Inorganic tin salts are poorly absorbed and rapidly excreted in the faeces; as a result they have a low toxicity. Only about 5 per cent is absorbed from the gastrointestinal tract, widely distributed in the body, then excreted by the kidney. Some tin is deposited in lung and bone. Some tin salts can cause renal necrosis after parenteral doses. Mutagenic studies on metallic tin and its compounds have been negative. Long-term animal carcinogenic studies have shown fewer malignant tumours in animals exposed to tin than in controls. Human volunteers developed mild signs of toxicity with tin, given in fruit juices, at a concentration of 1400 mg per litre. The WHO 1973 permissible limit for tin in tinned food is 250 micrograms per kg. The adult daily intake of tin was about 17 mg per day in 1940, but it has now decreased to about 3.5 mg, due to improvements in technique of tinning with enamel overcoat and crimped lids to minimize exposure to tin and lead solder. This level is well below the level of 5-7 mg per kg body weight shown to give rise to toxic symptoms. Tin deficiency has not been described in man. Amounts in excess of 130 mg per day have been shown to accumulate in liver and kidneys. Many of the organotin compounds are toxic; the most toxic being trimethyltin and triethyltin, which are well absorbed from the gastrointestinal tract. Most of the other alkyl and aryltin compounds are poorly absorbed from the gastrointestinal tract, and are therefore less toxic when given orally than when given parenterally. The main results of toxicity are skin and eye irritation; cholangitis of the lower biliary tract, and later hepatotoxicity; and neurotoxicity, which has been shown to be due to intramyelin oedema induced by triethyltin, and neuronal necrosis caused by trimethyltin. Many of the organotin compounds affect mitochondrial oxidative phosphorylation and alter membranes, but the contribution of these biochemical and membrane effects in the cause of intramyelin oedema and neuronal necrosis has not been fully clarified. Widespread degeneration results, especially with trimethyltin. Peripheral neuropathy has not been reported as occurring with either inorganic or organic tin in humans. Certain dialkyltin compounds have been shown to cause adverse effects on cell-mediated immunity, specifically on the T cell lymphocyte. Experimental studies have failed to reveal any evidence of carcinogenicity, mutagenicity, or teratogenicity. Recent studies suggest that tin compounds exhibit some antitumour activity and may have a future role in cancer diagnosis and chemotherapy, and in controlling hyperbilirubinaemia.