Endocrine-disrupting chemicals (EDCs) are considered a heterogeneous group of natural (e.g., plant phytoestrogens) or synthetic compounds (e.g., industrial solvents, plastics, heavy metals, pesticides/herbicides) that cause health problems in an intact organism and its progeny by changing endocrine function. By binding to hormone receptors, EDCs influence downstream patterns regulated by specific hormones and lead to an imbalance in metabolism [43,44]. Dioxin and dioxin-like compounds, plastic components such as bisphenol A (BPA) and phthalates, parabens, and various flame retardants represent different examples of EDCs. Although heterogeneous, EDCs display some general characteristics shared by different components of the group. For instance, EDCs promote their adverse effects even at very low doses of exposure, and their action is stronger if it takes place during critical developmental periods, such as fetal life, infancy, puberty, and pregnancy [45,46,47]. In addition, the onset of disease promoted by EDCs is evident many years after the exposure [48]. Although EDCs show a very low affinity for hormone receptors compared to natural ligands, they can cause profound damage in several tissues. In general, since different classes of EDCs are released by human activities into the environment, they all together contribute to the development of a disease, and it is difficult to predict the detrimental effect associated with a specific EDC [49]. A possible association between the increase of global obesity and the spread of industrial chemicals into the environment was initially proposed in the early 2000s [50]. Afterwards, Grun and Blumberg introduced the term “obesogens” to indicate “xenobiotic chemicals that can disrupt the normal developmental and homeostatic controls over adipogenesis and/or energy balance” [51]. The effects of obesogenic environmental pollutants on adipose tissue expansion are stronger if the exposure happens during the prenatal or early-life period [52]. Obesogens target transcription regulators that are involved in the control of lipid homeostasis as well as adipocytes’ proliferation and differentiation. Due to their lipophilic property, EDCs accumulate in the adipose tissue over the years [53,54]. This produces a continuous spiral, promoting the EDC-induced expansion of adipose tissue and therefore the possibility to store larger amounts of additional EDCs [19]. Several obesogenic EDCs are known to affect the activity of a group of nuclear hormone receptors known as peroxisome proliferator-activated receptors (PPARs). Among those, PPARγ is considered the master regulator of adipogenesis, and it is associated with the control of lipids and glucose metabolism [55,56,57]. PPARγ is therefore the main target of obesogenic EDCs. In addition, since PPARs heterodimerize with the retinoid X receptors (RXRs) to induce transcription, RXRs can also be a target of obesogenic EDCs [58,59]. Although epigenetic effects of EDCs have been well described, the exact mechanisms by which they interfere with epigenetic marks still remain unknown. In general, it has been proposed as a global action, where EDCs affect the abundance or the activity of epigenetic regulators, such as DNA methyltransferases, and/or their cofactors, such as methyl donor SAM (s-adenosylmethionine), or they could have a gene-specific action, influencing the regulation of locus-specific epigenetic patterns.