Prenatal and postnatal exposure to PFAS and cardiometabolic factors and inflammation status in children from six European cohorts
•PFAS mixture exposure was associated with higher HDL cholesterol and lower waist circumference.•Postnatal PFAS were the main contributors to the identified mixtures.•Prenatal PFOA was positively related with the pro-inflammatory biomarker IL-1beta. Developing children are particularly vulnerable to...
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| Published in: | Environment international Vol. 157; p. 106853 |
|---|---|
| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Netherlands
Elsevier Ltd
01.12.2021
Elsevier |
| Subjects: | |
| ISSN: | 0160-4120, 1873-6750, 1873-6750 |
| Online Access: | Get full text |
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| Abstract | •PFAS mixture exposure was associated with higher HDL cholesterol and lower waist circumference.•Postnatal PFAS were the main contributors to the identified mixtures.•Prenatal PFOA was positively related with the pro-inflammatory biomarker IL-1beta.
Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children.
We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins.
In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6–12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network.
Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC.
Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. |
|---|---|
| AbstractList | Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6-12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6–12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and metabolic syndrome (MetS) score in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range=6–12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LD-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma by protein panels and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances(PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associatedwith poor metabolic health in children.We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolichealth in children, and the role of inflammatory proteins.In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations ofPFAS in blood collected in pregnancy and at 8 years (range = 6–12 years). We applied Bayesian Kernel Machineregression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolicfactors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP),and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C)cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying roleof inflammatory status for the exposure-outcome association by integrating the three panels into a network.Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associatedwith WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture,prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC andthese were opposing directions from the overall mixture. Further, the network consisted of five distinct communitiesconnected with positive and negative correlations. The selected inflammatory biomarkers were positively,while the postnatal PFAS were negatively related with the included cardiometabolic factors, and onlyprenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC.Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorablelipidemic profile and adiposity in childhood. •PFAS mixture exposure was associated with higher HDL cholesterol and lower waist circumference.•Postnatal PFAS were the main contributors to the identified mixtures.•Prenatal PFOA was positively related with the pro-inflammatory biomarker IL-1beta. Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6–12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6-12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood.Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6-12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. |
| ArticleNumber | 106853 |
| Author | Chatzi, Lida Urquiza, Jose Wright, John Papadopoulou, Eleni Heude, Barbara McEachan, Rosemary R.C. Sabidó, Eduard Borràs, Eva Gražulevičienė, Regina Casas, Maribel Fossati, Serena Robinson, Oliver Maitre, Léa Vrijheid, Martine Stratakis, Nikos Roumeliotaki, Theano Zhao, Yinqi Conti, David V. Basagaña, Xavier Brantsæter, Anne Lise Småstuen Haug, Line Slama, Rémy Vafeiadi, Marina |
| AuthorAffiliation | 3. Department of Complex Genetics and Epidemiology, CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, The Netherlands 13. Team of Environmental Epidemiology applied to Reproduction and Respiratory Health, Inserm, CNRS, University Grenoble Alpes, Institute of Advanced Biosciences, Joint research center (U1209), La Tronche, Grenoble, France 2. Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA 7. Department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania 4. ISGlobal, Barcelona, Spain 6. CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain 10. MRC Centre for Environment and Health, School of Public Health, Imperial College London, UK 1. Norwegian Institute of Public Health, Oslo, Norway 11. Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece 9. Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Founda |
| AuthorAffiliation_xml | – name: 10. MRC Centre for Environment and Health, School of Public Health, Imperial College London, UK – name: 9. Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – name: 12. Proteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain – name: 1. Norwegian Institute of Public Health, Oslo, Norway – name: 5. Universitat Pompeu Fabra (UPF), Barcelona, Spain – name: 3. Department of Complex Genetics and Epidemiology, CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, The Netherlands – name: 2. Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA – name: 6. CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain – name: 11. Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece – name: 7. Department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania – name: 4. ISGlobal, Barcelona, Spain – name: 13. Team of Environmental Epidemiology applied to Reproduction and Respiratory Health, Inserm, CNRS, University Grenoble Alpes, Institute of Advanced Biosciences, Joint research center (U1209), La Tronche, Grenoble, France – name: 8. Centre for Research in Epidemiology and Statistics, INSERM, Université de Paris, INRAe, Paris, France |
| Author_xml | – sequence: 1 givenname: Eleni surname: Papadopoulou fullname: Papadopoulou, Eleni email: elpa@fhi.no organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 2 givenname: Nikos surname: Stratakis fullname: Stratakis, Nikos organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA – sequence: 3 givenname: Xavier surname: Basagaña fullname: Basagaña, Xavier organization: ISGlobal, Barcelona, Spain – sequence: 4 givenname: Anne Lise surname: Brantsæter fullname: Brantsæter, Anne Lise organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 5 givenname: Maribel surname: Casas fullname: Casas, Maribel organization: ISGlobal, Barcelona, Spain – sequence: 6 givenname: Serena surname: Fossati fullname: Fossati, Serena organization: ISGlobal, Barcelona, Spain – sequence: 7 givenname: Regina surname: Gražulevičienė fullname: Gražulevičienė, Regina organization: Department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania – sequence: 8 givenname: Line surname: Småstuen Haug fullname: Småstuen Haug, Line organization: Norwegian Institute of Public Health, Oslo, Norway – sequence: 9 givenname: Barbara surname: Heude fullname: Heude, Barbara organization: Centre for Research in Epidemiology and Statistics, INSERM, Université de Paris, INRAe, Paris, France – sequence: 10 givenname: Léa surname: Maitre fullname: Maitre, Léa organization: ISGlobal, Barcelona, Spain – sequence: 11 givenname: Rosemary R.C. surname: McEachan fullname: McEachan, Rosemary R.C. organization: Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – sequence: 12 givenname: Oliver surname: Robinson fullname: Robinson, Oliver organization: MRC Centre for Environment and Health, School of Public Health, Imperial College London, UK – sequence: 13 givenname: Theano surname: Roumeliotaki fullname: Roumeliotaki, Theano organization: Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece – sequence: 14 givenname: Eduard surname: Sabidó fullname: Sabidó, Eduard organization: Proteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain – sequence: 15 givenname: Eva surname: Borràs fullname: Borràs, Eva organization: Proteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain – sequence: 16 givenname: Jose surname: Urquiza fullname: Urquiza, Jose organization: ISGlobal, Barcelona, Spain – sequence: 17 givenname: Marina surname: Vafeiadi fullname: Vafeiadi, Marina organization: Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece – sequence: 18 givenname: Yinqi surname: Zhao fullname: Zhao, Yinqi organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA – sequence: 19 givenname: Rémy surname: Slama fullname: Slama, Rémy organization: Team of Environmental Epidemiology applied to Reproduction and Respiratory Health, Inserm, CNRS, University Grenoble Alpes, Institute of Advanced Biosciences, Joint research center (U1209), La Tronche, Grenoble, France – sequence: 20 givenname: John surname: Wright fullname: Wright, John organization: Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK – sequence: 21 givenname: David V. surname: Conti fullname: Conti, David V. organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA – sequence: 22 givenname: Martine surname: Vrijheid fullname: Vrijheid, Martine organization: ISGlobal, Barcelona, Spain – sequence: 23 givenname: Lida surname: Chatzi fullname: Chatzi, Lida organization: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA |
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| ContentType | Journal Article |
| Copyright | 2021 The Authors Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved. Distributed under a Creative Commons Attribution 4.0 International License |
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| Snippet | •PFAS mixture exposure was associated with higher HDL cholesterol and lower waist circumference.•Postnatal PFAS were the main contributors to the identified... Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting... Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances(PFAS), a group of endocrine disrupting... |
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| StartPage | 106853 |
| SubjectTerms | Adiposity Alkanesulfonic Acids Bayes Theorem Bayesian theory biomarkers BKMR Cardiometabolic risk Cardiovascular Diseases childhood children cholesterol environment Environmental Pollutants - toxicity exposome Female Fluorocarbons - toxicity HDL high density lipoprotein Humans Inflammation Inflammation - chemically induced interleukin-1beta Life Sciences low density lipoprotein perfluorohexane sulfonic acid PFAS Pregnancy Santé publique et épidémiologie waist circumference |
| Title | Prenatal and postnatal exposure to PFAS and cardiometabolic factors and inflammation status in children from six European cohorts |
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