Evidence map›Paper›PMID 39226441›Full record

ArticleEnvironmental science & technology2024

Exposure to Per- and Polyfluoroalkyl Substances and Timing of Puberty in Norwegian Boys: Data from the Bergen Growth Study 2.

Ingvild Halsør Forthun, Mathieu Roelants, Helle Katrine Knutsen, Line Småstuen Haug, Nina Iszatt, Lawrence M Schell, Astanand Jugessur, Robert Bjerknes, Ninnie B Oehme, Andre Madsen and 2 more

Abstract read
In one paragraph

Article in Environmental science & technology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Environmental factors trigger pubertal development.Current opinion in pediatrics · 2025
    Review
  5. 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

12 authors.

Ingvild Halsør ForthunDepartment of Clinical Science, University of Bergen, 5020 Bergen, Norway.ORCID 0000-0001-5577-0553
Mathieu RoelantsDepartment of Public Health and Primary Care, Centre for Environment and Health KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-3749-0475
Helle Katrine KnutsenDepartment of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.
Line Småstuen HaugDepartment of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.
Nina IszattDepartment of Food Safety, Norwegian Institute of Public Health, 0213 Oslo, Norway.
Lawrence M SchellDepartment of Epidemiology and Biostatistics, University at Albany, Albany, New York 12144, United States.
Astanand JugessurCentre for Fertility and Health, Norwegian Institute of Public Health, 0213 Oslo, Norway.
Robert BjerknesDepartment of Clinical Science, University of Bergen, 5020 Bergen, Norway.
Ninnie B OehmeChildren and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway.
Andre MadsenMedical Biochemistry and Pharmacology, Haukeland University Hospital, 5021 Bergen, Norway.
Ingvild Særvold BruserudChildren and Youth Clinic, Haukeland University Hospital, 5021 Bergen, Norway.
Petur Benedikt JuliussonDepartment of Clinical Science, University of Bergen, 5020 Bergen, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Per- and polyfluoroalkyl substances (PFAS) are widespread environmental contaminants with endocrine-disruptive properties. Their impact on puberty in boys is unclear. In this cross-sectional study, we investigated the association between PFAS exposure and pubertal timing in 300 Norwegian boys (9-16 years), enrolled in the Bergen Growth Study 2 during 2016. We measured 19 PFAS in serum samples and used objective pubertal markers, including ultrasound-measured testicular volume (USTV), Tanner staging of pubic hair development, and serum levels of testosterone, luteinizing hormone, and follicle-stimulating hormone. In addition to logistic regression of single pollutants and the sum of PFAS, Bayesian and elastic net regression were used to estimate the contribution of the individual PFAS. Higher levels of the sum of perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorohexanesulfonic acid (PFHxS) were associated with later pubertal onset according to USTV (age-adjusted odds ratio (AOR): 2.20, 95% confidence interval (CI): 1.29, 3.93) and testosterone level (AOR: 2.35, 95% CI: 1.34, 4.36). Bayesian modeling showed that higher levels of PFNA and PFHxS were associated with later pubertal onset by USTV, while higher levels of PFNA and perfluoroundecanoic acid (PFUnDA) were associated with later pubertal onset by testosterone level. Our findings indicate that certain PFAS were associated with delay in male pubertal onset.

Indexed as

PubertyAdolescentAlkanesulfonic AcidsChildCross-Sectional StudiesEnvironmental ExposureEnvironmental PollutantsFluorocarbonsHumansMaleNorwayAlkanesulfonic AcidsEnvironmental PollutantsFluorocarbonsperfluorooctane sulfonic acidadolescentchildendocrine disruptionenvironmental healthpuberty

Identifiers

PMID39226441
PMCPMC11411722

What Socratic 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 Socratic graph.