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Adverse respiratory health effects of competitive swimming: the prevalence of symptoms, illnesses, and… Potts, James Edward 1994

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ADVERSE RESPIRATORY HEALTH EFFECTS OF COMPETITIVE SWIMMING:THE PREVALENCE OF SYMPTOMS, ILLNESSES, AND BRONCHIALRESPONSIVENESS TO METHACHOLINE AND EXERCISEByJAMES EDWARD POTTSB.P.E., The University of British Columbia, 1983M.P.E., The University of British Columbia, 1985A THESIS SUBMITTED IN PARTIAL FULFILLMENT OFTHE REQUIREMENTS FOR THE DEGREE OFDOCTOR OF PHILOSOPHYinTHE FACULTY OF GRADUATE STUDIES(Department of Physiology)We accept this thesis as conf rming to the required standard:The University of British ColumbiaMay, 1994© James Edward Potts, 1994In presenting this thesis in partial fulfilment of the requirements for an advanceddegree at the University of British Columbia, I agree that the library shall make itfreely available for reference and study. I further agree that permission for extensivecopying of this thesis for scholarly purposes may be granted by the head of mydepartment or by his or her representatives. It is understood that copying orpublication of this thesis for financial gain shall not be allowed without my writtenpermission.(Signature)_________________Department of_______________The University of British ColumbiaVancouver, CanadaDate TifZ 14 jqqL}iDE-6 (2188)ABSTRACTIndoor swimming pools, with their high ambient temperatures and relative humidity,contain a number of volatile chemicals that are known irritants, sensitizing agents, and possiblecarcinogens. While swimming may improve fitness and reduce morbidity associated withasthma, there is both anecdotal and scientific information to suggest that there are health-relatedproblems associated with swimming in chemically-treated pooi water. Competitive swimmersare especially susceptible to the adverse effects of chemically-treated pooi water because of thenumber of hours they spend training in this environment and the increase in ventilation thatoccurs with exercise. While case reports of respiratory and other health-related problems arecommon, there have been no epidemiological studies that have surveyed competitive swimmersabout the prevalence of health-related problems or the prevalence and severity of clinicalsymptoms.The purpose of this study was to determine the prevalence of respiratory and other health-related symptoms, illnesses, and allergies among competitive swimmers using a questionnaire,and to establish whether the symptoms were associated with swimming-related exposure. Inorder to determine how these symptoms and illnesses manifest themselves clinically, a group oflower mainland swimmers and non-swimmers also completed pulmonary functions studies, amethacholine challenge test, and exercise studies in the laboratory and swimming pool.Our results show that competitive swimmers have a high prevalence of asthma that, innational and international level swimmers, appears to have developed after they begancompetitive swimming. There was also a high prevalence of exercise-related respiratorysymptoms that were strongly associated with swimming-related exposure. Nearly all of thecompetitive swimmers had normal pulmonary function tests, however, 60% of the swimmerswere found to have increased non-specific bronchial responsiveness (BHR) to methacholine.There was no difference in the prevalence of BHR among swimmers with or without asthmaand/or exercise-related symptoms, however, the prevalence of BHR was significantly higher inswimmers than in non-swimmers. The prevalence of exercise-induced asthma (ETA) was higherrunning or cycling in the laboratory than during tethered swimming in the pooi. There was nodifference in the prevalence of ETA among swimmers and non-swimmers during the laboratorytesting.These results suggest that swimming related exposure, as determined by the amount oftime spent swimming or the distance covered during training sessions in the swimming pool,increases non-specific bronchial responsiveness without affecting baseline pulmonary functionor short-term exercise responses. Longer exposures may lead to the development of upper andlower respiratory tract symptoms, and the adoption of a restrictive breathing pattern insusceptible individuals. We propose that differences in the clinical presentation of thesecompetitive swimmers may be dependent on the presence of atopy, underlying respiratoryillnesses such as asthma, the pre-existing level of bronchial responsiveness, and the extent of theswimming-related exposure. It is possible that chronic, low level exposure to the chemicals usedto disinfect swimming pooi water may, ultimately, be responsible for our clinical and exerciserelated findings.TABLE OF CONTENTSAbstract IIList of Tables VIList of Figures VIIIList of Abbreviations XIAcknowledgements XVIGeneral Introduction 1Chapter 1 The Prevalence of Respiratory Symptoms and Other Health-RelatedProblems in Competitive SwimmersAbstract 5Introduction 8Methods 15Results 22Discussion 46Conclusions 57References 60Chapter 2 The Prevalence of Increased Bronchial Responsiveness toMethacholine in a Select Group of Competitive Swimmersand Non-SwimmersAbstract 65Introduction 68Methods 83Results 92DiscUssion 99Conclusions 107References 109Chapter 3 The Prevalence of Exercise-Induced Asthma in a Select Groupof Competitive Swimmers and Non-SwimmersAbstract 118Introduction 121Methods 132Results 141Discussion 168Conclusions 177References 179General Summary and Conclusions 187Appendix A 194Appendix B 208LIST OF TABLESTable 1 Properties of halogenated hydrocarbons found in swimming poolwater 14Table 2 A summary of the descriptive characteristics and trainingrequirements of competitive swimmers 34Table 3 A comparison of chest illnesses reported by competitive swimmers 35Table 4 A comparison of respiratory and other health-related symptomsreported by competitive swimmers 36Table 5 Results of the univariate analysis comparing the presence ofswimming-related symptoms to the swimming-related exposure (Part I) .... 37Table 6 Results of the univariate analysis comparing the presence ofswimming-related symptoms to the swimming-related exposure (Part II)... 38Table 7 Results of the logistic regression analysis comparing each of theswimming-related symptoms to the swimmer’s age, sex, level of swimmingand swimming-related exposure (Part I) 39Table 8 Results of the logistic regression analysis comparing each of theswimming-related symptoms to the swimmer’s age, sex, level of swimmingand swimming-related exposure (Part II) 40Table 9 The prevalence of physician-diagnosed respiratory illnessesamong competitive swimmers 41Table 10 The prevalence of physician-diagnosed allergies amongcompetitive swimmers 42Table 11 A description of the smoking history of competitive swimmers 43Table 12 A comparison of prescription drug use among competitiveswimmers 44Table 13 A description of respiratory and other health-related symptomsthat competitive swimmers associate with a strong chemical odorin the swimming pool 45Table 14 A comparison of the physical characteristics of the athletesinvolved in methacholine and exercise challenge testing 94Table 15 A comparison of the environmental conditions in the laboratoryduring methacholine and exercise challenge testing 94Table 16 A comparison of the pulmonary function data collected on theathletes prior to methacholine and exercise challenge testing 95Table 17 The distribution of PC20 among the three groups of competitiveathletes 96Table 18 The mean values of the cardiorespiratory data collected duringduring the 8 minute exercise challenge test in the laboratory 143Table 19 The physical characteristics of the swimmers who participatedin the exercise challenge tests in the swimming pool 151Table 20 The mean values of the cardiorespiratory data collected duringthe 8 minute exercise challenge test in the swimming pool 152Table 21 A comparison of the environmental conditions in the laboratoryand swimming pool 157Table 22 A comparison of the cardiorespiratory data collected during thethe exercise challenge tests in the laboratory and swimming pool 158Table 23 The mean values of the cardiorespiratory data collected duringthe 45 minute exercise challenge test in the swimming pool 163Table 24 Calculation of the cumulative dose of methacholine for subjectswith asthma or symptoms suggestive of asthma while exercising 209Table 25 Calculation of the cumulative dose of methacholine for subjectswith no clinical history of asthma or symptoms suggestive ofasthma while exercising 209LIST OF FIGURESFigure 1 Calibration curves for the nebulisers used in methacholinechallenge testing 86Figure 2 A comparison of the dose-response curves for the athletesinvolved in methacholine challenge testing 97Figure 3 Individual dose-response curves for swimmers in theCase Group 97Figure 4 Individual dose-response curves for swimmers in theControl Group 98Figure 5 Individual dose-response curves for athletes in theNon-Swimming Control Group 98Figure 6 The mean heart rates of athletes involved in the8 minute exercise challenge test in the laboratory 144Figure 7 The mean yE of athletes involved in the 8 minuteexercise challenge test in the laboratory 144Figure 8 The mean VT of athletes involved in the 8 minuteexercise challenge test in the laboratory 145Figure 9 The mean respiratory frequency of athletes involvedin the 8 minute exercise challenge test in thelaboratory 145Figure 10 The mean “02 of athletes involved in the 8 minuteexercise challenge test in the laboratory 146Figure 11 The mean R of athletes involved in the 8 minuteexercise challenge test in the laboratory 146Figure 12 A comparison of the changes in FEy1 following the8 minute exercise challenge test in the laboratory 147Figure 13 The individual FEy1 plots for the Case Groupfollowing the 8 minute exercise challenge testin the laboratory 147Figure 14 The individual FEV1 plots for the Control Groupfollowing the 8 minute exercise challenge testin the laboratory 148Figure 15 The individual FEy1 plots for the Non-SwimmingControl Group following the 8 minute exercisechallenge test in the laboratory 148Figure 16 The mean heart rates of swimmers involved in the8 minute exercise challenge test in the swimming pooi 153Figure 17 The mean VE of swimmers involved in the 8 minuteexercise challenge test in the swimming pooi 153Figure 18 The mean VT of swimmers involved in the 8 minuteexercise challenge test in the swimming pooi 154Figure 19 The mean respiratory frequency of swimmers involvedin the 8 minute exercise challenge test in theswimming pool 154Figure 20 The mean V02 for swimmers involved in the 8 minuteexercise challenge test in the swimming pool 155Figure 21 The mean R for swimmers involved in the 8 minuteexercise challenge test in the swimming pool 155Figure 22 A comparison of the changes in FEV1 following the8 minute exercise challenge test in the swimming pool 156Figure 23 A comparison of heart rates during exercise challengetests in the laboratory and swimming pool 159Figure 24 A comparison of VE during exercise challenge tests inthe laboratory and swimming pool 159Figure 25 A comparison of VT during exercise challenge tests inthe laboratory and swimming pool 160Figure 26 A comparison of respiratory frequency during exercisechallenge tests in the laboratory and swimming pool 160Figure 27 A comparison of VU2 during exercise challenge tests inthe laboratory and swimming pool 161Figure 28 A comparison of R during exercise challenge tests inthe laboratory and swimming pool 161Figure 29 A comparison of the changes in FEy1 following exercisechallenge tests in the laboratory and swimming pool 162Figure 30 The mean heart rates of swimmers involved in the45 exercise challenge test in the swimming pooi 164Figure 31 The mean yE of swimmers involved in the 45 minuteexercise challenge test in the swimming pool 164Figure 32 The mean VT of swimmers involved in the 45 minuteexercise challenge test in the swimming pooi 165Figure 33 The mean respiratory frequency of swimmers involvedin the 45 minute exercise challenge test in theswimming pool 165Figure 34 The mean V02 of swimmers involved in the 45 minuteexercise challenge test in the swimming pool 166Figure 35 The mean R of swimmers involved in the 45 minuteexercise challenge test in the swimming pooi 166Figure 36 A comparison of the changes in FEy1 following the45 minute exercise challenge test in the swimmingpool 167LIST OF ABBREVIATIONSANOVA analysis of varianceATPS ambient temperature and pressure saturated with water vapourbetaBAL broncho-alveolar lavageBC British ColumbiaBHR bronchial hyperresponsivenessBTPS body temperature and pressure saturated with water vapourCA CaliforniaCCK cholecystokininCO2 carbon dioxideCOPD chronic obstructive pulmonary diseaseEIA exercise-induced asthmaCd4 carbon tetrachiorideCC13H 1,1, 1-trichioroethaneCC12HC1 trichloroethyleneCC12 tetrachioroethyleneCHBr3 bromoformCH2BrC1 bromochioromethaneCHBrC12 bromodichioromethaneCHBr21 chiorodibromomethaneCHC13 chloroformCH21 dichloromethaneCH21CH1 1 ,2-dichloroethanecm centimetresC degrees celsiusECG electrocardiographyf respiratory frequencyFEF2575 mid maximum expiratory flow rateFEy1 forced expiratory volume in 1 secondFVC forced vital capacitygm gramHOC1 hypochiorous acidHR heart rateHRF histamine releasing factorIgE immunoglobulin EIgG immunoglobulin G1gM immunoglobulin MIL IllinoisIL interleukinkg kilogramsL litresL/sec litres per secondLT leukotriennelog logarithmMETdose final cumulative dose of methacholinex meanmg milligrammicrogramsmm minutemL millilitreMMC metabolic measurement cartMN MinnesotaMO MissouriN2 nitrogenNANC non-adrenergic, non-cholinergicNC North CarolinaNCFA neutrophil chemotactic factor of anaphylaxisNH2C1 chioramideN}{C12 chiorimideNC North CarolinaNC13 chlorine azideNo. numberNO2 nitrogen dioxide02 oxygen03 ozoneOC1 hypochlorite ionON OntarioPAF platelet activating factorXIVPC20 provoking concentration of methacholine causing a 20% fall in FEV1PG prostaglandinppm parts per millionPQ Quebecprob probabilityR respiratory exchange ratioRADS reactive airways dysfunction syndromeRHL respiratory heat losstotal timeSO2 sulfur dioxideSEM standard error of the meanSVC slow vital capacitySD standard deviationTx thromboxaneUBC University of British ColumbiaUK United KingdomUS United StatesUSEPA United States Environmental Protection AgencyVCO2 carbon dioxide productionVii minute ventilationVIP vasoactive intestinal peptide‘‘max maximum expiratory flow rateV02 oxygen consumptionVO2max maximal oxygen consumptionVT tidal volumeWA WashingtonWI WisconsinXVIACKNOWLEDGEMENTSThe task of completing a doctoral thesis is not an easy one. When you attempt tocomplete an interdisciplinary thesis in an applied faculty it is even more difficult. The bestadvice I could give anyone who intends to complete such a thesis is to research their topicthoroughly and choose their research chairman and committee members judiciously! I amextremely grateful for the time and effort that my committee members were able to give me.Tn-spite of their hectic academic and clinical schedules, they always had time to discuss mythesis with me and resolve any problems that I had.I am particularly indebted to the chairman of my research committee, Dr. Sverre Vedal.More than anyone, Dr. Vedal is responsible for ensuring that this project was completed. Thankyou for your wisdom, guidance, and encouragement, but most of all, thank you for believingin me and my ability to complete this project. I am, and always will be, eternally grateful!I would like to thank Dr. Don McKenzie, Dr. Peter Pare, Dr. Gordon Pirie, and Dr. JamesFarmer for their technical advice during the planning, data collection, and writing phases of mythesis. All of your efforts are sincerely appreciated!I feel extremely fortunate to have been able to complete my doctoral studies in theDepartment of Physiology. I am indebted to all of the faculty, students, and staff for makingmy program such a positive and rewarding experience. In particular, I would like to thank Dr.Peter Vaughan for his work as my departmental supervisor. I sincerely appreciate yourguidance, support, and encouragement. To Dr. Ray Pederson and his wife Margaret, thank youfor all of the time you spend caring for the graduate students, both in your home and on MayneIsland. I would like to thank Dr. Carol-Ann Courneya for her endearing friendship. C.A. youare a wonderful role model for all of your colleagues and students. If only you knew where toshop! I would also like to thank John Sanker and Joe Tay for their technical support of mythesis.I would like to acknowledge the efforts of SWIM B.C. and, in particular, Paul McKinnonand Al Heather, for their administrative, technical, and logistic support of this project. Yourtime and effort are greatly appreciated. I would like to extend my best wishes to all of thesubjects who participated in this study. Without your support, this project would never havebeen completed! In addition, I would especially like to acknowledge the financial support of theBritish Columbia Health Research Foundation and Sport Canada.Finally, without the support of my family I would not have been able to survive the lastfour years. To my wife, Tern, and son, Joey, thank you for your love and encouragement, andfor giving me the time I needed to complete this thesis. I know how much you have sacrificedfor me! To dad, mom, and Linda thank you for your vigilance, love and affection, it has meantso much to me. When I started university you were thrilled, little did you know that the thrillwould last so long!GENERAL INTRODUCTIONAs we near the end of the 20th century, we are becoming increasingly aware of howenvironmental issues affect our health. This concern has evolved to include our workingenvironment and its potential for fostering occupational illnesses. The evidence is persuasivethat the workplace environment is responsible for occupational illnesses such as pneumoconioses(asbestosis, silicosis, berylliosis and other dust diseases of the lung), asthma, and a variety ofneurologic and psychological illnesses (Landrigan and Baker, 1991; Rom, 1983; Rutstein et al.,1983).Occupational illnesses are underdiagnosed and many are incorrectly attributed to othercauses (Landrigan and Baker, 1991). This reflects the fact that many work-related illnesses arenot clinically distinct from diseases due to other causes (Goldman and Peters, 1981), and becausethere is usually a long latency between exposure to the causative agent and the appearance ofsymptoms or the illness (Rosenstock and Landrigan, 1986). As a result of these concerns, thefocus of epidemiological research is shifting from the avoidance of disease among highlyexposed individuals toward the protection of the general population from an unacceptable burdenof disease at much lower exposures (Samet and Utell, 1991). In addition, the development ofmore sensitive methods for identifying causative agents is now allowing researchers to also focuson environmental exposures which may be associated with work-related illnesses.The study of environmental illnesses is now extended to include the milieu in which wepursue our recreational interests. We know that outdoor activities in cities with high levels ofphotochemical air pollution can be problematic and incite respiratory problems. However, thepossibility of occupational-like illnesses occurring in indoor recreational facilities is relativelynew and merits our scientific interest and intervention.One of the diseases with “environmental” causation is asthma. When asthma isdiagnosed, particularly in the young, physicians frequently advise against participating in certainforms of exercise in order to reduce the risk of the patient developing the symptoms associatedwith exercise-induced asthma (ETA). There are numerous scientific articles which have reportedthe beneficial effects of swimming in subjects with asthma. Training in the swimming pool hasbeen shown to improve the fitness level of asthmatics (Fitch et al., 1976; Schnall et aL, 1982)and to reduce the frequency of asthma attacks, airway resistance, frequency of wheezing, needfor medication, visits to the emergency room of a hospital, and absenteeism from school (Huanget at, 1989). While swim training may improve fitness and reduce morbidity associated withasthma, there is both anecdotal and scientific information to suggest that there are health-relatedproblems associated with swimming in chemically-treated pooi water.The indoor swimming pool environment, with its high ambient temperature and relativehumidity, contains a number of volatile chemicals that are known irritants, sensitizing agents andpossible carcinogens. Competitive swimmers are especially susceptible to the adverse effectsof chemically-treated pooi water because of the number of hours they spend swimming in thisenvironment and the increased minute ventilation that occurs with exercise. While anecdotalreports of respiratory and other health-related problems are common, there have been noepidemiological studies that have surveyed competitive swimmers about the prevalence ofrespiratory and other health-related problems or the prevalence and severity of clinicalsymptoms. The first Chapter of this thesis provides a descriptive profile of competitiveswimmers from Canada, the United States, and a number of Pacific Rim countries. Includedin the profiles of these swimmers are the prevalence of respiratory and other health-relatedsymptoms and illnesses, as well as information about their training.The chemicals used to treat the pooi water may cause irritation or sensitization of theairways. This may lead to the manifestation of respiratory symptoms and increased bronchialresponsiveness during or after exercise in the swimming pool. In the second chapter, theprevalence of bronchial hyperresponsiveness among two groups of competitive swimmers, thosewho have asthma and/or pool-associated symptoms and those who have neither asthma nor pool-associated symptoms, is determined using a methacholine challenge test. The prevalence ofbronchial hyperresponsiveness is also determined for a group of non-swimming, athletic controlsubjects in order to assess whether competitive swimmers have a higher prevalence of bronchialhyperresponsiveness than non-swimmers.The anecdotal reports of respiratory and other health-related symptoms may be due tochemical treatment of the pool water, exercise, or both. In the presence of chemical irritantsor sensitizing agents, an exercise broncho-provocation test in the swimming pooi may be usedto induce symptoms or changes in lung function that are not elicited during laboratory studies.In the third chapter, a standard clinical test is used to determine the prevalence of ETA in thelaboratory and in the swimming pool among two groups of competitive swimmers, those whohave asthma and/or pool-associated symptoms and those who have neither asthma nor pool-associated symptoms. The prevalence of ETA in the laboratory is also determined for a groupof non-swimming, athletic control subjects. In addition, a 45 minute exercise bronchoprovocation test will be used to evaluate the effects of continuous, low intensity swimming onpost-exercise lung function in both groups of competitive swimmers.Each of these studies was approved by the University of British Columbia’s ClinicalScreening Committee for Research and Other Studies Involving Human Subjects (CertificateC91-007).REFERENCESFitch, K., A.R. Morton and B.A. Blanksby. Effects of swimming training on children withasthma. Arch. Dis. Child. 1976;51: 190-194.Goldman, R.H. and J.M. Peters. The occupational and environmental health history. JAMA21981 ;46:2831-2836.Huang, S.W., R. Veiga, U. Sila, E. Reed and S. Hines. The effect of swimming in asthmaticchildren - participants in a swimming program in the city of Baltimore. J. Asthma 1989;26: 117-121.Landrigan, P.J. and D.B. Baker. The recognition and control of occupational disease. JAMA1991 ;266: 676-680.Rom, W.N. Environmental and Occupational Medicine. Little Brown & Co. Inc., Boston,1983.Rosenstock, L. and P.J. Landrigan. Occupational health: the intersection between clinicalmedicine and public health. Ann. Rev. Public Health 1986;7:337-356.Rutstein, D.D., R.J. Mullan, T.M. Frazier, W.E. Halperin, J.M. Melius and J.P. Sestito.Sentinel health events (occupational): a basis for physician recognition and public healthsurveillance. Am. J. Public Health 1983;73: 1054-1062.Samet, J.M. and M.J. Utell. The environment and the lung. Changing perspectives. JAMA1991;266:670-675.Schnall, R., P. Ford, I. Gillam and L. Landau. Swimming and dry land exercises in childrenwith asthma. Austral. Paed. J. 1982; 18:23-27.CHAPTER 1The Prevalence of Respiratory Symptoms and OtherHealth-Related Problems in Competitive SwimmersABSTRACTRespiratory illness associated with occupational or environmental exposures include awide variety of conditions, ranging from acute reversible symptoms to chronic disabling lungdisease. The indoor swimming pool environment, with its high ambient temperature and relativehumidity, contains a number of volatile chemicals that are known irritants, sensitizing agents,and possible carcinogens. Competitive swimmers are especially susceptible to the adverseeffects of chemically-treated pool water because of the number of hours they spend training inthis environment and the increase in ventilation that occurs with exercise. While anecdotalreports of respiratory and other health-related problems are common, there have been noepidemiological studies that have surveyed competitive swimmers about the prevalence ofrespiratory and other health-related problems or the prevalence and severity of clinicalsymptoms.The purpose of this study was to determine the prevalence of respiratory and other healthrelated symptoms, illnesses, and allergies among competitive swimmers from across Canada,the United States, and a number of Pacific Rim countries. In addition, we wanted to establishwhether the respiratory symptoms were associated with a swimming-related exposure asdetermined by the amount of time spent swimming, or the distance covered, during trainingsessions in the swimming pool.A total of 738 competitive swimmers completed the questionnaire which represents aparticipation rate of 65.8%. A high percentage (43.5%) of the swimmers had at least one chestillness that kept them from participating in their normal daily activities for 3 days or moreduring the past year. The overall prevalence of physician-diagnosed asthma among thecompetitive swimmers was 13.4 %, but was as high as 20.6% in swimmers who participated atan international level. Many of the younger swimmers had their asthma diagnosed before theystarted competitive swimming, while the older, more accomplished swimmers had their asthmadiagnosed after they started swimming. The prevalence of bronchitis (24.9%) and pneumonia(10.2%) is slightly higher, and hay fever (16.9%) slightly lower, than that reported for thegeneral population. The most common allergies reported were to dust, pollen, animal hair,grasses, and molds, and the prevalence of allergies is similar to those reported for highperformance athletes as well as the general population.Almost all of the exercise-related symptoms were associated with the swimming-relatedexposure. We also identified a number of gender- and age-related differences for several of theexercise-related symptoms. Female swimmers were more likely to cough, feel congested, havedifficulty breathing, and experience headaches. Older swimmers were more likely to feelcongested, sneeze, wheeze, have chest tightness or a sore throat, difficulty breathing, andheadaches. A majority of the swimmers with exercise-related symptoms reported that theirsymptoms were less severe, less noticeable, or absent if they spent several days away from theswimming pooi.Cigarette smoking is extremely uncommon among competitive swimmers and issignificantly lower than that reported for the general population. Prescription medication is usedby more than 21% of the swimmers, and the trend in medication use tends to support the highprevalence of asthma, allergies, and respiratory symptoms, among the swimmers. The use ofcertain medications is also suggestive of a number of skin-related problems such as eczema,contact dermatitis, and psoriasis. Finally, nearly 74% of the swimmers smell a strong chemicalodor in the swimming pooi that they associate with respiratory and other health-relatedsymptoms.INTRODUCTIONLittle is known about the effects of acute or chronic exposure to chemically-treated poolwater on the short- and long-term health of swimming pooi users. Competitive swimmers, tn-athletes, fitness swimmers, lifeguards, coaches, instructors and young children in swimmingclasses are examples of individuals who may be affected (Sutherland, 1992). Anecdotal reportsof respiratory distress and irritation of the airways and lungs are common among competitiveswimmers, although the prevalence of respiratory symptoms and illnesses has not beenestablished for this group. Competitive swimmers often complain of upper respiratory tract andother health-related symptoms such as coughing, chest tightness, wheezing, dyspnea, headaches,nausea, lethargy and irritation of the eyes, nose and throat.In some instances, competitive swimmers have stopped using swimming pooi facilitiesbecause of medical problems associated with the indoor pooi environment (Laverdure, 1991;Sutherland, 1992). Swimming-pool water is disinfected in the interests of public health, but itwould appear that disinfection of the pool water with chlorine may be the cause of therespiratory symptoms (Mustchin and Pickering, 1979; Palm, 1974; Penny, 1983; Zwick et al.,1990).Evidence suggests that exposure to chlorine, derivatives of chlorine, chloroform orchloramines causes edema of the mucous membranes of the respiratory tract and lung;alteration, degeneration and desquamation of the columnar epithelial cells; and severeinflammatory reactions (Kummer, 1975; Wood et al., 1987). The concentration of chloroformin alveolar air and blood samples of competitive swimmers has been found to vary directly withthat found in the pooi water and surrounding air, the number of swimmers in the pooi, thelength of time spent swimming and with the intensity of exercise (Aggazzotti et al., 1990;Aggazzotti et aL, 1993). Chloroform is not only a respiratory tract irritant, but is also asuspected carcinogen.Frequent exposure to these irritants may make the airways more susceptible to allergens,cause bronchial hyperresponsiveness, and may lead to the development of asthma (Penny, 1983;Zwick et al., 1990). Competitive swimmers have been shown to have a higher prevalence ofallergic diseases and sub-clinical sensitization to aeroallergens, disorders of the immune systemand bronchial hyperresponsiveness in comparison with control subjects (Mustchin and Pickering,1979; Zwick et al., 1990). The development of clinical symptoms and bronchialhyperresponsiveness may also be due to, or enhanced by, the presence of underlying respiratorydisease (Mustchin and Pickering, 1979).Rose (1992) has implicated extrinsic allergic alveolitis as a cause of swimming pool-related lung disease in a group of lifeguards who worked at an indoor swimming pool with poorair quality, a strong chloramine odor and numerous water sprays and fountains. The outbreakof extrinsic allergic alveolitis in these lifeguards was attributed to the presence of high levels ofan endotoxin, a component of gram negative bacterial cell walls, in both air and water samplestaken from the swimming pool.Indoor swimming pools, with their high ambient temperatures and relative humidity,represent an environment where operational failures in water quality management or deficienciesin the ventilation system could cause a number of health-related problems. Recent innovationsin aquatic recreation technology, increased use of existing facilities and the introduction of“energy efficient” ventilation systems complicate air and water quality management in thesefacilities.As discussed above, disinfection of the pool water with chlorine generates the chemicalirritants that are found in the water and air of indoor poois. Several other types of disinfectionare available. They include bromination, ozonation, ionization of silver and copper atoms,ultraviolet radiation and the use of hydrogen peroxide, iodine and chlorine dioxide. However,none has yet proved to be as effective or economical as chlorination.A number of chemicals are added to the pooi water to control the pH, alkalinity, andwater hardness. Swimmers add a number of contaminants to the pool water. These includesweat, urine, hair-spray, body lotion and other secretions. The chemicals used to treat the pooiwater mix with these contaminants and undergo a series of complex chemical reactions thatresult in the formation of simple and complex halogenated compounds and other organic andinorganic oxidation by-products.Since swimmers breathe the air just above the surface of the water they are exposed toa number of chemicals that could cause irritation of the airways and lungs. All of thesechemicals have the following properties: (1) high volatility; (2) chemical stability; and (3) ageneration process that is compatible with the environmental conditions of the pool water (Shaw,1987).Active chlorine species are found in measurable concentrations in indoor poolenvironments (Scotte, 1984). At the pH found in pooi water (7.2 to 7.8), chlorine is completelyhydrolysed to hypochiorous acid (HOC1) and hypochlorite ion (OC1). Of these, chlorine gasis not volatile, HOC1 has very low volatility and 0C1 is not volatile at all (Holzwarth et al.,1984). The relative distribution of HOC1 and 0C1 in the water is very important because HOC1is 40 to 80 times more effiéient as a disinfecting agent than 0C1 is (Metcalf and Eddy, 1979).The addition of cyanuric acid as a stabilizing agent for free chlorine has been widely usedin swimming pooi disinfection since the mid 1950s (Feldstein et aL, 1985). Cyanuric acid reactswith chlorine to form mono-, di- and trichloroisocyanurate depending on the pH of the water andthe concentration of free chlorine. Cyanuric acid acts as a reservoir for free chlorine insolution; that is, as free chlorine is consumed, more free chlorine is released from chlorinatedisocyanurates. Studies in swimming pools indicate that chlorinated isocyanurates are at least aseffective as chlorine in bactericidal efficiency (Linda and Hollenback, 1978). Chlorinatedisocyanurates are thought to generate HOC1.The irritating effects of the indoor pool environment are attributed to the presence ofchloramines (Jessen, 1986; Lahl et al., 1981; Metcalf and Eddy, 1979; Shaw, 1987). Theseinclude the inorganic compounds chioramide (NH2C1), chiorimide (NHC12), and chlorine azide(Nd3). These compounds are formed by the chlorination of ammonia derived from the urineand sweat of swimming pool users, however, they contain very small amounts of free ammonia.NH2C1 is stable only in the presence of an excess of ammonia, it has low volatility and it doesnot exist in the presence of free chlorine, so it is generally absent from pooi water. NHC12 isextremely unstable at the pH of pool water and in the presence of free chlorine, it is slightlymore volatile than NH2C1, but does not appear to persist in the atmosphere. NC13 is stable atlow concentrations in water only in the presence ofa large excess of free chlorine, is highlyvolatile, however, it does not appear to persist in the atmosphere (Shaw, 1987).Chlorine is known to react with specific amino acids to form either formaldehyde oracetaldehyde (Hrudey et al., 1988,1989; Laverdure, 1991). Under conditions of high chlorineto amino acid ratios, nitriles can also be formed (Hrudey et al., 1988, 1989). Formaldehydevapours are known to cause sore throats, nausea, and irritation of the respiratory tract and eyes.Contact with the skin causes irritation and allergic sensitization (EPS, 1985). These symptomsmay occur at airborne levels as low as 0.05 ppm in very sensitive individuals such as infants,children, the elderly and those with pre-existing allergies or respiratory illnesses. Chronic low-level exposure to formaldehyde may lead to the development of cancer (Turoski, 1985).Aldehydes are highly reactive reducing agents: acetaldehyde forms covalent bonds withmany biologically important organic molecules, destroying their function. At highconcentrations, acetaldehyde appears to paralyse respiratory muscles and its general narcoticaction prevents coughing. It is also known to cause irritation of the eyes and mucousmembranes, skin and respiratory tract (USEPA, 1987). Prolonged exposure causes headaches,sore throats, a decrease in red blood cell mass, an increase in heart rate and a sustained increasein blood pressure (Mark et aL, 1978).Research by several investigators has demonstrated the presence of a number ofhalogenated hydrocarbons in pool water. These chemicals are both volatile and chemicallystable. Their generation increases proportionally with the number of swimming pool users andthe available chlorine. Many of these chemicals cause acute respiratory distress and irritationof the eyes, nose and throat (see Table 1). These chemicals are also known to be commonindustrial and office air contaminants and are found in chlorinated drinking water (Cotruvo andWu, 1978; Otsonetal., 1983).Outbreaks of enteroviral infections, skin lesions and rashes, respiratory tract problems,fever, headaches and fatigue are also associated with the presence of micro-organisms in the poolwater (Davis, 1985; Laverdure, 1991; Lenaway et al., 1989). These usually occur in hot tubs,whirlpools and spa pools that are heated to a temperature above 37°C, but may also occur incommunity and private swimming pools where the water temperature is well below 37°C(Laverdure, 1991; Lenaway et al., 1989; Strauss et aL, 1988). Several microbial indicatorsof inadequate disinfection of swimming pool water have been reported in the literature. Elevatedlevels of total coliforms, faecal coliform, faecal streptococci, total bacterial counts and yeastsare associated with increased risk for infection (Tosti et al., 1988). Others have suggested thatelevated levels of pseudomonas aeruginosa, amoebae (Esterman et al., 1987) and mycobacteriummarinum may be problematic as well (Fisher, 1988).While anecdotal reports of respiratory and other health-related problems are common,there have been no epidemiological studies that have surveyed competitive swimmers about theprevalence of respiratory and other health-related problems or the prevalence and severity ofclinical symptoms. The purpose of this study was to determine the lifetime prevalence ofrespiratory and other health-related symptoms, illnesses, and allergies in competitive swimmersfrom across Canada, the United States, and a number of Pacific Rim countries. In addition, wewanted to establish whether the respiratory symptoms were associated with a swimming-relatedexposure as determined by the amount of time spent swimming, or the distance covered, duringtraining sessions in the swimming pool.Table1:Propertiesofvolatilehalogenatedhydrocarbonsfoundinswimmingpoolwater.Atvaluesabove10atmm3/mole,chemicalsarereadilyvolatilizedfromwater.(AdaptedfromLaverdure,1991;Shaw,1987).B.C.OccupationalLimitsCompoundsChemicalHenry’sLawConstantHealthEffectsinAir8hExposure15mmExposureFormulaatmm3/mole@25°Cppmmg/rn3ppmmg/rn3ChloroformCHCI34.35xi0eyeandmucousmembraneirritation1050BromodichioromethaneCHBrCI21.60xI0eyeandmucousmembraneirritationN/AN/AN/AN/AChlorodibromomethaneCHBr21eyeandmucousmembraneirritationN/AN/AN/AN/ABromoformCHBr3eyeirritationandlacrimation0.55BromochloromethaneCH2I3rC1eyeandmucousmembraneirritation20010502501300CarbonTetrachlorideCd43.04x10.2burningirritationofeyesandlacrimation106520130DichloromethaneCH212.68xiOrespiratorytractirritation2007002508701,2-DichloroethaneCH2ICHI9.77x10eye,noseandthroatirritation50200753001,1,1-TrichloroethaneCCI3H8.00x10eyeirritation35019004402380TrichloroethyleneCCI2HCI1.03x10.2eyeandrespiratorytractirritation100535150800TetrachloroethyleneCCI21.49x102burningirritationofeyes,lacrimation,1006701501000noseandthroatirritationN/ANotAvailableMETHODSSubjectsSeven hundred and thirty-eight competitive swimmers completed the self-administeredquestionnaire between May 1991 and August 1992. The swimmers were recruited from theLower Mainland and Fraser Valley regions of British Columbia (B.C.) and from threecompetitive venues: (1) the 1991 Canadian Summer National Swimming Championships inVancouver, B.C.; (2) the 1991 Pan Pacific Swimming Championships in Edmonton, Alberta;and (3) national team training camps hosted by United States Swimming.The swimmers from the Lower Mainland and Fraser Valley regions of B.C. wererecruited from 17 competitive swim clubs registered with the B.C. Section of the CanadianAmateur Swimming Association. A list of these clubs, their coaches, addresses, and phonenumbers was obtained from the B.C. Section Office and the coaches were initially informedabout the study by letter. A follow-up telephone call was made two weeks later to solicit thecooperation of the coaches and meetings were arranged with the coaches, the swimmers and theirparents. The questionnaire was administered to the swimmers at this time. Swimmers whowere unable to attend the meetings were given instructions on how to complete the questionnaireand were asked to complete the questionnaire at home. The Age Group Swimmers wereencouraged to complete the questionnaire with the help of a family member who might be morefamiliar with the swimmer’s medical history. Three hundred and seventy-five swimmerscompleted the questionnaire. To study these 375 swimmers we distributed questionnaires to 680eligible swimmers. This represents a participation rate of 66%.Swimmers who attended the 1991 Canadian Summer National Swimming Championshipsin Vancouver, B.C. were asked to complete the questionnaire. Prior to the competition, theHigh Performance Director for Swimming/Natation Canada, the national-governing body forcompetitive swimming in Canada, was contacted by letter to ask for his approval to conduct thesurvey. The coaches were approached prior to the competition to ask for their cooperation andmeetings were arranged with the coaches and swimmers. The swimmers completed thequestionnaire at these meetings which were held 2-3 days prior to the competition. Two hundredand fifty-one swimmers completed the questionnaire. To study these 251 swimmers wedistributed questionnaires to 300 eligible swimmers. This represents a participation rate of 84%.Swimmers who attended the 1991 Pan Pacific Swimming Championships in Edmonton,Alberta were also asked to complete the questionnaire. The High Performance Director forSwimming/Natation Canada and the Chairman of the Competition’s Organizing Committee werecontacted by letter to solicit their approval for conducting the survey. The national team coachesfrom the participating teams were contacted several days before the competition, informed aboutthe purpose of the study, and meetings were arranged with the swimmers and coaches. Theswimmers completed the questionnaire at these meetings which were held 2-3 days prior to thecompetition. Forty-six swimmers completed the questionnaire. To study these 46 swimmerswe distributed questionnaires to 69 eligible swimmers. This represents a participation rate of67%.Swimmers who attended United States (U.S.) Swimming National Team Training Campsin Colorado Springs, Colorado and Indianapolis, Indiana were also asked to complete thequestionnaire. The National Team Director and the Director of Sports Medicine Programs forU.S. Swimming were initially contacted by letter to inform them of the study and solicit theircooperation. We had originally planned to administer the questionnaire to the Americanswimmers at the Pan Pacific Championships in Edmonton, however, at that time it was decidedby the American coaches that it would be inappropriate to interfere with their swimmers’preparation for the competition. The National Team Director suggested that the questionnairecould be administered to the swimmers at two U.S. National Team Training Camps to be heldin the fall of 1991. At each of these training camps, meetings were arranged with theswimmers and their coaches and the questionnaire was completed at that time. Sixty-sixswimmers completed the questionnaire. To study these 66 swimmers we distributedquestionnaires to 72 eligible swimmers. This represents a participation rate of 92%. Theswimmers were informed about the purpose of the study and read and signed a consent formprior to completing the questionnaire.The QuestionnaireThe American Thoracic Society’s Respiratory Disease Questionnaires for Adults andChildren (Ferris, 1978) were modified and administered as a single questionnaire to thecompetitive swimmers. A copy of the questionnaire is included in this dissertation asAPPENDIX A.The identification section of the questionnaire included information about the swimmer’sclub or affiliation, his or her coach’s name, and the level of competition that the swimmerparticipated. The level of competition was determined by the swimmer’s age, the swimmermeeting a time standard to qualify for an individual event or events at a national championship,or if the swimmer participated on a national team at an international competition. Theswimmers were placed into one of three categories depending on the performance criteria thatthey met. If the level of competition was determined by the swimmer’s age, the swimmer wasclassified as an Age Group Swimmer. If the swimmer met a time standard and qualified toswim at a national championship meet, the swimmer was classified as a National Qualifier.Finally, if the swimmer participated on a national team at an international competition, theswimmer was classified as an International Level Swimmer.Information about the amount of exposure to chemically-treated pool water was elicitedfrom a series of questions about the swimmers’ experience as a competitive swimmer and theamount of training that he/she did. These questions included the training facility that theswimmer used, the number of years spent in competitive swimming, the number of workoutsper day, the number of days of training per week, the number of weeks of training per year, theaverage number of metres of swimming per week, and the time and length of each trainingsession. Whenever possible, the swimmer’s coach was asked to review his or her training logto estimate these training parameters.The number of chest illnesses that occurred in the past year and the average number ofcolds that the swimmer has each year were included in the questionnaire. In addition,respiratory symptoms such as coughing, congestion, the production of phlegm, sneezing,wheezing, chest tightness and difficulty breathing were reported during colds, apart from colds(allergies), during exercise other than swimming, and during swimming. Symptoms such as sorethroats, sore eyes, headaches, and ear infections were also reported during similar conditions.For the purposes of this study, only the swimming-related symptoms will be reported.Questions on respiratory illnesses such as asthma, bronchitis, croup, pneumonia, and hayfever, and allergies to dust, pollen, animals, grass, molds, tobacco smoke, air pollution, insectbites, food, and medication were included in the questionnaire. Each of these illnesses orallergies had to have been diagnosed by a physician in order to be considered to be present. Thenumber of years that the swimmer had the illness or allergy was also included. Similarquestions about family members with these illnesses or allergies was also included in thequestionnaire, but the results will not be discussed in this manuscript.The smoking history of the swimmer and his or her family was included in thequestionnaire. A swimmer was considered to be a smoker if he/she smoked more that 20cigarettes in a lifetime. This criterion is significantly different than the criterion outlined by theAmerican Thoracic Society (Ferris, 1978), but was instituted because of the younger age andathletic prowess of our subject population.The use of prescription medication and, in particular, medication used in the treatmentof respiratory problems was included in the questionnaire. A series of questions aboutsymptoms that the swimmer associated with a strong chemical odor were asked. Once again,respiratory symptoms such as coughing, congestion, sneezing, wheezing, chest tightness anddifficulty breathing, and other health-related symptoms such as sore throats, sore eyes,headaches, and nausea were included.The rationale and justification for using each of the components of the Adult andChildren’s Questionnaires are described by Ferris (1978). A number of questions that wereasked on the American Thoracic Society’s Respiratory Disease Questionnaires for Adults andChildren were omitted from our questionnaire. These include the name of the interviewer, themarital status, race, level of education and job history of the subject or his or her parents, anda number of questions related to the age of the youngest sibling or child, the number of childrensharing a bedroom, and the number of rooms in the house, etc. Optional questions such as thetype of home heating and fuels used, whether or not air conditions, humidifiers, and air filtersare used in the house, the month of the year when respiratory symptoms are worse, or if thereare pets living in the house were also omitted from our questionnaire.20Statistical AnalysisThe mean, standard deviation, standard error of the mean, and the range of values werecalculated for all of the descriptive variables. Chi-square analysis was used to determine theassociation between each of the symptoms of cough, congestion, sneezing, wheezing, chesttightness, difficulty breathing, sore throat, sore eyes, and headaches and the three categories ofcompetitive swimmers (Age Group Swimmers, National Qualifiers, and International LevelSwimmers). Initial analysis was completed using 2x3 contingency tables. If the overallassociation was statistically significant, 2x2 contingency tables were used to evaluate theassociation between each of the symptoms and individual categories of competitive swimmers.Independent t-tests and chi-square analysis were used to determine whether there was anassociation between the swimmers’ age, sex, and swimming-related exposure among swimmerswith and without swimming-related symptoms. The exposure variables included the number ofminutes of training per day, the number of days of training per week, the number of weeks oftraining per year, the number of years of competitive swimming, and the number of metres ofswimming per week. In addition, two aggregate measures of exposure were created. Trainingvolume was defined as the product of the number of metres of swimming per week and thenumber of weeks of training per year. The second variable, cumulative exposure, was definedas the product of the number of minutes of training per day, the number of days of training perweek, the number of weeks of training per year, and the number of years of competitiveswimming.Stepwise logistic regression (SAS Institute, Inc., 1987) was used to determine theprobability that asthma and each of the symptoms of cough, congestion, sneezing, wheezing,chest tightness, difficulty breathing, sore throat, sore eyes, and headache occurred as a function21of the swimmers’ age, sex, category, and swimming-related exposure. In this context, exposurereferred to the amount of time spent swimming, or the distance covered, during training sessionsin the swimming pooi.Because multiple comparisons were made, we adopted the following convention forinterpreting statistical significance: p values below 0.005 were considered statisticallysignificant; values between 0.005 and 0.05 were considered to indicate associations that wereof marginal statistical significance and worth further consideration; and values above 0.05 wereconsidered statistically non-significant. All statistical analyses were completed using the SAS®Statistical Software Package (SAS Institute, Inc., Cary, NC).22RESULTSOverviewA total of 738 competitive swimmers completed the questionnaire. Of these, 357(48.4%) were male and 381 (51.6%) were female. The average age of the male swimmers was15.10 ± 4.15 years and the average age of the female swimmers was 14.69 ± 3.60 years.Thirty-five swimmers, or 4.7% of those surveyed, were between the ages of 5-8 years, 187(25.3%) were between the ages of 9-12 years, 231 (31.3%) were between the ages of 13-16years, 215 (29.1%) were between the ages of 17-20 years, and 70 (9.6%) were 20 years of ageor older.There were a total of 348 Age Group Swimmers, 225 National Level Swimmers, and 165International Level Swimmers. These numbers represent 47.2%, 30.5%, and 22.3 % of the totalnumber of swimmers who completed the questionnaire. A total of 626 swimmers, or 84.9% ofthose surveyed, were from Canada. Sixty-six (8.9%) were from the United States, 36 (4.9%)were from Australia, 7 (0.9%) were from New Zealand, 2 (0.3%) were from Indonesia, and 1(0.1%) was from Hong Kong.The swimmers who completed the questionnaire had a wide range of experience incompetitive swimming. The swimmers had been involved in competitive swimming for 6.61± 3.95 years, trained an average of 5.34 ± 1.21 days per week, for 44.00 ± 4.51 weeks peryear. The swimmers spent an average of 190.80 ± 79.61 minutes per day training. Theaverage swimming distance covered during training was 36,665 ± 23,128 metres per week.Table 2 summarizes the descriptive characteristics and training parameters for the three groupsof competitive swimmers.The National Qualifiers and International Level Swimmers were older (p <0.0001), had23been involved in competitive swimming longer (p <0.0001 and p <0.0001, respectively), andtrained more weeks/year (p <0.0001 and p <0.0001, respectively), days/week (p <0.0001 andp < 0.0001, respectively), and minutes/day (p < 0.0001 and p < 0.0001, respectively) than theAge Group Swimmers. The National Qualifiers and International Level Swimmers also hadmore practices/day (p <0.0001 and p <0.0001, respectively) and swam greater distances(p <0.0001 and p <0.0001, respectively) than the Age Group Swimmers. Similarly, theInternational Level Swimmers were involved in competitive swimming longer (p < 0.0001) andswam greater distances (p <0.0001) than the National Level Swimmers.Three hundred and twenty-one swimmers, or 43.5% of those surveyed, reported havinga chest illness that kept them from participating in their normal daily activities for 3 days ormore during the past year. Of those reporting being ill, there were an average of 2.52 ± 2.06illnesses with only 1.01 ± 1.30 lasting more than 7 days. There was a strong overallassociation between the swimmer reporting a chest illness and his or her level of competitiveswimming (p <0.0001). Age Group Swimmers were more likely to report chest illnesses thanwere National Qualifiers or International Level Swimmers (p <0.0001). The swimmers alsoreported having an average of 3.26 ± 2.06 colds each year. International Level Swimmersexperienced fewer colds per year than did either Age Group Swimmers or National Qualifiers(p <0.0001). Table 3 summarizes the chest illnesses reported by the three groups of competitiveswimmers.Swimming-Related SymptomsThe number of swimmers who cough during exercise in the swimming pooi was 206(27.9%) while 186 (25.2%) cough after exercise in the swimming pooi. Overall, 36.4% of the24swimmers cough during or after exercise in the swimming pooi, while only 16.7% cough bothduring and after exercise in the swimming pooi. Only 11.2% of those who cough duringexercise in the swimming pooi had to stop swimming because of the severity of the cough. Ofthose swimmers who cough during or after exercise in the swimming pool, 72.9% claim thattheir cough gets better if they have not exercised in the swimming pool for several days.The number of swimmers who feel congested during exercise in the swimming pooi was126 (17.1%) while 113 (15.3%) feel congested after exercise in the swimming pooi. Overall22.8% of the swimmers feel congested during or after exercise in the swimming pooi while only9.6% feel congested both during and after exercise in the swimming pool. Only 12.7% of thosewho feel congested during exercise in the swimming pooi had to stop swimming because of theseverity of the congestion. Of those swimmers who feel congested during or after exercise inthe swimming pool, 80.4% claim that their congestion is improved if they have not exercisedin the swimming pool for several days.The number of swimmers who sneeze during exercise in the swimming pool was 227(30.8%) while 289 (39.2%) sneeze after exercise in the swimming pooi. Overall, 45.0% of theswimmers sneeze during or after exercise in the swimming pool while only 24.9% sneeze bothduring and after exercise in the swimming pooi. Only 3.1 % of those who sneeze duringexercise in the swimming pooi had to stop swimming because of the severity of the sneeze.The number of swimmers who wheeze during exercise in the swimming pooi was 167(22.6%) while 137 (18.6%) wheeze after exercise in the swimming pooi. Overall, 26.3% ofthe swimmers wheeze during or after exercise in the swimming pooi, while only 14.4% wheezeboth during and after exercise in the swimming pooi. Only 13.8% of those who wheeze duringexercise in the swimming pooi had to stop swimming because of the severity of the wheeze. Of25those swimmers who wheeze during or after exercise in the swimming pool, 90.7% claim thattheir wheeze is improved if they have not exercised in the swimming pool for several days.The number of swimmers who experience chest tightness during exercise in theswimming pool was 156 (21.1 %) while 118 (16.0%) experience chest tightness after exercisein the swimming pool. Overall, 24.8% of the swimmers have chest tightness during or afterexercise in the swimming pool, while only 12.3% wheeze both during and after exercise in theswimming pool. Only 16.0% of those who have chest tightness during exercise in the swimmingpool had to stop swimming because of the severity of the wheeze. Of those swimmers whowheeze during or after exercise in the swimming pool, 79.2% claim that their wheeze isimproved if they have not exercised in the swimming pool for several days.The number of swimmers who have difficulty breathing during exercise in the swimmingpooi was 266 (36.0%) while 156 (21.1%) have difficulty breathing after exercise in theswimming pool. Overall, 39.4% of the swimmers have difficulty breathing during or afterexercise in the swimming pooi, while only 17.8% have difficulty breathing both during and afterexercise in the swimming pool. Only 41 swimmers or 15.4% of those who have difficultybreathing during exercise in the swimming pool had to stop swimming because of the severityof their symptoms. Of those swimmers who have difficulty breathing during or after exercisein the swimming pooi, 66.7% claim that their breathing is improved if they have not exercisedin the swimming pool for several days.The number of swimmers who complain of a sore throat during exercise in the swimmingpool was 153 (20.7%) while 162 (22.0%) complain or a sore throat after exercise in theswimming pool. Overall, 27.1 % of the swimmers complain of a sore throat during or afterexercise in the swimming pool, while only 15.6% complain of a sore throat both during and26after exercise in the swimming pooi. Only 7.8% of those who complain of a sore throat duringexercise in the swimming pool had to stop swimming because of their sore throat. Of thoseswimmers who complain of a sore throat during or after exercise in the swimming pool, 52.0%claim that their sore throat is improved if they have not exercised in the swimming pool forseveral days.The number of swimmers who complain of sore eyes during exercise in the swimmingpooi was 186 (25.2%) while 243 (32.9%) complain of sore eyes after exercise in the swimmingpooi. Overall, 36.0% of the swimmers complain of sore eyes during or after exercise in theswimming pool, while only 22.1 % complain of sore eyes both during and after exercise in theswimming pooi. Only 7.5% of those who complain of sore eyes during exercise in theswimming pool had to stop swimming because of their sore eyes. Of those swimmers whocomplain of a sore eyes during or after exercise in the swimming pool, 75.2% claim that theirsore eyes are improved if they have not exercised in the swimming pool for several days. Therewas a moderate overall association between the swimmer complaining of sore eyes during orafter exercise in the swimming pool and his or her level of competitive swimming (p <0.01).Age Group Swimmers and National Qualifiers were more likely to complain of sore eyes duringor after exercise in the swimming pool than were International Level Swimmers (p <0.05 andp<O.Ol, respectively).The number of swimmers who complain of headaches during exercise in the swimmingpool was 216 (29.3%), while a similar number complain of headaches after exercise in theswimming pool. Overall, 35.9% of the swimmers complain of headaches during or afterexercise in the swimming pooi, while only 22.6% complain of headaches both during and afterexercise in the swimming pool. Only 57 swimmers or 26.4% of those who complain of27headaches during exercise in the swimming pool had to stop swimming because of theirheadache. Of those swimmers who complain of a headache during or after exercise in theswimming pool, 50.9% claim that their headache is improved if they have not exercised in theswimming pool for several days. A comparison of the swimming-related symptoms reported bythe competitive swimmers is presented in Table 4.Ear infections were reported by 551 swimmers or 74.7% of those surveyed. Amongthose swimmers who reported having an ear infection, the average number of ear infections was2.24 ± 2.08 per year. National Qualifiers and International Level Swimmers were more likelyto report ear infections than were Age Group Swimmers (p<0.0001 and p<O.000l,respectively).The Relationship Between Symptoms and the Swimming-Related &posureMost of the swimming-related symptoms were associated with the swimmers’ age, sex,level of competition, and swimming-related exposure. Older swimmers were more likely tocough, feel congested, sneeze, wheeze, and experience chest tightness, difficulty breathing, sorethroats, and headaches. Female swimmers were more likely to cough, feel congested, andexperience difficulty breathing and headaches. National Qualifiers were more likely to becongested (p <0.001 and p <0.001, respectively), wheeze (p < 0.001 and p <0.01, respectively),and have chest tightness (p < 0.001 and p < 0.05, respectively), difficulty breathing (p <0.001and p <0.001, respectively), and a sore throat (p <0.001 and p <0.001, respectively) than wereeither Age Group or International Level Swimmers. National Qualifiers were also more likelyto cough and have headaches than were Age Group Swimmers (p <0.001 and p <0.01,respectively). Age Group Swimmers were less likely to sneeze than were either National28Qualifiers or International Level Swimmers (p <0.001 and p <0.01, respectively).All of the swimming-related symptoms except for sore eyes, were strongly associatedwith the swimming-related exposure variables. This included not only the individual exposurevariables such as the number of minutes, days, weeks, and years of swimming or the numberof metres of swimming each week, but also the two aggregate measures of exposure whichincorporated the individual exposure variables. A summary of the univariate analyses andlogistic models is presented in Tables 5-8.Respiratoiy Illnesses and AllergiesA number of physician-diagnosed respiratory illnesses were included in the medicalhistory of the competitive swimmers. Asthma was reported by 99 swimmers or 13.4% of thoseresponding to the questionnaire. This number included 10.6% of Age Group Swimmers, 12.4%of National Qualifiers, and 20.6% of International Level Swimmers. Older swimmers andswimmers who swam more weeks per year, more metres per week, and who had higher trainingvolumes were more likely to report asthma. A summary of the univariate and logistic regressionanalyses relating asthma to the swimming-related exposure is presented in Tables 6 and 8,respectively. When the effect of age was removed from the logistic regression analysis, trainingvolume became the most important variable associated with the presence of asthma (p <0.0110).International Level Swimmers had a higher prevalence of asthma than did either the AgeGroup Swimmers or National Qualifiers (p <0.01 and p <0.05, respectively). Interestingly, ofthose swimmers who reported asthma, 35.1% of Age Group Swimmers, 78.6% of NationalQualifiers, and 70.6% of International Level Swimmers had their asthma diagnosed by aphysician after they began competitive swimming.29Bronchitis was reported by 184 swimmers or 24.9% of those surveyed. This numberincludes 22.4% of Age Group Swimmers, 26.2% of National Qualifiers, and 28.5% ofInternational Level Swimmers. There was no significant association between the swimmerreporting bronchitis and his or her level of competitive swimming.Pneumonia was reported by 75 swimmers or 10.2% of those surveyed. This numberincludes 8.3% of Age Group Swimmers, 13.3% of National Qualifiers, and 9.7% ofInternational Level Swimmers. There was no significant association between the swimmerreporting pneumonia and his or her level of competitive swimming.Hay Fever was reported by 125 swimmers or 16.9% of those responding to thequestionnaire. This number includes 15.2% of Age Group Swimmers, 17.8% of NationalQualifiers, and 19.4% of International Level Swimmers. Once again, there was no significantassociation between the swimmer reporting hay fever and his or her level of competitiveswimming. A total of 179 swimmers, or 24.3% of those responding to the questionnaire,reported other physician-diagnosed respiratory illnesses such as croup, the flu, andmononucleosis. Table 9 summarizes the respiratory illnesses reported by the three groups ofcompetitive swimmers.A number of physician-diagnosed allergies were also reported by the competitiveswimmers. Allergies to dust were reported by 154 swimmers or 20.9% of those who respondedto the questionnaire. This number includes 20.1% of Age Group Swimmers, 22.2%of National Qualifiers, and 20.6% of International Level Swimmers. There was no significantassociation between the swimmer reporting allergies to dust and his or her level of competitiveswimming.Allergies to pollen were reported by 142 swimmers or 19.2% of those surveyed. Thisnumber includes 16.1% of Age Group Swimmers, 23.6% of National Qualifiers, and 20.6% of30International Level Swimmers. There was no association between the swimmer reportingallergies to pollen and his or her level of competitive swimming.Allergies to animal hair were reported by 126 swimmers or 17.1 % of those surveyed.This number includes 16.4% of Age Group Swimmers, 17.8% of National Qualifiers, and17.6% of International Level Swimmers. There was no association between the swimmerreporting allergies to animal hair and his or her level of competitive swimming.Allergies to grasses were reported by 126 swimmers or 17.1 % of those surveyed. Thisnumber includes 16.1% of Age Group Swimmers, 17.8% of National Qualifiers, and 18.2% ofInternational Level Swimmers. There was no association between the swimmer reportingallergies to grasses and his or her level of competitive swimming.Allergies to molds were reported by 63 swimmers or 8.5% of those surveyed. Thisnumber includes 6.3 % of Age Group Swimmers, 9.8% of National Qualifiers, and 11.5% ofInternational Level Swimmers. Once again, there was no association between the swimmerreporting allergies to molds and his or her level of competitive swimming. A total of 349swimmers, or 47.3% of those surveyed, reported other physician-diagnosed allergies. Theseinclude allergies to smoke (10.0%), insect bites (7.0%), food (10.3%), and medication (10.4%).Table 10 summarizes the allergies reported by the three groups of competitive swimmers.Smoking HistoryOnly 31 swimmers, or 4.2% of those who completed the questionnaire, have smokedmore than 20 cigarettes in their lifetime. A majority (80.6%) of these swimmers were male.There was a moderate association between a swimmer smoking and his or her level ofcompetitive swimming. National Qualifiers and International Level Swimmers were more likely31to smoke than were Age Group Swimmers (p <0.01 and p <0.05, respectively). NationalQualifiers were also more likely to live with someone who smokes than were Age GroupSwimmers (p <0.01). Table 11 summarizes the data that we collected on the smoking historyof the swimmers.Use of MedicationPrescription medication was used by 156 swimmers or 21.1% of those surveyed. Thisincludes 14.1% of Age Group Swimmers, 24.4% of National Qualifiers, and 31.5% ofInternational Level Swimmers. There was a strong association between the use of prescriptionmedication and the swimmer’s level of competition (p <0.001). National Qualifiers andInternational Level Swimmers were more likely to use prescription medication than were AgeGroup Swimmers (p<0.01 and p<O.OOl, respectively).The most frequently prescribed medications were antibiotics (6.8% of the swimmers),I2 agonists (5.0%), topical corticosteroids (4.2%), ántihistamines (3.1%), non-steroidal antiinflammatory drugs (2.7%), inhaled corticosteroids (1.9%), mast cell stabilizers (1.5%),anticholinergic drugs (0.4%), and theophylline (0.3%). In addition, refined petrolatums,acne therapeutics, ulcerative colitis therapeutics, anti-depressants, anti-viral agents, antifungal agents, anti-hypertensives, thyroid hormones, estrogens, and migraine therapeuticswere also prescribed to the swimmers for medical reasons.The sample cell sizes were too small to perform statistical analysis on the associationbetween most of the prescription drugs and the three levels of competitive swimming, however,there was a marginal association between the use of 132-agonists and the swimmer’s level ofcompetitive swimming (p <0.05). International level swimmers were more likely to use j232agonists than were Age Group Swimmers or National Qualifiers (p <0.05 and p <0.05,respectively). Table 12 summarizes the use of the more commonly prescribed drugs among thethree groups of competitive swimmers.Symptoms Associated with a Strong Chemical OdorA total of 544 swimmers, or 73.8% of those who completed the questionnaire, havesmelled a strong chemical odor in the swimming pooi. This includes 64.1 % of Age GroupSwimmers, 87.1% of National Qualifiers, and 76.4% of International Level Swimmers. Therewas a strong overall association between smelling a strong chemical odor and the swimmer’slevel of competitive swimming (p <0.001). National Qualifiers and International LevelSwimmers were more likely to smell a strong chemical odor in the swimming pooi than wereAge Group Swimmers (p <0.001 and p <0.05, respectively). Similarly, National Qualifierswere more likely to smell a strong chemical odor in the swimming pooi than were InternationalLevel Swimmers (p<0.01).The swimmers associated a number of symptoms with the strong chemical odor. Theseincluded coughing (40.9%), difficulty breathing (36.4%), sore eyes (26.3 %), sneezing (25.2%),a sore throat (22.9%), headaches (22.0%), chest congestion (21.3 %), chest tightness (21.0%),wheezing (20.9%), and nausea (11.7%). There was a strong overall association between theswimmer complaining of symptoms in the presence of a strong chemical odor and his or herlevel of competitive swimming. National Qualifiers and International Level Swimmers weremore likely to cough, have difficulty breathing, sore eyes, a sore throat, headaches, chestcongestion, chest tightness, wheezing, or nausea than were Age Group Swimmers. NationalQualifiers were more likely to sneeze than were either International Level Swimmers or Age33Group Swimmers. There was no association between the swimmer becoming nauseated in thepresence of a strong chemical odor and his or her level of competitive swimming.The number of swimmers who have to stop swimming because of the severity of any ofthese symptoms was 136 or 18.4% of those surveyed. There was a strong overall associationbetween the swimmer having to stop swimming and his or her level of competitive swimming(p <0.001). National Qualifiers and International Level Swimmers were more likely to stopswimming than were Age Group Swimmers (p <0.001 and p <0.001, respectively). Table 13summarizes the swimmer’s beliefs about the symptoms they associate with a strong chemicalodor in the swimming pool.Table2:Asummaryofthedescriptivecharacteristicsandtrainingparametersforthethreegroupsofcompetitiveswimmers.Themeanvalueandthestandarddeviationarereported.Thepercentageofmaleandfemaleswimmersineachgroupisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofSubjects348225165MeanAge(years)11.93±3.0917.70±2.40*18.23±2.99*p<O.000lNo.ofMaleSwimmers169(48.6%)112(49.8%)76(46.1%)MeanAge(years)11.68±3.1318.65±2.37*19.50±2.83j-p<O.0001No.ofFemaleSwimmers179(51.4%)113(50.2%)89(53.9%)MeanAge(years)12.16±3.0516.75±2.03*17.15±2.69tp<O.000lAverageno.ofyearsofcompetitiveswimming3.80±2.628.73±2.94*9.67±3.40tp<0.0001Averageno.ofweeks/yearofcompetitiveswimming41.37±4.1946.13±2.97*46.65±3.78*p<O.000lAverageno.ofdays/weekofcompetitiveswimming4.59±1.395.97±0.27*6.05±0.41*p<O0001Averageno.ofminutes/dayofcompetitiveswimming131.15±67.19242.84±46.07*245.64±41.69*p<O.0001Averageno.ofpractices/day1.30±0.501.97±0.24*1.95±0.40*p<O.000lAverageno.ofmetres/week17,449±13,13151,098±13,301*57,515±17,048tp<O.000lTrainingVolume(kilometres/year)741±5872,362±676*2,695±857fp<0.0001CumulativeExposure(hours)2,325±2,8149,819±4,043*11,152±4,434fp<O.0001TrainingVolumeisdefinedastheproductofthenumberofmetresofswimmingperweekandthenumberofweeksofswimmingperyear.CumulativeExposureisdefinedastheproductofthenumberofminutesofswimmingperday,thenumberofdaysofswimmingperweek,thenumberofweeksofswimmingperyear,andthenumberofyearsofcompetitiveswimming.*ThemeanvalueforNationalQualifiersandInternationalLevelSwimmersissignificantlyhigherthanthemeanvalueforAgeGroupSwimmers.jThemeanvalueforInternationalLevelSwimmersissignificantlyhigherthanthemeanvalueforNationalQualifiersandAgeGroupSwimmers.Table3:Acomparisonofchestillnesses(pneumonia,bronchitis,asthma,andcolds)thathavekeptcompetitiveswimmersfromparticipatingindailyactivitiesfor3daysormoreduringthepastyear.Themeanvalueandthestandarddeviationarereported.Thepercentageofswimmersreportingillnessesineachgroupisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofSubjectsReportingChestIllnesses177(50.9%)85(37.8%)59(35.8%)p<O.000l*Averageno.ofillnesses2.47±2.082.51±2.222.70±1.78N.S.Averageno.ofillnesses>7days0.94±1.271.11±1.451.06±1.17N.S.Averageno.ofcolds/year3.41±2.253.38±2.052.76±1.55fp<O.0001*Thelevelofsignificanceindicatesastrongoverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.fInternationalLevelSwimmershavefewercoldsperyearthaneitherAgeGroupSwimmersorNationalQualifiers.N.S.NotStatisticallySignificantTable4:Acomparisonofrespiratoryandotherhealth-relatedsymptomsthatoccurredinthreegroupsofcompetitiveswimmersduringorafterexerciseintheswinuningpooi.Themeanvalueandstandarddeviationarereported.Thepercentageofswimmersreportingsymptomsineachgroupisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswhocough109(31.3%)100(44.4%)60(36.4%)p<O.OltAverageno.ofyears2.11±1.613.87±2.833.89±3.98No.ofsubjectswhohavecongestion65(18.7%)69(30.7%)34(20.6%)p<0.OltAverageno.ofyears2.07±1.553.87±2.574.66±3.73No.ofsubjectswhosneeze126(36.2%)132(58.7%)74(44.8%)p<O.0O1*Averageno.ofyears3.52±2.924.60±2.836.34±5.27No.ofsubjectswhowheeze60(17.2%)92(40.9%)42(25.5%)p<O.OO1*Averageno.ofyears2.65±2.054.76±3.165.00±4.32No.ofsubjectswhohavechesttightness63(18.1%)79(35.1%)41(24.8%)p<O.OO1*Averageno.ofyears2.71±2.453.80±2.635.40±4.43No.ofsubjectswhohavedifficultybreathing92(26.4%)132(58.7%)67(40.6%)p<O.OO1*Averageno.ofyears2.80±2.064.19±2.894.71±4.09No.ofsubjectswhohaveasorethroat67(19.3%)99(44.0%)34(20.6%)p<O.OOl*Averageno.ofyears2.28±1.714.66±3.434.52±3.63No.ofsubjectswhohavesoreeyes129(37.1%)93(41.3%)44(26.7%)p<0.01tAverageno.ofyears3.63±2.575.76±3.935.22±4.17No.ofsubjectswhohaveheadaches105(30.2%)97(43.1%)63(38.2%)p<O.OltAverageno.ofyears2.37±1.834.97±3.584.28±2.61*Thelevelofsignificanceindicatesastrongoverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.tThelevelofsignificanceindicatesamarginaloverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.Table5:Resultsoftheunivariateanalysisthatwasusedtodeterminewhethertherewasastrongassociationbetweentheswimmers’age,sex,andswimming-relatedexposureandthepresenceofswimming-relatedsymptoms(PartI).CoughingCongestionSneezingWheezingChestTightnessAge(Older>Younger)()p<O.O1O9(t)p<O.OO17(t)p<O.0001(t)p<O.0001(t)p<O.0001Sex(Female>Male)(t)p<O.OO1()p<O.OO7N.S.N.S.N.S.MinutesofTrainingperDay(t)p<O.0001()p<O.OO1(t)p<O.0001()p<O.0001()p<O.0001DaysofTrainingperWeek()p<O.0001(t)p<O.0002(t)p<O.0001(t)p<O.0001(f)p<O.0001WeeksofTrainingperYear(t)p<O.0007()p<O.0001(i)p<O.0001(t)p<O.0001(f)p<O.0001YearsofCompetitiveSwimming(t)p<O.OOS4()p<O.OO81()p<O.0001(t)p<O.0001(t)p<O.0002MetresofTrainingperWeek()p<O.0002(1’)p<O.OO52(t)p<O.0001()p<O.0001()p<O.0001TrainingVolume*()p<tJ0002(t)p<O.OO11(t)p<O.0001(t)p<O.0001(t)p<O.0001CumulativeExposuref(t)p<O.OO2S(t)p<O.OO41()p<O.0001(t)p<O.0001(t)p<O.0001(f)Increasedprevalenceofsymptomassociatedwithincreasedexposure*TrainingVolumeisdefinedastheproductofthenumberofmetresofswimmingperweekandthenumberofweeksofswimmingperyear.tCumulativeExposureisdefinedastheproductofthenumberofminutesofswimmingperday,thenumberofdaysofswimmingperweek,thenumberofweeksofswinuningperyear,andthenumberofyearsofcompetitiveswimming.N.S.NotStatisticallySignificant00Table6:Resultsoftheunivariateanalysisthatwasusedtodeterminewhethertherewasastrongassociationbetweentheswimmers’age,sex,andswimming-relatedexposureandthepresenceofswimming-relatedsymptomsorasthma(PartII).DifficultyBreathingSoreThroatSoreEyesHeadachesAsthmaAge(Older>Younger)(t)p<O.0001()p<O.0001N.S.(t)p<O.0002(t)p<O.OO1Sex(Female>Male)()p<O.OO3N.S.N.S.(t)p<O.OO1N.S.MinutesofTrainingperDay(t)p<O.0001(t)p<O.0001N.S.(t)p<O.0003N.S.DaysofTrainingperWeek(t)p<O.0001()p<O.0001N.S.(t)p<O.0001N.S.WeeksofTrainingperYear(t)p<O.0001()p<O.0002N.S.()p<O.0001(t)p<O.O437YearsofCompetitiveSwimming(t)p<O.0001(t)p<O.0001N.S.()p<O.OO89N.S.MetresofTrainingperWeek()p<O.0001(t)p<O.0001N.S.(t)p<O.0001()p<O.O289TrainingVolume*()p<O.0001()p<O.0001N.S.(t)p<O.0001(f)p<O.O2O4CumulativeExposuret(t)p<O.0001()p<O.0001N.S.()p<O.OO26N.S.()Increaseprevalenceofsymptomassociatedwithincreasedexposure*TrainingVolumeisdefmedastheproductofthenumberofmetresofswimmingperweekandthenumberofweeksofswimmingperyear.tCumulativeExposureisdefinedastheproductofthenumberofminutesofswimmingperday,thenumberofdaysofswimmingperweek,thenumberofweeksofswimmingperyear,andthenumberofyearsofcompetitiveswimming.N.S.NotStatisticallySignificant0Table7:Resultsofthelogisticregressionanalysisthatwasusedtodeterminetheprobabilitythateachoftheswimming-relatedexposurevariablesoccurredasafunctionoftheswimmers’age,sex,levelofswimming,andswimming-relatedexposure(PartI).SymptomParameterEstimateStandardErrorLevelofSignificanceOddsRatioCoughingY-Intercept2.32450.4267p<0.0001NumberofDaysperWeek0.37440.0749p<O.0l1.45Sex(Male)-0.54280.1592p<0.00070.58CongestionY-lntercept5.90481.1091p<0.0001NumberofWeeksperYear0.08450.0271p<O.00l81.09Sex(Male)-0.48100.1847p<0.00920.62InternationalLevelSwimmer-0.58750.2345p<O.01220.56NumberofDaysperWeek0.23010.1024p<O.02461.26SneezingY-Intercept4.36950.8463p<0.0001NumberofWeeksperYear0.06810.0213p<0.00141.07NationalLevelSwimmer0.46330.1771p<O.0O891.59NumberofDaysperWeek0.18790.0804p<0.O1831.21WheezingY-Intercept5.26681.0365p<O.000lNationalLevelSwimmer0.66810.1879p<O.00041.95NumberofWeeksperYear0.06260.0253p<0.O13S1.06NumberofDaysperWeek0.22140.1033p<0.03201.25ChestTightnessY-Intercept7.18851.0989p<0.0001NumberofWeeksperYear0.10930.0258p<0.000l1.12Age(Years)0.08690.0256p<0.00071.09InternationalLevelSwimmer-0.66010.2303p<0.00410.52Table8:Resultsofthelogisticregressionanalysisthatwasusedtodeterminetheprobabilitythateachoftheswimming-relatedexposurevariablesorasthmaoccurredasafunctionoftheswimmers’age,sex,levelofswimming,andswimming-relatedexposure(PartII).SymptomParameterEstimateStandardErrorLevelofSignificanceOddsRatioDifficultyBreathingY-Intercept3.15670.4888p<0.0001NationalLevelSwimmer0.70740.1831p<O.000l2.03NumberofDaysperWeek0.34260.1001p<000061.41Sex(Male)-0.57960.1679p<O.00060.56Age(Years)0.05770.0269p<O.03l91.06SoreThroatY-Intercept2.90450.5126p<0.0001NationalLevelSwimmer0.93870.1856p<O.000l2.56NumberofDaysperWeek0.28660.0933p<O.0O211.33SoreEyesY-Intercept1.23620.3071p<O.000lInternationalLevelSwimmer-0.74230.2144p<0.00050.48Age(Years)0.05410.0205p<0.OO841.06HeadachesY-Intercept2.59080.4435p<0.0001NumberofDaysperWeek0.41640.0776p<0.00011.52Sex(Male)-0.55210.1606p<0.00060.58AsthmaY-Intercept2.51490.5208p<0.0001Age(Years)0.14490.0341p<O.00011.16NumberofDaysperWeek-0.29820.1234p<O.O1570.74Table9:Acomparisonoftheprevalenceofphysician-diagnosedrespiratoryillnessesamongthreegroupsofcompetitiveswimmers.Thepercentageofswimmersfromeachgroupreportingrespiratoryillnessesisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswithasthma37(10.6%)28(12.4%)34(20.6%)p<O.OltNo.ofsubjectswithbronchitis78(22.4%)59(26.2%)47(28.5%)N.S.No.ofsubjectswithpneumonia29(8.3%)30(13.3%)16(9.7%)N.S.No.ofsubjectswithhayfever53(15.2%)40(17.8%)32(19.4%)N.S.No.ofsubjectswithotherillnesses13(3.7%)20(8.9%)4(2.4%)N.S.tThelevelofsignificanceindicatesamarginaloverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.N.S.NotStatisticallySignificantTable10:Acomparisonoftheprevalenceofphysician-diagnosedallergiesamongthreegroupsofcompetitiveswimmers.Thepercentageofswimmersfromeachgroupreportingallergiesisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswithallergiestodust70(20.1%)50(22.2%)34(20.6%)N.S.No.ofsubjectswithallergiestopollen56(16.1%)53(23.6%)33(20.6%)N.S.No.ofsubjectswithallergiestoanimals57(16.4%)40(17.8%)29(17.6%)N.S.No.ofsubjectswithallergiestograsses56(16.1%)40(17.8%)30(18.2%)N.S.No.ofsubjectswithallergiestomolds22(6.3%)22(9.8%)19(11.5%)N.S.N.S.NotStatisticallySignificantTable11:Adescriptionofthesmokinghistoryamongthreegroupsofcompetitiveswimmers.Subjectswereconsideredtobesmokersiftheysmokedmorethan20cigarettesintheirlifetime.Themeanvalueandthestandarddeviationarereported.Thepercentageofswimmersfromeachgroupwhosmokeorlivewithsomeonewhosmokesisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswhohavesmoked>20cigarettes6(1.7%)16(7.1%)9(5.5%)p<O.OltAverageno.ofcigarettessmoked2.50±2.072.07±2.974.75±6.90Averageageofsubjectwhenhe/shestartedsmoking13.50±2.3515.21±4.1713.63±2.88Averageageofsubjectwhenhe/shestoppedsmoking13.83±2.4017.42±3.3716.71±3.68No.ofsubjectswhocurrentlysmoke0(0%)2(0.9%)2(1.2%)No.ofsubjectswholivewithsomeonewhosmokes66(19.0%)64(28.4%)42(25.5%)p<O.O5ttThelevelofsignificanceindicatesamarginaloverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.Table12:Acomparisonofprescriptiondruguseamongthreegroupsofcompetitiveswimmers.Thepercentageofswimmersineachgroupwhouseprescriptionmedicationisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswhotakeprescriptionmedication49(14.1%)55(24.4%)52(31.5%)p<O.OOl*Bronchodilators132-AgonistsV13(3.7%)9(4.0%)15(9.1%)p<O.05tTheophyllineV1(0.3%)1(0.4%)Anticholinergics1(0.3%)1(0.4%)1(0.6%)MastCellStabilizers4(1.1%)1(0.4%)6(3.6%)InhaledCorticosteroids5(1.4%)3(1.3%)6(3.6%)TopicalCorticosteroids16(4.6%)12(5.3%)3(1.8%)VAntihistamines5(1.4%)9(4.0%)9(5.5%)Antibiotics12(3.4%)17(7.6%)21(12.7%)NSAIDs6(1.7%)5(2.2%)9(5.5%)*NationalQualifiersandInternationalLevelSwimmersweremorelikelytouseprescriptionmedicationthanwereAgeGroupSwimmers.tInternationalLevelSwimmersweremorelikelytouse/32-AgoniststhanwereAgeGroupSwimmersorNationalQualifiers.IrTable13:Adescriptionofrespiratoryandotherhealth-relatedsymptomsthatcompetitiveswimmersassociatewithastrongchemicalodorintheswinmiingpool.Thepercentageofswimmersreportingsymptomsineachgroupisinparenthesis.AgeGroupNationalInternationalLevelLevelofSwimmersQualifiersSwimmersSignificanceNo.ofsubjectswhosmellastrongchemicalodor223(64.1%)195(87.1%)126(76.4%)p<O.OOl*No.ofsubjectswhocough76(21.8%)136(60.4%)90(54.5%)p<O.OOl*No.ofsubjectswhohavecongestion37(10.6%)76(33.8%)44(26.7%)p<O.OOl*No.ofsubjectswhosneeze72(20.7%)75(33.3%)39(23.6%),<O.o0SfNo.ofsubjectswhowheeze37(10.6%)72(32.0%)45(27.3%)p.<0001*No.ofsubjectswhohavechesttightness39(11.2%)69(30.7%)47(28.5%)p<0.OOl*No.ofsubjectswhohavedifficultybreathing69(19.8%)121(53.8%)79(47.9%)p<O.OOl*No.ofsubjectswhohaveasorethroat48(13.8%)75(33.3%)46(27.9%)p<O.OOl*No.ofsubjectswhohavesoreeyes70(20.1%)74(32.9%)50(30.3%)p<O.OO1*No.ofsubjectswhohaveheadaches54(15.5%)64(28.4%)44(26.7%).p.<0.OOl*No.ofsubjectswhohavenausea34(9.8%)36(16.0%)16(9.7%)N.S.No.ofsubjectswithothercomplaints14(4.0%)11(4.9%)7(4.2%)N.S.No.ofsubjectswhohavetostopswimming38(17.0%)57(25.3%)41(24.8%)p<0.OOl**Thelevelofsignificanceindicatesastrongoverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.tThelevelofsignificanceindicatesamarginaloverallassociationbetweenthevariableofinterestandthelevelofcompetitiveswimming.N.S.NotStatisticallySignificant46DISCUSSIONThe purpose of this study was to determine the lifetime prevalence of respiratory andother health-related symptoms, illnesses, and allergies among competitive swimmers, and toestablish whether the symptoms are associated with a swimming-related exposures determinedby the amount of time spent swimming, or the distance covered, during training sessions in theswimming pool. Our results suggest that the prevalence of respiratory and other health-relatedsymptoms, illnesses, and allergies are extremely common among competitive swimmers. Inaddition, we found that many of the symptoms were strongly associated with the amount of timespent swimming, or the distance covered, during training sessions in the swimming pool. Wealso identified significant gender- and age-related differences for several of the exercise-relatedsymptoms. Although we have no objective information about the 34.2% of swimmers who didnot respond to the questionnaire, it is possible that there is a selection bias within our samplepopulation that has excluded swimmers who have no significant respiratory symptoms orillnesses.One of the most impressive characteristics of these competitive swimmers is the amountof training that they do. Some of the swimmers have participated in competitive swimming foras many as 20 years, they train up to 6 hours daily, for as many as 52 weeks of the year.During the course a of week they may swim up to 100 kilometres and may, over the course ofthe competitive season, swim as many as 5,200 kilometres. This exposure data suggests thatcompetitive swimmers are extremely susceptible to any adverse health effects of chemicallytreated pool water.A high percentage (43.5%) of the swimmers had a chest illness that kept them fromparticipating in their normal daily activities for 3 days or more during the past year. In addition,V 4713.9% of the swimmers complained of a cough, and 22.9% of the swimmers produced phlegm,on most days for 3 months or more during the past year. Clinical data from studies by Joki(1974) and Nieman and Nehisen-Cannarella (1992) suggest that competitive athletes may havea higher prevalence of infectious illnesses than non-athletes. One of the reasons for this is thatintense physical activity may depress non-specific cellular immunity and make the athlete moresusceptible to infection (Lewicki et al., 1987).Respiratoiy Illnesses and AllergiesThe overall prevalence of asthma among the 738 competitive swimmers was 13.4%.This included 10.6% of the Age Group Swimmers, 12.4% of the National Qualifiers, and 20.6%of the International Level Swimmers. The extremely high prevalence of asthma among theInternational Level Swimmers was associated with the use of j32-agonists among 9.1 % of theswimmers in this group. It has been suggested that the prevalence of asthma may be affectedby heredity, allergic conditions, and the environment (Gerstman et al., 1989). It ranges fromas low as 1.8% in Scandinavian countries (Haahtela et al., 1990) to 14.3% or higher in theSouth Pacific (Liard et al., 1988). Data from the National Health and Nutrition ExaminationSurvey showed that the lifetime prevalence of asthma among 3 to 17 year old American childrenand adolescents was 6.7% (Gergen et al., 1988). Heibling and Muller (1991) estimated theprevalence of asthma among German high performance athletes to be 7.1 %. The prevalence ofasthma among athletes on the 1976 and 1980 Australian Olympic Teams was 9.7% and 8.5%,respectively (Fitch, 1984).An interesting finding in our study was that among those swimmers who reported asthma,35.1% of Age Group Swimmers, 78.6% of National Qualifiers, and 70.6% of International48Level Swimmers had their asthma diagnosed after they began competitive swimming. Onepossible explanation for these results is that many of the younger swimmers were diagnosed withasthma and their physicians recommended swimming as a form of exercise that would be leastlikely to exacerbate their asthmatic symptoms. The National and International Level swimmersmay have developed exercise-related symptoms during swimming which were suggestive ofasthma, seen their physician, and had their asthma diagnosed after beginning swimming. Inaddition, it would be interesting to know how severe the asthma was in these competitiveswimmers. It is possible that these swimmers have remained in competitive swimming becausethey have a mild form of asthma that may be seasonal or well-controlled by medication, and thepresence of exercise-related symptoms does not severely effect their asthma or swimmingperformance. Those swimmers who had more severe forms of asthma may have been selectedout of the sport because they had chronic asthma that was not well-controlled by medication ortheir symptoms may have limited their performance.Among the other respiratory illnesses that we identified, the lifetime prevalence ofbronchitis was 24.9%. This is significantly higher than the 0.8 to 1.3% reported for 12 to 74year olds in the United States (Turkeltaub and Gergen, 1991) and the 9% reported for 35 to 66year olds in Sweden (Lundback et al., 1993). The prevalence of pneumonia among theswimmers was 10.2% which is slightly lower than the 14.6% reported for a cohort of 905patients by Heckerling et al. (1992). A history of hay fever was reported by 16.9% of theswimmers. This prevalence is significantly lower than the 42% reported for German highperformance athletes (Helbling and Muller, 1991), and slightly higher than the 9% to 15%reported for Welsh schoolchildren (Burr et al., 1989) and the 10% reported for 15 to 70 yearolds from Norway (Bakke et at, 1990).49The most common allergies among the competitive swimmers were to dust (20.9%),pollen (19.2%), animal hair (17.1%), grasses (17.1%), and molds (8.5%). It is estimated thatas many as 20% to 30% of the population of developed countries may suffer from allergies(Peshkin, 1965). Fitch (1984) reported the prevalence of allergies among high performanceathletes who participated on the 1976 and 1980 Australian Olympic Teams. Approximately20.0% of the athletes on the 1976 team and 19.8% of the athletes on the 1980 team hadallergies.Ear infections were reported by 74.7% of the competitive swimmers. Otitis externa or“swimmer’s ear” is quite common among athletes involved in aquatic sports (Strauss andDierker, 1987; Weinberg, 1986). The moisture and the warm environment of the ear canalmake it an ideal breeding ground for bacteria which generate debris and invade the lining of thecanal. The most common bacteria associated with otitis externa are staphylococcus aureus,streptococcus pyogenes, pseudomonas aeruginosa, and proteus (Harrison, 1977).Asthma, Exercise-Related Symptoms, and the Swimming-Related ExposureAsthma was more likely to occur in swimmers who were older and had higher trainingvolumes (a product of the number of weeks of training per year and the number of metres oftraining per week). Since International Level Swimmers were older and had a higher swimming-related exposure than either Age Group Swimmers or National Qualifiers, it is not surprisingthat they had a higher prevalence of asthma. It is interesting to note that the logistic regressionanalysis showed that swimmers with asthma were more likely to train fewer days per week thanwere swimmers without asthma. This would suggest that while asthmatic swimmers train fewerdays per week, they must train greater distances during each day of training than non-asthmatic50swimmers do. In fact, this effect was confounded by the age of the swimmer. When age wasremoved from the logistic regression analysis, higher training volumes became the mostimportant variable associated with asthma (p <0.011).The prevalence of exercise-related symptoms were common among the competitiveswimmers. The symptoms of coughing, wheezing, chest tightness, and difficulty breathing areoften associated with exercise-induced asthma (McKenzie, 1991; Mahier, 1993). AlthoughInternational Level Swimmers had the highest prevalence of asthma (20.6%), National Qualifiershad a higher prevalence of exercise-related symptoms suggestive of asthma than did theInternational Level Swimmers. This may suggest that the association between asthma andexercise-related symptoms is not well supported in our study. However, swimmers who areNational Qualifiers represent a wide range of age and abilities and there may, in fact, beminimal differences in the swimming-related exposure between the best National Qualifiers andthe International Level Swimmers. Another possible explanation for the dissociation of asthmafrom exercise-related symptoms suggestive of asthma is that younger, more inexperiencedswimmers may associate their symptoms with the intensity of exercise or the presence of astrong chemical odor in the swimming pooi as opposed to the presence of an obstructive airwaysdisease such as asthma. It is for this reason that they may be less concerned about theirsymptoms and less likely to make an appointment to see their family physician about theirsymptoms. The older, more experienced swimmers may realize that the exercise-relatedsymptoms are not typical of high intensity training, but may be associated with respiratoryproblems. If this scenario is true, it is possible that we may have underestimated the prevalenceof asthma among the National Qualifiers.All of the symptoms, except for sore eyes, were strongly associated with the swimming-51related exposure. The exposure variables that we used included the average number of minutesof training each day, the number of days of training each week, the number of metres swumeach week, the number of weeks of training each year, and the two composite measures ofexposure, training volume and cumulative exposure. Since all of the individual exposurevariables were strongly associated with the presence of exercise-related symptoms, and since thecomposite exposure variables were simply products of the individual exposure variables, thecomposite variables were also strongly associated with the presence of exercise-relatedsymptoms.We also identified age- and gender-related differences for several of the symptoms.Female swimmers were more likely to cough, feel congested, have difficulty breathing, andexperience headaches than were male swimmers. In addition, older swimmers were more likelyto cough, feel congested, sneeze, wheeze, have chest tightness, difficulty breathing, a sorethroat, and experience headaches than were younger swimmers. When interpreting these data,it is important to remember that the reported prevalences are lifetime prevalences, so that as theswimmers get older their prevalences can only increase, they can not decrease.The logistic regression analyses identified the variables that remained statisticallyimportant after adjusting for the effects of collinear or confounding variables. The effects of agebecame statistically non-significant when the data was stratified by using age group categoriesinstead of age by itself. The swimmers’ level of competition remained an important determinanton whether the swimmer presented with exercise-related symptoms. National Level Swimmerswere more likely to sneeze, wheeze, or have difficulty breathing or a sore throat, whileInternational Level Swimmers were more likely to feel congested, or have chest tightness orsore eyes.52Studies comparing the Prevalence of Exercise-Related SymptomsThe most common symptom, sneezing, was reported by 45.0% of the swimmers.Sneezing is often associated with allergies, chronic rhinitis (Katz, 1984), or exercise-inducedrhinitis (Silvers, 1992). Sneezing may also be induced by inhaling water through the nose andactivating irritant receptors in the nasal cavity. Wheezing is the symptom that is most closelyassociated with asthma and, in many studies, questions about the prevalence of asthma and/orwheezing are often asked. The prevalence of wheezing (26.3%) among the competitiveswimmers is significantly higher than that reported for the general population. In the SecondNational Health and Nutritional Examination Survey, the prevalence of frequent wheeze wasestimated to be between 6.2% and 9.3% among white and black children in the United States(Schwartz et al., 1990). Sennhauser and Guntert (1992) estimated the prevalence of wheezingin children from Switzerland. The lifetime prevalence of wheezing was 16.5%, with only 34%of those reporting a history of asthma. The authors also showed that night-time symptoms ofirritant cough, chest tightness, and wheezing were more frequent in children who lived in urbanareas and in households with smokers.Our results show that the prevalence of lower respiratory tract symptoms in competitiveswimmers is significantly higher than that reported for football and basketball players. Weileret al. (1986) reported the prevalence of exercise-related respiratory symptoms for collegefootball and basketball players at the University of Iowa. The prevalence of symptoms for thefootball and basketball players were coughing (14% and 0%, respectively), wheezing (7% and0%, respectively), chest tightness (9% and 12%, respectively), and dyspnea (6% and 0%).Following exposure to cold air, smoke, fumes, dust, or molds, the prevalence of chest symptoms53were reported by 35% and 38% of the football and basketball players, respectively.The prevalence of sore eyes and sore throats among the competitive swimmers were36.0% and 27.1%, respectively. Many of the chemicals used to disinfect the pooi water areknown irritants of the eyes, nose, and throat (Laverdure, 1991; Shaw, 1987). Exposure to thesechemicals may be responsible for the swimmer’s complaining of these symptoms. However,while there. was a strong statistical association between a swimmer complaining of a sore throatand the swimming-related exposure, a similar association did not exist for sore eyes. Analternative reason for the high prevalence of sore eyes among the competitive swimmers involvesthe use of swimming goggles. Swimming goggles are almost universally worn by swimmers andthe soft malleable foam padding in the goggles is composed of dibutyithiourea, an agent whichis known to irritate the eyes and cause contact dermatitis (Alomar and Vilatella, 1985). Thechemicals used to disinfect the pooi water have also been shown to cause conjunctivitis incompetitive swimmers (Weinberg, 1986).In our study, 35.9% of the subjects complained of a headache during or after exercisein the swimming pool. Coughing, sneezing, sexual activity, and exercise are all known to causebenign exertional headaches (Diamond and Medina, 1982; Indo and Takahashi, 1990; Powell,1982; Rasmussen and Olesen, 1992; Silbert et al., 1991). These headaches are characterizedby severe, short-lived pain and are thought to have a vascular origin. Rasmussen and Olesen(1992) assessed the prevalence of headache disorders in a sample of 25-64 year olds. Theirresults suggest that approximately 1 % of the general population suffer from benign exertionalheadaches. It has also been shown that exertional headaches are 4-5 times more common in menthan in women (Rooke, 1968; Silbert et al, 1991). In our study, headaches were more commonin female swimmers which suggests that the underlying mechanism that cause these headaches54may differ from benign exertional headaches. Three cases of sudden, severe headachesoccurring in swimmers have been reported by Indo and Takahashi (1990). In all three casesneurological, radiological, and hematological findings were normal and the patients’ outcomeswere good. It is possible that the headaches experienced by competitive swimmers may haveto do with entrainment of their breathing pattern to their stroke rate or, in some instances, to“breath-hold” training sets. In either case, exertional headaches may occur from the resultinghypercapnia.The nature of the symptom and its severity were important determinants of whether theswimmer could continue to exercise or not. Only 3.1% of the swimmers who sneeze duringexercise were compelled to stop swimming because of the nature and severity of their symptoms.This compares to 7.5% of the swimmers who have sore eyes, 7.8% who have sore throats,11.2% who cough, 12.7% who develop congestion, 13.8% who wheeze, 15.4% who havedifficulty breathing, 16.0% who have chest tightness, and 26.4% who have headaches.There is a general belief among the swimmers that if they don’t exercise in the swimmingpooi for several days, their symptoms will “get better”. This term was explained to theswimmers as meaning that when resuming training following periods away from the swimmingpool the symptom would be less severe, less noticeable, or absent. In those swimmers whoreported exercise-related wheezing, 90.7% felt their symptoms were less severe, less noticeable,or absent following periods away from the swimming pool. A high percentage of swimmerswho reported exercise-related congestion (80.4%), chest tightness (79.2%), sore eyes (75.2%),coughing (72.9%), difficulty breathing (66.7%), sore throat (52.0%), and headaches (50.9%)felt their symptoms were less severe, less noticeable, or absent following periods away from theswimming pool.55When we asked the swimmers whether they ever smelled a strong chemical odor in theswimming pool, 73.8% of the swimmers responded that they did. The most common exercise-related symptom associated with a strong chemical odor, coughing, was reported by 40.9% ofthe swimmers. Other symptom prevalences included difficulty breathing (36.4%), sore eyes(26.3%), sneezing (25.2%), sore throats (22.9%), headaches (22.0%), congestion (21.3%), chesttightness (21.0%), wheezing (20.9%), and nausea (11.7%). The nature and severity of thesymptoms associated with this strong chemical odor were significant enough to cause 18.4% ofthe swimmers to stop swimming at one time or another. It is important to remember that theseresults only reflect the swimmer’s beliefs about an association between a strong chemical odorand the development of respiratory symptoms.Studies Comparing the Use of Medication and Tobacco ProductsPrescription medication was used by 21.1% of the swimmers. Antibiotics (6.8%), /2-agonists (5.0%), topical corticosteroids (4.2%), antihistamines (3.1%), non-steroidal antiinflammatories (2.7%), inhaled corticosteroids (1.9%), mast cell stabilizers (1.5%),anticholinergic drugs (0.4%), and theophylline (0.3 %) were the medications most commonlyprescribed to the competitive swimmers. The trend in medication use tends to support the highprevalence of respiratory symptoms, asthma, and allergies among the competitive swimmers andis suggestive of a number of skin-related problems such as eczema, contact dermatitis, andpsoriasis. The chemicals used to disinfect the pool water have also been shown to causepersistent swelling of the lips and generalized pruritus in swimmers (Parks and Camisa, 1986).Only 4.2% of the competitive swimmers have smoked more than 20 cigarettes in theirlifetime. Of these, nearly 81% were male. Dim et al. (1991) estimated the prevalence ofsmoking among Israeli male athletes to be 15.5%. Among foreign-born Canadians, theprevalence of smoking is 16% and among native-born Canadians, the prevalence of smoking is25% (Millar, 1992). In the United States, a 1987 survey suggested that approximately 29% ofthe population were smokers, and the prevalence of smoking among 12-17 year old Australianstudents was estimated to be 27-30% (Hill et aL, 1990).5657CONCLUSIONSIn conclusion, this study shows that the prevalence of respiratory and other health-relatedsymptoms, illnesses, and allergies are extremely common among competitive swimmers. Theoverall prevalence of physician-diagnosed asthma among the 738 competitive swimmers was13.4%. This is significantly higher than the 7.1% to 9.7% reported for other competitiveathletes. There was a significant difference in the prevalence rates of asthma among the threegroups of competitive swimmers. The range of values include 10.6% of Age Group Swimmers,12.4% of National Qualifiers, and 20.6% of International Level Swimmers. The extremely highprevalence of asthma among the International Level Swimmers is associated with the use of 2-agonists among 9.1 % of the swimmers in this group.There was a tendency for Age Group Swimmers to have their asthma diagnosed beforethey began competitive swimming, and National Qualifiers and International Level Swimmersto have their asthma diagnosed after they began competitive swimming. This suggests that theswimming-related exposure may be responsible for the development of respiratory symptoms thatwere severe enough for the National Qualifiers and International Level Swimmers to have adiagnosis of asthma made by their physician. We also question whether or not the swimmingrelated exposure precludes severe asthmatics from participating in competitive swimming becauseof uncontrolled symptoms, poor exercise tolerance, and/or poor performance.Among the other respiratory illnesses that we identified, the prevalence of bronchitis(24.9%) and pneumonia (10.2%) were higher than that reported for the general population. Theprevalence of hay fever (16.9%) is significantly lower than that reported for other highperformance athletes, but is slightly higher than that reported for the general population. Themost common allergies among the competitive swimmers were to dust (20.9%), pollen (19.2%),58animal hair (17.1%), grasses (17.1%), and molds (8.5%). These prevalences appear to besimilar to those reported for high performance athletes as well as the general population.A high percentage (43.5%) of the swimmers had at least one chest illness that kept themfrom participating in their normal daily activities for 3 days or more during the past year. Theprevalence of swimming-related symptoms included sneezing (45.0%), difficulty breathing(39.4%), coughing (36.4%), sore eyes (36.0%), headaches (35.9%), sore throat (27.1 %),wheezing (26.3%), chest tightness (24.8%), and chest congestion (22.8%) and suggest that bothupper and lower respiratory tract irritation occurs as a result of the swimming-related exposure.All of the symptoms, except for sore eyes, were strongly associated with the swimming-related exposure. Congestion, sneezing, wheezing, chest tightness, difficulty breathing, sorethroats, and headaches were all associated with the average number of minutes spent trainingeach day, the number of days spent training each week, the number of metres swum each week,and the number of weeks of training each year. The remaining symptom, coughing, wasassociated with the average number of minutes spent training each day, the number of days oftraining each week, and the number of metres swum each week. These results suggest that thereis a dose-response relationship between the amount of training and the occurrence of symptoms.We identified a number of gender- and age-related differences for several of theswimming-related symptoms. Female swimmers were more likely to cough, feel congested,have difficulty breathing, and experience headaches. Older swimmers were more likely to feelcongested, sneeze, wheeze, have chest tightness, difficulty breathing, sore throats, andheadaches. A majority of the swimmers with swimming-related symptoms reported that theirsymptoms were less severe, less noticeable, or absent if they spent several days away from theswimming pool.59Cigarette smoking is extremely uncommon among competitive swimmers. Only 4.2%of the swimmers reported smoking more than 20 cigarettes in their lifetime. The prevalence ofsmoking among the swimmers is significantly lower than that reported for the generalpopulation. Just over 21 % of the competitive swimmers use prescription medication. The trendin medication use tends to support the high prevalence of respiratory symptoms, asthma, andallergy among the competitive swimmers and is suggestive of a number of skin-related problemssuch as eczema, contact dermatitis, and psoriasis.And finally, nearly 74% of the swimmers smell a strong chemical odor in the swimmingpooi that they associate with respiratory and other health-related symptoms. 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Lung 1990; 168:111-115.65CHAPTER 2The Prevalence of Increased Bronchial Responsiveness to Methacholine in aSelect Group of Competitive Swimmers and Non-SwimmersABSTRACTNon-specific bronchial hyperresponsiveness (BHR) is almost a universal finding inpatients with obstructive airways diseases such as asthma. In the workplace, inhalation ofagents that have known or suspected allergic properties may result in the development ofa variant of asthma known as occupational asthma. Over 200 compounds have beenreported to cause occupational asthma and, as in other obstructive airways diseases, almostall patients with symptomatic occupational asthma have BHR. Inhalation of respiratoryirritants may also result in the development of occupational asthma. Because of its non-immunological etiology this form of asthma is known as irritant-induced occupationalasthma.A number of studies have shown that chronic, low level exposure to environmentalirritants may cause a significant increase in BHR. These include a number of swimming-related studies that suggest chronic, low level exposure to the chemicals used to disinfectswimming pool water may be responsible for the development of asthma-like symptoms andBHR among competitive swimmers. Therefore, it was the purpose of this study to: (1)assess the prevalence of BHR in a group of 35 competitive swimmers from the lowermainland of British Columbia using a methacholine challenge test; and (2) determinewhether there are differences in the prevalence of BHR among competitive swimmers withasthma or swimming-related symptoms (Case Group) and those who have neither asthma66nor swimming-related symptoms (Control Group), and to compare their results with a groupof non-swimming athletes who have neither asthma nor swimming-related symptoms (Non-Swimming Control Group).Our results show that the prevalence of BHR (PC20 16 mg/mL) among lowermainland competitive swimmers is 60.0%. When the sensitivity of the methacholinechallenge test is decreased to include only those swimmers with a PC20 8 mg/mL, theprevalence of BHR is 34.3%. These values are significantly higher than the respective12.5% and 0% prevalences that were observed for 16 non-swimming athletes in our study,and the 11-14% prevalence reported in several population-based studies. There was nodifference in the prevalence of BHR between swimmers in the Case Group (61.1%) andswimmers in the Control Group (58.8%). When the sensitivity of the methacholinechallenge test is decreased to include only those swimmers with a PC2O 8 mg/mL, 33.3%of the swimmers in the Case Group and 35.3 % of the swimmers in the Control Groupdemonstrated BHR.The clinical manifestations of this swimming-related exposure, whether it is relatedto the chemical treatment of the pool water, exercise, or both, may simply be to increaseBHR and, in some individuals, cause swimming-related symptoms suggestive of asthma.What remains unknown is why some swimmers develop swimming-related symptomssuggestive of asthma and others do not. A possible explanation might be that swimmerswith swimming-related symptoms may have been exposed to higher concentrations of poolchemicals than those swimmers without swimming-related symptoms, however, this theoryremains speculative.The most likely mechanism for the increased BHR in these competitive swimmers67is that chronic, low level exposure to the chemicals used to disinfect the pool water maycause damage to the epithelial layer of the swimmer’s airways. This damage may result inincreased exposure of afferent receptors, increased sensitivity of the receptors, and enhancedaccessibility of bronchoconstrictor agents to bronchial smooth muscle and/or sensory nerveendings under the mucosa. The tracheo-bronchial irritant receptors and pulmonary C-fibersare likely involved in this physiological response which triggers an axon reflex resulting inthe release of several neuropeptides that enhance smooth muscle contraction andinflammation of the airways.While there is some clinical evidence from other studies to suggest that competitiveswimmers may have increased sensitization to a number of common aero-allergens, we areextremely hopeful that chronic, low level exposure to chemically-treated pool water does notresult in the severe pathological changes that occur to the airways of individuals withimmunological- or irritant-induced occupational asthma.68INTRODUCTIONNon-specific bronchial responsiveness is the complex and poorly understoodphysiological response of the airways to non-antigenic stimuli. The measurement of nonspecific bronchial responsiveness is widely used in the diagnosis of asthma and otherobstructive airways diseases and the grading of their severity. It is also used in occupationaland population-based studies to identify host characteristics and environmental exposuresthat increase the risk of developing chronic obstructive pulmonary disease (COPD).Bronchial responsiveness is not necessarily a static trait, but may be influenced by exposureto several modulating factors (Sparrow and Weiss, 1989). Spontaneous changes in bronchialresponsiveness occur in asthmatic, as well as non-asthmatic subjects, however, asthmaticspersistently have hyperresponsive airways. This suggests that asthma should be classified asa variable airways disease instead of a reversible airways disease (Vedal et al., 1988).Increased bronchial responsiveness (BHR) is almost a universal finding in patientswith asthma. Subjects with asthma develop bronchial narrowing to a greater extent inresponse to smaller quantities of pharmacological, physical, or chemical stimuli than donormal subjects (Hargreave et al., 1981). Methacholine and histamine are thepharmacological agents that are most commonly used to assess non-specific bronchialresponsiveness. Breathing cold air or solutions containing non-isotonic aerosols, voluntaryhyperventilation, and exercise are physical stimuli that can be used to assess non-specificbronchial responsiveness as well. The level of responsiveness to methacholine has beenshown to correlate with the level of responsiveness to histamine (Aquilina, 1983), exercise(Ahmed and Danta, 1988;), and hyperventilation of cold air (Ahmed and Danta, 1988;Aquilina, 1983). The use of gases such as sulfur dioxide (SO2), nitrogen dioxide (NO2), and69ozone (03), and specific challenge agents that are identified in the workplace are frequentlybeing used in studies of occupational asthma.The results of several studies suggest that the prevalence of BHR is between 11-14%in normal subjects (Burney et al., 1987; Cockcroft et al., 1992; Woolcock et al., 1987;); 47%of patients with cough and no other chest symptoms; 40% of patients with rhinitis andvague chest symptoms; and 22% of patients with rhinitis and no chest symptoms (Cockcroftet a!, 1977; Makino, 1966). Increased bronchial responsiveness is also reported in cigarettesmokers with normal lung function (Gerrard et al., 1980). The degree of airwayresponsiveness appears to be higher in children than in adults, and similar between malesand females (Weiss et aL, 1984).The clinical presentation of asthma may include episodes of coughing, dyspnea, chesttightness, or wheezing. It may also involve an exaggerated diurnal variability in airwaycaliber that leads to nocturnal and early morning breathlessness and chest tightness (Ryanet al., 1982). While the severity of BHR in asthma has been shown to be related to theseverity of the patient’s symptoms (Ryan et al., 1982), it has been suggested by Kennedy(1992) that the absence of respiratory symptoms does not necessarily rule out BHR in allpersons. Many studies have attempted to determine the underlying pathophysiology ofBHR. It has become evident that one single factor is not responsible forhyperresponsiveness, but rather there is a complex interaction of several factors involved(Postma et aL, 1989).Because changes in bronchomotor tone in asthma may occur rapidly, it has beensuggested that asthma, and in particular BHR, might be explained by an abnormality ofautonomic control (Postma et al., 1989). Several different autonomic abnormalities have70been proposed in the pathogenesis of asthma, including enhanced cholinergic, alphaadrenergic or non-cholinergic excitatory mechanisms, or reduced beta-adrenergic or noncholinergic inhibitory mechanisms (Nadel and Barnes, 1984).The autonomic nervous system plays an important role in the regulation of airwaycaliber in health and disease. In addition to regulation of airway smooth muscle tone,autonomic nerves may influence secretion of mucus from submucosal glands, transport offluid across airway epithelium, permeability and blood flow in the bronchial circulation, andrelease of mediators from mast cells and other inflammatory cells. An important functionof sensory nerves and their receptors is to protect the airway against inhalation of irritantand chemical particles. Apart from protective effects such as cough, airway irritation causeslocal defense reactions such as bronchoconstriction, vasodilatation, and increased vascularpermeability, resulting in an increased reflex bronchoconstriction due to stimulation ofsensory receptors by inflammatory mediators.Most theories relating epithelial damage and airway hyperresponsiveness are basedon the assumption that epithelial damage and loss result in increased exposure of afferentreceptors, increased sensitivity of those receptors, and enhanced accessibility ofbronchoconstrictor to smooth muscle and/or sensory nerve endings under the mucosa(Postma et al., 1989). Exposure of sensory nerves may bring on increased reflexbronchoconstriction via vagal, or local reflexes involving antidromic conduction alongsensory afferent fibers (Barnes, 1986).Slowly adapting stretch receptors are myelinated nerve terminals localized in thesmooth muscle of the trachea and larger bronchi. It has been postulated that thebronchopulmonary stretch receptors provide information about the degree of inflation of the71lung and may regulate the rate and depth of breathing to achieve the optimal combinationof mechanical work and/or inspiratory force. Slowly adapting receptors may be responsiblefor the bronchodilator response to lung inflation in humans, particularly after inducedbronchoconstriction (Barnes, 1991).Tracheo-bronchial irritant receptors are non-specialized nerve endings that arethought to terminate between the epithelial cells close to the mucosal surface of the airways.These fibers are rapidly adapting to a maintained stimulus and have an irregularspontaneous discharge. They are stimulated by large inflations or deflations of the lungsand by a large number of inhaled irritants such as ammonia, So2, 03, and inflammatorymediators such as histamine, serotonin, and prostaglandin (PG) F2a. Stimulation of theirritant receptors causes cough, hyperpnea, increased mucus secretion, as well as vagallymediated reflex bronchoconstriction and laryngeal constriction.Pulmonary and bronchial C-fibers arise from a wide area of the lung and bronchialtree. These non-myelinated nerve endings are thought to be stimulated by pulmonaryedema and congestion and by embolization of the pulmonary vascular bed. They are alsostimulated by capsaicin, bradykinin, histamine, PGF2a, PGE2, PGI2, and SO2. Stimulationcauses rapid, shallow breathing, bronchoconstriction and increased airway secretion and areoften associated with cardiovascular depressor effects.There is some indirect evidence of an increase in central vagal drive in patients withasthma or COPD (Kallenbach et al., 1985; Postma et al., 1985). Activation of afferent andefferent pathways may also lead to increased vagal tone. Human airway smooth musclesare almost completely devoid of adrenergic nerves, however, endogenous circulatingcatecholamines play an important role in inhibiting cholinergic neurotransmission in the72airways (Danser et al., 1987). Impaired circulation of epinephrine is known to occur inasthmatic subjects and may play a role in BHR (md et al., 1985).Since non-adrenergic, non-cholinergic (NANC) innervation is the sole inhibitorysystem from the large to small airways, it has been suggested that a defect of this systemmay contribute to BHR. There is increasing evidence to suggest that neuropeptides maybe involved in NANC neurotransmission. VIP and a related peptide, peptide histidinemethionine, are known to be potent relaxants of airway smooth muscle. VIP is a Co.transmitter with acetyicholine in airway cholinergic nerves and may act as a “braking”mechanism to excessive cholinergic bronchoconstriction (Barnes, 1987). VIP also inhibitsantigen-induced histamine release in the guinea-pig lung, suggesting that VIP-receptors maybe present on mast cells (Undem et a!., 1983).Perhaps a more likely abnormality in the modulation of airway responsiveness is anincrease in NANC excitatory mechanisms. NANC bronchoconstriction is due to release ofneuropeptides from C-fiber endings (Lundberg et al., 1988). It has been proposed by Barnes(1986) that when these nerve endings are exposed to epithelial-cell-damaging inflammatorymediators an axon reflex might be triggered, resulting in smooth muscle contraction,microvascular leakage, and hypersecretion of mucus. Substance P, Neurokinin A and B,Neuropeptide K, and Calcitonin Gene-Related Peptide are all neuropeptides that enhanceairway smooth muscle contraction and amplify neutrophil and eosinophil responses tochemotactic agents, thus magnifying the inflammatory response in the airways (Hua et a!.,1985; Lundberg et al., 1983; Saria et al., 1988).Recent studies have suggested that inflammation may play an important role in thedevelopment of BHR and the symptoms of chronic asthma (Barnes, 1989). Increasedvascular leakage through the basement membrane of the endothelium is now thought to play73an important role in the regulation of airway inflammation (Laitinen et aL, 1985). Themechanisms responsible appear to be independent of epithelial permeability (Hogg, 1981).The role of the epithelial barrier against physiologic, pathologic, and pharmacologic stimuliis becoming of interest to researchers because of two reasons: (1) permeability changes ofthe epithelium; and (2) mediator generation from the epithelium. In patients with asthmaor COPD, an increase in epithelial permeability may be present.Recently, epithelial cells have been identified as a possible source of mediatorsinvolved in smooth muscle contraction and inflammatory reactions. Epithelial cells mayrelease epithelium-derived relaxing factor (Flavahan and Vanhoutte, 1985), a relaxing factorfor airway smooth muscle. Epithelial cells are also able to produce LTB4 which attractsneutrophils, contracts smooth muscle, and increases BHR in some species (Holtzman et aL,1983 and O’Byrne et al., 1985). Damage to the epithelium may increase sensitivity toacetyicholine, serotonin, and histamine (Flavahan et al., 1985).The immunologic pathway that is classically implicated in asthma involves the releaseof mediators from mast cells. Mast cells are located throughout the bronchial tree, but aremainly located in the bronchial mucosa between the epithelium and basement membrane.IgE receptor-mediated stimulation results in the release of several vasoactive, spasmogenic,and chemotactic mediators including histamine, leukotriennes, prostaglandins, and plateletactivating factor (PAF). It appears that the release of mast cell mediators is important inmaintaining the early phase reactions of asthma (Deyzer et al., 1984), and attracting anumber of inflammatory cells that are responsible for the late phase reactions (Wenzel etal., 1988).Macrophages, eosinophils, and platelets also have been shown to have surface74receptors for IgE (Capron et aL, 1981; Joseph et al., 1983; Joseph et aL, 1986). Alveolarmacrophages are a rich source of arachidonic acid metabolites, producing PGD2,PGF2a, andTxA2. An increased number of eosinophils in the blood, sputum, and airways of patientswith asthma is common. Booy-Noord et al. (1972) noted that eosinophils increased inconcurrence with an increase in bronchial responsiveness in peripheral blood after late-phase allergen-induced reactions. Eosinophils may be attracted to the lung by severalchemotactic factors including PAF, PGD2 LTB4,histamine and serotonin (Digby and Nadel,1988) and are activated by IL-3 and IL-5 (Silberstein and David, 1987). Their location inthe airways makes them available for phagocytosis of inhaled particles; the nature of theirsecretory products makes them a likely candidate for involvement in BHR, both inincreasing responsiveness and in limiting the extent of the inflammation andpathophysiological consequences (Postma et al., 1989).Platelets are known to secrete chemotactic products for neutrophils, enhance theiradhesion to vascular walls, augment release of enzymes, and stimulate the production ofinflammatory mediators (Weksler, 1988). Day et al. (1975) suggest there is a relationshipbetween the late-phase reaction of asthma and platelet activation. The release of PAF andthe activation of the platelets may result in bronchoconstriction and BHR through aninflammatory reaction (Manzoni et al., 1985).Lymphocytes have been shown in several animal models to modulate IgE production.Antigen-activated lymphocytes may release lymphokines and stimulate the production ofneutrophils and macrophages by the bone marrow, chemotaxis of neutrophils to the site ofinflammation, and prime eosinophils and macrophages for heightened cytotoxic activity(Postma et al., 1989). Lymphocytes have also been shown to produce a histamine releasing75factor (HRF) for mast cells and basophils (Sedgwick et al., 1981).We still know very little about the factors that modulate the severity of bronchialresponsiveness. Exposure to allergens and occupational agents, a history of smoking, viralrespiratory infections, air pollution, and pre-existing airflow obstruction are thought toincrease bronchial responsiveness in asthma and COPD (Postma et al., 1989).Hypersensitivity to environmental antigens is often an important clinical feature ofasthma (Weiss et al., 1989). Antigen challenge and longitudinal clinical studies have shownthat allergy and allergen exposure may lead to increased non-specific bronchialresponsiveness in asthmatics (Cockcroft et al., 1977). The ability of an allergen to produceincreased airway responsiveness is dependent on the degree of allergy, the dose of antigen,and the degree of non-specific airway responsiveness (Cockcroft et al., 1979). In thelaboratory, a subject’s response to histamine or methacholine increases after allergenchallenge or occupational agent exposure. In sensitized patients, natural exposure toairborne allergens or occupational asthma-inducers may also lead to an increase in airwayresponsiveness (Vedal and Chan-Yeung, 1989). Conversely, removing the patient fromenvironmental exposure to domestic or occupational allergens often results in decreasedairway responsiveness. The magnitude and duration of the increased airway responsivenesshas been shown to correlated with the late-phase reaction of asthma (Durham, 1987).Bronchial inflammation resulting from antigen exposure is likely to be at least partlyresponsible for the association between allergy and heightened airway responsiveness to nonantigenic stimuli. This inflammatory response may result in damage to the respiratoryepithelium, submucosal edema, and alterations of the neural mechanism involved in theregulation of bronchial smooth muscle. Even in children who have been asymptomatic76throughout their lives and have no history of atopic disease, BHR appears to be closelylinked to total serum IgE levels (Sears et aL, 1991). Despite the association betweenheightened non-specific airway responsiveness and allergy, there have been no populationstudies that have related the degree of BHR to serum IgE levels (Burrows, 1989). Althoughallergen-induced airway hyperresponsiveness is the most studied of the airwayhyperresponsiveness syndromes, it is by no means the only type and may not be the mostcommon either epidemiologically or clinically (Postma et aL, 1989).Cigarette smoking has been shown to cause an acute increase in airway resistance tonon-smokers exposed in the laboratory (Nadel and Comroe, 1961). Several studies havealso shown increased BHR in smokers compared to non-smokers (Buczko et aL, 1984;Gerrard et al., 1980; Taylor et al., 1984). Taylor et al. (1985) found that the decline inFEV1 over a 7 year period was faster in smokers who had a PC20 <16 mg/mL whencompared to smokers who had lower bronchial responsiveness. In their study, 30% of thesmokers and 5% of non-smokers had a PC2O < 16 mg/mL. It has also been suggested thatexposure to cigarette smoke may predispose smokers and non-smokers to allergens (Tayloret al., 1985). Smokers also have a higher total serum IgE concentration and lower totalserum IgG and 1gM concentrations than non-smokers (Gerrard et al., 1980). Cigarettesmoking appears to predispose workers to sensitization to some compounds that areresponsible for occupational asthma (Vedal and Chan-Yeung, 1989). Smoking also appearsto play an important role in the development of COPD in asthmatic patients with markedBHR and atopy (Sparrow and Weiss, 1989).Population-based studies have provided conflicting evidence regarding the influenceof passive smoking on non-specific bronchial responsiveness and asthma among children.77O’Connor et al. (1987) found an association between BHR and maternal smoking in 21asthmatic children and young adults. They were unable to demonstrate a similar associationin non-asthmatic subjects, despite the occurrence of significantly lower levels of FEy1 andFEF2575% in association with maternal smoking. An association between parental smokingand symptoms of cough, phlegm, and wheeze were found in school children in two studies(Dodge, 1982; Weiss et al., 1980). Gortmaker et al. (1982) estimated that 18-34% ofchildhood asthma in a sample of children from Michigan and Massachusetts could beattributed to maternal smoking. In contrast to these results, Schenker et al. (1983) foundno association between parental smoking and wheezing or asthma.Several studies have suggested an association between viral respiratory infections inchildren, notably croup (Gurwitz et al., 1980; Zach et al., 1981) and bronchiolitis (Gurwitzet al., 1981; Pullan and Hey, 1982) and the subsequent development of increased levels ofbronchial responsiveness. Viral infections are known to increase the permeability of therespiratory epithelium and cause loss of columnar epithelium and i3-receptor downregulation (Busse, 1977). Respiratory illnesses are likely to exert their effects early in lifewhen the lung is more vulnerable, and may be more important in boys, especially those whoare atopic (Weiss et at., 1989). Weiss et al (1985) assessed the relationship betweenrespiratory illness and airway responsiveness and atopy in a cohort of 194 children betweenthe ages of 12-16 years. The results of their study suggest that respiratory illness in earlylife is associated with airway hyperresponsiveness as measured later in childhood. Theseresults are not universal, however, and some studies have failed to find significant effectsof viral infections using either histamine (Jenkins and Breslin, 1984) and cold air (Weiss etal., 1984).78In a cross-sectional study of the effects of air pollution on the chronic respiratoryhealth of children, Dockery et al. (1989) showed positive associations between theprevalence of chronic cough, bronchitis, and chest illness and all measures of particulatepollution and positive, but less strong, associations with the concentrations of two gases, SO2and NO2. No association was found between asthma, persistent wheeze, hay fever, ornonrespiratory illness, or between pulmonary function measures and the level of pollution.Air pollution measurements included total suspended particulates, particulate matter lessthan 15 m and 2.5 m aerodynamic diameter, fine fraction aerosol sulfate, SO2, NO2, andNon-specific bronchial hyperresponsiveness is partially determined by the prechallenge level of pulmonary function in both adults with intrinsic and extrinsic asthma(Ulrik, 1993). It has been suggested that the relationship between the baseline level ofpulmonary function and the degree of non-specific bronchial responsiveness is extremelycomplex (Weiss et al., 1989), however, it is probably the single best indicator of bronchialresponsiveness (Rijcken et al., 1988; Sparrow et aL, 1987). This may reflect baseline airwaycaliber, aerosol deposition, or other aspects of test performance, or alternatively, may reflecta causal relationship between airway responsiveness and lower levels of pulmonary function.Increased levels of airway responsiveness might lead to lower levels of pulmonary functionvia chronic inflammation or a change in mechanical factors linking increased levels of airwayresponsiveness with diminished lung elastic recoil (Rijcken et al., 1988; Sparrow et al., 1987).Several studies suggest that airway responsiveness is increased in the very young andthe elderly (Hopp et al., 1985; Rijcken et al., 1987; Weiss et al., 1984) and this may reflect79the lower levels of lung function that are common at the extremes of age. Children whohave symptoms early in life will have more severe asthma and more BHR (Seinra Mongeand Balvanera Ortiz, 1991; Sparrow et aL, 1987).In the workplace, inhalation of agents that have known or suspected allergic orirritant properties may result in the development of a variant of asthma known asoccupational asthma. Over 200 compounds have been reported to give rise to occupationalasthma (Chan-Yeung and Malo, 1994). Almost all patients with symptomatic occupationalasthma have increased bronchial responsiveness (Lam and Chan-Yeung, 1979). It has beenshown that removal of patients from the offending agents results in recovery inapproximately 40% of the patients, and this recovery is associated with gradualdisappearance of BHR (Paggiaro et al., 1984). Re-exposure of the patients to the sameworking environment leads to recurrence of asthmatic symptoms and to an increase inbronchial responsiveness (Hargreave et al., 1984). Because exposure to these irritants in theworkplace is common, a clear understanding of their role in occupational lung disease isimportant. If irritant exposures in the workplace can induce BHR, it is possible that theexposure may be implicated in the development of adult-onset asthma or COPD (Kennedy,1992).The agents that are responsible for occupational asthma can be divided into twocategories: high molecular weight compounds and low molecular weight compounds(MW< 1,000 daltons) (Vedal and Chan-Yeung, 1989). In occupational asthma caused byexposure to high molecular weight compounds, specific 1gB antibodies are found in the seraof affected patients. Skin tests with the extract of the appropriate allergen induce animmediate wheal and flare reaction. Clinically, the patients are usually atopic with a history80of allergic rhinitis and/or eczema and usually complain of asthma symptoms within a fewminutes of exposure. In contrast, in occupational asthma due to low molecular weightcompounds, specific IgE antibodies are either not found or found only in small proportionof the patients when the chemical is conjugated to a body protein (Vedal and Chan-Yeung,1989).Inhalation of respiratory irritants may also result in the development of occupationalasthma. Because of its non-immunological etiology this form of asthma is known as irritant-induced asthma or Reactive Airways Dysfunction Syndrome (RADS). RADS is notuncommon in patients who have been referred for assessment of occupational asthma. Itis estimated that between 2-6% of patients who are seen for assessment of occupationalasthma will be clinically diagnosed with RADS (Brooks et aL, 1985; Tarlo and Broder,1989).By definition, RADS occurs following a single, excessively high environmental oroccupational exposure to irritants in the form of gases, vapours, fumes, or smoke (Brookset al., 1985). Clinically, RADS is similar to asthma in that it is associated with symptomsof cough, dyspnea, and wheezing, and is almost universally associated with BHR. It differsfrom typical asthma in that it has a rapid onset, specific relationship to a singleenvironmental exposure, and has no apparent pre-existing period for sensitization to occur,with the apparent lack of an allergic or immunologic etiology. Typically symptoms occurwithin 24 hours of the exposure and persist for a minimum of 3 months. Pulmonarymechanics, diffusing capacity, and chest x-rays may be normal, but methacholine challengetesting is usually positive (Brooks et al., 1985).Most of the studies that have identified RADS have been case studies of patientsinvolved in exposure to a wide variety of chemicals. Inhalation of glacial acetic acid (Kern,811991), hydrochloric acid (Boulet, 1988; Promisloff et al., 1990), paint fumes, uraniumhexafluoride, floor sealant, hydrazine, metal coat remover, propylene glycol, alphachiorophane (Brooks et al., 1985; Brooks, 1985), epoxy resins (Lerman and Kipen, 1988),SO2 (Charan et aL, 1979; Rabinovitch et al, 1989), chlorine gas (Chester et aL, 1977; Mooreand Sherman, 1991; Schwartz et al., 1990), toluene diisocyanate (Boulet, 1988), ammonia(Bernstein and Bernstein, 1989), reactive dyes (Park et aL, 1990), latex (Tarlo et aL, 1990),aluminum (Soyseth et al., 1992), dusts and molds (Gilbert and Auchincloss, 1989), cleaningfluids (Murphy et al., 1976), and to the products of combustion and pyrolysis in fires(Sherman et al., 1989) have been implicated in the development of RADS.Mechanisms to explain the development of RADS have focused on the toxic effectsof the irritant exposure on the airways. The increase in bronchial responsiveness in RADSis probably due to an inhalation injury (Brooks et al., 1985; Flury et al, 1983). Bronchialbiopsies of RADS patients have shown damage to the respiratory epithelium with chronicnon-specific airway inflammation. Mild inflammatory infiltrates in bronchial and bronchiolarwalls have consisted mainly of lymphocytes and plasma cells. In addition, desquamation ofthe respiratory epithelium has occurred without significant increases in eosinophilic infiltrateor exudate, mucus gland hyperplasia, basement membrane thickening, or smooth musclehypertrophy (Brooks et al., 1985). It has been suggested that these changes may causealtered neural and vagal reflexes, modify beta-adrenergic sympathetic tone, and increase therelease of inflammatory mediators.While the definition of RADS is restrictive and requires the presence of a high levelexposure, it is conceivable that chronic, low level exposure could cause a similar process tooccur (Brooks et al., 1985; Kennedy, 1992). Kennedy (1992) reported that there was82convincing experimental evidence to show that increases in BHR can occur followingrelatively low level irritant exposure in the workplace and that asthma may occur followinghigh level irritant exposure. Exposure of healthy subjects to 0.6 ppm ozone for 2 hours hasbeen associated with an increase in BHR in all subjects, irrespective of their atopic status(Holtzman et al., 1979). Three studies have implicated poor air quality in the developmentof respiratory symptoms, sensitization to aero-allergens, and BHR in swimmers who wereexposed to low-levels of chemicals used in disinfecting pooi water (Mustchin and Pickering,1979; Penny, 1983; Zwick et al., 1990). The results of these last three studies suggest thatproblems in maintaining proper swimming pooi chemistry using disinfectants such aschlorine may result in poor air quality and the development of BHR. There is also someanecdotal evidence to suggest that BHR may occur in swimmers who train in properlymaintained facilities (Zwick et a!., 1990).Thus, chronic, low level exposure to chemical irritants can lead to increased BHRand the development of irritant-induced asthma. The purpose of this study was to: (1)determine the prevalence of BHR in a group of competitive swimmers using a methacholinechallenge test; and (2) determine whether there are differences in the prevalence of BHRamong competitive swimmers with asthma or swimming-related symptoms and those whohave neither asthma nor swimming-related symptoms, and to compare their results with agroup of non-swimming athletes who have neither asthma nor swimming-related symptoms.83METHODSSubjectsThe competitive swimmers were placed into either a Case Group or a Control Groupdepending on their responses to the questionnaire. A subject was considered eligible forthe Case Group if he/she had a medical history that included physician-diagnosed asthmaand/or symptoms suggestive of asthma (coughing, wheezing, chest tightness and difficultybreathing) while swimming in a pooi. A total of 28 lower mainland swimmers met thesecriteria. Of those, 18 had a medical history which included asthma. Eighteen swimmers(64.3% of eligible participants) agreed to participate in the study and formed the CaseGroup. A total of 58 lower mainland swimmers stated that they never had asthma orsymptoms suggestive of asthma while swimming in a pooi. These swimmers were consideredeligible for the Control Group and 17 (29.3% of eligible participants) agreed to participate.In addition to the swimmers, we recruited 16 competitive athletes who did not useswimming as part of their training to act as a non-swimming control group. Among thisgroups of athletes there were 6 soccer players, 5 middle distance runners, 2 cyclists, 1 rower,1 skater, and 1 field hockey player. Many of these athletes have participated inintercollegiate and national championships. None of the athletes had a medical history thatincluded physician-diagnosed asthma and/or symptoms suggestive of asthma while exercising.The subjects were informed about the purpose of the test and the procedures to befollowed. All of the subjects read and signed a consent form prior to participating in thestudy.84Preparation of the Methacholine SolutionAcetyl-3-methyl chloride (methacholine) solutions were prepared by the Pharmacyat University Hospital, U.B.C. Site. The following concentrations of methacholine wereproduced from stock methacholine powder (Valtec Labs, Montreal, PQ): 16.0 mg/mL, 8.0mg/mL, 4.0 mg/mL, 2.0 mg/mL, 1.0 mg/mL, 0.5 mglmL and 0.25 mg/mL. To prepare therequired concentrations of methacholine, the hospital pharmacy diluted 1,920 mg ofmethacholine powder with 28.08 mL of bacteriostatic normal saline solution to produce 30mL of 64.0 mg/mL methacholine solution. This solution was then diluted serially toproduce 30 mL of each of the required concentrations of methacholine. Each of themethacholine solutions was placed in a 30 mL bacteriostatic vial, labelled, and sealed in anamber bag. The vials were stored in a refrigerator at 4 C in order to reduce the risk ofchemical instability and contamination. The methacholine was removed from therefrigerator at least 30 minutes before testing and allowed to equilibrate to roomtemperature before use.Calibration of the NebulisersPrior to beginning the study, 2 Wright nebulisers (Aerosol Medical Ltd, Colchester,Essex, UK) were calibrated using the procedures outlined by Juniper, Cockcroft andHargreave (1991). Three mL of saline solution were placed into the vial of the nebuliser,the vial was attached to the nebuliser and weighed on an FX-40 analytical balance (ANOCompany Ltd, Tokyo, Japan) that was accurate to 0.001 gm. The flow rate was adjusted to7.0 L/min and the nebuliser was attached to the flow meter for exactly two minutes. Theflow meter was used to control the flow of medical air (Medigas Ltd, Vancouver, BC) to the85nebuliser. The nebuliser was disconnected from the flow meter and the nebuliser and vialwere weighed. The nebuliser output was determined from the difference in weight of thenebuliser and vial.These procedures were repeated five times at each of the following flow rates: 7Llmin, 8 L/min and 9 L/min. The mean value of the five measurements for each flow ratewas plotted against the flow rate in order to determine the flow rate that generated anoutput of 0.13 mL/min (Figure 1). Each set of measurements was reproducible to within± 0.006 gm. A flow rate of 7 L/min was found to generate an output of 0.13 mL/min andthis flow rate was used for all subsequent experiments.Calibration of the SpirometerA 1070 Pneumotach (Medical Graphics Corporation, St. Paul, MN) was used tomeasure lung function. The pneumotach was calibrated prior to testing the first subject.The barometric pressure, room temperature and valve dead space were entered into thecomputer program operating the pneumotach and the pneumotach was calibrated for bothexpiratory and inspiratory manoeuvers. A 3 litre syringe was connected to 1%” tubing thatwas attached to the pneumotach. The pneumotach was zeroed to ensure there was no biasflow through the system. The calibration syringe was used to inject five samples of air intothe pneumotach at varying flow rates. A calculated volume error of less than 2% wasconsidered acceptable. The pneurnotach was again zeroed and the calibration syringe wasused to withdraw five samples of air from the pneumotach at varying flow rates. Onceagain, a calculated volume error of less than 2% was considered acceptable. Theseprocedures were repeated every 3 hours.86Figure 1: Calibration of the Wright Nebulisers prior to methacholine challenge testing. Theflow rate of medical air necessary to generate a nebuliser output of 0.13 mL/minutewas determined for two nebulisers. Each of the nebulisers required a flow rate of7 L/minute to generate this output. Figure (a) represents the calibration resultsfor the first nebuliser and Figure (b) represents the calibration results for thesecond nebuliser.0.16‘ 0.15(a) EE; 0.11a)Z 0.100.09Li I I I I6.0 6.5 7.0 7.5 8.0Flow Rate (L/minute)0.160.15; o.n.z 0.100.09I I____I6.0 6.5 7.0 7.5 8.0Flow Rate (L/minute)87Test ProceduresPrior to methacholine challenge testing, the subjects were asked to refrain fromtaking medications that are known to inhibit the response of the airways to methacholine.These drugs include inhaled 13-agonists (8 hours), oral /3-agonists (12 hours), inhaledanticholinergics (12 hours), theophylline (24 hours), slow-release theophylline andcorticosteroids (48 hours) and antihistamines (4 days). The subjects were also asked torefrain from exercising or ingesting caffeine on the day of testing.Lung function was assessed using spirometry. Spirometry was performed usingcriteria outlined by the American Thoracic Society’s Standardization of Spirometry-1987Update (American Thoracic Society, 1987). The subjects initially performed a Slow VitalCapacity (SVC) manoeuver. They were asked to breath normally for 4-5 breaths. At theend of the last normal expiration, the subjects were asked to take a deep breath and filltheir lungs as completely as possible. When their lungs were completely full, the subjectswere asked to expire the air until they felt their lungs were completely empty. No time limitwas imposed on the manoeuver. They were then asked to take one more deep inspirationand fill their lungs as completely as possible. A minimum of 3 SVC manoeuvers wereperformed and the reported SVC was derived from the test that produced the largest SVC.The subjects then performed a Forced Vital Capacity (FVC) manoeuver. They wereasked to breath normally for 4-5 breaths. At the end of the last normal expiration, thesubjects were asked to take a deep breath and fill their lungs as completely as possible.When their lungs were completely full, the subjects were asked to expire the air as hard andas fast as possible until they felt their lungs were completely empty. They were then askedto take one more deep breath and fill their lungs as completely as possible. A flow-volume88curve was generated and displayed on the computer screen, with flow (L/sec) on theordinate and volume (L) on the abscissa. A minimum of 3 “acceptable” tests wereperformed. A test was considered acceptable if it met the following criteria: (1) a maximal,smooth effort was observed; (2) the subject did not cough, perform a valsalva manoeuver,prematurely stop his/her expiration or have an air leak; (3) the extrapolated volume wasless than 5% of the FVC or less than 100 mL, whichever was greater; and (4) at least twoout of the three tests were within ± 5% or ± 100 mL. The FVC, FEy1FEV1/FVC, MidMaximum Expiratory Flow Rate (FEF2575) and the Maximum Expiratory Flow Rate (VJwere recorded and displayed on the computer screen. The reported FVC was derived fromthe test that produced the largest FVC. The FEy1 was derived from the test that producedthe largest FEV1. The ratio of the FEV1/FVC was recorded as a percentage. The FEF75and‘fl1ax were taken from the test that produced the largest sum of FVC and FEy1. Thesevalues were entered into a database for statistical analysis.Once the spirometry had been completed, a face mask (Puritan Bennett Corp, LosAngeles, CA) was attached to the output port of the nebuliser. Using a 3 mL syringe andneedle, 3 mL of saline solution were placed into the nebuliser vial. The vial was attachedto the nebuliser and the nebuliser was handed to the subject. The subject was instructedto hold the nebuliser and not the vial in order to prevent warming of the solution in the vial.As the flow meter was turned on, the face mask was placed loosely over the subject’s noseand mouth. The subjects were instructed to relax and breathe quietly while they inhaled thesaline solution. After exactly 2 minutes the flow meter was turned off and the mask andnebuliser were removed from the subject’s face. The subject’s FEV1 was measured 30 and90 seconds after the end of the inhalation. During the expiratory portion of the spirometry89manoeuver, the subjects were asked not to expire to residual volume in order to preventfatigue or premature closure of the small airways. If the FEy1 at 90 seconds was the sameor lower than that at 30 seconds, the FEy1 was repeated at 3 minutes and, if needed, at 2minute intervals until the FEy1 started to increase. The FEy1 was only measured once ateach time interval to prevent tiring the subject, however, if the subject’s performance wasnot technically satisfactory, the FEy1 measurement was repeated after 10 seconds. Thelowest post-saline FEy1 was used as a baseline measurement for all subsequent calculations.The subjects were told that subsequent aerosols may produce a mild cough, chesttightness, wheezing or shortness of breath. They were instructed to remove the face maskand to stop inhaling the aerosol if any of these symptoms made them uncomfortable. Theinitial concentration of methacholine given to subjects who had asthma, or symptomssuggestive of asthma while swimming, was 0.25 mg/mL. All other subjects started at aconcentration of 1.0 mg/mL. The procedures that were outlined for administrating thesaline solution were repeated. The concentration of methacholine was doubled and givenat 5 minute intervals until the FEV1 fell by 20% from baseline (PC20), the FEy1 1.5 Lor the highest concentration of methacholine (16.0 mg/mL) had been given. All subjectswere then given 200 of Salbutamol (Glaxo Canada mc, Toronto, ON) and theirspirometry was repeated to ensure the subject’s pulmonary function had returned to normal.After each test, distilled water was placed in the nebuliser vial and the nebuliser wasoperated for at least 2 minutes in order to flush the methacholine from the nebuliser. Thenebuliser was then washed and rinsed thoroughly and allowed to dry before further use orstorage. The data was entered into a database for statistical analysis.90Statistical AnalysisA PC20 was calculated for all of the subjects who had a fall in FEV1 of at least 20%following methacholine challenge testing. The PC20 was calculated using the followingformula (Juniper et al., 1991):I (log C2 - log Cl) x (20 - Ri) 1PC20 antilog . log Cl +(R2-R1) Jwhere: Ci = second last concentration of methacholine (<20% fall in FEy1)C2 = last concentration of methacholine (>20% fall in FEy1)Ri % fall in FEV1 after CiR2 = % fall in FEV1 after C2A PC20 16 mg/mL was considered to represent increased bronchial responsiveness. Theprevalence of increased bronchial responsiveness was then determined for each group ofathletes. A dose-response slope was calculated for all of the subjects (O’Connor et al.,1987). The dose-response slope was expressed as the FEV1/METDOSe ratio, where FEy1 wasthe maximum decrease in FEy1 from the post-saline value and METDOSe was defined as thefinal cumulative dose of methacholine that was given to the subject. The tables forcalculating METo,e are presented in APPENDIX B.The mean, standard deviation, and standard error of the mean were calculated forall of the descriptive variables . Analysis of variance (ANOVA) was used to determinewhether there were statistical differences in the mean values of the dependent variables forthe three groups of athletes who participated in the study. If statistical differences werefound, a Student-Newman-Keuls multiple range test was used to determine which groupsdiffered.91Sensitivity and specificity were determined from 2 by 2 contingency tables in which“physician-diagnosed asthma” versus “no asthma” was tabulated against “positive test” and“negative test”. Sensitivity was defined as the percentage of athletes with asthma and/orsymptoms suggestive of asthma who had positive methacholine challenge tests (PC20 16mg/mL). Specificity was defined as the percentage of athletes with neither asthma norsymptoms suggestive of asthma who had negative methacholine challenge tests (PC20>16mg/mL).An alpha level of 0.05 (p <0.05) was considered to be statistically significant. Allstatistical analyses were completed using the SAS® Statistical Software Package (SASInstitute, Inc., Cary, NC).92RESULTSA total of 51 subjects (25 male and 26 female) completed baseline spirometry andmethacholine challenge testing. The physical characteristics of the subjects are presentedin Table 14. There were no statistically significant differences in the age, height, or weightbetween the three groups of athletes. A comparison of the environmental conditions in thelaboratory is presented in Table 15. The mean air temperature and relative humidity of thelaboratory were significantly higher during testing of the Non-Swimming Control Group thanduring testing of either of the swimming groups (p <0.0069 and p < 0.0004,respectively).The pulmonary function data are presented in Table 16. The SVC, FVC, and FEy1were significantly lower in the Non-Swimming Control Group when compared to either ofthe swimming groups (p <O.Ol76,p <0.0277,and p < 0.0207,respectively). These differencescould not be accounted for by differences in the subjects’ height or age, and statisticallysignificant differences between groups existed for SVC, FVC, FEV1 and Vmax when thepercentage of predicted values were calculated. Only one of the 51 subjects (2.0%) hadabnormal baseline spirometry. In this case the subject’s FEV1/FVC ratio was only 66%which is suggestive of a mild obstructive pattern.The overall prevalence of increased bronchial responsiveness (PC20 16 mg/mL)among the 51 athletes was 45.1 %. This included eleven swimmers from the Case Group(61.1%), ten swimmers from the Control Group (58.8%), and two athletes from the NonSwimming Control Group (12.5%). When we increased the specificity of the test to includeonly those athletes with a PC20 8 mg/mL, six swimmers from the Case Group (33.3%) andsix swimmers from the Control Group (35.3%) had increased bronchial responsiveness.None of the non-swimming athletes had a PC20 8 mg/mL. The distribution of PC20 among93the three groups of athletes is outlined in Table 17; A summary of the dose-response curvesfor the three groups of athletes who participated in the methacholine challenge testing ispresented in Figures 2-5.The dose-response slope was calculated to be -6.55 ± 10.53 for the Case Group, -6.23± 8.63 for the Control Group, and -1.22 ± 0.72 for the Non-Swimming Control Group. Thedose-response data were found to be positively skewed and was normalized by using thenatural logarithm of each dose-response slope value. The log of the dose-response slopewas 1.08 ± 1.36 for the Case Group, 1.01 ± 1.43 for the Control Group, and 0.01 ± 0.79for the Non-Swimming Control Group. The log of the dose-response slope was significantlylower in the Non-Swimming Control Group when compared to either of the swimminggroups (p<0.0257).The sensitivity and specificity of a PC20 16 mg/mL for identifying subjects withasthma or symptoms suggestive of asthma while swimming were 66.7% and 71.4%,respectively. The sensitivity and specificity of a PC20 8 mg/mL for identifying subjects withasthma or symptoms suggestive of asthma while swimming were 27.8% and 81.8%,respectively.0Table14:Acomparisonofthephysicalcharacteristicsofthe3groupsofcompetitiveathletes.Thex±SDarereported.CaseGroupControlGroupNon-SwimmingLevelofControlGroupSignificanceAge(years)17.56±2.9919.18±3.6120.50±4.76NSHeight(cm)174.43±8.04175.62±9.25173.94±7.36NSWeight(kg)67.88±11.4869.29±9.4969.02±9.02NSNS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.Table15:Acomparisonoftheenvironmentalconditionsinthelaboratoryduringmethacholinechallengetestingofthe3groupsofcompetitiveathletes.Thex±SDarereported.CaseGroupControlGroupNon-SwimmingLevelofControlGroupSignificanceBarometricPressure(torr)757.72±4.66754.94±8.26755.56±2.68NSAirTemperature(C)21.50±1.1021.12±0.7822.25±1.06p<O.OO69*RelativeHumidity(%)59.28±5.1458.06±3.9665.19±5.99p<O.0004**ThemeanairtemperatureandrelativehumiditywerehigherduringtestingoftheNon-SwimmingControlGroup.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.1j0Table16:Acomparisonofthepulmonaryfunctionvariablesforthe3groupsofcompetitiveathletes.Thex±SDarereported.Thepercentageofpredictedvalues(inparenthesis)werecalculatedusingequationsbyKnudsonetal.(1983)andKnudsonetal.(1976).CaseGroupControlGroupNon-SwimmingLevelofControlGroupSignificanceSVC(L)5.52±1.00(126%)5.99±1.30(131%)4.89±0.82(107%)p<O.Ol76*FVC(L)5.46±0.94(125%)5.89±1.26(128%)4.89±0.81(107%)p<O.O2’T7FEy1(L)4.47±0.75(117%)4.86±0.88(122%)4.10±0.58(103%)p<O.O2O7FEV1/FVC(%)82.17±5.4883.29±7.1684.25±6.07NSFEFu%75%(Lfsec)4.31±0.94(98%)4.79±1.02(105%)4.55±1.29(98%)NS“(L/sec)9.23±1.83(116%)10.73±2.70(129%)8.95±1.70(107%)NS*ThemeanSVC,FVC,andFEy1valuesoftheControlGroupwerehigherthanthemeanvaluesoftheNon-SwimmingControlGroup.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.0Table17:Theresultsofmethacholinechallengetesting.ThedistributionofPD,issummarizedforthethreegroupsofathletes.CaseGroupControlGroupNon-SwimningControlGroupPC2mgImL212<PC4mg/mL34<PC8mg/mL428<PC16mgImL542PC>16mg/mL771497C-)o Case GroupV Control Groupfl Non-Swimming Control GroupFigure 2: Dose-response curves for all three groups of athletes during methacholine challengetesting. The percentage change in FEV1 is plotted against the concentration ofmethacholine on a logarithmic scale.-25--20 -15 --10 --5 -0Sat’ 0.25 0.50 1 2 4 8 16Concentration of Methacholine (mglmL)Figure 3: Dose-response curve for the Case Group (n= 18) during methacholine challengetesting. The percentage change in FEV1 is plotted against the concentration ofmethacholine on a logarithmic scale.-40-35-30-25c)-15-20-1020-5050.25 0.50 1 2 4 8 16Concentration of Methacholine (mg/mL)>.-t1)-zU>-lU98Figure 4: Dose-response curve for the Control Group (n= 17) during methacholine challengetesting. The percentage change in FEy1 is plotted against the concentration ofmethacholine on a logarithmic scale.-40-35-30-25-20 Pc0-15-10-505Figure 5: Dose-response curve for the Non-Swimming Control Group (n= 16) duringmethacholine challenge testing. The percentage change in FEy1 is plotted against theconcentration of methacholine on a logarithmic scale.-40-35-30-25-20 PC20-15-10-5050.250.501 2 4 8 16Concentration of Methacholine (mg/mL)Salii’ 0.25 0.50 1 2 4 8 16Concentration of Methacholine (mg/mL)99DISCUSSIONThis study shows that the prevalence of BHR (PC 16 mg/mL) among competitiveswimmers in the lower mainland of British Columbia is approximately 60.0%. This includes61.1% of swimmers in the Case Group and 58.8% of swimmers in the Control Group. Whenthe sensitivity of the methacholine challenge test is increased to include only those swimmerswith a PC20 8 mg/mL, 33.3% of the swimmers in the Case Group and 35.3% of the swimmersin the Control Group demonstrated BHR. There does not appear to be any difference in theprevalence of BHR among swimmers who have asthma or complain of swimming-relatedsymptoms when compared to those that have neither asthma nor swimming-related symptoms.However, the prevalence of BHR among non-swimming athletes appears to be significantlylower than that of swimmers: only 12.5% of the non-swimmers had a PC20 16 mg/mL andnone had a PC20 8 mg/mL.Several studies have attempted to establish the prevalence of BHR in the normalpopulation. Cockcroft et al. (1992) conducted a survey of 500 college students and measuredtheir PC20 using histamine. BHR (PC20 8 mg/mL) was observed in only 11.6% of the students.Woolcock et al. (1987) estimated the prevalence of BHR in 876 subjects from Western Australiato be approximately 11.4%. Their study identified strong associations between BHR andrespiratory symptoms, atopy, smoking, and abnormal lung function, however, there was noassociation found between BHR and age, sex, or recent respiratory tract infections. Finally,Burney et al. (1987) estimated the prevalence of BHR to be 14% in 511 subjects from southernEngland. BHR was strongly associated with skin sensitivity to common allergens and a positivehistory of smoking. Both skin sensitivity and a history of smoking were dependent on age. Skinsensitivity was an important determinant of BHR in the young subjects and smoking was an100important determinant of BHR in the older subjects.BHR has been found to be unimodally distributed in population samples and is negativelyskewed, that is, skewed toward hyperresponsiveness (Cockcroft et at, 1983; Cockcroft et at,1992; O’Connor et al., 1987; Weiss et at, 1984). Our results show that while BHR isunimodally distributed among the competitive swimmers, the data are positively skewed orskewed toward non-responsiveness. In addition, while a PC20 8 mg/mL is often used clinicallyto represent increased bronchial responsiveness, our results and those of several other studieshave indicated the benefits of using a PC2O 16 mg/mL in population studies (Cockcroft et at,1992; Kennedy et al., 1990; Malo et al., 1991).In their study of the sensitivity and specificity of PC20 in 500 students, Cockcroft et al.(1992) demonstrated that with “current symptomatic asthma” as the diagnosis and PC20 8mg/mL as the positive test, the sensitivity was 100%, the specificity was 93%, the positivepredictive value was 29%, and the negative predictive value was 100%. If the cut-off point forthe positive test was reduced to a PC20 < 1 mg/mL, the sensitivity and negative predictive valuewere decreased to 41 % and 98%, respectively, and the specificity and positive predictive valuewere both increased to 100%. In our study, the sensitivity and specificity of a PC20 8 mg/mLfor identifying subjects with asthma or symptoms suggestive of asthma while swimming were27.8% and 81.8%, respectively. In addition, a comparison of our pulmonary function andmethacholine challenge results with those of Cockcroft et al. (1992) would suggest that amongthose swimmers with asthma or symptoms suggestive of asthma, very few are currentasthmatics.Our results suggest that the sensitivity and specificity of using a questionnaire to diagnoseasthma in competitive swimmers is not very good. Part of the reason is that the prevalence of101BJIR in swimmers who have neither asthma nor symptoms suggestive of asthma during exercise,whether you consider a positive test at a PC2O 16 mglmL or PC2O 8 mg/mL, is higher thanin the normal population and similar between our Case and Control Groups. Our results aresimilar to those of Malo et al. (1991) who assessed the validity of using a questionnaire todiagnose occupational asthma. Their results suggested that an open medical questionnaire is nota satisfactory means of diagnosing occupational asthma.One of the disadvanttges of using the PC20 as an index of responsiveness is that a numberof subjects will fail to experience a significant drop in their FEy1 and their data will be left outof any statistical analyses. O’Connor et al. (1987) have suggested that in a population study theloss of this information may be consequential to the results of the study. The authorsrecommended that the dose-response data be summarized by using the ratio of the percentdecrease in FEy1 over the cumulative dose of methacholine that was given (dose-responseslope). In population studies, calculation of the dose-response slope allows for the inclusion ofall of the individual dose-response data.O’Connor et al. (1987) have shown that there can be more than a 3,000-fold differencebetween the least and most responsive subjects using this method. In our study there wasapproximately a 363-fold difference between the least and most responsive subjects. When thedata were normalized by using the natural logarithm of each of the mean values, the doseresponse slope was found to be significantly lower in the non-swimmers than in either of theswimming groups. This indicates that bronchial responsiveness was significantly lower in thenon-swimmers.The remarkable differences in the prevalence of BHR between the swimmers and nonswimmers is one of the interesting findings of this study. To our knowledge, there are only two102other studies that have evaluated BHR among highly trained athletes. Zwick et al. (1990)studied 14 competitive swimmers and 14 matched control subjects and found that 78.6% of theswimmers and 35.7% of the control subjects had increased bronchial responsiveness after beinggiven 140 g, 1540 g, and 8540 g of nebulised methacholine. The increase in non-specificbronchial responsiveness in the swimmers was associated with conjunctival or respiratorysymptoms (78.6%), sensitization to aeroallergens (78.6%), and altered cellular immunity(50.0%). The control group had significantly lower prevalences of symptoms (21.4%),sensitization to aeroallergens (35.7%), and altered cellular immunity (14.3%). The authorsconcluded that frequent exposure to chlorine, chlorine gas, or their constituents may facilitatesensitization to different allergens and increase non-specific bronchial responsiveness.Weiler et al. (1986) tested college athletes and students at the University of Iowa andfound BHR in 50% of the football players, 25% of the basketball players, and 41% of thestudents. In their study, BHR occurred if the FEy1 fell by 20% or more after administrationof 150 breath units of nebulised methacholine (1 breath unit = 1 mg/mL). Only 12% of thefootball players and 7% of the students had a history of asthma. The athletes and studentswithout nasal symptoms (allergic rhinitis or hay fever) were less likely to have BHR than thosewith symptoms and, contrary to other studies that have been published, athletes and studentswith current or recent upper respiratory tract infections were no more likely to have BHR thanthose who did not. The authors suggested that the high prevalence of BHR among the footballplayers may have occurred as a result of living and exercising in a polluted or cold environment,deconditioning, or because of allergies.The extremely high prevalence of BHR among the competitive swimmers may result fromchronic, low level exposure to chemical irritants in pool water. While this theory is speculative,103there are a number of studies which have shown that competitive swimmers may develop mildbronchial irritation from chronic, low level exposure to chemical irritants in pool water.Mustchin and Pickering (1979) described the sudden onset of reversible airways disease in 3swimmers during a training session in a recently opened indoor pool. Many of the 24 swimmerswho were training in the pooi at the time of the incident developed a cough, sore throat, andchest tightness, and nearly half of the swimmers had to leave the water as a result. Thedevelopment of these symptoms were apparently associated with a strong chemical odor in thepooi. The authors suggested that low concentrations of chlorine gas may have resulted in a milddegree of bronchial irritation.Penny (1983) described a case report of a 57 year old man who also complained ofcoughing for 12-24 hours after swimming in a recently opened pool. He also noticed a strongchemical odor in the pooi. The patient’s symptoms were associated with a reduction in FEy1following an exercise challenge swim in the pooi. This facility used a heat reclamation systemthat recirculated a high proportion of the air in the pooi. Penny suggested that this irritantexposure also resulted in a mild degree of bronchial irritation and increased bronchialresponsiveness.Our results suggest that the swimming-related exposure results in increased non-specificbronchial responsiveness without causing any measurable change in baseline lung function amongthe competitive swimmers. What we do not know is why some swimmers have swimmingrelated symptoms suggestive of asthma and others do not. A possible explanation might be thatthose swimmers who have swimming-related symptoms may have higher training volumes orcumulative exposures, or may have been exposed to higher concentrations of pool chemicals thanthose swimmers without swimming-related symptoms. However, our data suggests that there104were no differences in the training volumes or cumulative exposures among the two groups ofswimmers. Whether or not swimmers with swimming-related symptoms were exposed to higherconcentrations of chemicals used to treat the pooi water remains speculative. The clinicalmanifestations of this swimming-related exposure, whether it is related to the chemical treatmentof the pool water, exercise, or both, may simply be to increase BHR and, in some individuals,to cause swimming-related symptoms suggestive of asthma.Kennedy (1992) has suggested that chronic, low level exposure to environmental irritantsmay cause a significant increase in non-specific bronchial responsiveness. She goes on tosuggest that persons who are exposed accidentally or episodically to irritants at higherconcentrations may also develop symptoms suggestive of asthma, variable airflow obstruction,and even greater BHR. Other studies have shown that chemical irritation of the respiratory tractmay damage the respiratory epithelium and cause chronic, non-specific airway inflammation(Brooks et al., 1985; Gautrin et al., 1994).Most theories that relate epithelial damage and airway responsiveness are based on theassumption that epithelial damage and loss result in increased exposure of afferent receptors,increased sensitivity of the receptors, and enhanced accessibility of bronchoconstrictor agentsto bronchial smooth muscle and/or sensory nerve endings under the mucosa (Brooks et al., 1985;Postma et al., 1989). Tracheo-bronchial irritant receptors and pulmonary C-fibers are likelyinvolved in the physiological response to these chemical irritants. In particular, when C-fibersare exposed to inflammatory mediators they may trigger an axon reflex which results in therelease of several neuropeptides that enhance smooth muscle contraction and inflammation(Barnes, 1986; Lundberg et al., 1988). We postulate that this mechanism may be responsiblefor the increased non-specific bronchial responsiveness found in the competitive swimmers105involved in our study.The possibility also exists that chronic, low level exposure to chemically-treated pooiwater may result in the development of occupational asthma. Bernstein et al. (1993) definedoccupational asthma as a disease that is “characterized by variable airflow limitation and/orbronchial hyperresponsiveness due to causes and conditions that are attributable to a particularoccupational environment and not to stimuli encountered outside of the workplace”. Zwick etal. (1990) have demonstrated that competitive swimmers have increased sensitization to aeroallergens and it is possible that the chemicals used to treat the pooi water are not only irritants,but sensitizing agents as well. In a recently published study by Gautrin et al. (1994), the authorsassessed the reversibility of airway obstruction, determined the prevalence of BHR, anddescribed the pathological changes that occurred in the airways of patients with immunologically-induced occupational asthma and a severe form of irritant-induced occupational asthma, RADS.The results of this study show that patients with occupational asthma have greaterreversibility of airway obstruction following the administration of the 132-adrenergic agent,albuterol, however, they also have more pronounced BHR. The average improvement in FEV1following the administration of albuterol was 19.4% and 9.6% in patients with occupationalasthma and RADS, respectively. The average PC20 in the patients with occupational asthma was0.4 mg/mL, while the average PC20 in the patients with RADS was 2.0 mg/mL. Thepathological data retrieved from BAL fluid and biopsy specimens from the subjects suggests thatpatients with RADS have an increased number of inflammatory cells (including lymphocytes),focal desquamation of the epithelial layer in association with squamous cell metaplasia and theloss of cilia, the presence of inflammatory cells (lymphocytes, polymorphonuclear neutrophilsand eosinophils, mastocytes and monocytes/macrophages), extensive reticulocollagenic fibrosis106of the bronchial wall, and severe thickening of the basement membrane (Gautrin et al., 1994).The authors concluded that occupational asthma and RADS can be distinguished bydifferences in airway reversibility, BHR, and some of their pathological features. They alsosuggested that patients with RADS who have normal airway caliber, mild BHR, and minimalfunctional changes in airway function, may also have extensive pathological changes to theirairways. While the competitive swimmers in our study appear to have normal airway caliberand mild BHR, it is hoped that chronic, low level exposure to chemically-treated pool water doesnot result in the severe pathological changes that occur to the airways of individuals withoccupational asthma or RADS.107CONCLUSIONSIn conclusion, this study shows that the prevalence of BHR (PC20 16 mg/mL) amonglower mainland competitive swimmers is 60.0%. When the sensitivity of the methacholinechallenge test was decreased to include only those swimmers with a PC20 8 mg/mL, theprevalence of BHR is 34.3%. These values are significantly higher than the 12.5% and 0%prevalences that were observed for 16 non-swimming athletes in our study and the 11-14%prevalence reported in several population-based studies. There was no difference in theprevalence of BHR among competitive swimmers who have a clinical history of asthma orsymptoms suggestive of asthma while exercising (61.1%) and those who have neither asthma norsymptoms (58.8%). When the sensitivity of the methacholine challenge test was decreased toinclude only those swimmers with a PC2O 8 mg/mL, 33.3 % of the swimmers in the CaseGroup and 35.3% of the swimmers in the Control Group demonstrated BHR.The use of the dose-response slope was effective in assessing differences in BHR amongthe three groups of athletes. In our study there was approximately a 363-fold difference betweenthe least and most responsive subjects using this method. The dose-response slope wassignificantly lower in the non-swimmers, indicating a lower prevalence of BHR in that groupof athletes. The use of a clinical history to identify subjects with asthma was extremely poorusing either a PC2O8 mg/mL or a PC20 16 mg/mL. As an example, in our study thesensitivity and specificity of a PC20 8 mg/mL for identifying subjects with asthma or symptomssuggestive of asthma were 27.8% and 81.8%, respectively. In addition, a comparison of ourpulmonary function and methacholine challenge test results with those of Cockcroft et al. (1992)suggests that among swimmers who reported asthma or symptoms suggestive of asthma, veryfew are current asthmatics.108The clinical manifestations of this swimming-related exposure, whether it is related tothe chemical treatment of the pool water, exercise, or both, may simply be to increase BHR and,in some individuals, cause swimming-related symptoms suggestive of asthma. What remainsunknown is why some swimmers develop swimming-related symptoms suggestive of asthma andothers do not. A possible explanation might be that swimmers with swimming-related symptomsmay have been exposed to higher concentrations of pool chemicals than those swimmers withoutswimming-related symptoms, however, this theory remains speculative.The most likely mechanism for the increased non-specific bronchial responsiveness inthese competitive swimmers is that chronic, low level exposure to the chemicals used to disinfectthe pool water may cause damage to the epithelial layer of the swimmer’s airways. This damagemay result in increased exposure of afferent receptors, increased sensitivity of the receptors, andenhanced accessibility of bronchoconstrictor agents to bronchial smooth muscle and/or sensorynerve endings under the mucosa. 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Lung 1990; 168:111-115.118CHAPTER 3The Prevalence of Exercise-Induced Asthma in aSelect Group of Competitive Swimmers and Non-SwimmersABSTRACTExercise has been shown to be a potent, non-antigenic, non-pharmacologic stimulus forassessing bronchial responsiveness. Exercise-induced asthma (ETA) is the manifestation ofincreased bronchial responsiveness and is characterized by reversible airflow obstructionfollowing several minutes of exercise. Exercise differs from other initiators of asthma in thatit does not produce any long-term sequelae and, in about 50% of subjects with ETA, there is asignificant refractory period during which repeated exercise will attenuate furtherbronchoconstriction. The underlying pathophysiology of ETA is that during exercise heat andwater are lost from the respiratory epithelium in warming the inspired air from ambient to bodyconditions. The net effect is to cool and dehydrate the airways which, in turn, leads to thedevelopment of the post-exercise symptoms and bronchoconstriction which are typical of ETA.A number of researchers have suggested that an increase in bronchial responsiveness mayalso occur in athletes without ETA who have been exposed to swimming pooi disinfectants suchas chlorine or chloramines, or photochemical air pollutants such as ozone, nitrogen dioxide, andsulphur dioxide. Concurrent with this hypothesis, we have previously shown that 60% of thecompetitive swimmers that were tested had increased non-specific bronchial responsiveness tomethacholine. What remained to be determined was whether this was a response to chronic, lowlevel exposure to chemical irritants in the water and air of the swimming pool, an exerciseresponse, or both.119Therefore, the purpose of this study was to: (1) establish the prevalence of ETA in agroup of competitive swimmers using a standard exercise challenge test in the laboratory; (2)establish the prevalence of EIA in the same group of swimmers using an exercise protocol inthe swimming pool; (3) determine whether there are differences in the prevalence of asthmaamong competitive swimmers with asthma or exercise-related symptoms and those who haveneither asthma nor exercise-related symptoms, and to compare their results with a group of nonswimming athletes who have neither asthma nor exercise-related symptoms; and (4) determinewhether a prolonged exercise challenge test in the swimming pool results in the development ofrespiratory symptoms and significant changes in pulmonary mechanics among the two groupsof competitive swimmers.Our results show that the prevalence of ETA among lower mainland competitiveswimmers is 9.8%. This value is within the 3-11% prevalence reported for other competitiveathletes, and is higher than. the 6.3% that was observed for the non-swimming athletes in ourstudy. The prevalence of ETA among the swimmers was also higher in the laboratory (9.8%)when compared to the swimming pooi (3.6%). Our results are in agreement with those of otherresearchers who have shown the lower asthmogenicity of swimming when compared to land-based activities. The mechanisms for this protective effect are not clear and, in our study, donot appear to be related to differences in the subjects’ ‘E or the temperature and relativehumidity of the inspired air. There were also no differences in the prevalence of EIA amongcompetitive swimmers who have asthma or exercise related symptoms (11.1 %) and those whohave neither asthma nor exercise-related symptoms (11.8%).While continuous submaximal swimming for 45 minutes results in the swimmerscomplaining of many of the symptoms reported on the questionnaire, we were unable todemonstrate significant pre- to post-exercise changes in FEy,. However, the swimmers in the120Case Group adopted a restrictive breathing pattern similar to that of athletes who are exposedto ozone during exercise. It is possible that this might be an early indicator of respiratorydistress. Finally, there is a remarkable discrepancy between the prevalence of BHR and EIAamong the competitive swimmers. These results provide us with substantial evidence that thereis something about the swimming-related exposure that increases non-specific bronchialresponsiveness, but does not incite ETA.121INTRODUCTIONExercise is a potent, naturally-occurring, non-antigenic, non-pharmacologic stimulus forassessing bronchial responsiveness in subjects with asthma, allergic rhinitis, hay fever, and inathletes with symptoms suggestive of asthma during or after exercise. Exercise-induced asthma(ETA) is the manifestation of increased bronchial responsiveness that occurs in response tophysical activity and is characterized by reversible airflow obstruction following several minutesof exercise.The prevalence of ETA in asthmatics, atopic individuals and athletes has been welldocumented. Theoretically, any subject with current symptoms of asthma should develop ETAif challenged under the appropriate exercise conditions, however, only 60-90% of asthmatics and35-40% of subjects with allergic rhinitis or hay fever develop ETA (Anderson, 1985; Bundgaard,1981; Chan-Yeung et al., 1971; Itkin and Nacman, 1966; James et al., 1976; Kawabori et aL,1976; McNeill et al., 1966; Rupp et al., 1992). The prevalence of ETA among athletes rangesbetween 3-11 % (Fitch, 1984; Helbling and Muller, 1991; Huftel et al., 1991; Rice et al., 1985;Voy, 1986) and is approximately 7% in healthy controls (Bierman et al., 1975). The wide rangeof values reported in the literature for asthmatics is probably due to variability in the type,intensity and duration of exercise that were used to assess ETA and to discrepancies in thedefinitions of asthma and a positive exercise test.The clinical presentation of ETA may vary among individuals. Its presentation may besimilar to an acute attack of asthma, with the subject developing symptoms of wheezing, chesttightness, dyspnea, sputum production and coughing. Others may develop breathlessness thatis inappropriate to the exercise task, demonstrate a transient post-exercise cough, or performpoorly (McKenzie, 1991). The pattern of response of the airways to exercise is well known.122There is mild bronchodilation of the airways during exercise that is followed bybronchoconstriction and an increase in airway resistance in the immediate post-exercise period(Morton et aL, 1981; Stirling et al., 1983). The increase in airway resistance reaches maximalvalues in 3-5 minutes in children and 5-7 minutes in adults (Gilbert et aL, 1988) and returns tonormal values in 30-90 minutes (McFadden, 1991; McKenzie, 1991).The use of an exercise challenge test offers the advantage that normal subjects do notrespond to the challenge with any significant change in their lung function (Deal et al., 1980;McFadden, 1991). A positive exercise challenge test is defined as either a 15-20% decrease inthe subject’s baseline FEV1 or a 35-40% decrease in the specific conductance of the airwaysfollowing 6-8 minutes of exercise at an intensity of 85-90% of the subject’s maximal heart rate(Eggleston et al., 1979; McFadden, 1991; McKenzie, 1991; Mahler, 1993).There is good correlation between the prevalence of increased bronchial responsivenessas determined by exercise, histamine challenge or methacholine challenge (O’Byme et al., 1982;Weiss et al., 1983). However, as McFadden (1991) points out, there is not one-to-onecorrespondence and individuals may be more sensitive to exercise than to pharmacologicalstimuli, and vice versa. His article suggests that a negative exercise challenge test does notnecessarily exclude the existence of increased bronchial responsiveness.Exercise differs from other initiators of asthma in that it does not seem to produce anylong-term sequelae and it has a refractory period. Asthmatic subjects who are exposed toallergens or occupational sensitizing agents develop acute bronchospasm that is associated withinflammation of the airways (Crirni et al., 1992; De Monchy et al., 1985; Rossi et al., 1991;Zawadski et al., 1988). One of the controversial issues surrounding ETA is whether a latephase, inflammatory response to exercise occurs. While exercise has been shown to be123associated with mast cell degranulation and the influx of eosinophils and other inflammatorymediators into the airway lumen, the delayed bronchoconstriction observed 3-6 hours afterexercise is now thought to be unrelated to exercise and is more likely related to underlyingairway inflammation and to the withdrawal of medication in asthmatic subjects (Crimi et aL,1992; Zawadski et al., 1988). Rubinstein et al. (1987) also suggested that the biphasic asthmaticresponse to exercise is uncommon and is related to the withdrawal of medication ormethodological problems in the experimental design of the study.Approximately 50% of all subjects with ETA demonstrate significant refractoriness torepeated exercise challenge (McNeill et al., 1966; Schoeffel et al., 1980; Anderson, 1984).During this refractory period, the response of the airways to exercise can be attenuated for aslong as 4 hours (Edmunds et al., 1978; McNeill et al., 1966; Schoeffel et al., 1980). It wasoriginally thought that the degree of refractoriness may be related to the severity of exercise andthe degree of bronchoconstriction and could be explained on the basis of respiratory heat loss(RHL) (Edmunds et al., 1978). This hypothesis has been rejected because we now know thata good warm-up prior to exercise, and breathing warm, humid air during exercise, may abolishETA even though refractoriness to further exercise is maintained (Ben-Dov, 1982). Also,Anderson and Schoeffel (1982) have shown that about 50% of asthmatic subjects who wereexposed to two exercise challenge tests 40-52 minutes apart had significant protection from ETAfollowing the second challenge even though the RHL was the same.The refractoriness to exercise can be blocked by indomethacin and acetylsalicylic acid,both of which are cyclo-oxygenase inhibitors. This suggests that prostaglandins may play a rolein mediating the bronchodilation that occurs during exercise and the subsequent refractorinessthat occurs after exercise (Hahn et al., 1984, 1985; Margoiskee et al., 1988; O’Byrne and Jones,1241986; Reiff et al., 1989). Manning et al. (1993) studied 14 asthmatic subjects who werechallenged with exercise or inhaled LTD4. Several of the subjects then took part in a series ofdouble-blind, randomized, cross-over studies with flurbiprofen, a prostaglandin synthetaseinhibitor, to determine whether cross-over refractoriness occurred between exercise and LTD4,whether flurbiprofen attenuated this effect, and whether flurbiprofen attenuated LTD4tachyphylaxis. The results of this study showed that there was a reduction in the intensity ofbronchoconstriction to the second challenge both with exercise (refractoriness) and with LTD4(tachyphylaxis). The authors suggested that LTD4 released in asthmatic airways as a result ofexercise stimulates prostaglandin release which is, in part, responsible for exerciserefractoriness.Beicher et al. (1988) have proposed that the refractory period in ETA is also not causedby the depletion of mediators such as histamine or neutrophil chemotactic factor of anaphylaxis(NCFA). An alternative hypothesis suggests that increased sympathoadrenal activity may beresponsible for the refractoriness following exercise. This hypothesis has yet to be provenbecause the measurement of circulating catecholamines (epinephrine and norepinephrine) hasshown only modest increases during exercise and are supposedly blunted in asthmatic subjects(Barnes et al., 1981; Beicher et al., 1988). Is the depletion of mediators from mast cells andother inflammatory cells or increased catecholamine release during exercise responsible for therefractory period following exercise? As we have not yet been able to identify the cause ofeither ETA or its refractoriness to further exercise, there may be a number of inter-related factorsthat are responsible (Reiff et al., 1989).One of the methods that is thought to induce refractoriness and attenuate the airways’response to exercise is to warm-up prior to participating in vigorous physical activity. Repeated125short sprints result in significantly less bronchoconstriction in asthmatic subjects (Schnall andLandau, 1980). Fifteen minutes of continuous treadmill running at an exercise intensity of 60%of maximal oxygen consumption (VO2max) (McLuckie, 1986) and for 30 minutes at asubmaximal intensity (Reiff et al., 1989) have both been shown to be effective in inducingrefractoriness and decreasing the level of bronchoconstriction in subsequent exercise sessions.A study by Morton et al. (1979) used three minutes of treadmill running at an exercise intensityof 60% “O2max to determine the effect of warm-up. Their study failed to show any benefit ofwarm-up, but suggested that the intensity and duration of the warm-up be increased beforerejecting the hypothesis of the benefits of warm-up on ETA.The type of physical activity also plays an important role in determining the degree ofbronchoconstriction that occurs following exercise. Early studies used a variety of methods toinduce ETA. These included ascending and descending stairs (Davies, 1968; Fisher et aL, 1970;McNeill et aL, 1966), running along hospital corridors (Pierson and Bierman, 1975), treadmillwalking (Sly, 1970), bicycle ergometry (Pierson et al., 1969) and swimming (Bar-Yishay et al.,1982; Fitch, 1975). It was soon realized that different modes of exercise did not producecomparable effects (Anderson et al., 1971). Outdoor running is considered to be the mostasthmogenic activity, followed by treadmill running, cycling, swimming and walking (Andersonet al., 1971; Fitch and Morton, 1971). Respiratory heat loss and exposure to cold and dry air,dust, and photo-chemical air pollution (Bar-Or et al., 1977; McKenzie et al., 1987; Strauss etal., 1977) may help to explain why some activities cause more or less bronchoconstriction thanothers.It has now been shown that intermittent exercise causes less bronchoconstriction thancontinuous exercise, although the differences can be minimized by equalizing the minute126ventilation (‘1E) and presumably equalizing the RHL (McKenzie, 1991; Noviski et al., 1987).Fitch and Godfrey (1976) and Godfrey (1984) have clearly demonstrated a lower prevalence ofETA among athletes involved in intermittent activities. Part of the reason for this is thatintermittent activities allow the athlete to work at a high intensity for a short period of time.Exercise intensities of between 65-75% of the subject’s ‘!O2max have been shown to result inthe greatest post-exercise bronchoconstriction, while exercise intensities above 85% of thesubject’s VO2max result in little or no change in the degree of bronchoconstriction (Silvermanand Anderson, 1972).In the past, a number of mechanisms have been proposed to explain the post-exercisebronchoconstriction that is typical of ETA. The underlying pathophysiology of ETA is that duringexercise heat and water are lost from the respiratory tract in warming the inspired air fromambient conditions (ATPS) to body conditions (BTPS). The net effect of this process is to cooland dehydrate the airways which, in turn, leads to the development of post-exercise respiratorysymptoms and bronchoconstriction. The question that remains to be answered is how thiscooling and dehydration of the airways triggers ETA. A number of hypotheses have beenproposed, but the scientific evidence is not currently supportive of one theory.Airway cooling was thought to have a direct bronchoconstrictor effect on bronchialsmooth muscle and was responsible for the conversion of f3-adrenergic receptors into aadrenergic receptors (Bleeker et al., 1983; Sly, 1983; Venugopalan et al., 1988) and anincreased sensitivity to cholinergic stimulation (Sly, 1983). This hypothesis is supported byscattered reports of the efficacy of alpha adrenergic receptor antagonists in preventing EIA.McFadden (1991) has suggested that while airway cooling may initiate ETA, other mechanismsare responsible for sustaining it. His hypothesis is supported by the fact that airway warming127is quite rapid following exercise, with resting airway temperatures being reached in 15-30seconds. Also, despite these thermal changes, increases in airway resistance develop over thistime and last for 30 minutes or more (Gilbert et al., 1988).The release of chemical mediators from mast cells has been proposed as a mechanismfor the development of ETA. Beicher et al. (1988) and Lee et al. (1984) have shown thatelevated levels of histamine and NCFA are associated with ETA. The leukotriennes C4, D4, andE4 are released from the mast cells during exercise and are thought to play a major role inpathogenesis of ETA. This hypothesis has been supported by the inhibitory effects of theleukotrienne D4 receptor antagonist, ICI 204219, on post-exercise bronchoconstriction (Finnertyet al., 1992). Pliss et al. (1990) showed increases in bronchoalveolar lavage (BAL)concentrations of leukotrienes, eosinophils, and epithelial cells and a trend towards significantincreases in neutrophils and prostaglandin D2. Neuman et al. (1984) suggested that elevatedkallikrein levels may trigger ETA. In asthmatics, pre-treatment with Hi receptor antagonists andcyclo-oxygenase inhibitors have both been shown to minimize the effects of histamine andprostaglandins on ETA (Finnerty and Holgate, 1990).In-spite of this supportive evidence, BAL studies of atopic subjects with ETA have shownno significant differences in pre- to post-exercise histamine or tryptase levels (Broide et a!.,1990; Jarjour and Calhoun, 1992). Finnerty et al. (1991) have shown that a thromboxaneantagonist, GR32191, has no effect on ETA. This suggests that prostaglandins that act via thethromboxane receptor do not have an important role in ETA. EIA does not produce an increasein either immediate or delayed non-specific bronchial responsiveness to methacholine in atopicasthmatics. Hence, if mediators are released during exercise they must function differently thanwhen released by antigen (Lin Ct al., 1991; Zawadski et al., 1988). These results suggest that128the manifestation of ETA is not dependent on the release of chemical mediators from mast cells.Hvidsten et al. (1986) have questioned the role of gastrointestinal regulatory peptides inthe pathogenesis of ETA. In a comparison of subjects with ETA and controls, plasma levels ofVasoactive Intestinal Polypeptide (VIP) and Cholecystokinin (CCK) were significantly higherafter 6 minutes of exercise. The plasma levels of somatostatin, secretin, pancreatic polypeptide,and motilin showed no significant differences between the groups. More research is needed todetermine what role, if any, the gastrointestinal regulatory peptides play in the pathogenesis ofETA.It has been proposed that stimulation of pulmonary C-fibres by a number of chemical andphysical factors results in the release of neuropeptides such as tachykinins and calcitonin gene-related peptide from synaptic vesicles (Solway and Leff, 1991). In the airways, these sensoryneuropeptides act on the bronchial smooth muscle, the mucosal vasculature and submucosalglands to promote airflow obstruction, hyperemia, increased permeability and increased mucoussecretion. In addition, tachykinins may potentiate cholinergic transmission and promote therecruitment, adherence, and activation of granulocytes (Solway and Leff, 1991).It has been suggested that asthmatic subjects may have a blunted catecholamine responseto exercise (Barnes et al., 1981). Berkin et al. (1988) and Gilbert et al. (1988) have clearlydemonstrated that asthmatics do not have a defect in catecholamine release during exercise. Intheir studies, epinephrine and norepinephrine levels rose with repetitive exercise and resulted inconcurrent bronchodilation. It has been proposed that, in addition to their effects on smoothmuscle relaxation, the alpha-adrenergic actions of the catecholamines are also responsible forreducing airway wall hyperemia and edema (Gilbert et al., 1988).As mentioned earlier, our current understanding of EIA suggests that the post-exercise129bronchoconstriction is initiated by thermal events. The severity of airway narrowing followingexercise has been shown to be a function of the yE and the temperature and water content of theinspired air (Deal et al., 1979). For a given set of inspired air conditions, high minuteventilations result in more obstruction than do low levels, and cooling and drying the air at anylevel of ventilation cause more obstruction than when breathing warm and humid air (Deal etal., 1979; McFadden, 1991; Strauss et al., 1978). ETA can virtually be abolished if subjectsbreathe air that has been warmed to BTPS (Deal et al., 1979).It has been suggested by McFadden et al. (1986) and McFadden (1991) that ETA is avascular event. This hypothesis suggests that asthmatics have a hyperplastic capillary bed intheir airway walls and during exercise airway cooling is followed by rapid rewarming in theimmediate-post exercise period. The rapid change in airway temperature leads to reactivehyperemia and edema of the bronchial vascular bed which, in turn, leads to physical obstructionof the airways. Gilbert and McFadden (1992) have shown that alterations in blood supplydirectly affect bronchial heat flux and influence obstruction following isocapnic hyperventilationof cold air. By reducing the mucosal blood supply of the airways with the administration ofnorepinephrine there was limited rewarming of the airways which attenuated the obstructiveresponse. Farley et al. (1988) also suggest that the rate of cooling of the upper airway is thepredominant stimulus in hyperventilation induced asthma in asthmatic and non-asthmatic subjectsexposed to isocapnic cold air hyperventilation.Anderson et al. (1989) suggest that the events that trigger ETA are not due to airwaycooling and rapid rewarming, but are due to airway drying and an increase in the osmolarity ofthe fluid lining the airway surface. These changes result in the degranulation of mast cells andrelease of chemical mediators such as histamine and NCFA. McFadden (1991) has been very130critical of these conclusions and has cited a number of reasons that support his criticism.Airway and esophageal temperatures fall whenever there is evaporative water loss, airwayobstruction does not occur in the absence of cooling and rewarming, and airway drying is nota feature of hyperpnea (Deal et aL, 1979; Gilbert et aL, 1987; 1988). Schmidt and Bundgaard(1986) studied asthmatic subjects who were administered inhaled aerosols of differentosmolarities. There were no differences in the response to the different aerosols and it wasconcluded that the osmolarity of the inhaled aerosol was of little or no importance in ETA.It has been suggested by Bar-Or and Inbar (1992), Frampton et al. (1991), McKenzie(1991), and Penny (1983) that an increase in bronchial responsiveness may also occur in athleteswithout ETA who have been exposed to swimming pool disinfectants such as chlorine orchioramines, or photochemical air pollutants such as ozone, nitrogen dioxide, and sulphurdioxide. In concurrence with this hypothesis, we have shown that 60% of the competitiveswimmers that we tested had increased non-specific bronchial responsiveness to methacholine.What remains to be determined is whether this is a response to chronic, low level exposure tochemical irritants in the water and air of the swimming pooi, an exercise response, or both. Ifthe prevalence of ETA is found to be relatively low compared with the high prevalence ofincreased non-specific bronchial responsiveness that we have shown, this may indicate that inthese competitive swimmers there are separate mechanisms involved in the pathogenesis of ETAand the increased non-specific bronchial responsiveness that we see. This would also indicatethat the increased non-specific bronchial responsiveness is likely due to chronic, low levelexposure to chemical irritants in the swimming pooi.The purpose of this study was to: (1) establish the prevalence of ETA in a group ofcompetitive swimmers using a standard exercise challenge test in the laboratory; (2) establish131the prevalence of EIA in the same group of swimmers using an exercise protocol in theswimming pool; (3) determine whether there are differences in the prevalence of asthma amongcompetitive swimmers with asthma or exercise-related symptoms and those who have neitherasthma or exercise-related symptoms, and to compare their results with a group of nonswimming athletes who have neither asthma or exercise-related symptoms; and (4) determinewhether a prolonged exercise challenge test in the swimming pooi results in the developmentrespiratory symptoms and significant changes in pulmonary mechanics among the two groupsof competitive swimmers.132METHODSLaboratory Testing for EIASubjectsThe 35 swimmers and 16 non-swimming control subjects who completed themethacholine challenge test agreed to participate in the laboratory test for ETA. The subjectswere asked to refrain from exercising or ingesting caffeine on the day of testing. They wereinformed about the purpose of the test and the procedures to be followed. All of the subjectsread and signed a consent form prior to participating in this study.Calibration of the SpirometerA 1070 Pneumotach was used to measure lung function. The pneumotach was calibratedprior to testing the first subject using procedures that were described in the previous chapter.The pneumotach was re-calibrated every 3 hours.Calibration of the Metabolic Measurement CartA Beckman Metabolic Measurement Cart (MMC) (Beckman Instruments mc, SchillerPark, IL) was used to collect the metabolic and respiratory variables during the exercise test.The MMC was calibrated prior to each exercise test. On the day before testing, the power tothe OM-1 1 Oxygen (02) Analyzer and the LB-2 Carbon Dioxide (C02)Analyzer was turned onto allow for proper warm-up of the analyzers. The power to the OM-1 1 and LB-2 Pickup Headswas turned on at least 1 hour prior to testing. The MMC barometric pressure and temperaturereadouts were adjusted to match the conditions in the laboratory.133The OM-1 1 and LB-2 analyzers were calibrated using a calibration gas containing15.95% 02, 4.06% CO2 and 79.99% N2. The calibration gas was turned on, adjusted to producea flow rate of 800 mL/min and connected to a sample line coming from the bottom of the dryingtube on the MMC. The OM-1 1 and LB-2 gain settings were adjusted to read 15.95% and4.06%, respectively. The calibration gas was then turned off and room air values of 20.93%and 0.03% for 02 and CO2 were obtained. Since CO2 is known to interfere with the operationof the OM-il analyzer, we had to wait several minutes before a room air value of 20.93% wasobtained.In order to ensure that there was no bias flow through the volume turbine, the sampleflow was adjusted so that there was no upscale or downscale drifting during a 30 secondcollection period. A two litre syringe was attached to the mouthpiece of a non-rebreathing valve(Hans-Rudolph Inc. Kansas City, MO). 1% inch tubing was connected between the expiratoryport of the mouthpiece and the mixing chamber of the MMC. The syringe was used to inject10 litres of air into the system at a flow rate and frequency approximating resting conditions.An additional 10 litres of air was then injected into the system at a higher flow rate andfrequency approximating exercise conditions. These procedures were repeated until a spancalibration of 10.00 ± 0.10 L was obtained for both conditions.The MMC was programmed to collect data every 30 seconds during the exercise tests.Expired air samples were averaged and the following variables were calculated by a Monroe1810 calculator integrated into the MMC: minute ventilation (‘1E), respiratory frequency (f),tidal volume (VT), oxygen consumption (V02) in mL/min and mL/min/kg, carbon dioxideproduction (VCO2), the respiratory exchange ratio (R), and total time (r). These values wereentered into a database for statistical analysis.134Test ProceduresPrior to beginning each test, a heart rate approximating 85% of the subject’s predictedmaximum was calculated using the following formula:Target Heart Rate = [210 - (0.65 x Age)] x 0.85The subjects performed baseline spirometry manoeuvers according to procedures that havepreviously been described. Their best FEy1 was recorded. Thirty-one of the 35 subjectsperformed the exercise test on a motor-driven treadmill (Quinton Instruments, Seattle, WA).The remaining 4 subjects performed the exercise test on an electronically-braked bicycleergometer (Mijnhardt KEM 3, Bunnik, Holland) because of lower leg injuries or a strongpreference for cycling over running. All 16 of the non-swimming control subjects performedthe exercise test on the electronically-braked bike.Diaphoretic electrodes (3M Ltd., St. Paul’s, MN) were placed on the subjects’ chest ina modified Lead II configuration. The heart rate was monitored by direct-leadelectrocardiography (ECG) using a Lifepac 6 cardioscope/recorder module (Physio-Control,Scarborough, ON). The subject was connected to the mouthpiece of the non-rebreathing valve.1% inch tubing was connected between the expiratory port of the mouthpiece and the mixingchamber of the MMC. During the first 2 minutes of the exercise test the speed of the treadmill,or the resistance on the bicycle ergometer, was adjusted in order to allow the subject to reachhis or her target heart rate. The elevation of the treadmill remained at a 0% grade. At the endof the first two minutes of exercise data collection was started and data was collected every 30seconds for six minutes. The speed of the treadmill, or the resistance on the bicycle ergometer,was continually adjusted in order to maintain the subject’s target heart rate. At the end of theexercise test the subject was disconnected from the non-rebreathing valve and ECG equipment.135Spirometry was performed immediately and 5, 10 and 15 minutes after exercise. During theexpiratory portion of the spirometry manoeuver, the subjects were asked not to expire to residualvolume in order to prevent fatigue or premature closure of the small airways.Heart rate, yE, f, VT, V02, R, ET, the baseline FEy1 and the post-exercise FEV1swererecorded for each subject and entered into a database for statistical analysis.Swimming Pool Testing for ETASubjectsSwimmers who completed the methacholine challenge test and the laboratory test for ETAwere considered eligible for the tethered swimming protocol to assess ETA. A total of 28 of the35 eligible subjects agreed to participate in this study. Seven subjects did not participatebecause of illness, injury, or non-compliance. Thirteen subjects formed the Case Group and 15subjects formed the Control Group. Six out of the 13 subjects in the Case Group had physician-diagnosed asthma, while the remaining 7 had symptoms suggestive of asthma while swimming.The subjects were asked to refrain from exercising or ingesting caffeine on the day of testing.They were informed about the purpose of the test and the procedures to be followed. All of thesubjects read and signed a consent form prior to participating in the remaining exercise studies.Calibration of the SpironieterA 2130 Dry-Rolling Seal Spirometer (SensorMedics Corporation, Yorba-Linda, CA)interfaced to an IBM-compatible 386DX computer was used to measure lung function. Thebarometric pressure and room temperature were entered into the computer program operatingthe spirometer. The spirometer bell was positioned at the mid-point of its operating range. A1363 litre syringe was connected to 2 inch tubing which was connected to the spirometer. Tocalibrate the spirometer six 3 litre samples of air were alternately injected and withdrawn fromthe spirometer at varying flow rates. These procedures were then repeated to verify thecalibration of the spirometer. The last four 3 litre samples were averaged and a correctionfactor introduced for all subsequent calculations. The spirometer was re-calibrated every 3hours.Calibration of the Metabolic Measurement CartA Beckman MMC was used to collect the metabolic and respiratory variables during thetethered swimming protocol. The MMC was calibrated prior to each exercise test usingprocedures that have previously been described.Test ProceduresIn order to equate the exercise intensity from the 8 minute laboratory test to the 8 minutetethered swimming protocol, the average VE from the laboratory test was recorded for eachsubject and an attempt was made to match this VE during the tethered swimming protocol. Thesubjects performed baseline spirometry manoeuvers according to procedures that have previouslybeen described. Their best FEV1 was recorded.Diaphoretic electrodes were placed on the. subjects’ chest in a modified Lead IIconfiguration. Water-proof plastic adhesive tape (Johnson and Johnson, Montreal, PQ) was thenplaced over each of the electrodes in order to prevent loss of the ECG signal. The heart ratewas monitored by direct-lead electrocardiography using a EK-lO ECG Module (BurdickCorporation, Milton, WI). A belt was placed around the waist of the subject. The belt was137attached to a tethering apparatus located on the side of the pool deck. The tethering apparatusconsisted of a pulley system that was attached to a bucket containing weighted sand bags. Theresistance of the tethering apparatus was controlled by either adding or removing sand bags.The subject was asked to get into the water and was then connected to a non-rebreathing valve.The subject breathed air through 1% inch tubing that was located 6 inches off the surface of thewater and connected to the inspiratory port of the mouthpiece. 1% inch tubing was alsoconnected between the expiratory port of the mouthpiece and the mixing chamber of the MMC.The subjects were instructed to swim in a stationary position over a marker that wasplaced on the bottom of the pooi. They were also instructed to use front crawl during thetethered swimming protocol because it is the stroke they use during most of their training.During the first 2 minutes of the exercise test the resistance of the tethering apparatus wasadjusted in order to reach the subject’s target yE. At the end of the first two minutes ofexercise, data collection was started and data was collected every 30 seconds for six minutes.The resistance of the tethering apparatus was continually adjusted in order to maintain thesubject’s target VE. At the end of the exercise test the subject was disconnected from the nonrebreathing valve, tethering apparatus and ECG equipment. Spirometry was performedimmediately and 5, 10 and 15 minutes after exercise. During the expiratory portion of thespirometry manoeuver, the subjects were asked not to expire to residual volume in order toprevent fatigue and premature closure of the small airways.Heart rate, yE, f, VT, ‘O2, R, T, the baseline FEV1 and the post-exercise FEV1swererecorded for each subject and entered into a database for statistical analysis.138The Prolonged Exercise Challenge Test in the Swimming PoolSubjectsThe 28 subjects who participated in the 8 minute tethered swimming protocol completedthe 45 minute protocol. The subjects were informed about the purpose of the test and theprocedures to be followed.Calibration of the SpirometerThe spirometry tests were performed using the System 2130 dry-rolling seal spirometer.The dry-rolling seal spirometer was calibrated prior to testing the first subject using proceduresthat have previously been described. The spirometer was re-calibrated every 3 hours.Calibration of the Metabolic Measurement CartA Beckman MMC was used to collect the metabolic and respiratory variables during thetethered swimming protocol. The MMC was calibrated prior to each exercise test usingprocedures that have previously been described.Test ProceduresPrior to beginning each test, a heart rate approximating 70% of the subject’s predictedmaximum was calculated using the following formula:Target Heart Rate [210- (0.65 x Age)] x 0.70The subjects performed baseline spirometry manoeuvers according to procedures that havepreviously been described. Their best FEy1 was recorded.139The tethered swimming protocol was performed using procedures that have previouslybeen described, except that data was collected for 30 seconds every 5 minutes during the 45minute test. Spirometry was performed immediately and 5, 10 and 15 minutes after exercise.During the expiratory portion of the spirometry manoeuvers, the subjects were asked not toexpire to residual volume in order to prevent fatigue and premature closure of the small airways.Heart rate, VE, f, V’r, V02 R, !T, the baseline FEV1 and the post-exercise FEV1s, andany symptoms reported by the swimmers during or after the test were recorded for each subjectand entered into a database for statistical analysis.Statistical AnalysisThe mean, standard deviation, and the standard error of the mean were calculated for allof the descriptive variables. Analysis of variance (ANOVA) was used to determine whetherthere were statistical differences in the mean values of the dependent variables for the threegroups of athletes who participated in the exercise challenge test in the laboratory. If statisticaldifferences were found, a Student-Newman-Keuls multiple range test was used to determinewhich groups differed. Independent t-tests were used to determine whether there were statisticaldifferences in the mean values of the dependent variables for the two groups of swimmers whoparticipated in the exercise challenge tests in the swimming pool.The prevalence of HA was calculated for each of the three groups of athletes. Theexercise test was considered to be positive if the pre- to post-exercise FEV1 fell by 15% ormore. Sensitivity and specificity were determined from 2 by 2 contingency tables in which“physician-diagnosed asthma” versus “no asthma” was tabulated against “positive test” and“negative test”. Sensitivity was defined as the percentage of athletes with asthma and/or140symptoms suggestive of asthma while exercising who had positive exercise tests (tFEV1 15%).Specificity was defined as the percentage of athletes with neither asthma nor symptomssuggestive of asthma while. exercising who had negative exercise tests.An alpha level of 0.05 (p <0.05) was considered to be statistically significant. Allstatistical analyses were completed using the SAS® Statistical Software Package (SAS Institute,Inc., Cary, NC).141RESULTSLaboratory Testing for EIAAll of the subjects who completed the methacholine challenge test completed the exercisechallenge test in the laboratory. Briefly, this study included fifty-one (25 male and 26 female)subjects who were divided into three groups. The Case Group was composed of 18 competitiveswimmers who had either physician-diagnosed asthma or symptoms suggestive of asthma whileswimming. The Control Group was composed of 17 swimmers who had neither physician-diagnosed asthma nor symptoms suggestive of asthma while swimming. The Non-SwimmingControl Group was composed of 16 non-swimming athletes who had neither physician-diagnosedasthma nor symptoms suggestive of asthma while exercising. The physical characteristics andlung function measurements of these subjects were reported in the previous chapter (Tables 14and 16). The environmental conditions during testing in the laboratory were also reported inthe previous chapter (Table 15).A comparison of the exercise data between the three groups of athletes is presented inTable 18. The mean predicted heart rate for the Case Group was statistically significantly higherthan that of the Non-Swimming Control Group (p <0.0449), but the difference was only 2 bpm.The mean heart rate calculated over the last 6 minutes of exercise was significantly higher in theCase Group when compared with either of the control groups (p <0.0029 and p <0.0001,respectively). Similarly, the mean heart rate of the Control Group was significantly higher thanthat of the Non-Swimming Control Group (p <0.0029) (Figure 6). There was no difference inthe mean values for yE, VT, f, and V02 calculated over the last 6 minutes of exercise betweenthe three groups of athletes (Figures 7-10). The mean R value calculated over the last 6 minutesof exercise for the Non-Swimming Control Group was significantly higher than either of the two142swimming groups (p <0.0001 and p <0.0001, respectively) (Figure 11).The overall prevalence of ETA among the 51 athletes was 9.8%. This included twoswimmers from the Case Group (11.1 %), two swimmers from the Control Group (11.8%), andone athlete from the Non-Swimming Control Group (6.3%). Neither of the swimmers in theCase Group who had positive exercise tests had physician-diagnosed asthma, but one of thesubjects had increased bronchial responsiveness with a PC20 of 1.36 mg/mL. Both of theswimmers in the Control Group who had positive exercise tests had increased bronchialresponsiveness with PC20s of 3.01 and 3.13 mg/mL, respectively. The one subject in the Non-Swimming Control Group who had a positive exercise test had normal bronchial responsivenesswith a PC20>16 mg/mL, but his baseline spirometry showed a mild obstructive pattern in hislarge airways (FEV1/ VC <70%). Figure 12 shows the mean percentage change in FEV1 valuesfollowing the 8 minute exercise challenge test in the laboratory. Figures 13-15 show theindividual post-exercise FEy1 plots for each of the groups of athletes. The sensitivity andspecificity of the laboratory test for ETA for identifying subjects with asthma or symptomssuggestive of asthma while exercising were 11.1 % and 90.9%, respectively.‘-4Table18:Themeanvaluesforthecardiorespiratoryvariablescollectedduringthe8minuteexercisechallengetestinthelaboratory.Thex±SDarereported.CaseGroupControlGroupNon-SwimmingLevelofControlGroupSignificancePredictedHeartRate(bpm)168.22±1.52167.53±2.00166.44±2.50<00449*ExerciseHeartRate(bpm)173.89±4.61168.35±5.47158.40±8.10p<O.0001tVE(L/min)76.62±16.1574.29±15.7582.24±18.14NSVT(mL)2,099.17±632.222,305.88±555.642,408.38±734.95NSf(b/niin)37.84±6.7932.85±5.6734.79±5.63NSV02(Llmin)2.79±0.702.85±0.592.77±0.78NS102(mL/min/kg)40.89±6.1540.92±5.2539.68±7.80NSR0.94±0.040.93±0.071.04±0.06p<O.0001**ThemeanpredictedheartrateoftheCaseGroupwassignificantlyhigherthanthatoftheNon-SwimmingControlGroup.ThemeanheartrateoftheCaseGroupwassignificantlyhigherthanthemeanheartrateofeitherofthecontrolgroups.Similarly,themeanheartrateoftheControlGroupwassignificantlyhigherthanthemeanheartrateoftheNon-SwimmingControlGroup.*ThemeanrespiratoryexchangeratiooftheNon-SwimmingControlGroupwassignificantlyhigherthanthemeanrespiratoryexchangeratiooftheCaseGroupandtheControlGroup.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.Figure 6: The mean heart rates measured during the last 6 minutes of the laboratory test forETA. Overall, the mean heart rate for the Case Group was significantly higher thanthat of either of the Control Groups (p <0.0029 and p <0.0001, respectively).Similarly, The mean heart rate for the Control Group was significantly higher thanthat of the Non-Swimming Control Group (p <0.0029). The ± SEM are reported.Figure 7: The mean VE values measured during the last 6 minutes of the laboratory test forETA. Overall, there was no difference in the mean ‘E value between the threegroups of athletes. The ± SEM are reported.0144I‘a)190180170160150140o Case GroupV Control GroupD Non-Swimming Control Group/I I I I I Exercise Time(Minutes)2 3 4 5 6 7 8100959085807570656O ///0 Case GroupV Control Group0 Non-Swimming Control Group3 4 5Exercise TimeI I I (Minutes)6 7 8Figure 8: The mean tidal volume (VT) values measured during the last 6 minutes of thelaboratory test for ETA. Overall, there was no difference in the mean VT valuebetween the three groups of athletes. The 5 ± SEM are reported.Figure 9: The mean respiratory frequency (f) values measured during the last 6 minutes of thelaboratory test for ETA. Overall, the mean f for the Case Group was significantlyhigher than that of the Control Group (p.< 0.0242). The ± SEM are reported.145C.)•:1)CO Case Group9 Control Group0 Non-Swimming Control GroupI I I I I Exercise Time(Minutes)C2700260025002400230022002100200019001800 /2 3 4 5 6 7 8Exercise Time(Minutes)45403530254 5 6 7 8Figure 11:3.5Ep0I2.51)CThe mean respiratory exchange ratio (R) values measured during the last 6 minutesof the laboratory test for ETA. Overall, the mean R value of the Non-SwimmingControl Group was significantly higher than that of either of the swimming groups(p <0.0001). The ± SEM are reported.1.1001.051)c0FL 1.0000.95Figure 10: The mean oxygen consumption (‘‘O2) values measured during the last 6 minutes ofthe laboratory test for ETA. Overall, there was no difference in the mean VO2value between the three groups of athletes. The ± SEM are reported.1462.0Case GroupControl GroupNon-Swimming Control GroupI I I I I I I Exercise Time(Minutes)3 4 5 6 7 80 Case Groupv Control GroupD Non-Swimming Control Group0.90A -I- I I I I Exercise Time(Minutes)2 3 4 5 6 7 8Figure 12: The mean FEV1 values following the 8 minute exercise challenge test in thelaboratory. The ± SEM are reported.>,-1)c-)Recovery Time(Minutes)147105-5o Case GroupV Control GroupNon-Swimming Control Group-10-15Figure 13:Baseline ImmediatePost-Exercise5 10 15The individual FEy1 plots for the Casechallenge test in the laboratory.Recovery Time(Minutes)Group following the 8 minute exercisePost-ExerciseFigure 14: The individual FEV1 plots for the Control Group following the 8 minute exercisechallenge test in the laboratory.c-)>,-ci)c)148105-5-10-15-205 10 15105Recovery TimeBaseline Immediate (Minutes)Post-ExerciseFigure 15: The individual FEV1 plots for the Non-Swimming Control Group following the 8minute exercise challenge test in the laboratory.Recovery Time(Minutes)-5-10-15-20Baseline Immediate 5 10 15Post-Exercise149Swimming Pool Testing for EIAThis study included twenty-eight (15 male and 13 female) competitive swimmers who hadparticipated in the previous study. The Case Group was composed of 13 competitive swimmersand the Control Group was composed of 15 swimmers. The criteria for placement into each ofthe groups remained the same. The physical characteristics of the subjects are presented inTable 19. There were no statistically significant differences in the mean values for age, height,and weight between the two groups of swimmers. During testing, the barometric pressure was758.11 ± 5.95 torr, the air temperature was 24.04 ± 0.43 C, the water temperature was 27.96± 0.19 °C, and the relative humidity was 59.75 ± 2.90 %. There were no statisticallysignificant differences in these values between the two groups of swimmers.A comparison of the exercise data between the two groups of swimmers is presented inTable 20. There was no difference in the mean values for heart rate, yE, VT, f, and “02calculated over the last 6 minutes of exercise between the two groups of swimmers (Figures 16-20). The mean R value calculated over the last 6 minutes of exercise for the Case Group wassignificantly higher than that of the Control Group (p <0.0029) (Figure 21). Figure 22 showsthe mean percentage change in FEy1 values following the 8 minute exercise challenge test in theswimming pool.The overall prevalence of EIA among the 28 swimmers was 3.6%. This included oneswimmer from the Case Group (7.7%) and no swimmers from the Control Group. The oneswimmer from the Case Group who had a positive exercise test did not have physician-diagnosedasthma, but had symptoms suggestive of asthma while swimming and increased bronchialresponsiveness with a PC20 of 9.51 mg/mL. Interestingly, this subject was not one of thesubjects who had a positive exercise test in the laboratory. The sensitivity and specificity of the150swimming pooi test for ETA for identifying swimmers with asthma or symptoms suggestive ofasthma while exercising were 6.7% and 100%, respectively.Table19:Thephysicalcharacteristicsofthe2groupsofcompetitiveswimmerswhoparticipatedintheexercisechallengetestsintheswimmingpool.Thex±SDarereported.CaseGroupControlGroupLevelofSignificanceAge(years)17.85±3.3919.80±3.36NSHeight(cm)174.46±8.42175.53±9.72NSWeight(kg)68.18±12.3469.76±9.64NSNS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.Table20:Themeanvaluesforthecardiorespiratoryvariablescollectedduringthe8minuteexercisechallengetestintheswimmingpooi.Thex±arereported.CaseGroupControlGroupLevelofSignificanceExerciseHeartRate(bpm)160.00±7.21158.40±8.10NSVE(L/min)78.14±16.7973.28±17.32NSVT(mL)2,158.92±706.822,132.60±572.50NSf(blmin)37.53±6.1435.48±7.71NSV02(Llmin)2.98±0.713.02±0.64NSV02(mL/min/kg)43.21±5.4443.09±5.85NSR0.96±0.050.90±0.04<00029**ThemeanrespiratoryexchangeratiooftheCaseGroupwassignificantlyhigherthanthatoftheControlGroup.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.153Figure 16: The mean heart rates measured during the last 6 minutes of the swimming pool testfor ETA. Overall, there was no difference in the mean heart rate between the twogroups of swimmers. The ± SEM are reported...10I I I I Exercise Time2 3 4 5 6 7 8(Minutes)Ici)190180170160150140 /o Case Groupv Control GroupFigure 17: The mean VE values measured during the last 6 minutes of the swimming pool testfor ETA. Overall, there was no difference in the mean VE value between the twogroups of swimmers. The ± SEM are reported.9085807570656055o Case GroupV Control Groupso7/ I I I I I I Exercise Time/ (Minutes)2 3 4 5 6 7 8Figure 18: The mean tidal volume (VT) values measured during the last 6 minutes of thelaboratory test for ETA. Overall, there was no difference in the mean VT valuebetween the two groups of swimmers. The ± SEM are reported.154260025002400EI-200019001800 /2 3 4 5 6 7 8Figure 19: The mean respiratory frequency (f) values measured during the last 6 minutes of theswimming pool test for ETA. Overall, there was no difference in the mean f valuebetween the two groups of swimmers. The 5 ± SEM are reported.4540o Case Groupv Control Group230022002100////I I I I I j Exercise Time(Minutes)E250 Case Groupv Control GroupI I I I I Exercise Time(Minutes)4 5 6 7 8155Figure 20: The mean oxygen consumption (‘‘O2) values measured during the last 6 minutes ofthe swimming pool test for EIA. Overall, there was no difference in the mean V02value between the two groups of swimmers. The ± SEM are reported.0I0 Case GroupV Control Group0 Case Group-_J_ V Control GroupNI-3.5__3.02.52.07/ I I I I I Exercise Time(Minutes)2 3 4 5 6 7 8Figure 21: The mean respiratory exchange ratio (R) values measured during the last 6 minutesof the swimming pooi test for ETA. Overall, the mean R value for the Case Groupwas significantly higher than that of the Control Group (p <0.0029). The ± SEMare reported.__________________1.0000.950.900.85/ /i Exercise Time34567 8(Minutes)156Figure 22: The mean FEy1 values following the 8 minute exercise challenge test in theswimming pool. The 5 ± SEM are reported.10 -5--10- 0 Case Groupv Control Group-15 -I I I Recovery TimeBaseline Immediate 5 10 15 (minutes)Post-ExerciseA Comparison of the Results from the Laboratory and Swimming Pool TestsA comparison of the environmental conditions during testing in the laboratory andswimming pool is presented in Table 21. The air temperature was significantly higher duringtesting in the swimming pool when compared to the laboratory (p < .000 1). A comparison ofthe exercise data during testing in the laboratory and swimming pool is presented in Table 22.The mean heart rate calculated over the last 6 minutes of exercise was significantly higher duringrunning or cycling when compared to swimming (p <0.0001) (Figure 23). There was nodifference in the mean values for ‘YE, VT, f, V02, and R calculated over the last 6 minutes ofexercise between the two groups of swimmers (Figures 24-28). Figure 29 compares the meanpercentage change in FEy1 values following each of the 8 minute exercise challenge tests.Table21:Acomparisonoftheenvironmentalconditionsduring8minuteexercisechallengetestsinthelaboratoryandswimmingpool.Thex±SDarereported.Running/CyclingSwimmingLevelofSignificanceBarometricPressure(torr)756.29±6.65758.11±5.95NSAirTemperature(C)21.42±0.8424.04±0.43p<O.000l*RelativeHumidity(%)58.71±5.0559.75±2.90NS*Themeanairtemperaturewassignificantlyhigherduringexercisechallengeintheswimmingpool.NS=Nostatisticallysignificantdifferenceswere.foundbetweengroups.00Table22:Acomparisonofthemeanvaluesforthecardiorespiratoryvariablescollectedduringtheexercisechallengetestsinthelaboratoryandintheswimmingpooi.Thex±SDarereported.Running/CyclingSwimmingLevelofSignificanceExerciseHeartRate(bpm)170.82±6.02159.14±7.60p<O.000l*VE(L/min)76.01±15.6475.54±16.94NSVT(mL)2,254.39±627.482,144.82±626.23NSf(b/min)34.92±6.8836.43±5.97NS‘O2(L/min)2.88±0.653.00±0.66NSV02(mL/min/kg)41.57±5.6543.15±5.56NSR0.94±0.0640.93±0.05NS*Themeanheartrateduringrunningorcyclingwassignificantlyhigherthanduringswimming.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.Figure 23: A comparison of the mean heart rates measured during the last 6 minutes of thelaboratory and swimming pool tests for ETA. Overall, the mean heart rate wassignificantly higher during tethered swimming in comparison with running orcycling (p <0.0001). The 5 ± SEM are reported.159I I I I I Exercise Time(Minutes)3 4 5 6 7 8Figure 24: A comparison of the mean yE measured during the last 6 minutes of the laboratoryand swimming pool tests for ETA. Overall, there was no difference in the mean yEvalue between the two groups of swimmers. The 5 ± SEM are reported.E0.,ci)>.___________________Ici)190180170160150140o Running/CyclingV Swimming85807570656055500 Running/CyclingV SwimmingI I I I I Exercise Time(Minutes)4 5 6 7 8160Figure 25: A comparison of the mean tidal volume (VT) values measured during the last 6minutes of the laboratory and swimming pooi tests for ETA. Overall, there was nodifference in the mean VT value between the two groups of swimmers. Thei ± SEM are reported.0r Running/CyclingV Swimming/ i I I I ExerciseTime(Minutes)3 4 5 6 7 8Figure 26:26002500E \/fl1900 - I0 Running/Cycling1800 / V Swimming7 I I I I Exercise Time/ “ (Minutes)2 3 4 5 6 7 8A comparison of the mean respiratory frequency (f) values measured during the last6 minutes of the laboratory and swimming pool tests for EIA. Overall, there wasno difference in the mean f value between the two groups of swimmers. The± SEM are. reported.45E 4025/IFigure 27: A comparison of the mean oxygen consumption (V02) values measured during thelast 6 minutes of the laboratory and swimming pool tests for EIA. Overall, therewas no difference in the mean V02 value between the two groups of swimmers.The ± SEM are reported.E0.0c-)I)C0.,1)C.)0161/0 Running/CyclingV Swimming3.53.02.52.0>I I I I I I ExerciseTime/ / (Minutes)2 3 4 5 6 7 8Figure 28: A comparison of the mean respiratory exchange ratio (R) values measured duringthe last 6 minutes of the laboratory and swimming pool tests for ETA. Overall, therewas no difference in the mean R value between the two groups of swimmers. The± SEM are reported.1.000.950.900.85 /0 Running/CyclingV Swimming/ I I Exercise Time(Minutes)2 3 4 5 6 7 8162Figure 29: A comparison of the mean FEy1 values following the 8 minute exercise challengetests in the laboratory and swimming pooi. The ± SEM are reported.10 -5--10- HE Running/CyclingI V Swimming-15 -__________________________________Recovery TimeBaseline Immediate 5 10 15 (Minutes)Post-ExerciseThe Prolonged Exercise Challenge Test in the Swhnming PoolA comparison of the exercise data between the two groups of swimmers is presented inTable 23. The mean predicted heart rate for the Case Group was significantly higher than thatof the Control Group (p <0.0444). There was no difference in the mean values for heart rate,yE, VT, f, V02, and R calculated over the 45 minutes of exercise between the two groups ofswimmers (Figures 30-35). Figure 36 shows the mean percentage change in FEV1 valuesfollowing the test. The most common symptom reported by the swimmers following theprolonged exercise challenge test was a sore throat (53.6% of participants). Other symptomsreported by the swimmers included coughing (25.0%), chest tightness or headache (14.3%), drymouth (10.7%), sneezing or chest congestion (7.1%), and sore eyes or nasal congestion (3.6%).A total of 8 swimmers (28.6%) reported no symptoms following the test.Table23:Themeanvaluesforthecardiorespiratoryvariablescollectedduringthe45minuteexercisechallengetestintheswimmingpooi.Thex±SDarereported.CaseGroupControlGroupLevelofSignificancePredictedHeartRate(bpm)138.69±1.44137.53±1.46<00444*ExerciseHeartRate(bpm)139.46±2.82137.20±5.00NSVE(L/min)50.40±8.3751.31±10.09NSVT(mL)1,719.54±505.661,877.40±512.57NSf(b/min)31.19±8.7228.40±5.94NSV02(L/min)2.26±0.472.24±0.43NSV02(mL/min/kg)33.14±4.6432.04±3.64NSR0.88±0.040.88±0.05NS*ThemeanpredictedheartratefortheCaseGroupwassignificantlyhigherthanthatoftheControlGroup.NS=Nostatisticallysignificantdifferenceswerefoundbetweengroups.164Figure 30: The mean heart rates measured during the 45 minute exercise challenge test.Overall, there was no difference in the mean heart rate value between the twogroups of swimmers. The 5 ± SEM are reported.I I I I I I I I Exercise Time5 10 15 20 25 30 35 40 45 (Minutes)Figure 31: The mean yE values measured during the 45 minute exercise challenge test.Overall, there was no difference in the mean VE value between the two groups ofswimmers. The ± SEM are reported.C4-.I)160150I:S 1401301201109zEEEZ2o Case GroupV Control Group6560555045403530 /• 0 Case Groupv Control Group/I I I I I I I I I Exercise Time5 10 15 20 25 30 35 40 45 (Minutes)Figure 32: The mean tidal volume (VT) values measured during the 45 exercise challenge test.Overall, there was no difference in the mean VT value between the two groups ofswimmers. The ± SEM are reported.E1)rJ02200210020001900180017001600150014001300165Io Case Groupv Control GroupFigure 33:1E0>I I I I I I I I Exercise Time0 5 10 15 20 25 30 35 40 45 (Minutes)The mean respiratory frequency (f) values measured during the 45 minute exercisechallenge test in the swimming pooi. Overall, there was no difference in the meanf value between the two groups of swimmers. The ± SEM are reported.4540353025o Case Groupv Control Group_________________________________________Exercise Time0 5 10 15 20 25 30 35 40 45 (Minutes)166Figure 34: The mean oxygen consumption (V02)values measured during the 45 minute exercisechallenge test in the swimming pooi. Overall, there was no difference in the meanV02 value between the two groups of swimmers. The ± SEM are reported.EI-10I_________Figure 35: The mean respiratory exchange ratio (R) values measured during the 45 minuteexercise challenge test in the swimming pool. Overall, there was no difference inthe mean R value between the two groups of swimmers. The ± SEM arereported.0g:0 0.90r.u0 0.85I I I Exercise Time0 5 10 15 20 25 30 35 40 45 (Minutes)3.02.52.01.570 Case GroupV Control GroupI I I I Exercise Time5 10 15 20 25 30 35 40 45 (Minutes)0.950.80 /0 Case Group7 Control Group167Figure 36: The mean FEV1 values following the 45. minute exercise challenge test in theswimming pooi. The ± SEM are reported.10 -5-10- 0 Case Groupv Control Group-15I I I I Recovery TimeBaseline Immediate 5 10 15 (minutes)Post-Exercise168DISCUSSIONThis study shows that the prevalence of ETA in competitive swimmers is within the 3-11 % range that has been reported for other competitive athletes (Fitch, 1984; Heibling andMuller, 1991; Huftel et aL, 1991; Rice et al., 1985; Voy, 1986). Overall, the prevalence ofEIA in the group of athletes that we tested was 9.8%. This includes 11.1% of the Case Group,11.8% of the Control Group, and 6.3% of the Non-Swimming Control Group. There do notappear to be differences in the prevalence of ETA among swimmers with asthma or exercise-related respiratory symptoms when compared to swimmers who have neither asthma norexercise-related symptoms. Also, the prevalence of ETA among swimmers appears to be similarto that of non-swimmers. Although we found a 3.5% higher prevalence rate in swimmers, thisdifference may partially be explained by differences in the mode of exercise used by the twogroups of athletes. Most of the swimmers were tested while running on a treadmill, while allof the non-swimmers were tested on a bicycle ergometer. Anderson et al. (1971) and Fitch andMorton (1971) have shown that treadmill running is more asthmogenic than bicycle ergometry.Our current understanding of ETA suggests that the post-exercise bronchoconstriction isinitiated by thermal events. Deal et al. (1979) suggest that the magnitude of RHL appears tobe directly related to the severity of ETA and Noviski et al. (1987) suggest that the intensity ofexercise determines and, climatic conditions modify, the severity of ETA. The severity ofairway narrowing has been shown to be a function of the yE and the temperature and watercontent of the inspired air. For a given set of inspired conditions, high minute ventilations resultin more obstruction than do low levels, and drying and cooling the air at any level of ventilationcause more obstruction than when breathing warm and humid air. Low inspired air temperaturesproduce greater convective cooling and low humidity enhances evaporative cooling of the airway169mucosa.In our study we did not measure either inspired or expired air conditions at the mouthand, therefore, we could not calculate RHL. Even though the temperature and relative humidityof the inspired air was higher in the non-swimming control group, it is likely that there wereminimal differences in RHL among the three groups of athletes who were tested for ETA in thelaboratory. Based on our results it could be suggested that the non-swimming control groupwould have a lower RHL, however, when we compare the differences between the ‘1E,temperature and relative humidity of the inspired air between the three groups of athletes thesedifferences are minimal, especially since we are only dealing with a 1 C difference intemperature and a 5% difference in relative humidity of the inspired air. Also, within the rangeof values that we measured, we are not dealing with extremes in either the temperature orrelative humidity of the inspired air.The prevalence of ETA among the swimmers appears to be dependent on whether theexercise protocol is performed in the laboratory or swimming pool. The prevalence of ETA washigher in the laboratory (9.8%) when compared to the swimming pool (3.6%). These resultsare similar to those of others in that they illustrate the lower asthmogenicity of swimming whencompared to land-based exercise (Anderson, 1972; Bar-Yishay et al., 1982). The mechanismsfor this protective effect of swimming are not clear, but a number of mechanisms have beenproposed.Inbar et al. (1980) conducted a study involving asthmatics in which they manipulated thehumidity of the inspired air between 25-30% during tethered swimming and treadmill runningand 80-90% during a second 8 minute tethered swimming protocol. Even though ‘E and “02were equated during each of the exercise sessions, ETA occurred following running, but neither170of the swimming protocols induced EIA, irrespective of the water content of the inspired air.Bar-Yishai et al. (1982) did a similar experiment in which asthmatics were asked to run andswim under two conditions. The humidity of the inspired air alternated between 8% and 100%and VE and ‘O2 were equated during each of the exercise sessions. Irrespective of the humidityof the inspired air, running induced greater bronchoconstriction than swimming. However, thehumidification of the inspired air reduced the post-exercise fall in FEy1 by 57%. Bundgaardet al. (1987) compared the effects of indoor cycling and swimming on ETA by administering dryair with a relative humidity of 15 % during both exercise sessions. Their results showed similarchanges in post-exercise PEFR. Boulet and Turcotte (1991) showed that bronchoconstrictioncould be minimized by exercising in humid air and recovering in dry air and was maximized ifthe exercise was performed. in dry air and recovery occurred in humid air. The results of thesestudies suggest that the high humidity of the inspired air in indoor swimming pools can onlypartially explain the lower asthmogenicity of swimming.A second possible mechanism for the protective effect of swimming may result from thesubjects being immersed in the water. Immersion in water is a simple and common maneuverthat is used to study physiological changes in cardiovascular, respiratory, renal, endocrine, andthermoregulatory function., These changes include increases in intrathoracic blood volume,stroke volume, and cardiac output, diuresis, natriuresis, kaliuresis, increases in plasma atrialnatriuretic peptide, inhibition of epinephrine, norepinephrine, renin, aldosterone, argininevasopressin, and an increase in the ambient temperature zone for thermoregulation. Threefactors are thought to be responsible for these changes: the high density of water supports theextra-thoracic blood vessels (analogous to a gravity-free state); the differential pressuredistribution over the body (which gives rise to negative-pressure breathing); and the high171thermoconductivity of water (Lin and Hong, 1984). Water immersion has also been shown toimprove gas diffusion and ventilation-perfusion matching in the lung (Arborelius et al., 1972;Löllgen et al., 1976). These immersion-related changes are thought to result from elevation ofthe diaphragm, a decrease in residual volume, and the influence of hydrostatic pressure on theblood vessels and thoracic wall (Lollgen et al., 1976). Kelly et al. (1986) suggested that theperipheral vasoconstriction and increase in central blood volume that occurs during immersionmay result in a lower RHL and less bronchoconstriction.Most of the research involving water immersion has been conducted with the subjects ina vertical orientation in the water. Exercise in the recumbent position has also been shown toimprove gas diffusion and ventilation-perfusion matching in the lung (Craig et al., 1971; Prefautet al., 1979). The effects of water immersion and posture on ETA were evaluated in two recentstudies. Inbar et al. (1991) studied the effects of upright and prone body positions on EIA andisocapnic hyperventilation in 12 asthmatic children. All of the subjects had their FEy1 testedbefore and after completing 8 minute exercise or isocapnic hyperventilation sessions in theupright and prone positions. The subjects’ ‘E was kept constant for each of the sessions andthe subjects were tested in an environmental chamber where the air temperature was 1O and therelative humidity was 31 %. No difference was found in the FEy1 between the prone andupright body positions following either exercise or isocapnic hyperventilation. The authorsconcluded that on land, body posture has no effect on the severity of bronchoconstriction inasthmatic children. However, the authors suggested that there may be some physiologicalbenefits of the prone position in water.Inbar et al. (1993) then studied the effects of prone immersion on isocapnichyperventilation in 12 asthmatic children. The subjects performed 8 minutes of isocapnic172hyperventilation on land (upright) and in the water (jrone) with the temperature and relativehumidity of the inspired air kept at 20°C and 10%, respectively. The subjects’ ‘E was similarduring each session and the authors observed similar decreases in FEy1 following each session.However, some of the subjects had less bronchoconstriction in the water and some had lessbronchoconstriction on land.In our study there was no difference in the relative humidity of the inspired air betweenthe laboratory (59%) and the swimming pool (60%). Similar results have been reported by BarYishay et al. (1982). As well, the mean value for yE between swimmers who completed boththe laboratory and swimming pool tests for ETA were similar. Even though the temperature ofthe air was 3°C higher in the swimming pool, it is unlikely that this difference alone couldaccount for significant differences in RHL between swimmers who completed both the laboratoryand swimming pool tests for ETA. Even though we were able to show that swimming isassociated with lower asthmogenicity than treadmill running or cycling in competitive swimmers,the pathophysiological mechanism of the lower asthmogenicity does not appear to be related toRHL. It appears that while the humidity of the inspired air can partially explain the lowerasthmogenicity of swimming, the effect of body position is not important and, based on the fewstudies that have been done, the effect of immersion is equivocal and varies among individuals.Our study was designed to match V02, and heart rate during exercise testing. Therewere no statistically significant differences in the mean values for and ‘c’02 between any ofthe 3 groups of athletes involved in the laboratory test for ETA, or for the 2 groups of swimmersinvolved in the swimming pooi test for ETA. However, the mean heart rate for the NonSwimming Control Group was significantly lower than the mean heart rate for either of the twoswimming groups, and the mean heart rate for the Control Group was significantly lower than173that of the Case Group. It is difficult to assess the importance of these findings given that therewere no differences in the mean values for ‘E and “02 between the three groups of athletes.However, because we were using heart rate to control for the intensity of exercise, it doessuggest that we were not able to control it very well during the laboratory test for EIA.The differences in heart rate could be due to differences in the aerobic fitness level ofthe athletes, the specificity of training on land as opposed to water, or to individual differencesamong the sample of subjects that were studied. If we evaluate the relationship between yE andheart rate (VE/HR) or V02 and heart rate (‘1O2/HR), we obtain a hierarchy of values thatsuggest the Non-Swimming Control Group may be more aerobically fit than the Control Group,and both of these groups are more aerobically fit than the Case Group. However, the mean Rvalues obtained during exercise testing would suggest otherwise. The mean R value of the Caseand Control Groups (0.94 and 0.93, respectively) were significantly lower than that of the Non-Swimming Control Group (1.04). The higher R values also suggest that at a given level of’’E,the non-swimmers are producing more VCO2 than are the swimmers which would result in alower VE/VCO2ratio.Clausen (1976), Holmer and Atrand (1972), and Saltin et al. (1976) have shown thatfollowing training V°2, heart rate, and R are lower at any level of submaximal exercise,all of which indicates an improvement in the aerobic fitness of the subject. These changes alsoindicate the importance of the specificity of training and since swimmers do not use running orcycling as an integral part of their training they may be expected to have higher heart rates thanindividuals who use either training methods extensively. This assumption does not explain thedifferences in heart rates between the two swimming groups. Thus, in the laboratory, thedifferences in the mean values for heart rate between, the three groups of athletes are not likely174due to differences in aerobic fitness, but may be due to the specificity of training among the non-swimmers and swimmers or to the sample population that represents each group of athletes.There was no difference in the mean heart rate between the Case and Control Groupsduring exercise challenge testing in the swimming pool. However, at a similar ‘E and ‘‘O2, themean heart rate in the swimming pooi was 11 beats/minute lower than in the laboratory. Lowerheart rates have been reported for many studies that have evaluated the physiological effects ofthe diving reflex or water immersion and comparative studies of exercise on land and in thewater. Although the diving reflex is thought to be weak in man, it is known to be associatedwith apnea, peripheral vasoconstriction, and bradycardia. Berk et al. (1991) have shown thatcold water facial immersion induces bradycardia. Immersion to the chest in thermoneutral wateror cold water may decrease resting heart rate by 15%; whereas, immersion to the chest in hotwater may increase heart rate by 32% (Bonde-Petersen et al., 1992).Inbar et al. (1980) found heart rates to be significantly lower during swimming thanduring treadmill running. A number of studies comparing water running to free or treadmillrunning have shown heart rates to be significantly lower during water running (Ritchie andHopkins, 1991; Svedenhag and Seger, 1992). Forgays and McClure (1988) found no differencein the heart rates of subjects immersed in water in either a vertical or horizontal position,suggesting that it is not the body position during immersion that accounts for the lower heartrates. Thus, the lower heart rates probably occur as a result of the diving reflex with facialimmersion as well as the effects of whole body immersion.Studies of occupational lung disease often use spirometry or peak flow measurements toassess lung function before and after work exposure. We attempted to assess the effects ofprolonged swimming on lung function by measuring FEy1 before and after a 45 minute exercise175challenge test. We were unable to detect any change in lung function following exercise,although the swimmers did complain of a number of respiratory and other health-relatedsymptoms. The prevalence of chest congestion, sneezing, chest tightness, sore eyes, andheadaches following the 45 minute swim was lower than the prevalence of post-exercisesymptoms reported on the questionnaire. Sore throats and a dry mouth were reported morefrequently following the 45 minute swim and this may be due to the fact that the swimmers hadto breathe air through a mouthpiece and a long section of tubing for the duration of the test.The intensity of the 45 minute exercise test was 15-20% lower than that of the 8 minute exercisechallenge test, which may partially explain the fact why none of the swimmers reportedwheezing or dyspnea.There was also an interesting trend in the “E and f data for the Case Group during the45 minute test. There was a progressive fall in VE and a continual rise in f which suggests thatthese swimmers were adopting a restrictive breathing pattern. This breathing pattern is similarto that reported for exercising athletes who are exposed to low level concentrations of ozone(Adams and Schelegle, 1983; Follinsbee et al., 1988; McKenzie et al., 1987). Symptoms ofsubsternal soreness, dyspnea, coughing, wheezing, congestion, sore throats, headaches, andnausea are common during exercise under these conditions. Perhaps prolonged exposure to thechemicals used to disinfect the pool water have a similar effect on breathing pattern andsymptom responses, and what we are seeing is an early indicator of respiratory distress.There is a remarkable discrepancy between the prevalence of BHR (60.0%) and ETA(9.8%) among these competitive swimmers. While the prevalence of BHR is significantly higherin swimmers than in non-swimmers, there is no difference in the prevalence of ETA among thetwo groups of athletes. We also know that the prevalence of BHR is similar between swimmers176with and without asthma and/or exercise-related symptoms, and even though swimmers have ahigh prevalence of exercise-related symptoms suggestive of asthma, these symptoms don’tmanifest themselves as ETA. These results provide us with substantial evidence that there issomething about the swimming-related exposure that increases non-specific bronchialresponsiveness, but does not incite ETA.177CONCLUSIONSIn conclusion, this study shows that the prevalence of ETA among lower mainlandcompetitive swimmers is 9.8%. This value is within the 3-11 % prevalence reported for othercompetitive athletes, and is similar to the 6.3% prevalence that was observed for 16 non-swimming athletes in our study. Our study also confirms the lower asthmogenicity of swimmingwhen compared to land-based activities. The prevalence of ETA was higher in the laboratory(9.8%) when compared to the swimming pool (3.6%). The mechanisms for this protective effectare not clear, but in our study it does not appear to be related to RHL or to differences in thetemperature or humidity of the inspired air. There were no differences in the prevalence of ETAamong competitive swimmers who have asthma or exercise-related symptoms (11.1 %) incomparison with those whO have neither asthma nor exercise-related symptoms (11.8%).Throughout this study we were able to match VE and V02 for the three groups of athletesinvolved in the laboratory study for ETA and the two groups of swimmers involved in theswimming pool study for ETA. Despite this, there were significant differences in heart rateamong the three groups of athletes involved in the laboratory study, and when comparing heartrates between the laboratory and pool studies. The mean heart rate of the Non-SwimmingControl Group was significantly lower than that of either of the swimming groups. Similarly,the mean heart rate of the Control Group was significantly lower than the Case Group. Thesedifferences are likely due to the specificity of training among the non-swimmers and swimmersor to differences in the sample population which represents each group of athletes. The meanheart rate of the swimmers during the swimming pool test for EIA was 11 beats/minute lowerthan during the laboratory test for ETA. This finding is similar to many of the comparativestudies that have evaluated the physiological effects of exercise on land and in the water. These178lower heart rates probably occur as a result of the diving reflex with facial immersion as wellas the effects of whole body immersion.Finally, while continuous submaximal swimming for 45 minutes results in the swimmerscomplaining of many of the symptoms reported on our questionnaire, there were no significantpre- to post-exercise changes in FEV1. 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Physiol. 1988;64:812-816.187GENERAL SUMMARY AND CONCLUSIONSThis study has provided us with the answers to a number of questions that originallyevolved from anecdotal reports of respiratory and other health-related problems amongcompetitive swimmers. In the first chapter, we determined the prevalence of respiratory andother health-related symptoms, illnesses, and allergies among competitive swimmers, andestablished whether the symptoms were associated with a swimming-related exposure as definedby the amount of time spent swimming, or the distance covered, during training sessions in theswimming pool. To accomplish these objectives, we modified the American Thoracic Society’sRespiratory Disease Questionnaire for Adults and Children into a single questionnaire andadministered it to 738 competitive swimmers from Canada, the United States, and a number ofPacific Rim countries.The prevalence of respiratory and other health-related symptoms, illnesses, and allergieswere extremely common among competitive swimmers. The overall prevalence of physician-diagnosed asthma among the 738 competitive swimmers was 13.4%. This is significantly higherthan the 7.1% to 9.7% reported for other competitive athletes. There was a significantdifference in the prevalence rates of asthma for the three groups of competitive swimmers thatwe identified. The range of values included 10.6% of Age Group Swimmers, 12.4% ofNational Qualifiers, and 20.6% of International Level Swimmers. The extremely highprevalence of asthma among the International Level Swimmers was associated with a highprevalence of swimming-related symptoms suggestive of asthma and the use of 32-agonistsamong 9.1 % of the swimmers in this group.188There was a tendency for Age Group Swimmers to have their asthma diagnosed beforethey began competitive swimming, while the National Qualifiers and International LevelSwimmers had their asthma diagnosed after they began competitive swimming. This suggeststhat a combination of exercise and the swimming-related exposure may have caused swimming-related respiratory symptoms that were severe enough for the swimmers to see their physicianfor medical advice.Among the other respiratory illnesses that we identified, the prevalence of bronchitis(24.9%) and pneumonia (10.2%) were higher than that reported for the general population. Theprevalence of hay fever (16.9%) was significantly lower than that reported for other highperformance athletes, but is slightly higher than that reported for the general population. Themost common allergies among the competitive swimmers were to dust (20.9%), pollen (19.2%),animal hair (17.1%), grasses (17.1%), and molds (8.5%). These prevalences appear to besimilar to those reported for high performance athletes as well as the general population.A high percentage (43.5%) of the swimmers had at least one chest illness that kept themfrom participating in their normal daily activities for 3 days or more during the past year. Theprevalence of swimming-related symptoms included sneezing (45.0%), difficulty breathing(39.4%), coughing (36.4%), sore eyes (36.0%), headaches (35.9%), sore throat (27.1 %),wheezing (26.3 %), chest tightness (24.8%), and chest congestion (22.8%). This suggests thatboth upper and lower respiratory tract irritation occurs as a result of the swimming-relatedexposure. All of the symptoms, except for sore eyes, were strongly associated with theswimming-related exposure. These results imply that there is a dose-response relationshipbetween the amount of training and the occurrence of symptoms.189We identified a number of gender- and age-related differences for several of theswimming-related symptoms. Female swimmers were more likely to cough, feel congested,have difficulty breathing, and experience headaches. Older swimmers were more likely to feelcongested, sneeze, wheeze, have chest tightness, difficulty breathing, sore throats, andheadaches. A majority of the swimmers with swimming-related symptoms reported that theirsymptoms were less severe, less noticeable, or absent if they spent several days away from theswimming pool.In the second chapter, we established the prevalence of bronchial hyperresponsiveness(BHR) in a group of competitive swimmers from the lower mainland using a methacholinechallenge test. In addition, we determined whether there were differences in the prevalence ofBHR among competitive swimmers with asthma or swimming-related symptoms (Case Group)and those who had neither asthma nor symptoms (Control Group), and compared their resultswith a group of non-swimming athletes who had neither asthma nor symptoms (Non-SwimmingControl Group).This study showed that the prevalence of BHR (PC20 16 mg/mL) among lower mainlandcompetitive swimmers was 60.0%. When the sensitivity of the methacholine challenge test wasdecreased to include only those swimmers with a PC20 8 mg/mL, the prevalence of BHR was34.3 %. These values are significantly higher than the 12.5% and 0% prevalences that wereobserved for 16 non-swimming athletes in our study and the 11-14% prevalence reported inseveral population-based studies. There was no difference in the prevalence of BHR amongcompetitive swimmers who have a clinical history of asthma or symptoms suggestive of asthmawhile swimming (61.1%) and those who have neither asthma nor symptoms (58.8%). When thesensitivity of the methacholine challenge test was decreased to include only those swimmers with190a PC2O 8 mg/mL, 33.3% of the swimmers in the Case Group and 35.3% of the swimmers inthe Control Group demonstrated BHR.The use of the dose-response slope was effective in assessing differences in BHR amongthe three groups of athletes. In our study there was approximately a 363-fold difference betweenthe least and most responsive subjects using this method. The dose-response slope wassignificantly lower in the non-swimmers, indicating a lower prevalence of BHR in that groupof athletes. The extremely high prevalence of BHR among the competitive swimmers whencompared to the non-swimmers leads us to believe that there is something about the swimming-related exposure that may be responsible for the BHR among the swimmers. These competitiveswimmers have a high prevalence of asthma, respiratory symptoms suggestive of asthma, andnon-specific BHR to methacholine. However, their lung function is normal and there is nodifference in the prevalence of BHR among swimmers with or without asthma or swimming-related symptoms. At this time, we can only speculate that the chemicals used to disinfect theswimming pool water are responsible for the development of BHR among the competitiveswimmers.In the third chapter, we established the prevalence of exercise-induced asthma (ETA) inthe same group of swimmers from the lower mainland using a standard exercise challenge testin the laboratory and a tethered swimming protocol in the swimming pool. We also determinedwhether there were differences in the prevalence of ETA among competitive swimmers in theCase and Control Groups and compared their results with the Non-Swimming Control Group.In addition, we determined whether a prolonged exercise challenge test in the swimming poolresulted in the development of respiratory symptoms and significant changes in pulmonarymechanics.191The prevalence of ETA among lower mainland competitive swimmers was 9.8%. Thisvalue was within the 3-11 % prevalence reported for other competitive athletes, and was similarto the 6.3% that was observed for the non-swimming athletes in our study. The prevalence ofETA among the swimmers was also higher in the laboratory (9.8%) when compared to theswimming pool (3.6%). Our results are in agreement with those of other researchers who haveshown the lower asthmogenicity of swimming when compared to land-based activities. Themechanisms for this protective effect are not clear and, in our study, do not appear to be relatedto respiratory heat loss (RHL) or to differences in VE or the temperature and humidity of theinspired air. There were also no differences in the prevalence of ETA among competitiveswimmers who have asthma or swimming-related symptoms (11.1 %) and those who have neitherasthma nor swimming-related symptoms (11.8%).Finally, while continuous submaximal swimming for 45 minutes results in the swimmerscomplaining of many of the symptoms reported on our questionnaire, there were no significantpre- to post-exercise changes in FEy1. However, the swimmers in the Case Group adopted arestrictive breathing pattern similar to that of athletes who are exposed to irritants such as SO2,NO2, and 03 during exercise. It is possible that this might be an early indicator of respiratorydistress.In summary, these results provide us with substantial evidence that there is somethingabout the swimming-related exposure that may cause a mild form of asthma in susceptibleswimmers, causes non-specific BHR in 60% of swimmers whether or not they have asthma orswimming-related symptoms, but does not appear to incite ETA. In fact, there is a remarkablediscrepancy between the prevalence of BHR and ETA among the competitive swimmers. Thisfinding is associated with a number of other interesting results. The presence of normal lung192among those swimmers with physician-diagnosed asthma suggests that many of the swimmersare not currently atopic or symptomatic. There was also a higher prevalence of BHR inswimmers when compared to non-swimmers, a similar prevalence of EIA among swimmers andnon-swimmers and, despite a low prevalence of EIA, there was a high prevalence of swimming-related symptoms among the swimmers. It is possible that individuals with unstable asthma orsevere swimming-related symptoms that affect performance may not be able to participate incompetitive swimming at the national or international level.These findings suggest that the underlying mechanism responsible for the BHR is relatedto a heightened cholinergic excitatory mechanism that increases non-specific bronchialresponsiveness to methacholine, but not to exercise. We speculate that chronic, low levelexposure to the chemicals used to disinfect the pool water may damage the respiratory epitheliumand expose bronchial irritant receptors and pulmonary C-fibers. This may trigger an axon reflexthat results in the release of chemical mediators that enhance smooth muscle contraction,inflammation, and BHR. Swimmers who complain of symptoms during training may have beenexposed to higher concentrations of these chemicals. Since the most common cause of asthmain young people is sensitization to inhaled allergens, there may be a relationship between atopyand the chemical irritants in the swimming pool. Knowing this relationship may have providedus with information about whether chemical irritants in the swimming pool increase thelikelihood of becoming atopic or, conversely, whether atopic individuals are more likely todevelop swimming-related symptoms. In retrospect, it would have been prudent to have assessedthe atopic status of the subjects from the lower mainland.193Future studies of competitive swimmers need to document the relationship between theclinical findings in our study and exposure to the chemicals used to disinfect swimming poolwater. This will need to be done using specific inhalation challenge tests with the chemicalirritants found in the water. In addition, studies need to evaluate the prevalence of respiratoryillnesses and symptoms, BHR, and ETA, longitudinally. These studies should attempt toestablish these prevalences at the onset of the swimmer’s career, and measure the change inprevalence at regular intervals during the competitive season and throughout the swimmer’scareer. Since a majority of swimmers feel that their symptoms improve if they do not exercisein the swimming pool for several days, it would also be interesting to monitor changes in theirpeak expiratory flow rates before and after training sessions and after prolonged periods awayfrom the swimming pool. These studies may provide us with information about any long-termhealth-related problems associated with competitive swimming and establish whether theswimming-related exposure results in the development of irritant-induced occupational asthmaor RADS.194APPENDIX ACompetitive Swimmer’s Respiratory HealthQuestionnaire (27/04/91)DEPARTMENT OF PHYSIOLOGYFACULTY OF MEDICINEUNIVERSITY OF BRITISH COLUMBIACOMPETITIVE SWIMMER’SRESPIRATORY HEALTH QUESTIONNAIRE27/04/91195NAME:ADDRESS:(Last) (First) (Middle)(Street)(City)(Telephone Number)(Province) (Postal Code)DATE OF BIRTH:(Year) (Month) (Day)GENDER:(M/F)SWIM CLUB:COACH’S NAME:(Last) (First)COMPETITIVE CATEGORY: 7-10 year olds11-17 year olds (not a national qualifier)18-over (not a national/university qualifier)University (not a national qualifier)National QualifierI.D. NumberCompetitive Swimmer’s 196Respiratory Health QuestionnairePage 2Today’s Date:_______________________________(Year) (Month) (Day)AGE: GENDER:Did you complete this questionnaire by yourself__or with the help of someone else_____?If someonehelped you complete this questionnaire, name that person: (please-../ below)(a) Mother__(d) Male Guardian_____(b) Father__(e) Coach(c) Female Guardian_(f) Other (specify)_ ___________________COMPETITIVE CATEGORY: 7-10 year olds11-17 year olds (not a national qualifier)18-over (not a national/university qualifier)University (not a national qualifier)National QualifierTRAINING FACILITY:___ _(1) How many years have you been a competitive swimmer?____(2) On average, how many times do you train in the water each day?_(3) On average, how many days do you train in the swimming pool each week?(4) On average, how many weeks do you train in the swimming pool each year?(5) On average, how many metres do you swim each week?(6) Are your training sessions early in the morning (5 am to 9 am)_ ___,mid-day (10 am to 2 pm)_____or late afternoon/early evening (3 pm to 7 pm)___ _?(please-./ appropriate times)(7) On average, how long are your training sessions?:(a) early morning training sessions hours(b) mid-day training sessions hours(c) late afternoon/early evening training sessions hoursI.D. NumberCompetitive Swimmer’s 197Respiratory Health QuestionnairePage 3(8) During the past year, have you had any chest illnesses(pneumonia, bronchitis, asthma, colds, etc.) that havekept you from participating in your daily activitiesfor 3 days or more?If you answered YES to (8), how many times did this occurduring the past year?_____If you answered YES to (8), how many times did theseillnesses last for 7 days or more?(9) On average, how many colds do you get each year?_____(10) Do you usually have a cough with colds?(11) Do you usually have a cough apart from colds?(12) If you answered YES to (10) or (11), do you cough on mostdays (4 or more days each week) for as much as 3 monthsof the year?(13) Do you usually cough during or after exercise other than swimming?(a) during exercise(b) after exerciseIf you answered YES to (13), please indicate the number of yearsyou have experienced this problem?If you answered YES to (13), does this cough usually prevent youfrom continuing to exercise?(14) Do you usually cough during or after exercise in the swimming pool?(a) during exercise(b) after exerciseIf you answered YES to (14), please indicate the number of yearsyou have experienced this problem?YESD NODNumber of illnessesNumber of illnessesNumber coldsYESD NODYESD NODYESD NODYESD NODYESD NODNumber of yearsYESD NODYESD NODYESD NODNumber of yearsI.D. NumberCompetitive Swimmer’s 198Respiratory Health QuestionnairePage 4If you answered YES to (14), does this cough usually prevent youfrom continuing to exercise?If you answered YES to (11),(13) or (14), does this coughget better when you have not exercised in the swimming pooi forseveral days?(15) Does your chest usually feel congested when you have a cold? YES D(16) Does your chest usually feel congested apart from colds? YES D(17) Does your chest usually feel congested during or after exercise other than swimming?(a) during exercise YES D(b) after exercise YES DIf you answered YES to (17), please indicate the number of yearsyou have experienced this problem?If you answered YES to (17), does this chest congestion usually YES Dprevent you from continuing to exercise?(18) Does your chest usually feel congested during or after exercise in the swimming pool?(a) during exercise YES D(b) after exercise YES 0YESDYESDNumber of yearsNODNODNODNODNODNODNODNODNODNODNODNODIf you answered YES to (18), please indicate the number of yearsyou have experienced this problem?If you answered YES to (18), does this chest congestion usuallyprevent you from continuing to exercise?If you answered YES to (16),(17) or (18), does thiscongestion get better after you have not exercised in theswimming pool for several days?(19) Do you usually bring up phlegm when you have a cold?Number of yearsYESOYESDYESDI.D. NumberCompetitive Swimmer’s 199Respiratory Health QuestionnairePage 5(20) Do you usually bring up phlegm apart from colds? YES ci NO ci(21) If you answered YES to (19) or (20), do you bring up phlegm YES ci NO cion most days (4 or more days each week) for as much as3 months of the year?(22) Do you usually sneeze when you have a cold? YES ci NO ci(23) Do you usually sneeze apart from colds? YES ci NO ci(24) Do you ever sneeze during or after exercise other than swimming?(a) during exercise YES ci NO ci(b) after exercise YES ci NO ciIf you answered YES to (24), please indicate the number of years Number of yearsyou have experienced this problem?If you answered YES to (24), does this sneezing usually prevent YES ci NO ciyou from continuing to exercise?(25) Do you ever sneeze during or after exercise in the swimming pool?(a) during exercise YES ci NO ci(b) after exercise YES ci NO ciIf you answered YES to (25), please indicate the number of years Number of yearsyou have experienced this problem?If you answered YES to (25), does this sneezing usually prevent YES ci NO ciyou from continuing to exercise?If you answered YES to (23),(24) or (25), does this YES 0 NO cicongestion get better after you have not exercised in theswimming pool for several days?(26) Does your chest ever sound “wheezy” when you have a cold? YES ci NO ciI.D. NumberCompetitive Swimmer’s 200Respiratory Health QuestionnairePage 6(27) Does your chest ever sound “wheezy” apart from colds? YES D NO DIf you answered YES to (27), does your chest sound “wheezy” YES 0 NO cion most days or nights?If you answered YES to (27), please indicate the number of years Number of yearsthat you have experienced this problem.(28) Does your chest ever sound “wheezy” during or after exercise other than swimming?(a) during exercise YES D NO 0(b) after exercise YES o NO ciIf you answered YES to (28), please indicate the number of years Number of yearsthat you have experienced this problem.If you answered YES to (28), please indicate whether this YES 0 NO 0“wheezing” usually prevents you from continuing to exercise?(29) Does your chest ever sound “wheezy” during or after exercise in the swimming pool?(a) during exercise YES 0 NO 0(b) after exercise YES ci NO 0If you answered YES to (29), please indicate the number of years Number of yearsthat you have experienced this problem.If you answered YES to (29), please indicate whether this YES 0 NO 0“wheezing” usually prevents you from continuing to exercise?If you answered YES to (27),(28) or (29), does this YES ci NO ci“wheezing” usually get better after you have not exercisedin the swimming pool for several days?(30) Do you usually have chest tightness with colds? YES 0 NO ci(31) Do you usually have chest tightness apart from colds? YES D NO 0I.D. NumberCompetitive Swimmer’s 201Respiratory Health QuestionnairePage7(32) Do you ever have chest tightness during or after exercise other than swimming?(a) during exercise YES D NO ci(b) after exercise YES ci NO ciIf you answered YES to (32), please indicate the number of years Number of yearsyou have experienced this problem.If you answered YES to (32), does this chest tightness usually YES ci NO ciprevent you from continuing to exercise?(33) Do you ever have chest tightness during or after exercise in the swimming pool?(a) during exercise YES ci NO ci(b) after exercise YES ci NO ciIf you answered YES to (33), please indicate the number of years Number of yearsthat you have experienced this problem.If you answered YES to (33), please indicate whether this YES C NO cichest tightness usually prevents you from continuing toexercise?If you answered YES to (31),(32) or (33), does this YES ci NO cichest tightness usually get better after you have not exercisedin the swimming pooi for several days?(34) Do you usually have difficulty breathing when you have a cold? YES ci NO ci(35) Do you usually have difficulty breathing apart from colds? YES ci NO ci(36) Do you ever have difficulty breathing during or after exercise other than swimming?(a) during exercise YES ci NO ci(b) after exercise YES ci NO ciIf you answered YES to (36), please indicate the number of years Number of yearsthat you have experienced this problem.I.D. NumberCompetitive Swimmer’s 202Respiratory Health QuestionnairePage 8If you answered YES to (36), does this difficulty breathing YES C NO Cusually prevent you from continuing to exercise?(37) Do you ever have difficulty breathing during or after exercise in the swimming pool?(a) during exercise YES D NO C(b) after exercise YES D NO CIf you answered YES to (37), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (37), does this difficulty breathing YES C NO Cusually prevents you from continuing to exercise?If you answered YES to (35),(36) or (37), does this YES C NO Cdifficulty breathing occur less frequently or with lessintensity after you have not exercised in the swimming pooifor several days?(38) Is your throat usually “raspy” or “ticklish” when you have YES C NO Ca cold?(39) Is your throat usually “raspy” or “ticklish” apart from colds? YES D NO C(40) Is your throat ever “raspy” or “ticklish” during or after exercise other than swimming?(a) during exercise YES C NO C(b) after exerciseV YES C NO oIf you answered YES to (40), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (40), does this “raspy” or “ticklish” throat YES C NO Cusually prevent you from continuing to exercise?I.D. NumberCompetitive Swimmer’s 203Respiratory Health QuestionnairePage 9(41) Is your throat ever “raspy” or “ticklish” during or after exercise in the swimming pool?(a) during exercise YES D NO D(b) after exercise YES ° NO DIf you answered YES to (41), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (41), does this “raspy” or “ticklish” throat YES o NO ousually prevent you from continuing to exercise?If you answered YES to (39),(40) or (41), does your throat YES D NO Dfeel better after not exercised in the swimming pool for severaldays?(42) Are your eyes usually itchy, watery, or puffy when you have YES D NO Ca cold?(43) Are your eyes usually itchy, watery, or puffy apart from colds? YES C NO C(44) Are your eyes ever itchy, watery, or puffy during or after exercise other than swimming?(a) during exercise YES C NO C(b) after exercise YES C NO CIf you answered YES to (44), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (44), do itchy, watery, or puffy eyes YES C NO Cusually prevent you from continuing to exercise?(45) Are your eyes ever itchy, watery, or puffy during or after exercise in the swimming pool?(a) during exercise YES C NO C(b) after exercise YES C NO CIf you answered YES to (45), please indicate the number of years Number of yearsthat you have experienced this problem?I.D. NumberCompetitive Swimmer’s 204Respiratory Health QuestionnairePage 10If you answered YES to (45), do itchy, watery, or puffy eyes YES 0 NO ciusually prevent you from continuing to exercise?If you answered YES to (43), (44) or (45), do your eyes YES 0 NO cifeel better after you have not exercised in the swimming pooifor several days?(46) Do you usually experience headaches when you have a cold? YES 0 NO ci(47) Do you usually experience headaches apart from when you YES 0 NO 0have colds?(48) Do you ever experience headaches during or after exercise other than swimming?(a) during exercise YES ci NO ci(b) after exercise YES ci NO ciIf you answered YES to (48), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (48), do these headaches usually prevent YES C NO ciyou from continuing to exercise?(49) Do you ever experience headaches during or after exercise in the swimming pool?(a) during exercise YES 0 NO ci(b) after exercise YES ci NO ciIf you answered YES to (49), please indicate the number of years Number of yearsthat you have experienced this problem?If you answered YES to (49), do these headaches usually prevent YES ci NO ciyou from continuing to exercise?If you answered YES to (47),(48) or (49), do these YES ci NO ciheadaches occur less frequently or with less intensityafter you have not exercised in the swimming pooi for several days?I.D. NumberCompetitive Swimmer’s 205Respiratory Health QuestionnairePage 11(50) Have you ever had an ear infection? YES D NO DIf you answered YES to (50), please indicate the average Number per yearnumber of ear infections you get each year?(51) Has a doctor ever told you that you have any of the following, and if you answer Yes, at what age wereyou when it was first diagnosed by the doctor?(a) Asthma YES ci NO ci Age_____(b) Bronchitis YES ci NO ci Age(c) Croup YES ci NO C Age(d) Pneumonia YES ci NO C Age(e) Hay Fever YES C NO C Age(f) Eczema YES C NO ci Age_(g) Other (specify)___________________________Age(52) Has a doctor ever said that any member of your family (mother, father, brother(s), or sister(s)) has everhad any of the following?(a) Asthma YES ci NO 0(b) Bronchitis YES I] NO C(c) Emphysema YES C NO C(d) Pneumonia YES C NO C(e) Hay Fever YES C NO 0(f) Eczema YES C NO 0(g) Other (specify)_(53) Has a doctor ever told you that you are allergic to any of the following, and if you answer YES, at whatage were you when you were told?(a) Dust YES C NO C Age(b) Pollen YES C NO C Age(c) Animals or Pets YES C NO C Age(d) Grasses YES C NO C Age(e) Molds YES C NO 0 Age(f) Tobacco Smoke YES C NO C Age(g) Air Pollution YES C NO C Age(h) Insect Bites YES C NO C Age(i) Food(s) YES C NO C Age(j) Medication(s) YES C NO C Age(k) Other (specify)_________ ___Age_____I.D. NumberCompetitive Swimmer’s 206Respiratory Health QuestionnairePage 12(54) Has a doctor ever said that any member of your family (mother, father, brother(s), or sister(s)) isallergic to any of the following?:(a) Dust YES C NO C(b) Pollen YES D NO 0(c) Animals or Pets YES D NO D(d) Grasses YES C NO C(e) Molds YES D NO D(f) Tobacco Smoke YES 0 NO 0(g) Air Pollution YES C NO 0(h) Insect Bites YES D NO 0(i) Food(s) YES 0 NO C(j) Medication(s) YES C NO C(k) Other (specify)_________________________(55) Are you sensitive to things that come into contact with your skin?(a) Underwrap YES C NO C(b) Tape YES C NO 0(c) Sweat Bands YES C NO 0(d) Deodorants YES C NO C(e) Cologne, Perfume, etc. YES C NO C(f) Other (specify)____(56) Have you ever smoked cigarettes (answer YES only if you have YES C NO 0smoked more than 20 cigarettes in your lifetime)?If you answered YES to (56), at what age did you start smoking? Age_____If you answered YES to (56), what is the average number of Numbercigarettes you smoke/smoked each day?(57) If you answered YES to (56), do you still smoke? YES 0 NO 0If you answered NO to (57), at what age did you quit smoking? Age_____I.D. NumberCompetitive Swimmer’s 207Respiratory Health QuestionnairePage 13(58) Do you live with anyone who smokes (cigarettes, cigars, pipe, etc.) YES D NO DIf you answered YES to (58), is that person your:(a) Mother YES 0 NO 0(b) Father YES 0 NO 0(c) Brother(s) YES 0 NO 0(d) Sister(s) YES C NO 0(e) Other (please specify)_____________________(59) Are you currently taking any prescription medication? YES 0 NO 0If you answered YES to (59), list the medications that you are currently taking.(60) Do you ever smell a strong chemical odor in the swimming pool YES 0 NO 0when you exercise?If you answered YES to (60), do you usually have any of the following symptoms when you smell astrong chemical odor in the swimming pool?(a) Coughing YES C NO C(b) Chest Congestion YES 0 NO 0(c) Sneezing YES 0 NO 0(d) Wheezing YES C NO 0(e) Chest Tightness YES C NO C(f) Difficulty Breathing YES NO C(g) “Raspy” or “Ticklish” Throat YES 0 NO C(h) Itchy, watery, or puffy eyes YES 0 NO 0(i) Headaches YES C NO C(j) Nausea YES C NO C(k) Other (specify)If you answered YES to (60), has this strong chemical odor ever YES 0 NO Cprevented you from continuing to exercise?I.D. Number208APPENDIX BTables for Calculating the Cumulative Doseof MethacholineCTable24:Calculationofthecumulativedoseofmethacholmeforsubjectswithasthmaorsymptomssuggestiveofasthmawhileexerclsmg.Thesevalueswereusedtocalculatethelinearslopeofthedoseresponsecurveforeachofthesubjects.ConcentrationNebulizerOutputTimeDoseCumulativeDose(mglmL)(mLlmin)(mm)(mg)(mg)Saline0.132000.250.1320.0650.0650.500.1320.1300.1951.000.1320.2600.4552.000.1320.5200.9754.000.1321.0402.0158.000.1322.0804.09516.000.1324.1608.255Table25:Calculationofthecumulativedoseofmethacholineforsubjectswithnoclinicalhistoryofasthmaorsymptomssuggestiveofasthmawhileexercising.Thesevalueswereusedtocalculatethelinearslopeofthedoseresponsecurveforeachofthesubjects.ConcentrationNebulizerOutputTimeDoseCumulativeDose(mglmL)(mLImin)(mm)(mg)(mg)Saline0.132001.000.1320.2600.2602.000.1320.5200.7804.000.1321.0401.8208.000.1322.0803.90016.000.1324.1608.060

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