Only 2-3% of absorbed MEK is exhaled unchanged (Liira et al., 1988a; 1988b). The concentration of MEK in expired air correlates with the exposure concentration (Tada et al., 1972; Perbellini et al., 1984). In volunteers exposed to MEK, a steady state concentration of MEK in the breath was reached after two hours and was 5-6% of the exposure concentration (Brown et al., 1987; Dick et al., 1988). MEK is rapidly eliminated from the lungs. In a volunteer study more than half the subjects had no detectable MEK in breath samples taken 90 minutes after cessation of exposure (Brown et al., 1987).

In a volunteer study following exposure to 200 ppm MEK for four hours, two elimination phases were identified in blood (Liira et al., 1988a). For the first phase (0-45 minutes after cessation of exposure) the half-life was 30 minutes and for the second (60-320 minutes post-exposure) it was 81 minutes. In another study the half-life of MEK was estimated to be 49 minutes (Dick et al., 1988).

Urinary excretion of MEK and 3-hydroxy-2-butanone only accounts for approximately 0.1% of the absorbed dose (Miyasaka et al., 1982; Perbellini et al., 1984). Only about 3% of MEK is excreted as 2,3-butanediol, however there is wide interindividual variation (Liira et al., 1988a; 1988b).

Using the data of Munies and Wurster (1965), Liira et al. (1988a) estimated that following ingestion of 375 mg of MEK in a gelatine capsule about 30% was excreted through the lungs. The half-life of MEK was 10.1 hours in an individual who intentionally ingested a glue containing 28% MEK, 18% acetone and 39% cyclohexanone and 15% polyvinyl chloride and drank ethanol (Sakata et al., 1989).

The urinary concentrations of both MEK (Miyasaka et al., 1982; Perbellini et al., 1984; Imbriani et al., 1989; Ong et al., 1991; Yoshikawa et al., 1995) and 3-hydroxy-2-butanone (Perbellini et al., 1984) are significantly correlated with the exposure concentration of MEK. However, breath concentrations of MEK do not correlate well with the urinary MEK concentration (Ong et al., 1991).

Accumulation of MEK over a working week is not expected because of the short elimination half-life (Liira et al., 1988a). The metabolism of MEK becomes saturated at relatively low concentrations and consequently a larger proportion would be expected to be excreted both through the lungs and the kidney at high exposure concentrations (IPCS, 1993).

Toxicology of Solvents Mode of action

There is only very limited information on the mode of action of MEK (IPCS, 1993). In cats and dogs, high concentrations (500-10,000 ppm) caused pulmonary vasoconstriction and hypertension (Zakhari et al., 1977). The main hazard of MEK is its ability to potentiate the effects, particularly the neurotoxicity, of other substances (IPCS, 1993).

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