Department of Occupational and Environmental Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.
Department of Occupational and Environmental Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.
Bone. 2021 Feb;143:115768. doi: 10.1016/j.bone.2020.115768. Epub 2020 Nov 21.
It is well known that high-level exposure to cadmium can cause bone disease such as osteoporosis, osteomalacia and fractures. However, the effect of low-level exposure, as found in the general population (mainly derived from diet and smoking), has only been assessed recently. The aim of this study was to examine if cadmium exposure in the general Swedish population causes other bone changes than decreased areal bone mineral density as measured by traditional DXA technology, e.g. changes in microstructure and geometry, such as cortical thickness or area, cortical porosity and trabecular bone volume. The study population consisted of 444 men, aged 70-81 years at inclusion year 2002-2004, from the Swedish cohort of the Osteoporotic Fractures in Men Study (MrOS). Cadmium was analyzed in baseline urine samples (U-Cd). Different parameters of bone geometry and microstructure were measured at the distal tibia at follow-up in 2009, including examination with high-resolution peripheral quantitative computed tomography (HR-pQCT). Associations between bone parameters and U-Cd in tertiles were estimated in multivariable analyses, including potential confounding factors (age, smoking, BMI, and physical activity). We found significant associations between U-Cd and several bone geometry or microstructure parameters, with 9% lower cortical thickness (p = 0.03), 7% lower cortical area (p = 0.04), and 5% lower trabecular bone volume fraction (p = 0.02) in the third tertile of U-Cd, using the first tertile as the reference. Furthermore, significant negative associations were found between log-transformed U-Cd and cortical thickness, cortical area, trabecular number and trabecular bone volume fraction, and a significant positive association with trabecular separation. The results indicate that low-level Cd exposure in the general population has negative effects on both cortical and trabecular bone.
众所周知，高水平的镉暴露会导致骨质疏松症、佝偻病和骨折等骨骼疾病。然而，最近才评估了在一般人群中（主要来自饮食和吸烟）低水平暴露的影响。本研究旨在检查在一般瑞典人群中，镉暴露是否会引起其他骨骼变化，而不仅仅是传统 DXA 技术测量的面积骨密度降低，例如微观结构和几何形状的变化，例如皮质厚度或面积、皮质孔隙率和小梁骨体积。研究人群由来自瑞典男性骨质疏松性骨折研究（MrOS）队列的 444 名年龄在 70-81 岁的男性组成，他们在 2002-2004 年纳入研究时采集了基线尿样（U-Cd）。在 2009 年随访时，在胫骨远端测量了不同的骨几何和微观结构参数，包括使用高分辨率外周定量计算机断层扫描（HR-pQCT）进行检查。在多变量分析中，根据 U-Cd 的三分位数估计了骨参数与 U-Cd 之间的关联，包括潜在的混杂因素（年龄、吸烟、BMI 和体力活动）。我们发现 U-Cd 与几个骨几何或微观结构参数之间存在显著关联，U-Cd 第三分位组的皮质厚度降低 9%（p=0.03），皮质面积降低 7%（p=0.04），小梁骨体积分数降低 5%（p=0.02），使用第一分位组作为参考。此外，log 转换后的 U-Cd 与皮质厚度、皮质面积、小梁数量和小梁骨体积分数呈显著负相关，与小梁分离呈显著正相关。结果表明，一般人群中低水平的 Cd 暴露对皮质骨和小梁骨均有负面影响。
