Choi Won-Jun, Kang Seong-Kyu, Ham Seunghon, Chung Wookyung, Kim Ae Jin, Kang Myunghee
Department of Occupational and Environmental Medicine, Gachon University College of Medicine, Gil Medical Center, 21, Namdong-daero 774beon-gil, Namdong-gu, Incheon, 21565, Republic of Korea.
Division of Nephrology, Department of Internal Medicine, Gachon University College of Medicine, Gil Medical Center, 21, Namdong-daero 774beon-gil, Namdong-gu, Incheon, 21565, Republic of Korea.
Saf Health Work. 2020 Jun;11(2):235-240. doi: 10.1016/j.shaw.2020.03.005. Epub 2020 Apr 5.
Cadmium exposure may induce chronic intoxication with renal damage. Silver soldering may be a source of cadmium exposure.
We analyzed working environment measurement data and periodic health screening data from a small-scale silver soldering company with ten workers. Concentrations of cadmium in air from working environment measurement data were obtained. Concentrations of blood and urinary cadmium, urine protein, and urine β2-microglobulin (β2M) were obtained. The generalized linear model was used to identify the association between blood and urine cadmium and urine β2M concentrations. Clinical features of chronic cadmium intoxication focused with toxicological renal effects were described.
The mean duration of work was 8.5 years (standard deviation [SD] = 6.9, range = 3-20 years). Cadmium concentrations in air were ranged from 0.006 to 0.015 mg/m. Blood cadmium concentration was elevated in all ten workers, with a highest level of 34.6 μg/L (mean = 21.288 μg/L, SD = 11.304, range = 9.641-34.630 μg/L). Urinary cadmium concentration was elevated in nine workers, with a highest level of 62.9 μg/g Cr (mean = 22.151 μg/g creatinine, SD = 19.889, range = 3.228-62.971 μg/g creatinine). Urine β2M concentration was elevated in three workers. Urinary cadmium concentration was positively associated with urine protein concentration (beta coefficient = 10.27, 95% confidence interval = [4.36, 16.18]). Other clinical parameters were compatible with renal tubular damage.
Cadmium intoxication may occur at quite low air concentrations. Exposure limit may be needed to be lowered.
接触镉可能会导致慢性中毒并损害肾脏。银焊可能是镉暴露的一个来源。
我们分析了一家有十名工人的小型银焊公司的工作环境测量数据和定期健康筛查数据。从工作环境测量数据中获取空气中镉的浓度。获取血液和尿液中镉的浓度、尿蛋白以及尿β2-微球蛋白(β2M)的浓度。使用广义线性模型来确定血液和尿液中镉与尿β2M浓度之间的关联。描述了以毒理学肾脏效应为重点的慢性镉中毒的临床特征。
平均工作时长为8.5年(标准差[SD]=6.9,范围=3 - 20年)。空气中镉浓度范围为0.006至0.015毫克/立方米。所有十名工人的血液镉浓度均升高,最高水平为34.6微克/升(均值=21.288微克/升,SD = 11.304,范围=9.641 - 34.630微克/升)。九名工人尿液镉浓度升高,最高水平为62.9微克/克肌酐(均值=22.151微克/克肌酐,SD = 19.889,范围=3.228 - 62.971微克/克肌酐)。三名工人的尿β2M浓度升高。尿液镉浓度与尿蛋白浓度呈正相关(β系数=10.27,95%置信区间=[4.36, 16.18])。其他临床参数与肾小管损伤相符。
在相当低的空气浓度下可能会发生镉中毒。可能需要降低接触限值。