Viaene M K, Masschelein R, Leenders J, De Groof M, Swerts L J, Roels H A
Department of Occupational Medicine, Catholic University of Leuven, Belgium.
Occup Environ Med. 2000 Jan;57(1):19-27. doi: 10.1136/oem.57.1.19.
A patient with unexplained minor behavioural changes associated with an axonal sensorimotor polyneuropathy had a history of chronic occupational exposure to cadmium (Cd). Although animal studies have shown that Cd is a potent neurotoxicant, little is known about its toxicity for the human central nervous system. The aim of this study was to investigate the toxic potential of chronic occupational exposure to Cd on neurobehavioural functions.
A cross sectional epidemiological study was conducted ina group of Cd workers and an age matched control group. Eighty nine adult men (42 exposed to Cd and 47 control workers) were given a blinded standardised examination that consisted of computer assisted neurobehavioural tests (neurobehavioural examination system), a validated questionnaire to assess neurotoxic complaints (neurotoxicity symptom checklist--60, NSC-60), and a standardised self administered questionnaire to detect complaints consistent with peripheral neuropathy and dysfunction of the autonomic nervous system. Historical and current data on biomonitoring of exposure to Cd, either the highest value of Cd in urine (CdU in microgram Cd/g creatinine) of each Cd worker during work (CdUmax) or the current value (CdUcurrent) of each control, were available as well as data on microproteinuria.
Cd workers (CdUmax: mean (range), 12.6 (0.4-38.4)) performed worse than the controls (CdUcurrent: mean (range), 0.7 (0.1-2.0)) on visuomotor tasks, symbol digit substitution (p = 0.008), and simple reaction time to direction (p = 0.058) or location (p = 0.042) of a stimulus. In multiple linear regression analysis, symbol digit substitution, simple direction reaction time test, and simple location reaction time test were significantly related to CdUmax, (beta = 0.35 (p < 0.001), beta = 0.25 (p = 0.012), and beta = 0.23 (p = 0.021) respectively). More complaints consistent with peripheral neuropathy (p = 0.004), complaints about equilibrium (p = 0.015), and complaints about concentration ability (p = 0.053) were found in the group exposed to Cd than in the control group, and these variables correlated positively with CdUmax (peripheral neuropathy: beta = 0.38, p < 0.001; equilibrium: beta = 0.22, p = 0.057; concentration ability: beta = 0.27, p = 0.020).
Slowing of visuomotor functioning on neurobehavioural testing and increase in complaints consistent with peripheral neuropathy, complaints about equilibrium, and complaints about concentration ability were dose dependently associated with CdU. Age, exposure to other neurotoxicants, or status of renal function could not explain these findings. The present study also indicates that an excess of complaints may be detected in Cd workers before signs of microproteinuria induced by Cd occur.
一名患有与轴索性感觉运动性多发性神经病相关的不明原因轻微行为改变的患者有长期职业性接触镉(Cd)的病史。尽管动物研究表明镉是一种强效神经毒物,但关于其对人类中枢神经系统的毒性知之甚少。本研究的目的是调查长期职业性接触镉对神经行为功能的潜在毒性。
对一组镉作业工人和年龄匹配的对照组进行了横断面流行病学研究。89名成年男性(42名接触镉的工人和47名对照工人)接受了一项盲法标准化检查,该检查包括计算机辅助神经行为测试(神经行为检查系统)、一份用于评估神经毒性主诉的有效问卷(神经毒性症状清单 - 60,NSC - 60)以及一份用于检测与周围神经病变和自主神经系统功能障碍相符的主诉的标准化自填问卷。可获得镉接触生物监测的历史和当前数据,即每位镉作业工人工作期间尿镉的最高值(以微克镉/克肌酐计的CdU,CdUmax)或每位对照的当前值(CdUcurrent),以及微量蛋白尿的数据。
在视觉运动任务、符号数字替换(p = 0.008)以及对刺激方向(p = 0.058)或位置(p = 0.042)的简单反应时间方面,镉作业工人(CdUmax:均值(范围),12.6(0.4 - 38.4))的表现比对照组(CdUcurrent:均值(范围),0.7(0.1 - 2.0))差。在多元线性回归分析中,符号数字替换、简单方向反应时间测试和简单位置反应时间测试与CdUmax显著相关(β分别为0.35(p < 0.001)、β为0.25(p = 0.012)和β为0.23(p = 0.021))。与对照组相比,接触镉的组中发现更多与周围神经病变相符的主诉(p = 0.004)、关于平衡的主诉(p = 0.015)和关于注意力集中能力的主诉(p = 0.053),并且这些变量与CdUmax呈正相关(周围神经病变:β = 0.38,p < 0.001;平衡:β = 0.22,p = 0.057;注意力集中能力:β = 0.27,p = 0.020)。
神经行为测试中视觉运动功能减慢以及与周围神经病变相符的主诉增加、关于平衡的主诉增加和关于注意力集中能力的主诉增加与CdU呈剂量依赖性相关。年龄、接触其他神经毒物或肾功能状态无法解释这些发现。本研究还表明,在镉诱导的微量蛋白尿迹象出现之前,镉作业工人中可能会检测到过多的主诉。