Prenatal and postnatal exposure to PFAS and cardiometabolic factors and inflammation status in children from six European cohorts.


Journal

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

Informations de publication

Date de publication:
12 2021
Historique:
received: 04 05 2021
revised: 27 08 2021
accepted: 30 08 2021
pubmed: 10 9 2021
medline: 21 10 2021
entrez: 9 9 2021
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 34500361
pii: S0160-4120(21)00478-5
doi: 10.1016/j.envint.2021.106853
pii:
doi:

Substances chimiques

Alkanesulfonic Acids 0
Environmental Pollutants 0
Fluorocarbons 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

106853

Subventions

Organisme : Department of Health
ID : RP-PG-0407-10044
Pays : United Kingdom
Organisme : NIEHS NIH HHS
ID : R01 ES029944
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030691
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030364
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES029681
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES028903
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES007048
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA196569
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA140561
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES016813
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES029944
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK048522
Pays : United States

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Eleni Papadopoulou (E)

Norwegian Institute of Public Health, Oslo, Norway. Electronic address: elpa@fhi.no.

Nikos Stratakis (N)

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA; Department of Complex Genetics and Epidemiology, CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, the Netherlands.

Xavier Basagaña (X)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Anne Lise Brantsæter (AL)

Norwegian Institute of Public Health, Oslo, Norway.

Maribel Casas (M)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Serena Fossati (S)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Regina Gražulevičienė (R)

Department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania.

Line Småstuen Haug (L)

Norwegian Institute of Public Health, Oslo, Norway.

Barbara Heude (B)

Centre for Research in Epidemiology and Statistics, INSERM, Université de Paris, INRAe, Paris, France.

Léa Maitre (L)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Rosemary R C McEachan (RRC)

Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.

Oliver Robinson (O)

MRC Centre for Environment and Health, School of Public Health, Imperial College London, UK.

Theano Roumeliotaki (T)

Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece.

Eduard Sabidó (E)

Proteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain.

Eva Borràs (E)

Proteomics Unit, Centre de Regulació Genòmica, Barcelona Institute of Science and Technology, Barcelona, Spain.

Jose Urquiza (J)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Marina Vafeiadi (M)

Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece.

Yinqi Zhao (Y)

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.

Rémy Slama (R)

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.

John Wright (J)

Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.

David V Conti (DV)

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.

Martine Vrijheid (M)

ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiologia y Salud Pública (CIBERESP), Madrid, Spain.

Lida Chatzi (L)

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.

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