Differences in sexual development (DSD) are congenital conditions characterised by abnormal patterns of sexual development. DSDs are among the most common human birth defects and are drastically increasing in prevalence over past decades. Although there is a known affiliation between DSDs and epigenetic mutations, the increasing incidence of DSDs is too rapid to be caused by genetic factors alone. Thus, DSDs are thought to be consequential of chemicals within the exposome that accumulate as disease risk factors. Exposure to endocrine disruptor chemicals (EDCs), which mimic or disrupt normal hormonal signalling, has been directly linked with an increased prevalence of DSDs. The synthetic oestrogen Diethylstilbesterol (DES) is a key example of this. DES exposure has been shown to induce adverse reproductive health effects for exposed individuals and unexposed individuals past the F3 generation through multi and transgenerational inheritance respectively. In this study, we examined the ovarian phenotype in F1-F3 generation exposed females to determine whether DES exposure predisposed females to polycystic ovarian syndrome (PCOS) and primary ovarian insufficiency (POI). To define the transgenerational reproductive impacts in females following DES exposure, gestating F0 female mice were exposed to 2.5L/g of DES. Ovaries were analysed in offspring at D21pp and in mature adults for the number of follicles, follicle atresia, and the formation of ovarian cysts. Significant differences were seen between generations in follicle populations for both the D21pp and mature adult cohorts. By examining the morphological effects of DES exposure in young and aged female mice (up to the F3 generation) we can define the reproductive consequences of DES exposure. Such findings have broad implications for the millions of female DES descendants, while further deepening our understanding of the consequences of EDC exposure upon the prevalence of DSDs such as PCOS and POI.