By David M. Bonnick, MCIWEM, CChem, MRSC

Awide range of pathogenic microorganisms such as viruses, bacteria, fungi and protozoa can contaminate swimming pool water. They enter the swimming pool via sweat, urine, mucus, saliva, hair, skin scales, fecal matter, vomit or general dirt. Other potential sources of contamination include faulty plumbing and, for outdoor pools, bird droppings, dust and insects.

Although encouraging swimmers to shower, use the toilet and soak in disinfected footbaths beforehand helps reduce a certain amount of pollution introduced into the pool, it is equally essential to provide a chemical environment that rapidly inactivates the broad pathogenic spectrum that could otherwise adversely affect pool water quality and swimmers’ health. Disinfection and filtration effectively inactivate these contaminants and provide a pleasant swimming experience without adverse long-term health effects. With these treatment methods, swimming pool-related infections are relatively uncommon.

To maintain effective control of disease-causing organisms in the swimming pool, it is also important to understand potential contamination sources, pathogenic organism types and their varying susceptibilities, infection routes and disinfection mechanisms. In addition, it is also imperative to be familiar with the chemistry of the disinfectant used and know how it could adversely affect the swimming environment which, in turn, could impact swimmers’ comfort and health.

Chlorine residual is the most common means of protecting against cross-swimmer infection. Chlorine may be supplied to the pool water in a variety of forms. Chlorine gas, sodium hypochlorite solution and calcium hypochlorite are the most commonly used, but chlorine dioxide is sometimes selected, while some pools instead use a combination of chlorine and bromide salts.

Chlorine gas and hypochlorites dissolve in water to produce the compound hypochlorous acid (HOCl). The HOCl is in equilibrium with its anion, hypochlorite. The proportions of each are determined by the pH, temperature and conductivity of the treated water. The ubiquitous DPD (diethyl-p-phenylene diamine) test for free chlorine residual measures both HOCl and hypochlorite ion.

HOCl is a much more effective disinfectant for swimming pools and spas than hypochlorite ion. The bactericidal effect of free chlorine residual may be accounted for almost entirely in terms of the hypochlorous acid concentration. Figure 1 shows the variation of HOCl as a proportion of the measured chlorine residual and demonstrates the importance of pH control for effective disinfection.

Chlorine reacts with a number of common swimming pool contaminants to produce a range of disinfection by-products (DBP). These include mono-chloramine, dichloramine, nitrogen trichloride and the trihalomethanes (THM) trichloromethane, tribromometh-ane, dibromochloromethane and di-chlorobromomethane. Some of these, such as the trihalomethanes and nitrogen trichloride, pose potential health risks, while the chloramines may adversely affect the comfort of swimmers and spectators by causing eye irritation.

Urine causes ammonia to form in pool water. Chlorine, in turn, reacts with ammonia to produce the chloramines shown in Figure 2.

The type of chloramine formed depends on the pH and the ratio of chlorine to ammonia. While monochloramine is not a particular problem, dichloramine results in a strong chlorine odor and may cause eye irritation. However, dichloramine should decompose rapidly if the pool pH level is within the correct range and excess free chlorine is available. The mass ratio of chlorine to ammonia to form monochloramine is approximately four to one. This means that relatively low concentrations of ammonia (< 0.2 mg/L) can result in significant effects on the swimming pool chemistry. Ammonia levels in swimming pools are normally high enough to form significant levels of chloramines. Germany’s DIN 19643 standard, which states that chloramines cannot exceed 0.20 mg/L, indicates the acceptable level of chloramines in the swimming pool environment.

Nitrogen trichloride is pungent and will cause extreme discomfort to swimmers and spectators, as well as swimming instructors, lifeguards and other poolside workers. If not properly ventilated, it is released into the atmosphere, where it accumulates. Levels of 0.1 to 0.57 mg/m3 have been detected.1 Several studies demonstrate a link between elevated nitrogen trichloride levels in the pool atmosphere and increased incidences of asthma.2,3

Correctly maintaining the pool environment with adequate ventilation, dilution, pH control and an adequate level of free chlorine can minimize the formation and accumulation of chloramines. The presence of free chlorine indicates the so-called breakpoint has been reached. In principle, this means that chloramines have been oxidized to innocuous compounds; however, in practice, a certain level of chloramines usually remains in the pool. Dosing powdered activated carbon onto the filters and adding ultraviolet (UV) treatment are further steps that may be taken to hold chloramines at acceptably low levels. The powdered activated carbon is used to adsorb chloramines and THMs. UV treatment acts to reduce chloramines by photolysis.

Other nitrogen-containing compounds such as creatinine and amino acids may be present in the pool as a result of the breakdown of urine and perspiration. These then react with chlorine to produce N-chloro (chloramine) compounds, which appear as combined chlorine in the DPD test. Many of these compounds are not removed by adding extra chlorine to the pool, as observed by Lomas.4 This was attributed to the presence of chloro-creatinine, which is only removed from the pool by dilution, carbon adsorption or ozone/UV oxidation (see Figure 3).

Chlorine may also react with organic contaminants to produce THMs. THMs in drinking water supplies have been shown to adversely affect health and their effect in swimming pool water is questionable. In particular, researchers are examining a possible link between THM exposure and bladder cancer,5 an increased number of birth defects6 and low birth weights.7 The concentration of chloroform and total THMs correlates to the number of swimmers and the total organic carbon (TOC) concentration. Testing on eight London pools8 gave an arithmetic mean concentration of 121.1 µg/L of chloroform. In Germany, the DIN 19643 standard stipulates a maximum level for THMs in swimming pools of 20 µg/L.

The pool’s chlorine residual affects each group of pathogens differently. Chlorine inactivates microorganisms similarly to how white blood cells (leukocytes) destroy potentially pathogenic organisms—by releasing oxidative toxins including hypochlorous acid.9,10 A number of recent medical studies are trying to discover how these toxins, particularly hypochlorous acid, inactivate their target.

Filtration and other disinfection methods
Adequate filtration is critical to a pool disinfection system. Without continuously removing suspended material from the pool, it would be impossible to maintain adequate disinfection, regardless of the process used. Filters must be sized to the pool’s capacity and loading, use appropriate coagulant aids in accordance with suppliers’ instructions and be routinely backwashed to remove filtrate buildup. Accumulated organic material must be removed from the filter during backwashing, as it may help THMs form. Post-filter chlorine dosing can help reduce THM levels. Properly operated filtration with coagulation can remove most pollution from the pool water, resulting in lower levels of organisms, lower chlorine demand and fewer DBPs.

A halogen-based disinfectant should quickly inactivate most potential pathogens in the pool and thus minimize the risk of cross-swimmer contamination. As the disinfectant used will most likely be some form of chlorine, careful consideration must be given to the element’s chemistry. While the pool pH must be maintained at a sufficiently low level to ensure that much of the free chlorine is in the HOCl form, the pH should not be low enough to cause discomfort to the swimmers or increase the likelihood of corrosion. An automated system should ideally control the pH level at a recommended range of 7.2 to 7.4 to maintain a consistent pH in the pool at all times.

If chlorine (or a chlorine donor) is used, the free chlorine residual should be monitored automatically and the signal used to maintain the residual at a level sufficient to ensure disinfection without causing discomfort to the swimmers. In a typical UK pool, this is likely to be between 1.0 and 1.2 mg/L free chlorine. Pools in other countries (such as Germany, where pool conditions are strictly controlled by the standard DIN 1964311) may operate at lower free chlorine residuals.

The Redox potential of the pool water provides a valuable additional control parameter. DIN 19643 states that the Redox potential should be between 750 and 770mV. Systems are available that use a combination of residual measurement and Redox potential to minimize the use of chlorine.

The level of contaminants entering the pool must be kept to a minimum. In addition to encouraging swimmers to shower, use the toilet or use a disinfected footbath beforehand, those with a known infectious waterborne disease should also be discouraged from using the pool. Policies that address fecal or vomiting incidents in the pool or add fresh water to the pool in proportion to the bathing load may further promote a healthy pool. For instance, the publication Swimming Pool Water12 recommends adding 30 L/day of fresh water for every swimmer using the pool.

Other approaches to maintaining low contaminant and DBP levels include using ozone, UV and activated carbon.

Ozone is used in conjunction with residual chlorination to improve the environment for swimmers and spectators. Using ozone with activated carbon filtration improves performance and prevents ozone from entering the swimming pool area.

UV treatment may be used to reduce chloramine levels in the pool. UV at relatively low doses can also inactivate Cryptosporidium oocysts (see Figure 4).

Activated carbon powder is mixed into a suspension that is dosed prior to sand filtration. If a uniform grade of sand is used, a layer of carbon can be formed in the filter. This adsorbs and breaks down chloramines in accordance with the reactions as shown in Figure 5.13

THMs are adsorbed and discarded with the waste carbon during backwashing. This system has been widely used in Germany in the last decade to ensure compliance with the stringent requirements of DIN 19643 that stipulates a maximum of 200 µg/L chloramines and 20 µg/L THM (as chloroform).

Adenovirus, hepatitis A virus (HAV), echovirus and norovirus are just a few viruses that have caused disease outbreaks in swimming pools.14 Viruses typically consist of genetic material (nucleic acid) surrounded by protective capsids that consist of protein sub-units. The nucleic acid may be either a single-strand RNA or a double-strand DNA. When combined, capsid and nucleic acid form a nucleocapsid. Infection is caused by the viral nucleic acid being released into the host cell and taking over the DNA to replicate the virus.

Li et al. note that HAV is somewhat more resistant to chlorine than other enteroviruses.15 They have demonstrated that chlorine inactivates the HAV by attacking a section of the nucleic acid known as 5’NTR. Li et al. found that a chlorine residual of at least 10 mg/L for 30 minutes is required to completely inactivate the HAV. However, Peterson et al. have shown that chlorine residuals of 0.5-1.5 mg/L for 30 minutes sufficiently inactivate almost all HAV infectivity in a purified solution while 2.0-2.5 mg/L completely destroyed the infectivity under the same conditions.16 They note, however that the levels of free residual chlorine required to inactivate HAV in the environment, protected by fecal material aggregated and dispersed in water, are unknown.

Engelbrecht et al. have reported considerable variations in the susceptibility of different viruses to chlorine.17 Virus type, pH and the ionic nature of the surrounding medium all affect the viruses’ susceptibility to chlorine disinfection. The viruses they investigated are all more rapidly inactivated by chlorine at lower pH values consistent with the greater reactivity of HOCl relative to hypochlorite ion. They also discovered that pH affects inactivation independently of the HOCl dissociation and that the presence of other ions, notably chloride, is very significant.

HAV, norovirus and echoviruses are largely spread by the fecal/oral route. For disease transmission to occur in a swimming pool, fecal matter or vomit has to be released into the water. At least one recorded HAV outbreak linked to swimming pools was related to accidental contamination by sewage.14

Adenoviruses may cause pharyngo-conjunctival fever, an infection of the pharynx and conjunctiva. Outbreaks of this disease have been associated with swimming pools with inadequate chlorination levels.14,18

Bacteria consist of a nucleoid containing DNA, ribosomes containing RNA, cytoplasm, a plasma membrane and a cell wall. The bacteria’s energy requirements are met when adenosine 5’ –triphosphate (ATP) is formed. ATP is either catalyzed by soluble enzymes present in the cell cytoplasm or by enzymes bound in the cell membrane.19

Mycobacterium marinum, Mycobacterium avium,20 Pseudomonas aeruginosa,21 Escherichia coli, Legionella spp. and Leptospira interrogans are all bacteria that have been linked to swimming pool- and spa-related disease.

Low concentrations of chlorine used to disinfect swimming pool and drinking water inhibits certain enzymes essential for bacterial cell survival. Knox et al.22 demonstrated that sulfhydryl enzymes were inhibited by chlorine. From their E.coli studies, Camper and McFeters23 postulated that chlorine attacked the sulfhydryl enzymes located in the cell membrane. Barrette et al.24 have shown that HOCl affects an enzyme in the cell membrane that is responsible for energy transport. The enzyme known as F1 –ATPase is required for synthesizing ATP. Inactivating the ATPase will diminish available energy, resulting in the bacterial cell’s death.

E.coli is very susceptible to chlorine disinfection and therefore is widely used as an indicator species to demonstrate effective disinfection. Most strains of E.coli are non-pathogenic and are commonly found in the gut. However, the serotype E.coli 0157 can cause serious illness, several outbreaks of which have been traced to swimming in untreated lakes and an untreated paddling pool.14

Pseudomonas aeruginosa is a common environmental bacterium found in a variety of habitats. P. aeruginosa can form bio-films and is very resistant to disinfection. An opportunistic pathogen that may cause infections in susceptible individuals, the bacteria is responsible for folliculitis outbreaks in whirlpools, hot-tubs and, less commonly, swimming pools.25

Inhaling aerosols contaminated with Legionella spp. bacteria may also cause infection. Legionella pneumophila is the species most commonly associated with infection. Legionellosis is a form of pneumonia that may result in mortality rates of up to 15 percent in hospitalized cases.14 Most Legionella outbreaks in recreational waters occur in spas.

Mycobacteria are particularly resistant to chlorine disinfection. The two main disease-causing species—M. tuberculum and M. leprae that cause typhoid and leprosy, respectively—are not of significance in swimming pool water. However, a range of environmental mycobacteria have infected people with impaired immunity. Although such mycobacteria are commonly found in swimming pools, they are not a significant cause of disease.26 They can, however, cause problems in some spas and hot tubs perhaps because of the higher bathing load to water ratio and the higher temperature. Mycobacteria’s resistant cell wall is waxy and hydrophobic, making the bacteria very resistant to disinfection. A study by Taylor et al.27 showed that CT values for chlorine of 51 to 204 were required for 99.9 percent inactivation of Mycobacterium avium. Lumb et al.28 showed that cases of lung disorders related to Mycobacterium avium were attributed to spas with inadequate disinfection.

Fungi may be found in several places in the swimming pool environment. In general, fungi are not responsible for spreading serious disease. A survey of fungal contamination in Iranian swimming pools29 indicated that fungal contamination in pools does not have a significant effect on health. People using swimming pools may be more susceptible to opportunistic fungal infections due to the effect of moist conditions on the skin. Changing room floors may well host dermatophytic fungi of the Trichophyton genus, which may cause Tinea pedis (athletes’ foot) infection. Proprietary disinfectants are available for controlling fungal contamination of changing room floors.30

This very diverse group of organisms contains a number of pathogens that create particular challenges for swimming pool disinfection.

The main disease-causing organisms are Cryptosporidium parvum, Giardia lamblia, Naegleria spp. and Acanthamoeba spp. Cryptosporidium and Giardia are fecally-transmitted organisms that can cause acute diarrheal illnesses (crypto-sporidiosis and giardiasis). The environmental form of the organism is resistant to chlorination. Giardia lamblia cysts require31 a free chlorine residual of 1.5 mg/L or greater at 25°C for 10 minutes to ensure 2.8-log10 reduction. Inactivation takes considerably longer at lower temperatures. Cryptosporidium parvum oocysts require levels of chlorine of 3,000 mg.min/L for one-log10 inactivation. They are more susceptible to other disinfectants, including chlorine dioxide and UV.32

Naegleria and Acanthamoeba amoebae may cause a serious disease called primary amoebic meningoencephalitis. Cursons et al. found that 0.79 mg/L total chlorine for 30 minutes gave a 4.3 log10 kill for Naegleria spp. while Acanthamoeba spp. required 1.25 mg/L for 30 minutes for the same level of inactivation.33

Organisms in combination
Many microorganisms have the tendency to form associations with other microorganisms. These associations are referred to as biofilms wherever they colonize a surface. A biofilm may consist of a wide range of species including bacteria, fungi, grazing protozoa and nematodes. Biofilms may make disinfection more difficult because of the protective effect of substances excreted by certain organisms. Biofilms secreted by P. aeruginosa and Klebsiella pneumoniae have been shown34 to reduce chlorine residuals to 20 to 30 percent of the bulk concentration of 2.5 mg/L at the film surface and falling to zero at deeper levels. Much higher chlorine residuals are required to completely penetrate and inactivate the biofilm.

Protozoa may act as infective hosts for other types of organisms. For example, Legionella pneumophila can infect the amoebae, Hartmanella vermiformis and Acanthamoeba polyphaga.35 The infected amoebae may, in turn, act as Legionella infective agents for humans.36

Biofilms may begin to form in areas where disinfection is inadequate, such as in poorly maintained filters. Once the biofilm is established, it may be difficult to remove and may release harmful microorganisms into the pool. Appropriate levels of disinfectant must be maintained at all times to prevent biofilms from becoming established.

Residual disinfection is essential for controlling the transmission of disease between swimmers. Disinfection can result in the formation of undesirable by-products that may affect the health and comfort of swimmers and pool staff. It is possible to provide safe and pleasant swimming conditions, provided the pool is properly maintained and treated.

Chlorine in the form of HOCl can affect different organisms in different ways. Bacteria like E.coli require relatively low doses, as they are inactivated by the damaging effect on enzymes in the cell membrane. Mycobacteria have much more resistant cell walls and require much higher doses of chlorine. Pseudomonas aeruginosa protects itself with extracellular polysaccharides, making it very resistant to chlorine. Viruses vary in their response, but chlorine appears to penetrate their protein coat to attack the DNA or RNA within. Fungi are not of major significance within the pool and can be controlled by fungicides applied to pool surroundings and changing room floors. Protozoa generally may be controlled by HOCl at typical pool water concentrations, but Cryptosporidium oocysts are resistant and need to be controlled by effective filtration, possibly in conjunction with UV.

A number of disinfection techniques are available for treating swimming pool water. These may greatly enhance the pool water quality in terms of swimmers’ comfort and well-being as well as the destruction of more chlorine-resistant organisms. However to be fully effective, these techniques generally need to be used in conjunction with some form of chlorine residual donor.


  1. Thickett, K.M., McCoach, J.S., Gerber, J.M., Burge, P.S. Occupational asthma caused by chloramines in indoor swimming-pool air Eur. Respir. J.; 2002; 19: 827-832.
  2. Massin, N., Bohadana, A.B., Wild, P., Herey, M., Toamain, J.P., Hubert, G. Respiratory symptoms and bronchial responsiveness in lifeguards exposed to nitrogen trichloride in indoor swimming pools. Occup. Environ. Med. 1998; 55; 258-263.
  3. Bernard. A., Carbonnelle, S., de Burbure, C., Buchet, J-P., Hermans, X., Doyle, I. Lung hyperpermeability and asthma prevalence in schoolchildren: unexpected associations with the attendance at indoor chlorinated swimming pools. Occup. Environ. Med. 2003; 60; 385-394.
  4. Lomas, P.D.R. The Combined Chlorine Residual of Swimming bath Water J. Assoc. Publ. Analysts, 1967, 5, 27. p. 27-36.
  5. Villaneuva, C.M., Cantor, K.P., Grimalt, J.O., Dosemeci, M., Malats, N., Real, F.X., Silverman, D., Tardon, A., Garcia-Closas, R., Serra, C., Carrato, A., Castano-Vinyals, G., Rothman, N., Kogevinas, M. Bladder Cancer and Exposure to Disinfection Byproducts in Water Through Ingestion, Bathing, Showering and Swimming in Pools: Findings from the Spanish Cancer Study. Epidemiology Vol. 15, No. 4, July 2004.
  6. Whitaker, H.J., Nieuwenhuijsen, M.J., Best, N.G. The Relationship between Water Concentraions and Individual Uptake of Chloroform: A Simulation Study. Environmental Health Perspectives, Vol. 111, No. 5, May 2003.
  7. Wright, J.M., Schwartz, J., Dockery, D.W. Effect of trihalomethane exposure on fetal development. Occup. Environ. Med. 2003; 60; 173-180.
  8. Chu, H., Nieuwenhuijsen, M. Distribution and determinants of trihalomethane concentrations in indoor swimming pools.Occup. Environ. Med. 2002; 59; 243-247.
  9. Hurst, K.J. Barrette, W.C. Leucocytic Oxygen Activation and Microbicidal Oxidative Toxins. Critical Reviews in Biochemistry and Molecular Biology, Vol. 24, Iss. 4 (1989) p. 271-328.
  10. Klebanoff, S.J. Phagocytic Cells: Products of Oxygen Metabolism. Inflammation: Basic Principles and Correlates. Eds. J.I Gallin, I.M. Goldstein and R. Snyderman. Raven Press, Ltd. New York. 1988.
  11. DIN 19643.
  12. Swimming Pool Water–Treatment and Quality Standards. Pool Water Treatment Advisory Group. 1999.
  13. Scaramelli, A.B. and DiGiacomo, F.A. Effect of sorbed organics on the efficiency of ammonia removal by chloramine-carbon surface reactions. J. Wat. Pollut. Control Fed., 1977, 49, No.4, 693-705.
  14. WHO. Guidelines for Safe Recreational-water Environments Final Draft for Consultation Vol. 2: Swimming Pools, Spas and Similar Recreational-water Environments August 2000.
  15. Li, J.W., Xin, Z.T., Wang, X.W., Zheng, J.L., Chao, F.H. Mechanisms of Inactivation of Hepatitis A Virus by Chlorine. Applied & Environmental Microbiology, Oct. 2002, p. 4951-4955. Vol. 68, No. 10.
  16. Peterson, D.A., Hurley, T.R., Hoff, J.C. and Wolfe, L.G. Effect of Chlorine Treatment on Infectivity of Hepatitis A Virus. Applied and Environmental Microbiology, Jan. 1983, p. 223-227. Vol. 45, No. 1.
  17. Engelbrecht, R.S., Weber, M.J., Salter, B.L. and Schmidt, C.J. Comparative Inactivation of Viruses by Chlorine. Applied and Environmental Microbiology, Aug. 1980, p. 249-256. Vol. 40, No.2.
  18. Harley, H., Harrower, B., Lyon, D., Dick, A. A primary school outbreak of pharyngo-conjunctival fever caused by adenovirus type 3. Commun. Dis. Intell 2001; 25: 9-12.
  19. Haddock, B.A. and Jones, C.W. Bacterial Respiration. Bacteriological Reviews, Mar. 1977, p.47-99, Vol. 41, No. 1.
  20. Lumb, R., Stapledon, R., Scroop, A., Bond, P., Cunliffe, D., Goodwin, A., Doyle, R., Bastian, I. Investigation of Spa Pools Associated with Lung Disorders Caused by Mycobacterium Avium Complex in Immunocompetent Adults. Applied and Environmental Microbiology, Aug. 2004, p. 4906-4910. Vol. 70, No. 8.
  21. Ratnam, S., Hogan, K., March, S.B., Butler, R.W. Whirlpool-Associated Folliculitis Caused by Pseudomonas aeruginosa: Report of an Outbreak and Review. Journal of Clinical Microbiology, Mar. 1986, p.655-659.
  22. Knox, W.E., Stumpf, P.K., Green, D.E. and Auerbach, V.H. The Inhibition of Sulfhydryl Enzymes as the Basis of the Bactericidal Action of Chlorine. J. Bacteriol. 1948, 55 (4) p. 451-458.
  23. Camper, A.K. and McFeters, G.A., Chlorine Injury and the Enumeration of Waterborne Coliform Bacteria. Applied & Environmental Microbiology. Mar. 1979, p.633-641. Vol. 37, No.3.
  24. Barrette, W.C., Hannum, D.M., Wheeler, D.W. and Hurst, J.K. General Mechanism for the Bacterial Toxicity of Hypochlorous Acid: Abolition of ATP Production. Biochemistry, Vol. 28, No. 23, 1989, p. 9172-9178.
  25. Ratnam et al. 1986.
  26. Leoni, E., Legnani, P., Mucci, M.T. and Pirani, R. Prevalence of mycobacteria in a swimming pool environment. Journal of Applied Microbiology 1999, 87, 683-688.
  27. Taylor, R.H., Falkinham, J.O., Norton, C.D., LeChevalier, M.W., Chlorine, Chloramine, Chlorine Dioxide and Ozone Susceptibility of Mycobacterium avium Applied and Environmental Microbiology, Apr. 2000, p. 1702-1705.
  28. Lumb, R., Stapledon, R., Scroop, A., Bond, P., Cunliffe, D., Goodwin, A., Doyle, R., Bastian, I. Investigation of Spa Pools Associated with Lung Disorders Caused by Mycobacterium Avium Complex in Immunocompetent Adults. Applied and Environmental Microbiology, Aug. 2004, p. 4906-4910. Vol. 70, No. 8.
  29. Nanbakhsh, H., Diba, K. Hazarti, K., Study of Fungal Contamination of Indoor Public Swimming Pools. Iranian J. Public Health, Vol. 33, No.1, pp. 60-65 2004.
  30. Bobichon, H., Dufour-Morfaux, F., Pitort, V. In Vitro Susceptibility of Public Indoor Swimming Pool Fungi to Three Disinfectants. Mycoses. 1993 Sep-Oct; 36 (9-10): 305-311.
  31. Jarroll, E.J., Bingham, A.K., & Meyer, E.A. Effect of Chlorine on Giardia lamblia Cyst Viability. Applied & Environmental Microbiology, Feb. 1981, p.483-487. Vol. 41, No.2.
  32. Morita, S., Namikoshi, A., Hirata, T., Oguma, K., Katayama,H., Ohgaki, S., Motoyama, N., Fujiwara, M., Efficacy of UV Irradiation in Inactivating Cryptosporidium parvum Oocycts. Applied & Environmental Microbiology, Nov. 2002, p. 5387-5393. Vol.68, No. 11.
  33. Cursons, R.T.M., Brown, T.J., Keys, E.A. Effect of Disinfectants on Pathogenic Free-Living Amoebae: in Axenic Conditions. Applied & environmental Microbiology, July 1980, p. 62-66 Vol. 40, No.1.
  34. De Beer, D., Srinivasan, R. & Stewart, P.S. Direct Measurement of Chlorine Penetration into Biofilms during Disinfection. Applied & Environmental Microbiology, Dec.1994, p. 4339-4344.
  35. Abu Kwaik, Yousef, Gao, Lian-Yong, Stone, B. J., Venkataraman, Chandrasekar, Harb, O. S. Invasion of Protozoa by Legionella pneumophila and Its Role in Bacterial Ecology and Pathogenesis Appl. Environ. Microbiol. 1998, 64: 3127-3133.
  36. Rowbotham, T.J., Preliminary report on the pathogenicity of Legionella pneumophila for freshwater and soil amoebae. Journal of Clinical Pathology, 1980; 33: 1179-1183.

* MCIWEM stands for Member of the Chartered Institution of Water & Environmental Management; CChem, for Chartered Chemist; and MRSC, for Member of the Royal Society of Chemistry.

Note: This paper was originally presented at CIWEM’s ‘Swimming Pools & Spa Baths–Effective Control of Water Quality and Public Health’ Conference at the Chancellors Hotel & Conference Centre in Manchester, England on November 30, 2005.

About the author
David M. Bonnick, MCIWEM, CChem, MRSC, is a Technology Manager for the Wallace & Tiernan product line at Siemens Water Technologies in Tonbridge, Kent, UK. He has a BS degree in Earth science from the University of Leicester and an MS degree in chemical research from the University College London. Bonnick can be reached at 44-0-1732-502024 or at [email protected].



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