Evidence map›Paper›PMID 31726365›Full record

ArticleEnvironment international2020

Prenatal dioxin exposure and glucose metabolism in the Seveso Second Generation study.

Marcella Warner, Stephen Rauch, Paolo Brambilla, Stefano Signorini, Paolo Mocarelli, Brenda Eskenazi

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

Article in Environment international, 2020. 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
1.5field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
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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

6 authors at 2 institutions in 2 countries.

Marcella WarnerCenter for Environmental Research and Children's Health (CERCH), School of Public Health, University of California at Berkeley, Berkeley, CA, USA. Electronic address: mwarner@berkeley.edu.
Stephen RauchCenter for Environmental Research and Children's Health (CERCH), School of Public Health, University of California at Berkeley, Berkeley, CA, USA.
Paolo BrambillaDepartment of Laboratory Medicine, University of Milano-Bicocca, School of Medicine, Hospital of Desio, Desio-Milano, Italy.
Stefano SignoriniDepartment of Laboratory Medicine, University of Milano-Bicocca, School of Medicine, Hospital of Desio, Desio-Milano, Italy.
Paolo MocarelliDepartment of Laboratory Medicine, University of Milano-Bicocca, School of Medicine, Hospital of Desio, Desio-Milano, Italy.
Brenda EskenaziCenter for Environmental Research and Children's Health (CERCH), School of Public Health, University of California at Berkeley, Berkeley, CA, USA.
Center for Environmental Health · USUniversity of Milano-Bicocca · IT

Funding

In Utero Dioxin Exposure in Seveso, Italy and Health of the Second GenerationR01ES007171 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI ESKENAZI, BRENDA · 1996 to 2017
$7.1M
ENDOMETRIOSIS AND DIOXIN EXPOSURE OF RESIDENTS OF SEVESOF06TW002075 · FIC · UNIVERSITY OF CALIFORNIA BERKELEY · PI ESKENAZI, BRENDA · 1994 to 1994
–
FIC NIH HHS F06 TW002075NIEHS NIH HHS R01 ES007171
6 · The paper itself

Abstract

backgroundExposure to endocrine disrupting compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during susceptible developmental windows may alter risk of metabolic disease later in life. Animal studies of in utero and lactational TCDD exposure report associations with alterations in insulin sensitivity and energy homeostasis, but epidemiologic evidence is limited. We examined the relationship of prenatal TCDD exposure with markers of glucose homeostasis in the Seveso Second Generation study, a unique cohort of children born to TCDD-exposed women resulting from a 1976 explosion in Seveso, Italy.

methodsWe included 426 children who were 18 years or older with complete follow-up data including a fasting blood draw. Insulin and glucose were measured and the updated homoeostatic model assessment was used to estimate insulin resistance (HOMA2-IR) and beta-cell function (HOMA2-B). Prenatal TCDD exposure was defined in two ways, as initial maternal serum TCDD concentration and TCDD estimated at pregnancy.

resultsThe children (222 female, 204 male) averaged 28.6 (±6.0) years. We found a 10-fold increase in TCDD estimated at pregnancy was inversely associated with insulin (adj-β = -1.24 μIU/mL, 95% confidence interval (CI): -2.38, -0.09) and HOMA2-B (adj-β = -10.2% decrease, 95% CI: -17.8, -1.9) among daughters, but not sons (insulin: adj-β = 0.57 μIU/mL, 95% CI: -0.84, 1.98, P for interaction = 0.04; and HOMA2-B: adj-β = 0.8% increase, 95% CI -10.7, 13.9, P for interaction = 0.11). Similar effect modification was observed for TCDD estimated at pregnancy and HOMA2-IR (P for interaction = 0.13). The models for initial maternal serum TCDD showed similar effect modification by child sex. The observed associations in daughters showed evidence of mediation by body mass index, which we have previously found to be associated with prenatal TCDD exposure in female offspring.

conclusionThese results suggest prenatal exposure to TCDD is associated with lower insulin resistance and beta compensation in female offspring, and show evidence of mediation by body mass index.

Indexed as

Prenatal Exposure Delayed EffectsAdolescentAdultChildDioxinsEndocrine DisruptorsFemaleGlucoseHumansItalyMalePolychlorinated DibenzodioxinsPregnancyYoung AdultDioxinsEndocrine DisruptorsGlucosePolychlorinated Dibenzodioxins2,3,7,8-Tetrachlorodibenzo-p-dioxinDioxinGlucose metabolism markersInsulinSevesoTCDD

Identifiers

PMID31726365
PMCPMC6904529
OpenAlexW2987442101

What OpenQuestion holds

Textmetadata
LicenceTDM
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.