A Single Oral Exposure to Polyethylene Terephthalate Microplastics Causes Mild Metabolic and Gastrointestinal Disruption: Dose and Sex Determinants
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Microplastics, derived largely from degraded household and commercial plastics, have become a pervasive environmental concern, and may pose health risks resulting from ingestion and accumulation in living organisms. Polyethylene terephthalate (PET) microplastics, commonly found in consumer products such as plastic bottles and clothing, have been detected in human arteries and brains among other tissues—although their health impacts remain unknown. This study aimed to evaluate 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 or 50 mg/kg of PET microplastics derived from cryomilling of plastic nurdles. Animals were monitored for ~ 18 hours in an indirect calorimetry apparatus beginning immediately after gavage for changes in metabolic rate. Tissue samples were collected the following morning after gavage to measure systemic indicators of inflammation and injury, changes in hormones related to metabolic function, and changes in gene expression in the liver and gastrointestinal tissue. Males exposed to low PET had significant decreases in metabolic rate, respiratory exchange ratio, and blood insulin, and significant changes in gene expression in the duodenum, whereas PET caused dose-dependent increases in serum platelets, LDL cholesterol and glucose. By contrast, females exposed to PET were limited to decreased metabolic rate with the high dose, and dose-dependent increases in serum LDL. These findings suggest that exposure to PET has the potential to cause mild metabolic dysfunction and systemic and organ toxicity in a dose- and sex-specific manner (Abstract does not reflect U.S. EPA policy).