Cadmium (Cd) is a prevalent environmental contaminant that exerts widespread toxic effects on human health through various biochemical and molecular mechanisms. This review highlights the primary pathways through which Cd inflicts damage, including oxidative stress induction, disruption of Ca²⁺ signaling, interference with cellular signaling pathways, and epigenetic modifications. The paper details the absorption, distribution, metabolism, and excretion (ADME) of Cd, along with its interactions with cellular components such as mitochondria and DNA, emphasizing the extensive damage caused by Cd²⁺ at the cellular and tissue levels. The role of Cd in inducing oxidative stress, a pivotal mechanism behind its toxicity, is discussed, focusing on how it disrupts the balance between oxidants and antioxidants, leading to cellular damage and apoptosis. Additionally, the review covers Cd’s impact on signaling pathways like Mitogen-Activated Protein Kinase (MAPK), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Tumor Protein 53 (p53) pathways, illustrating how its interference with these pathways contributes to pathological conditions and carcinogenesis. The epigenetic effects of Cd, including DNA methylation and histone modifications, are also explored to explain its long-term impact on gene expression and disease manifestation. This comprehensive analysis not only elucidates the mechanisms of Cd toxicity but also underscores the critical need for enhanced strategies to mitigate its public health implications.Cadmium (Cd) is a prevalent environmental contaminant that exerts widespread toxic effects on human health through various biochemical and molecular mechanisms. This review highlights the primary pathways through which Cd inflicts damage, including oxidative stress induction, disruption of Ca²⁺ signaling, interference with cellular signaling pathways, and epigenetic modifications. The paper details the absorption, distribution, metabolism, and excretion (ADME) of Cd, along with its interactions with cellular components such as mitochondria and DNA, emphasizing the extensive damage caused by Cd²⁺ at the cellular and tissue levels. The role of Cd in inducing oxidative stress, a pivotal mechanism behind its toxicity, is discussed, focusing on how it disrupts the balance between oxidants and antioxidants, leading to cellular damage and apoptosis. Additionally, the review covers Cd’s impact on signaling pathways like Mitogen-Activated Protein Kinase (MAPK), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Tumor Protein 53 (p53) pathways, illustrating how its interference with these pathways contributes to pathological conditions and carcinogenesis. The epigenetic effects of Cd, including DNA methylation and histone modifications, are also explored to explain its long-term impact on gene expression and disease manifestation. This comprehensive analysis not only elucidates the mechanisms of Cd toxicity but also underscores the critical need for enhanced strategies to mitigate its public health implications.