There is continuing interest, by health professionals and individuals, in the composition of mainstream tobacco smoke. Regular official surveys of tar, nicotine and carbon monoxide yields are from time to time supplemented by special surveys of specific components. In this study, gas chromatography-mass spectrometry was used to identify and quantify benzene and certain other volatile compounds of interest in the mainstream smoke of 26 cigarette brands on the UK market and of smoke from hand rolled tobacco. Validation of the method adopted demonstrated the ability to identify and to measure reliably the yields of benzene and seven other compounds: toluene, ethylbenzene, m/p-xylene, o-xylene, styrene, isoprene and acrylonitrile. Yields of these analytes were ranked and compared with the tar yields of the brands. In general terms, brands yielding < or = 3 mg of tar yielded proportionately more of the vapour phase analytes than did brands yielding > 3 mg of tar per cigarette. For many of the higher tar brands the yield of vapour phase analyte was approximately proportional to the tar yield. Smoking cigarettes with an average yield of 50 micron of benzene per cigarette has been compared with the occupational maximum exposure limit (16 mg m-3) concentration and with US studies on the home environment. Smoking the majority of brands examined could contribute significantly to the population exposure of benzene and the other volatile organic compounds considered in this study.

Arginase has therapeutic potential as a cytotoxic agent in some cancers, but this is unclear for precursor B acute lymphoblastic leukaemia (pre-B ALL), the commonest form of childhood leukaemia. We compared arginase cytotoxicity with asparaginase, currently used in pre-B ALL treatment, and characterised the forms of cell death induced in a pre-B ALL cell line 697. Arginase and asparaginase both efficiently killed 697 cells and mature B lymphoma cell line Ramos, but neither enzyme killed normal lymphocytes. Arginase depleted cellular arginine, and arginase-treated media induced cell death, blocked by addition of arginine or arginine-precursor citrulline. Asparaginase depleted both asparagine and glutamine, and asparaginase-treated media induced cell death, blocked by asparagine, but not glutamine. Both enzymes induced caspase cleavage and activation, chromatin condensation and phosphatidylserine exposure, indicating apoptosis. Both arginase- and asparaginase-induced death were blocked by caspase inhibitors, but with different sensitivities. BCL-2 overexpression inhibited arginase- and asparaginase-induced cell death, but did not prevent arginase-induced cytostasis, indicating a different mechanism of growth arrest. An autophagy inhibitor, chloroquine, had no effect on the cell death induced by arginase, but doubled the cell death induced by asparaginase. In conclusion, arginase causes death of lymphoblasts by arginine-depletion induced apoptosis, via mechanism distinct from asparaginase. Therapeutic implications for childhood ALL include: arginase might be used as treatment (but antagonised by dietary arginine and citrulline), chloroquine may enhance efficacy of asparaginase treatment, and partial resistance to arginase and asparaginase may develop by BCL-2 expression. Arginase or asparaginase might potentially be used to treat Burkitt lymphoma.

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