Associations of Prenatal Per- and Polyfluoroalkyl Substance (PFAS) Exposures with Offspring Adiposity and Body
Mingyu Zhang1,2, Sheryl L Rifas-Shiman1, Izzuddin M Aris1
1Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, USA.
Insights
Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) may increase obesity risk in adolescents. Higher PFAS levels were linked to increased obesity and BMI trajectories in a prospective cohort study.
Area of Science:
- Environmental health science
- Endocrinology
- Pediatric health
Background:
- Associations between prenatal per- and polyfluoroalkyl substances (PFAS) exposure and offspring adiposity are inconsistent.
- Limited research exists on whether these associations extend into adolescence.
Purpose of the Study:
- To investigate the associations between prenatal PFAS exposures and offspring adiposity and body composition in late adolescence.
- To examine PFAS mixture effects and BMI trajectories in relation to prenatal PFAS levels.
Main Methods:
- Studied 545 mother-child pairs from the Project Viva prospective cohort.
- Measured six PFAS in maternal plasma during early pregnancy.
- Assessed offspring obesity, adiposity, and body composition at 16-20 years using anthropometry, bioelectrical impedance, and DXA.
Main Results:
- Prenatal PFAS concentrations were associated with increased obesity risk (e.g., PFOS, PFOA, PFNA).
- Bayesian kernel machine regression indicated PFAS mixture effects and interactions (e.g., PFOA and PFOS).
- Higher prenatal PFOS, EtFOSAA, and MeFOSAA were linked to accelerated BMI increase from childhood.
Conclusions:
- Prenatal PFAS exposure may contribute to obesogenic effects persisting into late adolescence.
- These findings highlight potential long-term impacts of environmental chemical exposures on child development and metabolic health.
Background:
Findings on the associations between prenatal PFAS exposures and offspring adiposity are inconsistent. Whether such associations may extend to adolescence is especially understudied.
Objectives:
We investigated associations of prenatal PFAS exposures with offspring adiposity and body composition at 16-20 years of age.
Methods:
We studied 545 mother-child pairs in the prospective prebirth cohort Project Viva (Boston, Massachusetts). We measured six PFAS (PFOA, PFOS, PFNA, PFHxS, EtFOSAA, and MeFOSAA) in maternal early pregnancy (, range: 5.7-19.6 wk) plasma samples. At the late adolescence visit ( y, range: 15.9-20.0 y), we obtained anthropometric measures and assessed body composition using bioelectrical impedance analysis and dual-energy X-ray absorptiometry. We examined associations of individual PFAS with obesity [i.e., age- and sex-specific body mass index (BMI) percentile] and adiposity and body composition using multivariable Poisson and linear regression models, respectively. We assessed PFAS mixture effects using Bayesian kernel machine regression (BKMR) and quantile g-computation. We used fractional-polynomial models to assess BMI trajectories (at 3-20 years of age) by prenatal PFAS levels.
Results:
Thirteen percent () of the children had obesity in late adolescence. After multivariable adjustment, higher prenatal PFAS concentrations were associated with higher obesity risk [e.g., 1.59 (95% CI: 1.19, 2.12), 1.24 (95% CI: 0.98, 1.57), and 1.49 (95% CI: 1.11, 1.99) times the obesity risk per doubling of PFOS, PFOA, and PFNA, respectively]. BKMR showed an interaction between PFOA and PFOS, where the positive association between PFOS and obesity was stronger when PFOA levels were lower. Each quartile increment of the PFAS mixture was associated with 1.52 (95% CI: 1.03, 2.25) times the obesity risk and 0.52 (95% CI: , 1.06) higher BMI. Children with higher prenatal PFOS, EtFOSAA, and MeFOSAA concentrations had higher rates of BMI increase starting from 9-11 years of age.
Discussion:
Prenatal PFAS exposures may have obesogenic effects into late adolescence. https://doi.org/10.1289/EHP12597.
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