Chlorinated Pools Research Articles

Effects of UV254 irradiation on residual chlorine and DBPs in chlorination of model organic-N precursors in swimming pools

Ultraviolet (UV) irradiation is commonly applied as a secondary disinfection process in chlorinated pools. UV-based systems have been reported to yield improvements in swimming pool water and air chemistry, but to date these observations have been largely anecdotal. The objectives of this investigation were to evaluate the effects of UV irradiation on chlorination of important organic-N precursors in swimming pools.Creatinine, L-arginine, L-histidine, glycine, and urea, which comprise the majority of the organic-N in human sweat and urine, were selected as precursors for use in conducting batch experiments to examine the time-course behavior of several DBPs and residual chlorine, with and without UV254 irradiation. In addition, water samples from two natatoria were subjected to monochromatic UV irradiation at wavelengths of 222 nm and 254 nm to evaluate changes of liquid-phase chemistry. UV254 irradiation promoted formation and/or decay of several chlorinated N-DBPs and also increased the rate of free chlorine consumption. UV exposure resulted in loss of inorganic chloramines (e.g., NCl3) from solution. Dichloromethylamine (CH3NCl2) formation from creatinine was promoted by UV exposure, when free chlorine was present in solution; however, when free chlorine was depleted, CH3NCl2 photodecay was observed. Dichoroacetonitrile (CNCHCl2) formation (from L-histidine and L-arginine) was promoted by UV254 irradiation, as long as free chlorine was present in solution. Likewise, UV exposure was observed to amplify cyanogen chloride (CNCl) formation from chlorination of L-histidine, L-arginine, and glycine, up to the point of free chlorine depletion. The results from experiments involving UV irradiation of chlorinated swimming pool water were qualitatively consistent with the results of model experiments involving UV/chlorination of precursors in terms of the behavior of residual chlorine and DBPs measured in this study.The results indicate that UV254 irradiation promotes several reactions that are involved in the formation and/or destruction of chlorinated N-DBPs in pool settings. Enhancement of DBP formation was consistent with a mechanism whereby a rate-limiting step in DBP formation was promoted by UV exposure. Promotion of these reactions also resulted in increases of free chlorine consumption rates.

Can Indoor Swimming Alter Hormones in Boys?

Can Indoor Swimming Alter Hormones in Boys?

Heated indoor swimming pools, infants, and the pathogenesis of adolescent idiopathic scoliosis: a neurogenic hypothesis.

BackgroundIn a case-control study a statistically significant association was recorded between the introduction of infants to heated indoor swimming pools and the development of adolescent idiopathic scoliosis (AIS). In this paper, a neurogenic hypothesis is formulated to explain how toxins produced by chlorine in such pools may act deleteriously on the infant's immature central nervous system, comprising brain and spinal cord, to produce the deformity of AIS.Presentation of the hypothesisThrough vulnerability of the developing central nervous system to circulating toxins, and because of delayed epigenetic effects, the trunk deformity of AIS does not become evident until adolescence. In mature healthy swimmers using such pools, the circulating neurotoxins detected are chloroform, bromodichloromethane, dibromochloromethane, and bromoform. Cyanogen chloride and dichloroacetonitrile have also been detected.Testing the hypothesisIn infants, the putative portals of entry to the blood could be dermal, oral, or respiratory; and entry of such circulating small molecules to the brain are via the blood-brain barrier, blood-cerebrospinal fluid barrier, and circumventricular organs. Barrier mechanisms of the developing brain differ from those of adult brain and have been linked to brain development. During the first 6 months of life cerebrospinal fluid contains higher concentrations of specific proteins relative to plasma, attributed to mechanisms continued from fetal brain development rather than immaturity.Implications of the hypothesisThe hypothesis can be tested. If confirmed, there is potential to prevent some children from developing AIS.

Severe and rapid erosion of dental enamel from swimming: A clinical report

The diagnosis and treatment of a patient with excessive and rapid erosion of enamel is presented. Although the Center for Disease Control and the dental literature have reported on dental enamel erosion resulting from swimming pool chlorination, the awareness of such etiology among dental professionals may be limited. Common findings in these reports include cold sensitivity, a distinctive appearance resembling laminate veneer preparations of the facial surfaces of anterior teeth, occurrence of diastemas, and at times, a rough or gritty texture of the remaining tooth structure. Clinical presentations of erosive lesions can be diagnosed and the best course of treatment determined.

Exercise-Induced Bronchoconstriction in Children and Adolescents

Exercise-induced bronchoconstriction (EIB) is common in children. This article reviews the epidemiology, clinical presentation, pathophysiology, diagnosis, and treatment of EIB. EIB is caused by transient narrowing of the airways during or most often after exercise and indicates airway hyperresponsiveness. EIB is an important cause of exercise limitation in children. However, the diagnosis of EIB can be challenging because symptoms poorly predict the presence of EIB. Bronchial challenges, such as cardiopulmonary exercise testing, are required to document EIB. The severity of EIB is worsened by exposure to inhalational toxicants such as chlorine in pools and air pollution. In most children, EIB can be effectively prevented by both nonpharmacological means and medications. Educating the child, his/her family, and supervising adults about asthma triggers and management is important. Prompt recognition and treatment of an asthma attack associated with exercise is critical; bronchodilators should be on the sidelines at all times, and an asthma action plan should be in place.

Associations between testicular hormones at adolescence and attendance at chlorinated swimming pools during childhood

The goal was to evaluate the associations between testicular hormones at adolescence and the exposure to chlorination by-products when attending chlorinated swimming pools. We obtained serum samples from 361 school male adolescents (aged 14–18 years) who had visited swimming pools disinfected with chlorine or by copper–silver ionization. We analysed serum concentrations of inhibin B (two different assays), total and free testosterone, sex hormone-binding globulin, luteinizing hormone (LH), follicle stimulating hormone (FSH) and dehydroepiandrosterone sulphate (DHEAS). There were strong inverse associations between serum levels of inhibin B (both assays) or of total testosterone, adjusted or unadjusted for gonadotropins and the time adolescents had spent in indoor chlorinated pools, especially during their childhood. Adolescents having attended indoor chlorinated pools for more than 250 h before the age of 10 years or for more than 125 h before the age of 7 years were about three times more likely to have an abnormally low serum inhibin B and/or total testosterone (<10th percentile) than their peers who never visited this type of pool during their childhood (odds ratio, 95% CI, 2.83, 1.06–7.52, p = 0.04 and 3.67, 1.45–9.34, p = 0.006, respectively). Such associations were not seen with free testosterone, LH, FSH and DHEAS or with the attendance of outdoor chlorinated pools or of the copper–silver pool. Swimming in indoor chlorinated pools during childhood is strongly associated with lower levels of serum inhibin B and total testosterone. The absorption of reprotoxic chlorination by-products across the highly permeable scrotum might explain these associations.

Mysterious Foot Lesions in a Healthy Eight Year Old

Mysterious Foot Lesions in a Healthy Eight Year Old

Relationship between chlorinated pools and bronchial asthma

Relationship between chlorinated pools and bronchial asthma

Short-Term Changes in Respiratory Biomarkers after Swimming in a Chlorinated Pool

BackgroundSwimming in chlorinated pools involves exposure to disinfection by-products (DBPs) and has been associated with impaired respiratory health.ObjectivesWe evaluated short-term changes in several respiratory biomarkers to explore mechanisms of potential lung damage related to swimming pool exposure.MethodsWe measured lung function and biomarkers of airway inflammation [fractional exhaled nitric oxide (FeNO), eight cytokines, and vascular endothelial growth factor (VEGF) in exhaled breath condensate], oxidative stress (8-isoprostane in exhaled breath condensate), and lung permeability [surfactant protein D (SP-D) and the Clara cell secretory protein (CC16) in serum] in 48 healthy nonsmoking adults before and after they swam for 40 min in a chlorinated indoor swimming pool. We measured trihalomethanes in exhaled breath as a marker of individual exposure to DBPs. Energy expenditure during swimming, atopy, and CC16 genotype (rs3741240) were also determined.ResultsMedian serum CC16 levels increased from 6.01 to 6.21 μg/L (average increase, 3.3%; paired Wilcoxon test p = 0.03), regardless of atopic status and CC16 genotype. This increase was explained both by energy expenditure and different markers of DBP exposure in multivariate models. FeNO was unchanged overall but tended to decrease among atopics. We found no significant changes in lung function, SP-D, 8-isoprostane, eight cytokines, or VEGF.ConclusionsWe detected a slight increase in serum CC16, a marker of lung epithelium permeability, in healthy adults after they swam in an indoor chlorinated pool. Exercise and DBP exposure explained this association, without involving inflammatory mechanisms. Further research is needed to confirm the results, establish the clinical relevance of short-term serum CC16 changes, and evaluate the long-term health impacts.

Genotoxic Effects in Swimmers Exposed to Disinfection By-products in Indoor Swimming Pools

BackgroundExposure 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.ObjectivesWe evaluated adults who swam in chlorinated pools to determine whether exposure to DBPs in pool water is associated with biomarkers of genotoxicity.MethodsWe 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.ResultsAfter 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.ConclusionsOur 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.

Exercise-Induced Rhinitis in Competitive Swimmers

Elite swimmers are at increased risk of asthma, which has been related to chronic effects of pool chlorine environment. However acute effects of swimming on rhinitis remain unknown. We aimed to assess the nasal response to exercise in competitive swimmers compared with competitive runners. Measurements of nasal symptoms, peak nasal inspiratory flow, lung function, dyspnea, and of airway inflammation were obtained before and after a training session of 19 international-level swimmers and 13 professional runners. Exercise-induced rhinitis was defined as a fall in peak nasal inspiratory flow above 20% from baseline and atopy by positivity to skin-prick testing. Changes within groups were compared using paired t test and differences compared by analysis of covariance. Prevalence of exercise-induced rhinitis was similar between swimmers and runners, respectively 21% and 23%. Contrary to runners, swimmers experienced a decrease in nasal inspiratory flow levels and increase in sneezing, nasal congestion, itching, and postnasal drip after exercise. However, difference in changes was only significant for postnasal drip (p = 0.050). All subjects experiencing exercise-induced rhinitis were nonatopic. An overall improvement in nasal flows, sneezing, and itching after exercise was observed in atopic athletes, although no significant differences in changes compared with nonatopic athletes existed. Swimmers, contrary to runners, experience a worsening of nasal function after training. Although these differences were only significant for postnasal drip, our results provide support to the existence of a "swimming-induced rhinitis" independent of the atopic status of the athlete.

Exercise but not mannitol provocation increases urinary Clara cell protein (CC16) in elite swimmers

Elite swimmers have an increased risk of developing asthma, and exposure to chloramine is believed to be an important trigger factor. The aim of the present study was to explore pathophysiological mechanisms behind induced bronchoconstriction in swimmers exposed to chloramine, before and after swim exercise provocation as well as mannitol provocation. Urinary Clara cell protein (CC16) was used as a possible marker for epithelial stress. 101 elite aspiring swim athletes were investigated and urinary samples were collected before and 1h after completed exercise and mannitol challenge. CC16, 11β-prostaglandin (PG)F(2α) and leukotriene E(4) (LTE(4)) were measured. Urinary levels of CC16 were clearly increased after exercise challenge, while no reaction was seen after mannitol challenge. Similar to CC16, the level of 11β-PGF(2α) was increased after exercise challenge, but not after mannitol challenge, while LTE(4) was reduced after exercise. There was no significant difference in urinary response between those with a negative compared to positive challenge, but a tendency of increased baseline levels of 11β-PGF(2α) and LTE(4) in individuals with a positive mannitol challenge. The uniform increase of CC16 after swim exercise indicates that CC16 is of importance in epithelial stress, and may as such be an important pathogenic factor behind asthma development in swimmers. The changes seen in urinary levels of 11β-PGF(2α) and LTE(4) indicate a pathophysiological role in both mannitol and exercise challenge.

HEADS UP

HEADS UP

Infant swimming in chlorinated pools and the risks of bronchiolitis, asthma and allergy

Recent studies suggest that swimming in chlorinated pools during infancy may increase the risks of lower respiratory tract infection. The aim of the present study was to assess the influence of swimming in chlorinated pools on the risks of bronchiolitis and its late consequences. A total of 430 children (47% female; mean age 5.7 yrs) in 30 kindergartens were examined. Parents completed a questionnaire regarding the child's health history, swimming practice and potential confounders. Attendance at indoor or outdoor chlorinated pools ever before the age of 2 yrs was associated with an increased risk of bronchiolitis (OR 1.68; 95% CI 1.08-2.68; p = 0.03), which was exposure-dependent for both types of pool (p-value for trend <0.01). Associations persisted, and were even strengthened, by the exclusion of other risk factors. Among children with no parental antecedents of atopic disease or no day-care attendance, odds ratios for bronchiolitis amounted to 4.45 (1.82-10.9; p = 0.001) and 4.44 (1.88-10.5; p = 0.007) after >20 h spent in chlorinated pools during infancy. Infant swimmers who developed bronchiolitis also showed higher risks of asthma and respiratory allergies later in childhood. Swimming pool attendance during infancy is associated with a higher risk of bronchiolitis, with ensuing increased risks of asthma and allergic sensitisation.

Risks and Benefits of Pool Chlorination, with Manolis Kogevinas

Chlorine is one of the most common disinfectants used to kill microbes in water and make it safe for humans to swim in and drink. But when chlorine and other disinfectants combine with organic matter in pools such as sweat, urine, and skin cells, the results are disinfection by-products (DBPs), which have been linked with adverse health effects in animals and humans. In this podcast, Manolis Kogevinas discusses recent research on the carcinogenic and genotoxic potential of DBPs, but he also explains why people don't necessarily need to stop swimming in pools. Kogevinas is a professor and co-director of the Centre for Research in Environmental Epidemiology in Barcelona, Spain.

Impact of Chlorinated Swimming Pool Attendance on the Respiratory Health of Adolescents

The goal was to estimate the burden of allergic diseases associated with chlorinated pool exposure among adolescents. We examined 847 students, 13 to 18 years of age, who had attended outdoor or indoor chlorinated pools at various rates. Of them, 114 had attended mainly a copper-silver pool and served as a reference group. We measured total and aeroallergen-specific immunoglobulin E (IgE) levels in serum and screened for exercise-induced bronchoconstriction. Outcomes were respiratory symptoms, hay fever, allergic rhinitis, and asthma that had been diagnosed at any time (ever asthma) or was being treated with medication and/or was associated with exercise-induced bronchoconstriction (current asthma). Among adolescents with atopy with serum IgE levels of>30 kIU/L or aeroallergen-specific IgE, the odds ratios (ORs) for asthma symptoms and for ever or current asthma increased with the lifetime number of hours spent in chlorinated pools, reaching values of 7.1 to 14.9 when chlorinated pool attendance exceeded 1000 hours. Adolescents with atopy with chlorinated pool attendance of >100 hours had greater risk of hay fever (OR: 3.3-6.6), and those with attendance of >1000 hours had greater risk of allergic rhinitis (OR: 2.2-3.5). Such associations were not found among adolescents without atopy or with copper-silver pool attendance. The population attributable risks for chlorinated pool-related ever-diagnosed asthma, hay fever, and allergic rhinitis were 63.4%, 62.1%, and 35.0%, respectively. Chlorinated pool exposure exerts an adjuvant effect on atopy that seems to contribute significantly to the burden of asthma and respiratory allergies among adolescents.

Volatile disinfection by-product analysis from chlorinated indoor swimming pools

Chlorination of indoor swimming pools is practiced for disinfection and oxidation of reduced compounds that are introduced to water by swimmers. However, there is growing concern associated with formation for chlorinated disinfection by-products (DBPs) in these settings. Volatile DBPs are of particular concern because they may promote respiratory ailments and other adverse health effects among swimmers and patrons of indoor pool facilities. To examine the scope of this issue, water samples were collected from 11 pools over a 6 month period and analyzed for free chlorine and their volatile DBP content. Eleven volatile DBPs were identified: monochloramine (NH 2Cl), dichloramine (NHCl 2), trichloramine (NCl 3), chloroform (CHCl 3), bromoform (CHBr 3), dichlorobromomethane (CHBrCl 2), dibromochloromethane (CHBr 2Cl), cyanogen chloride (CNCl), cyanogen bromide (CNBr), dichloroacetonitrile (CNCHCl 2), and dichloromethylamine (CH 3NCl 2). Of these 11 DBPs, 10 were identified as regularly occurring, with CHBrCl 2 only appearing sporadically. Pool water samples were analyzed for residual chlorine compounds using the DPD colorimetric method and by membrane introduction mass spectrometry (MIMS). These two methods were chosen as complementary measures of residual chlorine, and to allow for comparisons between the methods. The DPD method was demonstrated to consistently overestimate inorganic chloramine content in swimming pools. Pairwise correlations among the measured volatile DBPs allowed identification of dichloromethylamine and dichloroacetonitrile as potential swimming pool water quality indicator compounds.

Chlorine in swimming pools

To the Editor: As a former competitive swimmer who is now involved in the health and fitness industry, I am often approached by swimmers and coaches to get my opinion on the water quality in swimming pools used for training by competitive swimmers. Many swimming clubs train in heated indoor pools, mostly in a gym environment, and most of the swimmers complain of a number of symptoms such as sinus problems, itchy skin and itchy ear channels as a result of spending several hours per week exposed to chlorinated water. The scientific literature around the topic of swimming and water quality focuses on asthma and allergies caused by chlorine in swimming pools. However, none of the studies mention any normative values for chemical levels in swimming pools.

Outdoor swimming pools and the risks of asthma and allergies during adolescence

Exposure to indoor chlorinated swimming pools can be detrimental to the airways of swimmers and increase asthma risks but it is unknown whether these effects concern outdoor pools. The present study examined 847 secondary school adolescents who had attended residential or nonresidential outdoor chlorinated pools at a variable rate. The main outcomes were: ever asthma (physician-diagnosed at any time); current asthma (ever asthma under medication and/or with exercise-induced bronchoconstriction); elevated exhaled nitric oxide; and aeroallergen-specific immunoglobulin (Ig)E in serum. The prevalence of ever and current asthma significantly increased with the lifetime number of hours spent in outdoor pools by up to four and eight times, respectively, among adolescents with the highest attendance (>500 h) and a low exposure to indoor pools (<250 h). Odds for asthma were significantly increased among adolescents with total serum IgE >25 kIU x L(-1), on average by 1-2 units for each 100-h increase in pool attendance. Use of residential outdoor pools was also associated with higher risks of elevated exhaled nitric oxide and sensitisation to cat or house dust mite allergens. Outdoor chlorinated swimming pool attendance is associated with higher risks of asthma, airways inflammation and some respiratory allergies.

Nitrosamine Carcinogens Also Swim in Chlorinated Pools

Highly carcinogenic N-nitrosodialkylamine (nitrosamine) disinfection byproducts were quantified in chlorinated swimming pools, hot tubs, and aquaria. N-Nitrosodimethylamine, the most abundant nitrosamine detected, was measured in swimming pools and hot tubs at levels up to 500-fold greater than the drinking water concentration of 0.7 ng/L associated with a one in one million lifetime cancer risk. Temperature, enclosure, amine and nitrite precursor loading, and the use of disinfection schemes with reduced chlorine doses contributed to statistically significant variability in its occurrence. N-Nitrosodibutylamine and N-nitrosopiperidine were also detected but together represented <5% of the total analyte distribution. The presence of N-nitrodimethylamine at levels comparable to N-nitrosodimethylamine points to a competition between the nitration and nitrosation of amines in chlorinated recreational waters. Since nitrosamines can cause bladder cancer, the significance of our measurements needs clarification with respect to recent epidemiological results that are suggestive of a link between swimming in chlorinated pools and bladder cancer.