2 research outputs found
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