ABSTRACT
The divalent metal cadmium (Cd) is used in multiple industrial processes. It has no known biological role in humans, and all of its perceptible effects are toxic. Although the metal can be inhaled in polluted air as Cd oxide, it is acquired primarily from food or tobacco grown in contaminated soil. Initially, it is stored in hepatocytes in complexes with the protein metallothionein (CdMT). Subsequently, hepatic CdMT is released into the circulation, filtered by renal glomeruli, and reabsorbed by proximal tubules. After a process requiring several steps, Cd is again stored as CdMT, but the small fraction that eludes complexation inflicts continuous injury, and the severity of the injury is proportional to the magnitude of the burden. That burden may increase for many years after cessation of exposure because of ongoing release from the liver. Functional expressions of Cd toxicity include spillage of intracellular proteins, defective reabsorption of multiple filtered substances, cell death, nephron loss, and consequent reduction of glomerular filtration rate. Cd is an important bone toxin. In high doses, it causes osteomalacia; in low doses and in multiple regions of the world, it is a highly prevalent cause of osteoporosis. Epidemiologic data suggest that Cd predisposes humans to hypertension, liver inflammation, macular degeneration, and Alzheimer’s disease. Cd is a carcinogen, especially in the lungs and kidneys, and it potentiates the renal effects of diabetes. Prevention of Cd toxicity requires minimization of environmental exposure, sufficient intake of Zn, and maintenance of adequate body content of iron.
