Dietary and Environmental Exposure to Toxic Elements in Endometriosis: A Missing Piece of the Etiological Puzzle?

Background/Objectives: Endometriosis is a chronic estrogen-dependent disease with a complex and incompletely understood etiology. Environmental exposure to toxic elements, including cadmium, lead, mercury, and arsenic, may contribute to its development and progression. Proposed mechanisms include endocrine disruption, oxidative stress, chronic inflammation, and epigenetic alterations. Methods: This narrative review was based on a structured literature search of the PubMed, Scopus, and Web of Science databases for studies published up to 15 June 2026. The search included the following keywords: endometriosis, cadmium, lead, mercury, arsenic, toxic elements, heavy metals, environmental exposure, diet, nutrition, and biomonitoring. Results: This review summarizes current evidence on the relationship between toxic element exposure and endometriosis, including sources of exposure, biomonitoring findings, proposed biological mechanisms, and human studies. The influence of nutritional status on metal bioavailability is also considered. Among the toxic elements reviewed, cadmium has been studied most extensively and shows the most consistent association with endometriosis. Evidence for lead is less consistent, whereas data on mercury and arsenic remain limited. Although the available epidemiological evidence does not establish a causal relationship, biomonitoring and experimental studies support a possible role of toxic elements in the development and progression of endometriosis. Conclusions: Current evidence supports a possible role of toxic elements in endometriosis, although a causal relationship has not been established. Cadmium has been investigated most extensively, while evidence for other toxic elements remains limited. Nutritional status should be considered when evaluating biomonitoring findings, particularly in relation to cadmium exposure.