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Health effects from swimming training in chlorinated pools and the corresponding metabolic stress pathways.

ABSTRACT: Chlorination is the most popular method for disinfecting swimming pool water; however, although pathogens are being killed, many toxic compounds, called disinfection by-products (DBPs), are formed. Numerous epidemiological publications have associated the chlorination of pools with dysfunctions of the respiratory system and with some other diseases. However, the findings concerning these associations are not always consistent and have not been confirmed by toxicological studies. Therefore, the health effects from swimming in chlorinated pools and the corresponding stress reactions in organisms are unclear. In this study, we show that although the growth and behaviors of experimental rats were not affected, their health, training effects and metabolic profiles were significantly affected by a 12-week swimming training program in chlorinated water identical to that of public pools. Interestingly, the eyes and skin are the organs that are more directly affected than the lungs by the irritants in chlorinated water; instead of chlorination, training intensity, training frequency and choking on water may be the primary factors for lung damage induced by swimming. Among the five major organs (the heart, liver, spleen, lungs and kidneys), the liver is the most likely target of DBPs. Through metabolomics analysis, the corresponding metabolic stress pathways and a defensive system focusing on taurine were presented, based on which the corresponding countermeasures can be developed for swimming athletes and for others who spend a lot of time in chlorinated swimming pools.

SUBMITTER: Li JH

PROVIDER: S-EPMC4351252 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Health effects from swimming training in chlorinated pools and the corresponding metabolic stress pathways.

Li Jiang-Hua JH Wang Zhi-Hui ZH Zhu Xiao-Juan XJ Deng Zhao-Hui ZH Cai Can-Xin CX Qiu Li-Qiang LQ Chen Wei W Lin Ya-Jun YJ

PloS one 20150305 3

Chlorination is the most popular method for disinfecting swimming pool water; however, although pathogens are being killed, many toxic compounds, called disinfection by-products (DBPs), are formed. Numerous epidemiological publications have associated the chlorination of pools with dysfunctions of the respiratory system and with some other diseases. However, the findings concerning these associations are not always consistent and have not been confirmed by toxicological studies. Therefore, the h ...[more]

PMID: 25742134

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Project description:BACKGROUND: Exposure to disinfection by-products (DBPs) in drinking water has been associated with cancer risk. A recent study (Villanueva et al. 2007; Am J Epidemiol 165:148-156) found an increased bladder cancer risk among subjects attending swimming pools relative to those not attending. OBJECTIVES: We evaluated adults who swam in chlorinated pools to determine whether exposure to DBPs in pool water is associated with biomarkers of genotoxicity. METHODS: We collected blood, urine, and exhaled air samples from 49 nonsmoking adult volunteers before and after they swam for 40 min in an indoor chlorinated pool. We estimated associations between the concentrations of four trihalomethanes (THMs) in exhaled breath and changes in micronuclei (MN) and DNA damage (comet assay) in peripheral blood lymphocytes before and 1 hr after swimming; urine mutagenicity (Ames assay) before and 2 hr after swimming; and MN in exfoliated urothelial cells before and 2 weeks after swimming. We also estimated associations and interactions with polymorphisms in genes related to DNA repair or to DBP metabolism. RESULTS: After swimming, the total concentration of the four THMs in exhaled breath was seven times higher than before swimming. The change in the frequency of micronucleated lymphocytes after swimming increased in association with higher exhaled concentrations of the brominated THMs (p = 0.03 for bromodichloromethane, p = 0.05 for chlorodibromomethane, p = 0.01 for bromoform) but not chloroform. Swimming was not associated with DNA damage detectable by the comet assay. Urine mutagenicity increased significantly after swimming, in association with the higher concentration of exhaled bromoform (p = 0.004). We found no significant associations with changes in micronucleated urothelial cells. CONCLUSIONS: Our findings support potential genotoxic effects of exposure to DBPs from swimming pools. The positive health effects gained by swimming could be increased by reducing the potential health risks of pool water.

Project description:Heat stress (HS) seriously affects animal performance. In view of global warming, it is essential to understand the regulatory mechanisms by which animals adapt to heat stress. In this study, our aim was to explore the genes and pathways involved in heat stress in sheep. To this end, we used transcriptome analysis to understand the molecular responses to heat stress and thereby identify means to protect sheep from heat shock. To obtain an overview of the effects of heat stress on sheep, we used the hypothalamus for transcriptome sequencing and identified differentially expressed genes (DEGs; false discovery rate (FDR) < 0.01; fold change > 2) during heat stress. A total of 1423 DEGs (1122 upregulated and 301 downregulated) were identified and classified into Gene Ontology (GO) categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Heat stress triggered dramatic and complex alterations in gene expression in the hypothalamus. We hypothesized that heat stress induced apoptosis and dysfunction in cells and vital organs and affected growth, development, reproduction, and circadian entrainment via the calcium signaling pathway, which influences ribosome assembly and function. Real-time PCR was used to evaluate the expression of the genes regulating important biological functions or whose expression profiles were significantly changed after acute heat stress (FDR < 0.01; fold change > 4), and the results showed that the expression patterns of these genes were consistent with the results of transcriptome sequencing, indicating that the credibility of the sequencing results. Our data indicated that heat stress induced calcium dyshomeostasis, blocked biogenesis, caused ROS accumulation, impaired the antioxidant system and innate defense, and induced apoptosis through the P53 signaling pathway activated by PEG3, decreased growth and development, and enhanced organ damage. These data is very important and helpful to elucidate the molecular mechanism of heat stress and finally to find ways to deal with heat stress damage in sheep.

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Health effects from swimming training in chlorinated pools and the corresponding metabolic stress pathways.

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Health effects from swimming training in chlorinated pools and the corresponding metabolic stress pathways.

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