Evidence map›Paper›PMID 29471507›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2018

Di(2-Ethylhexyl) Phthalate Exposure During Prenatal Development Causes Adverse Transgenerational Effects on Female Fertility in Mice.

Saniya Rattan, Emily Brehm, Liying Gao, Jodi A Flaws

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  9. Year-to-year variation in phthalate metabolites in the Midlife Women's Health Study.Journal of exposure science & environmental epidemiology · 2024
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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

4 authors at 1 institution in 1 country.

Saniya RattanDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802.
Emily BrehmDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802.
Liying GaoDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802.
Jodi A FlawsDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802.
University of Illinois Urbana-Champaign · US

Funding

Research Training Program in Toxicology and Environmental HealthT32ES007326 · NIEHS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI Jodi A. Flaws · 2000 to 2026
$8.7M
Project 3: Endocrine Disruptors and Diet: Effects on the Developing Cortex P01ES022848 · NIEHS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI FIESE, BARBARA H · 2013 to 2018
$4.2M
NIEHS NIH HHS P01 ES022848
6 · The paper itself

Abstract

Di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental toxicant and endocrine disrupting chemical, but little is known about its effects on female reproduction. Thus, we tested the hypothesis that prenatal exposure to DEHP accelerates the onset of puberty, disrupts estrous cyclicity, disrupts birth outcomes, and reduces fertility in the F1, F2, and F3 generations of female mice. Pregnant CD-1 mice were orally dosed with corn oil (vehicle control) or DEHP (20 and 200 µg/kg/day and 500 and 750 mg/kg/day) from gestation day 10.5 until birth. F1 females were mated with untreated males to obtain the F2 generation. F2 females were mated with untreated males to produce the F3 generation. In all generations, the onset of puberty, estrous cyclicity, select birth outcomes, and fertility-related indices were evaluated. In the F1 generation, prenatal DEHP exposure (200 µg/kg/day) accelerated the onset of puberty, it (200 µg and 500 mg/kg/day) disrupted estrous cyclicity, and it (20 and 200 µg/kg/day) decreased fertility-related indices. In the F2 generation, ancestral DEHP exposure (500 mg/kg/day) accelerated the onset of puberty, it (20 and 200 µg/kg/day) disrupted estrous cyclicity, it (20 µg and 500 mg/kg/day) increased litter size, and it (500 mg/kg/day) decreased fertility-related indices. In the F3 generation, ancestral DEHP exposure (20, 200 µg, and 500 mg/kg/day) accelerated the onset of puberty, it (20 µg/kg/day) disrupted estrous cyclicity, and it (750 mg/kg/day) decreased female pup anogenital index. Collectively, these data indicate that prenatal DEHP exposure causes female reproductive problems in a multigenerational and transgenerational manner.

Indexed as

AnimalsDiethylhexyl PhthalateDose-Response Relationship, DrugEndocrine DisruptorsFemaleFertilityMaternal ExposureMice, Inbred StrainsPregnancyPrenatal Exposure Delayed EffectsDiethylhexyl PhthalateEndocrine Disruptors

Identifiers

PMID29471507
PMCPMC5974785
OpenAlexW2792396355

What OpenQuestion holds

Textmetadata
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.