Chlorine Toxicity


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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.
  9. Exposure to swimming pool water increases the likelihood of some cancers.


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.


Kogevinas, M., Villanueva, C. M., Font-Ribera, L., Liviac, D., Bustamante, M., Espinoza, F., Nieuwenhuijsen, M. J., Espinosa, A., Fernandez, P., DeMarini, D. M., Grimalt, J. O., Grummt, T., & Marcos, R. (September 12, 2010). Genotoxic effects in swimmers exposed to disinfection by-products in indoor swimming pools. Environmental Health Perspectives, on line [].

“Exposure to disinfection by-products (DBPs) in drinking water has been associated with cancer risk. A recent study found an increased bladder cancer risk among subjects attending swimming pools relative to those not attending.” This study evaluated whether swimming in pools is associated with biomarkers of genotoxicity. Blood, urine, and exhaled air samples from non-smoking adult volunteers (N = 49) were taken before and after they swam for 40 minutes in an indoor chlorinated pool. It was estimated thatthere would be associations between the concentrations of four trihalomethanes in exhaled breath and changes in the following biomarkers: micronuclei and DNA damage (comet assay) in peripheral blood lymphocytes before and one hour after swimming, urine mutagenicity (Ames assay) before and two hours after swimming, and micronuclei in exfoliated urothelial cells before and two weeks after swimming. It was also estimated that there would be associations and interactions with polymorphisms in genes related to DNA repair or disinfection by-products metabolism.


After swimming, the total concentration of the four trihalomethanes in exhaled breath was seven times higher than before swimming. The change in the frequency of micronucleated lymphocytes after swimming increased in association with exhaled concentrations of the brominated trihalomethanes but not chloroform. Swimming was not associated with DNA damage detectable by the comet assay. Urine mutagenicity increased significantly after swimming in association with the concentration of exhaled CHBr3. No significant associations with changes in micronucleated urothelial cells were observed. [The reason that bromine trihalomines were evident as opposed to chlorine trihalomines was that the local water supply was high in bromine.]


Implication. There are potential genotoxic effects of exposure to disinfection by-products from swimming pools. The positive health effects gained by swimming could be increased by reducing the potential health risks of the traditional chlorine disinfection processes of pool water.



Font-Ribera, L., Kogevinas, M., Zock, J.-P., Gómez, F. P., Barreiro, E., Nieuwenhuijsen, M. J., Fernandez, P., Lourencetti, C., Pérez-Olabarría, M., Bustamante, M., Marcos, R., Grimalt, J. O., & Villanueva, C. M. (September 12, 2010). Short-term changes in respiraotry biomarkers after swimming in a chlorinated pool. Environmental Health Perspectives, on line [].

“Swimming in chlorinated pools involves exposure to disinfection by-products (DBPs) and has been associated with impaired respiratory health.” This study evaluated short-term changes in several respiratory biomarkers to explore mechanisms of potential lung damage related to swimming pool exposure. Measures were taken of lung function and biomarkers of airway inflammation (fractional exhaled nitric oxide – FeNO- and 8 cytokines and one growth factor (VEGF) in exhaled breath condensate), oxidative stress (8-isoprostane in exhaled breath condensate), and lung permeability (surfactant protein D-SPD- and the Clara cell secretory protein -CC16- in serum) in healthy non-smoking adults (N = 48) before and after swimming for 40 minutes in a chlorinated indoor swimming pool. The investigators measured trihalomethanes in exhaled breath as a marker of individual exposure to disinfection by-products. Energy expenditure during swimming, atopy, and CC16 genotype (rs3741240) were also determined.


Median serum CC16 levels increased from 6.01 to 6.21 ug/L (~ 3.3%), regardless of atopic status and CC16 genotype. This increase was explained both by energy expenditure and different markers of disinfection by-products exposure in multivariate models. FeNO was unchanged overall but tended to decrease among atopics. No significant changes in lung function, SP-D, 8-isoprostane, 8 cytokines, and VEGF were found.


Implication. A slight increase in serum CC16, a marker of lung epithelium permeability [an increase in the likelihood that toxins could enter through the lungs], was detected in healthy adults after swimming in an indoor chlorinated pool. Exercise and disinfection by-products exposure explained this association, without involving inflammatory mechanisms.



Richardson, S. D., DeMarini, D. M., Kogevinas, M., Fernandez, P., Marco, E., Lourencetti, C., Ballesté, C., Heederik, D., Meliefste, K., McKague, A. B., Marcos, R., Font-Ribera, L., Grimalt, J. O., & Villanueva, C. M. (September 12, 2010). What’s in the pool? A comprehensive identification of disinfection by-products and assessment of mutagenicity of chlorinated and brominated swimming pool water. Environmental Health Perspectives, on line [].

“Swimming pool disinfectants and disinfection by-products (DBPs) have been linked to human health effects, including asthma and bladder cancer, but no studies have provided a comprehensive identification of disinfection by-products in the water and related that to mutagenicity.” This study conducted a comprehensive identification of disinfection by-products and disinfectant species in waters from public swimming pools that disinfect with either chlorine or bromine in Barcelona, Catalonia, Spain.


Gas chromatography/mass spectrometry was used to measure trihalomines in water and gas chromatography with electron capture detection was used for air. Low and high resolution Gas chromatography/mass spectrometry was used to comprehensively identify disinfection by-products. Photometry was used to measure disinfectant species (free chlorine, monochloroamine, dichloramine, and trichloramine) in the waters, and an ion chromatography method was used to measure trichloramine in air. We assessed mutagenicity in the Salmonella mutagenicity assay was assessed.


More than 100 disinfection by-products were identified, including many nitrogen-containing disinfection by-products that were likely formed from nitrogen-containing precursors from human inputs, such as urine, sweat, and skin cells. Many disinfection by-products were new and had not been reported previously in either swimming pool or drinking waters. Bromoform levels were greater in the brominated vs. chlorinated pool waters, but many brominated disinfection by-products were also identified in the chlorinated waters. The pool waters were mutagenic at levels similar to that of drinking water.


Implication. This study discovered many new disinfection by-products not identified previously in swimming pool or drinking water and found that swimming pool waters are as mutagenic as typical drinking waters. [The greater exposure to swimming pool water in serious competitive swimmers could increase these toxins to dangerous levels. That is what separates swimming from drinking water.]



Cantor, K., Villanueva, C. M., Silverman, D. T., Figueroa, J. D., Real, F. X., Garcia-Closas, M., Malats, N., Chanock, S., Yeager, M., Tardon, A., Garcia-Closas, R., Serra, C., Carrato, A., Castano-Vinyals, G., Samanic, C., Rothman, N., Kogevinas, M. (September 12, 2010). Polymorphisms in GSTT1, GSTZ1, and CYP2E1, disinfection by-products, and risk of bladder cancer in Spain. Environmental Health Perspectives, on line [].

“Bladder cancer has been linked with long-term exposure to disinfection by-products (DBPs) in drinking water.” This study investigated the combined influence of disinfection by-products exposure and polymorphisms in genes (GSTT1, GSTZ1, CYP2E1) in the metabolic pathways of selected by-products on bladder cancer in a hospital-based case-control study in Spain.


Average trihalomine exposures (trihalomines are a surrogate for disinfection by-products), from age 15 were estimated for each S based on residential history and information on municipal water sources among 680 cases and 714 controls. Effects of trihalomines and GSTT1, GSTZ1, and CYP2E1 polymorphisms on bladder cancer were estimated using adjusted logistic regression models with and without interaction terms.


Trihalomine exposure was positively associated with bladder cancer. Associations between trihalomines and bladder cancer were stronger among Ss that were GSTT1 +/+ or +/- versus GSTT1-null, GSTZ1 rs1046428 CT/TT versus CC, and CYP2E1 rs2031920 CC versus CT/TT. Among the 195 cases and 192 controls with high risk forms of GSTT1 and GSTZ1 the odds ratios for quartiles 2, 3, and 4 of trihalomines were ~1.5, ~3.4, and ~5.9.


Implication. Polymorphisms in key metabolizing enzymes modified the disinfection by-products-associated bladder cancer risk. The consistency of these findings with experimental observations of GSTT1, GSTZ1, and CYP2E1 activity strengthens the hypothesis that disinfection by-products cause bladder cancer and suggests possible mechanisms as well as the classes of compounds likely to be implicated. [The greater exposure of serious competitive swimmers to these modifications is the reason for training in chlorinated pools being deemed dangerous.]


  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. It now appears that some cancer-risks are more likely because of increased exposures to chlorinated pools.

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

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