Evidence map›Paper›PMID 28558807›Full record

ArticleEnvironmental health : a global access science source2017

Genome-wide DNA methylation at birth in relation to in utero arsenic exposure and the associated health in later life.

Akhilesh Kaushal, Hongmei Zhang, Wilfried J J Karmaus, Todd M Everson, Carmen J Marsit, Margaret R Karagas, Shih-Fen Tsai, Hui-Ju Wen, Shu-Li Wang

Open access · goldAbstract read
In one paragraph

Article in Environmental health : a global access science source, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
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  8. Update of the risk assessment of inorganic arsenic in food.EFSA journal. European Food Safety Authority · 2024
    Article
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  10. Review
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  16. Inter- and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  17. Review
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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

9 authors at 5 institutions in 2 countries.

Akhilesh KaushalDivision of Epidemiology, Biostatistics, and Environmental Health, University of Memphis, Memphis, TN, 38152, USA.
Hongmei ZhangDivision of Epidemiology, Biostatistics, and Environmental Health, University of Memphis, Memphis, TN, 38152, USA. hzhang6@memphis.edu.
Wilfried J J KarmausDivision of Epidemiology, Biostatistics, and Environmental Health, University of Memphis, Memphis, TN, 38152, USA.
Todd M EversonDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Carmen J MarsitDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Margaret R KaragasDepartment of Epidemiology, Geisel School of Medicine at Dartmouth College, Hanover, NH, USA.
Shih-Fen TsaiNational Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli, Taiwan.
Hui-Ju WenNational Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli, Taiwan.
Shu-Li WangNational Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli, Taiwan.
University of Memphis · USEmory University · USNational Health Research Institutes · TWDartmouth College · USNational Defense Medical Center · TW

Funding

Project 3: Placental Biomarkers of Exposure and Outcome (Marsit)P01ES022832 · NIEHS · DARTMOUTH COLLEGE · PI MURRAY, CAROLYN J · 2013 to 2018
$4.7M
Does epigenetic methylation explain the gender-switch in adolescent asthma?R01AI121226 · NIAID · UNIVERSITY OF MEMPHIS · PI HOLLOWAY, JOHN W, ZHANG, HONGMEI · 2016 to 2020
$3.2M
Transgenerational epigenetic inheritance of allergy in a multigenerational cohortR01AI091905 · NIAID · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI KARMAUS, WILFRIED JJ · 2011 to 2015
$2.7M
NIAID NIH HHS R01 AI091905NIAID NIH HHS R01 AI121226NIEHS NIH HHS P01 ES022832
6 · The paper itself

Abstract

backgroundIn utero arsenic exposure may alter fetal developmental programming by altering DNA methylation, which may result in a higher risk of disease in later life. We evaluated the association between in utero arsenic exposure and DNA methylation (DNAm) in cord blood and its influence in later life.

methodsGenome-wide DNA methylation in cord blood from 64 subjects in the Taiwanese maternal infant and birth cohort was analyzed. Robust regressions were applied to assess the association of DNA methylation with in utero arsenic exposure. Multiple testing was adjusted by controlling false discovery rate (FDR) of 0.05. The DAVID bioinformatics tool was implemented for functional annotation analyses on the detected CpGs. The identified CpGs were further tested in an independent cohort. For the CpGs replicated in the independent cohort, linear mixed models were applied to assess the association of DNA methylation with low-density lipoprotein (LDL) at different ages (2, 5, 8, 11 and 14 years).

resultsIn total, 579 out of 385,183 CpGs were identified after adjusting for multiple testing (FDR = 0.05), of which ~60% were positively associated with arsenic exposure. Functional annotation analysis on these CpGs detected 17 KEGG pathways (FDR = 0.05) including pathways for cardiovascular diseases (CVD) and diabetes mellitus. In the independent cohort, about 46% (252 out of 553 CpGs) of the identified CpGs showed associations consistent with those in the study cohort. In total, 11 CpGs replicated in the independent cohort were in the pathways related to CVD and diabetes mellitus. Via longitudinal analyses, we found at 5 out of the 11 CpGs methylation was associated with LDL over time and interactions between DNA methylation and time were observed at 4 of the 5 CpGs, cg25189764 (coeff = 0.157, p-value = 0.047), cg04986899 (coeff. For interaction [coeff.int] = 0.030, p-value = 0.024), cg04903360 (coeff.int = 0.026, p-value = 0.032), cg08198265 (coeff.int = -0.063, p-value = 0.0021), cg10473311 (coeff.int = -0.021, p-value = 0.027).

conclusionIn utero arsenic exposure was associated with cord blood DNA methylation at various CpGs. The identified CpGs may help determine pathological epigenetic mechanisms linked to in utero arsenic exposure. Five CpGs (cg25189764, cg04986899, cg04903360, cg08198265 and cg10473311) may serve as epigenetic markers for changes in LDL later in life.

Indexed as

ArsenicEnvironmental PollutantsMaternal ExposureAdolescentChildChild, PreschoolCpG IslandsDNA MethylationEpigenesis, GeneticFemaleFetal BloodFetal DevelopmentHumansInfant, NewbornMaleNew HampshireArsenicEnvironmental PollutantsArsenicCpGDAVIDDNA methylationGenome-wideKEGG pathwayLdl

Identifiers

PMID28558807
PMCPMC5450181
OpenAlexW2619936702

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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 OpenQuestion graph.