Carbonnelle Sylviane, Bernard Alfred, Doyle Ian R, Grutters Jan, Francaux Marc
School of Public Health, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium.
Med Sci Sports Exerc. 2008 Aug;40(8):1472-6. doi: 10.1249/MSS.0b013e3181733159.
The purpose of this study was to examine whether a swimming session performed in a pool sanitized with chlorine-based agents induces lung inflammation, modifies lung epithelium permeability, and alters lung function.
Eleven volunteers performed two standardized swimming sessions: one in a nonchlorinated indoor swimming pool and the other one in a chlorinated indoor pool. Lung inflammation was assessed by fractional exhaled nitric oxide (FE(NO)). Changes in lung epithelium permeability were estimated by measuring the surfactant-associated proteins Type A and Type B (SP-A and SP-B), the Clara cell protein (CC16), and the Krebs von den Lungen-6 protein (KL-6). Lung function tests were also performed. All measurements were carried out in basal conditions, after training completion and 3 h postexercise. Nitrogen trichloride (NCl3), the most concentrated gas derived from pool water chlorination, was measured in each pool during the swimming sessions.
NCl3 ranged from 160 to 280 microg x m(-3) in the air of the chlorinated pool and was undetectable in the nonchlorinated one. Lung function was affected neither by the exercise session nor by the type of sanitation. Serum pneumoproteins were unchanged excepted SP-A which decreased by 8% after exercise in the chlorinated pool (P < 0.05). FE(NO) increased by 34% (P < 0.05) after exercise in the nonchlorinated pool, whereas it was unaffected in the chlorinated one.
At concentrations lower than 300 microg x m(-3), NCl3 in an indoor chlorinated pool, does not produce short-term changes in lung function or in epithelial permeability. The unchanged FE(NO) found in the chlorinated pool after exercise suggests that chlorination might inhibit NO-induced vasodilation observed during exercise.
本研究旨在探讨在使用氯基消毒剂消毒的泳池中进行游泳活动是否会引发肺部炎症、改变肺上皮通透性并影响肺功能。
11名志愿者进行了两次标准化游泳活动：一次在未用氯消毒的室内游泳池，另一次在经氯消毒的室内游泳池。通过呼出一氧化氮分数（FE(NO)）评估肺部炎症。通过测量表面活性物质相关蛋白A和B（SP-A和SP-B）、克拉拉细胞蛋白（CC16）以及克雷布斯冯登伦格-6蛋白（KL-6）来估计肺上皮通透性的变化。还进行了肺功能测试。所有测量均在基础状态下、训练结束后以及运动后3小时进行。在游泳活动期间，对每个泳池中的三氯化氮（NCl3）进行了测量，NCl3是泳池水氯化产生的最浓缩气体。
在经氯消毒的泳池空气中，NCl3浓度范围为160至280微克×立方米−3，在未用氯消毒的泳池中未检测到。肺功能既不受运动活动影响，也不受消毒类型影响。血清肺蛋白除了在经氯消毒的泳池中运动后SP-A下降8%（P < 0.05）外，其余均无变化。在未用氯消毒的泳池中运动后FE(NO)增加了34%（P < 0.05），而在经氯消毒的泳池中则未受影响。
在室内经氯消毒的泳池中，当NCl3浓度低于300微克×立方米−3时，不会引起肺功能或上皮通透性的短期变化。在经氯消毒的泳池中运动后FE(NO)未发生变化，这表明氯化作用可能会抑制运动期间观察到的一氧化氮诱导的血管舒张。
