PMID- 15036120 OWN - NLM STAT- MEDLINE DCOM- 20040823 LR - 20181113 IS - 0027-5107 (Print) IS - 0027-5107 (Linking) VI - 558 IP - 1-2 DP - 2004 Mar 14 TI - Lack of increased genetic damage in 1,3-butadiene-exposed Chinese workers studied in relation to EPHX1 and GST genotypes. PG - 63-74 AB - 1,3-Butadiene (BD) is an important industrial chemical and pollutant. Its ability to induce genetic damage and cause hematological malignancies in humans is controversial. We have examined chromosome damage by fluorescence in situ hybridization (FISH) and mutations in the HPRT gene in the blood of Chinese workers exposed to BD. Peripheral blood samples were collected and cultured from 39 workers exposed to BD (median level 2 ppm, 6 h time-weighted average) and 38 matched controls in Yanshan, China. No difference in the level of aneuploidy or structural changes in chromosomes 1, 7, 8, and 12 was detected in metaphase cells from exposed subjects in comparison with matched controls, nor was there an increase in the frequency of HPRT mutations in the BD-exposed workers. Because genetic polymorphisms in glutathione S-transferase (GST) enzymes and microsomal epoxide hydrolase (EPHX1) may affect the genotoxic effects of BD and its metabolites, we also related chromosome alterations and gene mutations to GSTT1, GSTM1 and EPHX1 genotypes. Overall, there was no effect of variants in these genotypes on numerical or structural changes in chromosomes 1, 7, 8 and 12 or on HPRT mutant frequency in relation to BD exposure, but the GST genotypes did influence background levels of both hyperdiploidy and HPRT mutant frequency. In conclusion, our data show no increase in chromosomal aberrations or HPRT mutations among workers exposed to BD, even in potentially susceptible genetic subgroups. The study is, however, quite small and the levels of BD exposure are not extremely high, but our findings in China do support those from a similar study conducted in the Czech Republic. Together, these studies suggest that low levels of occupational BD exposure do not pose a significant risk of genetic damage. FAU - Zhang, Luoping AU - Zhang L AD - School of Public Health, University of California, 140 Warren Hall, Berkeley, CA 94720-7360, USA. FAU - Hayes, Richard B AU - Hayes RB FAU - Guo, Weihong AU - Guo W FAU - McHale, Cliona M AU - McHale CM FAU - Yin, Songnian AU - Yin S FAU - Wiencke, John K AU - Wiencke JK FAU - Patrick O'Neill, J AU - Patrick O'Neill J FAU - Rothman, Nathaniel AU - Rothman N FAU - Li, Gui-Lan AU - Li GL FAU - Smith, Martyn T AU - Smith MT LA - eng GR - P42 ES004705/ES/NIEHS NIH HHS/United States GR - P42ES04705/ES/NIEHS NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - Netherlands TA - Mutat Res JT - Mutation research JID - 0400763 RN - 0 (Butadienes) RN - 0 (DNA Primers) RN - EC 2.4.2.8 (Hypoxanthine Phosphoribosyltransferase) RN - EC 2.5.1.18 (Glutathione Transferase) RN - EC 3.3.2.- (Epoxide Hydrolases) RN - JSD5FGP5VD (1,3-butadiene) SB - IM MH - Base Sequence MH - Butadienes/*toxicity MH - China MH - Chromosomes, Human, Pair 12 MH - Chromosomes, Human, Pair 8 MH - DNA Primers MH - Epoxide Hydrolases/*genetics MH - Genotype MH - Glutathione Transferase/*genetics MH - Humans MH - Hypoxanthine Phosphoribosyltransferase/genetics MH - In Situ Hybridization, Fluorescence MH - *Occupational Exposure PMC - PMC1249498 MID - NIHMS2763 EDAT- 2004/03/24 05:00 MHDA- 2004/08/24 05:00 PMCR- 2007/12/09 CRDT- 2004/03/24 05:00 PHST- 2003/08/13 00:00 [received] PHST- 2003/11/10 00:00 [revised] PHST- 2003/11/13 00:00 [accepted] PHST- 2004/03/24 05:00 [pubmed] PHST- 2004/08/24 05:00 [medline] PHST- 2004/03/24 05:00 [entrez] PHST- 2007/12/09 00:00 [pmc-release] AID - S1383571803003218 [pii] AID - 10.1016/j.mrgentox.2003.11.001 [doi] PST - ppublish SO - Mutat Res. 2004 Mar 14;558(1-2):63-74. doi: 10.1016/j.mrgentox.2003.11.001.