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综合关于炭黑致癌风险的研究:流行病学、动物暴露及作用机制。

Integrating studies on carcinogenic risk of carbon black: epidemiology, animal exposures, and mechanism of action.

作者信息

Valberg Peter A, Long Christopher M, Sax Sonja N

机构信息

Gradient Corporation, Cambridge, Massachusetts 02138-5756, USA.

出版信息

J Occup Environ Med. 2006 Dec;48(12):1291-307. doi: 10.1097/01.jom.0000215342.52699.2a.

Abstract

OBJECTIVE

We sought to address the toxicology literature on carbon black (CB) since 1996, when IARC reclassified CB from group 3 to group 2B.

METHODS

We reviewed epidemiology and laboratory studies from 1996 to 2006, focusing on new analyses of worker populations, on species differences in tumorigenicity of poorly soluble particles, and on the role of particle-bound organics in tumorigenicity.

RESULTS

Some epidemiology studies have reported positive associations between cancer risk and worker's possible exposure to CB, but larger studies, in more highly exposed populations, have not shown consistent patterns of either elevated risk or dose-response. High levels of inhaled CB were linked with rat lung tumors in 1996, but today scientists increasingly recognize that rats exhibit a unique lung tumor response to all inert inhaled particles that is unlikely to be relevant to humans. On mechanism of action, new reports have continued to show that CB has a high surface area of elemental carbon, and a low quantity of organic material, which is poorly bioavailable.

CONCLUSION

Overall, the new epidemiological evidence decreases concerns for cancer risk compared with pre-1996 evidence. Laboratory studies support a conclusion that the mechanism of tumorigenicity of CB in rats is no different from that of any poorly soluble particle, ie, toxicity results from the particle overload per se, and not from the particles' chemistry. Thus, research published after 1996 has not identified an increase in support for CB cancer risk, but rather, points to limited and inadequate evidence for carcinogenicity.

摘要

目的

自1996年国际癌症研究机构(IARC)将炭黑(CB)从3类重新分类为2B类以来,我们试图梳理有关炭黑的毒理学文献。

方法

我们回顾了1996年至2006年的流行病学和实验室研究,重点关注工人人群的新分析、难溶性颗粒致瘤性的物种差异以及颗粒结合有机物在致瘤性中的作用。

结果

一些流行病学研究报告了癌症风险与工人可能接触炭黑之间的正相关关系,但在暴露程度更高的人群中进行的更大规模研究并未显示出风险升高或剂量反应的一致模式。1996年,高剂量吸入炭黑与大鼠肺部肿瘤有关,但如今科学家越来越认识到,大鼠对所有吸入的惰性颗粒都表现出独特的肺部肿瘤反应,而这与人类不太可能相关。在作用机制方面,新的报告继续表明,炭黑具有高表面积的元素碳和低含量的有机物质,其生物利用度较差。

结论

总体而言,与1996年之前的证据相比,新的流行病学证据降低了对癌症风险的担忧。实验室研究支持这样一个结论,即炭黑在大鼠中的致瘤机制与任何难溶性颗粒的致瘤机制没有区别,也就是说,毒性是由颗粒过载本身导致的,而不是由颗粒的化学性质导致的。因此,1996年之后发表的研究并未发现更多支持炭黑致癌风险的证据,相反,指向了关于其致癌性的有限且不充分的证据。

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