Exposure to a mixture of non-persistent environmental chemicals and neonatal thyroid function in a cohort with improved exposure assessment.


Journal

Environment international
ISSN: 1873-6750
Titre abrégé: Environ Int
Pays: Netherlands
ID NLM: 7807270

Informations de publication

Date de publication:
03 2023
Historique:
received: 13 09 2022
revised: 13 02 2023
accepted: 17 02 2023
pubmed: 2 3 2023
medline: 22 3 2023
entrez: 1 3 2023
Statut: ppublish

Résumé

In vitro and toxicological studies have shown that non-persistent environmental chemicals can perturb thyroid hormone homeostasis. Epidemiological studies with improved exposure assessment (i.e., repeated urine samples) are needed to evaluate effects of these compounds, individually or as a mixture, in humans. We studied the associations between prenatal exposure to non-persistent environmental chemicals and neonatal thyroid hormones. The study population consisted of 442 mother-child pairs from the French SEPAGES mother-child cohort recruited between July 2014 and July 2017. For each participant, four parabens, five bisphenols, triclosan, triclocarban, benzophenone-3 as well as metabolites of phthalates and of di(isononyl)cyclohexane-1,2-dicarboxylate were assessed in two pools of repeated urine samples (median: 21 spot urines per pool), collected in the 2nd and 3rd trimesters of pregnancy, respectively. Thyroid stimulating hormone (TSH) and total thyroxine (T4) levels were determined in newborns from a heel-prick blood spot. Maternal iodine and selenium were assessed in urine and serum, respectively. Adjusted linear regression (uni-pollutant model) and Bayesian Kernel Machine Regression (BKMR, mixture model) were applied to study overall and sex-stratified associations between chemicals and hormone concentrations. Interaction with child sex was detected for several compounds. Triclosan, three parabens, and one phthalate metabolite (OH-MPHP) were negatively associated with T4 among girls in the uni-pollutant model. BKMR also suggested a negative association between the mixture and T4 in girls, whereas in boys the association was positive. The mixture was not linked to TSH levels, and for this hormone the uni-pollutant model revealed associations with only a few compounds. Our study, based on repeated urine samples to assess exposure, showed that prenatal exposure to some phenols and phthalates disturb thyroid hormone homeostasis at birth. Furthermore, both uni-pollutant and mixture models, suggested effect modification by child sex, while, to date underlying mechanisms for such sex-differences are not well understood.

Sections du résumé

BACKGROUND
In vitro and toxicological studies have shown that non-persistent environmental chemicals can perturb thyroid hormone homeostasis. Epidemiological studies with improved exposure assessment (i.e., repeated urine samples) are needed to evaluate effects of these compounds, individually or as a mixture, in humans. We studied the associations between prenatal exposure to non-persistent environmental chemicals and neonatal thyroid hormones.
METHODS
The study population consisted of 442 mother-child pairs from the French SEPAGES mother-child cohort recruited between July 2014 and July 2017. For each participant, four parabens, five bisphenols, triclosan, triclocarban, benzophenone-3 as well as metabolites of phthalates and of di(isononyl)cyclohexane-1,2-dicarboxylate were assessed in two pools of repeated urine samples (median: 21 spot urines per pool), collected in the 2nd and 3rd trimesters of pregnancy, respectively. Thyroid stimulating hormone (TSH) and total thyroxine (T4) levels were determined in newborns from a heel-prick blood spot. Maternal iodine and selenium were assessed in urine and serum, respectively. Adjusted linear regression (uni-pollutant model) and Bayesian Kernel Machine Regression (BKMR, mixture model) were applied to study overall and sex-stratified associations between chemicals and hormone concentrations.
RESULTS
Interaction with child sex was detected for several compounds. Triclosan, three parabens, and one phthalate metabolite (OH-MPHP) were negatively associated with T4 among girls in the uni-pollutant model. BKMR also suggested a negative association between the mixture and T4 in girls, whereas in boys the association was positive. The mixture was not linked to TSH levels, and for this hormone the uni-pollutant model revealed associations with only a few compounds.
CONCLUSION
Our study, based on repeated urine samples to assess exposure, showed that prenatal exposure to some phenols and phthalates disturb thyroid hormone homeostasis at birth. Furthermore, both uni-pollutant and mixture models, suggested effect modification by child sex, while, to date underlying mechanisms for such sex-differences are not well understood.

Identifiants

pubmed: 36857904
pii: S0160-4120(23)00113-7
doi: 10.1016/j.envint.2023.107840
pii:
doi:

Substances chimiques

Parabens 0
Triclosan 4NM5039Y5X
Thyroid Hormones 0
Hormones 0
Environmental Pollutants 0
Thyrotropin 9002-71-5
Phthalic Acids 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

107840

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Ophélie Coiffier (O)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Dorothy Nakiwala (D)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Matthieu Rolland (M)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Andres Malatesta (A)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Sarah Lyon-Caen (S)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Benoît Chovelon (B)

Département de Pharmacochimie Moléculaire, Université Grenoble Alpes, CNRS, UMR 5063, F-38041 Grenoble, France; Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France.

Patrice Faure (P)

Département de Pharmacochimie Moléculaire, Université Grenoble Alpes, CNRS, UMR 5063, F-38041 Grenoble, France; Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France.

Anne Sophie Gauchez (A)

Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France.

Dorra Guergour (D)

Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France.

Amrit K Sakhi (AK)

Norwegian Institute of Public Health, Oslo, Norway.

Azemira Sabaredzovic (A)

Norwegian Institute of Public Health, Oslo, Norway.

Cathrine Thomsen (C)

Norwegian Institute of Public Health, Oslo, Norway.

Isabelle Pin (I)

Pediatric Department, Grenoble University Hospital, 38700 La Tronche, France.

Rémy Slama (R)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France.

Christelle Corne (C)

Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France.

Claire Philippat (C)

University Grenoble Alpes, Inserm U1209, CNRS UMR 5309, Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Institute for Advanced Biosciences, 38000 Grenoble, France. Electronic address: claire.philippat@inserm.fr.

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Classifications MeSH