School of Public Health, Southern Medical University, Guangzhou, Guangdong, China.
Guangdong Provincial Center for Disease Control and Prevention, Guangzhou, Guangdong, China.
J Bone Miner Res. 2017 Oct;32(10):1990-2000. doi: 10.1002/jbmr.3151. Epub 2017 Jun 16.
This study aimed to assess the association between osteoporosis and long-term environmental Cd exposure through diet in southern China. A total of 1116 subjects from a Cd-polluted area and a non-Cd-polluted area were investigated. All subjects met the criteria of having been living in the investigated area for more than 15 years and lived on a subsistence diet of rice and vegetables grown in that area. Besides bone mineral density, the levels of urinary markers of early renal impairment, such as urinary N-acetyl-β-D-glucosaminidase (NAG), α -microglobulin, β -microglobulin, and urinary albumin, were also determined. Urinary Cd concentrations of all studied subjects ranged from 0.21 to 87.31 µg/g creatinine, with a median of 3.97 µg/g creatinine. Multivariate linear regression models indicated a significant negative association of urinary Cd concentrations with bone mineral density. In logistic regression models, both categorical and continuous urinary Cd concentrations were positively associated with osteoporosis. Subjects in the second, third, and fourth quartiles of urinary Cd concentration had greater odds of osteoporosis compared with subjects in the first quartile (odds ratio [OR] = 3.07, 95% confidence interval [CI], 1.77 to 5.33; OR = 4.63, 95% CI, 2.68 to 7.98; OR = 9.15, 95% CI, 5.26 to 15.94, respectively). Additional adjustment for levels of urinary markers did not attenuate the associations. No evidence existed of an interaction between urinary Cd concentration and renal function using levels of urinary markers, and estimated glomerular filtration rate (eGFR). In all subjects, the benchmark dose and benchmark dose lower bound were 1.14 (0.61) and 2.73 (1.83) µg/g creatinine, with benchmark response set at 5% and 10%, respectively. The benchmark dose of urinary Cd was lower in women than in men. This study demonstrated an inverse association between the body burden of Cd and osteoporosis. The toxic effect of Cd on bone may occur in parallel to nephrotoxicity. © 2017 American Society for Bone and Mineral Research.
本研究旨在评估中国南方地区通过饮食摄入长期环境镉暴露与骨质疏松症之间的关联。共调查了来自镉污染区和非镉污染区的 1116 名受试者。所有受试者均符合在调查地区居住 15 年以上并以该地区种植的水稻和蔬菜为主要生存饮食的标准。除骨密度外，还测定了尿早期肾损伤标志物的水平，如尿 N-乙酰-β-D-氨基葡萄糖苷酶（NAG）、α-微球蛋白、β-微球蛋白和尿白蛋白。所有研究对象的尿镉浓度范围为 0.21 至 87.31µg/g 肌酐，中位数为 3.97µg/g 肌酐。多变量线性回归模型表明，尿镉浓度与骨密度呈显著负相关。在逻辑回归模型中，尿镉浓度的分类和连续变量均与骨质疏松症呈正相关。与第一四分位组相比，尿镉浓度处于第二、三、四分位组的受试者患骨质疏松症的几率更高（比值比[OR] = 3.07，95%置信区间[CI]，1.77 至 5.33；OR = 4.63，95%CI，2.68 至 7.98；OR = 9.15，95%CI，5.26 至 15.94）。对尿标志物水平进行额外调整并未减弱相关性。在使用尿标志物和估计肾小球滤过率（eGFR）水平的情况下，未发现尿镉浓度与肾功能之间存在交互作用的证据。在所有受试者中，基准剂量和基准剂量下限分别为 1.14（0.61）和 2.73（1.83）µg/g 肌酐，基准反应设定为 5%和 10%。女性的尿镉基准剂量低于男性。本研究表明，体内镉负荷与骨质疏松症之间存在负相关。镉对骨骼的毒性作用可能与肾毒性同时发生。 © 2017 美国骨与矿物质研究协会。
