Gao M, Levy L S, Faux S P, Aw T C, Braithwaite R A, Brown S S
Institute of Occupational Health, University of Birmingham, Edgbaston.
Occup Environ Med. 1994 Oct;51(10):663-8. doi: 10.1136/oem.51.10.663.
Molecular epidemiological techniques, capable of detecting damage to DNA, were used to see if such damage occurred in the lymphocytes of a group of workers exposed to chromium. The two aims of this pilot study were to see if these new techniques might make useful biological monitoring tools for workers exposed to chromium and also, to help assess whether the current occupational exposure limit for chromium (VI) was sufficiently protective in this specific working situation.
Volunteer groups of 10 workers exposed to chromium and 10 non-exposed workers provided urine and blood samples towards the end of the working week. Chromium concentrations were measured in whole blood, plasma, lymphocytes, and urine. Lymphocytes were used to examine two forms of DNA damage in the two groups; these were the level of DNA strand breakage and, the production of 8-hydroxydeoxyguanosine.
Chromium concentration in whole blood, plasma, and urine of workers exposed to chromium was significantly raised (P < 0.01) compared with non-exposed controls, but in isolated lymphocytes, there was only a modest but significant (P < 0.05) increase in chromium in the group exposed to chromium. There was no difference in the levels of DNA strand breaks or 8-hydroxydeoxyguanosine between the groups. Air monitoring for chromium was not undertaken but current levels for the group exposed to chromium were reported to be around 0.01 mg/m3, which is 20% of the current United Kingdom occupational exposure limit.
We were unable to detect any damage in lymphocytic DNA due to exposure to chromium. This may have been due to the low chromium exposure (< 20% of the United Kingdom occupational exposure limit), the ability of plasma to detoxify chromium (VI) to chromium (III) before it reached the lymphocytes, or perhaps the insensitivity of the molecular techniques used. It is now important to test these and other such techniques on groups exposed to levels closer to the United Kingdom occupational exposure limit.
运用能够检测DNA损伤的分子流行病学技术,来观察一组接触铬的工人的淋巴细胞中是否发生此类损伤。这项初步研究的两个目的是,探究这些新技术能否成为接触铬工人有用的生物监测工具,以及帮助评估当前六价铬的职业接触限值在这种特定工作环境中是否具有足够的防护作用。
10名接触铬的工人和10名未接触铬的工人组成的志愿者小组在工作周结束时提供了尿液和血液样本。测量全血、血浆、淋巴细胞和尿液中的铬浓度。利用淋巴细胞检测两组中两种形式的DNA损伤;即DNA链断裂水平和8-羟基脱氧鸟苷的产生量。
与未接触铬的对照组相比,接触铬的工人的全血、血浆和尿液中的铬浓度显著升高(P < 0.01),但在分离出的淋巴细胞中,接触铬的组中铬仅有适度但显著的升高(P < 0.05)。两组之间的DNA链断裂水平或8-羟基脱氧鸟苷水平没有差异。未对空气中的铬进行监测,但据报告,接触铬的组当前的水平约为0.01 mg/m³,这是英国当前职业接触限值的20%。
我们未能检测到因接触铬而导致的淋巴细胞DNA损伤。这可能是由于铬接触水平较低(<英国职业接触限值的20%)、血浆在铬到达淋巴细胞之前将六价铬解毒为三价铬的能力,或者也许是所用分子技术不够灵敏。现在重要的是,对接触水平更接近英国职业接触限值的人群测试这些技术及其他此类技术。