SALICYLATE continues to be a leading cause of accidental poisoning in the United States; in 1964 there were more than 16,000 cases of accidental aspirin ingestion among all age groups, accounting for 25.8 per cent of all accidental poisonings reported1. Existing methods for the treatment of salicylate poisoning are aimed at alkalinization of the urine and extrarenal removal of the drug2,3. The natural elimination of salicylate in man is a slow process. The average half-life of a single 1 g dose of aspirin is reported to be 6 h (ref. 4), and high doses have given half-life values up to 19 h (ref. 5). Administration of salicylate labelled with carbon-14 to man6 has given the following metabolites (here reported as average mean values): free salicylate 61 per cent; salicylic phenolic glucuronide 22 per cent; salicyluric acid 8 per cent; salicylic acyl glucuronide 5 per cent; and gentisic acid 1 per cent. The conjugates of salicylic acid are less diffusible across cell membranes and thus have given higher clearances7. Furthermore, the excretion of salicyluric acid after administration of acetylsalicylate or salicylate is limited by the ability to conjugate salicylate with glycine rather than the excretion capacity of the kidneys8.