A biological exposure index for isopropanol has not been established by the ACGIH (ACGIH, 2000). The biological exposure index for acetone, the metabolite of isopropanol, is an end of shift urinary acetone concentration of 50 mg/l (ACGIH, 2000).

Isopropanol is a common industrial and laboratory solvent and is present in a wide range of domestic products and in some coolants and antifreezes. Historically, it was available as a 'rubbing alcohol' for the relief of rheumatic and muscular pain, and for cooling fevers in children (Garrison, 1953; Adelson, 1962). The medicinal uses of isopropanol are now limited owing to the potential for serious effects (Garrison, 1953; McFadden and Haddow, 1969). Despite the widespread use of isopropanol, there are very few reports of toxic effects following chronic or occupational exposures. It is considered to have a relatively low order of acute and chronic toxicity (Bevan, 2001). The majority of the information on toxicity, kinetics and clinical effects are known from acute cases including intentional ingestion as an ethanol substitute, intentional self-harm, excessive dermal application and therapeutic errors in administration (Garrison, 1953; Adelson, 1962; McFadden and Haddow, 1969; Alexander et al., 1982; Vicas and Beck, 1993).

Isopropanol is predominantly a central nervous system (CNS) depressant. However, toxicity following exposure to isopropanol is also related to its metabolite acetone, which is also a CNS depressant. It is controversial whether it is the parent compound or its metabolite that is responsible for the major CNS effects observed following exposure to isopropanol. An intentional ingestion by an individual with reduced alcohol dehydrogenase activity did not result in the profound CNS depressant effects expected for the volume consumed. The lack of serious effects was probably related to the reduced production of acetone (Chan et al., 1993). However, Gaudet and Fraser (1989) report a patient who was awake and conversant when his blood acetone concentration was at its peak (1,600 mg/l).

Following ingestion, isopropanol is rapidly absorbed, with signs and symptoms occurring within 30 minutes of ingestion (Lacouture et al., 1983; Pappas et al., 1991). In some cases absorption time is delayed, especially following ingestion of large volumes of isopropanol. Ingestion of as little as 20 ml can cause effects (Lacouture

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