Prenatal exposure to multiple organochlorine compounds and childhood body mass index.

Bayesian varying coefficient kernel machine regressions Bayesian weighted quantile sum regressions Body mass index Chemical mixture Organochlorine compounds Outcome trajectories

Journal

Environmental epidemiology (Philadelphia, Pa.)
ISSN: 2474-7882
Titre abrégé: Environ Epidemiol
Pays: United States
ID NLM: 101719527

Informations de publication

Date de publication:
Jun 2022
Historique:
received: 22 07 2021
accepted: 17 02 2022
entrez: 15 6 2022
pubmed: 16 6 2022
medline: 16 6 2022
Statut: epublish

Résumé

Prenatal exposure to organochlorine compounds (OCs) has been associated with increased childhood body mass index (BMI); however, only a few studies have focused on longitudinal BMI trajectories, and none of them used multiple exposure mixture approaches. To determine the association between We applied three approaches: (1) linear mixed-effect regressions (LMR) to associate individual compounds with BMI measures; (2) Bayesian weighted quantile sum regressions (BWQSR) to provide an overall OC mixture association with BMI measures; and (3)Bayesian varying coefficient kernel machine regressions (BVCKMR) to model nonlinear and nonadditive associations. In the LMR, yearly change of BMI measures was consistently associated with a quartile increase in hexachlorobenzene (HCB) (estimate [95% Confidence or Credible interval] BMI: 0.10 [0.06, 0.14]; BMI z-score: 0.02 [0.01, 0.04]). BWQSR results showed that a quartile increase in mixture concentrations was associated with yearly increase of BMI measures (BMI: 0.10 [0.01, 0.18]; BMI z-score: 0.03 [0.003, 0.06]). In the BVCKMR, a quartile increase in dichlorodiphenyldichloroethylene concentrations was associated with higher BMI measures at 4 years (BMI: 0.33 [0.24, 0.43]; BMI z-score: 0.19 [0.15, 0.24]); whereas a quartile increase in HCB and polychlorinated biphenyls (PCB)-118 levels was positively associated with BMI measures yearly change (BMI: HCB:0.10 [0.07, 0.13], PCB-118:0.08 [0.04, 012]; BMI z-score: HCB:0.03 [0.02, 0.05], PCB-118:0.02 [0.002,04]). BVCKMR suggested that PCBs had nonlinear relationships with BMI measures, and HCB interacted with other compounds. All analyses consistently demonstrated detrimental associations between prenatal OC exposures and childhood BMI measures.

Sections du résumé

Background UNASSIGNED
Prenatal exposure to organochlorine compounds (OCs) has been associated with increased childhood body mass index (BMI); however, only a few studies have focused on longitudinal BMI trajectories, and none of them used multiple exposure mixture approaches.
Aim UNASSIGNED
To determine the association between
Methods UNASSIGNED
We applied three approaches: (1) linear mixed-effect regressions (LMR) to associate individual compounds with BMI measures; (2) Bayesian weighted quantile sum regressions (BWQSR) to provide an overall OC mixture association with BMI measures; and (3)Bayesian varying coefficient kernel machine regressions (BVCKMR) to model nonlinear and nonadditive associations.
Results UNASSIGNED
In the LMR, yearly change of BMI measures was consistently associated with a quartile increase in hexachlorobenzene (HCB) (estimate [95% Confidence or Credible interval] BMI: 0.10 [0.06, 0.14]; BMI z-score: 0.02 [0.01, 0.04]). BWQSR results showed that a quartile increase in mixture concentrations was associated with yearly increase of BMI measures (BMI: 0.10 [0.01, 0.18]; BMI z-score: 0.03 [0.003, 0.06]). In the BVCKMR, a quartile increase in dichlorodiphenyldichloroethylene concentrations was associated with higher BMI measures at 4 years (BMI: 0.33 [0.24, 0.43]; BMI z-score: 0.19 [0.15, 0.24]); whereas a quartile increase in HCB and polychlorinated biphenyls (PCB)-118 levels was positively associated with BMI measures yearly change (BMI: HCB:0.10 [0.07, 0.13], PCB-118:0.08 [0.04, 012]; BMI z-score: HCB:0.03 [0.02, 0.05], PCB-118:0.02 [0.002,04]). BVCKMR suggested that PCBs had nonlinear relationships with BMI measures, and HCB interacted with other compounds.
Conclusions UNASSIGNED
All analyses consistently demonstrated detrimental associations between prenatal OC exposures and childhood BMI measures.

Identifiants

pubmed: 35702503
doi: 10.1097/EE9.0000000000000201
pmc: PMC9187184
doi:

Types de publication

Journal Article

Langues

eng

Pagination

e201

Informations de copyright

Copyright © 2022 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.

Déclaration de conflit d'intérêts

The authors declare that they have no conflicts of interest with regard to the content of this report.

Références

Environ Health Perspect. 2005 Jul;113(7):853-7
pubmed: 16002372
Toxicology. 2001 Feb 14;158(3):141-53
pubmed: 11275356
Mol Cell Biochem. 2012 Jun;365(1-2):275-8
pubmed: 22350817
Environ Int. 2010 Aug;36(6):577-83
pubmed: 20471680
PLoS One. 2011 Jan 26;6(1):e15977
pubmed: 21298090
Environ Int. 2021 Jun;151:106469
pubmed: 33711537
Toxicol In Vitro. 2011 Feb;25(1):394-402
pubmed: 21044676
Biochem Pharmacol. 2002 Mar 1;63(5):997-1007
pubmed: 11911853
Curr Opin Pediatr. 2020 Apr;32(2):315-320
pubmed: 31934891
Environ Health Perspect. 2010 May;118(5):712-9
pubmed: 20056561
Obesity (Silver Spring). 2014 Feb;22(2):488-96
pubmed: 23963708
Environ Health Perspect. 2015 Oct;123(10):1030-7
pubmed: 25956007
Environ Health Perspect. 2012 Feb;120(2):316-20
pubmed: 22204795
Am J Epidemiol. 2017 Jan 1;185(1):30-39
pubmed: 27927620
Prev Med. 2011 May;52(5):300-4
pubmed: 21371500
Int J Obes (Lond). 2011 Jul;35(7):891-8
pubmed: 20975725
Pediatrics. 1998 Mar;101(3 Pt 2):518-25
pubmed: 12224658
Int J Obes Relat Metab Disord. 1999 Mar;23 Suppl 2:S2-11
pubmed: 10340798
Environ Health Perspect. 2013 May;121(5):631-6
pubmed: 23512307
Environ Health Perspect. 2015 Oct;123(10):1015-21
pubmed: 25910281
Toxicol Lett. 2008 Dec 15;183(1-3):65-71
pubmed: 18992306
Arch Pediatr Adolesc Med. 2012 Oct;166(10):952-8
pubmed: 23367522
Int J Obes (Lond). 2013 Jan;37(1):94-100
pubmed: 22846775
Environ Int. 2018 Apr;113:231-239
pubmed: 29453090
J Pediatr Endocrinol Metab. 2005 Dec;18 Suppl 1:1145-55
pubmed: 16398443
Reprod Toxicol. 2017 Mar;68:3-33
pubmed: 27760374
Acta Paediatr. 2008 Oct;97(10):1465-9
pubmed: 18665907
JAMA. 2004 Jun 16;291(23):2847-50
pubmed: 15199035
Environ Health Perspect. 2009 Jan;117(1):122-6
pubmed: 19165398
Environ Health Perspect. 2013 Sep;121(9):1103-9
pubmed: 23799652
Environ Health Perspect. 2019 Feb;127(2):26001
pubmed: 30720337
Eur J Endocrinol. 2006 May;154(5):599-611
pubmed: 16645005
Environ Health. 2010 Sep 06;9:56
pubmed: 20819217
Epidemiology. 2013 Jan;24(1):1-9
pubmed: 23211345
Environ Int. 2019 Feb;123:325-336
pubmed: 30557812
Environ Health. 2019 Aug 28;18(1):76
pubmed: 31462251
J Chromatogr A. 2013 Sep 27;1309:48-55
pubmed: 23972455
Bull World Health Organ. 2007 Sep;85(9):660-7
pubmed: 18026621
Am J Clin Nutr. 2014 Jan;99(1):5-13
pubmed: 24153349
Environ Health Perspect. 2010 Sep;118(9):1235-42
pubmed: 20444671
Environ Health Perspect. 2016 Dec 1;124(12):A227-A229
pubmed: 27905274
Stat Med. 2018 Dec 30;37(30):4680-4694
pubmed: 30277584
J Expo Sci Environ Epidemiol. 2020 Jan;30(1):16-27
pubmed: 31548623
Am J Epidemiol. 2018 Nov 1;187(11):2292-2296
pubmed: 30099488
J Epidemiol Community Health. 2014 Jan;68(1):4-5
pubmed: 23486924
Int J Epidemiol. 2017 Oct 1;46(5):1392-1393k
pubmed: 29040580
Endocr Rev. 2009 Jun;30(4):293-342
pubmed: 19502515
Int J Environ Res Public Health. 2019 Nov 08;16(22):
pubmed: 31717330
Environ Health Perspect. 2011 Feb;119(2):272-8
pubmed: 20923745
Mol Cell Endocrinol. 2009 May 25;304(1-2):19-29
pubmed: 19433244
Environ Health Perspect. 2012 Mar;120(3):451-7
pubmed: 22027556
Int J Hyg Environ Health. 2016 Jul;219(4-5):331-42
pubmed: 27216159
Environ Epidemiol. 2020 Apr 30;4(3):e092
pubmed: 32613152
Int J Environ Res Public Health. 2011 Nov;8(11):4220-37
pubmed: 22163204
Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):1023-8
pubmed: 9023376
Environ Sci Pollut Res Int. 2016 Feb;23(3):2186-200
pubmed: 26300354
Reprod Toxicol. 2017 Mar;68:145-153
pubmed: 27496715
J Sex Med. 2012 Mar;9(3):941-2
pubmed: 22239867
Psychol Bull. 2007 Jul;133(4):557-80
pubmed: 17592956

Auteurs

Elena Colicino (E)

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York.

Katerina Margetaki (K)

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece.

Damaskini Valvi (D)

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York.

Nicolo Foppa Pedretti (NF)

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York.

Nikos Stratakis (N)

ISGlobal, Barcelona, Spain.

Marina Vafeiadi (M)

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

Theano Roumeliotaki (T)

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

Soterios A Kyrtopoulos (SA)

Institute of Chemical Biology, National Hellenic Research Foundation, Athens, Greece.

Hannu Kiviranta (H)

Department of Health Security, National Institute for Health and Welfare, Kuopio, Finland.

Euripides G Stephanou (EG)

Environmental Chemical Processes Laboratory, Department of Chemistry, University of Crete, Heraklion, Greece.

Manolis Kogevinas (M)

ISGlobal, Barcelona, Spain.
Universitat Pompeu Fabra, Barcelona, Spain.
CIBER Epidemiología y Salud Pública, Barcelona, Spain.

Rob McConnell (R)

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

Kiros T Berhane (KT)

Department of Biostatistics, Mailman School of Public Health, Columbia University, New York.

Leda Chatzi (L)

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

David V Conti (DV)

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York.

Classifications MeSH