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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.
  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.]


Päivinen, M. K., Putus, T., Kallliokoski, P, & Tikkanen, H. O. (2010). Respiratory symptoms, airways obstruction, and inflammation in competitive swimmers. Presentation 806 at the 2010 Annual Meeting of the American College of Sports Medicine, Baltimore, Maryland; June 2-5.

This study evaluated the prevalence of asthma, allergy, airways infections, and reported respiratory symptoms and combinations of these with measurements of swimming environment conditions, spirometry, and airways inflammation in elite competitive swimmers (M = 53; F = 47). Ss completed a questionnaire and were tested with flow-volume spirometry and exhaled nitric oxide.

The prevalence of physician diagnosed asthma and allergy was 25% (males) and 30% (females). Family history of asthma was reported by 23%, family history of allergy was 58%, and airways infection, sinusitis, or bronchitis was reported by 31%. Spirometry was normal in 85% of the Ss, but 15% had a finding suggesting airways obstruction. Prevalence of respiratory symptoms was 46%. Only 9 out of 46 symptomatic swimmers had obstruction. However, 37 out of 46 symptomatic swimmers had normal spirometry. The most significant risk factors for respiratory symptoms in swimming were asthma, allergies, airways infections, and family history of both asthma and allergy. Exposure to a swimming pool environment and findings in spirometry or exhaled nitric oxide were not associated with reported symptoms. Half of the swimmers with obstruction reported no symptoms at all and only one had an elevated exhaled nitric oxide level. All the swimmers with obstruction had asthma diagnosed or a family history of asthma.

Implication. Asthma, allergy, family history of both asthma and allergy, and airways infections are significant risk factors for respiratory symptoms in swimming. No association with environmental factors was observed. Screening of respiratory health is recommended for swimmers with asthma and a family history of asthma.


  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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Selected Replies and Comments (May 30, 1999)

A number of replies and comments about this problem were received from coaches from four countries. The general impressions of these inputs were as follows.

  1. Teams who train part of the year indoors and the other outdoors, have some swimmers and coaches who suffer respiratory problems while indoors but those problems disappear when they revert to an outdoor pool.
  2. Some swimmers are diagnosed with respiratory problems when indoors and use respiratory medications during practice. However, when they go outdoors the use of medications drops off markedly.
  3. Some swimmers who only train indoors in chlorinated pools become so ill that they no longer can compete or train effectively. They are chronically ill.
  4. Coaches are just as susceptible to chlorine toxicity indoors as are swimmers and suffer similar respiratory problems but also have their voice altered and cough more noticeably.
  5. Ozone water-treatment systems alleviate the chlorine-related problems in both coaches and swimmers.

January 27, 2000

From Edward P. Mjolsnes, P.E.
EMDS/Consulting Engineers
Anchorage, Alaska

"Ozone vs Chlorine

Over the past couple of decades the technology for ozone application in the areas of sanitizing liquid streams has made tremendous strides, both in effectiveness and cost reduction (installation and operating). There is a movement from chlorine usage to ozone application in both the municipal water supply and waste water treatment areas. The known hazards with the use of chlorine dictate the pursuit of other methods of achieving the same sanitizing results.

It is getting to the point that the trade-offs between ozone and chlorine for indoor swimming pool design is such that ozone is becoming the more economical. When you consider the economics and the health/safety issues it is getting to the point that some of us in the engineering field are saying that the failure to use both air to air heat exchangers and ozone in an indoor pool design constitutes 'professional negligence.' "

[Contact a local Mechanical Engineering Consultant for assistance in obtaining information on heat exchangers for heating indoor pool air and ozone sanitizing.]

April 12, 1999

From Dr. Larry Weisenthal, noted pathologist, oncologist, avid swimmer, and student of swimming, from Huntington Beach, California.

I have a study somewhere that examined the concentration of trihalomethanes in the zone immediately above the water, where the swimmer breathes. There was, I recall, a strong gradient, with very high levels in the breathing zone.

Our local swim club, which trains in a community college pool, used to have a number of kids with inhalers at the end of their lanes to treat their asthma. Two years ago, the college converted the pool to an ozone water disinfection system. Chlorine concentrations in the water are much lower, the pool is a joy in which to swim; the water "tastes" wonderfully clean and fresh, almost like a clean lake. There is little or no chlorine residue on the skin. The remarkable occurrence was that, after the pool was ozonated, every single one of the inhalers disappeared. They were no longer needed. Nine months later, a nationally ranked swimmer who made finals in several events in the 1997 Pan Pacs, transferred to our club. She had inhaler-dependent asthma. To her parent I predicted she would no longer require her medications after a couple of months in our pool. My prediction was correct.

I later learned that the Santa Barbara Swim Club trains out of two pools -- one chlorinated and the other ozonated. A number of swimmers training in the former pool require inhalers while there are none at the latter. When I discussed this on the Internet, I received a communication from Massachusetts, in which the respondent described the reverse of my own club's situation: they switched from ozone to conventional chlorine. They also had the emergence of new inhalers at the ends of lanes where they were previously not to be found.

So I think that the high incidence of asthma in swimmers is iatrogenic, rather than resulting from selection, or gravitation to the sport by asthmatics who find swimming to be less problematic for their asthma than they find land sports. Ironically, I believe that swimming in conventional chlorinated pool exacerbates exercise-related asthma, rather than diminishes it. So the answer is not necessarily with ventilation, although good ventilation is desirable for many other reasons, but with reducing the concentrations of halogenated organics in pool water through replacement of chlorine disinfection with alternatives. Ozone seems to be a desirable replacement

AN EXCHANGE -- July12, 1999


I have read with interest your papers discussing the quality of air in indoor heated swimming pools, a subject that is close to my heart at the moment. I am a member of the committee at the ------- Amateur Swimming Club, South Australia and we are having many problems with pool vapours during the southern hemisphere winter.

Reading the articles on your web site was like turning on the light in an otherwise dark (information) world. I have been having a hell of a time convincing local authorities that the swimming conditions at our pool during winter are becoming unhealthy for our young and old swimmers alike. Many times during our evening swimming sessions, swimmers have to stop mid-stroke to cough and splutter for oxygen. These children and adults are not asthmatics nor do they have any history of breathing difficulties. As a concerned parent, I have demanded that the sliding doors that surround our pool be opened by pool staff when the pool vapours are present. This temporary measure has met with resistance and has been stifled by the "pool bureaucrats" who insist that opening the doors raises the heating costs and sends learn-to-swim parents away from the pool in their droves affecting revenue. What do you suggest we do about this problem?

We have enlisted the assistance of a "pool consultant" but as yet his findings are inconclusive other than his statement that "breathing in chloramine vapour is not harmful to your health". Is this in fact true and has it been empirically tested?


I know the problem you are having with that quaint individual, the Australian facility supervisor. Your story is very similar to the Carlile experience at Narrabeen that eventually led to the termination of the careers of at least two top swimmers.

See if a lawsuit is possible? The endangerment of children's health in chlorinated environments is important. It is stupid for someone to say, "breathing in chloramine vapour is not harmful to your health." If it were not there would be no need for pool atmosphere standards.

The problem is that standards are developed for inactive individuals in a static environment. When individuals become active and the environment becomes turbulent (water is churned and the air circulates to produce a "toxic build-up") the poisoning is much worse. As you have pointed out the only solution in your situation is to reduce the irritation to breathing -- flushing the air as much as possible by diluting and/or removing it with "clean" air. At least that should reduce the toxicity.

COMMUNICATION -- December 25, 2000

I was reading the articles regarding chlorine effects with great interest. I realize that this was with acceptable levels of chlorine and how serious the effects are. I was exposed to a high concentration last year when I opened a poorly ventilated pool in which the chorine had built up overnight to about a level 10. I now have severe asthma and my doctor is not too forthcoming about what I can expect in the future. All I know is right now I can't work in indoor pools for the winter as I am super sensitive to chlorine (as you can imagine) and there are no ozone pools in my area. It has been heartbreaking to have to quit swimming, teaching, and coaching since the summer ended.

I am glad that I found your article. My brother is on the board at the YMCA where my accident happened. I have been trying to get across to them the importance of repairing their ventilation system before this happens to someone else. Maybe this article will help.

Thanks, BP


BP: Thanks for this. I do not know of any other references other than those I have in the SSJ. I am personally convinced that the reason so many swimmers have to use VENTOLIN is because of chlorine poisoning. I believe there is another alternative water treatment using hydrogen peroxide. With it, chlorine is still used at a concentration of .5, not the 3+ that seems to be prevalent today. Do you know that in the "old" days, the standard used to be .5 in indoor pools, and we never had respiratory problems? Since the concentration has risen so much, so have the respiratory problems.


June 2, 2003

It is good that there is finally some serious attention being paid (research-wise) to this obvious association.

After many years of training, my older (college-bound) daughter developed rather severe asthma (the real thing, with markedly elevated IgE levels and obstructive airway disease documented by spirometry and the need to take daily glucocorticoids, as well as bronchodilators, with asthma attacks occuring even on dry land, in the middle of the night, etc). She spent a "gap year" training at the British National "High Performance Training Centre" at the U of Bath, but then developed a severe shoulder injury in January, during a three week training trip in Australia. So she was out of the water between late January and just one week ago. Two weeks out of the water, she stopped taking all her meds and has not had a single episode of symptomatic airway obstruction or coughing ever since.

I am not, however, expecting this happy state of affairs to last, as she gets back intro training and especially when she goes to college in September and does all her training in indoor pools.

Even with the outdoor pools, it is very interesting. Most of her training (when she became frankly asthmatic) was in a college 65 meter outdoor pool, a beautiful facility with high gutters, which trapped the above water air and contained it, particularly in the morning workouts, occurring between 5 and 7 AM, when there is very little wind. I am pretty certain that there are more problems in such pools than in pools (for example, the "combat training tank" at the US Naval station down in San Diego (a very nice 25 meter by 50 meter pool with an underwater viewing tunnel...I'm guessing that you've been there) in which the water line is flush with the pool deck.


Anonymous Email; June, 2003

My daughter, a college swimmer, was diagnosed with laryngeal dyskinesia, which is brought on in pools with high chlorine levels. This condition is sometimes diagnosed as asthma. I was wondering if some other swimmers might have this condition?


Dear Dr.Rushall:

I am a Professor of Environmental Sciences and currently visiting San Diego. In the recent edition of the San Diego Union-Tribune (22 July, 2003), I saw the reference to your work on asthma and its relation to chlorinated water in swimming pools. I have observed this effect in so many children in India as we use excess of chlorine in our swimming pools.

I saw the clinching evidence last weekend. My nephew came from San Jose to see me in San Diego. He has a long history of asthma but has been normal over the last couple of years. He went swimming in a pool in San Diego where the water was chlorinated heavily. He enjoyed the swimming but that night he had a severe attack of asthma. Everybody suggested many reasons for the attack, but I am convinced it was due to the swimming pool water and chlorine. Few believed this explanation. However, because of today's paper and the story about "asthma" and chlorinated pools, everybody now accepts my theory/reason for the asthmatic attack.

I return to India shortly. I will plan a systematic study to evaluate more effects on children with a history of asthma as well as the relation of "swimmer's asthma" to chlorinated water. I will inform you of any significant observation I discover.

Best wishes,

Ashok Ghosh
Professor IC, Dept.of Environment and water Management
ANC.Magadh University, Patna - 800013, India


The World Today - Thursday, 29 May , 2003

HAMISH ROBERTSON: A new report has found that chlorine used to disinfect indoor swimming pools can increase the risk of asthma in children. The problem is caused by a gas that's formed when the chlorine mixes with urine or sweat from swimmers using the pool. The study, by Belgian scientists, has sparked concern among asthma organisations, which encourage children to swim as a way of controlling the disease.

Paula Kruger reports.

PAULA KRUGER: Swimming has long been promoted as the best form of exercise for young asthma sufferers. It is less likely than other aerobic activity to dry out the lungs and spark an attack.

But a new study by Belgian Scientists has found children using indoor swimming pools could be a greater risk from the disease. The research looked at the gas trichloramine, which is produced when chlorine in swimming pools mixes with urine, sweat and other human organic matter.

It found the gas increased the body's levels of certain proteins that can attack the lining of the lungs, making a person more prone to allergies and asthma. Australian asthma specialists say the dangers of chloramines have been know for some time.

Professor Charles Mitchell is a respiratory physician and member of the National Asthma Council.

CHARLES MITCHELL: Chlorine itself is an irritant, and in people with asthma, bad asthma, it can precipitate an attack. But the major concern is where chlorine combines with other organic material from sweat and particularly from urine to form chloramines, which are very potent irritants, and they have been known to actually cause asthma in workers working in an enclosed environment, in swimming pools.

PAULA KRUGER: Australian scientists are still analyzing the results of the Belgian study, but say it could expand our understanding of how chloramines affect the body.

But Professor Charles Mitchell says he still believes swimming is the best form of exercise for asthma sufferers.

CHARLES MITCHELL: So this now means that operators of swimming pools have to start to worry about not only the levels of chlorine in the water, in order to keep the water clean, but also to make sure that the area around swimming pools are adequately ventilated to keep chloramine levels down to acceptably low levels.

PAULA KRUGER: Asthma organizations say they are concerned about the findings of the report and are already monitoring the effect swimming in indoor swimming pools could have on children with asthma.

Suzie Lough is an education officer from the Asthma Foundation of New South Wales.

SUZIE LOUGH: Well we do know that chlorine can be an irritant to some people, and we do run a swimming program and with that we monitor our children very, very closely. We have stringent procedures in place for the pools for the programs and we make sure that the children have measurements before they go into the pool and after they come out of the pool.

PAULA KRUGER: The Asthma Foundation says it will review its swimming programs if they are proved to be unsafe for children suffering the disease.

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[The full text of the article, A report of the advantages of using a dual stage method of sanitation, that supports the contentions of this brief summary is available at:]

Chlorine is a deficient method of pool sanitation. Chlorine concentrations decline very quickly under a variety of swimming pool and environmental conditions. To combat the decline in effectiveness problem with chlorine alone, pool managers often over-chlorinate a pool (>3 ppm) to offset chlorine reduction. It is that heightened concentration that leads to excessive absorption through the skin and inspiration that leads to breathing problems in many swimmers.

The referenced article provides evidence that allows pool sanitation to remain at a high level of effectiveness while the level of chlorine is reduced, probably to a non-toxic level. The solution involves mixing silver and copper ions with reduced levels of chlorine.

Silver and copper attack and kill bacteria and viruses more effectively than chlorine. When added to lower than customary levels of chlorine (~.05 ppm), an extremely effective sanitation of swimming pools results. It is a better sanitation combination than chlorine alone.

Implication. Pool sanitation is improved when copper and silver ions are mixed with low levels of chlorine. This "dual method" is easy to implement and is within all known health laws. The potential to cause "swimmer's asthma" is likely to be reduced or eradicated.


A proposal by Richard Falk (December 21, 2009)

The possibility of using a small amount of cyanuric acid in indoor pools, probably not more than 20 ppm CYA with 4 ppm free chlorine (since one wants some reasonable oxidation capability), is proposed. In high bather load situations, supplemental oxidation is strongly recommended.

To read the full proposal click on this link and it will be downloaded to your computer in pdf file format.


Rushall, B. S. (September 18, 2005). Comparisons of Chlorine and MIOX Treated Pool Water. Consultant's Report.


To view the full Rushall article in .pdf format click on this link


Bradford, W. L., & Dempsey, R. (June 17, 2005). OBSERVATIONS ON THE USE OF MIXED OXIDANTS IN SWIMMING POOLS: Mechanisms for Lack of Swimmer’s Complaints in the Presence of a Persistent Combined Chlorine Measurement. Consultant's Report.

[Wesley L. Bradford, Ph.D., Los Alamos Technical Associates, Inc., Los Alamos, NM and Chief Scientist, Product Development for MIOX Corporation, Albuquerque, NM, and Rick Dempsey, President, Simply Water, LLC, Houston, TX]


Evidence from reports in the technical literature, laboratory research, and operational experience with the MIOX mixed-oxidant solution (MOS) in swimming pool water strongly indicates that MOS causes steady oxidation of organic nitrogen compounds and organic chloramines, and rapid completion of the breakpoint reaction on inorganic –N– fragments from that oxidation rather than allowing accumulation of them (including volatile NHCl2 and NCl3) in the pool water, as is likely the case using chlorine (to wit, the common swimmer's complaints of "chlorinous" odors and burning eyes when bleach/hypochlorite is used for disinfection). This steady removal of organic nitrogen and rapid completion of the breakpoint reaction would be expected to cause the following beneficial effects, as have been noted by swimmers in and operators of virtually all pools using MOS as a replacement for chlorine for disinfection:

Better disinfection, although not as yet studied directly in pools, is also expected because: 1) the MOS has been shown in numerous studies to be a better disinfectant than chlorine alone; and 2) the bulk of the disinfection residual in the pool water is present as FAC not the combined chlorines (chloramines as both inorganic and organic).

Studies recently completed on two MOS-treated pools revealed three striking features:

  1. Nitrate expressed as nitrogen (NO3 - -N) concentrations do NOT accumulate in the MOS-treated pool waters, in contrast to literature reports on bleach-treated pools. This observation suggests a chemical mechanism for the degradation of organic nitrogen compounds by MOS that is different from that of bleach;
  2. The accumulated Total Organic Carbon (TOC) concentrations from the Body Fluid Analog (BFA) added continuously by bathers are MUCH lower than those reported in the literature for bleach-treated pools; and
  3. The cause for persistent positive biases in the Combined Chlorine (CC) measurements, which are observed in some MOS-treated pools, is most likely slow degradation of some organic nitrogen (organic–N) components of the BFA. This results in small concentrations being observed (in the Total Kjeldahl Nitrogen analysis) at any time, and formation of organic chloramines – a persistent CC measurement arising from this mechanism is equivalent to a "nuisance residual".

To view the full Bradford and Dempsey article in .pdf format click on this link

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[June, 2001]

[Adapted from a publication of the Amateur Swimming Association of Great Britain]


One in seven children and one in twenty-five adults in Great Britain have asthma and the number is growing. Thus, every swim squad or club will have a number of asthmatics. It is important for coaches and club officials to have at least a basic knowledge of the condition.

Asthma is a disorder of the small airways of the lungs, which become sensitive to certain triggers, leading to their narrowing when they become inflamed. This results in the child or adult becoming wheezy, short of breath, or coughing. The underlying causes are partly genetic and partly environmental.

The triggers vary from patient to patient but often include colds and viral infections, pollens and moulds, pets, dust, tobacco smoke, emotion and stress, cold air and some medications, such as aspirin. Unfortunately for swimmers, chlorine can also be a trigger. Some people's airways narrow during exercise. This is known as EIA or exercise-induced asthma, which typically appears after 5-10 minutes of a training session.

However, swimming is a sport in which asthmatics can and often do excel, as the warm moist air of the indoor pool doesn't trigger an attack. Some members of the current British team have asthma and at least six Olympic Gold medallists in the aquatic events have been sufferers.

How is it diagnosed?

By asking a person to breathe as hard as they can into a meter, it is possible to measure how quickly they can expel air from their lungs. This is known as a "peak flow test". By relating this information to an individual's age and height, it can be determined if a person is asthmatic. Diagnosis is confirmed if after exercise or treatment by inhaler, there is a 15% variation from the person's optimum or "predicted" peak flow. People can also detect such variations themselves by carrying out regular peak flow tests and maintaining a record of test results.


Once asthma has been diagnosed, it is mandatory that the swimmer or his/her parents or coach declares this to the governing swimming association together with details of prescribed medications. This is essential to avoid violating Doping Control rules. Notification of the condition and treatments must be done annually. Any subsequent changes in medication should be indicated.

Remember: it is a swimmer's responsibility to keep the swimming association informed.

How is the condition managed?

Modern management of asthma is a shared-care process with the patient taking some responsibility for the condition in conjunction with the general practitioner. Nurse-led asthma clinics at most G.P. surgeries help to maintain good control, check inhaler technique, and monitor progress. The peak flow meter, which every asthmatic should have, is the cornerstone of management. This measures the performance of the lungs and if charted gives a clear idea of the effectiveness of attempted control. The peak flow reading varies with the age, sex, and height of the patient. It can also be calculated from charts. Each asthma sufferer should know their optimum reading and have a self-management plan.

Types of treatment

There are two types of medication to treat asthma: relievers and preventers. Both are inhalers and they are color coded to help identification. There has been a move to CFC inhalers over the last two years.

  1. Relievers: Inhalers are color-coded blue - e.g. salbutamol (Ventolin). They work to open the airways. They are also known as bronchodilators (or beta-2 agonists). These are mostly used after symptoms appear but sometimes give brief protection against triggers such as exercise. It is important NOT to exceed the maximum dose of two puffs four times daily.
  2. Preventers: If taken regularly, these can prevent an asthma attack occurring. They protect the lining of the airways and make them less likely to narrow when triggered. There are two main types: -

Preventers should not be used for treating an acute attack, as they do not bring immediate relief. They can take about 14 days to be fully effective if taken regularly.

Other long acting inhalers and oral tablets form a second line treatment if the above do not adequately control the condition.

The Step Care approach to treatment

The current treatment of asthma follows guidelines laid down by the British Thoracic Association. They take the form of a step care plan now known as the British Guidelines for the Management of Asthma. This involves stepping up the level of treatment until satisfactory control is achieved. It is important not to over-treat. Stepping down is just as important if the asthma is well controlled.

Step 1. Use an inhaled short acting bronchodilator (e.g., salbutamol) for symptom relief up to once or twice daily. If you need more than this, move to step 2.

Step 2. Use an inhaled short-acting bronchodilator for symptom relief plus a regular low dose inhaled steroid twice daily (e.g., beclomethasone, or in some cases the regular preventer cromoglycate).

Step 3. Use an inhaled short acting bronchodilator for symptom relief plus either a regular high dose inhaled steroid via a large volume spacer, or low dose steroids and a long acting bronchodilator.

For patients who present more of a management problem, two higher steps are available. It is also worthwhile for all asthma sufferers to have a flu vaccine.

Which drugs are legal and which illegal?

The rescue inhalers such as salbutamol (Ventolin) and terbutaline (Bricanyl) are permitted substances under ASA and FINA law as are the common steroid based inhalers such as beclomethasone (Pecotide), budenoside (Pulmicort) and fluticasone (Flixotide).

The preventative inhaler cromoglycate (Intal) can be used legally as can the recently introduced oral leukotrine antagonists such as montelukast (Singulair) and salmeterol (Serevent) inhalers.

However for the competitive swimmer, salbutamol tablets are NOT permitted and the older inhalers (although very rarely used) such as isoprenaline, ephedrine, orciprenaline are banned.

Sometimes a short course of oral corticosteroid drugs is necessary to bring the asthma under control. If this is the case, the swimmer must not compete until at least two weeks after the course has finished.

The reason why declaration of asthma is essential is that the beta-agonists and steroid drugs may enhance performance (by stimulatory and anabolic effects on the body) if used by an athlete without asthma.

The Medical Commission of the International Olympic Committee has recently toughened its stance against the misuse of asthma medication. In the future, Olympic athletes seeking authorization to use asthma medication during an Olympic Games will be required to produce clinical and laboratory proof of their ailment.

When tested at doping control you must declare the asthma medication you are taking.

Never let another swimmer use your inhaler for fun. Believe it or not, this does happen sometimes and the consequences can be extremely serious.

List of Asthma Drugs that are permitted in Sport

There is a maximum permitted level of salbutamol. The recommended dosage of the salbutamol inhaler is two puffs four times daily and must not be exceeded.

What delivery devices are available?

A number of delivery systems are available to meet individual requirements. The commonest are simple meter dose aerosol inhalers but there are also breath-activated inhalers and ones that employ dry powders. The aerosols are currently being switched to CFC. with new propellants to avoid damaging the ozone layer. For younger patients or people who have trouble getting on with inhalers or higher dose steroid the dose can be given via a spacer device (large chamber - volumatic).

How do you know if the asthma is not well controlled?

Measuring the peak flow is one of the best ways of determining good control. Detection of a lower than optimum level or a declining level should prompt an active review of treatment. The swimmer may complain of nighttime coughing or wheezing or may have to get out of a training session due to wheezing, coughing, or shortness of breath.

When should the swimmer take their inhaler relative to training or an event?

The relief inhaler (e.g. salbutamol or Ventolin) should be taken if necessary between 15 and 30 minutes before training or competing to allow maximum time to work properly. One to two puffs is particularly useful in those patients who suffer from exercise induced asthma. A swimmer should not keep getting in and out of the water during a training session for a quick puff of their inhaler. Coaches should actively discourage this habit. This usually means that the asthma is not well controlled and the treatment needs to be reviewed. A swimmer's "rescue" inhaler should always be ready at hand in case it is needed. Swimmers should never share inhalers.

What to do if a swimmer has an asthmatic attack in the water.

The swimmer concerned should be removed immediately from the water. The swimmer should be reassured and calmed, advised not to hyperventilate and given one to two puffs of their usual rescue inhaler. If there is no reaction after 10 minutes this can be repeated. If, after this has been done, the swimmer is still distressed, unduly short of breath, has a rapid pulse or respiratory rate, or is blue (cyanosed), medical help should be sort urgently and if necessary an ambulance called. If available, oxygen can be given whilst awaiting help.

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