Morgan K T, Gross E A, Patterson D L
Toxicol Appl Pharmacol. 1986 Dec;86(3):448-56. doi: 10.1016/0041-008x(86)90372-8.
A previous report of inhalation exposure of F-344 rats to formaldehyde gas, using a whole-body exposure system, described the induction of regional inhibition of nasal mucociliary function, with a clear concentration-response relationship. A head-only exposure system was subsequently developed in order to facilitate the present study of reversibility of acute effects of formaldehyde on the nasal mucociliary apparatus. This study also included an examination of more extensive areas of the nose than those reported in the previous work. Male F-344 rats were exposed to 2 or 15 ppm formaldehyde gas for 10, 20, 45, or 90 min or 6 hr with recovery groups examined 1 hr after the end of the 90-min and 6-hr exposures. No effects were observed in rats exposed to 2 ppm formaldehyde. In rats exposed to 15 ppm, the extent of formaldehyde-induced inhibition of mucociliary function detected in specific regions of the nose was time dependent, with increasing areas of mucostasis and ciliastasis being induced during a 6-hr exposure period. A 1-hr room-air exposure, following exposure to 15 ppm formaldehyde, resulted in marked recovery of mucociliary function, indicating the value of a head-only exposure system for rapid examination of mucociliary function following exposure. Recovery of mucociliary function occurred especially in the more posterior areas of affected regions of the nose. However, in areas of recovery mucus flow rate was reduced compared to unexposed control rates, indicating incomplete recovery of function in these areas. Regions of formaldehyde-induced inhibition of mucociliary function correlated well with the previously reported distribution of formaldehyde-induced nasal squamous cell carcinomas, with the exception of effects on the medial aspect of the maxilloturbinate. These findings were considered to provide further support for the proposal that both regional exposure and local tissue susceptibility may be responsible for the distribution of formaldehyde-induced nasal squamous cell carcinomas. It was also postulated, on the basis of mucus flow patterns derived from control animals in this study, that flow relationships between nasal mucus and inspired air form a countercurrent system which may optimize clearance of inhaled air contaminants.
先前一份关于使用全身暴露系统让F-344大鼠吸入甲醛气体的报告描述了鼻腔黏液纤毛功能的局部抑制诱导情况,且存在明确的浓度-反应关系。随后开发了仅头部暴露系统,以促进目前对甲醛对鼻腔黏液纤毛装置急性效应可逆性的研究。本研究还对鼻子更广泛区域进行了检查,比先前工作报道的区域更广泛。雄性F-344大鼠暴露于2或15 ppm甲醛气体中10、20、45或90分钟或6小时,在90分钟和6小时暴露结束后1小时检查恢复组。暴露于2 ppm甲醛的大鼠未观察到影响。在暴露于15 ppm的大鼠中,在鼻子特定区域检测到的甲醛诱导的黏液纤毛功能抑制程度与时间有关,在6小时暴露期间,黏液停滞和纤毛停滞的区域增加。在暴露于15 ppm甲醛后进行1小时的室内空气暴露,导致黏液纤毛功能明显恢复,表明仅头部暴露系统对于暴露后快速检查黏液纤毛功能的价值。黏液纤毛功能的恢复尤其发生在鼻子受影响区域的更靠后部位。然而,在恢复区域,黏液流速与未暴露的对照流速相比有所降低,表明这些区域的功能未完全恢复。甲醛诱导的黏液纤毛功能抑制区域与先前报道的甲醛诱导的鼻腔鳞状细胞癌的分布密切相关,但对上颌鼻甲内侧的影响除外。这些发现被认为进一步支持了这样的提议,即局部暴露和局部组织易感性可能是甲醛诱导的鼻腔鳞状细胞癌分布的原因。还根据本研究中对照动物的黏液流动模式推测,鼻腔黏液与吸入空气之间的流动关系形成了一个逆流系统,这可能优化吸入空气污染物的清除。