Cadmium (Cd) is a heavy metal that poses significant health risks due to its widespread environmental presence and toxic effects on human health. This review summarizes the mechanisms and pathways of Cd toxicity, including oxidative stress, disruption of calcium signaling, interference with cellular signaling pathways, and epigenetic modifications. Cd is primarily absorbed through inhalation and dietary intake, with long-term exposure leading to kidney damage, osteoporosis, and cardiovascular issues. The absorption, distribution, metabolism, and excretion (ADME) of Cd are critical factors in its toxic effects, with Cd accumulating in the kidneys, liver, and bones. Cd induces oxidative stress by increasing reactive oxygen species (ROS) and decreasing antioxidant defenses, leading to cellular damage and apoptosis. It also disrupts signaling pathways such as MAPK, NF-κB, and p53, contributing to pathological conditions and carcinogenesis. Epigenetic changes, including DNA methylation and histone modifications, further impact gene expression and disease development. The review highlights the need for enhanced strategies to mitigate Cd's public health implications. Cd exposure is linked to various health issues, including inflammation, DNA damage, and epigenetic alterations, which contribute to diseases like cancer, osteoporosis, and kidney disease. The study emphasizes the importance of monitoring Cd levels in the environment and developing effective prevention and treatment strategies to reduce its health risks.Cadmium (Cd) is a heavy metal that poses significant health risks due to its widespread environmental presence and toxic effects on human health. This review summarizes the mechanisms and pathways of Cd toxicity, including oxidative stress, disruption of calcium signaling, interference with cellular signaling pathways, and epigenetic modifications. Cd is primarily absorbed through inhalation and dietary intake, with long-term exposure leading to kidney damage, osteoporosis, and cardiovascular issues. The absorption, distribution, metabolism, and excretion (ADME) of Cd are critical factors in its toxic effects, with Cd accumulating in the kidneys, liver, and bones. Cd induces oxidative stress by increasing reactive oxygen species (ROS) and decreasing antioxidant defenses, leading to cellular damage and apoptosis. It also disrupts signaling pathways such as MAPK, NF-κB, and p53, contributing to pathological conditions and carcinogenesis. Epigenetic changes, including DNA methylation and histone modifications, further impact gene expression and disease development. The review highlights the need for enhanced strategies to mitigate Cd's public health implications. Cd exposure is linked to various health issues, including inflammation, DNA damage, and epigenetic alterations, which contribute to diseases like cancer, osteoporosis, and kidney disease. The study emphasizes the importance of monitoring Cd levels in the environment and developing effective prevention and treatment strategies to reduce its health risks.