Nordberg Gunnar F, Nordberg Monica
Department of Epidemiology and Global Health, Umeå University, SE-90185 Umeå, Sweden.
Institute of Environmental Medicine, Karolinska Institutet, SE-17177 Stockholm, Sweden.
Biomolecules. 2025 Jul 26;15(8):1083. doi: 10.3390/biom15081083.
Cadmium is widely recognized as an important environmental toxicant that may give rise to kidney dysfunction, bone disease, and cancer in humans and animals. Kidney dysfunction occurs at very low exposures and is often considered as the most sensitive or critical effect. Cadmium exposures of concern occur in many countries. In low- and middle-income countries with small-scale mining, excessive exposure to cadmium and other metals occurs in occupational and environmental settings. This is of particular importance in view of the growing demand for metals in global climate change mitigation. Since the 1970s, the present authors have contributed evidence concerning the role of metallothionein and other factors in influencing the toxicokinetics and toxicity of cadmium, particularly as it relates to the development of adverse effects on kidneys in humans and animals. The findings gave a background to the development of biomarkers employed in epidemiological studies, demonstrating the important role of metallothionein in protection against cadmium-induced kidney dysfunction in humans. Studies in cadmium-exposed population groups demonstrated how biomarkers of kidney dysfunction changed during 8 years after drastic lowering of environmental cadmium exposure. Other epidemiological studies showed the impact of a good zinc status in lowering the prevalence of cadmium-related kidney dysfunction. Increased susceptibility to Cd-induced kidney dysfunction was shown in a population with high exposure to inorganic arsenic when compared with a group with low such exposure. Several national and international organizations have used part of the reviewed information, but the metallothionein-related biomarkers and the interaction effects have not been fully considered. We hope that these data sets will also be included and improve risk assessments and preventive measures.
镉被广泛认为是一种重要的环境毒物，可导致人类和动物出现肾功能障碍、骨骼疾病和癌症。在极低的暴露水平下就会发生肾功能障碍，通常被认为是最敏感或最关键的影响。许多国家都存在令人担忧的镉暴露情况。在小规模采矿的低收入和中等收入国家，职业和环境环境中会出现镉和其他金属的过度暴露。鉴于全球减缓气候变化对金属的需求不断增加，这一点尤为重要。自20世纪70年代以来，本文作者提供了有关金属硫蛋白和其他因素在影响镉的毒代动力学和毒性方面作用的证据，特别是与人类和动物肾脏不良反应的发展有关的证据。这些发现为流行病学研究中使用的生物标志物的发展提供了背景，证明了金属硫蛋白在保护人类免受镉诱导的肾功能障碍方面的重要作用。对镉暴露人群组的研究表明，在环境镉暴露大幅降低后的8年里，肾功能障碍生物标志物是如何变化的。其他流行病学研究表明，良好的锌状态对降低镉相关肾功能障碍的患病率有影响。与低无机砷暴露组相比，高无机砷暴露人群对镉诱导的肾功能障碍的易感性增加。几个国家和国际组织已经使用了部分审查信息，但与金属硫蛋白相关的生物标志物和相互作用效应尚未得到充分考虑。我们希望这些数据集也能被纳入，以改进风险评估和预防措施。
