Endometriosis and infertility is more of a loose-canon fraternity however, in which the nature and hierarchy of mechanisms by which endometriosis interferes with reproduction are still the source of fierce debates. At the heart of these enduring powwows, 2 effects of endometriosis strike out as mainstay paradigms by which endometriosis causes infertility: (i) Pelvic inflammation interferes with sperm-oocyte interaction and thus, hampers in vivo – but not in vitro fertilization (IVF). (ii) Alterations of the eutopic endometrium encountered in case of endometriosis interfere to various extents with embryo implantation, an effect particularly preeminent in IVF. Amongst the scores of candidate factors – spanning from genetic to immunological ones – purported as causing or facilitating endometriosis, the role played by the environment is an emerging domain with mushrooming implications of public health relevance. The recent years have indeed unveiled that chemicals in our environment can affect reproduction and reproductive hormones related disorders such as endometriosis by mimicking hormones and interacting with hormone receptors and/or modify gene expression by DNA-methylation. One putative mechanism put forth for explaining these disruptions of reproductive-hormone related functions is altered gene expression mediated by inappropriate activation or deactivation of hormone receptors that act as transcription factors. The aim of this review is to determine whether and to which extent environmental factors may be associated with, let alone cause endometriosis and/or partake in its impact on female fecundity by compounding any of the disease’s effects on human reproduction.