Kutzman R S, Drew R T, Shiotsuka R N, Cockrell B Y
J Toxicol Environ Health. 1986;17(2-3):175-89. doi: 10.1080/15287398609530814.
Fischer-344 rats were exposed to 0.0, 0.3, 1.0, or 2.0 mg Cd/m3 as CdCl2 aerosol for 6 h/d, 5 d/wk, for 62 exposure days. Exposure to 2.0 mg Cd/m3 resulted in rapid weight loss, and all of the animals died within the first 45 exposure days. As a group, female rats survived significantly longer than the males. Exposure to Cd resulted in dose-dependent increases in lung weight. The increased weight was the result of additional tissue mass rather than edema. Both connective-tissue components, elastin and collagen, were significantly increased in the 1.0-mg/m3 group when these components were expressed on the basis of dry weight. Dose-dependent changes at the terminal bronchioles consisted of hyperplasia and flattening of type II cells, inflammation, and the proliferation of fibroblasts. Exposure to Cd also resulted in the development of intralymphatic microgranulomas in the perivascular and peribronchiolar lymphoid tissues.
将Fischer - 344大鼠暴露于浓度为0.0、0.3、1.0或2.0毫克氯化镉/立方米的氯化镉气溶胶中,每天暴露6小时,每周暴露5天,共暴露62天。暴露于2.0毫克氯化镉/立方米会导致体重迅速下降,所有动物在最初的45个暴露日内死亡。作为一个群体,雌性大鼠的存活时间明显长于雄性大鼠。镉暴露导致肺重量呈剂量依赖性增加。重量增加是额外组织质量而非水肿的结果。当以干重为基础表示时,在1.0毫克/立方米组中,弹性蛋白和胶原蛋白这两种结缔组织成分均显著增加。终末细支气管的剂量依赖性变化包括II型细胞增生和扁平、炎症以及成纤维细胞增殖。镉暴露还导致血管周围和细支气管周围淋巴组织中出现淋巴管内微肉芽肿。