Asthma and Recreational SCUBA Diving

Sports Med 2003; 33 (2): 109-116REVIEW ARTICLE 0112-1642/03/0002-0109/$30.00/0

© Adis Data Information BV 2003. All rights reserved.

Asthma and RecreationalSCUBA DivingA Systematic Review

Michael Koehle, Rob Lloyd-Smith, Don McKenzie and Jack Taunton

Allan McGavin Sports Medicine Centre, Department of Family Practice and the School of HumanKinetics, University of British Columbia, Vancouver, British Columbia, Canada

Contents

Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1091. Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1102. Review Methodology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1103. Review Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

3.1 Selected Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1103.2 Critical Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111

4. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Asthma has traditionally been a contraindication to recreational self-containedAbstractunderwater breathing apparatus (SCUBA) diving, although large numbers ofpatients with asthma partake in diving. The purpose of this paper is to review allthe research relevant to the issue of the safety of asthma in divers.

MEDLINE and MDConsult were searched for papers between 1980–2002.Keywords used for the search were ‘asthma’, ‘SCUBA’ and ‘diving’. Additionalreferences were reviewed from the bibliographies of received articles.

A total of fifteen studies were identified as relevant to the area. These includedthree surveys of divers with asthma, four case series and eight mechanisticinvestigations of the effect of diving on pulmonary function. The survey datashowed a high prevalence of asthma among recreational SCUBA divers, similar tothe prevalence of asthma among the general population. There was some weakevidence for an increase in rates of decompression illness among divers withasthma. In healthy participants, wet hyperbaric chamber and open-water divingled to a decrease in forced vital capacity, forced expired volume over 1.0 secondand mid-expiratory flow rates. In participants with asymptomatic respiratoryatopy, diving caused a decrease in airway conductivity.

There is some indication that asthmatics may be at increased risk of pulmonarybarotrauma, but more research is necessary. Decisions regarding diving participa-tion among asthmatics must be made on an individual basis involving the patientthrough informed, shared decision making.

110 Koehle et al.

The issue of asthma and self-contained underwa- equalisation is not allowed, a pressure differentialter breathing apparatus (SCUBA) diving is a contro- will be created which can lead to barotrauma.versial one. Historically, asthma or a past history of Common sites of barotrauma are the middle ear,asthma has been considered an absolute contraindi- sinuses and the lungs. When barotrauma occurs incation for diving.[1] Recently, many experts in the the lungs, the expanding air can rupture alveoli,field have been revisiting their views on this is- leading to pneumothorax, pneumomediastinum,sue.[1-5] There is a lack of concrete evidence to back subcutaneous emphysema and arterial gas embolismeither side of this debate. Since prospective recrea- (AGE). These four entities are represented by thetional divers may come to their physician for advice term pulmonary barotrauma (PBT). At shallowerand medical clearance, the clinician must have an depths the changes in pressure are more pro-understanding of the issues and research related to nounced. For example, the pressure doubles whenasthma and diving. In this article, the relevant litera- travelling from the surface (1 atm) to 10m (2 atm),ture on the subject of asthma and recreational diving whereas it is only increased by 20% when descend-will be reviewed and discussed. ing from 40m (5 atm) to 50m (6 atm). Theoretically,

the greatest risk for PBT occurs as the diver ap-proaches the surface.[5] The concern with asthmatic1. Physiologydivers is that they may experience airway obstruc-

In this paper various pressure units are used, tion at depth, putting them at higher risk of gasreflecting the different units employed in the origi- trapping, and therefore PBT.nal articles. They reflect either a direct pressure Decompression sickness (DCS) is a separatemeasurement or an indirect pressure measurement pathological entity. DCS occurs when dissolved ni-in terms of depth. One atmosphere (atm) refers to trogen comes out of solution in tissues to formthe atmospheric pressure at sea level, equivalent to bubbles. Symptoms vary according to the location760 torr or 760mm Hg (millimetres of mercury). of the bubbles and can include joint pain, impairedAlternatively, pressure can be described indirectly vision, deafness and paralysis. As gas trapping is notusing depth. As a diver descends, the ambient pres- a potential cause for decompression sickness, theresure increases due to the column of water between is less concern about asthma causing DCS.the diver and the surface. At a depth of 10 metres (ofsea water), the ambient pressure doubles from 1 atm 2. Review Methodologyto 2 atm. This value is increased by 1 atm for every

MEDLINE and MDConsult databases were used10m the diver descends. Thus, the pressure andto search the keywords ‘asthma’, ‘SCUBA’ anddepth can be described in both atmospheres and‘diving’ from 1980–Feb 2002. Bibliographies ofmetres of seawater. Seawater is specified, as itsarticles selected were used to find additional perti-density is less than that of freshwater due to thenent articles. Preference was given to primary refer-salinity. As ambient pressure increases with depth,ences, including surveys, case reports and originalthere is a proportionate increase in the pressure ofresearch. The search was also limited to articles inthe air that the diver breathes. Boyle’s law states thatthe English language. A total of 25 articles andat a constant temperature, pressure is inversely pro-abstracts met these criteria.portional to volume. Therefore, in a submerged div-

er at 10m (2 atm), a given amount of air would be3. Review Findingscompressed to half the volume that it would occupy

at the surface. Conversely, on ascent to the surfacefrom a depth of 10m, a volume of gas would double. 3.1 Selected StudiesWhen the diver changes depth, the pressure of thebody’s gas-filled spaces must be equalised to the A total of fifteen studies[3,5-18] were identified asambient pressure. If a pocket of gas is trapped, and being relevant to the safety of asthma in SCUBA

© Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (2)

Asthma and Recreational SCUBA Diving 111

Table I. Summary of surveys of asthma in divers

Reference Sample Survey type Results Comment

Farrell and Glanvill[3] 104 divers with asthma Questionnaire in Diver 70% wheezed >12 × year; 89% Large number of dives(100 between ages magazine (circ 38 000); had asthma since childhood; no with low incidence of DCS16–40y) 12 864 dives logged cases of PBT; one diver had two and no PBT. Relatively

episodes of DCS; 96% take β- high frequency ofagonists before a dive; 21% dive wheezing. Many diverswithin 12 hours of wheezing diving with recent

wheezing

Bove et al.[6] 10 422 divers Survey in Skin Diver 8.3% answered ‘yes’ to ‘have you Proportion of asthmaticmagazine (circ 211 041) ever had asthma?’; 2.6% stated respondents not dissimilar

that they dive with asthma; 3.3% to general populationstated that they currently haveasthma

Corson et al.[7] 279 divers with asthma Survey in Alert Diver 56 334 dives in 269 divers; 88.7% Odds ratio 4.16. Relativelymagazine (75 000 mailed) took medications for asthma; high proportion of divers

55.8% took medications pre-dive; with severe asthma26.4% had been hospitalised forasthma; 11 cases of DCI reportedin 8 participants

circ = circulation; DCI = decompression illness; DCS = decompression sickness; PBT = pulmonary barotrauma.

diving. These included three surveys, four case se- 3.2 Critical Reviewries and eight mechanistic investigations of the ef-fect of diving on pulmonary function. These investi- The three surveys were quite similar in that theygations are summarised in tables I to III, re- involved voluntary responses to questionnaires dis-spectively. tributed through recreational diving magazines.[3,6,7]

Table II. Summary of case series of asthma in diving

References Number of cases Data source Results Comment

Leitch and Review of 12 cases Institute of Naval No cases reported asthma as a factor Retrospective study; did not findGreen[8] of recurrent PBT Medicine in England spirometry screening affected

1965–1985 PBT rate

Corson et al.[7] Review of 1213 Cases reported to 16 AGE cases had Hx of asthma, 7 Odds ratio was not significantcases of DCI Divers Alert Network were current asthmatics. Odds Ratio(including 196 cases 1987–1990 for current asthmatics was 1.98of AGE). Compared (0.65–2.59)with 696 surveyrespondents

Weiss and Van Two cases of likely Patients presenting to First case: 32-year-old female with Incidents occurred at shallowMeter[5] cerebral air embolismthe emergency Hx of asthma-like symptoms depths in swimming pool.

from diving in a department at developed pre-syncope, nausea, Second case lost to follow-up,swimming pool Louisiana State paraesthesias after dive to 3.6m. so Dx of cerebral air embolism

University School of Second case: 33-year-old female with not confirmedMedicine lifelong asthma developed vomiting,

pre-syncope and confusion after diveto 5.4m

Tetzlaff et al.[9] 15 consecutive casesComparison of divers 2/15 PBT cases had asthma. 14/15 PBT cases had riskof PBT; 15 with PBT to divers with Comparison of PFTs for all cases factors (pre-existing disease,consecutive cases of DCS. All were patients showed that PBT cases had a lower low MEF25, or lung cysts).DCS referred to the Naval MEF25 than DCS cases. High MEF25 is a non-specific and

Medical Institute in Kiel, incidence of lung cysts identified on insensitive test and cannot beGermany CT in PBT cases used to screen for PBT risk[4]

AGE = arterial gas embolism; CT = computed tomography; DCI = decompression illness; DCS = decompression sickness; Dx = diagnosis;Hx = history; MEF25 = mid-expiratory flow at 25% of forced vital capacity; PBT = pulmonary barotrauma; PFTs = pulmonary function testing.


112 Koehle et al.

Table III. Summary of physiologic investigations of pulmonary function in diving

Reference Sample Methods Results Comment

Catron et al.[12] 10 male active Simulated dive to 285 feet in a dry No change in FVC, FEV1.0, FEV1.0/FVC No demonstrable changeor former US recompression chamber for 10 min. after dive; two participants had mild in lung function thatNavy divers Pre- and post-dive spirometry and DCS; four participants had audible could be attributed to

precordial Doppler bubble signals on Doppler dive

Jammes et 1) 8 adult 1) Tracheotomised preparation, 1) RL increased 16% with N2O2 and Different gas mixtureal.[13] rabbits measured RL at varying T with 36% with HeO2 between surface and

N2O2 and HeO2 depth

2) 3 male 2) Measured RL while breathing 2) No change in RL with cold air, buthumans cold air at surface and cold HeN2O2 there was a 30–55% increase with the

mixture at simulated depths HeN2O2 mixture at depth

Thorsen et 7 (6 men, 1 Crossover design; warm dry gas vs Reduction in FEV1.0 of 4% (dry gas) Divers not blinded to dryal.[14] women) non- warm humid gas. 1) 30 min bottom and 1.1% (humid gas). Reduction in vs humid. Volumes

smoking divers time, 117 (pool), 375 and 600 kPa FEF25-75 of 8.6% (dry gas) and 0.9% decrease with depth,with no history (hyperbaric chamber); swimming (humid gas). No change in FVC. dryness andof pulmonary against resistance. 2) 240 min Decrease in volumes related to bronchoreactivitypathology bottom time 135 kPa in pool; 3 × 15 increasing pressure (p < 0.02),

min exercise bouts increased response to methacholine (p< 0.01)

Dujic et al.[15] 10 Navy divers 46 min dive to 5.5 bar in hyperbaric No change in spirometry post-dive. Decrease in DLCO likelychamber. Spirometry, blood gases PaO2 decreased 20 torr in air related to presence ofand DLCO measured pre and post, decompression group, no change in O2 venous gas embolialong with pre-cordial Doppler. group. DLCO decreased in all airDecompression was with either air decompression divers correlating toor O2 bubble signal on Doppler, no change in

O2 group

Thorsen et 12 male divers Two simulated dives to 39m with No change in spirometry after simulated Spirometry unchanged.al.[16] either slow or rapid decompression. dives. VGE noted in 1/6 divers on slow VGE likely cause of

Precordial Doppler, spirometry decompression, and all divers on fast decreased DLCO

decompression. DLCO decreased post-dive in proportion to amount of VGE

Skogstad et 1) 9 male divers1) Open sea dive to 10m (32–62 1) Decrease in FVC (5.8%), FEV1.0 Presence of VGE notal.[17] min) (6.6%), FEF25–75 (10.3%) and DLCO assessed. Shallower

(11.3%) dives have larger effecton spirometry

2) 17 male 2) Open sea dive to 50m (26–76 2) Smaller decrease in FVC (1.8%),divers min). Both used umbilical demand FEV1.0 (2.7%), FEF25–75 (5.2%) and

equipment similar decrease in DLCO (12.8%)

Tetzlaff et 1) 10 control, 1) Dive 50m in wet chamber at 2 1) Decrease in FVC, FEV1.0, MEF75 Decompression wasal.[10] 10 cold temperatures and no change in DLCO prolonged in all cases,

likely explainingunchanged DLCO

2) 15. All 2) Dives to 10m and 50m in wet 2) No difference in volumes between 2groups healthy chamber in cold conditions depthsmale divers

Tetzlaff et 9 participants Dives to 50m in wet chamber 3% reduction in FVC in both RV, FEV1.0, MEF50,al.[11] with hay fever DLCO changes were not

significant

9 healthy PFTs, methacholine challenge pre- Airway conductance decreased 15% incontrols and post-dive (3h and 24h) atopics at 24h post-dive

DCS = decompression sickness; DLCO = lung diffusing capacity; FEF25–75 = forced mid-expiratory flow at 75% forced vital capacity; FEV1.0

= forced expired volume in 1 second; FVC = forced vital capacity; MEF50 = mid-expiratory flow at 50% forced vital capacity; MEF75 = mid-expiratory flow at 75% forced vital capacity; PaO2 = arterial partial pressure of oxygen; PFTs = pulmonary function testing; RL = lungresistance; RV = residual volume; T = temperature; VGE = venous gas embolism.



The survey by Bove et al.[6] aimed to characterise the same institute in the 13 years before and the 7the incidence of asthma in active divers. Of 10 422 years following institution of mandatory pre-partici-respondents, 8.3% endorsed a past history of asth- pation spirometry. They found no improvement inma, while 3.3% admitted to being current asthmat- the incidence of AGE. Weiss and Van Meter[5] re-ics. These values are within the range of incidence ported two cases of cerebral air embolism in patientsof asthma in the general US population (4–7%).[6,19] with a history consistent with asthma. The strikingThe other two surveys only solicited responses from factor about these two cases was that they bothasthmatics. Farrell and Glanvill[3] catalogued 104 occurred at shallow depths in a swimming pool.divers with asthma for a total of 12 864 dives. There Tetzlaff et al.[4,9,21] attempted to identify risk factorswere no cases of PBT but two cases of DCS (in the for PBT by retrospectively examining 15 cases thatsame diver). Corson et al.[7] reported higher injury had been consecutively referred to the Naval Med-rates. In a total of 56 334 dives among 279 divers, ical Institute in Kiel, Germany. They examined11 cases of decompression illness (DCI) were re- medical history, radiological findings (including aported among eight participants. The authors com- computed tomography [CT] scan in 12 patients) andpared these data with the estimated risk in un- pulmonary function testing. In 14 of 15 cases, PBTselected divers from another study[20] to derive an risk factors were identified. These factors includedodds ratio of 4.16. However, there are several flaws medical history of asthma (two cases), lung cystswith this approach. The term DCI is a broad term visualised on CT (five cases) and a decreased mid-that comprises both DCS and PBT. Corson et al.[7] expiratory flow at 25% of capacity (MEF25) in tendid not differentiate between these two entities, so it of the cases. This group was compared with a groupis not clear how many cases of PBT actually oc- of 15 consecutive cases of DCS, who demonstratedcurred among these divers. The validity of compar- no prior medical history, no evidence of lung cystsing results from a self-report survey to another study and a decreased MEF25 in only one patient. Due tois questionable. With 75 000 questionnaires mailed the retrospective study design, the investigatorsout, and only 279 asthmatic respondents, the re- were unable to determine whether the cysts weresponse rate is exceedingly low. Assuming 8% of present before, or resultant from the barotrauma.survey recipients (6000 individuals) were asthmatic, Thus, the significance of these cysts remains un-the 279 responses represent a response rate of ap- clear. Using these results, the authors proposed thatproximately 5%. Of the divers who responded, MEF25 may be a good screening tool for divers to26.4% had been hospitalised for asthma, indicating reduce the risk of PBT.[9,21]

that the survey respondents likely represented a rela- This proposition was disputed by Neuman andtively severe subpopulation of asthmatics. The odds Clausen,[4] who took issue with the statistical analy-ratio quoted by this study must not be considered to sis of such a small sample size, asserting that thebe very reliable. decreased MEF25 was not in fact significant. They

In summary, we can conclude from these surveys also maintained that MEF25 is neither specific (ex-that there is a sizeable subpopulation of divers who cluding 25% of the general population) nor sensi-have asthma. There is not as yet, rigourous epidemi- tive, missing a third of the individuals in the PBTological evidence for an increased relative risk of group. Based on this work, it is therefore unlikelyPBT among divers with asthma. that MEF25 can provide a reliable screening tool for

predicting PBT risk.Four case series have been published on the issueof asthma and SCUBA diving. Leitch and Green[8] The Divers Alert Network (DAN), a US-basedreviewed all cases of recurrent PBT from non-profit organisation promoting diver safety, has1965–1985 at the Institute of Naval Medicine in the conducted the most systematic case review.[18] TheyUK. Asthma was not a causative factor in any of the retrospectively reviewed all cases of DCI reported tocases. The investigators also looked at AGE rates at DAN from 1987–1990. A total of 1213 cases of


114 Koehle et al.

DCI, including 196 cases of AGE had been reported. breathing a cold HeN2O2 mixture at 2, 3.5 and 8Sixteen (8.2%) of the divers who experienced AGE atm. They found no increase in RL with cold air at 1had a history of asthma, with seven of those divers atm, but a 30–55% increase in RL when breathingbeing currently asthmatic at the time of injury. To the mixture at 8 atm. The airway resistance rosecompare these data with the general asthma preva- further to 38–95% at 25 atm. These data are difficultlence among divers, DAN sent out 1000 question- to interpret, as there is more than one uncontrollednaires to a randomly selected group of DAN mem- variable between the two conditions (depth, inspiredbers, receiving 696 responses. The odds ratio was gas). Moreover, there were three participants ex-calculated for AGE among all asthmatics and the posed to 8 atm while only two participants weresubgroup of participants who were currently asth- tested at 25 atm. Thorsen et al.[14] hypothesised thatmatic. The odds ratio for current asthmatics was dry air may have more of an effect than humidified1.98 with a 95% CI of 0.51–2.59. The investigators air. Using a crossover design in seven divers, theywere therefore unable to demonstrate significance. exposed them to simulated diving with both dry andA larger sample size is definitely needed before any humidified air. A reduction in forced expired vol-reliable conclusions can be made. Another limita- ume in 1 second (FEV1.0) was present in both situa-tion of the study is that the control group was tions, but the reduction was significantly largercomprised of DAN members. Divers who become when the divers were breathing dry air.members of a safety promotion organisation would Three newer studies have looked at pulmonarylikely be safer, more responsible divers than the function under more realistic conditions, using ei-general population. A more representative control ther a wet hyperbaric chamber, or with actual open-group is therefore needed. sea diving.[10,11,17] In 1996, Skogstad et al.[17] exa-

mined pulmonary function after open-sea diving inIn summary, although there are some trends indi-healthy professional dive school students. Nine di-cating that asthma increases the risk of PBT invers dove to 10m, and a separate group (n = 17)divers, these case series do not provide solid evi-performed a dive to 50m. Pulmonary function wasdence. DAN is currently conducting a larger study inassessed before and after diving. Significant de-an attempt to better characterise the odds ratio ofcreases were found in forced vital capacity (FVC),AGE in divers with asthma.FEV1.0, forced mid-expiratory flow at 75% forcedAnother approach to the question of diving safetyvital capacity (FEF25–75) and DLCO at both depths,in asthmatics has been to look at the effects of thebut the changes were actually greater at shallowerhyperbaric environment on pulmonary function.depths. However, this study had several limitations.Several studies have used simulated diving in aFirstly, the divers were using umbilical demandhyperbaric chamber in a dry environment[12,15,16] toequipment, instead of the SCUBA equipment typi-depths of up to 285 feet (87m). These studies havecally used by recreational divers. Secondly, the sam-failed to demonstrate a change in spirometry post-ple was different between the two groups. Althoughdive. They have, however, demonstrated a drop inthe groups were anthropometrically similar, thethe lung diffusing capacity (DLCO) of 3–15%,sample sizes were different. Therefore, some of thewhich reverted to normal at 24 hours post-dive. Thisdisparity in pulmonary function between the divesalteration in DLCO has been attributed to the asymp-may be attributable to inter-group differences.tomatic presence of venous gas microemboli enter-

In a well-designed, two-part study, Tetzlaff eting the pulmonary circulation and reducing gas dif-al.[10] tried to assess the effects of cold on pulmonaryfusion. In 1988, Jammes et al.[13] tried to examinefunction at depth. Two matched groups of non-the effect of cold air on airway resistance (RL) inasthmatic sport divers completed simulated dives torabbits and humans. In an odd design, they com-50m in a wet hyperbaric chamber. The control grouppared airway resistance in humans breathing cold airwas exposed to ‘comfortable’ temperature (25°C)at atmospheric pressure with resistance when



while wearing a full 7mm wetsuit. The experimental • The prevalence of asthma in the diving popula-group was exposed to ‘cold’ temperature (only 5°C tion appears to resemble that in the general popu-colder) wearing a 3mm ‘shorty’ wetsuit that covered lation.only the trunk. Pulmonary function assessed before • There may be an increased odds ratio for PBT inand after diving showed a decrease in FVC, FEV1.0 divers with current asthma.and mid-expiratory flow at 75% of capacity

• Diving produces transient decreases in FVC,(MEF75) [1 hour post-dive] in both groups with noFEV1.0 and mid-expiratory flow rates post-divesignificant difference between groups. Pulmonarywhich are not exacerbated by cold temperature orfunction returned to normal by 24 hours post-dive.increasing depth. Diving may cause a decrease inTo truly test the effect of temperature under theseairway conductance in divers with asymptomaticconditions, this experiment should be repeated withrespiratory atopy at 24 hours post-dive.a larger temperature difference between the two

groups. The second part of the study involved 15 There is a definite need for more research in thisparticipants diving in ‘cold’ conditions to simulated area before an evidence-based decision can be madedepths of 10m and 50m in a wet hyperbaric cham- regarding the risks of asthma in recreational diving.ber. Again, there were decreases in FVC, FEV1.0 Both epidemiological studies and physiological ex-and MEF75 but there were no differences between periments are currently insufficient to address thisthe two depths. These ‘wet’ studies provide more issue. Although the DAN study may provide anconvincing evidence for alterations in pulmonary indication of increased risk for PBT in asthmatics,function with diving than the previous ‘dry’ studies. we currently cannot reliably estimate their relativeThere does not seem to be solid evidence that in- risk. Considering that the overall rate of dive injuriescreasing depth potentiates these changes, with one is approximately 0.53–3.4 per 10 000 dives,[22] westudy supporting that notion,[14] while others contra- can assume that the absolute risk is still quite low.dict it.[10,17]

Local guidelines are quite varied. For example,Only one study has examined the effects of div-the British Sub-Aqua Society allows well-controlleding on those with a history of respiratory atopy.asthmatics to dive; providing they have not needed aTetzlaff et al.[11] compared simulated wet chamberbronchodilator within the preceding 48 hours anddiving to 50m in nine divers with hay fever with athat they do not have cold-, exercise- or emotion-group of matched controls. The investigators per-induced asthma.[23] The South Pacific Underwaterformed pulmonary function testing including theMedicine Society requires ‘risk stratification’ formeasurement of specific airways conductance, pre-asthmatics, including history, physical and oftenand post-dive. In both groups, there was a similarpulmonary function testing with or without provoca-3% decrease in FVC at 24h post-dive, but moretion testing.[24] As there is a large variation in policy,significantly, there was a 15% decrease in airwayit is often difficult for the clinician to make a judge-conductance in the atopic group only. This study isment. When discussing the risks of asthma andthe only investigation to look into the effect ofrecreational SCUBA diving with a patient, perhapsdiving on atopic divers. The resulting difference inthe most appropriate approach is that of informed,airway conductance post-dive provides the first di-shared decision making. In this process, the patientrect evidence that diving adversely affects pulmona-becomes educated (with the physician’s assistance)ry function in atopic individuals.on the relevant knowledge related to the issue, andhow it relates to the patient’s individual medical4. Conclusionhistory. The patient and physician then jointly makea decision based on all the available information. InAfter examining the current body of research onthis way, the patient has an understanding of thethe relationship between asthma and diving, theissues at play and is able to share the responsibilityfollowing conclusions can be made:


116 Koehle et al.

13. Jammes Y, Burnet H, Cosson P, et al. Bronchomotor responseof making a decision that best suits their individualto cold air or helium-oxygen at normal and high ambient

situation. pressures. Undersea Biomed Res 1988; 15 (3): 179-92

14. Thorsen E, Ronnestad I, Segadal K, et al. Respiratory effects ofwarm and dry air at increased ambient pressure. Undersea

Acknowledgements Biomed Res 1992; 19 (2): 73-83

15. Dujic Z, Eterovic D, Denoble P, et al. Effect of a single air diveon pulmonary diffusing capacity in professional divers. J Appl

Dr Koehle received funding from the Department of Fam- Physiol 1993; 74 (1): 55-61ily Practice, University of British Columbia and the British

16. Thorsen E, Risberg J, Segadal K, et al. Effects of venous gasColumbia Sports Medicine Research Foundation. The authorsmicroemboli on pulmonary gas transfer function. Underseahave no conflicts of interest that are directly relevant to theHyperb Med 1995; 22 (4): 347-53

content of this manuscript.17. Skogstad M, Thorsen E, Haldorsen T, et al. Divers’ pulmonary

function after open-sea bounce dives to 10 and 50 meters.Undersea Hyperb Med 1996; 23 (2): 71-5

References 18. Corson K, Dovenbarger J, Moon R, et al. Risk assessment of1. Van Hoesen K, Neuman T. Asthma and SCUBA diving. Immu- asthma for decompression illness [abstract]. Undersea Biomed

nol Allergy Clin North Am 1996; 16 (4): 917-28 Res 1991; 18S: 162. Badier M, Guillot C, Delpierre S, et al. Value of bronchial 19. Wolf SL, Twarog F, Weiler JM, et al. Discussion of risk of

challenge in scuba diving candidates. J Asthma 2000; 37 (8):scuba diving in individuals with allergic and respiratory dis-661-5eases: SCUBA subcommittee. J Allergy Clin Immunol 1995;

3. Farrell PJ, Glanvill P. Diving practices of scuba divers with 96 (6 Pt 1): 871-3asthma. BMJ 1990; 300 (6718): 166

20. Wilmshurst P. Analysis of decompression accidents in amateur4. Neuman TS, Clausen JL. Recommend caution in defining riskdivers. Prog Underwater Sci 1990; 15: 31-7factors for barotrauma in divers. Chest 1998; 114 (6): 1791-3

5. Weiss LD, Van Meter KW. Cerebral air embolism in asthmatic 21. Bove AA. Pulmonary barotrauma in divers: can prospectivescuba divers in a swimming pool. Chest 1995; 107 (6): 1653-4 pulmonary function testing identify those at risk? Chest 1997;

6. Bove A, Neuman T, Kelsen S, et al. Observations on asthma in 112 (3): 576-8the recreational diving population [abstract]. Undersea Bi-

22. Strauss MB, Borer Jr RC. Diving medicine: contemporary top-omed Res 1992; 19S: 18ics and their controversies. Am J Emerg Med 2001; 19 (3):7. Corson K, Moon R, Nealen M, et al. A survey of diving232-8asthmatics [abstract]. Undersea Biomed Res 1992; 19S: 18-9

23. British Sub-Aqua Club. Respiratory system: asthma and diving8. Leitch DR, Green RD. Recurrent pulmonary barotrauma. AviatSpace Environ Med 1986; 57 (11): 1039-43 [online]. Available from URL: http://www.bsac.org/medical/

r_asthma.htm/ [Accessed 2002 Aug 16]9. Tetzlaff K, Reuter M, Leplow B, et al. Risk factors for pulmo-nary barotrauma in divers. Chest 1997; 112 (3): 654-9 24. Gorman D, Veale A. SPUMS Policy on asthma and fitness for

10. Tetzlaff K, Friege L, Koch A, et al. Effects of ambient cold and diving [online]. Available from URL: http://www.spums. or-depth on lung function in humans after a single scuba dive. Eur g.au/SPUMS_policy_asthma.htm/ [Accessed 2002 Aug 16]J Appl Physiol 2001; 85 (1-2): 125-9

11. Tetzlaff K, Staschen CM, Struck N, et al. Respiratory effects ofa single dive to 50 meters in sport divers with asymptomatic Correspondence and offprints: Michael Koehle, Allan McGa-respiratory atopy. Int J Sports Med 2001; 22 (2): 85-9

vin Sports Medicine Centre, 3055 Wesbrook Mall, Vancou-12. Catron PW, Bertoncini J, Layton RP, et al. Respiratory mechan-ver, BC V6T 1Z3, Canada.ics in men following a deep air dive. J Appl Physiol 1986; 61

(2): 734-40 E-mail: [email protected]


Documents

Asthma and Recreational SCUBA Diving