Early-Life Environmental Exposures and Blood Pressure in Children.
Blood Pressure
/ drug effects
Blood Pressure Determination
/ methods
Built Environment
Child
Dichlorodiphenyl Dichloroethylene
/ analysis
Environmental Exposure
/ adverse effects
Environmental Pollutants
/ adverse effects
Europe
/ epidemiology
Female
Holistic Health
Humans
Hypertension
/ diagnosis
Insecticides
/ adverse effects
Male
Meteorological Concepts
Polychlorinated Biphenyls
/ analysis
Pregnancy
Prenatal Exposure Delayed Effects
/ blood
blood pressure
chemicals
children
cohort
environment
epidemiology
exposome
Journal
Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365
Informations de publication
Date de publication:
10 09 2019
10 09 2019
Historique:
received:
05
12
2018
revised:
26
04
2019
accepted:
24
06
2019
entrez:
7
9
2019
pubmed:
7
9
2019
medline:
20
5
2020
Statut:
ppublish
Résumé
Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously. This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children. Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously. Decreases in systolic BP were observed with facility density (β change for an interquartile-range increase in exposure: -1.7 mm Hg [95% confidence interval (CI): -2.5 to -0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (-1.4 mm Hg [95% CI: -2.6 to -0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: -1.6 mm Hg [95% CI: -2.4 to -0.7 mm Hg]), hexachlorobenzene (-1.5 mm Hg [95% CI: -2.4 to -0.6 mm Hg]), and mono-benzyl phthalate (-0.7 mm Hg [95% CI: -1.3 to -0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (-1.4 mm Hg [95% CI: -2.3 to -0.5 mm Hg]) and child DDE concentrations (-1.1 mm Hg [95% CI: -1.9 to -0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: -0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg]). This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children.
Sections du résumé
BACKGROUND
Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously.
OBJECTIVES
This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children.
METHODS
Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously.
RESULTS
Decreases in systolic BP were observed with facility density (β change for an interquartile-range increase in exposure: -1.7 mm Hg [95% confidence interval (CI): -2.5 to -0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (-1.4 mm Hg [95% CI: -2.6 to -0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: -1.6 mm Hg [95% CI: -2.4 to -0.7 mm Hg]), hexachlorobenzene (-1.5 mm Hg [95% CI: -2.4 to -0.6 mm Hg]), and mono-benzyl phthalate (-0.7 mm Hg [95% CI: -1.3 to -0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (-1.4 mm Hg [95% CI: -2.3 to -0.5 mm Hg]) and child DDE concentrations (-1.1 mm Hg [95% CI: -1.9 to -0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: -0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg]).
CONCLUSIONS
This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children.
Identifiants
pubmed: 31488269
pii: S0735-1097(19)35959-5
doi: 10.1016/j.jacc.2019.06.069
pmc: PMC8713646
mid: NIHMS1759258
pii:
doi:
Substances chimiques
Environmental Pollutants
0
Insecticides
0
Dichlorodiphenyl Dichloroethylene
4M7FS82U08
Polychlorinated Biphenyls
DFC2HB4I0K
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1317-1328Subventions
Organisme : NIEHS NIH HHS
ID : P30 ES007048
Pays : United States
Organisme : Medical Research Council
ID : MR/K021656/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/K006665/1
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : U01 NS047537
Pays : United States
Organisme : NIEHS NIH HHS
ID : N01ES75558
Pays : United States
Organisme : Medical Research Council
ID : G0601712
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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