Citation

Gaum PM, Gube M, Esser A, Schettgen T, Quinete N, Bertram J, Putschögl FM, Kraus T, Lang J. Int. J. Environ. Res. Public Health 2019; 16(6): e16060950.

Affiliation

Institute for Occupational, Social and Environmental Medicine, RWTH Aachen University, Pauwelsstraße 30, 52074 Aachen, North Rhine Westphalia, Germany. jlang@ukaachen.de.

Copyright

(Copyright © 2019, MDPI: Multidisciplinary Digital Publishing Institute)

DOI

10.3390/ijerph16060950

PMID

30884813

Abstract

Polychlorinated biphenyls' (PCB) exposure has been reported to be associated with depressive symptoms, which is correlated to lower dopamine- (DA) and thyroxine-concentrations (T4). T4 is necessary for DA-synthesis and it binds to transthyretin (TTR) being transported into the brain. PCBs can displace T4 by binding to TTR itself, being transported into the brain and disturbing DA-synthesis, where depressive symptoms might occur. Consequently, the free T4-concentration (fT4) increases when PCBs bind to TTR. The interaction of PCBs with fT4 and its associations with the main DA metabolite, homovanillic acid (HVA), and depressive symptoms were investigated. In total, 116 participants (91.6% men) were investigated, who took part in three annual examinations (t1⁻t3) of the HELPcB health surveillance program. Blood was collected for measuring PCBs, hydroxy PCBs (OH-PCBs), and fT4 and urine for HVA. Depressive Symptoms were assessed with a standardized questionnaire. Interactions were tested cross-sectionally with multiple hierarchical regressions and longitudinally with mixed effect models. Related to HVA, an interaction was cross-sectionally found for lower-chlorinated PCBs (LPCBs) and dioxin-like PCBs (dlPCBs); longitudinally only for LPCBs. Related to depressive symptoms, the interaction was found for LPCBs, dlPCBs, and OH-PCBs; longitudinally again only for LPCBs. The results give first hints that a physiological process involving the thyroid and DA system is responsible for depressive symptoms after PCB exposure.

Language: en

Keywords

depression; free T4, occupational exposure; homovanillic acid; pathomechanism; polychlorinated biphenyls