DOI 10.1378/chest.111.3.816 1997;111;816-819 Chest

 Michael J. Burns and Christopher H. Linden  

Acid ExposureSecondary to Bromine and Hydrobromic Another Hot Tub Hazard: Toxicity

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and change the filters. This may be all that is necessary to

prevent the buildup of M avium complex in hot tubs. Mavium complex is resistant to chlorination and so it is foundin domestic water.32 The high chlorine concentrationsneeded for sterilization may be unpleasant for hot tub use.

Superheating the water, if possible, to 70°C for up to an hourmay help.3-5 If our findings prove to occur more frequently inhot tubs, then a study of how to control the growth of Mavium complex must be done.

ACKNOWLEDGMENT: We acknowledge the consultationfrom Dr. A. Pan on the first case, the radiologic assistance of Dr.B. Maycher for the CT scan, the work of Ms. J. Wolfe in theMycobacterial Laboratory, Winnipeg, and the expertise of Char¬lotte Smith for serologic testing in the Centers for DiseaseControl and Prevention, Atlanta.

References1 Scully RE, Mark EJ, McNeely WF, et al. Case 6-1996. Case

records of the Massachusetts General Hospital. N Engl J Med1996; 334:521-26

2 Prince DS, Peterson DD, Steiner RM, et al. Infection withMycobacterium avium complex in patients without predispos¬ing conditions. N Engl J Med 1989; 321:863-68

3 von Reyn CF, Maslow JN, Barber TW, et al. Persistentcolonisation of potable water as a source of Mycobacteriumavium infection in AIDS. Lancet 1994; 343:1137-41

4 Marinkovich VA, Novey HS. Humidifier lung. Clin RevAllergy 1983; 1:533-36

5 du Moulin GC, Stottmeier KD, Pelletier PA, et al. Concen¬tration of Mycobacterium avium by hospital hot water sys¬tems. JAMA 1988; 260:1599-1601

6 Yakrus MA, Reeves MW, Hunter SB. Characterization ofisolates of Mycobacterium avium serotypes 4 and 8 frompatients with AIDS by multilocus enzyme electrophoresis.J Clin Microbiol 1992; 30:1474-78

7 Gruft H, Katz J, Blanchard DC. Postulated source ot Myco¬bacterium intracellulare (Battey) infection. Am J Epidemiol1975; 102:311-18

8 Wendt SL, George KL, Parker BC, et al. Epidemiology ofinfection by nontuberculous Mycobacteria: III. Isolation ofpotentially pathogenic mycobacteria from aerosols. Am RevRespir Dis 1980; 122:259-63

9 Parker BC, Ford MA, Gruft H, et al. Epidemiology ofinfection by nontuberculous Mycobacteria: IV. Preferentialaerosolization of Mycobacterium intracellulare from naturalwaters. Am Rev Respir Dis 1983; 128:652-56

10 Rosenzweig *DY. Pulmonary mycobacterial disease due to My¬cobacterium intracellulare-avium complex: clinical features andcourse in 100 consecutive cases. Chest 1979; 75:115-19

11 Engback HC, Vergmann B, Bentzon MW. Lung diseasecaused by Mycobacterium avium/Mycobacterium intracellu¬lare. An analysis of Danish patients during the period 1962-76. Eur J Resp Dis 1981; 62:72-83

12 Hawkins CC, Gold JWM, Whimbey E, et al. Mycobacteriumavium complex infection in patients with the acquired immu¬nodeficiency syndrome. Ann Intern Med 1986; 105:184-88

13 Teirstein AS, Damsker B, Kirschner PA, et al. Pulmonaryinfection with Mycobacterium avium-intracellulare: diagnosis,clinical patterns, treatment. Mt Sinai J Med 1990; 57:209-15

14 Banaszak EF, Thiede WH, Fink JN. Hypersensitivity pneu¬monitis due to contamination of an air conditioner. N EnglJ Med 1970; 283:271-76

15 Hodges GR, Fink JN, Schlueter DP. Hypersensitivity pneu¬monitis caused by a contaminated cool mist vaporizer. AnnIntern Med 1974; 80:501-04

16 Miller MM, Patterson R, Fink JN, et al. Chronic hypersen¬sitivity lung disease with recurrent episodes of hypersensitiv¬ity pneumonitis due to a contaminated central humidifier.Clin Allergy 1976; 6:451-62

17 Friend JAR, Pickering CAC, Palmer KNV, et al. Extrinsicallergic alveolitis and contaminated cooling-water in a factorymachine. Lancet 1977; 1:297-300

18 Muittari A, Kuusisto P, Virtanen P, et al. An epidemic ofextrinsic allergic alveolitis caused by tap water. Clin Allergy1980; 10:77-90

19 Lynch DA, Rose CS, Way D, et al. Hypersensitivity pneumo¬nitis: sensitivity of high-resolution CT in a population-basedstudy. AJR 1992; 159:469-72

20 Metzger WJ, Patterson R, Fink J, et al. Sauna-takers diseases:hypersensitivity pneumonitis due to contaminated water in a

home sauna. JAMA 1976; 236:2209-1121 Atterholm I, Hallberg T, Ganrot-Norlin K, et al. Unexplained

acute fever after a hot bath. Lancet 1977; 2:684-8622 Coleman A, Colby TV. Histologic diagnosis of extrinsic

allergic alveolitis. Am J Surg Pathol. 1988; 12:514-1823 Baur X, Behr J, Dewair M, et al. Humidifier lung and

humidifier fever. Lung 1988; 166:113-2424 Solley GO, Hyatt RE. Hypersensitivity pneumonitis induced by

Penicillium species. J Allergy Clin Immunol 1980; 65:65-7025 Edwards JH, Griffiths AJ, Mullins J. Protozoa as sources of

antigen in "humidifier fever." Nature 1976; 264:438-3926 Kane GC, Marx JJ, Prince DS. Hypersensitivity pneumonitis

secondary to Klebsiella oxytoca: a new cause of humidifierlung. Chest 1993; 104:627-29

27 Muittari A, Rylander R, Salkinoja-Salonen M. Endotoxin andbath water [letter]. Lancet 1980; 2:89

28 Sausker WF, Aeling JL, Fitzpatrick JE, et al. Pseudomonasfolliculitis acquired from a health spa whirlpool JAMA 1978;239:2362-65

29 Rose HD, Franson TR, Sheth NK, et al. Pseudomonaspneumonia associated with use of a home whirlpool spa.JAMA 1983; 250:2027-29

30 Aubuchon C, Hill JJ, Graham DR. Atypical mycobacterialinfection of soft tissue associated with use of a hot tub. J BoneJoint Surg 1986; 68A:766-68

31 Montecalvo MA, Forester G, Tsang AY, et al. Colonisation ofpotable water with Mycobacterium avium complex in homesof HIV-infected patients [letter]. Lancet 1994; 343:1639

32 Pelletier PA, du Moulin GC, Stottmeier KD. Mycobacteria inpublic water supplies: comparative resistance to chlorine.Microbiol Sci 1988; 5:147-48

Another Hot Tub Hazard*Toxicity Secondary to Bromine andHydrobromic Acid ExposureMichael J. Burns, MD; andChristopher H. Linden, MD

We describe the clinical course of two patients whodeveloped acute pneumonitis followed by reactive

*From the Section in Toxicology, Division of Emergency Medi¬cine, Beth Israel Hospital, Boston (Dr. Burns); and the Depart¬ment of Emergency Medicine, Division of Toxicology, Univer¬sity of Massachusetts Medical Center, Worcester (Dr. Linden).Manuscript received April 29, 1996; revision accepted Sep¬tember 19.Reprint requests: Dr. Michael Burns, 26 Edmunds Way, North-boro, MA 01532

816 Selected Reports

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airways dysfunction syndrome after bathing in a hottub. Additional findings were present and suggestedthat exposure to a corrosive agent was responsible.Bromine and hydrobromic acid generated from a

widely used water disinfectant were implicated as

the underlying cause. Physicians should be alert tothe possibility that such exposures may initiate or

exacerbate inflammatory pulmonary disease.(CHEST 1997; 111:816-19)

Key words: bromine; hot tub; hydrobromic acid; RADS

Abbreviations: Br2=aqueous or gaseous bromine; HBr=hydro-bromic acid; HOBr=hypobromous acid; HOCl=hypochlorousacid; RADS=reactive airways dysfunction syndrome

TT ot tub bathing is a popular recreational activity.-¦¦"¦-Although generally considered safe, public facilitiesusually have signs warning against hot tub use by individ¬uals who are pregnant, take certain medicines, or havediabetes or cardiovascular disease. A variety of medicalproblems have been linked to hot tub bathing.13 Exceptfor hypersensitivity pneumonitis due to the fungus, Cla-dosporium, however, pulmonary complications have notbeen described previously (to our knowledge).4 We de¬scribe two patients who developed signs and symptoms ofacute bromine toxicity followed by reactive airways dys¬function syndrome (RADS) after bathing in a hot tub anddiscuss the pathogenesis and pathophysiology of theirdisease.

Case ReportsCase 1

A 42-year-old woman presented with burning eyes, chest, andthroat, shortness of breath, and wheezing that began during a

10-min bath in a hot tub 2 h earlier. She reported a strong odorof "bleach" in the hot tub area, a glass-enclosed room measuring8X11 feet, located inside a local health club. Black discolorationof her gold jewelry and green bathing suit was also noted. She hadbeen in good health previously and did not smoke. Mild inspira¬tory stridor, expiratory wheezing, and a bleach-like odor to thebreath were noted on examination. Vital signs were normal andthe eyes, nose, throat, and skin were unremarkable. Oxygensaturation was 98% on room air. Chest radiograph and results ofroutine laboratory analyses were unremarkable. She was treatedwith humidified oxygen and nebulized albuterol during a 24-hhospitalization.

She reported intermittent rectal bleeding and generalizedalopecia during the following week and month, respectively.Dyspnea and chest burning continue to occur on exertion andexposure to cold air and strong odors. Symptoms respond toinhaled albuterol. Pulmonary function tests performed 3 and 10months after exposure revealed normal results of spirometry andlung volumes with a strongly positive methacholine challenge.The provocative doses required to produce a 20% fall in FEVXwere 0.008 and 0.007 |jimol, respectively. An c^-antitrypsin levelwas normal. Flexible sigmoidoscopy performed 13 months afterher exposure revealed nonspecific proctitis.Case 2

A 32-year-old woman presented with burning eyes, throat, andchest; hoarseness; nonproductive cough; and mild dyspnea that

developed during a single 5-min bath in the same hot tub at thesame time as patient 1. She, too, reported a strong acrid odorwhile bathing in the hot tub. She was previously healthy and didnot smoke. Results of physical examination were normal. Oxygensaturation was 99% on room air. Chest radiograph and results ofarterial blood gas analysis were normal. No treatment was

administered. Cough, sore throat, and hoarseness persisted for 7months. She continues to have chest burning with exertion.

Pulmonary function tests performed 10 months after exposurerevealed normal lung volumes and normal results of spirometrybut a strongly positive methacholine challenge (provocative doserequired to produce a 20% fall in FEVl5 0.447 |jimol).

DiscussionClinical manifestations and the temporal course of

events suggested exposure to an irritant chemical in thehot tub water and atmosphere as the etiology of our

patients' signs and symptoms. Bleach (hypochlorous acid,HOCl) or a chlorine-based disinfectant was initially sus¬

pected. Investigation, however, revealed that a bromine-based agent was used in the hot tub in question.

Three brominating compounds are available for recre¬

ational hot tub, spa, and swimming pool sanitation: elementalbromine, sodium bromide/monopotassium persulfate, andbromochlorodimethylhydantoin. All three compounds gen¬erate aqueous hypobromous acid (HOBr), the primary bac¬tericidal agent, when dissolved in water.

In the present incident, l-bromo-3-chloro-5,5-dimeth-ylhydantoin ("Brom Tabs," "Brominating Tablets") was

identified as the brominating agent. When added to poolwater, this compound hydrolyzes to HOBr and HOCl.5Bromide ions are subsequently generated when HOBrreacts with microorganisms. In an acidic pH, as occurs at

high concentrations, bromide also exists as hydrobromicacid (HBr). Unless the pH is kept relatively neutral (eg, byadding potassium carbonate), these two compoundsreadily react to form aqueous bromine (Br2). The subse¬quent liberation of Br2 (and possibly HBr) vapors in¬creases as water temperatures increase. Chlorine gas is not

generated because HOCl reacts with bromide ions result¬ing in the reformation of HOBr.5

Pool water bromination is achieved similarly with thesodium bromide/monopotassium persulfate method.When these compounds are added to water, bromide ionsare oxidized by monopotassium persulfate to HOBr.5Subsequent reactions are the same. Aqueous Br2 concen¬

trations between 2 and 4 ppm are recommended forresidential spas and 4 to 6 ppm for commercial spas.5Water pH should be between 7.2 and 7.6 optimally.

Br2 and HBr liquids and their vapors are skin andmucous membrane irritants. The extent of tissue injury is

dependent on their concentration, duration of contact, andwater content of exposed tissue. Pathologic effects includeedema, inflammation, and necrosis. Exposure to atmo¬

spheric concentrations of 10 ppm of Br2 is consideredimmediately dangerous to life and 0.3 ppm is the currentshort-term (15-min) exposure limit.6 Human volunteerscould not tolerate a Br2 concentration of 0.9 ppm forgreater than 5 min.7 Br2 is two to three times more

corrosive than HBr. Nasal irritation occurs at HBr vaporconcentrations of 5 to 6 ppm.8

CHEST / 111 / 3 / MARCH, 1997 817

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Like chlorine, the major cytotoxic effects of Br2 are

presumed to be secondary to the oxidizing effects ofnascent oxygen.9 Br2 reacts rapidly with tissue water toform HBr and HOBr. HOBr may subsequently breakdown into HBr and oxygen free radicals.10 The corrosiveaction of the acids generated and reaction of Br2 and theseacids with cellular proteins to form bromamine and thiolradicals may contribute to toxicity. Greater water solubil¬ity, and, thus, tissue permeability may explain why bro¬mine is more toxic than chlorine.

Clinical manifestations usually begin immediately aftervapor inhalation but may be delayed for up to 10 h.11Generally, low-concentration exposures will result in eye,nose, and upper airway injury and higher concentrationswill additionally result in lower airway damage. Sequelaeare infrequent and usually consist of subjective complaintswithout objective findings to correlate with symptoms.12One patient developed chemical pneumonitis and a

restrictive pattern of pulmonary dysfunction followingshort-term exposure to a mixture of HBr and phosphorustribromide.13 Persistent bronchiolar spasm has been ob¬served in animals exposed to Br2 vapors but not inhumans.14

Both patients described fulfill the criteria for RADS.15The abrupt onset of irritant symptoms within minutes of a

single bath suggest high-concentration irritant exposure.Circumstances strongly implicate exposure to bromineand HBr as the precipitating event. Allergic asthma (hy¬persensitivity pneumonitis) was not considered likely be¬cause it is typically insidious in onset, requiring repetitiveexposures to elicit an inflammatory reaction. Even withacute hypersensitivity pneumonitis, symptoms do not de¬velop until 4 to 6 h after exposure. In addition, patientswith hypersensitivity pneumonitis typically have constitu¬tional symptoms, abnormal chest radiographs, and restric¬tive pulmonary disease, findings that were not seen in our

patients.The pathophysiologic state of RADS has not been fully

elucidated. Nonspecific bronchial hyperresponsiveness isoperative and may be mediated by structural airwayabnormalities, immunogenic inflammation, and dysregu-lation of neurogenic inflammation.16 Bronchial biopsyspecimens from patients with RADS have revealed epi¬thelial destruction, squamous cell hyperplasia, subepithelialbasement membrane and connective tissue thickening, andvariable nonspecific inflammatory cell response (lymphocytesand plasma cells).151718 Structural bronchial damage isclosely linked to heightened airway responsiveness.RADS has been reported following inhalation of chlo¬

rine gas19 and pulmonary toxic reactions have resultedfrom the inhalation of vapors generated by swimming poolchlorinating tablets.10 Given the widespread use of bro¬mine compounds as bathing water disinfectants, the lackof previously reported cases of toxic reactions from bro¬minating agents is surprising, particularly in the setting ofhot tub use, where high water temperatures would beexpected to promote the liberation of toxic vapors. Thismay reflect greater safety of bromine-containing disinfec¬tants as compared with chlorinated ones. The greaterwater solubility of bromine allows for less vapor liberation

from aqueous solutions. Alternatively, similar cases mayhave occurred but gone unrecognized or unreported.We suspect that the bromine concentration and pH of

the hot tub water in which our patients bathed were

higher and lower, respectively, than recommended. Thejewelry and bathing suit discoloration noted by patient 1supports this contention. We were unable, however, toobtain any information from the health club managementin regards to these parameters. Although not previouslydescribed, alopecia and proctitis are also consistent withthe known toxicity (ie, corrosive effects) of bromine and itshalogen acid and exposure by way of immersion.An abnormally high bromine concentration or abnor¬

mally low pH in the hot tub water would also have resultedin greater production and liberation of Br2 and HBrvapors, and, hence, respiratory tract exposure. The factthat the hot tub was located in a small room rather thanoutdoors or in a larger (eg, poolside) indoor area may havecreated a situation similar to that of smoke inhalation,where exposure in an enclosed space is well known toincrease the risk of respiratory tract injury. Since both ofour patients reported that no one else was present in thehot tub at the same time as they were, we were unable todetermine whether other people used the hot tub inquestion and were similarly affected. We suspect thatwhen our patients reported their symptoms to the healthclub management at the time of exposure, the hot tub area

was closed to use until the situation could be investigatedand corrected.The known chemistry of brominating compounds, their

reported use in the hot tub in question, the temporalrelationship between exposure and toxic effects, clinicalsigns and symptoms that were consistent with the knowntoxicity of halogen gases and their acids, and the absenceof alternative explanations strongly implicate Br2 and HBras the cause of our patients' illnesses. Bromine poisoningshould be added to the list of potential hot tub hazards. Aswith chlorine gas exposure, inhalation of Br2 and HBrvapors may cause RADS. Patients with new-onset RADSor exacerbation of preexisting pulmonary disease shouldbe questioned about hot tub use and exposure to halogengases or vapors as a precipitating factor. Further study isnecessary to determine the incidence of poisoning result¬ing from such exposures.

References1 Press E. The health hazards of saunas and spas and how tominimize them. Am J Public Health 1991; 81:1034-37

2 Sausker WF, Aeling JL, Fitzpatrick JE, et al. Pseudomonasfolliculitis acquired from a health spa whirlpool. JAMA 1978;239:2362-65

3 Spitalny KC, Vogt RL, Witherell LE. National survey on

outbreaks associated with whirlpool spas. Am J Public Health1984; 74:725-26

4 Jacobs RL, Thorner RE, Holcomb JR, et al. Hypersensitivitypneumonitis caused by Cladosporium in an enclosed hot-tubarea. Ann Intern Med 1986; 105:204-06

5 Mitchell PK. The proper management of pool and spa water:

catalog 88-83735. Decatur, Ga: Hydrotech Chemical Corpo¬ration, 1988; 17-28

6 Stokinger HE. The halogens and the nometals boron andsilicon. In: Clayton GD, Clayton FE, eds. Patty's industrial

818 Selected Reports

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hygiene and toxicology. 3rd ed (vol IIB). New York: JohnWiley, 1981; 2965-72

7 Rupp H, Henschler D. Wirkungen geringer chlor- undbrom-konzentrationen auf den Menschen. Int Arch Gewer-

bepathologie Gewerbehygiene 1967; 23:79-908 Alexandrov DD. Bromine and compounds. In: Parmeggiani

L, ed. Encyclopedia of occupational health and safety. 3rd ed(vol 1). Geneva, Switzerland: International Labour Organisa¬tion, 1983; 326-29

9 Decker WJ, Koch HF. Chlorine poisoning at the swimmingpool: an overlooked hazard. Clin Toxicol 1978; 13:377-81

10 Wood BR, Colombo JL, Benson BE. Chlorine inhalationtoxicity from vapors generated by swimming pool chlorinatortablets. Pediatrics 1987; 79:427-30

11 Champeix J, Catilina P, Andraud G, et al. Etude clinique et

experimentale de l'intoxication par vapeurs de brome. Pou-mon Coeur 1970; 26:895-903

12 Carel RS, Belmaker I, Potashnik G, et al. Delayed healthsequelae of accidental exposure to bromine gas. J ToxicolEnviron Health 1992; 36:273-77

13 Kraut A, Lilis R. Chemical pneumonitis due to exposure tobromine compounds. Chest 1988; 94:208-10

14 Schlagbauer M, Henschler D. Toxicitat von chlor und brombei einmaliger und wiederholter Inhalation. Int Arch Gewer-bepathologie Gewerbehygiene 1967; 23:91-8

15 Brooks SM, Weiss MA, Berstein IL. Reactive airways dys¬function syndrome (RADS): persistent asthma syndromeafter high level irritant exposures. Chest 1985; 88:376-84

16 Meggs WJ. RADS and RUDS.the toxic induction of asthmaand rhinitis. Clin Toxicol 1994; 32:487-501

17 Deschamps D, Soler P, Rosenberg N, et al. Persistent asthmaafter inhalation of a mixture of sodium hypochlorite andhydrochloric acid. Chest 1994; 105:1895-96

'

18 Gautrin D, Boulet LP, Boutet M, et al. Is reactive airwaysdysfunction syndrome a variant of occupational asthma?J Allergy Clin Immunol 1994; 93:12-22

19 Decker WJ. Reactive airway dysfunction syndrome (RADS)following single acute exposure to chlorine gas [abstract]. VetHum Toxicol 1988; 30:344

Neurocardiogenic Syncope andPrinzmetal's Angina AssociatedWith Bronchogenic Carcinoma*Paolo Angelini, MD; and Paul Y. Holoye, MD

A clinical case is presented illustrating a previouslyunreported association of (1) neurocardiogenic syn¬cope of new onset in a 57-year-old man, (2) Prinz¬metal's angina, and (3) bronchogenic carcinoma ofthe lung. Initiation of aggressive chemotherapy re¬

sulted in immediate suppression of both cardiacmanifestations. This newly described paraneoplastic*From the Departments of Adult Cardiology (Dr. Angelini) andMedical Oncology (Dr. Holoye), St. Luke's Episcopal Hospitaland the Texas Heart Institute, and the Department of InternalMedicine, Baylor College of Medicine, Houston.Manuscript received January 10, 1996; revision acceptedApril 24.Reprint requests: Dr. Angelini, Leachman Cardiology Associates,PO Box 20206, Houston, TX 77225-0206

syndrome is discussed.(CHEST 1997; 111:819-22)

Key words: bronchogenic carcinoma; neurocardiogenic syncope;Prinzmetal's angina

T^T eurocardiogenic syncope is a well-defined cardiovas-¦** ^ cular condition; its cause, however, is still poorlyunderstood.12 Although several pathophysiologic interpre¬tations regarding its cause have been proposed, variousmechanisms may contribute to the cause in differentpatients or even simultaneously in one patient.24 Wepresent an unusual case of neurocardiogenic syncope,which was associated with a malignant form of Prinzmet¬al's angina. In this patient, the causative factor, broncho¬genic carcinoma, could be substantiated by empirical andclinical proof. Treatment of carcinoma by chemotherapywas indeed sufficient for prompt elimination of the car¬

diovascular symptoms.

Case ReportA 67-year-old Hispanic man, who was a long-time cigarette

smoker (2 packs per day), was well until February 1995 when hebegan to experience episodes of syncope. Initially, he related thesyncope to changing from the supine to the erect position;eventually, he began to experience these episodes even duringbed rest. On March 30, 1995, he was admitted to a hospital inMexico City because of prolonged resting pain, accompanied bynear syncope. After the ECG showed anterior ST-T segmentchanges, he was immediately taken to the catheterization labo¬ratory; a tentative diagnosis was made of acute anterior myocar¬dial infarction. During the catheterization procedure, the patientwas sedated and the pain disappeared. At that time, coronaryangiography revealed a normal coronary flow pattern, with theappearance of a left anterior descending coronary artery lesionthat showed about 50% diameter narrowing. While the patientwas being prepared for balloon angioplasty, he again complainedof chest pain and developed severe hypotension and bradycardia.New coronary angiograms clearly revealed an uneven flow pat¬tern with slow flow limited to the left anterior descendingcoronary artery7 territory, without discrete narrowing. The ECGshowed anterior T-wave changes and mild ST elevation, withadvanced atrioventricular block. Intracoronary nitroglycerin andtemporary ventricular pacing alleviated the bradycardia andischemia. The new angiograms revealed no fixed stenosis andbrisk flow in all the coronary branches. The procedure was thusaborted. Because of recurrent episodes of syncope and atrioven¬tricular block with long periods of asystole, the patient eventuallyreceived a permanent atrioventricular sequential pacemaker.Medications were changed to disopyramide (100 mg, 3 times a

day), fludrocortisone (0.1 mg daily), famotidine (40 mg daily), andsedatives. The patient continued to be bedridden because ofrecurrent dizziness and chest pain until his admission to St.Luke's Episcopal Hospital on May 5, 1995. At that time, physicalexamination revealed an anxious, diaphoretic, acutely ill patient.No significant abnormalities were discovered at the time ofphysical examination, which included a detailed neurologic ex¬

amination. BP was 110/70 mm Hg. ECGs obtained over the nextseveral days (Fig 1) showed sinus or electronic pacemaker atrialrhythm or intermittent atrial fibrillation, with normally con¬

ducted QRS complex and transient T-wave changes that corre¬

lated with chest pain. A chest x-ray film was read as normal, withpossible linear atelectasis in the left perihilar region.

CHEST/111 /3/MARCH, 1997 819

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DOI 10.1378/chest.111.3.816 1997;111;816-819 Chest

Michael J. Burns and Christopher H. Linden Hydrobromic Acid Exposure

Another Hot Tub Hazard: Toxicity Secondary to Bromine and

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