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Endocrine Disruption- Chemical Causation and Mixtures

Through controlled exposures we have proven that feminisation of wild roach living in UK rivers is caused by exposure to treated sewage effluents. Using a targeted biological screening of chemically fractionated bile from effluent exposed fish, with collaborators (University of Sussex) we have also identified a suite of feminising chemicals in effluent discharges, principally environmental oestrogens, that contribute to the feminisation of wild fish in UK rivers. Our laboratory studies have subsequently proven that some of these chemicals, notably natural and synthetic steroid oestrogens and alkylphenolic compounds, can induce some of the endocrine disrupting effects seen in fish at environmentally relevant concentrations. This has been shown both in laboratory models (zebrafish and fathead minnow) and indigenous UK fish (roach). We have conducted long term, including multigenerational exposures, to show that the synthetic oestrogen pharmaceutical, ethinyloestradiol, used in the contraceptive pill, can have severe detrimental reproductive effects in fish at an exposure concentration of only 1 part per billion. Furthermore, our laboratory studies have recently shown that exposure to ethinyloestradiol during early life sensitizes fish to oestrogen in later life and this is likely to have significant and wide impact for toxicology research. Our laboratory has also studied the biological effects of weaker environmental oestrogens found in effluents, including some of the most widely used industrial chemicals such as bisphenol A, phthalates, and some pesticides. Some of our data have been instrumental in establishing an environmental quality standard for endocrine active chemicals and highlighted other chemicals for further hazard identification. Thus, our research findings have served to improve environmental quality standards.

Recently we have further discovered that effluents from STWs contain substantial amounts of anti-androgenic activity (which may similarly induce feminising effects) and with collaborators at Sussex University we are now tracking down the identity of these compounds and their significance in contributing to the feminisation of wild fish.  

Some of our work on endocrine disruption has focused on mixture effects of endocrine active chemicals. With collaborators (e.g. Bremen University), and combining empirical studies with models including Concentration Addition/Joint Independent Action, we have established that endocrine active chemicals can be additive in their effects and these findings have had a widespread and international influence (with further highly cited papers).   

Complimenting our work on endocrine disruption, EABRG has projects assessing the wider health implications of exposure to various chemicals including pharmaceuticals and effluents in fish, investigating for immumotoxicity and genotoxicity. The EABRG has also worked on tumourigenesis and was the first to clone and sequence some of the p53 tumour suppresser genes in fish.