Submitted to: Risk Assessment Conference Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 8/26/2003
Publication Date: 9/4/2003
Citation: Chaney, R.L., Ryan, J.A., Reeves, P.G. 2003. Cadmium risk perception and assessment-principles and procedures. [abstract]. Abstracts of the SCOPE Workshop on Risk Assessment and Management of Environmental Cadmium. Interpretive Summary:
Technical Abstract: Cadmium consumed in foods grown on soils contaminated by industrial Cd+Zn discharges has caused renal tubular dysfunction in exposed humans in discrete situations. However, lack of understanding about environmental Cd has caused wide concern that general populations may be at risk from soil Cd. Discovery of Cd disease in Japan was the impetus to search for other locations with Cd disease. In other cases where rice-Cd was high because of paddy soil contamination, more human Cd disease was identified. However, other sources of dietary Cd were not found to cause Cd disease (oysters in NZ; gardens in UK, Germany, USA, and The Netherlands). Other studies where differences in the excretion of Cd or ß2-microglobulin among various populations occurred also suggested Cd disease, but these urinary indicators remained within the normal range for individuals over 50 years of age. Because secretion of these proteins in urine is the diagnostic test best associated with Cd disease in humans, and persons with unequivocal disease secrete on the order of 100,000 'g ß2-M/g creatinine, concern about persons exceeding the 95th percentile of a normal distribution are hardly relevant to diagnosis of Cd disease. Thus, it became evident that individuals consuming polished rice grain grown on industrially-contaminated flooded soils for many years suffered Cd disease in many locations, but that individuals consuming garden foods grown in even more highly contaminated soils suffered no Cd disease. What is the explanation for this discrepancy? At the same time, important public health aspects of low bioavailable Fe and Zn in polished rice were recognized, and a program was initiated to breed rice with higher bioavailable Fe and Zn. Studies by Reeves and Chaney confirmed work by Fox et al., which indicated that marginal deficiency of Fe and Zn could cause over 10-fold increase in net absorption of dietary Cd. Coupled with the public health evidence that subsistence rice consumers commonly suffer frank Fe and Zn deficiencies, this information provides an alternative explanation for how and where Cd disease will occur. Further, in contrast with other staple grains, rice grown on Cd+Zn contaminated fields rejects Zn from the grain but not Cd. Thus, flooded rice can comprise high Cd risk when soils are contaminated with Cd+Zn from mining and smelting. In some locations, Cd contamination is accompanied by little Zn, which could allow Cd transfer in food-chains to be much greater; fortunately these sources have not contaminated large land areas. Similarly, Cd applied in P-fertilizers comprise less risk than some have estimated because they ignored these soil and crop factors which affect Cd bioavailability and risk A fuller understanding of food-chain transfer of soil Cd in relation to soil Zn and a realization of the many crop and dietary factors that affect the bioavailability of Cd, Zn and Fe in regional diets, support a new paradigm for risk assessment for soil Cd. Accordingly, regulation of crop Cd limits should take into account both the differences in Cd bioavail-ability and the presence of co-contaminating Zn at high levels that can reduce Cd risk for most crops. A one-size-fits-all regulation of soil or crop Cd is no longer appropriate.