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Maternal co-exposure to polystyrene microplastics and DEHP impairs thyroid function in adult rat offspring
Summary
When pregnant rats were exposed to microplastics and DEHP (a common plastic-softening chemical found in food packaging and personal care products) together, their offspring showed worse thyroid problems than exposure to either substance alone, including disrupted thyroid hormone levels and changes in gut bacteria linked to thyroid function. This matters because it suggests real-world plastic pollution, which almost always involves multiple chemicals mixing together, may pose bigger risks to developing babies than studies testing one chemical at a time have shown, and effects may differ between males and females.
Maternal combined exposure to polystyrene microplastics (PS-MPs) and di-(2-ethylhexyl) phthalate (DEHP) poses potential risks to offspring endocrine development; however, the combined effects of these two contaminants remain poorly characterized. Pregnant rats were exposed to PS-MPs, DEHP or a combination of both throughout pregnancy and lactation. The hypothalamic-pituitary-thyroid (HPT) axis function and gut microbiota composition were then assessed in adult offspring. Single-contaminant exposure altered thyroid hormone levels and HPT axis gene expression. Co-exposure exacerbated these disruptions, producing greater TSH suppression, elevated thyroid hormone levels, and uniform downregulation of Nis expression in offspring of both sexes. Sex-specific differences in hypothalamic and pituitary gene expression were observed, suggesting that upstream HPT axis regulation was disrupted via sex-divergent mechanisms. The combined exposure also induced morphological disruption of thyroid follicular epithelial cells and elevated oxidative stress markers. In co-exposed offspring, gut microbiome profiling revealed Bacteroides depletion and Enterococcus enrichment as the most prominent taxa-level shifts. The parallel perturbations in gut microbiome composition and HPT axis function across treatment groups support a proposed disruption model of the gut-brain-thyroid axis. Our findings demonstrate that maternal co-exposure to PS-MPs and DEHP induces sex-divergent thyroid endocrine disruption in offspring, driven by a complex integration of additive and synergistic toxicities. Consequently, relying exclusively on single-pollutant models likely underestimates the developmental health threats of real-world plastic mixtures, highlighting the critical need to incorporate mixture interactions and sex-specific vulnerabilities into future environmental risk assessments.