley A. Lewis, Adam Biales, Colette N. Miller, Wendy M. Oshiro, Tracey E. Beasley, Mette C. Schladweiler, Georges-Marie Momplaisir, Robert L. Flick, Mary Jean See, Weichun Huang, Wanda C. Williams, Makala L. Moore, Gary S. Casuccio, Long Li, Michael J. Deible, Rachel D. Grindstaff, Thomas W. Jackson, Mehdi S. Hazari, Kim R. Rogers, Kay Ho, Aimen K. Farraj

Summary

Researchers gave male and female rats a single oral dose of PET microplastics derived from cryomilled nurdles and monitored metabolic rate, gene expression, and blood biomarkers for 18 hours, finding sex- and dose-dependent effects including decreased metabolic rate, altered duodenal gene expression in males, and elevated LDL in females, suggesting mild but measurable systemic disruption.

Polyethylene terephthalate (PET) microplastics, derived from consumer products such as plastic bottles and clothing, are pervasive in the environment with documented detection in human arteries and brains among other tissues, although their health impacts remain unclear. This study evaluated the biological effects of a single oral exposure to PET microplastics in female and male rats. Three-month-old Sprague-Dawley rats were exposed once via oral gavage to sterile water vehicle, or 5 mg/kg (low PET), or 50 mg/kg (high PET) of PET microplastics derived from cryomilling of plastic nurdles. Immediately after exposure, animals were monitored for ∼18 hours in an indirect calorimetry apparatus for changes in metabolic rate, respiratory exchange ratio, and differences between light and dark periods. At the end of the monitoring period, tissue samples were collected to measure systemic indicators of inflammation and injury, metabolic function, and changes in gene expression in the liver and gastrointestinal tissue. The findings indicate that males exposed to low PET, but not high PET, had significant decreases in metabolic rate, respiratory exchange ratio, and blood insulin. Low PET also caused significant changes in gene expression in the duodenum in males. However, males had dose-dependent increases in serum platelets. Females exposed to PET were limited to decreased metabolic rate with high PET, and dose-dependent increases in serum LDL. In summary, although there was variability across dose and sex, these findings suggest that exposure to PET has the potential to cause mild metabolic dysfunction and systemic and organ toxicity.

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