Polybrominated Diphenyl Ethers (PBDEs) in Aborted Human Fetuses and Placental Transfer during the First Trimester of Pregnancy

Data on early human fetal exposure to polybrominated diphenyl ethers (PBDEs) is limited. However, early pregnancy, in particular the first trimester, is critical for fetal development. We investigated exposure to PBDEs and placental transfer during early pregnancy by analyzing PBDEs in paired aborted fetuses (<i>n</i> = 65), placentas (<i>n</i> = 65), and maternal blood samples (<i>n</i> = 31) at 10–13 weeks gestation, which were collected in a hospital near electronic wastes (e-wastes) recycling sites in Taizhou, China. Mean total PBDE (∑PBDE) concentrations were 4.46, 7.90, and 15.7 ng/g of lipid weight (lw) in the fetuses, placentas, and blood, respectively. The three matrices had roughly similar PBDE congener profiles, dominated by BDE-209, BDE-197, BDE-153, BDE-47, and BDE-28. Significant correlations were found between ∑PBDE concentrations in the paired matrices. Comparing the concentration ratios between the paired samples, we observed significantly higher fetus/blood and fetus/placenta ratios for BDE-28, BDE-99, and BDE-47 than for BDE-197, BDE-209, and BDE-153, while opposite results were found in placenta/blood ratios. Our results indicate that PBDEs can enter the fetus during the first trimester and low-brominated congeners cross the placenta more easily than high-brominated congeners, which tend to remain in the placenta. This phenomenon is consistent with findings at the end of pregnancy

TBBPA and Its Alternatives Disturb the Early Stages of Neural Development by Interfering with the NOTCH and WNT Pathways

Tetrabromobisphenol A (TBBPA), as well as its alternatives Tetrabromobisphenol S (TBBPS) and Tetrachlorobisphenol A (TCBPA), are widely used halogenated flame retardants. Their high detection rates in human breast milk and umbilical cord serum have raised wide concerns about their adverse effects on human fetal development. In this study, we evaluated the cytotoxicity and neural developmental toxicity of TBBPA, TBBPS, and TCBPA with a mouse embryonic stem cell (mESC) system, at human body fluid and environmental relevant doses. All the three compounds showed similar trends in their cytotoxic effects. However, while TBBPA and TBBPS stimulated ESC neural differentiation, TCBPA significantly inhibited neurogenesis. Mechanistically, we demonstrated that, as far as the NOTCH (positive regulator) and WNT (negative regulator) pathways were concerned, TBBPA only partially and slightly disturbed them, whereas TBBPS significantly inhibited the WNT pathway, and TCBPA down-regulated the expression of NOTCH effectors but increased the WNT signaling, actions which both inhibited neural specification. In conclusion, our findings suggest that TBBPS and TCBPA may not be safe alternatives to TBBPA, and their toxicity need to be comprehensively evaluated