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?

In silico prediction of nuclear receptor binding to polychlorinated dibenzofurans and its implication on endocrine disruption in humans and wildlife

“…The computational results presented in this paper also indicate that PCDFs bind to androgen receptor with binding affinities that are lower than the binding affinities of testosterone and bicalutamide. This finding is consistent with previously reported results for other low-molecular weight exogenous chemicals that act as endocrine disruptors—they generally act as weak agonists or antagonists with binding affinities several orders of magnitude lower than the binding affinities of endogenous hormones ( Autrup et al, 2020 , Balaguer et al, 2017 , Shanle and Xu, 2011 , Lee et al, 2013 ). The relatively lower binding affinities of PCDFs and other low-molecular weight EDCs may be due to the fewer contacts that these EDCs made within the binding cavities of the receptors on account of their small sizes ( Balaguer et al, 2017 ).…”

Endocrine disruptors concentrations in drinking water samples from México and their health implications

“…Previous studies have shown that NP is ubiquitous in baby food representing a daily intake from 0.23 to 0.65 µg kg − 1 bw d − 1 (Raecker et al 2011). However, low concentrations in humans may have virtually no chance to compete with natural hormones in the unions of free receptors, implying that the health risks of endocrine disruptors may be insigni cant (Autrup et al 2020). Therefore, exposure effects of endocrine disruptors at low doses during the development of humans have been underestimated (Welshons et al 2006).…”

Endocrine-Disrupting Chemicals: Science and Policy

“…It has been argued that EDCs may bind NHRs with lower affinity than endogenous hormones, leading to the conclusion that the risk of certain EDCs is minimal at environmentally relevant doses because it is not high enough to competitively bind the NHR (e.g., Autrup et al, 2020; Castelain & Castelain, 2012; Okubo et al, 2001). This argument lacks validity when considering that physiological hormone-receptor interactions may not align with standard toxicity testing and that certain life stages are at increased susceptibility to endocrine disruption (discussed below).…”