Evidence map›Paper›PMID 34839469›Full record

ArticleAmerican journal of perinatology2024

Do Genetic Variants Modify the Effect of Smoking on Risk of Preeclampsia in Pregnancy?

Anna E Bauer, Christy L Avery, Min Shi, Clarice R Weinberg, Andrew F Olshan, Quaker E Harmon, Jingchun Luo, Jenny Yang, Tracy Manuck, Michael C Wu and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of perinatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Alzheimer's disease multi-ancestry genome-wide interaction and stratified study with smoking.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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

14 authors at 4 institutions in 2 countries.

Anna E BauerDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID 0000-0002-7771-930X
Christy L AveryDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Min ShiBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Durham, North Carolina.
Clarice R WeinbergBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, Durham, North Carolina.
Andrew F OlshanDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Quaker E HarmonEpidemiology Branch, National Institute of Environmental Health Sciences, Durham, North Carolina.
Jingchun LuoMammalian Genotyping Core, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Jenny YangDepartment of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Tracy ManuckDepartment of Obstetrics and Gynecology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Michael C WuBiostatistics and Biomathematics Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Kari KlungsøyrDivision for Mental and Physical Health, Norwegian Institute of Public Health, Oslo, Norway.
Lill TrogstadDivision for Mental and Physical Health, Norwegian Institute of Public Health, Oslo, Norway.
Per MagnusCentre for Fertility and Health, Norwegian Institute of Public Health, Oslo, Norway.
Stephanie M EngelDepartment of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
University of North Carolina at Chapel Hill · USNational Institute of Environmental Health Sciences · USNorwegian Institute of Public Health · NOFred Hutch Cancer Center · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
Gene-Environment Interactions in an Autism Birth CohortU01NS047537 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIPKIN, W. IAN · 2003 to 2013
$27.0M
Training Program in Reproductive, Perinatal, and Pediatric EpidemiologyT32HD052468 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Julie L Daniels · 2008 to 2026
$3.8M
Prenatal Smoking, Maternal & Fetal Genetic Variation & Risk of PreeclampsiaR01HD058008 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ENGEL, STEPHANIE · 2008 to 2012
$2.7M
Applications of methods in collaborative scienceZIAES103086 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI WEINBERG, CLARICE · 2012 to 2025
$986k
Intramural NIH HHS ZIA ES103086NICHD NIH HHS R01 HD058008NICHD NIH HHS R01HD058008NICHD NIH HHS T32 HD052468NIEHS NIH HHS N01 ES075558NIEHS NIH HHS P30 ES010126NIEHS NIH HHS Z01-ES103086NINDS NIH HHS U01 NS047537
6 · The paper itself

Abstract

objectiveMaternal smoking is associated with as much as a 50% reduced risk of preeclampsia, despite increasing risk of other poor pregnancy outcomes that often co-occur with preeclampsia, such as preterm birth and fetal growth restriction. Researchers have long sought to understand whether this perplexing association is biologically based, or a result of noncausal mechanisms. We examined whether smoking-response genes modify the smoking-preeclampsia association to investigate potential biological explanations. STUDY

designWe conducted a nested case-control study within the Norwegian Mother, Father and Child Birth Cohort (1999-2008) of 2,596 mother-child dyads. We used family-based log-linear Poisson regression to examine modification of the maternal smoking-preeclampsia relationship by maternal and fetal single nucleotide polymorphisms involved in cellular processes related to components of cigarette smoke (

resultsThree polymorphisms showed overall (

conclusionEvidence for gene-smoking interaction was limited, but differences by smoking cessation warrant further investigation. We demonstrate the potential utility of expanded dyad methods and gene-environment interaction analyses for outcomes with complex relationships between maternal and fetal genotypes and exposures. KEY POINTS: · Maternal and fetal genotype may differentially influence preeclampsia.. · Smoking-related genes did not strongly modify smoking-preeclampsia association.. · Smoking cessation reduced strength of gene by smoking interactions..

Indexed as

Pre-EclampsiaPremature BirthCase-Control StudiesFemaleGenetic Predisposition to DiseaseHumansInfant, NewbornPolymorphism, Single NucleotidePregnancySmoking

Identifiers

PMID34839469
PMCPMC10127527
OpenAlexW3215475531

What OpenQuestion holds

Textmetadata
LicenceTDM
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.