循环铅修饰铬酸盐暴露人群中六价铬诱导的遗传损伤：一项流行病学研究。
Circulating lead modifies hexavalent chromium-induced genetic damage in a chromate-exposed population: An epidemiological study.
机构信息
School of Medical Science and Engineering, Beihang University, Beijing 100191, China; Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China; Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing 100191, China.
Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, China.
出版信息
Sci Total Environ. 2021 Jan 15;752:141824. doi: 10.1016/j.scitotenv.2020.141824. Epub 2020 Aug 21.
Chromium (Cr) can coexist with other heavy metals in the blood of chronically chromate-exposed individuals. However, few studies have explored the health impacts of other hazardous metals after exposure to hexavalent chromium [Cr(VI)]. This study aimed to assess the modification effects of blood lead (Pb) on the genetic damage induced by Cr(VI). During 2010-2019, 1000 blood samples were collected from 455 workers exposed to chromate and 545 workers not exposed to chromate from the same factory with similar labor intensity. The levels of Cr and Pb were measured in whole blood samples. Micronucleus frequency (MNF) and urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured to reflect different types of genetic damage. Multivariate linear regression analyses were performed to evaluate the associations between hazardous metals and the modification effects of Pb on genetic damage. The geometric mean levels of Cr and Pb in the exposure group were significantly higher than those in the control group [Cr: 6.42 (6.08- 6.79) vs. 1.29 (1.22- 1.36) μg/L; Pb: 38.82 (37.22- 40.50) vs. 34.47 (33.15- 35.85) μg/L]. The geometric means of urinary 8-OHdG and MNF in exposure group were 4.00 (3.64- 4.40) μg/g and 5.40 (4.89- 5.97) ‰, respectively, significantly higher than the 3.20 (2.94- 3.48) μg/g and 4.57 (4.15- 5.03) ‰, respectively, in control group. logCr was independently and positively associated with urinary 8-OHdG (β = 0.143, 95% CI: 0.082- 0.204) and MNF (β = 0.303, 95%CI: 0.020- 0.587). With the change in circulating Pb levels, the types of genetic damage induced by Cr(VI) were different. At low levels of circulating Pb (<30.80 μg/L), chromate mainly caused changes in 8-OHdG, while at high circulating Pb levels (≥44.88 μg/L), chromate induced alterations in MNF. The findings suggested that chromate exposure could cause multiple types of genetic damage, and circulating Pb might modify the association between circulating Cr and the form of genetic damage.
铬（Cr）可以与长期接触铬酸盐的个体血液中的其他重金属共存。然而，很少有研究探讨六价铬[Cr(VI)]暴露后其他有害金属对健康的影响。本研究旨在评估血铅（Pb）对 Cr(VI)诱导遗传损伤的修饰作用。在 2010 年至 2019 年期间，从同一工厂中具有相似劳动强度的 455 名接触铬酸盐的工人和 545 名未接触铬酸盐的工人中采集了 1000 份血样。测量全血样本中的 Cr 和 Pb 水平。微核频率（MNF）和尿 8-羟基脱氧鸟苷（8-OHdG）用于反映不同类型的遗传损伤。进行多变量线性回归分析以评估危险金属与 Pb 对遗传损伤的修饰作用之间的关联。暴露组中 Cr 和 Pb 的几何均数水平明显高于对照组[Cr：6.42（6.08-6.79）vs.1.29（1.22-1.36）μg/L；Pb：38.82（37.22-40.50）vs.34.47（33.15-35.85）μg/L]。暴露组尿 8-OHdG 和 MNF 的几何均值分别为 4.00（3.64-4.40）μg/g 和 5.40（4.89-5.97）‰，明显高于对照组的 3.20（2.94-3.48）μg/g 和 4.57（4.15-5.03）‰。logCr 与尿 8-OHdG（β=0.143，95%CI：0.082-0.204）和 MNF（β=0.303，95%CI：0.020-0.587）呈独立正相关。随着循环 Pb 水平的变化，Cr(VI)诱导的遗传损伤类型也不同。在低循环 Pb 水平（<30.80μg/L）下，铬酸盐主要引起 8-OHdG 的变化，而在高循环 Pb 水平（≥44.88μg/L）下，铬酸盐引起 MNF 的改变。结果表明，铬酸盐暴露可引起多种类型的遗传损伤，循环 Pb 可能会改变循环 Cr 与遗传损伤形式之间的关系。
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