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There are extensive data available from animal models and in vitrowork on the toxicokinetics of propylene oxide that indicate that about 25% of inhaled propylene oxide is absorbed(Csanádyand Filser, 2006; Morris et al., 2004; Morris and Pottenger, 2006).

Two studies investigated upper respiratory uptake of propylene oxide in rats and mice. Rats were exposed to 300 ppm propylene oxide for 15, 30, 45, or 60 min at a flow rate of 200 ml/min or 50 ml/min (Morris et al., 2004). The uptake average was approximately 25% efficient at 50 ml/min flow rate compared to approximately 11% efficient at 200 ml/min flow rate, regardless of the exposure concentration. In this study at concentrations of 100 ppm or more, propylene oxide exposure resulted in significant depletion of nasal respiratory mucosal nonprotein sulfhydryls (NPSH), providing strong evidence that direct reaction and/or conjugation of propylene oxide with glutathione and/or other NPSH groups occurred. Propylene oxide exposure was shown to also deplete nasal NPSH levels in the mouse. Olfactory NPSH content averaged 63 and 48% of control in the 300- and 500-ppm groups. (Morris and Pottenger, 2006). Average uptake was similar to that observed in rats with 29% efficient at 12 ml/min flow rate and approximately 11% efficient at 50 ml/min flow rate, regardless of the exposure concentration.

Propylene oxide is demonstrated to berapidly biotransformed by rats. Only a small fraction (3%) was exhaled unchanged (Golkaet al., 1989); the majority of absorbed propylene oxideis widely distributed throughout the organism following inhalation exposure to high levels, based on adduct formation in proximal and distant tissues (Osterman-Golkar et al., 2003; Rios-Blancos et al., 1997, 2000, 2003). The absorbed propylene oxide is available for detoxificationviaglutathione-S-transferase-mediated conjugation with glutathione (GSH) or hydrolysisviaEpoxide Hydratase (EH) (Faller et al., 2001; Lee et al, 2005).  Propylene oxide also binds with cellular macromolecules, including hemoglobin and DNA (Osterman-Golkar et al., 1999, 2003; Rios-Blancos et al., 1997, 2000, 2002, 2003). Such data provide important dosimetry information on the internal dose and distribution of propylene oxide, including calculation of the half-life of 3 days for the predominant DNA adduct formed, the N7-hydroxypropylguanine (Segerback et al., 1994, 1998; Plna et al., 1999).

The limited data available from worker populations (Boogaardet al., 1999;Czèneet al., 2002; Schettgenet al., 2002) indicate that propylene oxide is absorbed and that adduct formation occurs in humans exposedviainhalation, similar to the animal data.

Based on the information available, propylene oxide is expected to be readily absorbed through the gastrointestinal and respiratory tracts and widely distributed to the major organs. There is no data available for dermal absorption but acute dermal toxicity data indicate the potential for dermal absorption of the liquid. No information is available regarding the potential for dermal absorption of the vapour.