Vitamin D, a fat-soluble vitamin primarily synthesized in the skin upon exposure to ultraviolet B radiation, known for its crucial role in phospho-calcium homeostasis and bone health, elicits numerous extra-skeletal benefits, such as anti-inflammatory, antioxidant, anti-infectious, anti-proliferative, and immunomodulatory effects. These effects are mediated via the canonical, vitamin D receptor (VDR)–mediated genomic and non-genomic pathways but also via non-canonical pathways activated by several metabolites. Emerging evidence indicates that endocrine disruptors (EDs), exogenous compounds that interfere with hormonal signaling, can negatively impact vitamin D metabolism and function, potentially contributing to a range of adverse health outcomes. Compounds such as phthalates, bisphenol A, polychlorinated biphenyls, certain pesticides, etc. have been associated with alterations in vitamin D pathways, either by affecting its metabolism or by disrupting VDR-mediated signaling. Furthermore, EDs decrease the circulating levels of vitamin D through inhibition of key enzymes involved in its synthesis and activation. Conversely, vitamin D may exert a protection against the detrimental influence of EDs, owing to its anti-inflammatory, antioxidant, and immunomodulatory properties. Ensuring sufficient plasma level of vitamin D could therefore represent a one approach to mitigate the health risks associated with exposure to EDs. A deeper understanding of the interplay between vitamin D and endocrine-disrupting chemicals is crucial for the development of preventive/therapeutic strategies aimed at reducing the burden of chronic diseases and also for informing public health policies. Further research is warranted to clarify the molecular mechanisms underlying their interaction and define the serum levels of the vitamin required to prevent the deleterious effects of persistent exposure to EDs, particularly in vulnerable populations.