Evidence map›Paper›PMID 36608759›Full record

ArticleEnvironmental research2023

Networks of placental DNA methylation correlate with maternal serum PCB concentrations and child neurodevelopment.

Julia S Mouat, Xueshu Li, Kari Neier, Yihui Zhu, Charles E Mordaunt, Michele A La Merrill, Hans-Joachim Lehmler, Michael P Jones, Pamela J Lein, Rebecca J Schmidt and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Environmental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
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

17 citing papers in PubMed, 24 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Julia S MouatDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA, USA; Perinatal Origins of Disparities Center, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA.
Xueshu LiDepartment of Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, IA, USA.
Kari NeierDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA, USA; Perinatal Origins of Disparities Center, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA.
Yihui ZhuDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA, USA; Perinatal Origins of Disparities Center, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA.
Charles E MordauntDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA, USA; Perinatal Origins of Disparities Center, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA.
Michele A La MerrillPerinatal Origins of Disparities Center, University of California, Davis, CA, USA; Department of Environmental Toxicology, University of California, Davis, CA, USA.
Hans-Joachim LehmlerDepartment of Occupational and Environmental Health, College of Public Health, University of Iowa, Iowa City, IA, USA.
Michael P JonesDepartment of Biostatistics, College of Public Health, University of Iowa, Iowa City, IA, USA.
Pamela J LeinPerinatal Origins of Disparities Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA; Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, USA.
Rebecca J SchmidtPerinatal Origins of Disparities Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA; Department of Public Health Sciences, School of Medicine, University of California, Davis, CA, USA.
Janine M LaSalleDepartment of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA, USA; Perinatal Origins of Disparities Center, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA; MIND Institute, University of California, Davis, CA, USA. Electronic address: jmlasalle@ucdavis.edu.
University of California, Davis · USUniversity of Iowa · US

Funding

Training CoreP42ES013661 · NIEHS · UNIVERSITY OF IOWA · PI HANS-JOACHIM LEHMLER · 2006 to 2026
$60.3M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
Research Project: Pathologic Significance of Maternal AutoantibodiesP50HD103526 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEONARD J. ABBEDUTO, Melissa Dawn Bauman · 2020 to 2026
$9.7M
ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
PCB Epigenomic Brain & Behavior Lasting Effects Study (PEBBLES)R01ES029213 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Janine M LaSalle, Pamela J Lein · 2018 to 2026
$6.5M
BUILDS MARBLES: Biorepository Upkeep and Infrastructure for Longitudinal Data Sharing for MARBLESR24ES028533 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Brittany D. Chambers Butcher, Rebecca Jean Schmidt · 2017 to 2026
$2.3M
BUILDS MARBLES: Biorepository Upkeep and Infrastructure for Longitudinal Data Sharing for MARBLESU24ES028533 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHAMBERS BUTCHER, BRITTANY D., SCHMIDT, REBECCA JEAN · 2023 to 2025
$1.2M
NICHD NIH HHS P50 HD103526NIEHS NIH HHS P30 ES005605NIEHS NIH HHS P30 ES023513NIEHS NIH HHS P42 ES013661NIEHS NIH HHS R01 ES029213NIEHS NIH HHS R24 ES028533NIEHS NIH HHS T32 ES007059NIEHS NIH HHS U24 ES028533
6 · The paper itself

Abstract

backgroundGestational exposure to polychlorinated biphenyls (PCBs) has been associated with elevated risk for neurodevelopmental disorders. Placental epigenetics may serve as a potential mechanism of risk or marker of altered placental function. Prior studies have associated differential placental DNA methylation with maternal PCB exposure or with increased risk of autism spectrum disorder (ASD). However, sequencing-based placental methylomes have not previously been tested for simultaneous associations with maternal PCB levels and child neurodevelopmental outcomes.

objectivesWe aimed to identify placental DNA methylation patterns associated with maternal PCB levels and child neurodevelopmental outcomes in the high-risk ASD MARBLES cohort.

methodsWe measured 209 PCB congeners in 104 maternal serum samples collected at delivery. We identified networks of DNA methylation from 147 placenta samples using the Comethyl R package, which performs weighted gene correlation network analysis for whole genome bisulfite sequencing data. We tested placental DNA methylation modules for association with maternal serum PCB levels, child neurodevelopment, and other participant traits.

resultsPCBs 153 + 168, 170, 180 + 193, and 187 were detected in over 50% of maternal serum samples and were highly correlated with one another. Consistent with previous findings, maternal age was the strongest predictor of serum PCB levels, alongside year of sample collection, pre-pregnancy BMI, and polyunsaturated fatty acid levels. Twenty seven modules of placental DNA methylation were identified, including five which significantly correlated with one or more PCBs, and four which correlated with child neurodevelopment. Two modules associated with maternal PCB levels as well as child neurodevelopment, and mapped to CSMD1 and AUTS2, genes previously implicated in ASD and identified as differentially methylated regions in mouse brain and placenta following gestational PCB exposure.

conclusionsPlacental DNA co-methylation modules were associated with maternal PCBs and child neurodevelopment. Methylation of CSMD1 and AUTS2 could be markers of altered placental function and/or ASD risk following maternal PCB exposure.

Indexed as

Autism Spectrum DisorderPolychlorinated BiphenylsAnimalsChildDNA MethylationFemaleHumansMaternal ExposureMicePlacentaPregnancyPolychlorinated BiphenylsAutism spectrum disordersDNA methylationPlacentaPolychlorinated biphenylsWGCNAWhole genome bisulfite sequencing

Identifiers

PMID36608759
PMCPMC10518186
OpenAlexW4313530679

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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 OpenQuestion graph.