Safe levels of cadmium intake to prevent renal toxicity in human subjects

Abstract

The present review attempts to provide an update of the scientific knowledge on the renal toxicity which occurs in human subjects as a result of chronic ingestion of low-level dietary Cd. It highlights important features of Cd toxicology and sources of uncertainty in the assessment of health risk due to dietary Cd. It also discusses potential mechanisms for increased susceptibility to Cd toxicity in individuals with diabetes. Exposure assessment on the basis of Cd levels in foodstuffs reveals that vegetables and cereals are the main sources of dietary Cd, although Cd is also found in meat, albeit to a lesser extent. Cd accumulates particularly in the kidney and liver, and hence offal contains relatively high amounts. Fish contains only small quantities of Cd, while crustaceans and molluscs may accumulate larger amounts from the aquatic environment. Data on Cd accumulation in human kidney and liver obtained from autopsy studies are presented, along with results of epidemiological studies showing the relationship between renal tubular dysfunction and kidney Cd burden. These findings suggest that a kidney Cd level of 50 μg/g wet weight is a maximum tolerable level in order to avoid abnormal kidney function. This renal Cd burden corresponds to a urinary Cd excretion of 2 μg/d. Accordingly, safe daily levels of Cd intake should be kept below 30 μg per person. Individual variations in Cd absorption and sensitivity to toxicity predicts that a dietary Cd intake of 30 μg/d may result in a slight renal dysfunction in about 1 % of the adult population. The previous guideline for a maximum recommended Cd intake of 1 μg/kg body weight per d is thus shown to be too high to ensure that renal dysfunction does not occur as a result of dietary Cd intake.

The Co-Induced Effects of Molybdenum and Cadmium on the Trace Elements and the mRNA Expression Levels of CP and MT in Duck Testicles

“…Bersényi reported that Mo can reduce the contents of Zn in the liver and muscle [7]. Cd can replace Cu and Zn to bind with MT which leads to Zn being redistributed in plasma/serum [49]. The result of the present study showed a significant decrease in the content of Zn in Mo + Cd groups, which indicated that combined action of Mo and Cd may reduce the content of Zn in duck testicles.…”

Chronic renal failure among farm families in cascade irrigation systems in Sri Lanka associated with elevated dietary cadmium levels in rice and freshwater fish (Tilapia)

“…The prevalent high Xuoride content in ground water that is used as drinking water by some farmers would also appear to facilitate Cd absorption through the gastrointestinal tract as Xuoride (JEFCA 2004) compounds of Cd, leading to the present outbreak of CRF in the NCP. The existing situation demands more intensive protective measures in view of the observations made by Satarug et al (2000): "If Cd pollution continuous to increase, so will human dietary Cd exposure, and renal tubular dysfunction is likely to become more prevalent in human populations in the next 10-20 years, particularly in high-risk groups such as those with diabetics and those with poor vitamin C status, low body Fe stores. "…”

The influence of iron stores on cadmium body burden in a Thai population

“…It accumulates in various tissues and organs with the most extensive accumulation occurring in the kidney cortex. Cadmium nephrotoxicity has been detected at renal cadmium concentrations of C50 lg/g wet tissue weight (Satarug et al 2000(Satarug et al , 2003. Cadmium persists in the kidney of humans for many years (half-life of 30 years).…”