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将遗传学和基因组学纳入吸入性锰风险评估:从数据到政策。

Incorporating genetics and genomics in risk assessment for inhaled manganese: from data to policy.

作者信息

Curran Christine P, Park Robert M, Ho Shuk-mei, Haynes Erin N

机构信息

Department of Biological Sciences, Northern Kentucky University, SC342 Nunn Drive, Highland Heights, KY 41099, United States.

出版信息

Neurotoxicology. 2009 Sep;30(5):754-60. doi: 10.1016/j.neuro.2009.07.013. Epub 2009 Jul 29.

DOI:10.1016/j.neuro.2009.07.013
PMID:19646473
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2765692/
Abstract

Manganese is an essential nutrient, and a healthy human with good liver and kidney function can easily excrete excess dietary manganese. Inhaled manganese is a greater concern, because it bypasses the body's normal homeostatic mechanisms and can accumulate in the brain. Prolonged exposure to high manganese concentrations (>1mg/m(3)) in air leads to a Parkinsonian syndrome known as "manganism." Of greatest concern are recent studies which indicate that neurological and neurobehavioral deficits can occur when workers are exposed to much lower levels (<0.2mg/m(3)) of inhaled manganese in welding fumes. Consequently, researchers at NIOSH are conducting a risk assessment for inhaled manganese. Novel components of this risk assessment include an attempt to quantify the range of inter-individual differences using data generated by the Human Genome Project and experimental work to identify genetically based biomarkers of exposure, disease and susceptibility. The difficulties involved in moving from epidemiological and in vivo data to health-based quantitative risk assessment and ultimately enforceable government standards are discussed.

摘要

锰是一种必需营养素,肝功能和肾功能良好的健康人能够轻松排出过量的膳食锰。吸入的锰更令人担忧,因为它绕过了人体正常的稳态机制,可能在大脑中蓄积。长期暴露于空气中的高锰浓度(>1毫克/立方米)会导致一种称为“锰中毒”的帕金森综合征。最令人担忧的是最近的研究表明,当工人接触焊接烟雾中低得多的吸入锰水平(<0.2毫克/立方米)时,可能会出现神经和神经行为缺陷。因此,美国国家职业安全与健康研究所的研究人员正在对吸入锰进行风险评估。这项风险评估的新内容包括尝试利用人类基因组计划生成的数据量化个体间差异的范围,并通过实验工作确定基于基因的接触、疾病和易感性生物标志物。文中讨论了从流行病学和体内数据转向基于健康的定量风险评估以及最终可执行的政府标准所涉及的困难。

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