Tates A D, van Dam F J, de Zwart F A, Darroudi F, Natarajan A T, Rössner P, Peterková K, Peltonen K, Demopoulos N A, Stephanou G, Vlachodimitropoulos D, Srám R J
MGC-Department of Radiation Genetics and Chemical Mutagenesis, Leiden University, Leiden, The Netherlands.
Toxicology. 1996 Oct 28;113(1-3):91-9. doi: 10.1016/0300-483x(96)03432-4.
Blood samples were collected twice (in 1993 and 1994) from 19 workers exposed to 1,3-butadiene and 19 matched controls. Three exposed and three control subjects were the same in 1993 and 1994. Personal passive dosimetry was performed in 1993 and twice in 1994 on the day preceding blood sampling. Mean exposure level in 1994 was 1.76 +/- 4.20 ppm (S.D.) and individual exposure levels ranged between 0.012 ppm (detection limit) and 19.77 ppm. Using the clonal assay, geometric mean of hprt mutant frequencies adjusted for cloning efficiency, age and smoking were, respectively, 7.85 (+/- 7.09) x 10(-6) and 10.14 (+/- 9.16) x 10(-6) in pooled (1993 plus 1994) exposed and control subjects. The difference was not statistically significant indicating that 1,3-butadiene did not induce a detectable increase in mutations at the hprt locus. A similar result was obtained for the 1994 subjects alone. There was no difference between adjusted geometric mean mutant frequencies of exposed and unexposed non-smokers or between exposed and unexposed smokers. Analysis of chromosomal aberrations in lymphocytes from 1994 subjects indicated that the percentage of aberrant cells was significantly enhanced in exposed subjects. In 1993 (data not shown), it was impossible to demonstrate a significant increase of aberrant cells in subjects exposed to 1,3-butadiene. Frequencies of micronuclei in cytochalasin-B blocked binucleate lymphocytes in exposed and unexposed 1994 subjects were not significantly different. This was also the case for earlier samples analyzed in the same plant. Using the comet assay for 1994 subjects, no statistically significant difference was found between the whole group of exposed and unexposed subjects. This was true for both the comet tail length and the percentage of DNA in the tail. In exposed smokers, however, the comet tail length was significantly longer than in unexposed smokers. Unexpectedly, in unexposed smokers the tail length was significantly shorter than in unexposed non-smokers. It was also unexpected that the percentage of DNA in the comet tail was significantly lower in exposed non-smokers than in unexposed non-smokers.
1993年和1994年，从19名接触1,3 - 丁二烯的工人和19名配对对照者身上采集了两次血样。1993年和1994年有3名接触者和3名对照者相同。1993年进行了个人被动剂量测定，1994年在采血前一天进行了两次。1994年的平均暴露水平为1.76 +/- 4.20 ppm（标准差），个体暴露水平在0.012 ppm（检测限）至19.77 ppm之间。使用克隆分析方法，对克隆效率、年龄和吸烟情况进行校正后，1993年和1994年合并的接触组和对照组中，hprt突变频率的几何平均值分别为7.85（+/- 7.09）x 10^(-6)和10.14（+/- 9.16）x 10^(-6)。差异无统计学意义，表明1,3 - 丁二烯未在hprt基因座诱导可检测到的突变增加。仅对1994年的受试者进行分析也得到了类似结果。接触组和未接触组的非吸烟者或吸烟者校正后的几何平均突变频率之间没有差异。对1994年受试者淋巴细胞染色体畸变的分析表明，接触组中异常细胞的百分比显著增加。在1993年（数据未显示），无法证明接触1,3 - 丁二烯的受试者中异常细胞有显著增加。1994年接触组和未接触组中细胞松弛素 - B阻断的双核淋巴细胞中的微核频率无显著差异。在同一工厂分析的早期样本中也是如此。对1994年受试者使用彗星试验，接触组和未接触组的整个群体之间未发现统计学上的显著差异。彗星尾长和尾中DNA百分比均是如此。然而，在接触组吸烟者中，彗星尾长显著长于未接触组吸烟者。出乎意料的是，在未接触组吸烟者中，尾长显著短于未接触组非吸烟者。同样出乎意料的是，接触组非吸烟者彗星尾中DNA的百分比显著低于未接触组非吸烟者。
