Evidence map›Paper›PMID 39884538›Full record

ArticleEnvironmental research2025

Sex-specific effects of in utero exposure to per- and polyfluoroalkyl substances on placental development.

Cynthia Perez, Neha Sehgal, Stephanie M Eick, Dana Boyd Barr, Parinya Panuwet, Volha Yakimavets, Kelsey Chen, Kartik Shankar, Kevin J Pearson, Aline Andres and 1 more

Abstract read
In one paragraph

Article in Environmental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Stress-activated pathways mediate PFAS effects on human placental syncytiotrophoblast cells.Toxicological sciences : an official journal of the Society of Toxicology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Cynthia PerezGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Neha SehgalGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Stephanie M EickGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA; Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Dana Boyd BarrGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Parinya PanuwetGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Volha YakimavetsGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Kelsey ChenGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA.
Kartik ShankarUSDA Agricultural Research Service, Responsive Agricultural Food Systems Research Unit, College Station, TX, USA.
Kevin J PearsonDepartment of Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, USA.
Aline AndresDepartment of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Arkansas Children's Nutrition Center, Little Rock, AR, USA.
Todd M EversonGangarosa Department of Environmental Health, Emory University Rollins School of Public Health, Atlanta, GA, USA; Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, USA. Electronic address: Todd.M.Everson@Emory.edu.

Funding

Pilot Project ProgramP30ES019776 · NIEHS · EMORY UNIVERSITY · PI William Michael Caudle · 2013 to 2026
$22.6M
Pilot Project ProgramP30ES026529 · NIEHS · UNIVERSITY OF KENTUCKY · PI Erin N Haynes · 2017 to 2026
$15.4M
Graduate and Postdoctoral Training in ToxicologyT32ES012870 · NIEHS · EMORY UNIVERSITY · PI Carmen Joseph Marsit · 2004 to 2026
$9.1M
Growth and metabolic programming from prenatal PFAS exposure: examining the roles of placental functional genomics and protection by maternal exerciseR01ES032176 · NIEHS · UNIVERSITY OF KENTUCKY · PI ANDRES, ALINE, EVERSON, TODD M · 2021 to 2023
$1.9M
Perinatal PFAS Impact Children's Development: Examining the Roles of Placental Functional Multiomics and Protection by Maternal ExerciseR01ES036986 · NIEHS · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI Aline Andres, Todd M Everson · 2025 to 2026
$1.4M
NIEHS NIH HHS P30 ES019776NIEHS NIH HHS P30 ES026529NIEHS NIH HHS R01 ES032176NIEHS NIH HHS R01 ES036986NIEHS NIH HHS T32 ES012870
6 · The paper itself

Abstract

backgroundPer- and polyfluoroalkyl substances (PFAS) are persistent organic pollutants that may impact placental function, and potentially gestational age acceleration (GAA), a deviation from reported and predicted gestational age. GAA potentially represents differences in cell maturation in response to a challenging environment.

objectiveThis study aimed to characterize the effects of individual and mixtures of PFAS on GAA, cell composition, birth length, and birthweight.

methodsPregnant peoples were recruited from around Little Rock, Arkansas, United States between 2011 and 2014. We utilized placental DNA methylation profiles of 153 healthy pregnancies to calculate GAA and estimate the proportions of six placental cell types. PFAS were quantified in homogenized placental tissue using high-performance liquid chromatography-tandem mass spectrometry. Five PFAS were detected in over 70% of samples. We studied these five PFAS individually using multiple linear regression and as a mixture using quantile g-computation, while adjusting for confounders. The dependent variables in our models included GAA, cell proportions, birthweight, and birth length.

resultsWe did not observe associations between PFAS and any of our outcomes in our primary models. While GAA in male placentas were not significantly affected by PFAS, the PFAS mixture associated with decreased syncytiotrophoblast proportion (Ψ = -0.018, 95% CI [-0.032, -0.004]). PFAS mixture did not alter cell proportions in female placentas but was associated with increased GAA (Ψ = 0.269, 95% CI [0.026, 0.513]). Similarly, for females, greater GAA was associated with PFOA (β = 0.141, 95% CI [-0.016,0.040]) and PFOS (β = 0.205, 95% CI [-0.020,0.0416]). DISCUSSION: We illustrate that PFAS may influence placental development in a sex specific manner. Suggested by decrease in syncytotrophoblast, male placenta may experience a more stunted development due to PFAS exposure. Alternatively, female placentas exhibited increased GAA, a plausible marker of elevated developmental maturation in the face of environmental adversity.

Indexed as

Environmental PollutantsFluorocarbonsMaternal ExposurePlacentationAdultArkansasBirth WeightDNA MethylationFemaleGestational AgeHumansInfant, NewbornMalePlacentaPregnancySex FactorsEnvironmental PollutantsFluorocarbonsEpigenetic age accelerationEpigeneticsPFASPlacentaPrenatal

Identifiers

PMID39884538
PMCPMC12482962

What Socratic holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.