Prenatal and Early Life Exposure to Polychlorinated Dibenzo-p-Dioxins, Dibenzofurans and Biphenyls May Influence Dehydroepiandrosterone Sulfate Levels at Prepubertal Age: Results from the Duisburg Birth Cohort Study

Abstract

Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/F) and polychlorinated biphenyls (PCB) are postulated to act as endocrine disrupters. In the ongoing Duisburg birth cohort study, started in 2000–2002, influence of persistent organic pollutants (POP) on child development was monitored. For the first time, associations were reported between prenatal and postnatal PCDD/F and PCB exposures and early endocrinological changes concerning adrenarchal development. PCDD/F and PCB concentrations were measured in blood samples taken in wk 32 of pregnancy and in breast milk using gas chromatography and high-resolution mass spectrometry (GC/HRMS). At the age of 6–7 and 8–9 yr, serum samples were collected from 111 children. The samples were assayed for the sex hormones testosterone, estradiol, dehydroepiandrosterone sulfate (DHEA-S), and 17-OH-progesterone (17-OHP) by using an automated chemiluminescence assay system. Analyses of repeated measurements of DHEA-S serum levels were performed by linear regression analysis using generalized estimating equations (GEE). Linear regression analysis showed a positive association between DHEA-S and breast milk levels of PCDD/F and PCB expressed as toxicity equivalents according to toxicity equivalent factors published by the World Health Organization (WHO) in 2005 (WHO₂₀₀₅-TEq) (increase of 29%, geometric mean ratio, GMR: 1.29, 95% CI 1.06–1. 58 per doubling of PCDD/F + PCB WHO₂₀₀₅-TEq levels). Results for the association with the WHO₂₀₀₅-TEq levels in blood of mothers were in the same direction (increase of 15%, GMR 1.15, 95% CI 0.93–1.42 per doubling of PCDD/F + PCB WHO₂₀₀₅-TEq levels), but not significant. Data indicate that PCDD/F and PCB exposure in infancy may influence DHEA-S serum levels in prepubertal children. Increased DHEA-S serum levels are considered to indicate acceleration of the adrenal maturation.

Acknowledgments

We thank the North Rhine-Westphalia State Environment Agency for the initiation of the study, the German Federal Environment Agency for financial support of the follow-up. Thanks to all participants and the health authorities in Duisburg. We thank Michaela Greshake and Jochen Scheld for their outstanding engagement. We thank Alma Vogelsang Stiftung Bochum for financial support of A. Rennert.