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Cardiometabolic diseases, including cardiovascular disease, type 2 diabetes mellitus (T2DM), obesity-related metabolic dysfunction, and hypertension, remain major causes of global morbidity and mortality. Beyond traditional risk factors, environmental exposure to toxic metals is increasingly recognized as a contributor to vascular and metabolic injury. Lead, cadmium, arsenic, and mercury are persistent toxicants that may accumulate in human tissues and interfere with essential trace-element homeostasis. This narrative review examines how toxic metal exposure disrupts the biological balance of iron, zinc, copper, and selenium, thereby weakening mitochondrial function, antioxidant defense, endothelial regulation, and metabolic stability. A central focus is ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation and failure of protective systems such as the selenium-GPX4-glutathione axis. Toxic metal-essential trace-element imbalance may create a pro-ferroptotic environment that promotes endothelial dysfunction, nitric oxide impairment, vascular stiffness, atherosclerotic plaque instability, myocardial ischemic vulnerability, insulin resistance, β-cell dysfunction, and cardiometabolic clustering. This review reframes heavy metal-associated cardiometabolic disease as a consequence of toxic metal-essential trace-element dyshomeostasis rather than direct toxicity alone. Clinically, this framework supports targeted exposure history, careful interpretation of metal and trace-element biomarkers, correction of documented deficiencies, and avoidance of indiscriminate supplementation. Future studies integrating exposomics, metallomics, ferroptosis biomarkers, and longitudinal cardiometabolic outcomes are needed to clarify causality and guide prevention.