All are hepatotoxic except

Isoflurane is metabolized to trifluoroacetic acid. Although serum fluoride fluid levels may rise, nephrotoxicity is extremely unlikely, even in the presence of enzyme inducers. Prolonged sedation (>24 h at 0.1-0.6% isoflurane) of critically ill patients has resulted in elevated plasma fluoride levels (15-50 mmol/L) without evidence of kidney impairment. Similarly, up to 20 MAC-hours of isoflurane may lead to fluoride levels exceeding 50 mmol/L without detectable postoperative kidney dysfunction. Its limited oxidative metabolism also minimizes any possible risk of significant hepatic dysfunction. Total hepatic blood flow (hepatic aery and poal vein flow) may be reduced during isoflurane anesthesia. Hepatic oxygen supply is better-maintained with isoflurane than with halothane, however, because hepatic aery perfusion is preserved. Liver function tests are usually not affected. The major effect of acute inhalation of chloroform is central nervous system depression. At concentrations from 1,500-30,000 ppm, chloroform exposure can induce anesthesia; at concentrations exceeding 40,000 ppm, it can be fatal. Chronic inhalation of chloroform in humans results in hepatotoxicity and central nervous symptoms such as depression and irritability. Meanwhile, chronic oral exposure to chloroform in humans results in effects on the blood, livers, and kidneys. Ref: Miller's anesthesia 8th edition Ref: Morgan & Mikhail's clinical anesthesiology 6e