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Abstracts
24 September 2018
ISES-ISEE 2018 Joint Annual Meeting: Addressing Complex Local and Global Issues in Environmental Exposure and Health

The Early Life Exposome: Associations with Child Lipid Profile

Publication: ISEE Conference Abstracts
Volume 2018, Issue 1

Abstract

Background: High cholesterol levels during childhood have been associated with increased risk of atherosclerosis later in life. Apart from traditional risk factors for dyslipidemia, such as high fat diet and obesity, the contribution of environmental exposures on variations in lipid levels in childhood, is unclear.Aim: To assess the impact of a wide array of environmental exposures during pregnancy and childhood on lipid profiles in children using an exposome-wide approach.Methods: Within the HELIX exposome project, we measured over 90 prenatal and 110 childhood environmental exposures in 1,301 mother-child pairs from 6 European countries. We also measured in 2-hour fasting plasma samples, total (TC), high-density (HDL), low-density (LDL) lipoprotein cholesterol, and triglyceride (TG) levels at the age of 6-11 years. Associations were assessed using agnostic exposome-wide analyses (ExWAS) correcting for multiple comparisons.Results: Childhood exposure to organochlorine compounds was associated with increased lipids. Exposure to hexachlorobenzene (HCB) was associated with higher TC, LDL and TG levels (mean change per IQR increase: 6.6 mg/dL, 95% CI: 4.4 to 8.8; 5.7 mg/dL, 95% CI: 3.6 to 7.8 and 6.0 mg/dl, 95% CI: 2.6 to 9.4 respectively) after multiple testing correction. Dichlorodiphenyltrichloroethane (DDT) and polychlorinated biphenyls (PCBs) childhood levels were also associated with increased TGs (6.9 mg/dl, 95% CI: 3.4 to 10.4 and 9.6 mg/dl, 95% CI: 5.4 to 13.9 respectively). Childhood exposure to polybrominated diphenyl ether (PBDE 153) was associated with a 5.2 mg/dL change in TC (95% CI: 2.6 to 7.8), while copper exposure was associated with a -1.7 mg/dL change in HDL (95% CI: -2.7 to -0.8) and a 3.3 mg/dL change in LDL (95% CI: 1.5 to 5.1).Conclusions: Children with higher exposure to organochlorine compounds and copper had higher levels of lipids. Further work is needed to examine the underlying mechanisms and to exclude the role of reverse causation.

Information & Authors

Information

Published In

ISEE Conference Abstracts
Volume 2018Issue 124 September 2018

History

Published online: 24 September 2018

Keywords

  1. Biomarkers/Biomonitoring/Exposome
  2. Children
  3. Endocrine Disrupters

Authors

Affiliations

Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece, [email protected]
Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece, [email protected]
Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Greece, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
Department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
Team of Environmental Epidemiology applied to Reproduction and Respiratory Health, U1209, Inserm (Institut national de la santé et de la recherché médicale), IAB (Institute for Advanced Biosciences), CNRS (Centre national de la recherche scientifique), University Grenoble Alpes, Grenoble, France, [email protected]
Department of Environmental Exposure and Epidemiology, Division of Infection Control, Environment and Health, Norwegian Institute of Public Health, Oslo, Norway, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, United Kingdom, [email protected]
ISGlobal, Insititute for Global Health, Barcelona, Spain, [email protected]
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, United States, [email protected]

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