There is growing evidence that various female reproductive syndromes may be due to environmental chemicals, as is Testis Dysgenesis Syndrome. The detrimental effects of exposure to environmental chemicals include developmental abnormalities, adult dysfunction and cancers in the ovary, urogenital tract, genitalia, mammary gland and hypothalamus/pituitary. Some symptoms, especially premature menarche and premature ovarian ageing, are of considerable concern. This is especially true in countries where women delay childbirth until they reach ages where fecundity would de-facto be reduced even without exposure to environmental chemicals. It is now many years since ovarian formation was thought to be simply due to the absence of SRY and testosterone. We now know that the process leading to a functional ovary in the adult includes complex endocrine signalling. Therefore, the fetal ovary is susceptible to endocrine disruption during development and its controlled development in-utero is critical for the reproductive health of the adult female. Indeed, in women, and model experimental species such as the sheep, the fetal ovary contains the machinery for oestradiol production and reception prior and during to primordial follicle formation. Both real life and experimental exposures have highlighted key mechanisms that are sensitive to environmental chemicals. These include: i) establishment of somatic cell numbers, ii) primordial follicle formation, ii) follicle activation and iv) maintenance of follicle health. All these processes play an important role in the establishment of fecundity in the female and their disturbance by endocrine disruptors is of serious concern.