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item Chaney, Rufus
item Reeves, Phillip

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/2/2005
Publication Date: 3/8/2005
Citation: Chaney, R.L., Reeves, P.G. 2005. Risk assessment for soil cd should consider soil and crop variation and cd bioavailability. [abstract]. Conference Program for PROLAND OECD Conference. Pulawy, Poland, March 8-13, 2005. p. 46.

Interpretive Summary: --

Technical Abstract: Human disease from soil Cd was first recognized in 1969 in Toyoma, Japan where farm families subsisting on rice experienced both renal tubular dysfunction and osteomalacia. Agricultural and nutritional scientists conducted significant research to understand better the specifics of this case. How did soil Cd move from soil to rice grain and to kidney of consumers? Because there was so little basic knowledge about Cd at that time, conservative assessments were used to prevent new occurrences of Cd disease. In addition, analytical errors were common in measuring Cd at the concentrations present in foods. Toxicologists and epidemiologists built careers on this problem. Their research was important, but they assumed that Cd from different foods had equal bioavailability and caused equal risk despite early evidence that nutritional interactions were very important in Cd absorption and risk. Over time, other populations were studied, but no Cd disease was found even though individuals ingested as much Cd as the Japanese farm families. Oyster fisherpersons and families in New Zealand, gardeners on smelter and mine waste contaminated soils in Europe and the US consumed high amounts of Cd daily but had no adverse effects. By using maximum normal urinary Cd and low molecular weight protein as indicators of Cd toxicity, some toxicologists defined individuals as low as the 90th percentile of normal to be suffering Cd health effects. This was contrary to measurements of actual tubular function. The discrepancy between expected widespread Cd disease and that found only in subsistence rice consumers forced researchers to characterize soil Cd transfer to crops, and to determine the bioavailability of dietary Cd from different types of foods. Although some Cd contamination is from Cd-only sources, an overwhelming majority of all Cd contaminated soils are from Zn-Pb ores (geogenic); such geogenic sources usually contain 100-200 times more Zn than Cd. Agronomically, Zn inhibits Cd uptake by plants, and inhibits Cd transport to storage tissues of plants; conditions which increase Zn and Cd uptake kill plants with Zn phytotoxicity before crop Cd is very increased. Further, increased crop Zn inhibits accumulation of crop Cd in the intestine. Rice is unusual in its handling of soil Cd, and important progress has been made in understanding how this occurs. First, flooded soils form insoluble metal sulfides and raise soil pH to neutral; farmers drain the fields at mid-flowering to improve yields, but this also allows rapid oxidation of CdS which makes the Cd highly phytoavailable; aeration of the soil causes oxidation of Fe and Mn which lowers soil pH. Together these changes after draining fields cause the Cd to be highly phytoavailable to rice. Perhaps more important is the observation that Zn and Fe are excluded from rice grain even in highly Zn contaminated soils. Animal feeding studies to model subsistence rice diets have shown that diets with "marginal" supply of Fe, Zn and Ca can cause 10-20 fold higher Cd absorption than "adequate" diets. In addition, in other studies, it has been found that 100-fold or higher amount of Zn accompanying food Cd inhibits Cd absorption. We have recently completed a study that assessed the role of the metallothionein (MT) genes in Cd absorption in animals. Wild type and MT-null animals fed "marginal" and "adequate" amounts of Zn-Fe-Ca in rice based diets were compared. The presence of MT genes had no effect on Cd absorption or distribution in mice fed food-Cd at concentrations normally found in food. This was in strong contrast with toxicological tests with much higher levels of dietary Cd. These findings should prompt those concerned about risk from soil Cd to human health to reassess the large number of toxicology studies where the Cd dose bore no relationship to that usually found in the human dietary. Many of