ArticleToxicological sciences : an official journal of the Society of Toxicology2025
Distribution of polybrominated diphenyl ethers (PBDEs) in placental tissues of maternal and fetal origin in exposed Wistar rats and associations with thyroid hormone levels.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Developmental PBDE exposure persistently impairs mast cell function in vivo and drives sex-specific morphological and transcriptional changes in bone marrow-derived mast cells.Environmental research · 2026Article
- Mechanisms of Flame Retardant Toxicity and Their Impacts on Anxiety and Cognition in the Brain.Endocrinology · 2025Review
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7 authors.
Funding
Abstract
In utero exposure to polybrominated diphenyl ethers (PBDEs) is linked to adverse pregnancy and fetal health outcomes, including altered thyroid hormone (TH) levels. Despite their phase-out, PBDEs are still commonly detected in newborn cord blood. While PBDEs can cross the placenta, few studies have separately assessed PBDEs or THs in the maternal and fetal placental tissues. Additionally, no studies have separately assessed THs in these tissues across mid- and late gestation, during the onset of fetal TH synthesis. To address these gaps, we conducted a study with Wistar rats and examined PBDE accumulation in the maternal and fetal placenta. Pregnant dams were exposed daily to sesame oil vehicle, a low dose, or high dose PBDE mixture. At GD15 and 20, dams were sacrificed and placental tissues were collected. Tissues were analyzed for PBDEs, T3, rT3, and T4 using mass spectrometry. BDE-47, -99, -100, and -209 were frequently detected in both the fetal and maternal placenta. At GD15, higher concentrations of BDE-99, -100, and -209 were measured in the fetal placenta; however, this trend reversed by GD20, with higher maternal placental concentrations. Placental T3 and T4 were significantly impacted by exposure, tissue, and exposure × tissue at GD15, with significant reductions in both THs following low-dose exposure in the maternal placenta. By GD20, maternal placental T3 was only significantly reduced in the high exposure groups and there was no effect on placental T4. Overall, these results highlight the rapid developmental changes that occur throughout gestation between the maternal and fetal placenta, and the differential impacts of gestational PBDE exposure on placental T3 and T4 across mid- and late gestation.
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