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Cancer Epidemiology Biomarkers & Prevention 16, 796-802, April 1, 2007. doi: 10.1158/1055-9965.EPI-06-0915
© 2007 American Association for Cancer Research

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Exposure to Ethylene Oxide in Hospitals: Biological Monitoring and Influence of Glutathione S-Transferase and Epoxide Hydrolase Polymorphisms

Vincent Haufroid1, Brigitte Merz2, Annette Hofmann2,3, Alois Tschopp4, Dominique Lison1 and Philippe Hotz1,2

1 Industrial Toxicology and Occupational Medicine Unit, Catholic University of Louvain, Brussels, Belgium and 2 Occupational and Environmental Medicine Unit, 3 Staff Safety and Environment, and 4 Department of Biostatistics, University of Zurich, Zurich, Switzerland

Requests for reprints: Philippe Hotz, Occupational and Environmental Medicine Unit, University of Zurich, Medizinische Poliklinik USZ, Rämistrasse 100, CH-8091 Zurich, Switzerland. Phone: 41-44-255-97-47; Fax: 41-44-255-98-52. E-mail: philipp.hotz{at}usz.ch

Ethylene oxide is considered as a human carcinogen. A biomarker of exposure would be a useful instrument to assess the risk in occupationally exposed workers. This cross-sectional study aimed at examining (a) whether the urinary excretion of a metabolite of ethylene oxide, 2-hydroxyethyl mercapturic acid (HEMA), could be used for monitoring occupational exposure and (b) whether glutathione S-transferase (GST) and epoxide hydrolase genotypes influenced biological monitoring. Exposure to ethylene oxide was measured by personal sampling in 80 hospital workers (95% of those eligible). HEMA concentrations were determined in three urine samples (baseline, end of shift, and next morning) by liquid chromatography with tandem mass spectrometry. GSTs (GSTT1, GSTM1, and GSTP1) and epoxide hydrolase (EPHX1) were also genotyped. The influence of exposure, genotypes, and several other factors was examined in multiple regression analyses. Exposure was always <1 parts per million. On a group basis, exposure and a non-null GSTT1 genotype increased the HEMA concentrations in the urine sample collected at the end of the shift and these factors remained statistically significant after considering possible confounding or modifying factors. (Cancer Epidemiol Biomarkers Prev 2007;16(4):796–802)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2007 by the American Association for Cancer Research.