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1,3 - 丁二烯在实验动物中,在百万分之6.25至8000的所有浓度下都会诱发癌症。

1,3-Butadiene induces cancer in experimental animals at all concentrations from 6.25 to 8000 parts per million.

作者信息

Melnick R L, Huff J E

机构信息

Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.

出版信息

IARC Sci Publ. 1993(127):309-22.

PMID:8070878
Abstract

1,3-Butadiene, a chemical produced in large volumes, induces cancer in many organs in rats (at 1000 and 8000 ppm) and mice (at 6.25 to 1250 ppm); however, the sites of tumour induction (seven in rats and nine in mice) and the magnitudes of response differ between the two species. Particularly noteworthy in the studies of mice exposed by inhalation were the early, extensive induction of malignant lymphomas, the induction of uncommon haemangiosarcomas of the heart and the development of malignant lung tumours at 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. In order to account for the impact of early mortality on the expression of late development of tumours, survival-adjusted tumour rates were computed for mice exposed to butadiene at 6.25-625 ppm. The results provide a more accurate characterization of concentration-dependent responses for butadiene-induced cancers. Stop-exposure studies revealed that the atmospheric concentration of butadiene was a greater contributing factor to the development of lymphomas than was duration of exposure. The studies in mice show a good correspondence with the reported associations between occupational exposure to butadiene and excess mortality from lymphatic and haematopoietic cancers; mice are thus a better experimental surrogate for humans. Although further work is needed to improve our understanding of the mechanisms of tumour induction by butadiene, pursuit of that research must not delay reduction of human exposure to this carcinogenic chemical.

摘要

1,3 - 丁二烯是一种大量生产的化学物质,可在大鼠的许多器官(1000 ppm和8000 ppm)和小鼠的许多器官(6.25至1250 ppm)中诱发癌症;然而,两种物种的肿瘤诱发部位(大鼠有七个,小鼠有九个)和反应程度有所不同。在吸入暴露的小鼠研究中,特别值得注意的是早期广泛诱发恶性淋巴瘤、诱发罕见的心脏血管肉瘤以及在6.25 ppm(该气体长期致癌性研究中使用过的最低浓度)时出现恶性肺肿瘤。为了说明早期死亡对肿瘤晚期发生表达的影响,计算了暴露于6.25 - 625 ppm丁二烯的小鼠的生存调整肿瘤发生率。结果更准确地描述了丁二烯诱发癌症的浓度依赖性反应。停止暴露研究表明,丁二烯的大气浓度对淋巴瘤发生的影响比暴露持续时间更大。小鼠研究与所报道的职业性接触丁二烯与淋巴和造血系统癌症超额死亡率之间的关联表现出良好的一致性;因此,小鼠是更适合人类的实验替代物。尽管需要进一步开展工作以增进我们对丁二烯诱发肿瘤机制的理解,但开展该研究绝不能拖延减少人类对这种致癌化学物质的接触。

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