Finley B L, Scott P K, Norton R L, Gargas M L, Paustenbach D J
ChemRisk Division of McLaren/Hart Environmental Engineering Corporation, Cleveland, Ohio 44122, USA.
J Toxicol Environ Health. 1996 Aug 9;48(5):479-99. doi: 10.1080/009841096161195.
In this study, we evaluate the significance of increased urinary chromium concentrations as a marker of chromium exposure and potential health risk. Six human volunteers ingested trivalent chromium [Cr(III)] and hexavalent chromium [Cr(VI)] at doses that are known to be safe but are much higher than typical dietary levels. The following dosing regimen was used: d 1-7, 200 micrograms/d chromium picolinate (a dietary supplement); d 8-10, Cr(VI) ingestion at the U.S. Environmental Protection Agency (EPA) reference dose (RfD) of 0.005 mg/kg/d; d 11-13, no dose; d 14-16, Cr(III) ingestion at the U.S. EPA RfD of 1.0 mg/ kg/d; and d 17-18, postdose. Urine voids were collected throughout the dosing periods and analyzed for chromium. Our findings are as follows: (1) ingestion of 200 micrograms/d of chromium picolinate yielded significantly elevated urine concentrations such that each participant routinely exceeded background, (2) ingestion of the Cr(VI) RfD (0.005 mg/kg/d) yielded individual mean urinary chromium levels (1.2-23 micrograms/L) and a pooled mean urinary chromium level (2.4 micrograms/L) that significantly exceeded background, and (3) ingestion of the Cr(III) RfD yielded no significant increase in urinary chromium concentrations, indicating that little, if any, absorption occurred. Our work identified three critical issues that need to be accounted for in any future studies that will use urinary chromium as a marker of exposure. First, a minimum urinary chromium concentration of approximately 2 micrograms/L should be used as a screening level to critically identify individuals who may have experienced elevated exposures to chromium. Second, if Cr(III) levels in soils are known to be less than 80,000 ppm and the Cr(III) is insoluble, urinary chromium concentrations are not an appropriate marker of exposure. Third, newer forms of chromium supplements that contain organic forms of Cr(III) must be considered potential confounders and their contribution to residential chromium uptake must be carefully evaluated.
在本研究中,我们评估了尿铬浓度升高作为铬暴露标志物及潜在健康风险的意义。六名人类志愿者摄入了已知安全但远高于典型饮食水平剂量的三价铬[Cr(III)]和六价铬[Cr(VI)]。采用了以下给药方案:第1 - 7天,每天200微克吡啶甲酸铬(一种膳食补充剂);第8 - 10天,以美国环境保护局(EPA)参考剂量(RfD)0.005毫克/千克/天摄入Cr(VI);第11 - 13天,无剂量摄入;第14 - 16天,以美国EPA RfD 1.0毫克/千克/天摄入Cr(III);第17 - 18天,给药后。在整个给药期间收集尿液并分析其中的铬。我们的研究结果如下:(1)每天摄入200微克吡啶甲酸铬使尿铬浓度显著升高,以至于每个参与者的尿铬浓度经常超过背景值;(2)摄入Cr(VI)的RfD(0.005毫克/千克/天)使个体尿铬平均水平(1.2 - 23微克/升)和合并尿铬平均水平(2.4微克/升)显著超过背景值;(3)摄入Cr(III)的RfD未使尿铬浓度显著增加,表明几乎没有吸收(如果有吸收也是极少的)。我们的研究确定了在未来任何将尿铬用作暴露标志物的研究中都需要考虑的三个关键问题。首先,应将约2微克/升的最低尿铬浓度用作筛查水平,以严格识别可能经历过铬暴露升高的个体。其次,如果已知土壤中Cr(III)水平低于80,000 ppm且Cr(III)不溶,则尿铬浓度不是合适的暴露标志物。第三,含有有机形式Cr(III)的新型铬补充剂必须被视为潜在的混杂因素,必须仔细评估它们对居民铬摄入量的贡献。