The majority of absorbed MEK is metabolised, but the metabolic pathways have not been fully elucidated. The metabolites of MEK found in experimental animals (DiVincenzo et al., 1976; Dietz and Traiger, 1979) and humans (Perbellini et al., 1984; KeZic and Monster, 1988) are 2-butanol, 3-hydroxy-2-butanone (acetylmethylcarbinol) and 2,3-butanediol.

MEK is reduced to 2-butanol which can be converted back to MEK by alcohol dehydrogenase. MEK is also oxidised by carbon chain ra-1 hydroxylation (probably catalysed by the microsomal monooxygenase system) to 3-hydroxy-2-butanone which is then reduced to produce 2,3-butanediol. In humans less than 5% of the absorbed dose is exhaled as MEK and only about 3% is excreted as 2,3-butanediol. The majority of absorbed MEK is thought to be metabolised to 2,3-butanediol, which then enters the general metabolic pathways and is transformed to simple compounds such as water and carbon dioxide (IPCS, 1993).

Experimental data has shown that at high doses the kinetics of MEK are dose-dependent and saturation kinetics may be reached at 50-100 ppm, depending on the workload (Liira et al., 1990b).

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