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For much of the 1990s the plausibility of the endocrine disrupter hypothesis (EDH) as a useful model for the aetiology of a number of disorders of hormonally regulated biological systems in nature, and ultimately the relevance of the EDH to human disease, has preoccupied interested biologists, toxicologists, and epidemiologists. There is an ever increasing battery of evidence for environmental and industrial chemicals, which show evidence of hormonal activity in vitro, and there is considerable observational evidence of sexuality modifying effects of these chemicals in wildlife. Secular trend data in disorders of hormonally controlled physiological systems in humans have also been examined to identify likely candidate human outcomes for endocrine disruption. The now well rehearsed list of such disorders includes testicular cancer (for which there is convincing evidence of a rise in prevalence over the past century); decreasing sperm counts (for which there is less convincing evidence); and also the congenital anomalies hypospadias and cryptorchidism (for which there is the least convincing evidence).
Skakkebaek et al have suggested that these disorders are related and may usefully be considered as part of a syndrome which they have termed “testicular dysgenesis sydrome”.1 Sharpe and colleagues2,3 have recently reported a putative animal model for this syndrome where offspring rats display all or some of these outcomes (excluding testicular …