Renne R A, Brown H R, Jokinen M P
Battelle, Pacific Northwest Laboratories, Richland, Washington 99352.
Toxicol Pathol. 1992;20(3 Pt 1):416-25. doi: 10.1177/019262339202000311.
Chronic (24-month) inhalation exposure to 5 or 10 ppm allyl glycidyl ether (AGE) induced nasal lesions in Osborne-Mendel rats and B6C3F1 mice. Inflammation, degeneration, regeneration, metaplasia, hyperplasia, and neoplasia were observed in the nasal mucosa. Squamous metaplasia and hyperplasia of the respiratory epithelium and degeneration and regeneration with subsequent squamous and/or respiratory metaplasia of the olfactory epithelium were observed in many AGE-exposed animals. Three primary nasal neoplasms (1 papillary adenoma, 1 squamous cell carcinoma, and 1 olfactory epithelial carcinoma) were observed in rats exposed to 10 ppm AGE, and 1 nasal papillary adenoma was observed in a rat exposed to 5 ppm. Four papillary adenomas and 2 hemangiomas were observed in the noses of mice exposed to 10 ppm AGE. Although the incidence of primary nasal tumors in AGE-exposed rats or mice was not statistically significant compared to the incidence in concurrent controls, the relative rarity of primary nasal tumors in historical controls and the concurrent presence of metaplastic and hyperplastic nasal lesions similar to those reported to be associated with induced tumors of nasal epithelia by other chemicals suggest that the nasal tumors observed may be related to AGE exposure. It was concluded that, in addition to lesions indicating a toxic effect on the nasal mucosa, inhalation exposure to AGE for 24 months resulted in some evidence of carcinogenicity of AGE for male mice, equivocal evidence of carcinogenicity for female mice and male rats, and no evidence of carcinogenicity for female rats.
将奥斯本-孟德尔大鼠和B6C3F1小鼠慢性（24个月）吸入5或10 ppm烯丙基缩水甘油醚（AGE）可诱发鼻腔病变。在鼻黏膜中观察到炎症、变性、再生、化生、增生和肿瘤形成。在许多暴露于AGE的动物中观察到呼吸上皮的鳞状化生和增生，以及嗅上皮的变性和再生，随后出现鳞状和/或呼吸化生。在暴露于10 ppm AGE的大鼠中观察到3个原发性鼻腔肿瘤（1个乳头状腺瘤、1个鳞状细胞癌和1个嗅上皮癌），在暴露于5 ppm的1只大鼠中观察到1个鼻腔乳头状腺瘤。在暴露于10 ppm AGE的小鼠鼻腔中观察到4个乳头状腺瘤和2个血管瘤。尽管与同期对照组相比，暴露于AGE的大鼠或小鼠原发性鼻腔肿瘤的发生率无统计学意义，但历史对照组中原发性鼻腔肿瘤相对罕见，且同时存在与其他化学物质诱发的鼻腔上皮肿瘤相关的化生和增生性鼻腔病变，这表明观察到的鼻腔肿瘤可能与AGE暴露有关。得出的结论是，除了表明对鼻黏膜有毒性作用的病变外，24个月吸入AGE还导致有一些证据表明AGE对雄性小鼠有致癌性，对雌性小鼠和雄性大鼠有模棱两可的致癌性证据，而对雌性大鼠没有致癌性证据。
