Polybrominated diphenyl ethers (PBDEs) and hydroxylated PBDE metabolites (OH-PBDEs) in maternal and fetal tissues, and associations with fetal cytochrome P450 gene expression
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Background Human fetal exposures to polybrominated diphenyl ethers (PBDEs) and their metabolites (OH-PBDEs) are unique from adults, and in combination with a different metabolic profile, may make fetal development more sensitive to adverse health outcomes from these exposures. However, we lack data to characterize human fetal PBDE exposures and the metabolic factors that can influence these exposures. Objective We examined differences between 2nd trimester maternal and fetal exposures to PBDEs and OH-PBDEs. We also characterized fetal cytochrome P450 (CYP) mRNA expression and its associations with PBDE exposures. Methods We collected paired samples of maternal serum and fetal liver (n=86) with a subset having matched placenta (n=50). We measured PBDEs, OH-PBDEs, and mRNA expression of CYP genes (e.g. CYP1A1, -2E1, -2J2, -2C9) in all samples. As a sensitivity analysis, we measured PBDEs and OH-PBDEs in umbilical cord serum from a subset (n=22). Results BDE-47 was detected in ≥96% of all tissues. Unadjusted ∑PBDEs concentrations were highest in fetal liver (geometric mean (GM)=0.72ng/g), whereas lipid-adjusted concentrations were highest in cord serum (111.12ng/g lipid). In both cases, fetal concentrations were approximately two times higher than maternal serum levels (GM=0.33ng/g or 48.75ng/g lipid). ΣOH-PBDEs were highest in maternal and cord sera and 20-200 times lower than PBDE concentrations. In regression models, maternal BDE-47 explained more of the model variance of liver than of placenta BDE-47 concentrations (adjusted R 2=0.79 vs 0.48, respectively). In adjusted logistic regression models, ∑PBDEs were positively associated with expression of CYP2E1 and -2J2 (placenta), and -1A1 (liver) (p<0.05). Conclusion Our findings suggest that under normal conditions of mid-gestation, the human fetus is directly exposed to concentrations of PBDEs that may be higher than previously estimated based on maternal serum and that these exposures are associated with the expression of mRNAs coding for CYP enzymes. These results will help frame and interpret findings from studies that use maternal or cord blood as proxy measures of fetal exposures, and will inform the molecular pathways by which PBDEs affect human health.
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Zota et al. found a significant correlation between fetal liver burden of PBDE and expression of CYP1A1, but no correlation to any other studied CYPs.
“Zota et al. found significant correlation between fetal liver burden of PBDE and expression of CYP1A1 , but no correlation to any other studied CYPs (Zota et al., 2018).”
From Pregnancy-related maternal physiological adaptations and fetal chemical exposure (2023) · cites this paper as Zota et al., 2018
The Results report a positive association between fetal-liver PBDE levels and CYP1A1 expression, but its 95% confidence interval in the full sample includes 1 (OR 2.36, 95% CI 0.98–5.68); it was significant in the analysis restricted to never-smokers. The Results also describe a suggestive, non-significant association with liver CYP2J2, so saying there was no correlation with any other studied CYP overstates the finding. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe largest study included 85 fetuses, while the median sample size of the reported studies was 44.
“The largest study included 85 fetuses (Zota et al., 2018), while the median sample size of the reported studies was 44 (Table 1).”
From Pregnancy-related maternal physiological adaptations and fetal chemical exposure (2023) · cites this paper as Zota et al., 2018
The Study Population section reports two cohorts of 36 and 50 women, and the Cytochrome P450 mRNA expression section reports 84 fetal-liver samples examined. These passages establish a study of roughly the stated size but do not substantiate exactly 85 fetuses. The median of 44 is attributed to the citing paper’s Table 1, not to Zota et al. (LLM, conf=0.82)
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- Authors
- Zota, A. R., Mitro, S. D., Robinson, J. F., Hamilton, E. G., Park, J.-S., Parry, E., Zoeller, R. T., & Woodruff, T. J.
- Affiliations
- George Washington University (US)
- University of California, San Francisco (US)
- California Department of Toxic Substances Control (US)
- University of Massachusetts Amherst (US)
- Corresponding author
- Woodruff, Tracey J.
- ORCID
- Venue
- Environment International
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 112
- Pages
- 269-278
- ISSN
- 0160-4120 (ISSN-L)
- PMC
- PMC6561508
- OpenAlex
- W2781803153
- Cited by
- 95
- References
- 45
- Citations by year
- 2026: 2 · 2025: 16 · 2024: 16 · 2023: 8 · 2022: 9 · 2021: 21 · 2020: 15 · 2019: 6 · 2018: 1 · 2017: 1
- FWCI
- 5.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Environment International (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Environmental Health Sciences (P01ES022841, R21ES022422, R01ES010026, R00ES019881)
- U.S. EPA-Science to Achieve Results (STAR) (83543301)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Keywords
- polybrominated diphenyl ethers, prenatal exposure, maternal-fetal transfer, BDE-47, fetal liver, placenta, umbilical cord serum, cytochrome P450 gene expression, CYP1A1, CYP2E1, CYP2J2, CYP2C9, fetal development
- MeSH terms
- Cytochrome P-450 Enzyme System, Female, Fetus, Humans, Hydroxylation, Liver, Pregnancy, Maternal Exposure, Halogenated Diphenyl Ethers
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