Occurrence of styrene-7,8-oxide and styrene glycol in mouse after the administration of styrene.

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Abstract
Styrene-7,8-oxide and its hydrated product styrene glycol were determined in mouse tissues at different times (0.5-5 h) after the i.p. administration of 7-[14C]-styrene (3.8 mmol/kg). In a study of the influence of dose on the metabolite pattern of styrene, mice were killed 2 h after a dose of 1.1, 2.3, 3.4, and 5.1 mmol/kg, respectively. The mouse tissues studied (blood, liver kidney, lung, brain, subcutaneous adipose tissue) were isolated and extracted first with hexane to remove styrene and styrene-7,8-oxide and then with ethyl acetate to remove styrene glycol. .beta.-Glucuronidase was used to liberate conjugated styrene glycol. A gas-liquid chromatographic method based on the use of an electron capture detector (GLC-EC) was used to quantify styrene glycol, as well as styrene-7,8-oxide, after hydrolysis. In addition all homogenates and extracts were assayed by radioactivity counting. Styrene-7,8-oxide and styrene glycol reached maximum concentrations within 2 h. The highest levels of styrene-7,8-oxide were detected in the kidneys and subcutaneous adipose tissue, while the lungs showed the lowest levels. Styrene glycol was found in the highest concentrations in the kidneys, liver, blood, and lungs. The concentration of unmetabolized styrene increased exponentially at higher doses. There seemed to be a linear increase with the dose of styrene-7.8-oxide and styrene glycol in all the tissues studied. The more polar metabolites occurred at relatively lower levels in the liver and kidneys at higher doses. Ina completentary study the epoxide hydratase inhibitor trichloropropene oxide was added to the removed tissues, and the hexane extracts were analyzed for styrene-7,8-oxide both by CLC-EC and mass spectrometry (GLC-MS). [Implications for human industrial exposure are discussed.].

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