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首页> 外文期刊>Archives of Toxicology >Subchronic inhalation exposure to 2-ethyl-1-hexanol impairs the mouse olfactory bulb via injury and subsequent repair of the nasal olfactory epithelium
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Subchronic inhalation exposure to 2-ethyl-1-hexanol impairs the mouse olfactory bulb via injury and subsequent repair of the nasal olfactory epithelium

机译：亚慢性吸入暴露于2-乙基-1-己醇会通过损伤和随后的鼻嗅上皮修复来损害小鼠嗅球

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摘要

The olfactory system can be a toxicological target of volatile organic compounds present in indoor air. Recently, 2-ethyl-1-hexanol (2E1H) emitted from adhesives and carpeting materials has been postulated to cause "sick building syndrome." Patients' symptoms are associated with an increased sense of smell. This investigation aimed to characterize the histopathological changes of the olfactory epithelium (OE) of the nasal cavity and the olfactory bulb (OB) in the brain, due to subchronic exposure to 2E1H. Male ICR mice were exposed to 0, 20, 60, or 150 ppm 2E1H for 8 h every day for 1 week, or 5 days per week for 1 or 3 months. After a 1-week exposure, the OE showed inflammation and degeneration, with a significant concentration-dependent reduction in the staining of olfactory receptor neurons and in the numbers of globose basal cells at a parts per thousand yen20 ppm. Regeneration occurred at 1 month along with an increase in the basal cells, but lymphocytic infiltration, expanded Bowman's glands, and a decrease in the olfactory receptor neurons were observed at 3 months. Intriguingly, the OB at 3 months showed a reduction in the diameters of the glomeruli and in the number of olfactory nerves and tyrosine hydroxylase-positive neurons, but an increased number of ionized calcium-binding adaptor molecule 1-positive microglia in glomeruli. Accordingly, 2E1H inhalation induced degeneration of the OE with the lowest-observed-adverse-effect level of 20 ppm. The altered number of functional cell components in the OB suggests that effects on olfactory sensation persist after subchronic exposure to 2E1H.
机译：嗅觉系统可能是室内空气中挥发性有机化合物的毒理学目标。最近，已经假定从粘合剂和地毯材料中散发出的2-乙基-1-己醇（2E1H）会导致“病态建筑综合症”。患者的症状与嗅觉增加有关。这项研究旨在表征由于亚慢性暴露于2E1H而引起的鼻腔嗅上皮（OE）和脑中嗅球（OB）的组织病理学变化。将雄性ICR小鼠每天暴露于0、20、60或150 ppm 2E1H 8小时，持续1周，或每周5天，持续1或3个月。在暴露1周后，OE显示出炎症和变性，嗅觉受体神经元的染色和球状基底细胞数量的浓度依赖性地显着降低，每千日元的浓度为20 ppm。再生在1个月时发生，同时基底细胞增加，但在3个月时观察到淋巴细胞浸润，鲍曼氏腺扩张和嗅觉受体神经元减少。有趣的是，3个月的OB显示肾小球直径的减少以及嗅觉神经和酪氨酸羟化酶阳性神经元的数量减少，但是肾小球中的电离钙结合衔接子分子1阳性小胶质细胞的数量增加了。因此，2E1H吸入诱导的OE变性，观察到的最低不良反应水平为20 ppm。 OB中功能细胞成分数量的变化表明，亚慢性暴露于2E1H后，对嗅觉的影响仍然存在。

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