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Review

Disinfection byproducts in swimming pool: Occurrences, implications and future needs Shakhawat Chowdhury a,*, Khalid Alhooshani b, Tanju Karanfil c a Department of Civil and Environmental Engineering, Water Research Group, King Fahd University of Petroleum and Minerals, Dhahran 31261, Saudi Arabia b Department of Chemistry, King Fahd University of Petroleum and Minerals, Dhahran 31261, Saudi Arabia c Department of Environmental Engineering and Earth Sciences, Clemson University, SC, USA

article info

abstract

Article history:

Disinfection of swimming pool water is essential to deactivate pathogenic microorganisms.

Received 7 October 2013

Many swimming pools apply chlorine or bromine based disinfectants to prevent microbial

Received in revised form

growth. The chlorinated swimming pool water contains higher chlorine residual and is

7 January 2014

maintained at a higher temperature than a typical drinking water distribution system. It

Accepted 8 January 2014

constitutes environments with high levels of disinfection by-products (DBPs) in water and

Available online 21 January 2014

air as a consequence of continuous disinfection and constant organic loading from the bathers. Exposure to those DBPs is inevitable for any bather or trainer, while such expo-

Keywords:

sures can have elevated risks to human health. To date, over 70 peer-reviewed publications

Chlorinated swimming pool

have reported various aspects of swimming pool, including types and quantities of DBPs,

DBPs formation

organic loads from bathers, factors affecting DBPs formation in swimming pool, human

Human exposure

exposure and their potential risks. This paper aims to review the state of research on

Continuous disinfection

swimming pool including with the focus of DBPs in swimming pools, understand their

Constant organic load

types and variability, possible health effects and analyze the factors responsible for the formation of various DBPs in a swimming pool. The study identifies the current challenges and future research needs to minimize DBPs formation in a swimming pool and their consequent negative effects to bathers and trainers. ª 2014 Elsevier Ltd. All rights reserved.

Contents 1. 2. 3. 4. 5. 6. 7.

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69 DBPs in swimming pools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Precursors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 DBPs formation pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Uptake of DBPs in swimming pools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Human health effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Analysis of findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 7.1. Indoor and outdoor pools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

* Corresponding author. Tel.: þ966 13 860 2560; fax: +966 13 860 2879. E-mail addresses: [email protected], [email protected] (S. Chowdhury). 0043-1354/$ e see front matter ª 2014 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.watres.2014.01.017

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69

7.2. Freshwater and seawater pools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 7.3. Hot tub and spa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 7.4. Exposure and risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 8. Anticipated challenges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 9. Recommendations and future research needs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 10. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Acknowledgment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Disinfection byproducts in swimming pools: role of bathers, disinfectants and strategies to minimize DBPs formation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

1.

Introduction

Chlorination as a disinfection approach for water was first introduced in 1902 in Middlekerke, Belgium (MWH, 2005). Since then, chlorination has been known as an efficient disinfection approach for municipal water (Chlorine Chemistry Council, 2003; Health Canada, 2009; USEPA, 2006; WHO, 2011). Other disinfectants, such as, chloramine, chlorine dioxide, ozone and UV irradiation are also applied for water disinfection (AWWA, 2000; MOE, 2007). Disinfection of swimming pool water is essential to prevent outbreaks of infectious illnesses (Geldreich, 1989; USCDC, 1997; MOE, 2002; MWH, 2005; CDC, 2007; HaitiLibre, 2010). While disinfectants inactivate pathogens in swimming pools, unintended reactions between disinfectants (e.g., chlorine, chloramines, ozone, or chlorine dioxide) and natural organic matter (NOM), bromide/iodide and human inputs (e.g., constituents of sweat and urine, skin particles, hair, microorganisms, cosmetics, and other personal care products) form disinfection by-products (DBPs) (Weisel et al., 2009). The types and concentrations of DBPs depend on several factors, including the type and amount of disinfectant used, characteristics of the swimming pool and pool water and users’ hygiene (Zwiener et al., 2007). In swimming pools, chlorine is the most commonly used disinfectant. The types of chlorine generally used are sodium hypochlorite (liquid bleach), calcium hypochlorite, or chlorine gas for the indoor pools (Ford Red, 2007), and stabilized chlorine products (e.g., stabilized chlorine granules, chlorinated isocyanurates, chlorine tablets) are typically used for outdoor swimming pools. The swimming pool waters generally have higher temperature leading to the higher rates of chlorine decay. To compensate for the chlorine demand, swimming pools use relatively higher doses of chlorine to ensure free residuals in the pool water (Richardson et al., 2010; Weisel et al., 2009). Higher free residual chlorine (FRC), higher temperature, constant organic loads, contact of water surface with air and water recirculation can affect DBPs formation in swimming pool. More than 600 DBPs have been identified in chlorinated waters, and many of them are mutagenic or carcinogenic (Richardson et al., 2007). Swimming pools constitute environments with high levels of DBPs in water and air due to continuous disinfection and constant organic load from bathers (Kim et al., 2002;

LaKind et al., 2010). To date, the DBPs identified in the swimming pool are trihalomethanes (THMs), haloacetic acids (HAAs), haloacids, halodiacids, iodo-THMs, haloaldehydes, halonitriles, haloketones (HKs), halonitromethanes, bromate, haloamides, haloalcohols, nitrosamines, combined available chlorine, and 3-chloro-4-(dichloromethyl)-5hydroxy-2(5H)-furanone (MX) and MX homologues, etc. (Richardson et al., 2010). The most prevalent DBPs in swimming pool are chloramines, THMs and HAAs, (Chu and Nieuwenhuijsen, 2002; Kim et al., 2002). Chloramines are also an important group of disinfectants, which may also form some DBPs in swimming pools (e.g., iodinated DBPs, NNitrosodimethylamine [NDMA]). Given the high nitrogen content of organic matter from bathers, nitrogenous DBPs such as, haloacetonitriles, nitrosamines (e.g., NDMA) can also be formed. In addition, elevated levels of ammonia in urine react with chlorine and lead to formation of chloramines, which are also found at high concentrations in swimming pools (Richardson et al., 2010; Zwiener et al., 2007; Walse and Mitch, 2008). Ammonia is also produced during ammonification of urea in biofilms. Past studies have reported the presence of biofilms in both chlorinated and unchlorinated swimming pools (Keuten et al., 2009; Schets et al., 2011; Casanovas-Massana and Blanch, 2013). The bacteria in the biofilms utilize urea as a nutrient and release ammonia as a residual. In addition, the dead cells separated from the biofilms add organic substances into the pool water. The addition of organics from the dead cells is nearly constant at a relatively low concentration. The biofilms and the separation of dead cells from the biofilms can play an important role in the formation and distribution of DBPs in swimming pools. Many DBPs, especially nitrogenous ones, are more cyto- and genotoxic than the regulated DBPs (i.e., THM and HAA) (Richardson et al., 2010). Therefore, it is not surprising that pool water is found to be more genotoxic than the source tap water, and that the type of disinfectant and illumination conditions altered the genotoxicity (Liviac et al., 2010). The genotoxicity study of swimming pool water reported that the pool water induced DNA damage in Hep-G2 cells (comet assay), and that most of the genotoxicity was associated with lower-molecular-weight ( THMs. Another interesting finding was that the genotoxicity was strongest in the low-molecular weight fraction of DBPs (Glauner et al., 2005), while removal of these DBPs requires membranes with low-molecular weight cut offs down to 200 g/mol. In assessing human health effects, most of past studies have focused on specific group of populations. The compositions of the populations (e.g., male versus female, swimmers versus non-swimmers, adults versus kids, etc.) were different. Further, their exposure conditions and environmental conditions of the exposed locations were different. To have a concluding remarks, it is important to analyze the results from studies, which are consistent with respect to participants, environmental conditions, disinfection practices, source water, pool water volume, total pool hall volume, pool locations (indoor versus outdoor) and operational conditions. Further, consistency among the dosing equipment and maintenance practices is also important for comparison purposes. Better understanding is warranted to develop the framework for minimizing human exposure and risks.

7.

Analysis of findings

7.1.

Indoor and outdoor pools

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THMs and HAAs in the indoor and outdoor swimming pools showed variable patterns. The seawater fed indoor swimming pools in the southwest of France had HAAs to THMs ratio as 1.1e3.8, while brominated THMs and HAAs were the major fractions in the total THMs and HAAs respectively (Parinet et al., 2012). For the swimming pools fed with municipal water distribution systems (MWDS), 15 indoor pools in Quebec, Canada, had HAAs to THMs ratio of 4.1e8.7, while in the 39 outdoor pools fed with the same MWDS, HAAs to THMs ratio were 6.7e14.1 (Simard et al., 2013). The ratios of THMs in the outdoor to indoor pools were 0.6e2.6, indicating that THMs in the outdoor pools can be lower than the indoor pools (Table 1). In contrast, HAAs were always higher in the outdoor pools (634e983 mg/L) than the indoor pools (348e510 mg/L) with the ratios of outdoor to indoor as 1.5e2.5 (Simard et al., 2013). Higher concentrations of TOC and higher pH in the outdoor pools could have partially increased the formation of these DBPs (Simard et al., 2013). In addition, the outdoor pools are subjected to prolong exposure to sunlight, which could have increased THMs and HAAs (Liu et al., 2006). Due to its conservative nature, HAAs remained in water while much of the THMs were volatilized, which might have led to higher ratios of HAAs to THMs in the outdoor pools than the indoor pools. The log octanolewater partition coefficients for THM compounds are 1.97 (chloroform) to 2.38 (bromoform), while for most of the HAAs, it ranges from 0.22 (MCAA) to 1.33 (TCAA), indicating that significant fractions of THMs can be partitioned from water to air, while HAAs are non-volatile. This also justifies higher ratios between HAAs to THMs in the outdoor pool water. Cardador and Gallego (2011) reported higher levels of DCAA in the outdoor pools (148  15 mg/L) than those in the indoor pools (83  14 mg/L), while TCAA were almost similar in the indoor and outdoor pools (117  21 and 118  11 respectively). Past studies reported that increase in temperature can promote the transformation of TCAA into CHCl3 and CO2, while CHCl3 can be volatilized from pool water (Wu et al., 2001), which could reduce TCAA concentrations in the outdoor pools. In contrast, Lee et al. (2010) showed that DCAA could be much lower than TCAA in the chlorinated, ozone/chlorinated and EGMO treated indoor pools. The variable patterns of THMs and HAAs in the indoor and outdoor pools indicate that few factors (e.g., sunlight, BFA) might have role on the concentrations of THMs and HAAs in the pools, while such effects are not well explained to date. Pool water containing anthropogenic pollutants exhibit different rates of THMs and HAAs formation (Kanan and Karanfil, 2011), while the causes of such differences have not been well investigated. Future study may look into these points. In addition, higher levels of volatile compounds (TCA, THMs, etc.) in the indoor pool air have been documented in literature (Richardson et al., 2010; Bessonneau et al., 2011), indicating that the indoor swimming pool premise might need better ventilation system.

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However, research to date has not gained sufficient knowledge to design a proper ventilation system for swimming pools. Pool ventilation is regulated both by temperature and humidity. Pool hall sensors measure the actual conditions and adjust the settings of the ventilation system. The pool air temperature is normally set to 1e2  C above pool water temperature. Due to public demands, the pool water temperature has been rising during the past decade, resulting in a more than equal rising for the pool air. Instead of recirculating the pool hall, the hot pool air rises like a hot air balloon to the top of the pool hall and volatile DBPs near the pool water surface are accumulating. The regulation on minimal requirements for a swimming pool ventilation system is not available. Better understanding on pool ventilation system and setting of regulation can better protect human health. In addition, increase in pool water temperature following the public demands in the recent years, might have increased DBPs formation in the pool water and the transfer of volatile DBPs from water to air. Understanding of such effects is also important.

7.2.

Freshwater and seawater pools

Formation of THMs and HAAs were several times higher in the saline water pools than the freshwater pools. THMs in saline water pools were 4.2 times the THMs in the freshwater pools, while the dominant species were CHBr3 and CHCl3 respectively (Beech et al., 1980). In freshwater pools, brominated THMs were 7.1e33.3% of total THMs, while in the saline water pools, these were more than 95% (Beech et al., 1980; Lahl et al., 1981; Chu and Nieuwenhuijsen, 2002). Similar results were observed for HAAs (Parinet et al., 2012). If bromide is present in the source water and/ or treated with HOBr or EGMO, brominated THMs and HAAs are likely to be formed (Richardson et al., 2010; Judd and Jeffry, 1995; Lourencetti et al., 2012). In the presence of bromide, HOBr is formed, which forms brominated species. However, in the literature, it was not ascertained whether the substitution reactions were the only pathway of increased formation of brominated THMs and/or HAAs in the saline water swimming pools. Furthermore, it could not be confirmed whether the increase in total THMs and HAAs (by weight) was due to the substitution of chloride by bromide. Chowdhury et al. (2010) indicated possible additional pathway of formation of brominated DBPs in presence of bromide, where the authors indicated that the low molecular weight NOM might have preferential reactions with HOBr to form brominated species. To better understand the formation pathways of brominated THMs and HAAs in saline water pools, control study by varying bromide content and BFA can be performed in future.

7.3.

Hot tub and spa

In addition to swimming pools, hot tub and spas in hotels and beach are the regularly visited places for relaxing and curing treatments. Several therapeutic gels, oil and medicines are typically used in the hot tubs and spas for enhanced performance (e.g., shower gels, bath oil). Some of the compounds in these gels and oil are reactive with

chlorine (e.g., citric acid, glycerol, preservative), which can form several DBPs (Judd and Jeffrey, 1995; Florentin et al., 2011; Weng and, Blatchley, 2011. 2011). The pharmaceutically active compounds are often released into the hot tubs and spas during the relaxing seasons. Implications of using these medicines, gels and oil in context to DBPs formation have not been well explored to date. Future studies may better explain their effects on DBPs formation and human health risk.

7.4.

Exposure and risk

Exposure to DBPs in swimming pools and hot tubs is highly likely. The findings to date have indicated possible association of swimming pool exposure with several sub-chronic and chronic effects to human. Past studies have reported higher toxicity of swimming pool water than the source tap water (Saito et al., 1996; Panyakapo et al., 2008; Plewa et al., 2011). Toxicity of bromide containing swimming pool water was much higher (27 times) than the toxicity of swimming pool water without bromide (Hansen et al., 2011). The seawater swimming pools are likely to have much higher brominated DBPs, which can have higher risks than the chlorinated counterparts (Hansen et al., 2011). Increased risks of bladder cancer from exposure to swimming pool DBPs have been anticipated in few studies (Zwiener et al., 2007; Panyakapo et al., 2008; Lee et al., 2009; Chen et al., 2011). Walse and Mitch (2008) observed much higher concentrations of NDMA, which is a potential human carcinogen. Other than the cancer risk, increased risks of airway inflammation, chest tightness, coughing, respiratory problems, red eyes, itching and asthma have been reported from exposure to swimming pool DBPs (Bernard et al., 2006; Uyan et al., 2009; Weisel et al., 2009). The indoor pool premises often have inadequate ventilation system to remove the partitioned DBPs (e.g., TCA, THMs, etc.) from pool air instantly, which can increase human exposure to the volatile DBPs. To date, little is known on the potential effects from exposure to mixture of DBPs in swimming pools. In addition, exposure and risk assessment are associated with uncertainties from several sources. Inclusion of uncertainties in the assessment process can improve the current level of understanding on human exposure and risk from DBPs in swimming pools.

8.

Anticipated challenges

To confirm safe disinfection requirements, it is essential to maintain FRC. The lowest levels of FRC to be maintained in pool water vary in the range of 0.3e1.0 mg/L, which is a wide range. Maintaining minimal levels of FRC (e.g., 0.5 mg/L) might assist in lowering DBPs formation. However, it is essential to prevent sudden loss of FRC in the pool water, which can be obtained through a robust pool water treatment and monitoring system, such as, online monitoring of FRC and chlorine dosing systems. Many countries do not have robust systems, which often require higher FRC levels to maintain minimal disinfection. A level for acceptable risk has to be set to explain the safe level of disinfection. Future research is necessary to

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set the acceptable level of risk and FRC. Inadequate disinfection may lead to an increased incidence of waterborne diseases as a result of increased exposure to pathogenic microorganisms, and thus, it would pose a greater risk to human health. The filling water for the pools inevitably contains NOM, in particular, the low molecular weight NOM (Liang and Singer, 2003). Continuous loading from bathers adds an appreciable amount of human input to the pool water, while these are typically rich in organic nitrogen. The pool air temperature needs to be 1e2  C higher than the pool water to avoid a misty layer in the pool hall. However, in some pools, pool water temperature has been reported to be higher than the pool air (e.g., Pardo et al., 2007), while such scenarios should be avoided. Different pools and/or hot tubs use different types of source water (seawater, freshwater, municipal water, own water well), disinfectants and additional chemicals depending on the purpose. Swimming pools are one of the most visited recreation centers, where people of all ages and sexes could spend few hours per week. Furthermore, swimming is often recommended as a means of physical exercise (Agopian et al., 2013). Swimming is advised as the most appropriate sport for asthmatic children (Fitch et al., 1976). It is essential for the elite athletes and swimming competitors (Fitch et al., 2008). Swimming pool activities have been reported to contribute positively to the children with autism (Yilmaz et al., 2004). In swimming pools, HAAs are likely to be higher (60.8e72.6% of total DBPs), followed by THMs (13.7e25.5%), CH (7.1e10.3%), HANs (3.4e6.6%) and other DBPs respectively (Lee et al., 2010). However, in the filling water, THMs generally constitute the higher fractions (MOE, 2007). This variability can be explained by the higher partitions of THMs from pool water to air as well as higher formation potential for HAAs. The higher temperature of pool water might explain the watereair partitions of THMs. When the source water contains bromide or treated with bromide based disinfectants, formation of brominated THMs and HAAs can constitute the major fractions of THMs and HAAs. Swimming pool water always contains chloramines (MCA, DCA and TCA) when chlorine and swimmers are or have been present, while higher concentrations of TCA in pool air have been widely reported (Richardson et al., 2010). TCA has been reported as an agent of respiratory irritation. However, a recent review of Heederik and Jacobs (2013) presented in the Rome Conference indicates that swimming in the pools does not increase the risk of having asthma later in life. Brominated and nitrogenous DBPs are noted to have much higher levels of genotoxic effects than the chlorinated counterparts (Richardson et al., 2007; Florentin et al., 2011; Hansen et al., 2011). Furthermore, a recent study demonstrated that most of the estimated cytotoxicity of pool water without bromide (63e92%) could be attributed to HANs (Hansen et al., 2012). The low molecular DBPs might have higher genotoxicity, while removal of these DBPs requires membranes with low-molecular weight cut offs (Glauner et al., 2005). Higher temperature in swimming pools often leads to higher rates of DBPs formation, while lowering pool water temperature is not recommended to avoid other physical implications, such as comfort, hypothermia, etc. Hypothermia usually occurs from long exposure to low

81

temperature water without physical exercise. Normal body temperature in humans is 36.5e37.5  C. Hypothermia is defined as a core body temperature below 35  C. It may be graded as mild (32e35  C), moderate (28e32  C) or severe (26e49 and >49 mg/L. Duration of chlorinated surface water in the residence, Average ingestion THMs exposure and duration of shower and bath were also divided into four groups. Long-term THM exposure was associated with a twofold bladder cancer risk, with an odds ratio of 2.10 (95% CI: 1.09e4.02) for average household THM levels of >49 versus 8 mg/L. Compared with subjects not drinking chlorinated water, subjects with THM exposure of >35 mg/day through ingestion had an odds ratio of 1.35 (95% CI: 0.92e1.99). The odds ratio for duration of shower or bath weighted by residential THM level was 1.83 (95% CI: 1.17e2.87) for the highest compared with the lowest quartile. Swimming in pools was associated with an odds ratio of 1.57 (95% CI: 1.18e2.09). Bladder cancer risk was associated with long-term exposure to THMs in chlorinated water at levels regularly occurring in industrialized countries

Comments

Historical THM levels were estimated by municipality under the assumption that THM level remained unchanged for a constant water source. Incorporation of THMs variability through uncertainty analysis might provide enhanced understanding on the potential risks of THMs. Further, presence of other DBPs could also have affects, which were not isolated in this study.

Averages of THMs in municipal water in Oct. Nov.eDec. and Apr.eMay were 61.3, 45.1 and 54.5 mg/L respectively. Average THM level in swimming pools was 80.4 (63.5e97.6) mg/L. Concentrations of CHCl3, BDCM, DBCM and CHBr3 in swimming pool were 66.5 (47e81.7), 9.3 (5.1e11.9), 3.2 (1.4e4.6) and 1.4 (1e1.9) mg/L respectively. Average water consumption during pregnancy was 1.9 L/day. The source of the household drinking water was 90% bottled, 8% municipal and 2% from other sources. Forty-seven percent attended swimming pools during pregnancy. The geometric mean of total THM uptake was 0.93 mg/day. Showering contributed 64%, swimming in pools 23%, bathing 12%, and drinking water 1% to the total THM uptake. Geographical variability was low and characteristics of the household did not influence THM levels. Within-subject variability in THM levels was three times higher than between-subject variability.

THMs uptakes from swimming were reported to be much higher in some studies. Further, the low contribution through ingestion of drinking water might be due to the habit of drinking bottled water.

Membrane filtration has emerged as a promising treatment method as an alternative to flocculation and traditional filtration with sand or diatomaceous earth. It can reduce DOC to a much greater extent and does not produce much waste compared to the suspension/filtration. Children swimmers have an increased risk of developing asthma and infections of the respiratory tract and ear. A 1.6e2.0-fold increased risk for bladder cancer has been associated with swimming or showering/bathing with chlorinated water. Bladder cancer risk from THM exposure (all routes combined) was greatest among those with the GSTT1-1

Efficient DOC and TOX removal requires filtration with a much lower molecular weight cut off (MWCO). Only about 30% of TOX was found in the 5 years versus 0 years).

Some degree of outcome misclassification may be present as the researchers did not have clinical measurements of respiratory and allergic symptoms. Needs of future study was stressed.

The model was developed to predict CHCl3 in swimming pool air through combining environmental conditions, Occupant activities and the airflow recycle effect. The good agreement between model simulation and measured data demonstrates the feasibility of using the presented model for indoor air quality management, operational guidelines and health-related risk assessment

To the best of the knowledge, it was the first model to predict air-phase CHCl3 in the swimming pool air. However, model predictions were way different than the measure values, indicating that the model might need improvement. Use of ozone/chlorine seems to form much lower THMs than the chlorine and EGMO treated pools. However, characterization of emerging DBPs is essential to better understand their risks. EGMO produces higher fractions of brominated THMs. It is likely that it might produce higher fractions of brominated HAAs as well. The brominated DBPs are known to have higher toxic effects to human.

The geometric means of THMs in the swimming pool waters were 32.9  2.4 mg/L (range: 1.8e104.3 mg/L) for chlorine, 23.3  2.2 mg/L (range: 0.2e68.5 mg/L) for ozone/chlorine, and 58.2  1.7 mg/L (12.6e135.2 mg/L) for EGMO treated pools. In the chlorine pools, concentrations of CHCl3, BDCM, DBCM and CHBr3 in the pool water were 40.7 (range: 0.2e101.7), 3.0 (range: ND-10.5), 0.5 (range: ND-5.6) and ND mg/L respectively. In the ozone/chlorine pools, concentrations of CHCl3, BDCM, DBCM and CHBr3 in the pool water were 28.5 (range: 0.2e64.9), 2.4 (range: ND-5.7), 0.2 (range: ND-3.4) and ND mg/L respectively. In the EGMO pools, concentrations of CHCl3, BDCM, DBCM and CHBr3 in the pool water were 27.3 (range: 6.8e55.6), 9.8 (range: 1.6e26.9), 9.1 (range: ND-30.1) and 18.8 (range: ND-36.2) mg/L respectively. The patterns of THM concentrations were similar for chlorinated and ozone-chlorinated swimming pool water (almost 90% CHCl3), while EGMO disinfection resulted in lower CHCl3 and higher concentrations and wider variations of brominated THMs (almost 45.5% CHCl3). The lifetime cancer risk estimation showed that, while risks from oral ingestion and dermal exposure to THMs are mostly less than 106,

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Appendixe (continued ) Sl.

Author (Year)

37

Uyan et al. (2009)

38

Weaver et al., 2009

39

Weisel et al. (2009)

40

Aprea et al. (2010)

Model description

Findings

(electrochemically generated mixed oxidants). This study discussed on the effects of chlorine derivatives in different categories of people routinely attending swimming pools.

however swimmers can be at the greater risk from inhalation exposure (7.77  104e1.36  103). Lifeguards of both sexes exposed to trichloramine in SP were at risk of developing acute irritant related eye, nose and throat symptoms. Long-term exposure to chlorine compounds might contribute to the occurrence of airway inflammation and increased bronchial responsiveness in highly trained swimmers. This study advised to perform comprehensive studies to establish whether or not a causeeeffect relationship really exists between recreational swimming and asthma development.

This study investigated the formation of volatile DBPs in indoor SP. Water samples were collected from 11 pools over a 6 month period (FebeAug, 2008) and analyzed for free chlorine and DBPs. Eleven volatile DBPs were identified: NH2Cl, NHCl2, NCl3, CHCl3, CHBr3, BDCM, DBCM, CNCl, CNBr, DCAN and CH3NCl2. A total of 25e40 samples were analyzed from each pool. This study explored the potential for swimming pool DBPs, which are respiratory irritants, to cause asthma in young children. The authors have described the state of the science on methods for understanding children’s exposure to DBPs and biologics at swimming pools and associations with newonset childhood asthma and recommend a research agenda to improve the understanding of this issue. The data source was the workshop, held in Leuven, Belgium, 21e23 August 2007. This study investigated exposure of bathers and pool employees to THMs in four indoor SP in Siena, Italy. The pools have the volumes of 400, 470, 476.3 and 700 m3. These pools had variable levels of nitrates (0.7e15 mg/L), isocyanic acid (65. The children in age group 1e4 had the highest dose of THMs (1.18 mg/kg/day).

Comments

Better understanding is necessary on the effects of cumulative exposure to DBPs in SP. Exposure during infancy and childhood needs to be comprehensively evaluated.

A good correlation between urine and water sample levels was obtained in all cases. However, the correlations in swimmers were lower (average correlation coefficient for TCAA, DCAA and MCAA, rw0.81) than those found in workers (average correlation coefficient for DCAA and TCAA, r w0.95).

The carcinogenicity of CHCl3 is under reassessment. Prediction of cancer risks from CHCl3 needs to be reviewed

The models may needs few critical updates in context to fresh air recirculation rate and continuous formation of THMs in SP. In an SP, THMs formation is likely to be a continuous process, which has not been addressed adequately in this model. Further, THMs

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Findings

collected from each pool once per month over a year (Jan. 2007eFeb. 2008). A level III fugacity model was developed to estimate inhalation, dermal contact and ingestion exposure doses.

54

Florentin et al. (2011)

This study investigated the health effects of DBPs in SP water. Release of urea, ammonia, amino-acids, creatinine, total nitrogen and other compounds by swimmers into the SP was summarized. This study also summarizes typical concentrations of THMs and HAAs in SP water and air.

55

Font-Ribera et al., 2011

56

Hansen et al., 2011

This study examined the association of swimming in infancy and childhood with asthma and allergic symptoms at age 7 and 10 years. The analysis was performed for 5738 children in Avon, UK. Data on swimming were collected by questionnaire at 6, 18, 38, 42, 57, 65, and 81 months. Data on rhinitis, wheezing, asthma, eczema, hay fever, asthma medication and potential confounders were collected through questionnaires at 7 and 10 years. Spirometry and skin prick testing were performed at 7e8 years. This study investigated the effect of chlorination of artificial body fluid analogue at different pHvalues between 6 and 8. Deionized water was buffered with phosphate buffer at pH 6.0, 6.5, 7.0, 7.5, and 8.0. The water was added body-fluid analogue (BFA) prepared as suggested by Judd and Bullock (2003) corresponding to 1 mg TOC/ L in the experiments. A constant start

This study shows that release of urea, ammonia, aminoacids, creatinine, total nitrogen and other compounds by swimmers are in the ranges of 320e840, 30e60, 15e50, 10e25, 400e1000 and 20e45 mg/swimmer respectively. This study showed that the concentrations of THMs and HAAs can vary considerably in the SP water. Presence of brominated species was reported to be significant. This study showed that the risk of colorectal cancer might increase with increased concentrations of THMs and exposure duration. This study reported that genotoxicity was associated with brominated THMs, not CHCl3. The chlorinated atmosphere of SP can be detrimental to the lung by increasing the risk of asthma, bronchial hyper reactivity and airways inflammation. The children are over-risked if they are exposed to swimming pool DBPs. Exposition to trichloramine in higher concentrations can harm the lung epithelium and promote the development of asthma, particularly among children Higher social class and maternal education were associated with a higher frequency of swimming. This study observed no increase in risk of asthma, atopy, or any respiratory and allergic symptom from swimming in British children. Swimming was associated with increased lung function and with a decreased prevalence of current asthma among children with previous respiratory conditions. Children with asthma with a high versus low cumulative swimming had an odds ratio for current asthma at 10 years of 0.34 (0.14 e0.80). Children with a high versus low cumulative swimming pool attendance from birth to 7 years had an odds ratio of 0.88 (95%confidence interval, 0.56e1.38) and 0.50 (0.28e0.87), respectively, for ever and current asthma at 7 years.

Chlorination of BFA (without bromide addition) formed THMs, HANs and HAAs. Increase in pH increased THMs but decreased HANs. Variation of pH did not affect the formation of HAAs. Addition of bromide formed brominated DBPs and influenced the amount of DBPs formed. At pH 7, HAA was decreased with presence of bromide from 0.27 to 0.11 mmol/L, whereas THM and HAN were increased (THMs from 0.077 to 0.11 mmol/L and HANs from 0.025 to 0.056 mmol/L). A decrease in the HAA5 (sum of MCAA, BCAA, DCAA, DBAA, TCAA) with increasing bromide level was found. When pH was changed from 6 to 7, the genotoxic potency of water was reduced by half. However when pH was increased to 8, genotoxicity remains almost constant. Presence of bromide in the water increased the genotoxic potency. At pH 7 without bromide the toxicity was

Comments typically need several minutes to achieve steady state condition between the upper and lower layers of stratum corneum of human skin. As such, dermal exposure needs both unsteady and steady state assessment depending on exposure duration. It is to be noted that microbiological safety of SP water must not be compromised under any circumstance.

Levels of DBPs in pool water and/or air has not been reported in this study, while exposure to some DBPs might be associated with several symptoms. Association with the levels of DBPs.

This study found that the genotoxic potency of the water increases when lowering the pH. The experiments are laboratory batch experiments. Future research is warranted for better understanding of genotoxic effects and HAAs formation due to the variation of pH in SP water.

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Author (Year)

57

De Laat et al., 2011

58

Kanan and Karanfil (2011)

59

Mukiibi et al. (2011)

60

Plewa et al., 2011

Model description concentration of free chlorine was set to 35 mg/L. The experiments were repeated with 1 mg Br-/L added. Formation of THMs, HAAs, HANs was measured This study investigated the reactivity of chlorine with urea in swimming pool water. Chlorination of urea (Urea ¼ 10 mMe1 mM) was carried out for the Cl2/urea molar ratio of 0.5e15. A total of 50 swimming pool water samples were collected from 17 indoor SP located at Poitiers or near Poitiers to determine the concentrations of urea in the swimming pool water.

The contribution and role of different precursors in the formation of three classes of DBPs (THMs, HAAs and HNMs) in swimming pool waters were examined using filling waters obtained from five drinking water treatment plant (WTP) effluents and three body fluid analogs (BFAs). Three BFAs were prepared using distilled and deionized water following their recipes in literature. The Filling water NOM samples were collected from five drinking water treatment plants after conventional clarification processes (i.e., after coagulation, flocculation, and sedimentation before any oxidant or disinfectant addition) in South Carolina, US: Spartanburg (SP), Startex-Jackson-WellfordDuncan (SJWD), Greenville (GV), Myrtle Beach (MB), and Charleston (CH). This article addressed the advantages and disadvantages of using chlorine for disinfection. Effect of warm climate was discussed. This study investigated chronic in vitro mammalian

Findings

Comments

2.4  1005 but with bromide, toxicity was 6.5  1004 (27 times different). In the experiment without bromide, only the HANs contributed to the genotoxicity.

Mean concentrations of urea and TOC were equal to 1.08 mg/L (std. dev. 0.7) and 3.5 mg C/L (std. dev. 1.6) respectively. Average value for the urea contribution to TOC was 6.3%. Introduction of urea and TOC from 10:00 am to 8:00 pm were nearly equal to 11.1  0.6 g and 12.4  0.5 g respectively. Decrease of urea due to chlorination was 11.2% (range: 3.6e15.4%) after a reaction time of 11 h in the presence of 1.6e1.8 mg Cl2/L. Urea showed very slow degradation in a swimming pool condition. The long term chlorine demand of urea was approximately 5 mol Cl2/mol of urea. Chlorination formed 0.7e0.8 mol NO3/mol of urea for chlorine dose of 8e10 mol/mol. With urea, the fastest chlorine consumption was observed at pH 7.5e8 and the reactions were relatively slow under acidic and alkaline pH values. TN removals were equal to 85, 70 and 62% for applied chlorine doses of 4.1, 8.15 and 15.3 mol/mol, respectively. Nitrate yields of 0.1, 0.27 and 0.76 mol/mol of urea were measured for chlorine doses of 3, 4 and 10 mol Cl2/mol of urea, respectively. BFAs exerted higher chlorine demands (17e25 mg Cl2/mg TOC) as compared to NOM in filling waters (2e8 mg Cl2/mg TOC). BFAs exhibited higher HAA formation potentials than THM formation potentials, while the opposite was observed for the filling water NOM. There was no appreciable difference in the HNM formation potentials of BFAs and filling water NOM. Different components in the BFAs tested exhibited different degree and type of DBP formation. Citric acid had significantly higher THM and HAA yields than other BFA components. The effect of temperature was more pronounced on CHCl3 than DCAA and TCAA formation, while incubation time had more impact on HAA than THM formation. BFAs were more reactive toward chlorine than filling water NOM. This study demonstrated that individual reactivity of BFA components is important to consider and will determine the DBP formation and speciation of a particular BFA mixture.

This study indicated that the municipal water entering swimming pool may not be free from organic matter. Further, homeowners often apply higher doses of chlorine to ensure microbial safety. As such, formation of DBPs is more likely in the SP. Further, the warm climate can accelerate DBPs formation in the SP. TOC in the swimming pool extracts were in the range of 5.2e124.8 mg/L, while the tap water TOC was 1.2 mg/L.

Decay of urea is very slow indicating that exchange of the pool water by the tap water may reduce much of the chlorine demands exerted by urea.

This study compared the contributions of different sources of DBPs precursors. More comprehensive study to better understand the formation of other DBPs will assist in better explaining their exposure and risks.

No case or real evidence on the effects of warm climate was provided. Understanding the effects of warm climate on the formation of DBPs in SP is essential. All disinfected recreational pool water samples were

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Author (Year)

Model description

Findings

Comments

cell cytotoxicity of different recreational waters with varied environmental conditions that were derived from a common tap water source.

Levels of free residual chlorine in the tap water and swimming pools were 1.4 and 1.4e3.7 mg/L respectively. Recreational waters were significantly more toxic than their tap water source (on Chinese Hamster Ovary cell: CHO cell). A direct significant association was observed between cytotoxicity and genomic DNA damage in CHO cells. Pools subjected to a combination of ultraviolet light and free chlorine disinfection indoors, or outdoor sunlight exposure exhibited lower cytotoxicity than their indoor counterparts disinfected with free chlorine. Toxicity of pools disinfected with free chlorine alone was approximately 3 times higher than the pool disinfected with free chlorine and UV. Among indoor pools at room temperature, the pool disinfected with bromochloro dimethylhydantoin (BCDMH) exhibited cytotoxicity comparable to those disinfected with free chlorine, even though BCDMH treated pool exhibited a TOC at least four times higher than all other pools. Temperature and total organic carbon content, as an indirect measure of DBP precursors, were less important. Swimming frequency for the adult men was found to follow a negative binomial distribution with parameters of (0.83, 0.06), (1.2, 0.15) and (1.4, 0.18) for swimming pool, freshwater and seawater respectively. For the adult women, these parameters were (0.84, 0.05), (1.3, 0.17) and (1.5, 0.21) respectively, while for the children, these were (1.0, 0.04), (1.3, 0.14) and (1.5, 0.17) respectively. Swimming duration (min) for the adult men was found to follow lognormal distribution with parameters of (4.1, 0.57), (3.6, 0.85) and (3.5, 0.85) for swimming pool, freshwater and seawater respectively. For the adult women, these parameters were (4.0, 0.55), (3.5, 0.94) and (3.2, 0.94) respectively, while for the children, these were (4.2, 0.55), (4.1, 0.80) and (3.8, 0.80) respectively. Volume of swallowed water during swimming (mL) for the adult men was found to follow Gamma distribution with parameters of (0.48, 71), (0.45, 60) and (0.45, 60) for swimming pool, freshwater and seawater respectively. For the adult women, these parameters were (0.52, 45), (0.51, 35) and (0.51, 35) respectively, while for the children, these were (0.81, 63), (0.64, 58) and (0.58, 55) respectively. Presence of Cryptosporidium and Giardia in a swimming pool were reported to follow Gamma distributions with parameters (0.19, 1.6) and (0.11, 0.24) respectively. Their averages in swimming pool were 0.3/L and 0.025/L respectively. In four recreational lakes, Cryptosporidium and Giardia also follow Gamma distributions with parameters (0.11e2.3, 0.02e0.58) and (0.27 e4.1, 0.0096e0.44) respectively. In the swimming pool, the estimated infection risk for Cryptosporidium was about 1.1032.103 whereas for Giardia it was about 1.1052.105, per swimming event per person. This study found urea, ammonium ions and a-amino acids as the most important NCl3 precursors. For urea, a relative NCl3 formation of 96 and 76% was determined for pH of 2,5 and 7.1 respectively. Urea, ammonia and creatinine are the major compounds in human urine and sweat. This study observed decrease in NCl3 with increase in pH. At pH 7.1, the decreasing order of NCl3 precursors are urea, ammonia, formamide, glycine, and histidine. For a typical SP, concentration of urea was measured up to 2 mg/L. The transfer of NCl3 from water to air of a swimming pool would take 5.8 d or 20 h for smooth or rough water surface, respectively, indicating that this transfer is a slow process. This study demonstrates that NCl3 exposure to the bathers

more cytotoxic than the source tap water. The outdoor pool exposed to sunlight featured lower cytotoxicity than the same pool under indoor conditions, indicating that the UV light assisted disinfection (in combination with free residual chlorine) might reduce the overall toxic effects.

61

Schets et al., 2011

This study investigated on the volume of water swallowed and frequency and duration of swimming events in freshwater, seawater and swimming pools. Data were collected through questionnaires to a group of approximately 60,000e75,000 peoples in the Netherlands. The time spent in the water could be reported in classes of minutes of water contact (0 e30, 30e60, 60e120 and 120 e300 min) for each type of water. A total of 119 persons took part in a test to understand the swallowed volume of water. The risk of infection from Cryptosporidium oocysts and Giardia cysts in a swimming pool was predicted.

62

Schmalz et al. (2011)

This study investigated formation and mass transfer of trichloramine (NCl3) in the SP. The major reactions processes involved in the formation of trichloramine in SP were identified. Effects of acid amides and pH on the formation of NCl3.

Children are more susceptible to microbial contamination than the adults. Microbial risks might be more detrimental than the chemical risks in the swimming pool. Proper disinfection must not be compromised. However, it is not clear whether the swimming pool was disinfected.

A more cost efficient and quantitative decomposition process for urea and other precursors in pool water treatment need to be developed in the future.

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63

Weng and Blatchley (2011)

This study investigated the dynamics of DBPs in indoor SP under condition of heavy use (e.g., National swimming competition). Water chemistry was monitored in a chlorinated, indoor pool before and during a national swimming competition, a period of heavy, intense use in March 2010.

64

Hansen et al., 2012

65

Keuten et al., 2012

Formation of THMs, HAAs, HANs, NCl3, trichloronitromethane, dichloropropanone, and trichloropropanone were investigated during chlorination of filter particles from swimming pools under variable pH and controlled chlorination condition. The particles were collected from a hot tub with a drum micro filter. In addition, toxicities of these DBPs were estimated. This study was carried out in a typical swimming pool in Denmark. This study quantified the initial anthropogenic pollutant release in swimming pools. This study used a standardized shower cabin and a standardized showering protocol in laboratory time-series experiments and on-site experiments in swimming pools. A total of 18e20 water samples were taken per participant. All samples

Findings can be minimized by (i) reducing urea due to its slow reaction kinetics of NCl3 formation; and (ii) and degrading NCl3 due to its slow mass transfer from water to air. Both processes are slower than a typical treatment cycle, which typically ranges between 6 and 8 h. During competition, bather loads were typically 150-200 swimmers during warm up sessions, which was 5e10 times the normal bather loads. The discharges of sweat and urine into the pool water were 823e1760 and 54.7e117 mL/person/ day respectively. Considering 0.68 g urea/L of sweat and 10.245 g urea/L of urine, this study estimated the discharge of urea in the range of 0.56e1.2 g/person/day. The daily urea concentration increases ranged from 72.4 mg/L to 155 mg/L during the heavy use period. Urea concentration in nearsurface water showed a pattern of steady increase during each day of the competition, with a decrease at night. The chlorine demands were doubled at this time. Concentrations of NCl3 were double after the first day, and increased by a factor of 3e4 over the 4 days of competition. Urea, which is the main precursor of NCl3, was increased during the day and decreased during night. CHCl3 concentration trended upward during the competition and showed a consistent diurnal pattern: decrease in the daytime and increase overnight. Trend for BDCM was less distinct than CHCl3. DBCM and CHBr3, concentrations were much lower. CNCHCl2 and CH3NCl2 concentrations both increased by a factor of 2e3 during the course of the meet. CNCHCl2 increased steadily with no diurnal variations. CH3NCl2 concentrations were lowest near mid-day and showed steady increase overnight. No consistent trend was observed for CNCl, while it can be strongly influenced by maintenance practices that influence residual (free) chlorine. This study observed increased formation of THMs and HAAs, and decreased formation of HANs with the increase of pH. The body fluid analogue (dissolved organic matter from sweat and urine, and the particles consisting of hair and skin cells) showed increased formation of CHCl3 when pH was increased from 6 to 8. Formation of HAAs was increased with increase in pH. In contrast, HANs formation were reduced with the increase in pH from 6 to 8. HAAs/ THMs ratio was 2e3.5 for materials of human origin, while for the NOM, this ratio was 0.4. This study observed that the contribution of THMs to the overall solution toxicity was negligible compared to the other groups. The toxicity of the HANs comprised 63e92% of the total estimated cytotoxicity. The order of toxicity was HANs > HAAs > THMs. Increase in pH increases the absolute value of THMs toxicity.

The data showed that 70e90% of TOC, TN and cATP were released within the first 60 s of showering. The average initial (within first 60 s of controlled showering) anthropogenic pollutant release were 211 mg TOC, 46 mg TN, 1.6 mg cATP and 155  103 particles per person. TOC, TN and turbidity released during showering were strongly correlated (r > 0.8). The R2 values for the multiple regression models were 0.97, 0.96 and 0.95 for predicting TOC, TN and cATP respectively, indicating that these models have strong capabilities of predicting the release of these pollutants. Anthropogenic pollutant releases for male and female participants were only slightly different. This study showed that the time after last shower and physical activities can

Comments

The decrease in urea that was observed overnight is believed to be attributable to mixing of near-surface water with water from other parts of the pool (i.e., deeper water), where urea input would be negligible, and daytime concentration was likely to be lower. Water quality deteriorated during the course of the competition, as represented by increases in the concentrations of volatile DBPs, thereby leading to enhanced DBP exposure by swimmers, pool employees, and spectators at the competition.

Limited information is available on the concentrations of HANs in SP. Systematic monitoring of HANs and their effects to human health may provide better protection of human health.

The models were not calibrated for different environments. As such, predictive ability of these models under different environmental conditions could not be understood. Hygiene parameters, such as, time after last showering, levels of activities need to be better understood.

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Author (Year)

66

Lourencetti et al. (2012)

67

Parinet et al. (2012)

Model description

Findings

were placed in cold storage (3e5  C) immediately after sampling. Samples were analyzed for chemical and microbiological parameters. Models were developed to predict the release of TOC, TN and cATP. This study investigated air ewater distribution of THMs in chlorine and bromine disinfected swimming pool and assessed their exposure to humans. Two swimming pools from Barcelona, Catalonia, Spain, using chlorination or bromination agents for water disinfection were selected for study. Air samples were obtained by pulling air through 0.5 cm diameter and 9 cm long stainless steel tubes containing 0.18 g of Tenax TA. Composite water samples (250 mL) were collected at the four swimming pool corners, resulting in combined samples of 1 L. At least 3 composite samples were collected during each sampling day. A survey has been conducted in 8 swimming pools fed with seawater (Mediterranean Sea) and devoted to relaxing and cure treatments in Southeast of France. Measurements were performed for brominated THMs and HAAs. The correlations between these DBPs and other environmental factors such as nitrogen, pH, temperature, free residual chlorine, UV254, chloride and bromide concentrations, and daily frequentation were examined.

affect the release of TOC, TN and cATP. For greater time after last shower, release of higher amounts of TOC, TN and particulates were reported. For a gap of less than 12 h between showering, TOC, TN, cATP and particle release was 252 mg, 66 mg, 538 mg and 3.8  107 respectively. When the gap was more than 12 h, these values were 327 mg, 84 mg, 887 mg and 6.3  107 respectively.

Comments

CHCl3 and CHBr3 are the dominant species in chlorinated and brominated swimming pools respectively. Concentrations of CHCl3, BDCM, DBCM and CHBr3 in this pool were 15 (8.5e20), 14 (9.4e25), 13 (6.7e23) and 7.2 (3.1 e16) mg/L respectively. Concentrations of CHCl3, BDCM, DBCM and CHBr3 in the brominated pool water were 0.21 (0.08e0.29), 0.41(0.23e0.6), 2.4 (2.1e2.6) and 60 (52e61) mg/L respectively. Concentrations of CHCl3, BDCM, DBCM and CHBr3 in the chlorinated pool air were 32 (18e61), 15 (8.2e23), 14 (6.4e22) and 11(5.9e22) mg/m3 respectively. Concentrations of CHCl3, BDCM, DBCM and CHBr3 in the brominated pool air were 4.5 (1.8e6.9), 3 (1.9e4.2), 7.3 (6.4 e8.7) and 75 (55e92) mg/m3 respectively. In the chlorinated pool CHCl3, BDCM, DBCM and CHBr3 in the exhaled air were 65, 20, 10 and 5% respectively, while in the brominated pool these were 15, 7, 8 and 70% respectively. In the air and water of the brominated pool, CHBr3 were approximately 80 and 94% respectively, indicating that proportionately lower percentages were available in the air. DBPs in the pool water and exhaled air had R2 values in the ranges of 0.33e0.57 and 0.73e0.94 for the chlorinated and brominated pools respectively. DBPs in the pool air and exhaled air had R2 values in the ranges of 0.31e0.62 and 0.67e0.94 for the chlorinated and brominated pools respectively.

Understanding of the distributions of other DBPs in water and air phases is essential to better explain human exposure to DBPs from swimming pool.

Average concentrations of bromide ions in all 8 pools were in the range of 68.1e106.7 mg/L. Average concentrations of THMs in six SP water were in the range of 233.5e995.6 mg/L. Concentrations of CHCl3, BDCM, DBCM and CHBr3 were in the ranges of 0.03e0.29, 0.05e1.1, 13.6e63.6 and 219.5 e930.7 mg/L respectively. Average concentrations of HAAs in six SP water were in the range of 323.2e2232.9 mg/L. Concentrations of MCAA, MBAA, DCAA, TCAA, BCAA, DBAA, BDCAA, CDBAA, TBAA were 2.2e96.4, 8.2e155.1, 2.2 e8.7, 2.9e86.8, 27.4e216.1, 131.9e1088.6, 5.2e20.2, 72.5 e242.8 and 48.7e427.6 mg/L respectively. The two pools disinfected by dichloroisocyanuric acid had THMs and HAAs concentrations in the ranges of 32.2e77.7 and 84.1e123.1 mg/L respectively. Concentrations of HAAs were almost 1.5 fold (HAAs: median: 419 mg/L; maximum: 2233 mg/L and THMs: median: 287 mg/L; maximum: 995.6 mg/L). Brominated THMs and HAAs contributed the major fractions of the total THMs and HAAs. In THMs, DBCM and CHBr3 represented 4.1e9.3 and 89e95% respectively, while CHCl3 and BDCM were negligible. In HAAs, the most abundant HAA were DBAA (147 mg/L median, 1088.6 mg/L maximum), TBAA (97.9 mg/L median, 167.0 mg/L maximum), CDBAA (77.1 mg/L median, 242.7 mg/L maximum), and MBAA (27.1 mg/L median, 155.1 mg/L maximum). One SP pool had very high TOC (8.6  1.5 mg/L), which formed the highest amounts of THMs and HAAs (995.6 and 2232.9 mg/L) respectively. The other SP had TOC of 3.6e4.6 mg/L and their corresponding THMs and HAAs were in the ranges of 233.5 e325.4 and 323.2e626.3 mg/L respectively.

Recent study compares chronic cytotoxicity and acute genomic DNA damaging capacity in mammalian cells and ranks by order of chronic cytotoxicity in Chinese Hamster ovary cells: MBAA > TBAA > CDBAA > DBAA > BDCAA > BCAA > MCAA > TCAA > DCAA and by order of genotoxicity as MBAA > MCAA > DBAA > TBAA > BCAA > CDBAA. For many of these DBPs, slope factors are not available till date. It is essential to set their cancer potency (if there is any) to better understand their risks through different exposure pathways.

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Author (Year)

68

Weng et al., 2012.

69

Xiao et al., 2012.

70

Agopian et al., 2013.

71

Simard et al., 2013

Model description

Findings

Comments

This study evaluated the effects of UV irradiation on chlorination of important organic-N precursors in swimming pools. Creatinine, L-arginine, L-histidine, glycine, and urea were selected as precursors for use in conducting batch experiments 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 liquidphase chemistry. The initial precursor concentration was 1.8  105 M in each experiment, while free chlorine was added at target chlorine: precursor (Cl:P) molar ratios of nominally 1.5 or 3.0. Samples from each pool were collected from 30 cm below the water surface In this study, several new halogenated DBPs in SP water were detected. Permeability of these new DBPs through human skin was measured. The effects of chlorine on human skin were also investigated. Pool samples were collected from an outdoor pool in Sep. 2008 and an indoor pool in Nov. 2008. The pool water came from local tap water and was further treated. Bromide concentration in the pool source water was w6 mg/L, which were spiked to a level of 400 mg/L. This was disinfected for 24 h with NaOCl at a total dose of 5 mg/L as Cl2. This study evaluated the relationship between maternal swimming pool use during early pregnancy and risk for select birth defects in offspring. Data were evaluated for nonsyndromic cases with one of 16 types of birth defects and controls. This study investigated the presence of DBPs, such as THMs, HAAs and inorganic

Concentrations of TN, urea, creatinine, amino acid, glycine, histidine and arginine in urine were reported to be 664, 278, 10.7, 24, 1.72, 0.77 and 0.017 mmol/L respectively. In sweat, concentrations of TN, urea, creatinine and amino acid were 16e30, 19.6, 0.041 and 0.7e7 mmol/L respectively. The rate of decay of chlorine was much slower for urea than the other precursors. 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. Dichloroacetonitrile (CNCHCl2) formation (from L-histidine and L-arginine) was promoted by UV254 irradiation, as long as free chlorine was present in solution. From L-histidine, about 2 mg/L of CNCHCl2 was formed as a result of chlorination (Cl/P ¼ 3), while UV254 irradiation yielded a CNCHCl2 formation of 14 mg/L. For L-arginine, this increase was 5 folds. Likewise, UV exposure was observed to amplify cyanogen chloride (CNCl) formation from chlorination of Lhistidine, L-arginine, and glycine, up to the point of free chlorine depletion. The enhancements of CNCl formation were 7 times and 9 times higher for L-arginine and Lhistidine, respectively, in UV-chlorination experiments than in chlorination experiments. Dichloromethylamine (CH3NCl2) formation from creatinine was promoted by UV exposure (10e150% increase), when free chlorine was present in solution; however, when free chlorine was depleted, CH3NCl2 photo decay was observed.

In order to maintain the microbial safety of swimming pools, there must be some free residual chlorine in the pool water on continuous basis. As such, expecting the photoreductions for nitrogenous DBPs may not be realistic in many swimming pools. Despite, the UV irradiation decreases NCl3, increase in dichloroacetonitrile cyanogen chloride and dichloromethylamine can be a concern. It is essential to better understand the overall risks prior to introducing the UV irradiation.

TOC were 2.8 and 3.2 mg/L as C in the outdoor and indoor pools, respectively. Identified several new halo (nitro) phenols in pool water, resulting from chlorination of human body substances (such as urine) in presence of bromide. Among these new DBPs, 2,4-dibromophenol, 2,4dichlorophenol, 2-bromophenol, 2,6-dibromo-4nitrophenol, 2-bromo-6-chloro-4-nitrophenol, and 2,6-dichloro-4-nitrophenol were fully identified. For the exposure time of 64 h, permeability of 2,4-dibromophenol, 2,4-dichlorophenol and 2-bromophenol through human skin were to be 0.031  0.004, 0.021  0.003 and 0.023  0.003 cm/h, respectively. For a man with an estimated skin surface area of 18,900 cm2 (180 cm in height and 80 kg in weight), this man is estimated to contribute 17 mg CHCl3 and several mg HAAs to a pool after 2 h swimming (for 400 mg/L Br and 2 mg/L Cl2 dosage). Many nitrogenous brominated DBPs were generated during chlorination of human body substances in the presence of Br indicating that human body substances in pools are important sources of nitrogenous DBPs.

This paper showed many un-identified peaks for DBPs after reactions with human body materials and skins. Understanding of these DBPs may provide better insights on the toxic effects of swimming pool water and air.

No significant positive association between any or frequent pool use and any of the types of birth defects were observed. Frequent pool use was significantly negatively associated with spina bifida. Among offspring of women 20 years, pool use was associated with gastroschisis, though not significantly so.

Little evidence suggesting teratogenic effects of swimming pool use.

Average concentrations of THMs in the indoor and outdoor pools were 63.7 and 97.9 mg/L respectively. For HAAs, averages were 412.9 and 807.6 mg/L in the indoor and

High volatility of THMs might have lowered THMs in water. However, no data

105

w a t e r r e s e a r c h 5 3 ( 2 0 1 4 ) 6 8 e1 0 9

Appendixe (continued ) Sl.

72

Author (Year)

Soltermann et al., 2013

Model description

Findings

chloramines. Fifty-four swimming pools (outdoor: 39; indoor: 15) in Quebec city (Canada) were investigated over a period of one year (monthly or biweekly sampling, according to the type of pool) for the occurrence of DBPs. All pools were disinfected with hypochlorite-based disinfectant.

outdoor pools respectively, while chloramines were 0.8 and 1.0 mg/L in these pools respectively. In THMs, CHCl3 were approximately 97% of THMs, while DCAA and TCAA comprised approximately 93% of HAAs, indicating low levels of bromide ions in the source water. THMs in the water distribution systems in Des ˆılets, Lac des E´rables, Que´bec, Ste-Foy and Val-Be´lair were 110  70, 81  51, 26  10, 37  14 and 13  7 mg/L respectively. HAAs in these samples were 113  53, 78  42, 29  12, 34  10 and 12  7 mg/L respectively. In indoor swimming pools, THMs and HAAs were 117  35, 49  17, 50  31, 57  15 and 69  28 mg/L; and 474  290, 428  225, 348  157, 415  126 and 510  242 mg/L respectively. In outdoor swimming pools, THMs and HAAs were 68  45, 50  24, 131  75, 95  51 and 83  14 mg/L; and 962  365, 634  274, 874  538, 678  400 and 983  616 mg/L respectively. THMs in the distribution systems and indoor and outdoor pools were comparable, while HAAs in the pools were 4e80 times higher than the HAAs in the distribution systems. Chloramines in the indoor and outdoor swimming pools were 736  280 and 142  116 mg/L respectively. UV irradiation of solutions containing CL-DMA and NH2Cl resulted in a temporarily high, UV dose-dependent NDMA formation. NDMA concentration increased in a first phase (UV dose < 350 mJ/cm2) and remained on a high level (350 mJ/cm2 < UV dose < 700 mJ/cm2) before it decreased. UV-induced NDMA formation or NDMA degradation is not significantly influenced by pH changes in the range of 6.5e8. However, pH-dependence of NDMA formation in the blank (without UV irradiation) was much more pronounced in the pH range 6.5e8, with a maximum at pH 7.5. NDMA concentration increased linearly with the initial CL-DMA and NH2Cl concentration for stoichiometric ratios

Disinfection byproducts in swimming pool: occurrences, implications and future needs.

Disinfection of swimming pool water is essential to deactivate pathogenic microorganisms. Many swimming pools apply chlorine or bromine based disinfec...
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