Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

In Utero Exposure to Persistent Organic Pollutants and Childhood Lipid Levels

Version 1 : Received: 3 September 2021 / Approved: 3 September 2021 / Online: 3 September 2021 (13:56:53 CEST)

A peer-reviewed article of this Preprint also exists.

Boutot, M.E.; Whitcomb, B.W.; Abdelouahab, N.; Baccarelli, A.A.; Boivin, A.; Caku, A.; Gillet, V.; Martinez, G.; Pasquier, J.-C.; Zhu, J.; Takser, L.; St-Cyr, L.; Suvorov, A. In Utero Exposure to Persistent Organic Pollutants and Childhood Lipid Levels. Metabolites 2021, 11, 657. Boutot, M.E.; Whitcomb, B.W.; Abdelouahab, N.; Baccarelli, A.A.; Boivin, A.; Caku, A.; Gillet, V.; Martinez, G.; Pasquier, J.-C.; Zhu, J.; Takser, L.; St-Cyr, L.; Suvorov, A. In Utero Exposure to Persistent Organic Pollutants and Childhood Lipid Levels. Metabolites 2021, 11, 657.

Abstract

Animal studies have shown that developmental exposures to polybrominated diphenyl ethers (PBDE) permanently affect blood/liver balance of lipids. No human study has evaluated associations between in utero exposures to persistent organic pollutants (POPs) and later life lipid metabolism. In this pilot, maternal plasma levels of PBDEs (BDE-47, BDE-99, BDE-100, and BDE-153) and polychlorinated biphenyls (PCB-138, PCB-153, and PCB-180) were determined at delivery in participants of GESTation and Environment (GESTE) cohort. Total cholesterol (TCh), triglycerides (TG), low and high density lipoproteins (LDL-C and HDL-C), total lipids (TL), and PBDEs were determined in serum of 147 children at ages 6-7. General linear regression was used to estimate the relationship between maternal POPs and child lipid levels with adjustment for potential confounders, and adjustment for childhood POPs. In utero BDE-99 was associated with lower childhood levels of TG (p=0.003), and non-significantly with HDL-C (p=0.06) and TL (p=0.07). Maternal PCB-138 was associated with lower childhood levels of TG (p=0.04), LDL-C (p=0.04), and TL (p=0.02). Our data indicate that in-utero exposures to POPs may be associated with long-lasting decrease in circulating lipids in children, suggesting increased lipid accumulation in the liver, a mechanism involved in NAFLD development, consistent with previously reported animal data.

Keywords

dyslipidemia; fetal programing; lipid metabolism; NAFLD; persistent organic pollutants

Subject

Medicine and Pharmacology, Pharmacology and Toxicology

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