{"title":"在实验室模型系统中吸入气态次氯酸及其对人类呼吸道上皮细胞的影响。","authors":"Takashi Muramatsu, Kazuya Kodama, Tetsuyoshi Yamada, Atsushi Yamada, Satoshi Fukuzaki","doi":"10.4265/jmc.29.1_39","DOIUrl":null,"url":null,"abstract":"<p><p>During the disinfection of indoor spaces using gaseous hypochlorous acid (HOCl<sub>(g)</sub>), inhalation is the most common route of exposure for humans. In this study, an artificial human respiratory tract model was exposed to 12-140 ppb HOCl<sub>(g)</sub> at an aspiration flow rate of 800 mL/s for 15 h in a 1 m<sup>3</sup> chamber. The respiratory tract model was equipped with 5th order bronchi and all gas-contact parts were made of silicone rubber with no other chlorine-consuming substances. The concentration of HOCl<sub>(g)</sub> reaching the lung pseudo-space was approximately 47.4% of the HOCl<sub>(g)</sub> concentrations in the chamber and was calculated to be very close to zero when the chamber concentration was less than 20.5 ppb. The disappearance of HOCl<sub>(g)</sub> during inhalation is likely due to the adsorption of HOCl<sub>(g)</sub> on the gas-contact silicone rubber surfaces. The cytotoxicity of HOCl<sub>(g)</sub> on respiratory epithelial cells was also examined using human air-liquid-interface airway tissue models. Human nasal epithelium and bronchiolar epithelium were exposed to 100 ppb and 500 ppb HOCl<sub>(g)</sub> for 8 h and 5 d, respectively. No significant effects of HOCl<sub>(g)</sub> on cell viability and ciliary activity were observed in any cell type, indicating that low concentrations of HOCl<sub>(g)</sub>, less than 500 ppb, had no cytotoxic effect.</p>","PeriodicalId":73831,"journal":{"name":"Journal of microorganism control","volume":"29 1","pages":"39-44"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Inhalation of gaseous hypochlorous acid and its effect on human respiratory epithelial cells in laboratory model systems.\",\"authors\":\"Takashi Muramatsu, Kazuya Kodama, Tetsuyoshi Yamada, Atsushi Yamada, Satoshi Fukuzaki\",\"doi\":\"10.4265/jmc.29.1_39\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>During the disinfection of indoor spaces using gaseous hypochlorous acid (HOCl<sub>(g)</sub>), inhalation is the most common route of exposure for humans. In this study, an artificial human respiratory tract model was exposed to 12-140 ppb HOCl<sub>(g)</sub> at an aspiration flow rate of 800 mL/s for 15 h in a 1 m<sup>3</sup> chamber. The respiratory tract model was equipped with 5th order bronchi and all gas-contact parts were made of silicone rubber with no other chlorine-consuming substances. The concentration of HOCl<sub>(g)</sub> reaching the lung pseudo-space was approximately 47.4% of the HOCl<sub>(g)</sub> concentrations in the chamber and was calculated to be very close to zero when the chamber concentration was less than 20.5 ppb. The disappearance of HOCl<sub>(g)</sub> during inhalation is likely due to the adsorption of HOCl<sub>(g)</sub> on the gas-contact silicone rubber surfaces. The cytotoxicity of HOCl<sub>(g)</sub> on respiratory epithelial cells was also examined using human air-liquid-interface airway tissue models. Human nasal epithelium and bronchiolar epithelium were exposed to 100 ppb and 500 ppb HOCl<sub>(g)</sub> for 8 h and 5 d, respectively. No significant effects of HOCl<sub>(g)</sub> on cell viability and ciliary activity were observed in any cell type, indicating that low concentrations of HOCl<sub>(g)</sub>, less than 500 ppb, had no cytotoxic effect.</p>\",\"PeriodicalId\":73831,\"journal\":{\"name\":\"Journal of microorganism control\",\"volume\":\"29 1\",\"pages\":\"39-44\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of microorganism control\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4265/jmc.29.1_39\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of microorganism control","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4265/jmc.29.1_39","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Inhalation of gaseous hypochlorous acid and its effect on human respiratory epithelial cells in laboratory model systems.
During the disinfection of indoor spaces using gaseous hypochlorous acid (HOCl(g)), inhalation is the most common route of exposure for humans. In this study, an artificial human respiratory tract model was exposed to 12-140 ppb HOCl(g) at an aspiration flow rate of 800 mL/s for 15 h in a 1 m3 chamber. The respiratory tract model was equipped with 5th order bronchi and all gas-contact parts were made of silicone rubber with no other chlorine-consuming substances. The concentration of HOCl(g) reaching the lung pseudo-space was approximately 47.4% of the HOCl(g) concentrations in the chamber and was calculated to be very close to zero when the chamber concentration was less than 20.5 ppb. The disappearance of HOCl(g) during inhalation is likely due to the adsorption of HOCl(g) on the gas-contact silicone rubber surfaces. The cytotoxicity of HOCl(g) on respiratory epithelial cells was also examined using human air-liquid-interface airway tissue models. Human nasal epithelium and bronchiolar epithelium were exposed to 100 ppb and 500 ppb HOCl(g) for 8 h and 5 d, respectively. No significant effects of HOCl(g) on cell viability and ciliary activity were observed in any cell type, indicating that low concentrations of HOCl(g), less than 500 ppb, had no cytotoxic effect.