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对接触苯乙烯和苯乙烯-7,8-氧化物的工人多种生物标志物的调查。

An investigation of multiple biomarkers among workers exposed to styrene and styrene-7,8-oxide.

作者信息

Rappaport S M, Yeowell-O'Connell K, Bodell W, Yager J W, Symanski E

机构信息

School of Public Health, University of North Carolina, Chapel Hill 27599-7400, USA.

出版信息

Cancer Res. 1996 Dec 1;56(23):5410-6.

PMID:8968094
Abstract

Investigations of cancer and cytogenetic damage among reinforced-plastics workers have produced contradictory results. In all studies, the focus has been on styrene rather than the carcinogen, styrene-7,8-oxide (SO), traces of which are generated during the manufacturing process. Because styrene is present at very high levels and is metabolized almost exclusively through SO, coexposures to SO have been discounted. This study investigated the relative contributions of airborne styrene and SO and of smoking toward several SO-specific biomarkers (DNA and albumin adducts) and sister chromatid exchanges in the blood of 48 reinforced-plastics workers. Among individual subjects, albumin and DNA adducts as well as sister chromatid exchanges were significantly correlated with styrene exposure. However, among the 20 subjects with measurements to both styrene and SO, albumin adducts were significantly correlated with exposure to SO but not to styrene. Finally, among the 10 job groups, surprisingly strong correlations (0.709 < or = r < or = 0.966) were found between all SO biomarkers and exposure to SO but not to styrene. Calculations suggest that SO was about 2000 times more effective than styrene in producing SO biomarkers. After accounting for the disparate exposures to the two chemicals, a typical worker received 71% of the systemic dose of SO via inhalation; nonetheless, 5 of the 20 subjects received the majority of the SO dose from styrene. Cigarette smoking increased levels of SO-albumin and SO-DNA adducts, suggesting that SO was a constituent of tobacco smoke. We conclude that inhalation of SO should be considered in any interventions to reduce health risks.

摘要

对增强塑料工人的癌症和细胞遗传学损伤调查产生了相互矛盾的结果。在所有研究中,重点都放在了苯乙烯而非致癌物苯乙烯 - 7,8 - 氧化物(SO)上,在制造过程中会产生痕量的SO。由于苯乙烯含量极高且几乎完全通过SO代谢,因此对SO的共同暴露被忽视了。本研究调查了空气中苯乙烯和SO以及吸烟对48名增强塑料工人血液中几种SO特异性生物标志物(DNA和白蛋白加合物)和姐妹染色单体交换的相对影响。在个体受试者中,白蛋白和DNA加合物以及姐妹染色单体交换与苯乙烯暴露显著相关。然而,在20名同时测量了苯乙烯和SO的受试者中,白蛋白加合物与SO暴露显著相关,而与苯乙烯暴露无关。最后,在10个工作小组中,令人惊讶的是,所有SO生物标志物与SO暴露之间发现了很强的相关性(0.709≤r≤0.966),但与苯乙烯暴露无关。计算表明,在产生SO生物标志物方面,SO的效力比苯乙烯高约2000倍。在考虑了两种化学物质的不同暴露情况后,一名典型工人通过吸入获得了71%的SO全身剂量;尽管如此,20名受试者中有5名从苯乙烯中获得了大部分SO剂量。吸烟会增加SO - 白蛋白和SO - DNA加合物的水平,这表明SO是烟草烟雾的一种成分。我们得出结论,在任何降低健康风险的干预措施中都应考虑吸入SO的因素。

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