Risk Evaluation Branch, Education and Information Division, NIOSH, Centers for Disease Control and Prevention, Cincinnati, Ohio 45226, USA.
J Occup Environ Med. 2009 Oct;51(10):1125-36. doi: 10.1097/JOM.0b013e3181bd8114.
The exposure-response relationship for manganese (Mn)-induced adverse nervous system effects is not well described. Symptoms and neuropsychological deficits associated with early manganism were previously reported for welders constructing bridge piers during 2003 to 2004. A reanalysis using improved exposure, work history information, and diverse exposure metrics is presented here.
Ten neuropsychological performance measures were examined, including working memory index (WMI), verbal intelligence quotient, design fluency, Stroop color word test, Rey-Osterrieth Complex Figure, and Auditory Consonant Trigram tests. Mn blood levels and air sampling data in the form of both personal and area samples were available. The exposure metrics used were cumulative exposure to Mn, body burden assuming simple first-order kinetics for Mn elimination, and cumulative burden (effective dose). Benchmark doses were calculated.
Burden with a half-life of about 150 days was the best predictor of blood Mn. WMI performance declined by 3.6 (normal = 100, SD = 15) for each 1.0 mg/m3 x mo exposure (P = 0.02, one tailed). At the group mean exposure metric (burden; half-life = 275 days), WMI performance was at the lowest 17th percentile of normal, and at the maximum observed metric, performance was at the lowest 2.5 percentiles. Four other outcomes also exhibited statistically significant associations (verbal intelligence quotient, verbal comprehension index, design fluency, Stroop color word test); no dose-rate effect was observed for three of the five outcomes.
A risk assessment performed for the five stronger effects, choosing various percentiles of normal performance to represent impairment, identified benchmark doses for a 2-year exposure leading to 5% excess impairment prevalence in the range of 0.03 to 0.15 mg/m3, or 30 to 150 microg/m3, total Mn in air, levels that are far below those permitted by current occupational standards. More than one-third of workers would be impaired after working 2 years at 0.2 mg/m3 Mn (the current threshold limit value).
锰（Mn）诱发的不良神经系统影响的暴露-反应关系尚不清楚。以前有报道称，2003 年至 2004 年间，在建造桥墩的焊工中出现了与早期锰中毒相关的症状和神经心理学缺陷。本研究使用改进的暴露、工作历史信息和多种暴露指标进行了再分析。
检查了 10 项神经心理学表现指标，包括工作记忆指数（WMI）、言语智商、设计流畅性、斯特鲁普颜色词测试、雷氏复杂图形和听觉辅音三连音测试。可获得 Mn 血水平和以个人和区域样本形式的空气采样数据。使用的暴露指标包括 Mn 的累积暴露、假设 Mn 消除为简单一级动力学的身体负荷以及累积负荷（有效剂量）。计算了基准剂量。
半衰期约为 150 天的负荷是血 Mn 的最佳预测因子。对于每 1.0 mg/m3 x mo 的暴露（P = 0.02，单侧），WMI 性能下降 3.6（正常= 100，SD = 15）。在组平均暴露指标（负荷；半衰期= 275 天）下，WMI 性能处于正常的最低第 17 百分位，在最大观察到的指标下，性能处于最低的 2.5%。其他四个结果也表现出统计学上显著的相关性（言语智商、言语理解指数、设计流畅性、斯特鲁普颜色词测试）；五个结果中的三个没有观察到剂量率效应。
对于五个较强的效应进行风险评估，选择不同的正常表现百分位来表示损伤，确定了 2 年暴露的基准剂量，导致 5%的超额损伤流行率在 0.03 至 0.15 mg/m3 范围内，或空气中总 Mn 为 30 至 150 µg/m3，这些水平远低于当前职业标准允许的水平。超过三分之一的工人在接触 0.2 mg/m3 Mn 工作 2 年后会受到损伤（当前的阈限值）。
