The feeding of housed lambs on conserved forages and pelleted rations is accompanied by a high risk of chronic copper (Cu) poisoning (CCP) which might be reduced by selecting sires for low liver Cu status. Livers were therefore retrieved from Suffolk, Texel and Charollais lambs, slaughtered during the course of a performance trial, to ascertain sire and possibly breed effects on the rate of Cu accretion in the liver. In total, 160 livers were obtained, 100 from Suffolk, 40 from Texel and 20 from Charollais lambs, the progeny of 14, eight and eight sires, respectively. Lambs came from three separately managed flocks but were brought together at 8 weeks of age, weaned onto a common complete diet containing 6·1 mg Cu per kg dry matter (DM) and offered ad libitum. One-fifth of each breed group was slaughtered at 14, 18 or 22 weeks and the remaining 40% at 26 weeks of age. Mean (s.e. ) liver Cu concentrations at those ages were 3220 (450), 4639 (464), 6426 (468), and 6513 (370) µmol/kg DM for Suffolk, and 5843 (811), 6579 (857), 8017 (811) and 10406 (589) µmol/kg DM for Texel, respectively. The pattern of liver Cu accretion differed, the Suffolk starting at a low value yet reaching a plateau at about 22 weeks of age (significant quadratic regression coefficient), the Texel, continually increasing from a high initial value at an average rate of 53·7 (s.e.10·6) µmol/kg DM per day. There was a significant effect of sire on liver Cu in the Suffolk (P 0·05) with a heritability of 0·85 (s.e. 0·44); in the Suffolk and Texel combined, the heritability was 0·60 (s.e. 0·33). The data available on the Charollais were too limited to test for sire effects but at 26 weeks of age, where most information was available, the mean liver Cu concentration was 7285 (s.e.826) µmol/kg DM. At a given age, food intake, liver weight and live weight were each lowest in the Texel but when expressed as a proportion of live weight (LW), both food intake (43 g/kg LW) and liver weight (5·15 g DM per kg LW) were similar among breeds (P 0·05). Thus, differences in liver Cu accretion are unlikely to reflect differences in Cu intake per unit liver weight. There was a tendency for liver size per kg LW to decrease as liver Cu rose in the Texel but not in the Suffolk. Continued hepatic Cu accretion in the Texel may reflect a breed-specific inability to cope with Cu overload. Increases in liver Cu to marginally toxic levels in some Suffolk, some Charollais and most Texel lambs, and to a level commonly associated with toxicity in one Texel lamb, on a ration of moderate Cu concentration highlights the difficulty of controlling risk of CCP by manipulating dietary composition. The current EC limit for Cu in ovine diets, 17 mg Cu per kg DM, is clearly too high for the breeds and dietary conditions used in this study. However a safe limit would be hard to achieve and hence the need to exploit sire variation in propensity to accumulate liver Cu to reduce disease risk.