loendothelial cells and hepatocytes (Harris et al. 1998). An issue that merits investigation is the extent to which aceruloplasminemia might modulate an individual's susceptibility to copper toxicity.

Between about 1900 and 1980, 138 infants and young children died in the Tyrolean area of western Austria from liver cirrhosis; that syndrome has been termed Tyrolean infantile cirrhosis (TIC) (Müller et al. 1996). The pathology of TIC is indistinguishable from Indian childhood cirrhosis and other forms of hepatic copper toxicosis (see descriptions below) (Müller et al. 1996). A common feature among the infants and young children with TIC was having been fed a one-to-one mixture of unpasteurized cow's milk with water heated for about 20 min in old copper pots (Müller et al. 1996). Such a preparation results in a high concentration of copper in the milk (Müller et al. 1996). Copper cooking utensils were common in the Tyrolean area because of an extensive copper mining industry that was present until about 1926. The disease appears to be an autosomal recessive disorder (Müller et al. 1996), whose manifestations might be due to a combination of a genetic predisposition and a high intake of copper. Reports of this syndrome have essentially disappeared since about 1980, probably as copper cooking utensils were gradually replaced in the region by modern cooking utensils in the mid-to-late 1960s.

The etiology of Indian childhood cirrhosis (ICC) appears to be similar to that of TIC (Bavdekar et al. 1996; Bhave et al. 1982; Pandit and Bhave 1996; Popper et al. 1979; Tanner et al. 1983; Tanner et al. 1979). ICC occurs in India in infants and very young children fed milk stored in brass or copper containers. Copper might have a role in the disease for the following reasons: milk stored in that manner is very high in copper (Popper et al. 1979; Tanner et al. 1979; Bhave et al. 1982; Tanner et al. 1983; Bavdekar et al. 1996; Pandit and Bhave 1996); high copper concentrations have been found in the livers of ICC patients (Bavdekar et al. 1996; Bhave et al. 1982; Pandit and Bhave 1996; Popper et al. 1979; Tanner et al. 1983; Tanner et al. 1979); penicillamine treatment rapidly improves the symptoms (Bavdekar et al. 1996; Bhave et al. 1982; Pandit and Bhave 1996; Popper et al. 1979; Tanner et al. 1983; Tanner et al. 1979); and other possible causes of liver disease have been ruled out in most of the patients (Bavdekar et al. 1996; Bhave et al. 1982; Pandit and Bhave 1996; Popper