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Endocrine-Related Cancer 5 (2) 69-96    DOI: 10.1677/erc.0.0050069
Copyright © 1998 by the Society for Endocrinology.
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Environmental oestrogens and human reproductive cancers

W R Miller 1 and R M Sharpe 2

1 Breast Research Unit, Paderewski Building, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK
2 MRC Reproductive Biology Unit, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9EW, UK

Introduction

The past four years have seen an explosion of interest and concern with respect to ‘environmental hormone disruptors’, particularly environmental oestrogens. This is a consequence of (i) the discovery that a range of widely- used man-made chemicals (including certain pesticides, alkyphenols, phthalate esters and phenolic compounds), to which we are exposed daily, can act as weak oestrogens, and (ii) their hypothetical links to an increase in disorders of reproductive development and function in the human male and in some species of wildlife (Toppari et al. 1996). Additionally, several other ubiquitous chemicals to which man has had considerable exposure over the past half-century are potent anti-androgens (notably the fungicide vinclozolin (Kelce et al. 1994) and the principle, and most persistent, metabolite of DDT in the body, p,p-DDE (Kelce et al. 1995)). These discoveries have prompted numerous television programmes, government-funded enquiries and reports and have even led to legislative changes in the USA. Inevitably, speculation and exaggerated claims have appeared in the popular press, these have generally not been based on solid scientific foundation (see Kavlock et al. 1996, Ashby et al. 1997). On the other hand, the coincidence is striking between human exposure to these man-made chemicals and the apparent increase in prevalence of a range of hormone-dependent human cancers of reproductive tissues (breast, prostate, endometrium, testis and ovary). We therefore need to know whether these chemicals are directly involved in the aetiology of any of these cancers, so that human exposure to such chemicals can be reduced. Unfortunately, as this review will demonstrate, obtaining the data which would enable unequivocal, informed risk assessment is anything but straightforward (Kavlock et al. 1996, Ashby et al. 1997).

Note:

Acknowledgements

We are appreciative of the extreme tolerance of the Editor, Professor Vivian James, throughout the passing of many missed deadlines for submission of this review.




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