Prenatal metal mixtures and child blood pressure in the Rhea mother-child cohort in Greece.


Journal

Environmental health : a global access science source
ISSN: 1476-069X
Titre abrégé: Environ Health
Pays: England
ID NLM: 101147645

Informations de publication

Date de publication:
06 01 2021
Historique:
received: 07 08 2020
accepted: 07 12 2020
entrez: 7 1 2021
pubmed: 8 1 2021
medline: 31 8 2021
Statut: epublish

Résumé

Child blood pressure (BP) is predictive of future cardiovascular risk. Prenatal exposure to metals has been associated with higher BP in childhood, but most studies have evaluated elements individually and measured BP at a single time point. We investigated impacts of prenatal metal mixture exposures on longitudinal changes in BP during childhood and elevated BP at 11 years of age. The current study included 176 mother-child pairs from the Rhea Study in Heraklion, Greece and focused on eight elements (antimony, arsenic, cadmium, cobalt, lead, magnesium, molybdenum, selenium) measured in maternal urine samples collected during pregnancy (median gestational age at collection: 12 weeks). BP was measured at approximately 4, 6, and 11 years of age. Covariate-adjusted Bayesian Varying Coefficient Kernel Machine Regression and Bayesian Kernel Machine Regression (BKMR) were used to evaluate metal mixture impacts on baseline and longitudinal changes in BP (from ages 4 to 11) and the development of elevated BP at age 11, respectively. BKMR results were compared using static versus percentile-based cutoffs to define elevated BP. Molybdenum and lead were the mixture components most consistently associated with BP. J-shaped relationships were observed between molybdenum and both systolic and diastolic BP at age 4. Similar associations were identified for both molybdenum and lead in relation to elevated BP at age 11. For molybdenum concentrations above the inflection points (~ 40-80 μg/L), positive associations with BP at age 4 were stronger at high levels of lead. Lead was positively associated with BP measures at age 4, but only at high levels of molybdenum. Potential interactions between molybdenum and lead were also identified for BP at age 11, but were sensitive to the cutoffs used to define elevated BP. Prenatal exposure to high levels of molybdenum and lead, particularly in combination, may contribute to higher BP at age 4. These early effects appear to persist throughout childhood, contributing to elevated BP in adolescence. Future studies are needed to identify the major sources of molybdenum and lead in this population.

Sections du résumé

BACKGROUND
Child blood pressure (BP) is predictive of future cardiovascular risk. Prenatal exposure to metals has been associated with higher BP in childhood, but most studies have evaluated elements individually and measured BP at a single time point. We investigated impacts of prenatal metal mixture exposures on longitudinal changes in BP during childhood and elevated BP at 11 years of age.
METHODS
The current study included 176 mother-child pairs from the Rhea Study in Heraklion, Greece and focused on eight elements (antimony, arsenic, cadmium, cobalt, lead, magnesium, molybdenum, selenium) measured in maternal urine samples collected during pregnancy (median gestational age at collection: 12 weeks). BP was measured at approximately 4, 6, and 11 years of age. Covariate-adjusted Bayesian Varying Coefficient Kernel Machine Regression and Bayesian Kernel Machine Regression (BKMR) were used to evaluate metal mixture impacts on baseline and longitudinal changes in BP (from ages 4 to 11) and the development of elevated BP at age 11, respectively. BKMR results were compared using static versus percentile-based cutoffs to define elevated BP.
RESULTS
Molybdenum and lead were the mixture components most consistently associated with BP. J-shaped relationships were observed between molybdenum and both systolic and diastolic BP at age 4. Similar associations were identified for both molybdenum and lead in relation to elevated BP at age 11. For molybdenum concentrations above the inflection points (~ 40-80 μg/L), positive associations with BP at age 4 were stronger at high levels of lead. Lead was positively associated with BP measures at age 4, but only at high levels of molybdenum. Potential interactions between molybdenum and lead were also identified for BP at age 11, but were sensitive to the cutoffs used to define elevated BP.
CONCLUSIONS
Prenatal exposure to high levels of molybdenum and lead, particularly in combination, may contribute to higher BP at age 4. These early effects appear to persist throughout childhood, contributing to elevated BP in adolescence. Future studies are needed to identify the major sources of molybdenum and lead in this population.

Identifiants

pubmed: 33407552
doi: 10.1186/s12940-020-00685-9
pii: 10.1186/s12940-020-00685-9
pmc: PMC7789252
doi:

Substances chimiques

Environmental Pollutants 0
Metals, Heavy 0
Selenium H6241UJ22B
Arsenic N712M78A8G

Banques de données

figshare
['10.6084/m9.figshare.13535273.v1']

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

1

Subventions

Organisme : NIEHS NIH HHS
ID : R00 ES030400
Pays : United States
Organisme : NIEHS NIH HHS
ID : R00 ES024144
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030691
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01ES029944
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030364
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES028903
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 : R21 ES029681
Pays : United States
Organisme : NIEHS NIH HHS
ID : K99 ES030400
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES007048
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA196569
Pays : United States

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Auteurs

Caitlin G Howe (CG)

Department of Epidemiology, Geisel School of Medicine at Dartmouth, Dartmouth College, 1 Medical Center Dr, Lebanon, NH, 03766, USA. Caitlin.G.Howe@Dartmouth.edu.
Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA. Caitlin.G.Howe@Dartmouth.edu.

Katerina Margetaki (K)

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

Marina Vafeiadi (M)

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

Theano Roumeliotaki (T)

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

Marianna Karachaliou (M)

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

Manolis Kogevinas (M)

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

Rob McConnell (R)

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

Sandrah P Eckel (SP)

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

David V Conti (DV)

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

Maria Kippler (M)

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

Shohreh F Farzan (SF)

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

Leda Chatzi (L)

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

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