Low air levels of benzene: Correlation between biomarkers of exposure and genotoxic effects
Low air levels of benzene: Correlation between biomarkers of exposure and genotoxic effects
复制标题
DOI：
10.1016/j.toxlet.2009.04.028
复制
发表时间：
2010-01-15
影响因子：
3.5
通讯作者：
Manno, Maurizio
中科院分区：
文献类型：
--
作者：
Fracasso, Maria Enrica;Doria, Denise;Manno, Maurizio
通过GC-FID分析，对33名石油化工作业人员(PIO)、28名加油站值班员(SSA)、21名汽油泵维修工(GPMW)和51名非接触苯工人进行了苯暴露检测，以确定接触低苯工人的有用生物标志物，并评价这些指标之间的相关性。使用个人被动采样器(Radiello(R))采集样本。采集末班尿样，用高效液相色谱法测定t，t-肉桂酸(t，t-MA)，用高效液相-质谱仪测定S-苯硫尿酸(S-PMA)。彗星试验碱性版，19例SSA组和16名对照组的外周血淋巴细胞染色体畸变率(CA)和谷胱甘肽(GSH)水平明显高于对照组。与对照组相比，t，t-MA和S-PMA的SSA和PIO的尿量显著增加(t，t-MA和S-PMA分别为p=0.0258和p=0.0001)和PIO(t，t-MA和S-PMA分别为p=0.0013和p=0.0001)，而不连续且仅发生在特定工作日的GPMW组未见明显增加。彗星分析发现，与对照组相比，SSA(TM和TL分别为0.0001和0.008)和PIO(TM和TL分别为0.0001和0.0001)的DNA损伤显著增加。PIO组的彗星细胞数也显著增加(p<；0.0001)。吸烟习惯似乎不会干扰任何一组人的这些结果。接触组与对照组CA患病率差异无统计学意义。在所有组中，苯暴露与更具代表性的彗星参数TM显著相关(在SSA、GPMW和PIO中分别为r=0.509，p=0.007；r=0.525，p=0.017和r=0.420，p=0.046)。接触工人的DNA损伤与GSH、尿S-PMA呈负相关。综上所述，在目前的研究中，尿S-PMA和彗星试验的DNA损伤都对低水平的苯暴露敏感，GSH似乎对苯依赖的DNA损伤起着重要的防御作用。(C)2009爱思唯尔爱尔兰有限公司。保留所有权利。
This study was aimed to identify useful biomarkers of exposure and effect in workers exposed to low levels of benzene, and to evaluate any correlations existing between these parameters.Benzene exposure was measured in 33 petrochemical industry operators (PIO), 28 service station attendants (SSA), 21 gasoline pump maintenance workers (GPMW) and 51 non-exposed controls by GC-FID analysis. Samples were collected with personal passive samplers (Radiello (R)). End-shift urine samples were collected for t,t-muconic acid (t,t-MA) determination by HPLC and for S-phenylmercapturic acid (S-PMA) measurement by HPLC-MS/MS. The alkaline version of the comet assay and, in a subgroup of 19 SSA and 16 control subjects, chromosomal aberrations (CA) and glutathione (GSH) levels were measured in peripheral blood lymphocytes.Personal benzene exposure was significantly higher in PIO, SSA and GPMW as compared to controls. The urinary excretion of the two metabolites showed a significant increase in SSA (p = 0.0258 and p = 0.0001, for t,t-MA and S-PMA, respectively) and in PIO (p = 0.0013 and p = 0.0001, for t,t-MA and S-PMA, respectively) as compared with the control group, while no such increase was observed for GPMW, for whom occupational exposure was not continuous and occurred on specific working days only. Significant increases of DNA damage were found by the comet assay for tail moment (TM) and tail length (TL) in SSA (p < 0.0001 and p = 0.008, for TM and TL, respectively) and PIO (p < 0.0001 and p < 0.0001, for TM and TL, respectively) when compared with controls. The PIO group also displayed a significant increase in the number of cells with comet (p < 0.0001). Smoking habits did not appear to interfere with these results in any of the groups. No difference was found in percentage of CA between exposed workers and controls. Significant correlations were found, in all groups, between benzene exposure and the more representative comet parameter TM (r = 0.509, p = 0.007; r = 0.525, p = 0.017 and r = 0.420, p = 0.046 in SSA, GPMW, and PIO, respectively). A trend of negative correlation was observed between DNA damage and either GSH or urine S-PMA for exposed workers. In summary, in present study urinary S-PMA and DNA damage by the comet assay were both sensitive to exposure to low levels of benzene, and GSH seems to play an important defence role against benzene-dependent DNA damage. (C) 2009 Elsevier Ireland Ltd. All rights reserved.