Siwińska E, Mielzyńska D, Kapka L
Institute of Occupational Medicine and Environmental Health, 13 Kościelna St, 41-200 Sosnowiec, Poland.
Occup Environ Med. 2004 Mar;61(3):e10. doi: 10.1136/oem.2002.006643.
To investigate whether current occupational exposure of coke oven workers to polycyclic aromatic hydrocarbons (PAHs) results in genotoxic effects measured in peripheral blood lymphocytes and whether these biomarkers are associated with the biomarkers of exposure.
Blood and urine samples were collected immediately after a shift at the end of a working week from 50 coke oven workers and 50 control workers not exposed to PAHs. Methods included: (1) biomarkers of exposure: urinary 1-hydroxypyrene (HpU), urinary mutagenicity by the plate Salmonella test with strains TA98 and YG1024 after metabolic activation, expressed as mutagenic rate (MR98 and MR1024, respectively), urinary cotinine; and (2) biomarkers of biological effects in peripheral blood lymphocytes (PBL): sister chromatid exchanges (SCE/cell), cells of high frequency of SCE (% HFC), micronuclei (MN/1000 cells), chromosomal aberrations (CA/100 cells), and DNA damage by the Comet assay.
Occupational exposure to PAH resulted in significantly increased levels of HpU and mutagenic effect of urine. Median values of these biomarkers in coke oven workers were: 9.0 micromol/mol creatinine for HpU, 2.7 for MR98, and 8.2 for MR1024, compared to the controls: HpU = 0.6 micromol/mol creatinine, MR98 = 1.2, and MR1024 = 5.5. Occupational exposure caused significant induction of SCE, HFC, and MN in coke oven workers: median SCE = 5.9, HFC = 12.0%, MN = 6.0 compared to the controls: 3.9, 5.0%, and 3.0, respectively. No effect of occupational exposure was found in relation to CA and DNA damage measured with the Comet assay. HpU concentration was positively associated with SCE and HFC. The concentration of urinary 1-hydroxypyrene corresponding to a 5% probability of increased SCE was 1.0 micromol/mol creatinine.
The occupational exposure to PAHs resulted in measurable biological effects (SCE, HFC, MN). In coke oven workers an increased level of SCE was not observed below the level of 1.0 micromol HpU/mol creatinine.
调查当前焦炉工人职业性接触多环芳烃(PAHs)是否会在外周血淋巴细胞中产生遗传毒性效应,以及这些生物标志物是否与接触生物标志物相关。
在工作周结束时的一个班次后,立即采集50名焦炉工人和50名未接触PAHs的对照工人的血液和尿液样本。方法包括:(1)接触生物标志物:尿中1-羟基芘(HpU)、经代谢活化后用TA98和YG1024菌株的平板沙门氏菌试验检测的尿致突变性,以致突变率(分别为MR98和MR1024)表示、尿可替宁;(2)外周血淋巴细胞(PBL)中的生物学效应生物标志物:姐妹染色单体交换(SCE/细胞)、高频率SCE细胞(%HFC)、微核(MN/1000细胞)、染色体畸变(CA/100细胞)以及彗星试验检测的DNA损伤。
职业性接触PAH导致HpU水平显著升高和尿液致突变效应。焦炉工人这些生物标志物的中位数分别为:HpU为9.0微摩尔/摩尔肌酐、MR98为2.7、MR1024为8.2,而对照组分别为:HpU = 0.6微摩尔/摩尔肌酐、MR98 = 1.2、MR1024 = 5.5。职业性接触导致焦炉工人的SCE、HFC和MN显著增加:SCE中位数为5.9、HFC为12.0%、MN为6.0,而对照组分别为3.9、5.0%和3.0。未发现职业性接触对用彗星试验检测的CA和DNA损伤有影响。HpU浓度与SCE和HFC呈正相关。对应SCE增加5%概率的尿中1-羟基芘浓度为1.0微摩尔/摩尔肌酐。
职业性接触PAHs导致可测量的生物学效应(SCE、HFC、MN)。在焦炉工人中,当HpU水平低于1.0微摩尔/摩尔肌酐时,未观察到SCE水平升高。