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?. Issue 13 (17th July 2020)

• Record Type: Journal Article
• Authors: Autrup, Herman; Barile, Frank A.; Berry, Sir Colin; Blaauboer, Bas J.; Boobis, Alan; Bolt, Herrmann; Borgert, Christopher J.; Dekant, Wolfgang; Dietrich, Daniel; Domingo, Jose L.; Gori, Gio Batta; Greim, Helmut; Hengstler, Jan; Kacew, Sam; Marquardt, Hans; Pelkonen, Olavi; Savolainen, Kai; Heslop-Harrison, Pat; Vermeulen, Nico P.
• Is Part Of: Journal of toxicology and environmental health. Volume 83:Issue 13/14(2020)
• Page Start: 485
• Page End: 494
• Publication Date: 2020-07-17
• Subjects: Endocrine disruption -- risk characterization -- testing; Toxicology -- Periodicals; Environmental health -- Periodicals; 615.90205
• DOI: 10.1080/15287394.2020.1756592
• Languages: English
• ISSNs: 1528-7394

Abstract

ABSTRACT: 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 than S-EDCs. 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.