The liver is the major site of endogenous and exogenous drug metabolism. The primary result of drug metabolism is the production of more water-soluble and therefore more easily excreted drug metabolites. Drugs are sometimes biotransformed into more reactive metabolites, which may lead to toxicity. Volatile anesthetics, like most drugs, undergo metabolism in the body and are sometimes associated with toxic reactions. Here, author will discuss the metabolism and hepatic toxicity of inhaled anesthetics. Toxicity and liver injury have been reported after repeated exposure on subsequent occasions to different fluorinated anesthetics. This phenomenon of cross-sensitization has also been reported with the chlorofluorocarbon(CFC) replacement agents, the hydrochlorofluorocarbons(HCFCs). Halothane, enflurane, sevoflurane, isoflurane, desflurane are all metabolized to trifluoroacetic acid, which have been reported to induce liver injury in susceptible patients. The propensity to produce liver injury appears to parrel metabolism of the parent drug: halothane(20%) >>>> enflurane(2.5%) >> sevoflurane(1%) > isoflurane(0.2%) > desflurane(0.02%). The use of any anesthetic must be based on its benefits and risks, how it may produce toxicity, and in which patients it may be most safely administered. Nonhalogenated inhaled anesthetics (nitrous oxide, xenon) chemically inert and not metabolized in human tissue. The perfect anesthetic agents dose not exist. But ongoing research attempts to uncover emerging toxicities. Xenon is not currently approved for clinical use. Other than the expense associated with its use, it may be the most ideal anesthetic agent. In general, surgical manipulation or disturbance of the surgical site appears to be more important in decreasing hepatic blood flow than current anesthetic agents such as isoflurane, sevoflurane, and desflurane or technique. However, the clinician is challenged to balance new information with current clinical practices and choice the safest, most effective agents for each patient.