Evidence map›Paper›PMID 39615256›Full record

ArticleEnvironment international2024

Cord plasma metabolomic signatures of prenatal per- and polyfluoroalkyl substance (PFAS) exposures in the Boston Birth Cohort.

Zeyu Li, Mingyu Zhang, Xiumei Hong, Guoying Wang, Giehae Choi, Kari C Nadeau, Jessie P Buckley, Xiaobin Wang

Abstract read
In one paragraph

Article in Environment international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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

8 authors.

Zeyu LiCenter on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Mingyu ZhangDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Xiumei HongCenter on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Guoying WangCenter on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Giehae ChoiDepartment of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Kari C NadeauDepartment of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Jessie P BuckleyDepartment of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: jessie.buckley@unc.edu.
Xiaobin WangCenter on the Early Life Origins of Disease, Department of Population, Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: xwang82@jhu.edu.

Funding

Preterm Birth, Maternal and Cord Blood Metabolome, and Child Metabolic RiskR01HD041702 · NICHD · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI Frank B Hu, XIAOBIN WANG · 2001 to 2026
$11.1M
Immune Development Across the Life Course: Integrating Exposures and Multi-Omics in the Boston Birth CohortU01ES034983 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI Hongkai Ji, Harry Benjamin Larman · 2022 to 2026
$3.9M
Endocrine disrupting chemical mixtures and bone health in adolescenceR01ES033252 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUCKLEY, JESSIE P · 2021 to 2025
$3.0M
Inter-generational Link of Cardio-Metabolic Risk: Integrate Multi-OMICs with Birth CohortR01HD098232 · NICHD · JOHNS HOPKINS UNIVERSITY · PI LIANG, LIMING, WANG, XIAOBIN · 2019 to 2022
$2.7M
Early Life Phthalate and Perfluoroalkyl Substance Exposures and Childhood Bone HealthR01ES030078 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUCKLEY, JESSIE P · 2019 to 2023
$2.1M
Functional RNA Modifications, Micronutrient Exposure, Developmental DisabilitiesR01ES031521 · NIEHS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI WANG, XIAOBIN, XIE, HEHUANG · 2020 to 2024
$1.9M
Maternal Exposure to Low Level Mercury, Metabolome, and Child Cardiometabolic Risk in Multi-Ethnic Prospective Birth CohortsR01ES031272 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI WANG, GUOYING, WANG, XIAOBIN · 2020 to 2024
$1.2M
Maternal exposure to chemicals and offspring neurodevelopmental disabilities: informing public health actions by understanding nutritional modifiers and simulating interventionsK99ES035464 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI CHOI, GIEHAE · 2023 to 2023
$98k
American Heart Association-American Stroke Association 24CDA1257852NICHD NIH HHS R01 HD041702NICHD NIH HHS R01 HD098232NIEHS NIH HHS K99 ES035464NIEHS NIH HHS R01 ES030078NIEHS NIH HHS R01 ES031272NIEHS NIH HHS R01 ES031521NIEHS NIH HHS R01 ES033252NIEHS NIH HHS U01 ES034983
6 · The paper itself

Abstract

backgroundPrenatal per- and polyfluoroalkyl substance (PFAS) exposures are associated with adverse offspring health outcomes, yet the underlying pathological mechanisms are unclear. Cord blood metabolomics can identify potentially important pathways associated with prenatal PFAS exposures, providing mechanistic insights that may help explain PFAS' long-term health effects.

methodsThe study included 590 mother-infant dyads from the Boston Birth Cohort. We measured PFAS in maternal plasma samples collected 24-72 h after delivery and metabolites in cord plasma samples. We used metabolome-wide association studies and pathway enrichment analyses to identify metabolites and pathways associated with individual PFAS, and quantile-based g-computation models to examine associations of metabolites with the PFAS mixture. We used False Discovery Rate to account for multiple comparisons.

resultsWe found that 331 metabolites and 18 pathways were associated with ≥ 1 PFAS, and 38 metabolites were associated with the PFAS mixture, predominantly amino acids and lipids. Amino acids such as alanine and lysine and their pathways, crucial to energy generation, biosynthesis, and bone health, were associated with PFAS and may explain PFAS' effects on fetal growth restriction. Carnitines and carnitine shuttle pathway, associated with 7 PFAS and the PFAS mixture, are involved in mitochondrial fatty acid β-oxidation, which may predispose higher risks of fetal and child growth restriction and cardiovascular diseases. Lipids, such as glycerophospholipids and their related pathway, can contribute to insulin resistance and diabetes by modulating transporters on cell membranes, participating in β-cell signaling pathways, and inducing oxidative damage. Neurotransmission-related metabolites and pathways associated with PFAS, including cofactors, precursors, and neurotransmitters, may explain the PFAS' effects on child neurodevelopment. We observed stronger associations between prenatal PFAS exposures and metabolites in males.

conclusionsThis prospective birth cohort study contributes to the limited literature on potential metabolomic perturbations for prenatal PFAS exposures. Future studies are needed to replicate our findings and link prenatal PFAS associated metabolomic perturbations to long-term child health outcomes.

Indexed as

Environmental PollutantsFetal BloodFluorocarbonsMaternal ExposureMetabolomicsAdultBirth CohortBostonCohort StudiesFemaleHumansInfant, NewbornMaleMetabolomePregnancyPrenatal Exposure Delayed EffectsEnvironmental PollutantsFluorocarbonsFetal growth and developmentMechanismMetabolomicsMixturePFASPrenatal exposure

Identifiers

PMID39615256
PMCPMC11721280

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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.