Exposure to a mixture of non-persistent environmental chemicals and neonatal thyroid function in a cohort with improved exposure assessment
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,...
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| Published in: | Environment international Vol. 173; p. 107840 |
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| Main Authors: | , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Elsevier Ltd
01.03.2023
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| ISSN: | 0160-4120, 1873-6750, 1873-6750 |
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| Abstract | 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. |
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| AbstractList | 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, tri- closan, 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. 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.BACKGROUNDIn 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.METHODSThe 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.RESULTSInteraction 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.CONCLUSIONOur 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. 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. 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. 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. |
| ArticleNumber | 107840 |
| Author | Malatesta, Andres Philippat, Claire Pin, Isabelle Sakhi, Amrit K. Sophie Gauchez, Anne Guergour, Dorra Coiffier, Ophélie Sabaredzovic, Azemira Nakiwala, Dorothy Rolland, Matthieu Faure, Patrice Slama, Rémy Corne, Christelle Lyon-Caen, Sarah Chovelon, Benoît Thomsen, Cathrine |
| Author_xml | – sequence: 1 givenname: Ophélie surname: Coiffier fullname: Coiffier, Ophélie organization: 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 – sequence: 2 givenname: Dorothy surname: Nakiwala fullname: Nakiwala, Dorothy organization: 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 – sequence: 3 givenname: Matthieu surname: Rolland fullname: Rolland, Matthieu organization: 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 – sequence: 4 givenname: Andres surname: Malatesta fullname: Malatesta, Andres organization: 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 – sequence: 5 givenname: Sarah surname: Lyon-Caen fullname: Lyon-Caen, Sarah organization: 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 – sequence: 6 givenname: Benoît surname: Chovelon fullname: Chovelon, Benoît organization: Département de Pharmacochimie Moléculaire, Université Grenoble Alpes, CNRS, UMR 5063, F-38041 Grenoble, France – sequence: 7 givenname: Patrice surname: Faure fullname: Faure, Patrice organization: Département de Pharmacochimie Moléculaire, Université Grenoble Alpes, CNRS, UMR 5063, F-38041 Grenoble, France – sequence: 8 givenname: Anne surname: Sophie Gauchez fullname: Sophie Gauchez, Anne organization: Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France – sequence: 9 givenname: Dorra surname: Guergour fullname: Guergour, Dorra organization: Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France – sequence: 10 givenname: Amrit K. orcidid: 0000-0002-2918-323X surname: Sakhi fullname: Sakhi, Amrit K. organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 11 givenname: Azemira surname: Sabaredzovic fullname: Sabaredzovic, Azemira organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 12 givenname: Cathrine orcidid: 0000-0002-6889-7868 surname: Thomsen fullname: Thomsen, Cathrine organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 13 givenname: Isabelle surname: Pin fullname: Pin, Isabelle organization: Pediatric Department, Grenoble University Hospital, 38700 La Tronche, France – sequence: 14 givenname: Rémy surname: Slama fullname: Slama, Rémy organization: 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 – sequence: 15 givenname: Christelle orcidid: 0000-0003-1424-8157 surname: Corne fullname: Corne, Christelle organization: Service de Biochimie SB2TE, Institut de Biologie et Pathologie CHU Grenoble Alpes, France – sequence: 16 givenname: Claire orcidid: 0000-0002-4959-6648 surname: Philippat fullname: Philippat, Claire email: claire.philippat@inserm.fr organization: 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 |
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| Copyright | 2023 The Authors Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved. Distributed under a Creative Commons Attribution 4.0 International License |
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| Keywords | MEHP oxo-MINCH DiNP MMCHP Heel-prick blood spot Mixture MBzP oxo-MiNP Bisphenols ΣDiNP DEHP OH-MPHP Thyroid hormones ΣDINCH T3 WHO LOD T4 MEOHP MEHHP TSH MnBP Oh-MINCH Phthalates DINCH DEP MiBP Parabens LOQ Oh-MiNP BKMR ΣDEHP MECPP MEP cx-MiNP |
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| Snippet | In vitro and toxicological studies have shown that non-persistent environmental chemicals can perturb thyroid hormone homeostasis. Epidemiological studies with... Background: In vitro and toxicological studies have shown that non-persistent environmental chemicals can perturb thyroid hormone homeostasis. Epidemiological... |
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| StartPage | 107840 |
| SubjectTerms | Bayes Theorem Bayesian theory benzophenones Bisphenols blood serum children DINCH environment Environmental Exposure - adverse effects Environmental Pollutants - urine Environmental Sciences exposure assessment Female Heel-prick blood spot homeostasis Hormones Humans Infant, Newborn iodine Male maternal exposure metabolites Mixture Parabens Parabens - analysis Phthalates Phthalic Acids - toxicity Phthalic Acids - urine Pregnancy Prenatal Exposure Delayed Effects regression analysis selenium thyroid function Thyroid Gland Thyroid Hormones Thyrotropin thyroxine triclosan Triclosan - toxicity urine |
| Title | Exposure to a mixture of non-persistent environmental chemicals and neonatal thyroid function in a cohort with improved exposure assessment |
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