Prenatal exposure to organochlorine pesticides is associated with increased risk for neural tube defects.


Journal

The Science of the total environment
ISSN: 1879-1026
Titre abrégé: Sci Total Environ
Pays: Netherlands
ID NLM: 0330500

Informations de publication

Date de publication:
20 May 2021
Historique:
received: 22 11 2020
revised: 14 01 2021
accepted: 14 01 2021
pubmed: 31 1 2021
medline: 19 3 2021
entrez: 30 1 2021
Statut: ppublish

Résumé

Neural tube defects (NTDs) are among the most common and disabling fetal congenital defects. Organochlorine pesticides (OCPs) are ubiquitous in the environment. In this study, 119 women who had NTD-affected pregnancies (cases) and 119 women who delivered healthy neonates (controls) were recruited in a rural area of Northern China. We used concentrations of OCPs in umbilical cord tissue as markers of prenatal exposure to investigate the association between in utero exposure to OCPs and NTD risk. Concentrations of 20 OCPs were quantified by gas chromatography-mass spectrometry, and 16 of the 20 OCPs were included in the analyses. Odds ratios and 95% confidence intervals (95% CIs) for the associations between levels of individual OCPs and NTD risk were estimated separately with logistic regression adjusting for potential confounders. The combined effects of exposure to the 16 OCPs as a mixture were analyzed with Bayesian kernel machine regression (BKMR). Logistic regression showed that the risk for NTDs increased 5.44-fold (95% CI, 2.21-13.41) for β-hexachlorocyclohexane, 2.51-fold (95% CI, 1.07-5.86) for endosulfan I, 3.78-fold (95% CI, 1.60-8.89) for endosulfan II, 3.42-fold (95% CI, 1.44-8.12) for ο,ρ'-dichlorodiphenyldichloroethane, and 2.89-fold (95% CI, 1.22-6.86) for ρ,ρ'-dichlorodiphenyltrichloroethane when the concentration of each of these OCPs was above its median (exposed) compared to below its median (non-exposed). Other OCPs were not associated with NTD risk in multivariate models. In BKMR, NTD risk increased almost linearly with concentrations of the 16 OCPs as a mixture, which suggests joint effects on NTD risk. Exposure to α-hexachlorocyclohexane, β-hexachlorocyclohexane, endosulfan II, ο,ρ'-dichlorodiphenyldichloroethane, and ρ,ρ'-dichlorodiphenyldichloroethane was associated with an increased risk for NTDs when levels of the remaining 15 OCPs were taken into account. Taken together, these findings show that prenatal exposure to OCPs is associated with increased risk for NTDs.

Identifiants

pubmed: 33515890
pii: S0048-9697(21)00350-8
doi: 10.1016/j.scitotenv.2021.145284
pii:
doi:

Substances chimiques

Hydrocarbons, Chlorinated 0
Pesticides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

145284

Informations de copyright

Copyright © 2021 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Shengju Yin (S)

Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China; Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China.

Ying Sun (Y)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Jinhui Yu (J)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Zaiming Su (Z)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Mingkun Tong (M)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Yali Zhang (Y)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Jufen Liu (J)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Linlin Wang (L)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Zhiwen Li (Z)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.

Aiguo Ren (A)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China. Electronic address: renag@bjmu.edu.cn.

Lei Jin (L)

Institute of Reproductive and Child Health, National Health Commission Key Laboratory of Reproductive Health, Peking University, Beijing, China; Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China. Electronic address: jinlei@bjmu.edu.cn.

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