Our understanding of endocrine disruption in the aquatic environment has progressed considerably in the last few years, and is likely to improve further in the foreseeable future, as the intensive research activity underway presently in many countries comes to fruition. It is also likely that the ongoing research efforts will raise (possibly unexpected) new issues, which will in turn need exploring. I suspect that a great deal more research will be required (particularly in areas relatively uninvestigated presently, such as endocrine disruption in invertebrates) before it is possible to answer the many important questions that have arisen. Presently, the list of things that we do not know is much longer than the list of things we do know! The most important of these unanswered questions is whether or not endocrine disruption leads to population-level effects. In some cases it undoubtedly does; the example of TBT and its effects on molluscs should serve as a constant reminder that unexpected effects can be devastating. However, our understanding of the major factors (such as disease, habitat loss and over exploitation) controlling population numbers of most organisms (e.g. fish) is often very poor, and hence it will not be an easy task to put the importance of endocrine disruption into context with these other factors. Our aim should be to have enough understanding and knowledge to be able to prevent catastrophes, such as the complete elimination of some mollusc populations by TBT.

Endocrine disruption research is already having broad impact, and this is likely to increase. For example, the realisation that TBT causes imposex in many species of molluscs, leading ultimately to population-level declines, has led already to severe restrictions on the use of antifoulants containing TBT, and a worldwide ban on their use now looks, not before time, to be achievable. The rapidly increasing body of knowledge about the oestrogenic effects of nonylphenol (and related chemicals) has led already to a reassessment of the hazard posed by these chemicals to aquatic wildlife, and this is likely to lead to further restrictions in the permitted uses of the parent alkylphenol poly-ethoxylates from which nonylphenol derives. In other cases, where endocrine disruption is caused by natural chemicals (e.g. oestrogens excreted by humans and farm animals) or synthetic chemicals of profound importance, and where no obvious substitute exist (e.g. ethinyl oestradiol), the only feasible regulatory approach is to improve waste treatment processes, and hence increase the degradation of chemicals prior to their release (in effluents) to the aquatic environment. Thus, one of the outcomes of our rapidly increasing understanding of endocrine disruption will be further pressure to improve waste water treatment processes (this will have the added advantage of lowering the concentrations of other, non-endocrine active, chemicals entering the aquatic environment). This situation of regulatory action following conclusive evidence of adverse effects on wildlife caused by EDCs is reminiscent of the processes that followed the realisation many years ago that many chlorinated pesticides (e.g. PCBs and DDT) posed significant risks to wildlife, and in this regard endocrine disruption is no different from many other ecotoxicological issues.

Acknowledgement. I thank all my colleagues and students who have done all of the research which has come from my laboratory.

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