Evidence map›Paper›PMID 30862909›Full record

ArticleScientific reports2019

Prenatal Tobacco Exposure Modulated the Association of Genetic variants with Diagnosed ADHD and its symptom domain in children: A Community Based Case-Control Study.

Yanni Wang, Dan Hu, Wenjing Chen, Hongli Xue, Yukai Du

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 3 pooled it
2.3field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 3 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
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  8. Article
  9. Review
  10. Prenatal risk factors and genetic causes of ADHD in children.World journal of pediatrics : WJP · 2022
    Review
  11. Article
  12. Attention-deficit/hyperactive disorder updates.Frontiers in molecular neuroscience · 2022
    Review
  13. Article
  14. 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

5 authors at 3 institutions in 1 country.

Yanni WangDepartment of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China.
Dan HuDepartment of Child Health Care, Hospital of Maternal and Child Health of Dalian, Dalian, Liaoning, P. R. China.
Wenjing ChenDepartment of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China.
Hongli XueDepartment of Maternal, Child and Adolescent Health, School of Public Health, Lanzhou University, Lanzhou, Gansu, P. R. China.
Yukai DuDepartment of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P. R. China. 1978020507@hust.edu.cn.ORCID 0000-0003-3493-5165
Huazhong University of Science and Technology · CNDalian Maternal and Child Health Hospital · CNLanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of our study was to test the hypothesis that prenatal tobacco smoking exposure (PSE) could modulate the association of genetic variants with ADHD. A community based case-control study was conducted among Chinese children and 168 ADHD patients and 233 controls were recruited by using combination diagnosis of DSM-IV, SNAP-IV and semi-structured clinical interview. Logistic regression analysis was performed to estimate the effect of prenatal tobacco smoking exposure and genotype frequencies on ADHD susceptibility individually by adjustment for potential confounders. Multiplicative and additive interaction analysis were performed to evaluate the interactions between risk genes and PSE with regard to ADHD. Prenatal tobacco smoke exposure was a significant risk factor of ADHD even after adjusted for other potential confounders. ADRA2A rs553668, DRD2 rs1124491 and SLC6A4 rs6354 were identified to be associated with ADHD. A significant multiplicative and additive gene-environment interactions were observed between the PSE and the ADRA2A rs553668 in relation to ADHD and ADHD-ODD. The risk of the genetic variants in ADHD was increased significantly if the child had prenatal tobacco exposure. The genetic risk for ADHD could be influenced by the presence of environmental risks. The environmental and the genetic risks are not distinct to each other. More gene-environment interaction studies were needed to reveal the etiology of ADHD.

Indexed as

Attention Deficit Disorder with HyperactivityCase-Control StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMalePolymorphism, Single NucleotidePregnancyPrenatal Exposure Delayed EffectsReceptors, Adrenergic, alpha-2Receptors, Dopamine D2Serotonin Plasma Membrane Transport ProteinsTobacco Smoke PollutionADRA2A protein, humanDRD2 protein, humanReceptors, Adrenergic, alpha-2Receptors, Dopamine D2Serotonin Plasma Membrane Transport ProteinsSLC6A4 protein, humanTobacco Smoke Pollution

Identifiers

PMID30862909
PMCPMC6414688
OpenAlexW2921812615

What OpenQuestion holds

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LicenceCC BY
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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.