A number of my patients are competitive swimmers. Every winter, many of them tell me “there is this certain indoor pool that really bothers my lungs. But when I swim in the summer in an outdoor pool, I feel fine.” Is this a biologically-supported phenomenon? Or is it a reflection of the general depression that many Chicagoland people feel with our winter season of cold, bleak days with all-too-little sunshine? There is a body of research on this topic and it is very interesting.
In the case of elite swimmers, who can spend up to 40 hours per week swimming, there is ample evidence for airway inflammation (involving a mix of different types of white blood cells called eosinophils and neutrophils) and airway hyperresponsiveness. While the rate of asthma in the general population is under 10%, the risk of asthma is especially increased among competitive swimmers, of whom 36% to 79% show bronchial hyperresponsiveness to methacholine or histamine (this hyperresponsiveness suggests, but does not prove, that these individuals have asthma). In swimmers, the risk of asthma is closely associated with allergy and its severity.
In one study, 23 elite swimmers were compared to age-matched mild asthmatics and to non-asthmatics. The elite swimmers had increased airway mucosa eosinophilia and mast cell counts than controls (in other words, there were increased counts of inflammatory cells in the inner surfaces of the lungs). They also had more goblet cell hyperplasia and higher mucin expression (which indicates a type of inflammation) than the mild asthmatics or non-asthmatics. Swimmers also had more submucosal type I and III collagen expression and tenascin deposition (which indicates that there was some structural “hardening” of the lungs). However, exhaled nitric oxide (which indicates inflammation) and airway responsiveness to methacholine or eucapnic voluntary hyperpnea challenge (these are methods used to determine if someone’s lungs are hypersensitive, which would be typical for asthma) did NOT correlate with these inflammatory and remodeling changes. Therefore, as the authors concluded, intense, long-term swim training in indoor chlorinated pools is associated with airway changes similar to those seen in mild asthma, but with higher mucin expression. But these changes were independent from airway hyperresponsiveness.
A study from 2009 included 32 swimmers, 32 cold-air athletes, 32 mild asthmatics, and 32 non-asthmatics. 69% of swimmers and 28% of cold-air athletes had airway hyperresponsiveness. Sputum neutrophil count correlated with the number of training hours per week in both swimmers and cold-air athletes. Eosinophil counts, in sputum, were higher in swimmers than non-asthmatics, but lower than in asthmatic subjects. These eosinophil counts correlated with airway hyperresponsiveness only in swimmers. Finally, bronchial epithelial cell count was not correlated with airway hyperresponsiveness but was significantly increased in swimmers (the finding of elevated bronchial epithelial cells in sputum suggests that the inner surfaces of the lungs had been injured and were “shedding” these cells).
Another study included 16 adult elite swimmers and 33 adolescent elite swimmers. 8 (50%) of the adult elite swimmers were found to have bronchial hyperresponsiveness. The adolescent elite swimmers were compared to asthmatic adolescents and unselected adolescents. The author found no differences in the prevalence of airway hyperresponsiveness among the three adolescent groups. Furthermore, there were no differences among the three adolescent groups in measures of inflammation, such as exhaled nitric oxide, pH of exhaled breath condensate, or the cellular composition of the sputum. Therefore, the author concluded that there was a high prevalence of airway hyperresponsiveness among adult elite swimmers, but neither an increase in airway hyperresponsiveness nor measures of inflammation in adolescent elite swimmers. These findings appear to suggest that airway hyperresponsiveness among swimmers only starts to occur after a certain number of years or volume of exposure to chlorinated pools.
There was another study published that appeared to show that the potentially damaging effects of swimming in chlorinated pools can be reversible. In this study, 42 elite swimmers were followed for 5 years prospectively. 16 had continued to compete at the endpoint at 5 years, but 26 had stopped competing for more than 3 months before the endpoint. Bronchial hyperresponsiveness was measured with testing to inhaled histamine. This bronchial hyperresponsiveness was increased in 7 (44%) of ongoing swimmers at baseline and 8 (50%) of these swimmers at the endpoint. In contrast, bronchial hyperresponsiveness was increased in 8 (31%) at baseline of the swimmers who later stopped competing and just 3 (12%) of these swimmers at the endpoint. This is a statistically significant difference in bronchial hyperresponsiveness between the ongoing swimmers and past competitors (it should be pointed out, of course, that just because the second cohort was no longer competing, this did not mean that they stopped swimming altogether). Current asthma, which was defined as bronchial hyperresponsiveness along with exercise-induced bronchial symptoms, was observed in 5 (31%) of the ongoing swimmers at baseline and 7 (44%) at the endpoint. In contrast, of the past competitors, asthma was observed in 6 (23%) at baseline and 1 (4%) at the endpoint. This was also a statistically significant difference between these groups. Also of interest, the sputum counts of eosinophils increased significantly at the endpoint for active swimmers, but dropped (although the change did not reach statistical significance) in past competitors at the endpoint. However, the sputum eosinophil counts did differ, with statistical significance, between the two groups at the endpoint. The authors concluded that bronchial hyperresponsiveness and asthma attenuated or even disappeared once swimmers stopped competing. This suggests that “swimmers’ asthma” has some reversibility. However, eosinophilic airway inflammation appeared to worsen among swimmers who continued to compete.
Pharmacologic management of asthma associated with exercise, such as swimming, can be difficult. Bronchospasm associated with exercise can be prevented or reduced with premedication with inhaled beta-2 agonists (like albuterol). However, in asthma associated with exercise, preventative maintenance medications, such as inhaled corticosteroids and oral leukotriene antagonists, have been less effective than anticipated to treat airway inflammation, bronchial hyperresponsiveness, and symptoms. Because it is difficult to change the “natural course” of asthma in athletes by anti-inflammatory treatments, some authors have suggested switching training to less irritating environments.
So, competitive swimmers, should you get out of the pool?
One important consideration is assigning causality. Just because rates of bronchial hyperreactivity and asthma are elevated in competitive swimmers, is this proof that chlorinated water is the cause? The thinking surrounding this concept is that competitive swimmers can get a form of irritant asthma due to exposure to large quantities of chlorine by-products. Since ventilation in adults who are swimming competitively can increase up to up to 200 L/min, this can lead to aspiration of water droplets and inhalation of large amounts of air floating just above the water surface and, therefore, rich in chlorine by-products. This, aspiration can, in turn, lead to lung damage and respiratory symptoms. This model is further supported by the evidence that inhalation of chlorine, in pool-related accidents involving over-chlorination, can lead to damage of the lungs that can take months to heal.
However, while one line of thinking approaches chlorinated pools as a source of damage to the lungs, another line of thinking is quite different. To quote Uyan et al in a recent review on this subject “swimming is recommended as one of the most appropriate sports in asthmatic children since the humid environment of the swimming pool is considered protective against exercise-induced bronchoconstriction.” In fact, there are several studies that have shown improvement in asthma in children who swim.
My interpretation of the current evidence is that swimming, like other exercise, when directed and monitored by a health care provider as part of a fitness program, is probably helpful for most people with asthma. However, chlorine can cause respiratory damage and, if inhaled in large quantities, such as in the case of an elite swimmer, probably does cause such damage. This respiratory damage, represented by increased levels of inflammatory cells, shedding of respiratory epithelial cells, and bronchial hyperresponsiveness, is probably not permanent, but will improve or resolve once an athlete reduces the amount of exposure he or she has to chlorinated water.
As a parting thought, consider this idea. Perhaps it is time that high-level swimming programs, including college and Olympic programs, consider replacing chlorinated pools with non-chlorinated (but more expensive) options. Maybe this will allow more elite swimmers to compete without unfair disadvantages.
Published February 23, 2015
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