Archive for July, 2010


Swimmer’s Asthma
[Research Paper]
Research Testimonies and Anecdotes Sanitization Alternatives Asthma Drug Guidelines


In the course of preparing materials for the Swimming Science Journal, I came across the following articles concerning chlorinated pools. Abstracts of contents and appropriate comments are included below. Please read the discussion points and articles that follow the abstracts.


  1. Exercising competitive swimmers absorb toxic levels of chlorine products in the course of a training session.
  2. Training two or more times a day will not allow the toxins to be completely cleared from the body in most swimmers.
  3. Children inhale more air per unit of body weight than mature persons, and have lesser developed immune and defense systems.
  4. Young children absorb relatively greater amounts of toxins than older swimmers and therefore, are at greater risk.
  5. In hyper-chlorinated pools, even dental enamel can be eroded because of the increased acidity in swimmers in training.
  6. Exercise intensity and number of sessions increase the toxic concentrations in competitive swimmers.
  7. Greater toxin absorption occurs through the skin than through breathing. However, the breathing action alone is sufficient to cause hypersensitivity and “asthma-like” respiratory conditions in at least some swimmers. The percentage of asthma-like symptoms in swimmers that is attributable to exposure to chlorinated hydrocarbons versus being unrelated to chlorine exposure is presently unknown. This is an area clearly deserving of further research.
  8. Overchlorination is particularly hazardous to the health of swimmers.


Clifford, P. W., Richardson, S. D., Nemery, B., Aggazzotti, G., Baraldi, E., Blatchley, E. R., Blount, B. C., Carlsen, K., Eggleston, P. A., Frimmel, F. H., Goodman, M., Gordon, G., Grinshpun, S. A., Heederik, D., Kogevinas, M., LaKind, J. S., Nieuwenhuijsen, M. J., Piper, F. C., & Sattar S. A. (2009). Childhood asthma and environmental exposures at swimming pools: State of the science and research recommendations. Environmental Health Perspectives, 117, 500-507.

Recent studies have explored the potential for swimming pool disinfection by-products (DBPs), which are respiratory irritants, to cause asthma in young children. This review describes the state of the science on methods for understanding children’s exposure to DBPs and biologics at swimming pools and associations with new-onset childhood asthma. A research agenda to improve our understanding of this issue is recommended.

A workshop was held in Leuven, Belgium, 21–23 August 2007, to evaluate the literature and to develop a research agenda to better understand children’s exposures in the swimming pool environment and their potential associations with new-onset asthma. Participants, including clinicians, epidemiologists, exposure scientists, pool operations experts, and chemists, reviewed the literature, prepared background summaries, and held extensive discussions on the relevant published studies, knowledge of asthma characterization and exposures at swimming pools, and epidemiologic study designs.

Childhood swimming and new-onset childhood asthma have clear implications for public health. If attendance at indoor pools increases risk of childhood asthma, then concerns are warranted and actions are necessary. If there is no relationship, these concerns could unnecessarily deter children from indoor swimming and/or compromise water disinfection.

Conclusions: Current evidence of an association between childhood swimming and new-onset asthma is suggestive but not conclusive. Important data gaps need to be filled, particularly in exposure assessment and characterization of asthma in very young persons. It was recommended that additional evaluations using a multidisciplinary approach are needed to determine whether a clear association exists.


Bernard, A., Carbonnelle, S., Michel, O., Higuet, S., de Burbure, C., Buchet, J-P., Hermans, C., Dumont, X., & Doyle, I. (2003). Lung hyperpermeability and asthma prevalence in schoolchildren: unexpected associations with the attendance at indoor chlorinated swimming pools. Occupational and Environmental Medicine, 60, 385-394.

This study assessed whether exposure to nitrogen trichloride in indoor chlorinated pools may affect the respiratory epithelium of children and increase the risk of some lung diseases such as asthma.

Healthy children (N = 226), were measured for serum surfactant associated proteins A and B (SP-A and SP-B), 16 kDa Clara cell protein (CC16), and IgE. Lung specific proteins were measured in the serum of 16 children and 13 adults before and after exposure to NCl3 in an indoor chlorinated pool. The relation between pool attendance and asthma prevalence were studied in 1881 children. Asthma was screened with the exercise induced bronchoconstriction test (EIB).

Pool attendance was the most consistent predictor of lung epithelium permeability. A positive dose-effect relation was found with cumulated pool attendance and serum SP-A and SP-B. Serum IgE was unrelated to pool attendance, but correlated positively with lung hyperpermeability as assessed by serum SP-B. Changes in serum levels of lung proteins were reproduced in children and adults attending an indoor pool. Serum SP-A and SP-B were significantly increased after one hour on the poolside without swimming. Positive EIB and total asthma prevalence were significantly correlated with accumulated pool attendance indices.

Implications. Regular attendance at chlorinated pools by young children is associated with an exposure-dependent increase in lung epithelium permeability and increase in the risk of developing asthma, especially in association with other risk factors. It is postulated that increased exposure of children to chlorination products in indoor pools might be an important cause of the rising incidence of childhood asthma and allergic diseases in industrialized countries. Further epidemiological studies should be undertaken to test this hypothesis.


Aggazzotti, G., Fantuzzi, G., Righi, E., & Predieri, G. (1998). Blood and breath analyses as biological indicators of exposure to trihalomethanes in indoor swimming pools. Science of the Total Environment, 217, 155-163.

In this article, exposure to trihalomethanes (THMs) in indoor swimming pools as a consequence of water chlorination was reported.

Environmental and biological monitoring of THMs assessed the uptake of these substances after a defined period in competitive swimmers (N = 5), regularly attending an indoor swimming pool to train for competition during four sampling sessions. Analyses were performed by gas-chromatography and the following THMs were detected: chloroform (CHC13), bromodichloromethane (CHBrC12), dibromochloromethane (CHBrsC1) and bromoform (CHBr3). CHC13 appeared the most represented compound both in water and in environmental air before and after swimming. CHBrC1w and CHBr2C1 were always present, even though at lower levels than CHC13, CHBr3, was rarely present. In relation to biological monitoring, CHC13, CHBrC12 and CHBr2C1 were detected in all alveolar air samples collected inside the swimming pool. Before swimming, after one hour at rest at the pool edge, the mean values were 29.4 +/- 13.3, 2.7 +/- 1.2 and 0.8 +/- 0.8 micrograms/m3, respectively, while after spending one hour of swimming, higher levels were detected (75.6 +/- 18.6, 6.5 +/- 1.3 and 1.4 +/- 0.9 micrograms/m3, respectively). Only CHC13 was detected in all plasma samples (mean: 1.4 +/- 0.5 micrograms/1) while CHBrC1x and CHBr2C1 were observed only in few samples at a detection limit of 0.1 micrograms/1. After one at rest, at an average environmental exposure of approx. 100 micrograms/m3, the THM uptake was approx. 30 micrograms/h (26 micrograms/h for CHC1c, 3 micrograms/h for CHBrC12 and 1.5 micrograms/h for CHBr2C1). After one hour of swimming, the THM uptake was approximately seven times higher than at rest: a THM mean uptake of 221 micrograms/h (177 micrograms/h, 26 micrograms/h and 18 micrograms/h for CHC13, CHBrC12 and CHBr2C1, respectively) was evaluated at an environmental concentration of approx. 200 micrograms/m3.

Implication. Training for swimming in a poorly ventilated indoor swimming pool has the potential to cause illness through breathing undesirable concentrations of mainly chloroform.


Lindstrom, A.B., Pleil, J.D., & Berkoff, D.C. (1997). Alveolar breath sampling and analysis to assess trihalomethane exposures during competitive swimming training. Environmental Health Perspectives, 105(6), 636-642

Alveolar breath sampling was used to assess trihalomethane (THM) exposures encountered by collegiate swimmers during a typical 2-hr training period in an indoor natatorium.

Breath samples were collected at regular intervals before, during, and for three hours after a moderately intense training session. Integrated and grab whole-air samples were collected during the training period to help determine inhalation exposures, and pool water samples were collected to help assess dermal exposures.

Resulting breath samples collected during the workout demonstrated a rapid uptake of two THMs (chloroform and bromodichloromethane), with chloroform concentrations exceeding the natatorium air levels within eight minutes after the exposure began. Chloroform levels continued to rise steeply until they were more than two times the indoor levels, providing evidence that the dermal route of exposure was relatively rapid and ultimately more important than the inhalation route in this training scenario. Chloroform elimination after the exposure period was fitted to a three compartment model that allowed estimation of compartmental half-lives, resulting minimum blood borne dose, and an approximation of the duration of elevated body burdens. It was estimated that dermal exposure route accounted for 80% of the blood chloroform concentration and the transdermal diffusion efficiency from the water to the blood was in excess of 2%. Bromodichloromethane elimination was fitted to a two compartment model that provided evidence of a small, but measurable, body burden of this THM resulting from vigorous swim training.

These results suggest that trihalomethane exposures for competitive swimmers under prolonged, high-effort training are common and possibly higher than was previously thought and that the dermal exposure route is dominant. The exposures and potential risks associated with this common recreational activity should be more thoroughly investigated.

Implication. In this study the greater importance of transdermal (via the skin) uptake of chlorinated hydrocarbons compared to the respiratory route is demonstrated. This indicates that improved ventilation alone will not have a major impact on exposure to these materials because it is being immersed in the liquid that is the greatest threat. In contrast, ozonation allows markedly reduced levels of chlorine in the pool water.


Drobnic, F., Freixa, A., Casan, P., Sanchis, J., & Guardino, X. (1996). Assessment of chlorine exposure in swimmers during training. Medicine and Science in Sports and Exercise, 28(2), 271-274.

The presence of a high prevalence of bronchial hyperresponsiveness and asthma-like symptoms in swimmers has been recently reported. Chlorine, a strong oxidizing agent, is an important toxic gas that a swimmer can breath during training in chlorinated pools.

Measurements of the chlorine concentration in the breathing zone above the water (< 10 cm) were obtained randomly during five nonconsecutive days in four different swimming pool enclosures. The mean level in all the swimming pools was 0.42 +/- 0.24 mg/m3, far below the threshold limited value (TLV) of 1.45 mg/m3 for the work places for a day of work (8 h). The TLV could be reached and even exceeded if we consider the total amount of chlorine that a swimmer inhales in a daily training session of two hours (4-6 g) compared with a worker during eight hours at the TLV (4-7 g). Low correlation was observed with the number of swimmers in the swimming pool during the measurements (0.446) and other variables as the water surface area of the pool, volume of the enclosure, and the chlorine-addition system in the swimming pool. A low turnover rate in the air with an increase of chlorine levels through the day was observed in all pools.

The concentration of chlorine in the microenvironment where the swimmer is breathing is below the TLV concentration limit, but nevertheless results in a high total volume of chlorine inhaled by the swimmers in a given practice session.

The possible role of chlorine in producing respiratory symptoms in swimmers needs further investigation.

Implication. Even though chlorine concentrations in a pool environment are at acceptable “safe” levels, it is a swimmer’s exercising that produces abnormal levels of exposure to this toxin.

There has not been sufficient research to even begin understanding the health effects of this repetitive exposure.


Cammann, K., & Hubner, K. (1995). Trihalomethane concentrations in swimmers’ and bath attendants’ blood and urine after swimming or working in indoor swimming pools. Archives of Environmental Health, 50(1), 61-65

The influence of working or swimming in indoor swimming pools on the concentrations of four trihalomethanes (haloforms) in blood and urine was investigated. Different groups (bath attendants, agonistic swimmers, normal swimmers, sampling person) were compared.

The proportions of trihalomethanes in blood and urine correlated roughly with those in water and ambient air. Higher levels of physical activity were correlated with higher concentrations. Within one night after exposure in the pool the blood concentrations usually were reduced to the pre-exposure values. Secretion of trichloromethane in urine was found to be less than 10%.

Implication. Exercising in a chlorinated pool increases the levels of assimilation of chlorine related gases. The greater the amount of exercise, the greater the concentrations. Thus, hard training swimmers are at greater risk than more sedentary pool attendants and coaches.

It takes at least one night for absorbed substances to be removed. If insufficient time exists between training sessions the possibility of toxic build-up is real.


Aiking, H., van Acker, M.B., Scholten, R.J., Feenstra, J.F., & Valkenburg, H.A. (1994). Swimming pool chlorination: a health hazard? Toxicology Letters, 72(1-3), 375-380.

A pilot study addressed potential effects of long-term exposure to chlorination products in swimming pools.

The indicator compound chloroform was detectable in blood from competitive swimmers in an indoor pool (mean = 0.89 +/- 0.34 microgram/l; N = 10), but not in outdoor pool swimmers. No hepatotoxic effect was indicated by serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) or gamma-glutamyl transpeptidase (gamma-GT) enzyme levels. beta-2-microglobulin, an indicator of renal damage, was significantly elevated in urine samples of the slightly, but significantly, younger indoor swimmers.

The precise ratio between these two possible causes, age and chloroform exposure, as well as the mechanism of the former, remain to be elucidated.

Implication. The toxic effects of chlorine products in swimmers training in indoor pools are greater in younger than older swimmers. Young swimmers are therefore at a greater health risk.


Wood, B.R., Colombo, J.L., Benson, B.E. (1987). Chlorine inhalation toxicity from vapors generated by swimming pool chlorinator tablets. Pediatrics, 79(3), 427-430.

The authors presented two cases of serious respiratory injury after brief exposure to vapors from solid chlorine compounds. No previous reports of such accidents were located and, therefore, this paper related these cases to alert the medical community. It was recommend that physicians caring for children include warnings about these preparations in their routine counseling of parents.

Implication. Chlorinator tablets are of such a concentration that acute exposure to them is hazardous.


Centerwall, B.S., Armstrong, C.W., Funkhouser, L.S., & Elzay, R.P. (1986). Erosion of dental enamel among competitive swimmers at a gas-chlorinated swimming pool. American Journal of Epidemiology, 123(4), 641-647.

In September 1982, two Charlottesville, Virginia, residents were found by their dentists to have general erosion of dental enamel consistent with exposure to acid. Both patients were competitive swimmers at the same private club pool. No other common exposure could be determined. An epidemiologic survey was made of 747 club members.

Symptoms compatible with dental enamel erosion were reported by 3% of non-swimmers (9/295), 12% of swimmers who were not members of the swim team (46/393), and 39% of swim team members (23/59). All four swimmers with clinically verified dental enamel erosion had trained regularly in a particular pool. That pool was compared to one that had eight equivalent swimmers without enamel erosion. Examination of the implicated swimming pool revealed a gas-chlorinated pool with corrosion of metal fixtures and etching of cement exposed to the pool water. A pool water sample had a pH of 2.7, i.e., an acid concentration approximately 100,000 times that recommended for swimming pools (pH 7.2-8.0). A review of pool management practices revealed inadequate monitoring of pool water pH.

Acid erosion of dental enamel — “swimmer’s erosion” — is a painful, costly, irreversible condition which can be caused by inadequately maintained gas-chlorinated swimming pools.

Implication. Overchlorinated pools that produce excessively elevated levels of acidity can contribute to dental enamel erosion in competitive swimmers. Individuals who frequent pools less are less likely to be threatened.


Reuters Health, March 21, 2001.

A study presented [03/20/2001] in New Orleans at the 57th Annual Meeting of the American Academy of Allergy, Asthma and Immunology, strongly suggested that swimming pool environments adversely affect the lung function of competitive swimmers. Dr. Stephen J. McGeady, and colleagues, from Thomas Jefferson University in Wilmington, Delaware, measured the lung function (FEV1) of competitive swimmers (N = 28) before and after cycle ergometer testing in swimming pool and laboratory settings. The study was motivated by observations of university team swimmers displaying significant airway obstruction and the number of reports that many swimmers use beta-agonist inhalers.

Ss’ mean FEV1 was significantly lower in the pool than in the laboratory. Some swimmers (14%), not previously asthmatic, displayed airway obstruction at baseline. Exercise-induced bronchospasm occurred in a further 11% of swimmers not known to have that problem or asthma. Swimmers known to have asthma seemed to do better than swimmers who were not diagnosed with asthma. Exercise-induced bronchospasm negatively affected performance.

Implications. Swimming is worse on bronchospasm than other endurance sports, a paradox since swimming is supposed to promote health. The facility/exercise setting is implicated as the cause of these respiratory afflictions. Because of swimming pool environments, competitive swimming could be bad for one’s health!

[Thanks to Johnny Morton, former collegiate swimmer, current parent, official, coach and interested observer, for bringing this to my attention — BSR]


Williams, A., Schwellnus, M. P., & Noakes, T. (2004). Increased concentration of chlorine in swimming pool water causes exercise-induced bronchoconstriction (EIB). Medicine and Science in Sports and Exercise, 36(5) Supplement abstract 2046.

This study assessed whether chlorine exposure during swimming at the same exercise intensity in swimming pools with different chlorine levels provokes Exercise Induced Bronchoconstriction (EIB) in well-trained swimmers with and without a past history of EIB. Trained swimmers (N = 21) with a history of EIB and trained swimmers (N = 20) with no history of EIB served as subjects. Ss were randomly exposed to four different exercise tests of the same intensity (minimum of 6-8 min at 60-80% of the target heart rate) and duration:

The percent of Ss with a positive test for EIB was significantly higher in the high chlorine condition (No-history = 60, History = 67), compared with the low chlorine (No-history = 10, History = 0), no-chlorine (No-history = 18, History = 17), and exercise (No-history = 3, History = 12) conditions. There was no difference in the frequency of EIB between the No-history and History groups.

Implication. Competitive swimmers exposed to chlorine concentrations in pool water (> 1ppm) have a higher risk of developing EIB irrespective of past history with EIB.


  1. Beech, J.A., Diaz, R., Ordaz, C., & Palomeque, B. (1980). Nitrates, chlorates and trihalomethanes in swimming pool water. American Journal of Public Health, 70(1), 79-82.
  2. Water from swimming pools in the Miami area was analyzed for nitrates, chlorates and trihalomethanes. The average concentrations of nitrate and chlorate found in freshwater pools were 8.6 mg/liter and 16 mg/liter respectively, with the highest concentrations being 54.9 mg/liter and 124 mg/liter, respectively. The average concentration of total trihalomethanes found in freshwater pools was 125 micrograms/liter (mainly chloroform) and in saline pools was 657 micrograms/liter (mainly bromoform); the highest concentration was 430 micrograms/liter (freshwater) and 1287 micrograms/liter (saltwater). The possible public health significance of these results is briefly discussed.

  3. Mustchin, C.P., & Pickering, C.A. (1979). “Coughing water”: bronchial hyper-reactivity induced by swimming in a chlorinated pool. Thorax, 34(5), 682-683.
  4. Decker, W.J., & Koch, H.F. (1978). Chlorine poisoning at the swimming pool: an overlooked hazard. Clinical Toxicology, 13(3), 377-381.


Governmental regulation agencies have standards for PASSIVE air in enclosed swimming pools. At least that was the case the Carlile Organization experienced at Narrabeen several years ago when many of its top swimmers were ill. The supervising staff did all the environmental testing and the air was deemed to be safe and within published guidelines. Even after the declaration that the air was “good” swimmers remained ill particularly with upper respiratory problems.

However, according to the above research an exercising athlete increases the toxicity of the chlorinated pool atmosphere by 700%! That should be a high-level health risk! Safety accrediting agencies need to upgrade their standards to be reflected in active alveolar air, not passive environmental air.

People in swimming over the past decade have become alarmed at the high proportion of training swimmers who are diagnosed/treated asthmatics. However, “swimming asthma” might well be hypersensitivity to chloroform and the other gases as explained in the abstract and not truly asthma.

Is it possible that our sport might be generating life-long health problems purely because of the environment in which swimmers are continually exercised? If that is so there is a MAJOR PROBLEM WITH OUR SPORT.

I would appreciate hearing of any learned writings or investigations on this matter.

Brent S. Rushall

Chlorine, Swimsuits, and the Five Stages of Grief

Every person has experienced it, that feeling of rapturous joy as you open a new summer season with the absolute perfect swimming suit. After months and months of shopping, far too many dressing room visits to count, and hours of strenuous gym training, you are finally ready to hit the pool in that perfectly form-fitting, wonderfully flattering swimsuit. Unfortunately, the euphoria of owning the perfect, new swimsuit (as you bask in the admiring gazes of handsome onlookers) lasts approximately one month into the summer. It is then that you notice that the swimsuit that had been so bright and beautiful just four weeks ago is now starting to look fairly dull, and the elastic just does not seem to hug your body like it used to. That perfect swimming suit is already starting to sag, and there are still two sun-soaked months of summer left to enjoy.

So, what do you do? Chalk up the loss to another inevitable case of chlorine damage and hit the stores to search for the not quite so perfect replacement? Simply admit to the fact that all things (including swimsuits) eventually fade and lose their luster? Sadly enough, you will most likely be forced to accept these facts and move on with your life and your summer. However, to help you through the journey of swimsuit grief, from the initial shock to the eventual acceptance, we have provided a few tips to prolonging the life of your swimsuit and to accepting its eventual demise.

In this day and age, chlorinated swimming pool water is a necessary evil. Germs and other pathogens can quickly travel from body to body in a swimming pool, and chlorine, dangerous as it is in other aspects, helps to protect our bodies from these pathogens. Still, as chlorine kills and/or damages bacteria and viruses that occur in swimming pool water, it also kills and/or damages cells in the body. More important to the focus of this article, chlorine damages swimsuits to an almost irreparable extent. Swimming in a chlorinated swimming pool is effectively equivalent to soaking your swimsuit in bleach for a couple of hours. Needless to say, this is hardly a practice that encourages the durability and color-fastness of your swimsuit.

Interestingly, the eventual acceptance of the inevitable decline of your swimsuit closely follows the well-known five stages of grief. First, there is the initial denial that your perfect, beautiful swimsuit could actually be fading. Perhaps it is just a trick of the light? Then, there is the anger at having something so beautiful and flattering taken away from you so soon. Why did I spend so much money on such a piece of junk? Then, the inevitable bargaining…I promise I’ll do 50 crunches every day for the rest of my life if you (the swimsuit) will only last throughout the summer. Bargaining is followed by depression. Why should I have expected to make a splash at the pool this summer in my new swimsuit? It really doesn’t matter anyway. Finally, acceptance, the most helpful and constructive step, comes along. I know that chlorine is an inevitable factor in the life of my swimsuit. Now, what can I do about it?

Despite the fact that an eventual trip for your swimsuit or bikini to that big swimming pool in the sky (or the big landfill south of town) is inevitable, there are a few steps you can take to prolong the life of your swimsuit. Chlorine will always be the eventual victor; it is too powerful of a poison to vanquish entirely. Still, attentive care to the washing of your swimsuit can help to ensure that it maintains its life and vitality throughout the summer.

If you have accepted the ultimate demise of your beautiful swimsuit but are not yet willing to give up the fight, here is what you can do to prolong the life of your swimsuit, despite constant dippings in chlorinated water. First of all, you must truly accept the fact that your swimsuit is not meant to last forever. While there are fabrics that are treated for chlorine resistance, no fabric can entirely resist chlorine’s damaging effects. Second, you should make a consistent effort to take care of your swimsuit. After swimming, rinse your swimsuit as soon as possible in cold water. This act will remove much of the chlorine before it has too much of an impact. Also, when washing your swimsuit, be sure to hand wash or run it through the gentle cycle of your washing machine in cold water. In addition, you should never put your swimsuit in the dryer; the dryer will tend to exacerbate any fading that may occur.

With careful attention to the care of your swimsuit and a general acceptance of the inevitable decline of that swimsuit, you should be able to safely travel through the five stages of swimsuit grief and enjoy one, glorious summer with the swimsuit of your dreams.

Ventilation for Indoor Pools

From DesertAire

Irritant Effect of Disinfection Byproducts in Swimming Pool Water

Irritant Effect of Disinfection Byproducts in Swimming Pool Water Hyg. Umweltmed. 200, 491-503
© Gustav Fischer Verlag 1997/98
Zentralblatt für Hygiene und Umweltmedizin
Hygiene Institute of Heidelberg University Medical Center, Department of Hygiene and Medical Microbiology
Lothar Erdinger, Frank Kirsch, and Hans-Günther Sonntag
Abstract [original English]
Compounds which can occur as disinfection by-products (DBP’s) in swimming pool water were examined for their mucous membrane irritating potential. Previous studies using the rabbit eye test (Draizé [1] test) have shown that the irritating potential of typical concentrations of free and combined chlorine are insufficient to explain the degree of eye irritation that can result from exposure to swimming pool water. Other DBP’s which may be responsible for eye irritation include halogenated carboxyl compounds (HCC’s) which act as precursors during the formation of chloroform. In this study, a modified HET-CAM Test (Hens Egg Test at the Chorion Allantois Membrane) has been used to investigate the mucous membrane irritating effects of HCC’s. Some of the compounds tested were found to have a significantly increased irritating effect when compared to a chlorine/chloramine mixture of the same concentration, several mixtures of HCC’s where [sic] even more active at lower concentrations than single compounds. However, the irritating effects of individual compounds as well as of mixtures of HCC’S were not sufficiently intense to allow the identification of those compounds specifically responsible for the overall observed increase in irritation. HCC’s were therefore tested in the presence of aqueous chlorine solution. When combined with aqueous chlorine, a number of compounds exhibited significantly enhanced effects. Our results show that the eye irritating effects of low concentrations of DBP’s can be investigated using a modified HET-CAM assay. Moreover, results obtained using this assay suggest that the mucous membrane irritating potential of swimming pool water is a consequence of the effects and synergistic action of a number of DBP’s in the presence of chlorine. Further work should be carried out in order to establish an indicator for eye irritating effects of swimming pool water.

In one study conducted on the effect of swimming pool water on the cornea, 68% of the test subjects reported that after swimming they saw rainbows and/or halos around light sources, and 94% exhibited epithelial erosion [9]. These events were at least partially attributed to the hypotonic effect of swimming pool water. In other studies, it could also be shown that in pools with 0.5% NaCl content, less damage to the cornea occurred [14] than in pools operated without
salt added. In addition, chloramines have been suspected for a long time to be responsible for the irritant effects [5]. In one study back in 1951, it was found that different water treatment methods had different impacts on the irritant effect [15]. But for the most part, chlorine (the most commonly used disinfectant) was held responsible for the effects.
But chlorine is currently the only water disinfectant that meets the requirements necessary from a hygiene standpoint for safe use in swimming pools.
The mechanism by which chlorine inactivates microorganisms is to a large extent unknown [6]. It stands to reason that we should look for a fundamental cause in the chemical reactivity of chlorine. This high reactivity, however, also leads to byproducts, where organic matter contained in the water is chemically altered by the disinfectant. In addition to chloroform, many other byproducts are formed which have been only partially identified. For drinking water applications, in the USA detailed studies were conducted back in the beginning of the 1980s, where various compounds were quantitated.
Chloroform and other byproducts are inevitably also formed in swimming pool water. But since chloroform represents the end product of a multistep chain of reactions, more byproducts must be contained in the water.
As has already been mentioned, the most important disinfection byproduct for swimming pool water is chloroform, which can affect the swimmer through the water and through the air [11, 3]. The best known reaction mechanism by which chloroform can be formed using chlorine from organic compounds is the haloform reaction. This reaction occurs via several steps, where carbonyl compounds with methyl groups in the α position are converted first to α-chlorinated ketones and ultimately to chloroform and an organic acid.
While the toxicological properties of chloroform have been relatively well studied [2] and sufficient data are also available concerning its uptake in swimming pools [16], not much information is available concerning the type and concentration of its immediate precursors. However, in principle, compounds with a halogen atom in an α position relative to a double bond are regarded as having irritant effects on mucous membranes.
Chloroacetone was used as a chemical warfare agent for this reason, because of its severe irritant effect in the gaseous state.
Within this study, tests were conducted on the irritant activity relative to mucous membranes for substances that sometimes already had been detected in swimming pool water. Other compounds were taken as model compounds in the study, in order to be able to take into account their effects. The goal was to determine the threshold concentration for the effect of these substances, so we could demonstrate their fundamental significance in the origin of eye irritation in swimming pools while taking into account realistic exposure times.
We were able to show that under the indicated test conditions, the reaction in the HET-CAM test is somewhat more sensitive than in the Draize test. From this we conclude that this model is suitable in principle for detecting the effect of low material concentrations of compounds with an irritant effect.
In the test, the studied individual halogenated organic compounds proved to be irritants only in concentrations that are not usually found in swimming pools. The concentrations found so far in swimming pools are considerably lower. However, higher concentrations could be measured in outdoor swimming pools than in indoor pools, where concentrations of up to 100 μg/L could be detected.
Based on our results, it is therefore likely that the irritant effect occurring in swimming pools is not due to one individual compound, but rather many compounds present in the water contribute to this effect. At the same time, the concentrations of these compounds are dependent
on pool load and can fluctuate considerably over the day [8]. From personal experience, eye irritation is also dependent on pool load. Since the chlorine concentration in modern pools is automatically regulated and generally is not subject to large fluctuations, this can also be considered as evidence that the irritant effect is primarily due to other compounds.
Concerning the question of the extent to which other classes of compounds (besides halogenated organic keto compounds) also contribute to the irritant effect, at the moment we can only speculate. Since the oxidizing agents used in water treatment (chlorine and if necessary ozone) are very reactive, byproducts possibly having activity can also be formed by an oxidative route [18].
In continuing investigations, the model for studying irritant effects should be developed further so that it can be used for directly testing swimming pool water.
In order to develop simple prevention strategies, the mechanism for chloroform formation in swimming pools and especially the resulting intermediates should be studied. Ultimately, effective countermeasures can be further developed only if we know these interrelationships.