The ACGIH biological exposure index for MEK is an end of shift urinary MEK concentration of 2 mg/l (ACGIH, 2000).

MEK is of relatively low toxicity (Yang, 1986). There is no record of MEK having caused death or a large scale industrial accident (IPCS, 1993). There is limited information on exposure to MEK alone; most cases involve exposure to mixed solvents. The main hazard of MEK is its ability to potentiate the effects, particularly the neurotoxicity, of other substances (IPCS, 1993). There are many reports in the literature of interactions between MEK and other solvents, including occupational surveys and animal and volunteer studies (reviewed in Noraberg and Arlien-Soborg, 2000).

The pulmonary retention of MEK varies between 41-59% (Liira et al., 1988a, 1988b; Imbriani et al., 1989; Liira et al., 1990a). The concentration of MEK in blood correlates with the exposure concentration (Perbellini et al., 1984; Brown et al., 1987; Ong et al., 1991).

Dermal absorption of MEK is rapid. In a volunteer study MEK was detected in expired air 15 minutes after 100 ml was applied to normal skin of the forearm. A steady state concentration was achieved within 2-3 hours. The moisture content of the skin determined the rate of absorption. Absorption was slow through dry skin and the plateau did not occur until 4-5 hours after application. With moist skin, absorption was very rapid and MEK was detected in expired air within 30 seconds. The maximum concentration averaged four times the plateau concentration for normal and dry skin. However, absorption subsequently declined as MEK desiccated the skin (Munies and Wurster, 1965).

Ingestion of an unknown quantity of a MEK containing glue resulted in a blood MEK concentration of 950 mg/l (13.2 mmol/l) (Kopelman and Kalfayan, 1983). Following ingestion of approximately 240 ml of an ink cleaning solution thought to contain 47% MEK and 45% methanol the blood concentration of MEK was 1,240 mg/l (17 mmol/l) with 240 mg/l (3.3 mmol/l) 2-butanol (Price et al., 1994).

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