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[神经毒性职业性物质:I. 金属及其化合物。1970年至1982年文献综述]

[Neurotoxic occupational substances: I. Metals and their compounds. A literature review of the years 1970 to 1982].

作者信息

Triebig G, Büttner J

出版信息

Zentralbl Bakteriol Mikrobiol Hyg B. 1983 Jan;177(1-2):11-36.

PMID:6322474
Abstract

The knowledge of the neurotoxicity to the peripheral nervous system of arsenic, lead, thallium and mercury as well as their compounds is reviewed according to the literature of the period 1970-1982. - First acute and chronic intoxications are described with special reference of the neurological symptoms. Then we review the results of electromyographic, neurophysiological and histological investigations. Field studies in occupationally exposed groups and evaluation of dose-response-relationships are specified in detail. Further the presented results are discussed according to aspects in occupational medicine. The following conclusions can be drawn: Neuropathies after arsenic intoxications are characterized by symmetric sensory symptoms as usually numbness and paresthesiae of the distal extremities, but the neurophysiological and histological studies showed a great variety of results. In a former study a significant dose-response-relationship between arsenic load and evidence of neuropathy in workers was demonstrated. The onset of impairments of the peripheral nervous system caused by chronic lead exposure is discussed controversially. Some reports showed a dose-response-relationship between a slowering of nerve conduction velocities and an increase of the lead body burden. Proposals of threshold values ranged between 50 to 80 micrograms lead/dl blood. Other authors did not confirm these results. Longitudinal studies are, with one exception, not available at present. Thus a relevant evaluation, particularly regarding relevance and prognosis of a mild slowering of nerve conduction velocity, can not be given now. The neurotoxicity of mercury and its compounds is well demonstrated. In case of the metal and the inorganic compounds a direct damage of the peripheral nerve is possible, whereas for organic compounds the pathophysiological mechanism is unclear. Studies concerning dose-response-relationships as well as evaluation of threshold values in chronically exposed workers are limited. It seems at present not possible to define a threshold value for the neurotoxic effects of mercury according to peripheral nervous system. Thallium caused peripheral neuropathy is described in many casuistics But to our knowledge there are no reports of neurophysiological studies in occupationally exposed groups.

摘要

根据1970 - 1982年期间的文献,对砷、铅、铊和汞及其化合物对周围神经系统的神经毒性知识进行了综述。 - 首先描述了急性和慢性中毒情况,并特别提及了神经症状。然后我们回顾了肌电图、神经生理学和组织学研究的结果。详细说明了职业暴露人群的现场研究以及剂量 - 反应关系的评估。此外,根据职业医学的各个方面对所呈现的结果进行了讨论。可以得出以下结论:砷中毒后的神经病变以对称性感觉症状为特征,通常是远端肢体麻木和感觉异常,但神经生理学和组织学研究显示结果差异很大。在之前的一项研究中,证明了工人砷负荷与神经病变证据之间存在显著的剂量 - 反应关系。慢性铅暴露导致周围神经系统损伤的发病情况存在争议。一些报告显示神经传导速度减慢与铅体内负荷增加之间存在剂量 - 反应关系。阈值建议范围为每分升血液50至80微克铅。其他作者未证实这些结果。目前,除了一个例外,没有纵向研究。因此,现在无法给出相关评估,特别是关于神经传导速度轻度减慢的相关性和预后。汞及其化合物的神经毒性已得到充分证明。对于金属和无机化合物,可能直接损伤周围神经,而对于有机化合物,其病理生理机制尚不清楚。关于长期暴露工人的剂量 - 反应关系研究以及阈值评估有限。目前似乎无法根据周围神经系统确定汞神经毒性作用的阈值。铊导致的周围神经病变在许多病例报告中都有描述,但据我们所知,没有关于职业暴露人群神经生理学研究的报告。

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