ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), Carlos III Institute of Health, Madrid, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain.
Institute of Environmental Assessment and Water Research (IDÆA-CSIC), Barcelona, Spain.
Environ Int. 2019 Oct;131:104988. doi: 10.1016/j.envint.2019.104988. Epub 2019 Jul 16.
Swimming in pools is a healthy activity that entails exposure to disinfection by-products (DBPs), some of which are irritant and genotoxic.
We evaluated exposure to DBPs during swimming in a chlorinated pool and the association with short-term changes in genotoxicity and lung epithelium permeability biomarkers.
Non-smoker adults (N = 116) swimming 40 min in an indoor pool were included. We measured a range of biomarkers before and at different times after swimming: trihalomethanes (THMs) in exhaled breath (5 min), trichloroacetic acid (TCAA) in urine (30 min), micronuclei in lymphocytes (1 h), serum club cell protein (CC16) (1 h), urine mutagenicity (2 h) and micronuclei in reticulocytes (4 days in a subset, N = 19). Several DBPs in water and trichloramine in air were measured, and physical activity was extensively assessed. We estimated interactions with polymorphisms in genes related to DBP metabolism.
Median level of chloroform, brominated and total THMs in water was 37.3, 9.5 and 48.5, μg/L, respectively, and trichloramine in air was 472.6 μg/m. Median exhaled chloroform, brominated and total THMs increased after swimming by 10.9, 2.6 and 13.4, μg/m, respectively. Creatinine-adjusted urinary TCAA increased by 3.1 μmol/mol. Micronuclei in lymphocytes and reticulocytes, urine mutagenicity and serum CC16 levels remained unchanged after swimming. Spearman correlation coefficients showed no association between DBP exposure and micronuclei in lymphocytes, urine mutagenicity and CC16. Moderate associations were observed for micronuclei in reticulocytes and DBP exposure.
The unchanged levels of the short-term effect biomarkers after swimming and null associations with personal estimates of exposure to DBPs suggest no measurable effect on genotoxicity in lymphocytes, urine mutagenicity and lung epithelium permeability at the observed exposure levels. The moderate associations with micronuclei in reticulocytes require cautious interpretation given the reduced sample size.
游泳是一种有益健康的活动,但会使人接触到消毒副产物(DBPs),其中一些具有刺激性和遗传毒性。
我们评估了在氯化泳池游泳时接触 DBPs 的情况,并研究了其与遗传毒性和肺上皮细胞通透性生物标志物短期变化的相关性。
纳入 116 名不吸烟的成年人,让他们在室内泳池游泳 40 分钟。我们在游泳前和游泳后不同时间测量了一系列生物标志物:呼气中的三卤甲烷(THMs)(5 分钟)、尿液中的三氯乙酸(TCAA)(30 分钟)、淋巴细胞中的微核(1 小时)、血清克拉细胞蛋白(CC16)(1 小时)、尿液致突变性(2 小时)以及网织红细胞中的微核(在亚组中,N=19,4 天)。我们还测量了水中的几种 DBPs 和空气中的三氯胺,并广泛评估了体力活动情况。我们还估计了这些与 DBPs 代谢相关基因的多态性之间的相互作用。
水中的氯仿、溴化和总 THMs 中位数水平分别为 37.3、9.5 和 48.5μg/L,空气中的三氯胺中位数水平为 472.6μg/m。游泳后,呼气中的氯仿、溴化和总 THMs 分别增加了 10.9、2.6 和 13.4μg/m。尿液中肌酐调整后的 TCAA 增加了 3.1μmol/mol。游泳后,淋巴细胞和网织红细胞中的微核、尿液致突变性和血清 CC16 水平均无变化。Spearman 相关系数显示,DBP 暴露与淋巴细胞中的微核、尿液致突变性和 CC16 之间无关联。网织红细胞中的微核与 DBP 暴露之间存在中度关联。
游泳后短期效应生物标志物水平无变化,且与个人 DBPs 暴露估计值之间无关联,表明在观察到的暴露水平下,DBPs 对淋巴细胞遗传毒性、尿液致突变性和肺上皮细胞通透性没有可测量的影响。由于样本量较小,需要谨慎解释与网织红细胞中的微核存在中度关联的结果。