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镉及其他重金属暴露人群的早期肾脏损伤

Early kidney damage in a population exposed to cadmium and other heavy metals.

作者信息

Thomas Laura D K, Hodgson Susan, Nieuwenhuijsen Mark, Jarup Lars

机构信息

Small Area Health Statistics Unit, Imperial College London, London, United Kingdom.

出版信息

Environ Health Perspect. 2009 Feb;117(2):181-4. doi: 10.1289/ehp.11641. Epub 2008 Sep 9.

DOI:10.1289/ehp.11641
PMID:19270785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2649217/
Abstract

BACKGROUND

Exposure to heavy metals may cause kidney damage. The population living near the Avonmouth zinc smelter has been exposed to cadmium and other heavy metals for many decades.

OBJECTIVES

We aimed to assess Cd body burden and early signs of kidney damage in the Avonmouth population.

METHODS

We used dispersion modeling to assess exposure to Cd. We analyzed urine samples from the local population (n = 180) for Cd (U-Cd) to assess dose (body burden) and for three biomarkers of early kidney damage [N-acetyl-beta-d-glucosaminidase (U-NAG), retinol-binding protein, and alpha-1-microglobulin]. We collected information on occupation, intake of homegrown vegetables, smoking, and medical history by questionnaire.

RESULTS

Median U-Cd concentrations were 0.22 nmol/mmol creatinine (nonsmoking 0.18/smoking 0.40) and 0.34 nmol/mmol creatinine (nonsmoking 0.31/smoking 0.46) in non-occupationally exposed men and women, respectively. There was a significant dose-response relationship between U-Cd and the prevalence of early renal damage-defined as U-NAG > 0.22 IU/mmol-with odds ratios of 2.64 [95% confidence interval (95% CI), 0.70-9.97] and 3.64 (95% CI, 0.98-13.5) for U-Cd levels of 0.3 to < 0.5 and levels >or= 0.5 nmol/mmol creatinine, respectively (p for trend = 0.045).

CONCLUSION

U-Cd concentrations were close to levels where kidney and bone effects have been found in other populations. The dose-response relationship between U-Cd levels and prevalence of U-NAG above the reference value support the need for measures to reduce environmental Cd exposure.

摘要

背景

接触重金属可能导致肾脏损害。居住在埃文茅斯锌冶炼厂附近的人群数十年来一直暴露于镉和其他重金属中。

目的

我们旨在评估埃文茅斯人群体内镉的负荷以及肾脏损害的早期迹象。

方法

我们使用扩散模型评估镉暴露情况。我们分析了当地人群(n = 180)的尿液样本中的镉(尿镉)以评估剂量(体内负荷),并分析了三种早期肾脏损害生物标志物[N-乙酰-β-D-氨基葡萄糖苷酶(尿NAG)、视黄醇结合蛋白和α-1-微球蛋白]。我们通过问卷调查收集了职业、自种蔬菜摄入量、吸烟情况和病史等信息。

结果

非职业暴露男性和女性的尿镉浓度中位数分别为0.22 nmol/mmol肌酐(非吸烟0.18/吸烟0.40)和0.34 nmol/mmol肌酐(非吸烟0.31/吸烟0.46)。尿镉与早期肾损害患病率(定义为尿NAG>0.22 IU/mmol)之间存在显著的剂量反应关系,尿镉水平为0.3至<0.5以及≥0.5 nmol/mmol肌酐时的比值比分别为2.64 [95%置信区间(95%CI),0.70 - 9.97]和3.64(95%CI,0.98 - 13.5)(趋势p值 = 0.045)。

结论

尿镉浓度接近在其他人群中发现肾脏和骨骼效应的水平。尿镉水平与尿NAG高于参考值的患病率之间的剂量反应关系支持采取措施减少环境镉暴露的必要性。

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