The historical background, clinical features, morphology, epidemiology and aetiology of halothane hepatitis have been presented. Animal models of halothane hepatotoxicity have been described, although their application to humans is of doubtful significance. Two, probably distinct, forms of liver damage associated with halothane have been identified. The much more common mild form may result from reductive biotransformation of halothane, possibly influenced by genetic factors, or reduced liver oxygenation, whereas the rare fulminant form is most likely to be immune-mediated. The role of altered calcium homeostasis has not yet been established. In addition, a common mechanism for liver dysfunction associated with halogenated volatile anaesthetic agents has been proposed. The hepatotoxicity of enflurane cannot be excluded; while hepatic dysfunction after isoflurane or nitrous oxide is considered unlikely, further attention is necessary. It is too soon to comment on the hepatotoxic potential of sevoflurane or desflurane.