Evidence map›Paper›PMID 30348172›Full record

ArticleBMC medicine2018

Maternal smoking and high BMI disrupt thyroid gland development.

Panagiotis Filis, Sabine Hombach-Klonisch, Pierre Ayotte, Nalin Nagrath, Ugo Soffientini, Thomas Klonisch, Peter O'Shaughnessy, Paul A Fowler

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in BMC medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07201181 (Association of Prenatal Tobacco Exposure Verified by Maternal Urinary Cotinine With Umbilical Cord Blood Lactate, Fetal Carboxyhemoglobin, and Early Neonatal Outcomes), which is not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 11% 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.

NCT07201181 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Association of Prenatal Tobacco Exposure Verified by Maternal Urinary Cotinine With Umbilical Cord Blood Lactate, Fetal Carboxyhemoglobin, and Early Neonatal Outcomes: A Prospective Single-Center Observational Study

TypeobservationalSponsorHaseki Training and Research HospitalRan2026 to 2027Enrolled126ConditionsTobacco Smoke Pollution, Maternal Exposure During Pregnancy, Infant, Newborn, Carbon Monoxide PoisoningArmsMaternal Urinary Cotinine Assessment
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. 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

8 authors at 4 institutions in 2 countries.

Panagiotis FilisInstitute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK. pfilis@abdn.ac.uk.ORCID 0000-0002-4121-9354
Sabine Hombach-KlonischDepartment of Human Anatomy and Cell Science, Rady College of Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Pierre AyotteCentre de toxicologie, Institut National de Santé Publique du Québec, Quebec, QC, G1V 5B3, Canada.
Nalin NagrathInstitute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK.
Ugo SoffientiniInstitute of Biodiversity, Animal Health & Comparative Medicine (IBAHCM), College of Medical, Veterinary & Life Sciences, University of Glasgow, Garscube Campus, Bearsden Rd, Glasgow, G61 1QH, UK.
Thomas KlonischDepartment of Human Anatomy and Cell Science, Rady College of Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada.
Peter O'ShaughnessyInstitute of Biodiversity, Animal Health & Comparative Medicine (IBAHCM), College of Medical, Veterinary & Life Sciences, University of Glasgow, Garscube Campus, Bearsden Rd, Glasgow, G61 1QH, UK.
Paul A FowlerInstitute of Medical Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK.
University of Aberdeen · GBUniversity of Glasgow · GBUniversity of Manitoba · CAInstitut National de Santé Publique du Québec · CA

Funding

Medical Research Council MR/L010011/1
6 · The paper itself

Abstract

backgroundMaternal lifestyle factors, including smoking and increased body weight, increase risks of adult diseases such as metabolic syndrome and infertility. The fetal thyroid gland is essential for the control of fetal metabolic rate, cardiac output, and brain development. Altered fetal thyroid function may contribute to increased disease onset later in life. Here, we investigated the impact of maternal smoking and high maternal weight on human fetal thyroid function during the second trimester.

methodsThyroid glands and plasma were collected from fetuses electively terminated in the second trimester (normally progressing pregnancies). Plasma total triiodothyronine (T3) and total thyroxine (T4) were measured by solid-phase extraction-liquid chromatography-tandem mass spectrometry. Fetal plasma thyroid-stimulating hormone (TSH) levels were measured using a multiplex assay for human pituitary hormones. Histology and immunolocalization of thyroid developmental markers were examined in thyroid sections. Transcript levels of developmental, functional, apoptotic, and detoxification markers were measured by real-time PCR. Statistical analyses were performed using multivariate linear regression models with fetal age, sex, and maternal smoking or maternal body mass index (BMI) as covariates.

resultsMaternal smoking was associated with significant changes in fetal plasma T4 and TSH levels during the second trimester. Smoke-exposed thyroids had reduced thyroid GATA6 and NKX2-1 transcript levels and altered developmental trajectories for ESR2 and AHR transcript levels. Maternal BMI > 25 was associated with increased fetal thyroid weight, increased plasma TSH levels, and abnormal thyroid histology in female fetuses. Normal developmental changes in AHR and ESR1 transcript expression were also abolished in fetal thyroids from mothers with BMI > 25.

conclusionsFor the first time, we show that maternal smoking and high maternal BMI are associated with disturbed fetal thyroid gland development and endocrine function in a sex-specific manner during the second trimester. These findings suggest that predisposition to post-natal disease is mediated, in part, by altered fetal thyroid gland development.

Indexed as

Body Mass IndexAdultFemaleHumansObesityPregnancySmokingThyroid GlandDevelopmentFetusHumanMaternal obesityMaternal smokingThyroidThyroid hormones

Identifiers

PMID30348172
PMCPMC6198368
OpenAlexW2896387834

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.