Nakashima H, Omae K, Sakai T, Yamazaki K, Sakurai H
Department of Preventive Medicine and Public Health, School of Medicine, Keio University, Japan.
Arch Toxicol. 1994;68(5):277-83. doi: 10.1007/s002040050069.
To clarify the acute and subchronic inhalation toxicity of tetraethoxysilane [TEOS, Si(OC2H5)4], groups of ten male ICR mice (SPF grade) were exposed to 1000 ppm TEOS for 1,2,4 or 8 h (acute inhalation study), or to 200 ppm of TEOS for 6 h/day, 5 days/week, for 2 or 4 weeks (subchronic inhalation study). The numbers of mice that died during 2 weeks of observation were 0, 1, 1 and 6 in the 1-, 2-, 4- and 8-h inhalation experiments and zero in the subchronic inhalation study. In the acute inhalation study, body weight decreased after TEOS exposure and did not reach the level of control mice during 2 weeks of observation except in the 1-h inhalation study. In the subchronic exposure study, weight gain was suppressed during the exposure period. Body weight in mice exposed for 2 weeks reached the level of non-exposed mice during the 2-week observation period, but did not do so in mice exposed for 4 weeks. Acute tubular necrosis (ATN) and acute splenic atrophy (ASA) were observed in all dead mice in the acute inhalation study, and tubulointerstitial nephritis (TIN) was frequently found in the surviving mice in both the acute and subchronic studies. However, blood biochemical examinations revealed no evidence of renal dysfunction. The olfactory epithelium was necrotic in all dead mice. In the subchronic inhalation study, infiltration of polymorphonuclear neutrophils in the nasal mucosa was observed in all mice killed 1 day after exposure. These results indicate that the LCL0 for 1-h exposure to TEOS and LC50 for 4-h exposure are greater than 1000 ppm, and that the kidney and nasal mucosa are the target organs for TEOS inhalation.
为阐明四乙氧基硅烷[TEOS，Si(OC₂H₅)₄]的急性和亚慢性吸入毒性，将十只雄性ICR小鼠（无特定病原体等级）分为几组，分别暴露于1000 ppm的TEOS中1、2、4或8小时（急性吸入研究），或暴露于200 ppm的TEOS中，每天6小时，每周5天，持续2或4周（亚慢性吸入研究）。在1小时、2小时、4小时和8小时吸入实验中，观察的2周内死亡的小鼠数量分别为0、1、1和6只，亚慢性吸入研究中死亡小鼠数量为零。在急性吸入研究中，TEOS暴露后体重下降，除1小时吸入研究外，在2周观察期内体重未恢复到对照小鼠水平。在亚慢性暴露研究中，暴露期间体重增加受到抑制。暴露2周的小鼠体重在2周观察期内恢复到未暴露小鼠水平，但暴露4周的小鼠未恢复。在急性吸入研究中，所有死亡小鼠均出现急性肾小管坏死（ATN）和急性脾萎缩（ASA），在急性和亚慢性研究的存活小鼠中均经常发现肾小管间质性肾炎（TIN）。然而，血液生化检查未发现肾功能障碍迹象。所有死亡小鼠的嗅上皮均坏死。在亚慢性吸入研究中，暴露1天后处死的所有小鼠鼻黏膜均观察到多形核中性粒细胞浸润。这些结果表明，TEOS 1小时暴露的最低致死浓度（LCL₀）和4小时暴露的半数致死浓度（LC₅₀）均大于1000 ppm，肾脏和鼻黏膜是TEOS吸入的靶器官。
