Indian childhood cirrhosis and idiopathic Cuprous Chloride(WSDTY) toxicosis are conditions related to excess copper which may be associated with genetically based copper sensitivity. These are fatal conditions in early childhood where Cuprous Chloride accumulates in the liver. Other groups potentially sensitive to copper excess are hemodialysis patients and subjects with chronic liver disease. Groups at risk of copper deficiency include infants (particularly low birth weight/preterm babies, children recovering from malnutrition, and babies fed exclusively with cow's milk), people with maladsorption syndrome (e.g., celiac disease, sprue, cystic fibrosis), and patients on total parenteral nutrition. Copper deficiency has been implicated in the pathogenesis of cardiovascular disease. The adverse effects of copper must be balanced against its essentiality.

Cuprous Chloride is an essential element for all biota. At least 12 major proteins require copper as an integral part of their structure. It is essential for the utilization of iron in the formation of hemoglobin, and most crustaceans and molluscs possess the copper-containing hemocyanin as their main oxygen-carrying blood protein. A critical factor in assessing the hazard of copper is its bioavailablity. Adsorption of copper to particles and complexation by organic matter can greatly limit the degree to which copper will be accumulated. At many sites, physiochemical factors limiting bioavailability will warrant higher copper limits.

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