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Maternal co-exposure to polystyrene microplastics and DEHP impairs thyroid function in adult rat offspring
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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.
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Researchers exposed pregnant rats to a mixture of phthalates and nanoplastics, both separately and in combination, to study effects on the placenta and fetal development. They found that combined exposure caused more severe damage to placental structure and antioxidant defenses than either contaminant alone. The study suggests that simultaneous exposure to these common plastic-derived pollutants during pregnancy may compound risks to maternal and fetal health.
Polystyrene microplastics and di-2-ethylhexyl phthalate co-exposure: Implications for female reproductive health
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When rats were exposed to both polystyrene microplastics and the common plasticizer DEHP together, they developed significantly more ovarian damage -- including increased cystic follicles, fibrosis, and hormone imbalance -- than from either substance alone. The combined exposure activated a specific signaling pathway (TGF-beta1/Smad3) linked to ovarian fibrosis and may increase the risk of polycystic ovary syndrome, raising concerns about real-world co-exposure in women.
Differential parental exposure to polystyrene microplastics from weaning period to maturity: Immune homeostasis dysregulation in F1 offspring
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When rat parents drank water containing microplastics for three months, their babies were born with disrupted gut bacteria and weaker immune systems, even though the babies themselves were never directly exposed. Interestingly, the effects differed depending on whether the mother, father, or both parents were exposed, with mother's exposure causing the most damage to offspring's immune organs and gut health. While this is animal research, it raises concerns that microplastic exposure before pregnancy could affect children's immune development in ways that might not show up until later.
Co-exposure to microplastic and plastic additives causes development impairment in zebrafish embryos
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When zebrafish embryos were exposed to mixtures of polystyrene microplastics combined with common plastic additives (BPS and a phthalate), the combination was far more toxic than any single chemical alone. Even at individually non-toxic doses, the mixtures caused significant developmental abnormalities, oxidative stress, and disrupted thyroid hormone genes. This highlights that real-world exposure to microplastics plus their chemical additives may be more dangerous than studies of individual plastics suggest.
The single and combined effects of decabromodiphenyl ethane and mixed microplastics on male mice reproductive toxicity
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Researchers investigated the combined reproductive toxicity of mixed microplastics and the flame retardant DBDPE in male mice over seven weeks. The study found that DBDPE alone decreased sex hormone levels and sperm count, and when combined with microplastics, the effects on testicular damage, sperm malformation, and oxidative stress were compounded, suggesting that microplastics may amplify the toxicity of co-occurring chemical contaminants.
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