Considerable concern has been raised in recent publications that oestrogen-like compounds in either food or the environment cause adverse effects on reproductive health. There is clear evidence that reproductive disruption in wildlife may be caused by environmental pollutants and more specifically by endocrine-disrupting compounds. The increase in the incidence of disorders of the male reproductive tract (e.g. testicular cancer, cryptorchidism, hypospadias) and the possible decline of sperm quality led to the hypothesis in 1993 that the reported increases stem from fetal or neonatal exposure of the developing male to oestrogens. Cryptorchidism, hypospadias, testicular cancer and poor semen quality have also been proposed to be symptoms of one underlying cause, the testicular dysgenesis syndrome, which may develop during fetal life under the influence of environmental factors. However, there is only circumstantial evidence in humans that exposure to endocrine disrupters, especially diethylstilbestrol, during pregnancy causes problems of reproductive health. Oestrogen-like effects have been reported for a variety of naturally occurring oestrogens (so-called phytoestrogens) and for numerous synthetic compounds. The critical issue is whether there are sufficiently high levels of endocrine disrupters in the ambient environment to exert adverse health effects on the general population.