Kalina I, Brezáni P, Gajdosová D, Binková B, Salagovic J, Habalová V, Mracková G, Dobiás L, Srám R J
Department of Medical Biology, School of Medicine, P.J. Safárik University, Tr.SNP 1, 040 66, Kosice, Slovak Republic.
Mutat Res. 1998 Sep 1;417(1):9-17. doi: 10.1016/s1383-5718(98)00089-8.
Cytogenetic markers (chromosomal aberrations, sister chromatid exchanges (SCE), cells with high frequency of SCE (HFC), the heterogeneity index SCE (SCE-H) and genetic polymorphism of genotypes GSTM1 and NAT2 were evaluated in the peripheral lymphocytes of 64 coke oven workers and 34 control subjects from the same plant. Personal monitors were used to evaluate exposure to eight carcinogenic (polycyclic aromatic hydrocarbons) PAHs, including B[a]P, during an 8-h working shift. Smoking habits were checked by urinary cotinine measurement. The exposure among coke oven workers ranged widely from 0.6 to 547 microgram/m3 and 2 to 50 137 ng/m3, for carcinogenic PAHs and B[a]P, respectively. The respective values in controls were 0.07 to 1.51 microgram/m3 and from 2 to 63 ng/m3. The results of biomonitoring in exposed vs. control subjects were as follows: frequency of chromosomal aberrations (% AB.C.), 2. 30% AB.C. vs. 1.09% AB.C. (P<0.05); sister chromatid exchanges, 7.47 SCE/cell vs. 5.49 SCE/cell (P<0.05); HFC, 5.94% vs. 2.06% (P<0.05) and SCE-H index, 1.49 vs. 1.01 (P<0.05). All the cytogenetic markers were significantly increased in the exposed vs. control groups. The effect of smoking was observed only in SCE when evaluated as HFC. Using individual exposure data for carcinogenic PAHs, a significant correlation between exposure and %AB.C. (r=0.372, P=0.0002), SCE/cell (r=0.331, P=0.001), HFC (r=0.467, P=0.007) and SCE/H (r=0. 286, P=0.004) was found. No effects of GSTM1 and NAT2 genotypes, individually or in combination, on the cytogenetic markers was observed. It is concluded that occupational exposure of coke oven workers involved in this study resulted in an increased level of chromosomal aberrations and SCE. The frequency of AB.C. and SCE/cell was found to be related to exposure to carcinogenic PAHs.
对来自同一工厂的64名焦炉工人和34名对照者的外周血淋巴细胞进行了细胞遗传学标志物(染色体畸变、姐妹染色单体交换(SCE)、SCE高频细胞(HFC)、SCE异质性指数(SCE-H)以及基因型GSTM1和NAT2的基因多态性)评估。使用个人监测仪评估了8小时工作班次期间对包括苯并[a]芘在内的8种致癌性(多环芳烃)PAHs的暴露情况。通过测定尿中可替宁来检查吸烟习惯。焦炉工人中致癌性PAHs和苯并[a]芘的暴露范围分别为0.6至547微克/立方米和2至50137纳克/立方米。对照组的相应值分别为0.07至1.51微克/立方米和2至63纳克/立方米。暴露组与对照组的生物监测结果如下:染色体畸变频率(%AB.C.),2.30%AB.C.对1.09%AB.C.(P<0.05);姐妹染色单体交换,7.47次SCE/细胞对5.49次SCE/细胞(P<0.05);HFC,5.94%对2.06%(P<0.05)以及SCE-H指数,1.49对1.01(P<0.05)。与对照组相比,所有细胞遗传学标志物在暴露组中均显著增加。当将吸烟作为HFC进行评估时,仅在SCE中观察到吸烟的影响。利用致癌性PAHs的个体暴露数据,发现暴露与%AB.C.(r=0.372,P=0.0002)、SCE/细胞(r=0.331,P=0.001)、HFC(r=0.467,P=0.007)和SCE/H(r=0.286,P=0.004)之间存在显著相关性。未观察到GSTM1和NAT2基因型单独或联合对细胞遗传学标志物有影响。得出的结论是,本研究中涉及的焦炉工人的职业暴露导致染色体畸变和SCE水平升高。发现AB.C.频率和SCE/细胞与致癌性PAHs的暴露有关。