Fetal development is a period of heightened sensitivity to hormones that regulate the differentiation of tissues. An example showing that very small differences in testosterone (T) and estradiol (E₂) during fetal life can lead to changes in the life history of males and females is the intrauterine position phenomenon or IUP. Developing between fetuses of the same or opposite sex in species in which there are multiple fetuses (polytocous species) results in very small differences in fetal serum T and E₂ and differences in the development of tissues, including the brain, responsive to these sex steroids. For example, in mice, 2F males (located in utero between 2 females) have elevated serum E₂ during fetal life and in adulthood show an increase in sexual behaviors relative to 2M males (located between 2 males); 2M males have elevated serum T during fetal life and in adulthood are more aggressive than 2F males. Similarly, 2F female mice are more sexually attractive to males and more sexually receptive, but less aggressive, than their 2M female siblings. There are now numerous environmental chemicals that have been found to bind to estrogen receptors and disrupt normal estrogen signaling. The best studied of these estrogenic endocrine-disrupting chemicals is bisphenol A or BPA. Developmental exposure to BPA has been related to numerous changes in brain structure, function, and behavior in both males and females. Of great interest is the finding that the magnitude of the sex differences in some behaviors observed in untreated rats and mice is reduced or eliminated as a result of exposure to doses of BPA that are relevant to exposures experienced by humans based on biomonitoring studies. While there is less information regarding the effects of endocrine disrupting chemicals such as BPA in farm animals relative to rodents or humans, there is evidence for effects of fetal exposure to BPA on neuroendocrine function in sheep. There is also evidence for transgenerational transmission of altered phenotype, including behavior, caused by exposure to endocrine disrupting chemicals during the period of germ cell epigenetic programming.