In my personal opinion the risk assessment for endocrine disrupting chemicals should not be any different to any other risk assessment, e.g. the comparison of the lowest biologically significant and endocrine active endpoint to a predicted environmental concentration, but in order to get to this stage, several hurdles have to be overcome:

Firstly, test designs need to be appropriate to identify at what point in-vivo alterations to the endocrine system lead to effects at the population and finally the ecosystem level. A small toolbox of useful regulatory tests are available however, they do not provide definitive solid evidence that can be used to extrapolate to field scenarios. In addition laboratory based endocrine responses are a product of using an absolute worst case scenario, high doses and continuous exposure, given the sensitivity of many ED responses there is a high probability that many false/exaggerated positives could be generated using current tests and subsequently overly conservative values used for risk assessment and therefore I would also question whether the traditional method of continuous dosing at concentrations exceeding environmental realism is appropriate to generate endpoints used in risk assessment.

Secondly, we live in a chemical stew surrounded by chemicals that influence the endocrine system from various anthropogenic (effluents, PCPs, PPPs, pharmaceuticals) and natural (pine pollen, soy, hops, coffee, liquorice etc.) sources. Clearly this presents a major problem for risk assessment which aims to mitigate and prevent risk. However, some natural molecules with ED potential may have equal or greater potency than the anthropogenic sources that we aim to regulate and therefore what criteria should be used to identify what is considered to be an acceptable endocrine active substance and one that is not acceptable?

Over the last 20 years, it appears that an assumption has been made that the situation is “black and white” EDC or non-EDC respectively, but science has progressed and it has become more apparent that the situation is “grey” or “black” and in fact it is very difficult to find molecules that can be categorised as “white” and I believe that we have to tread very carefully or we may find common / natural products (e.g. coffee, beer, wine, tea, nuts, spinach, organic tomatoes) being categorised and labelled as endocrine disruptors due to them containing molecules that have activity on endocrine systems.

In conclusion, evidence indicates that molecules interfere with endocrine receptors and I am in agreement that risk assessment methods have to be developed but the method developed has to be inclusive of a molecules benefits, abundance, severity and specificity to allow identification of potent endocrine active molecules that need to be controlled based on a weight of evidence however, until there are agreed regulatory criteria, definitions of “Endocrine Disruption”, “acceptable potency levels” and differentiation between “modulation” vs “disruption” “acceptable effects” vs “non-acceptable effects” production of a meaningful and useful risk assessment approach will be a challenge.

Whatever risk assessment method is developed it needs to be consistent and standardised across all chemical sectors and regulations. It should ensure that mitigation is not applied to anthropogenic endocrine active chemicals with lower potencies than naturally occurring endocrine active molecules, cost-benefit analysis and weight of evidence will also be key. Finally in my opinion our understanding of this science is still in its infancy and small steps on solid foundations have to be taken to ensure intelligent decisions are made.