Children may be exposed to arsenic during contact with structures treated with chromated copper arsenate (CCA). A high frequency of hand-to-mouth activity may increase their risk of ingesting arsenic. Previous work showed that arsenic concentrations in the hand-wash samples of children playing on CCA playgrounds were four times higher than those playing on non-CCA playgrounds. It is not clear whether playing on CCA playgrounds results in elevated overall exposure to arsenic. The objective of this study was to perform arsenic biomonitoring in children to determine whether playing on CCA-treated playgrounds substantially contributes to their overall exposure to arsenic. One hundred and twenty five saliva samples from 61 children and 101 urine samples from 45 children were collected after children played on 8 CCA and 8 non-CCA playgrounds. Arsenic speciation analysis was conducted using high performance liquid chromatography combined with inductively coupled plasma mass spectrometry. The arsenic species detected in the urine and saliva samples from children playing on CCA and non-CCA playgrounds were similar. Dimethylarsinic acid and arsenobetaine were the main arsenic species found in urine samples. The sum of inorganic trivalent and pentavalent arsenic, monomethylarsonic acid, and dimethylarsinic acid in urine was 15 +/- 28 microg/L in the CCA group and 12 +/- 23 microg/L in the non-CCA group (p = 0.60). The sum of these species in saliva was 1.1 +/- 2.1 microg/L in the CCA group and 1.4 +/- 1.1 microg/L in the non-CCA group (p = 0.32). These results show that there is no significant difference in the concentration or speciation of arsenic between the samples from children playing on CCA and non-CCA playgrounds. Contact with CCA playgrounds is not likely to significantly contribute to the overall arsenic exposure in children; other sources such as dietary arsenic may be a main contributor to their overall exposure.

High levels of benzo(a)pyrene diol epoxide (BPDE)-DNA adducts in white blood cells have been indicated as a risk factor for lung cancer. Sensitive, specific, fast and cost-efficient techniques for the detection of BPDE-DNA adducts in white blood cells are required for routine human biomonitoring. In the present study, an immunoassay based on CE/LIF was developed for the detection of BPDE-DNA adducts in mononuclear white blood cells (MNCs). Although glutathione (GSH) conjugation catalyzed by glutathione-S-transferase (GST) is considered to be the major pathway for inactivating BPDE, the effect of GSH depletion on BPDE-DNA adduct formation in MNCs has not been assessed. Therefore, we applied the newly developed method to study the effect of GSH depletion by D,L-buthionine-[S,R]-sulfoximine (BSO) on the level of DNA adducts. We found that pretreatment of MNCs with 150 microM BSO for 2 h prior to BPDE exposure increased the level of BPDE-DNA adducts appreciably (by approximately 70%). Further investigations revealed that the 2-h BSO treatment neither decreased the GSH level instantly nor affected GST activity; rather, it prevented the induction of GSH in response to subsequent BPDE incubation. The blocked synthesis of GSH might be responsible for the elevated level of BPDE-DNA adducts in MNCs after BSO and BPDE treatment.

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