Cadmium (Cd) is a toxic, non-essential transition metal that poses significant health risks to both humans and animals. It is naturally present in the environment, primarily from agricultural and industrial sources, and is mainly ingested through contaminated food and water, with inhalation and cigarette smoking also contributing. Cd accumulates in plants and animals with a half-life of about 25–30 years. Epidemiological data suggest that Cd exposure is linked to various cancers, including breast, lung, prostate, nasopharynx, pancreas, and kidney cancers. It is also a risk factor for osteoporosis. The liver and kidneys are highly sensitive to Cd toxicity due to their ability to synthesize metallothioneins (MT), which bind Cd and protect cells. Cd induces oxidative stress, mitochondrial damage, and epigenetic changes, contributing to various diseases. Recent studies show that Cd induces epigenetic modifications, including DNA methylation, histone modifications, and miRNA regulation, which may lead to cancer. Cd is also associated with reproductive and developmental issues, including osteoporosis and fetal development problems. Cd exposure can lead to renal and hepatic dysfunction, pulmonary edema, testicular damage, and adrenal and hematopoietic system damage. Cd is a known human carcinogen, and its exposure is linked to various cancers. Cd is removed from the environment through phytoremediation, nanoparticles, and microbial fermentation. Cd toxicity is managed through chelation therapy with agents like EDTA, BAL, DMSA, and DMPS. Cd exposure can also lead to oxidative stress, DNA damage, and epigenetic changes, contributing to cancer and other diseases. The review highlights the cellular and molecular effects of Cd exposure, focusing on mitochondrial dysfunction, apoptosis, and epigenetic changes. The study emphasizes the need for further research to understand the mechanisms of Cd toxicity and develop effective prevention and treatment strategies.Cadmium (Cd) is a toxic, non-essential transition metal that poses significant health risks to both humans and animals. It is naturally present in the environment, primarily from agricultural and industrial sources, and is mainly ingested through contaminated food and water, with inhalation and cigarette smoking also contributing. Cd accumulates in plants and animals with a half-life of about 25–30 years. Epidemiological data suggest that Cd exposure is linked to various cancers, including breast, lung, prostate, nasopharynx, pancreas, and kidney cancers. It is also a risk factor for osteoporosis. The liver and kidneys are highly sensitive to Cd toxicity due to their ability to synthesize metallothioneins (MT), which bind Cd and protect cells. Cd induces oxidative stress, mitochondrial damage, and epigenetic changes, contributing to various diseases. Recent studies show that Cd induces epigenetic modifications, including DNA methylation, histone modifications, and miRNA regulation, which may lead to cancer. Cd is also associated with reproductive and developmental issues, including osteoporosis and fetal development problems. Cd exposure can lead to renal and hepatic dysfunction, pulmonary edema, testicular damage, and adrenal and hematopoietic system damage. Cd is a known human carcinogen, and its exposure is linked to various cancers. Cd is removed from the environment through phytoremediation, nanoparticles, and microbial fermentation. Cd toxicity is managed through chelation therapy with agents like EDTA, BAL, DMSA, and DMPS. Cd exposure can also lead to oxidative stress, DNA damage, and epigenetic changes, contributing to cancer and other diseases. The review highlights the cellular and molecular effects of Cd exposure, focusing on mitochondrial dysfunction, apoptosis, and epigenetic changes. The study emphasizes the need for further research to understand the mechanisms of Cd toxicity and develop effective prevention and treatment strategies.