This review article discusses the molecular and cellular mechanisms of carcinogenicity for metals and their compounds, including arsenic, antimony, beryllium, cadmium, chromium, cobalt, lead, nickel, and vanadium. Physicochemical properties determine the uptake, intracellular distribution, and binding of these compounds. While interactions with proteins, such as zinc finger structures, are more relevant than DNA binding, metal genotoxicity is generally caused by indirect mechanisms. Three predominant mechanisms are identified: (1) interference with cellular redox regulation and induction of oxidative stress, which may cause oxidative DNA damage or trigger signaling cascades leading to cell growth stimulation; (2) inhibition of major DNA repair systems, resulting in genomic instability and accumulation of critical mutations; and (3) deregulation of cell proliferation through signaling pathway induction or inactivation of growth controls such as tumor suppressor genes. Specific metal compounds have unique mechanisms, such as cadmium disrupting cell-cell adhesion, trivalent chromium directly binding to DNA, and vanadate interacting with phosphate binding sites of protein phosphatases. Carcinogens are classified by scientific committees and regulatory agencies. The International Agency for Research on Cancer (IARC) and the German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area (MAK commission) classify metals and metalloids as carcinogenic to humans or possibly carcinogenic. The classification depends on scientific evaluations and national policies. Metals may be carcinogenic in the form of free ions, metal complexes, or particles of metals and poorly soluble compounds. Their toxicity is governed by physicochemical properties, including ion charge, oxidation state, ionic radii, coordination number, geometry, and ligand type. Particle size and crystal structure are also important for poorly soluble compounds. Toxic metal cations and essential transition metal ions bind to biological ligands, forming complexes with oxygen, sulfur, and nitrogen groups of biomolecules. If toxic metal ions have similar physicochemical properties as essential ions, they may compete for biological binding sites, causing structural perturbations and aberrant function of biochemical macromolecules. Examples include Be²⁺ competing with Mg²⁺ and Cd²⁺ having similar ionic radii to Ca²⁺.This review article discusses the molecular and cellular mechanisms of carcinogenicity for metals and their compounds, including arsenic, antimony, beryllium, cadmium, chromium, cobalt, lead, nickel, and vanadium. Physicochemical properties determine the uptake, intracellular distribution, and binding of these compounds. While interactions with proteins, such as zinc finger structures, are more relevant than DNA binding, metal genotoxicity is generally caused by indirect mechanisms. Three predominant mechanisms are identified: (1) interference with cellular redox regulation and induction of oxidative stress, which may cause oxidative DNA damage or trigger signaling cascades leading to cell growth stimulation; (2) inhibition of major DNA repair systems, resulting in genomic instability and accumulation of critical mutations; and (3) deregulation of cell proliferation through signaling pathway induction or inactivation of growth controls such as tumor suppressor genes. Specific metal compounds have unique mechanisms, such as cadmium disrupting cell-cell adhesion, trivalent chromium directly binding to DNA, and vanadate interacting with phosphate binding sites of protein phosphatases. Carcinogens are classified by scientific committees and regulatory agencies. The International Agency for Research on Cancer (IARC) and the German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area (MAK commission) classify metals and metalloids as carcinogenic to humans or possibly carcinogenic. The classification depends on scientific evaluations and national policies. Metals may be carcinogenic in the form of free ions, metal complexes, or particles of metals and poorly soluble compounds. Their toxicity is governed by physicochemical properties, including ion charge, oxidation state, ionic radii, coordination number, geometry, and ligand type. Particle size and crystal structure are also important for poorly soluble compounds. Toxic metal cations and essential transition metal ions bind to biological ligands, forming complexes with oxygen, sulfur, and nitrogen groups of biomolecules. If toxic metal ions have similar physicochemical properties as essential ions, they may compete for biological binding sites, causing structural perturbations and aberrant function of biochemical macromolecules. Examples include Be²⁺ competing with Mg²⁺ and Cd²⁺ having similar ionic radii to Ca²⁺.