Related Experiment Video
Updated: Mar 18, 2026

The 4-vessel Sampling Approach to Integrative Studies of Human Placental Physiology In Vivo
Published on: August 2, 2017
PFAS Across the Placenta and Its Potential Impact on Glucose Imbalance and Infant Growth
Rongrong Xuan1, Jialin Li1, Yanqiu Feng2,3,4
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Ningbo University, Ningbo 315010, China.
Insights
Per- and polyfluoroalkyl substances (PFASs) cross the placenta, impacting neonatal growth and development. Maternal glucose regulation plays a key role in mediating these harmful effects, highlighting the need for PFAS regulation.
Area of Science:
- Environmental Health
- Toxicology
- Developmental Pediatrics
Background:
- Per- and polyfluoroalkyl substances (PFASs) are persistent environmental pollutants.
- PFASs are known to cross the placental barrier, but their transfer dynamics and effects on fetal development are not fully understood.
Purpose of the Study:
- To quantify PFAS levels in maternal and cord serum and placental tissues.
- To assess PFAS transfer efficiencies across the maternal-fetal interface.
- To investigate the association between prenatal PFAS exposure and neonatal growth, 12-month development, and maternal glucose regulation.
Main Methods:
- Quantification of 16 PFASs in maternal serum, cord serum, and placental tissues from 102 mother-infant pairs.
- Calculation of PFAS transfer efficiencies from mother to fetus.
- Mediation analysis to evaluate the role of maternal glucose regulation in linking PFAS exposure to growth outcomes.
Main Results:
- All 16 PFASs were detected, with significant concentrations found in maternal serum, cord serum, and placental tissues.
- High transfer efficiencies of PFASs from mother to fetus were observed, with some exceeding 100%.
- Prenatal PFAS exposure was associated with elevated glucose levels and reduced postnatal growth, with maternal glucose mediating a significant portion of this effect.
Conclusions:
- PFAS exposure during pregnancy poses risks to fetal development, potentially through pathways involving glucose dysregulation.
- Comprehensive analysis of matched biospecimens provides crucial insights into PFAS transport across the placenta.
- Findings underscore the necessity for stricter PFAS regulation and monitoring of metabolic health in infants exposed prenatally.
Abstract:
Per- and polyfluoroalkyl substances (PFASs) are persistent pollutants that cross the placental barrier, yet their transfer dynamics and developmental impacts remain unclear. We quantified 16 PFASs in maternal serum, cord serum, and maternal/fetal placental surfaces from 102 mother-infant pairs, calculated transfer efficiencies, and evaluated associations with neonatal growth and 12-month development. Mediation analysis assessed the role of maternal glucose regulation in linking PFAS exposure to early life growth outcomes. All 16 PFASs were detected, with mean ∑16PFAS concentrations of 5.26 ng/mL in maternal serum, 3.52 ng/mL in cord serum, and 1.15 and 0.97 ng/g on maternal and fetal placental surfaces, respectively. Average transfer efficiencies were 45% (maternal to cord) and 73% (maternal to fetal surface), with several PFASs exceeding 100%. Prenatal PFAS exposure correlated with elevated maternal, fetal, and neonatal glucose and reduced postnatal growth, with maternal glucose mediating up to 23.19% of the effect, implicating glucose dysregulation a key pathway. The findings provide quantitative evidence implicating glucose-regulatory pathways in PFAS-induced maternal-fetal health effects and, using multiple matched biospecimens per mother-infant pair, offer a comprehensive view of PFAS transport across the maternal-fetal interface. A 12-month follow-up confirmed persistent growth impairment, reinforcing the need to regulate emerging PFAS and monitor metabolic outcomes.
Related Concept Videos
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Teratogenicity
Inborn Errors of Metabolism
Glucose Transporters
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Diabetes Mellitus: Type 2 and Gestational
Pharmacokinetics in Pediatric Patients: Drug Metabolism

