Abstract
Human beings are normally exposed to only a very small amount of environmental cadmium (Cd) in food,leading to gradual Cd accumulation in their bodies,especially in the liver and kidneys, with aging due to the long biological half-life of Cd. The sentinel sign of adverse effect is renal tubular dysfunction, which is characterized by low-molecular-weight proteinuria, and can occur in concert with anemia or bone mineral loss if the exposure level is high, known as Itai-itai disease; it is found in a heavily Cd-polluted area. The accumulation of Cd in the kidneys to some extent without apparent toxic effect is because of the formation of metallothionein, a metal-protein complex. However, when the levels of Cd exceed the critical concentration, the release of free Cd from the complex causes dysfunction of proximal tubular reabsorption of low molecular weight proteins. In general, current exposure levels of Cd among Japanese is sufficiently lower than current provisional tolerable monthly intake (PTMI). But there exist concerns on adverse health effects especially among farmers in Cd-high farmland, because there are small margin of exposure.
