Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium
Measurement of vitamin D3 metabolites in smelter workers exposed to lead and cadmium
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DOI：
10.1136/oem.55.7.446
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发表时间：
1998-07-01
影响因子：
4.9
通讯作者：
Barltrop, D
中科院分区：
文献类型：
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作者：
Chalkley, SR;Richmond, J;Barltrop, D
目的：探讨铅、镉对维生素D-3代谢途径的影响。方法：对59名铅、镉职业接触工人进行血镉、尿镉及尿总蛋白测定。对其中19名工人的血浆维生素D-3代谢产物25-羟基胆钙化醇（25 OHD_3）、24 R，25-二羟基胆钙化醇（24 R，25（OH）（2）D-3）和1 α，25-二羟基胆钙化醇（1 α，25（OH）（2）D-3）与血铅进行了测定。结果血浆25（OH）D-3、24 R、25（OH）（2）D-3和1 α，25（OH）（2）D-3的范围分别为1.0-51.9 ng/ml、0.6-5.8 ng/ml和0.1-75.7 pg/ml。血铅的范围为1- I.mu/l（21-76 μ g/dl），血镉为6-145 nmol/l，尿镉为3-161 nmol/l。随机尿样中的总蛋白为2.1-32.6 mg/dl。血铅与尿镉浓度无相关性（相关系数为-0.265），但血镉与尿镉浓度有极显著相关性。无论铅浓度如何，随着血镉和尿镉的增加，24 R，25（OH）（2）D-3的浓度降低至正常范围以下。当铅浓度为1.9 μ mol/l时，高镉浓度与血浆1 α，25（OH）（2）D-3降低相关，Kruskal-Wallis方差分析（K-W ANOVA）χ（2）=10.3，p=0.006。血浆25（OH）D与尿总蛋白、尿镉呈负相关，与血浆24 R、25（OH）（2）D-3、l α、25（OH）（2）D-3、血铅、血镉无相关性。血镉浓度可由尿镉浓度预测（回归系数+0.35SE0.077）。单独接触镉会降低1 α，25（OH），D和24 R，25（OH）（2）D-3的浓度，而同时接触镉和铅会增加1 α，25（OH）（2）D-3的浓度。有人建议，镉和铅相互作用与肾脏线粒体羟化酶的维生素D，内分泌复合物。镉对维生素D代谢途径的干扰可能会导致健康影响，如骨质疏松症或骨软化症，铅的存在可能会增加这些风险。
Objectives-To investigate the effects of lead and cadmium on the metabolic pathway of vitamin D-3.Methods-Blood and urinary cadmium and urinary total proteins were measured in 59 smelter workers occupationally exposed to lead and cadmium. In 19 of these workers, the plasma vitamin D-3 metabolites, (25-hydroxycholecalciferol (25 OHD3), 24R, 25-dihydroxycholecalciferol (24R,25(OH)(2)D-3) and l alpha, 25-dihydroxycholecalciferol (1 alpha,25(OH)(2)D-3)) were measured together with blood lead. Vitamin D-3 metabolites were measured by radioimmunoassay, (RIA), lead and cadmium by atomic absorption spectrophotometry, and total proteins with a test kit.Results-Ranges for plasma 25(OH)D-3, 24R,25(OH)(2)D-3 and 1 alpha,25(OH)(2)D-3 were 1.0-51.9 ng/ml, 0.6-5.8 ng/ml, and 0.1-75.7 pg/ml, respectively. Ranges for blood lead were 1-3.7 I.mu mol/l, (21-76 mu g/dl), blood cadmium 6-145 nmol/l, and urinary cadmium 3-161 nmol/l. Total proteins in random urine samples were 2.1-32.6 mg/dl. Concentrations of lead and cadmium in blood showed no correlation (correlation coefficient -0.265) but there was a highly significant correlation between blood and urinary cadmium. Concentrations for 24R,25(OH)(2)D-3 were depressed below the normal range as blood and urinary cadmium increased, irrespective of lead concentrations. High cadmium concentrations were associated with decreased plasma l alpha,25(OH)(2)D-3 when lead concentrations were 1.9 mu mol/l, Kruskal-Wallis analysis of variance (K-W ANOVA) chi(2)=10.3, p=0.006. Plasma 25(OH)D, was negatively correlated with both urinary total proteins and urinary cadmium, but showed no correlation with plasma 24R,25(OH)(2)D-3, l alpha,25(OH)(2)D-3, blood lead, or blood cadmium.Conclusion-Continuous long term exposure to cadmium may result in a state of equilibrium between blood and urinary cadmium. Cadmium concentrations in blood could be predicted from the cadmium concentration of the urine, (regression coefficient +0.35 SE 0.077). Exposure to cadmium alone decreased the concentrations of 1 alpha,25(OH),D, and 24R,25(OH)(2)D-3, whereas exposure to both cadmium and lead increased the concentrations of 1 alpha,25(OH)(2)D-3. It has been suggested that cadmium and lead interact with renal mitochondrial hydroxylases of the vitamin D, endocrine complex. Perturbation of the vitamin D metabolic pathway by cadmium may result in health effects, such as osteoporosis or osteomalacia, risks which are possibly increased in the presence of lead.