Evidence map›Paper›PMID 40254104›Full record

ArticleReproductive toxicology (Elmsford, N.Y.)2025

Psychosocial stress and associations with inflammation in mid-gestation maternal, fetal, and placental tissue.

Neha Sehgal, Lin Li, Dana E Goin, Jessica Chen, Unurzul Jigmeddagva, Rachel Morello-Frosch, Tracey J Woodruff, Stephanie L Gaw, Joshua F Robinson, Stephanie M Eick

Abstract read
In one paragraph

Article in Reproductive toxicology (Elmsford, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

10 authors.

Neha SehgalGangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Lin LiCenter for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Dana E GoinDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
Jessica ChenCenter for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Unurzul JigmeddagvaCenter for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Rachel Morello-FroschProgram on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Department of Environmental Science, Policy and Management and School of Public Health, University of California, Berkeley, CA, USA.
Tracey J WoodruffProgram on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Stephanie L GawCenter for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Division of Maternal Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Joshua F RobinsonCenter for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Program on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.
Stephanie M EickGangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. Electronic address: stephanie.marie.eick@emory.edu.

Funding

Pilot Project ProgramP30ES019776 · NIEHS · EMORY UNIVERSITY · PI William Michael Caudle · 2013 to 2026
$22.6M
UCSF Environmental Research and Translation for Health Center (EaRTH Center)P30ES030284 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Rashmi Joglekar · 2020 to 2026
$11.2M
Graduate and Postdoctoral Training in ToxicologyT32ES012870 · NIEHS · EMORY UNIVERSITY · PI Carmen Joseph Marsit · 2004 to 2026
$9.1M
The UCSF Pregnancy Exposures to Environmental Chemicals (PEEC) Children's CenterP01ES022841 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOODRUFF, TRACEY J. · 2013 to 2018
$3.9M
Prenatal stress exposures and fetal inflammation during mid-gestationR21HD109723 · NICHD · EMORY UNIVERSITY · PI EICK, STEPHANIE MARIE, ROBINSON, JOSHUA FREDERICK · 2023 to 2024
$450k
NICHD NIH HHS R21 HD109723NIEHS NIH HHS P01 ES022841NIEHS NIH HHS P30 ES019776NIEHS NIH HHS P30 ES030284NIEHS NIH HHS T32 ES012870
6 · The paper itself

Abstract

backgroundInflammation has been implicated as an intermediary between psychosocial stress and adverse birth outcomes. However, prior work has mostly relied on maternal inflammation as a proxy for fetal inflammation mid-gestation or measured fetal inflammation in cord blood and placenta obtained at delivery. No studies have examined psychosocial stress in relation to fetal inflammation mid-gestation.

methodsTwenty cytokines were measured in matched maternal blood, cord blood, and placenta obtained mid-gestation from a socio-demographically diverse group of pregnant participants undergoing elective second-trimester pregnancy terminations (N = 106). Corticotropin-releasing hormone, a proposed biomarker of gestational length, was measured in maternal blood. Perceived stress, and exposure to stressful life events, job strain, and social support were measured via questionnaires. We used linear regression to estimate associations between individual stressors and inflammatory biomarkers in each biomatrix and principal component analysis to assess groups of inflammatory biomarkers.

resultsWe observed many matrix-specific associations between psychosocial stressors and inflammatory biomarkers. For example, low versus high social support was associated with significantly decreased levels of maternal blood CCL3 (β=-0.53; 95 % confidence interval [CI]=-0.98,-0.07), CCL4 (β=-0.26; 95 % CI=-0.47,-0.04), IL8 (β=-0.79; 95 % CI=-1.47,-0.11), CXCL9 (β=-0.47; 95 % CI=-0.89,-0.06), IFNγ (β=-2.28; 95 % CI=-3.60,-0.96), IL4 (β=-1.07; 95 % CI=-1.88,-0.26); and cord blood IFNγ (β=-0.83; 95 % CI=-1.52,-0.14). Social support was not associated with placental inflammation.

conclusionsDuring mid-pregnancy, psychosocial stress─ particularly low social support─ was associated with maternal blood levels of select cytokines, suggesting a potential pathway linking social stress and inflammation. Our results indicate that the placenta may buffer these inflammatory effects on the fetus.

Indexed as

InflammationPlacentaStress, PsychologicalAdultBiomarkersCytokinesFemaleFetal BloodFetusHumansPregnancyPregnancy Trimester, SecondSocial SupportYoung AdultBiomarkersCytokinesChemokinesCytokinesFetal healthInflammationInterferonsPlacentaStress

Identifiers

PMID40254104
PMCPMC12146064

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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.