Endocrine disruption is a specific form of toxicity, where natural and/or anthropogenic chemicals, known as “endocrine disruptors” (EDs), trigger adverse health effects by disrupting the endogenous hormone system. There is need to harmonize guidance on the regulation of EDs, but this has been hampered by what appeared as a lack of consensus among scientists. This publication provides summary information about a consensus reached by a group of world-leading scientists that can serve as the basis for the development of ED criteria in relevant EU legislation. Twenty-three international scientists from different disciplines discussed principles and open questions on ED identification as outlined in a draft consensus paper at an expert meeting hosted by the German Federal Institute for Risk Assessment (BfR) in Berlin, Germany on 11–12 April 2016. Participants reached a consensus regarding scientific principles for the identification of EDs. The paper discusses the consensus reached on background, definition of an ED and related concepts, sources of uncertainty, scientific principles important for ED identification, and research needs. It highlights the difficulty in retrospectively reconstructing ED exposure, insufficient range of validated test systems for EDs, and some issues impacting on the evaluation of the risk from EDs, such as non-monotonic dose–response and thresholds, modes of action, and exposure assessment. This report provides the consensus statement on EDs agreed among all participating scientists. The meeting facilitated a productive debate and reduced a number of differences in views. It is expected that the consensus reached will serve as an important basis for the development of regulatory ED criteria.

The metabolism of ( ¹⁴ C)aflatoxin B ₁ (AFB ₁ ) was studied in liver postmitochondrial supernatants. Livers of untreated as well as phenobarbital and Aroclor 1254 pretreated male rats, and those of untreated female rats and mice of both sexes were used. Aflatoxin B ₁ (AFB ₁ ), aflatoxin Q ₁ , aflatoxin M ₁ and aflatoxin P ₁ were identified and determined in lipophilic extracts by t.l.c. and h.p.l.c. These compounds accounted for more than 90% of the extracted radioactivity. The major watersoluble metabolite was the 8, 9-dihydro-8-(S-glutathionyl)-9-hydroxy-AFB ₁ which accounted for more than 80% of hydrophilic radioactivity in some experiments. Overall metabolic conversion of AFB ₁ in liver preparations was higher in mice than in untreated rats. Sex differences were not observed in mice but were apparent in rats, with females having the lower metabolic activity. For the purpose of comparison, values for metabolic activation and metabolic inactivation have been estimated. They indicate that mouse liver preparations have a potential for production of AFB ₁ -8,9-epoxide that is similar to that of uninduced or induced rat liver preparations; the mouse liver preparations, however, are 2, or 4, times more active in conjugating the epoxide with glutathione than those of untreated male or female rats, respectively. Pretreatment of rats with phenobarbital or Aroclor increased the overall rate of metabolism, but not the fraction of epoxide formed, whereas the fraction of the GSH-conjugate was doubled. If these results were to apply to the in vivo situation, the more efficient inactivation of AFB ₁ -epoxide by conjugation with glutathione could explain the lower susceptibility of mice as compared to rats against AFB ₁ toxicity, the lower susceptibility of female as compared to male rats, and the decrease of toxicity in rats by phenobarbital pretreatment. It could also contribute towards an understanding of species differences in tumor susceptibility.