Toraason M, Hayden C, Marlow D, Rinehart R, Mathias P, Werren D, Olsen L D, Neumeister C E, Mathews E S, Cheever K L, Marlow K L, DeBord D G, Reid T M
National Institute for Occupational Safety and Health, Cincinnati, OH 45226, USA.
Int Arch Occup Environ Health. 2001 Aug;74(6):396-404. doi: 10.1007/s004200100238.
To determine the potential for asphalt fume exposure to increase DNA damage, we conducted a cross-sectional study of roofers involved in the application of roofing asphalt.
DNA strand breaks and the ratio of 8-hydroxydeoxyguanosine (8-OHdG) to 2-deoxyguanosine (dG) were measured in peripheral blood leukocytes of roofers. In addition, urinary excretion of 8-OHdG and 8-epi-prostaglandin F2alpha (8-epi-PGF) was also measured. The study population consisted of 26 roofers exposed to roofing asphalt and 15 construction workers not exposed to asphalt during the past 5 years. A subset of asphalt roofers (n = 19) was exposed to coal-tar pitch dust (coal tar) during removal of existing roofs prior to applying hot asphalt. Personal air monitoring was performed for one work-week to measure exposure to total particulates, benzene-soluble fraction of total particulates, and polycyclic aromatic compounds (PACs). Urinary 1-OH-pyrene levels were measured as an internal biomarker of PAC exposure.
Full-shift breathing zone measurements for total particulates, benzene-solubles and PACs were significantly higher for coal-tar exposed workers than for roofers not exposed to coal tar. Similarly, urinary 1-OH-pyrene levels were higher in coal-tar exposed roofers than roofers not exposed to coal tar. Total particulates or benzene-soluble fractions were not associated with urinary 1-OH-pyrene, but PAC exposure was highly correlated with urinary 1-OH-pyrene. When stratified by 1-OH-pyrene excretion, DNA strand breaks increased in a dose-dependent manner, and leukocyte 8-OHdG/dG decreased in a dose-dependent manner. Significant changes in DNA damage appeared to be linked to PACs from coal-tar exposure, although asphalt fume alone was associated with a small but significant increase in urinary 1-OH-pyrene and DNA strand breaks.
Results are consistent with previous reports that asphalt or coal-tar exposure can cause DNA damage. Urinary 8-epi-PGF remained relatively constant during the week for virtually all subjects, regardless of exposure indicating that neither asphalt nor coal-tar exposure induces an overt oxidative stress. A small, but statistically significant increase in 8OHdG was evident in end-of-week urine samples compared with start-of-week urine samples in roofers exposed to coal-tar. The increase in urinary 8OHdG coupled with the decrease in leukocyte 8-OHdG/dG, suggests that coal-tar exposure induces protective or repair mechanisms that result in reduced levels of steady-state oxidative-DNA damage.
为了确定接触沥青烟是否会增加DNA损伤，我们对参与屋面沥青施工的屋顶工进行了一项横断面研究。
测量屋顶工外周血白细胞中的DNA链断裂情况以及8-羟基脱氧鸟苷（8-OHdG）与2-脱氧鸟苷（dG）的比率。此外，还测量了尿中8-OHdG和8-表前列腺素F2α（8-epi-PGF）的排泄量。研究人群包括26名接触屋面沥青的屋顶工和15名在过去5年中未接触沥青的建筑工人。一部分沥青屋顶工（n = 19）在涂抹热沥青之前拆除现有屋顶时接触了煤焦油粉尘（煤焦油）。进行了为期一周的个人空气监测，以测量总颗粒物、总颗粒物的苯可溶部分和多环芳烃（PACs）的接触情况。测量尿中1-羟基芘水平作为PACs接触的内源性生物标志物。
接触煤焦油的工人全工作日呼吸带的总颗粒物、苯可溶物和PACs测量值显著高于未接触煤焦油的屋顶工。同样，接触煤焦油的屋顶工尿中1-羟基芘水平高于未接触煤焦油的屋顶工。总颗粒物或苯可溶部分与尿中1-羟基芘无关，但PACs接触与尿中1-羟基芘高度相关。按1-羟基芘排泄量分层时，DNA链断裂呈剂量依赖性增加，白细胞8-OHdG/dG呈剂量依赖性降低。DNA损伤的显著变化似乎与煤焦油接触产生的PACs有关，尽管仅沥青烟就与尿中1-羟基芘和DNA链断裂的小幅但显著增加有关。
结果与先前关于接触沥青或煤焦油会导致DNA损伤的报道一致。几乎所有受试者在一周内尿中8-epi-PGF保持相对恒定，无论接触情况如何，这表明接触沥青和煤焦油均未诱导明显的氧化应激。与接触煤焦油的屋顶工一周开始时的尿样相比，一周结束时的尿样中明显出现了8OHdG的小幅但具有统计学意义的增加。尿中8OHdG的增加与白细胞8-OHdG/dG的降低相结合，表明煤焦油接触诱导了保护或修复机制，导致稳态氧化DNA损伤水平降低。
