Human exposure to synthetic endocrine disrupting chemicals (S-EDCs) is generally negligible as compared to natural compounds with higher or comparable endocrine activity: how to evaluate the risk of the S-EDCs?

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisLederForskningpeer review

DOI

  • Herman Autrup
  • Frank A. Barile, St. John's University
  • ,
  • Sir Colin Berry, Queen Mary University of London
  • ,
  • Bas J. Blaauboer, Utrecht University
  • ,
  • Alan Boobis, Imperial College London
  • ,
  • Herrmann Bolt, Dortmund University
  • ,
  • Christopher J. Borgert, Applied Pharmacology and Toxicology, Inc.
  • ,
  • Wolfgang Dekant, University of Würzburg
  • ,
  • Daniel Dietrich, University of Konstanz
  • ,
  • Jose L. Domingo, Pere Virgili Health Research Institute
  • ,
  • Gio Batta Gori, Regulatory Toxicology and Pharmacology
  • ,
  • Helmut Greim, Technical University of Munich
  • ,
  • Jan Hengstler, Dortmund University
  • ,
  • Sam Kacew, University of Ottawa
  • ,
  • Hans Marquardt, Toxicology
  • ,
  • Olavi Pelkonen, University of Oulu
  • ,
  • Kai Savolainen, Finnish Institute of Occupational Health
  • ,
  • Pat Heslop-Harrison, University of Leicester
  • ,
  • Nico P. Vermeulen, Vrije Universiteit Amsterdam

Theoretically, both synthetic endocrine disrupting chemicals (S-EDCs) and natural (exogenous and endogenous) endocrine disrupting chemicals (N-EDCs) can interact with endocrine receptors and disturb hormonal balance. However, compared to endogenous hormones, S-EDCs are only weak partial agonists with receptor affinities several orders of magnitude lower. Thus, to elicit observable effects, S-EDCs require considerably higher concentrations to attain sufficient receptor occupancy or to displace natural hormones and other endogenous ligands. Significant exposures to exogenous N-EDCs may result from ingestion of foods such as soy-based diets, green tea and sweet mustard. While their potencies are lower as compared to natural endogenous hormones, they usually are considerably more potent than S-EDCs. Effects of exogenous N-EDCs on the endocrine system were observed at high dietary intakes. A causal relation between their mechanism of action and these effects is established and biologically plausible. In contrast, the assumption that the much lower human exposures to S-EDCs may induce observable endocrine effects is not plausible. Hence, it is not surprising that epidemiological studies searching for an association between S-EDC exposure and health effects have failed. Regarding testing for potential endocrine effects, a scientifically justified screen should use in vitro tests to compare potencies of S-EDCs with those of reference N-EDCs. When the potency of the S-EDC is similar or smaller than that of the N-EDC, further testing in laboratory animals and regulatory consequences are not warranted.

OriginalsprogEngelsk
TidsskriftArchives of Toxicology
Vol/bind94
Nummer7
Sider (fra-til)2549-2557
ISSN0340-5761
DOI
StatusUdgivet - jul. 2020

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