Witschi Hanspeter, Espiritu Imelda, Uyeminami Dale, Suffia Marie, Pinkerton Kent E
Center for Health and the Environment, University of California, Davis, California 95616, USA.
Inhal Toxicol. 2004 Jan;16(1):27-32. doi: 10.1080/08958370490258372.
Male strain A/J mice were exposed for 5 mo in a whole-body inhalation chamber to 3 different concentrations of a mixture of cigarette sidestream and mainstream smoke (99, 120, and 176 mg/m(3) of total suspended particulate material, TSP). After an additional 4-mo recovery period in air, lung tumor multiplicities and incidences were determined. The two highest smoke concentrations produced significantly more lung tumors than did the low dose and control groups, although the response to the high was slightly less than to the medium dose. Lung tumor incidences were in all three groups significantly higher than in controls. Lung displacement volume was increased in a dose-dependent manner, but morphometric analysis of the tissues failed to provide evidence for airspace enlargement. Plasma cotinine levels were dose-dependent and similar after 1-day and 5-day exposure. The shape of the dose-response curve and a comparison with previous data suggest that cigarette smoke is only a comparatively weak mouse lung carcinogen.
雄性A/J品系小鼠在全身吸入舱中暴露于3种不同浓度的香烟侧流烟和主流烟混合物(总悬浮颗粒物TSP浓度分别为99、120和176 mg/m³)5个月。在空气中额外恢复4个月后,测定肺肿瘤的多发性和发生率。与低剂量组和对照组相比,两个最高烟雾浓度组产生的肺肿瘤明显更多,尽管高剂量组的反应略低于中剂量组。所有三组的肺肿瘤发生率均显著高于对照组。肺置换体积呈剂量依赖性增加,但组织形态计量分析未提供气腔扩大的证据。血浆可替宁水平呈剂量依赖性,且在暴露1天和5天后相似。剂量反应曲线的形状以及与先前数据的比较表明,香烟烟雾只是一种相对较弱的小鼠肺致癌物。