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Long man-made fibers and lung cancer risk.

机译:人造纤维过多和患肺癌的风险。

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We show that available experimental data from long-term oncogenicity experiments in Fisher rats are consistent with the hypothesis that the oncogenic potential of long man-made mineral fibers is determined mainly by their biopersistence. We present analyses of these data within the initiation-promotion-progression paradigm of carcinogenesis. Our method of analysis can take the temporal pattern of the burden of long fibers in the lungs of individual animals into explicit account. For this analysis, the temporal pattern of lung burden for each animal was imputed from the information obtained from sacrificed animals. The data are consistent with the hypothesis that fibers act as initiators in the rat lung. We present an estimate of the dose-dependent initiation parameter that is based on all the available data. Copyright 2001 Academic Press.
机译:我们表明,来自费舍尔大鼠长期致癌性实验的可用实验数据与以下假设相符:长人造矿物纤维的致癌潜力主要取决于它们的生物持久性。我们目前在致癌的起始-促进-进展范式内对这些数据进行分析。我们的分析方法可以明确考虑单个动物肺部长纤维负担的时间模式。为了进行此分析,根据从处死动物中获得的信息来估算每只动物的肺部负担的时间模式。数据与纤维充当大鼠肺中的引发剂的假设一致。我们提出了基于所有可用数据的剂量依赖性起始参数的估计。版权所有2001学术出版社。

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