Mercury rising: response to the EPA assessment of mercury exposure
Mercury rising: response to the EPA assessment of mercury exposure
复制标题
汞含量上升：对 EPA 汞暴露评估的回应
作者：
D. Laks
2013年11月，美国环境保护署（EPA）发布了一项关于国家健康和营养调查（NHANES）数据集的研究（EPA 2013），声称随着时间的推移，人类中的汞浓度正在下降。事实上，他们的数据支持相反的结论。血液中无机汞水平（IHg）的未报告上升表明，随着时间的推移，人口中的慢性汞暴露有所增加。汞的性质，长期暴露于这种强大的神经毒素是难以衡量的。美国环保署选择了不合适的汞的有机形式，甲基汞（MeHg），作为他们的接触生物标志物。虽然甲基汞是鱼类体内汞的主要形式，但有充分的证据表明，摄入甲基汞后，甲基汞在血液中的存在时间很短，在血液中的半衰期约为2个月。因此，甲基汞更多地是衡量近期接触的指标，而不是长期、慢性接触汞的指标。在许多关于有机汞接触的研究中，在停止接触后，血液和组织中的甲基汞水平会消失。我的比喻是，使用甲基汞作为汞暴露的生物标志物，就像看油箱，以测定一个人开了多远。甲基汞只是最近接触的一种生物标志物，因为油箱只能表明一个人多久以前加满了油箱。相比之下，血液中的无机汞（IHg）水平是长期接触汞的更好的生物标志物。IHg作为一种生物标志物，类似于通过观察机油来确定一个人驾驶了多远;它可能表明一个人积累了多少暴露量。甲基汞在人体组织中转化为IHg，随后IHg在组织中沉积多年。Sallsten等人（1993年）发现体内组织中存在碘汞的长期沉积，他们发现汞在长期接触后会被人体保留（Sallsten等人，1993年）。在Vahter等人（1994年）的研究中，他们证明有机汞（甲基汞）会脱甲基转化为无机汞（IHg），并在血液中检测到（Vahter等人，1994年）。此外，在一种情况下，血液中的无机汞即使在停止接触之后仍然升高，而有机汞总是被消除。因此，碘汞可以作为慢性接触的更好的生物指示剂，因为它本身可以在接触停止后很长时间内留在血液中。此外，有一种灵长类动物在接触有机汞后出现肝损伤，其IHg升高，但甲基汞没有升高。这表明IHg是汞暴露毒性效应的更好生物指示剂。一些甲基汞，有机汞，将自然退出人体通过消除，而一些甲基汞将生物转化为IHG，无机汞。血液中的有机汞水平是暂时的;它要么是在离开身体的路上，要么是在成为IHG的路上。D. R.美国加州大学洛杉矶分校生物化学系，379神经科学研究大楼，379室，635查尔斯E。Young Drive South，洛杉矶，CA 90095-7332，USA电子邮件：dlaks@mednet.ucla.edu
In November 2013, the United States EPA (Environmental Protection Agency) released a study (EPA 2013) of the NHANES (National Health and Nutrition Examination Survey) dataset claiming that mercury concentrations were decreasing in the human population over time. In fact, the opposite conclusion is supported by their data. The unreported rise in blood inorganic mercury levels (IHg) indicates a rise of chronic mercury exposure in the population over time. Mercurial by nature, chronic exposure to this potent neurotoxin is difficult to measure. The EPA chose the ill suited organic form of mercury, methyl mercury (MeHg), as their biomarker of exposure. Although MeHg is the primary form of mercury in fish, it is well documented that MeHg is only a fleeting occurrence in the blood after ingestion, with a half-life of around 2 months in blood. Therefore, MeHg is more a measure of recent exposure than it is of long term, chronic exposure to mercury. In numerous studies of organic mercury exposure, MeHg levels vanish from blood and tissue after cessation of exposure. My metaphor is that using MeHg as a biomarker for Hg exposure is like looking at the gas tank in order to assay how far a person has driven. MeHg is merely a biomarker of recent exposure, as a gas tank is only indicative of how long ago a person filled up their tank. In contrast, blood inorganic mercury (IHg) levels serve as a better biomarker for long-term exposure to mercury. IHg, as a biomarker, is akin to looking at the engine oil in order to determine how far a person has driven; it may signify how much a person has accumulated exposure. Methyl mercury is converted to IHg in the body tissue and subsequently IHg is deposited in the tissue for years. Long term deposition of IHg in tissues of the body was detected by Sallsten et al. in (1993) when they showed that mercury was retained by the body after chronic exposure (Sallsten et al. 1993). In Vahter et al. (1994) they demonstrated that organic mercury, MeHg, demethylates into inorganic mercury, IHg, and is detected in the blood (Vahter et al. 1994). Furthermore, inorganic mercury in the blood, in one instance, remained elevated even after cessation of exposure while organic mercury was always eliminated. Therefore, IHg served as a better bioindicator of chronic exposure because it alone could remain in the blood long after cessation of exposure. Moreover, the one primate that developed liver damage after exposure to organic mercury had elevated IHg but not MeHg. This indicates that IHg is a better bioindicator of the toxic effects of mercury exposure. Some MeHg, Organic Mercury, will naturally exit the body through elimination, while some MeHg will biotransform into IHG, Inorganic Mercury. Blood organic mercury levels are transitory; either it is on its way out of the body or on its way to becoming IHG. D. R. Laks (&) Department of Biological Chemistry, UCLA, 379 Neuroscience Research Bldg, Suite 379, 635 Charles E. Young Drive South, Los Angeles, CA 90095-7332, USA e-mail: dlaks@mednet.ucla.edu
影响因子：
3.8
作者：
VAHTER, M;MOTTET, NK;BURBACHER, T
通讯作者：
BURBACHER, T
影响因子：
3.8
作者：
VAHTER, ME;MOTTET, NK;BURBACHER, TM
通讯作者：
BURBACHER, TM