Subchronic dietary exposure of rats to cadmium alters the metabolism of metals essential to bone health.

Cadmium (Cd) was recently identified as a risk factor for osteoporosis. Skeletal damage may be the critical effect of low-level long-term exposure to Cd in the general population exposed via food, but the mechanisms behind this are not clearly understood. We investigated the effect of dietary Cd exposure on metals involved in bone turnover. Female rats received a Cd-supplemented diet (0, 10, 50, or 200 CdCl2 mg/kg diet) for 13 weeks. Cd and essential metals stored in the liver were measured by ICP-MS multianalysis. Mineral content of the livers was modified according to Cd level: iron, magnesium and selenium decreased while copper, zinc and manganese increased with increasing Cd levels. Iron was the most strikingly affected metal, falling to one-fifth of control values at high dietary Cd exposure. In this dosage group, selenium decreased to 36% of mean control concentrations while zinc increased to 168%. This mineral imbalance, especially depleted iron stores, can contribute, at least in part, to the Cd-associated risk of osteoporosis. The association between iron metabolism and Cd exposure should be investigated in humans, as Cd and low iron stores could act synergistically as risk factors for osteoporosis.