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.0 ~ L!~&L T Mc-b Vol 2t)0 Nir I (i l c9 .5MOMIItiG AND ~nN(;INn~ - n~lct~~~~(>tiw NIO T I~~CzF EFFECT OF PASSIVE SMOKING ON ANGINA PECTORIS WILBERT S. ARONOW, .VI'.D. Abstract The effect of passive smoking on exercise- induced' angina in a well ventilated and in an unven- tilated room was evaluated in 10 patients with angina. Patients exposed to 15 cigarettes smoked wlthln two hours in a weill ventilate6 room or an unventllated room increased their resting heart rate, systolic and diastolic blood', pressure, and venous carboxyhemo- glbbin and d'ecreased' their heart rate and systolic blood pressure at angina. Patients exposed'to passive smoking in an unventilated room had a larger in- PASSI!VE smoking is the breathing of smoke-con- taining air composed of mainstream smoke ex- haled by smokers and! of sidestrearn smoke, which leaves the burning, end of the tobacco product during puff intermissions: The amount of' smoke produced,the dep(h~ of'inhalation on the part of the smoker„ the ventilation available for the removal or dispersion of the smoke„ the nearness of the nonsmoker to the smoker and' the duration of the exposure to the pol- lutants in tobacco smoke influence the passive smok- er's absorption of the atmospheric pollutants caused by smoking.' In patients with angina pectoris anginal pain develops sooner after exercise when they have smoked high-nicotine ci,arettes,= low-nicotine cigarettes' or non-nicotine cigarettes.' The effect of'passive smoking on duration of exercise until angina pectoris also needed' to be investigated. Therefore, I performed a randomized study evaluating the effect of passive smoking, in a ventilated room~ and in an unventilared room om d'uration of exercise until the onset of angina pectoris. The data from this study are reported below. MATERIALS AND METHODS Ten men, ,. ith a mean age of 5s 3 t8. 1 years Ct 1 S D. ), who had classic stable exertional'angtna pectoris and angiographic evidence of savere coronarc-artery disease with >7i per cent narrowinq,ofat least one malor coronary, vessei! were subjects. Eight subjects were cx-smokcrs. Two subjects smoked two to four eit;arettes datiy but did! not smoke for at least 16 hours before the study or during the study on each of the three stud'y mornings. After careful explanatton of the risks involved, written informed consent was obtained from all 10'men ..-nh angina pectoris who participated inrthis study. t'he subjects understood the expcrimentai,destt{m,Care was utkrn dur- intt the informed-consent discussion non to introduce psycholugtc factors related to:the risk of passive smoking. Thr I Il: suhirrts were familiartzrd with the equiltm •ni and i hr prucedures and pracuccdexerctstn¢ upright on a(Cull!ns• cun,,tant- load bicycle crgometer before the study began. The study was per- formed on three consecutive mornings. From ihe.CardtuvasculariSccuon, Medical'$erwce. Long. Beach'iVeterans. Admtntstratton HuspnalJJ andd the University of CeliforniaCullbµe of. Medicine. Itvtne taddressreprtnt requests to Dr. Aronowat the Cardtovas-cviar Section. Veterans Administration Hospital. Long Beach. CA 908224 'wirrcn,E. Collins, Ihc.- Bratntree. MA.. This material may be proteded: by copyrjght law (Title 17 U'.S.. Co::.:j crease in resting, heart rate. systolic and diastol- ic blood pressure, and venous carboxyhemoglobin an6 a greater reducpon in heart rate and systolic blbod pressure at angina. The duratton ofi exercise untii angina was decreased 22 per cent after passive smoking in a well ventilated room (P<0.001); and de- creased 38 per cent after passive smoking in, an unventilated room (P<0.001); Passive smoking ag- gravates angina pectoris. (N Engl J Med 299:21-24, 1978) On three successive study rnornings.,at a o'clock. wtth the sublpct in the fasnn¢ state. ~enous bloodiwas drawn and anah•zed'for car- boxvhcmu¢lobin and hemo¢iohin lescis with a 182 Co-Owrmetcr * Thcn. Leadfr 2 and Vr wcre simultaneously recorded with an rlcc- trocardiograpfi with the patient sitting on the bic.c!e erttnmeter l hc resting heart rate was obtained from this c!cctrueardru¢ram The resting blood pressure was then measured with a mcrcur} sphy'¢momanometer Each subject then exercised upright an the bicycle er¢ometrr with a progressive work loadlunttl the onscrof angina pertnris. and the duration of exercise was recorded with a stopwatch, The pattent was monitored by telemetry with,Leads 2 and:V;:throughout,exer- cise.,An clectrocardiogram with Leads 2 and V, simultaneously was recorded at the onset of angina pectoris. The heart rate was ob- tained from this deetrocardiottram. The blood pressure was recorded at the onset ofantttna pectorts, wrth the patient conttnu- int; tu exerc,ce until the b!txtd prrssurc was ohtaincd 1'n a room 3.31 meters ('11S ft) long, 3.20 meters (1(1!3 ft) w~idc and 2:74lmeters (f7!fl,fl) high, near the research exercise laboratnrn. the subject then sat with thrce asymptomattc volunteers for two houPs. The patiem and'asymptomatic volunteers talked. rca&ncws- papcrs or magazines or listened to music. On one morning. thr, asymptomauc volunteers did! not smoke. On a second morntnQ, each of'the asvmptomatic volunteers smoked five cigarettes. his or her own brand; durtng, the two hours., The room was weJl, vrn- tilated. with a ventilation rate of 11.4 volumetric air changes per hour. On a third morntn¢- each ofl the asvmptomatic volun- teers smnked flve cigarettes. his or her own brand, durnn¢ the two hours, -nh the room unventilated. The order of exposure of thc paucntss with angina pro.torns to no smuking; smoking tn~ a well venttlated room or smoking in an unvcnulated room,v.as random- izcd. After exposure to no smoking for two hours, exposure to passive smoking for two hours in awell venti!ated room, and exposure to, passive smoking,for two hours in an unventtlated room, the paurnt sat an the bicycle ergometer and had an eiectrtxardiogram wtth Leads 2 and' V; simultaneouslv recorded. The heart rate was measured from this electrocardiogram. Then, the hlnnd: pressure was rrcurded with a mercury sphvKmumanometer. Vfrtous bluwril was next drawn and analyzed fur carboxyhemoglobin and: hemoglobin levels. tiuhsrr!uently. the patient exercised upri¢ht on the birvclr crionmetcr untiLthrnnsct nf .intztna pcrurns„and the duratton,nflex- erase was recorded wttti a stopwatch. An electrocardiogram wtth Lead! 2 an&V, was simuuanenusly recnrd'ed at the onset of angina Ircrtnns. Che heart rate was ohtatncd from this eiectrocardih¢ram.. Ihc blood pressure was recorded' at the onsat, of angina pcctorts, wtth the patucnt,continutn¢ to exereue unttl'.the blood pressure was obtained. The physician who performed' the exercise tests kncw ..hether the patients were exposed to no smoking. smoking in a well ventilated room or smoking m an unvcnnlated room. fIhstrumcntatton Laooratory. Inc., llcstngton„ MA. 2023512192

T,. 1'1f!F. NEW F.NCLAN1) Jt7t.`'RtiAL OF Mk!)ICaNE lulv G. I'r'.y In the asymptomatic volunteer smokers venous blood was drawn and analvzed fbr eartioxvhernoglohln bcfure and after smoking of five cigarettes each durln¢ two hours. The same smuking,vcilunteers werc present for thc successive study mornings. Written informed consent was obtained from these volunteers. The data were analyzed with Student's t-test for correlatcd mea ns. R ESUi:TS Tahle 1 indicates the duration of exercise in seconds until the onset of angina pectoris for each~ patient and the mean exercise duration ±1 SID. in the three con- trol periods, after exposure to no smoking, after ex- posure to smoking in a well ventilated'room and'after exposure to~smoking irnan unventilated room. Table 1 also presents the statistical analysis ofl the differences shown. Table 2 shows the resting mean heam rate, systolic and diastolic blood'pressure„prod'uct of systolic blood pressure X heart rate/1(V0; and venous carhoxvhemo- globin t 1' S.D. in the three controll periods, after ex- posure to no smoking, after exposure to smoking in a well ventilated room and after exposure to smoking,in an unventilated' room. Table 2 also presents the statistical analysis of the differences shown. Table 3 indicates the mean heart rate, systolic and diastolic blood pressure, product of systolic blood pressure X' heart rate/ 100 and amount of exercise- induced'ST-segment depression at the onset of angina: pectoris ± I S:D. in the three control periods, after ex- posure to no smoking, after exposure to smoking in a well! ventilated room and after exposure to smoking in, an unventiiate& room. Table 3 also: presents the sta- t'isaical analysis of the differences shown, The mean venous car.boxvhemoglobin in the vol- unteer smokers rose from 5.87t&90 per celtt hefiltc to 9.75±1.05 per cent after smoking in; the well ven- tilated room (P<0.001): The mean venuus r~,rbt,av- hcmoglobin in the volunteer smoker;s tcs :c II flm 3.92tf1.93 per centbefore smoking in the u(,vciltilz.cd room to 9;83'f 1. 19' per cent alter smoking, in the un- ventilated room (f'<0.009)I Premature ventricular beats were not recordccl in the electrocardiogram before exercise or after exercise in any patient d'uring,the threecontrol periods or after exposure to no smoking or to passive smoking in a well venrilated! room After exposure to passive smoking in~ an unvenuilated rooml one of 1i0'patients (1'0 percenl)r had: three premature ventricular beats lper rnirulta recorded in the electrocardiogram before cxerc isc, r.,,;i three of 10, patients (,30 per cent), had ptcrnaturc ventricular beats recordedl in the electrocardibgram after exercise. One patient had~seven prcrroature ven- tricular beats immediately after exercise, with pre- mature ventricular beats lasting for flve minutes; one patient had 10 premature ventricular beats per minute immediately after exercise, with premature ventricular beats lasting for eight minutes, and one patient had 12 premature ventricular beats per minute immediately after exercise, with premature ventricular beats lasting for 14 minutes. Table 1. Duration of Exercise until Angina in, the Control Periodse and after Exposure to No Smoking. Smoking in a Well Ventilated' Room and Smoking in an Unvenniated Poom., C.sE'Dt.t, nuI uF.txtacist IStcII lin: FxFOSItt TO \UfVU[r.\(:' - C/S~ r laN. FlIOSltt Tf), \U51/11t1\G ttt•Ir\LtFTO \MUl\I~r.IV '~ t1. L vf',r r(t ~ rEll i trn1V ~ (:fl~rtUl. 1TRNllF TO SMUe11U1V `~rEl.L, vFtftl.urEo rM'/Y FtFnLtF TO SWlll.\41!r. l1\t.1Tt1.nTlD .UUV - E'r/~ltrl/. EiFUSt.at TO SYUtI\(:IN UI\'E`I.TILnTED tUUV 1 193' 217, 191 149 202 127, 2 206 214 203' 169' 189 130 3 188 197, 181 145 192 128 /. '+ ... 4 ' 375 412 400 306 387 230 T , l L' 5 204 199 .111 ' 170 196 132 to 6 287 310 304 243 312 198 V1 7 221 215 213 158 232 135 W a 216 223 207 155 209 12a 9. 195 zoa 186 144 :00 129. 10 231 :24 227 171, 218 125 Mean, 231.6 241.9 232.3 181.It 233:7 145 8*>: W : SD' t57:9 x671 . i6a l s52.a t6a:8 s36.9 •Cunuol .aluo +<re musured'nn.<aeh wf 1he Ihroedaf nefonc e\pa.+wee ornnn<.p..wre al mute •1-<Unlll furc\pu>u e lu'.mntrnEln .<lu •crtulaEed ruumminun- rnf+ecll.<.umr,rr~„, mruNlu etlwnu<e w no.muimq m,nu.s rnpecure comrul'ec for exporurc lu nnaCGnp In un•enulytrd room minus r<.pectt.e aomrul as com(tured to cEpauur< to' iru cm„Lmt m.nrt rmCtclne camrol: jP<0 001 (or.etposurr 10 tmotSnt in unleeltllaEed room minus resptetl.a control a.cumpared lue.pwurc to smotrnt in +ell .emllacdroom minus respe:u.a- control.

PASSIVE SMUKINC AND Atit;11A - AItQ)NOw Vul. 294) No. I 23 Table 2. Resting Mean Heart Rate. Systolic and Diastolic Blood Pressure,Productof'Systolic Blbod Pressure X Heart Ratet10C1' and Venous Carboxyhemoglobin in the Control Periods and after Exposure to No Smoking, Smoking in a Well Ventllated~ Room and Smoking in an Uhventilated Room (±1 S.D.)I. hYtaut- .r' tsre/sue. Ta~ NO S.rt141,4. F..n.acae tu'. VU Svt141IG FtrntustTU~. Sw+lu.c I. hhn~stu.rn hvusUa.ru. S»ncr...,. Ftr.a.av rn S.tt... i. eart rate -CIl\TF1I4 2.4 0.6 N.~rrl v.aoa.u X:u~.v.- (rl.nm. 72.1 M>rl Y,vnti.nu~. X,..r. 77,2 rill KIM~.w- (.uwreol~ 72.9 Xl~~r 80 5 fbeats/mtnl t7.7 t7.1 t7 3 t6xt t7.8 t75+3 SBP Imm Hgl 122.8 122,0 122.6 127~5 127.2 1130:7. t4.9 t+.5 ±5.6 t5.9t _a 4 t1 6+q DBP(mm Hg) 79.2 78.6' 794 82.9' 79 8 85:1 ±2.5 t2.5 _3.3 t].tt t2,0 t I 8t~, Heart rate 89.0 86.2 88.4' 98.5 89 8 105 2 x SBP/100 tl ILO t9.6 z10.3' zl0.lt t't0.2 tI0!2+t Carboxt hemo• 1.29 1.26 1.25 1.77' 1.30 2.28'. gfobin (°r) ±0.22 x0:18 t0!'_0 ±'A!INr ±0.18 t0:15'ti "SBP dMutn s.~•lulncblood pressure & UNP dlastohc blood pres.wa. •P<-0.001 fuc espusure:lo smokln`.In.elt •enulated room minus ropectrrc conlral as compared to crtpoeure tuo nosmotlnF minus respecure controd orfor erposure ta smoc'tng in unrenulacd room minus respective conuud as compared toecpwsure to no smuaInE min.uss respeeu.o control' jP<0.0Ui fuaatoosurc to smokln6 In un.eatdated room minus respectlvc control as.compared lo.anposare to smoEln~ in .cll rentdatcd ruum mmus respeeb.e contrul. ;P<0.005 far esposure to smoking in unvenulated room minus rnpecsl•e control as.com,pared to.esposureto smoking Inweil rentdatcd room mtnus respeattre control. Discussiort, The data from this study clcarly demonstrate that under the conditions of this experiment, passive smoking causes anginal pain to develop'sooner after exercise. The duration of exercise untii angina pec- toris is also decreased more after passive smoking, in an unventilated room than after passive smoking in a ventilated room. Smoking higti-nicotineT•s•6 or low-nicotine''•'' ciga- rettes causes an increase in resting heart rate and im systolic and diastolic blood pressure in patients winhangina pectoris, increasing their myocardial oxygen dernand. This increase in heart'rate and iniblood pres- sure does not occur after smokin¢' of non-nicotine cigarettes" or after breathing of carbon monoxide." The increase in heart rate and systolic and diastolic blbod pressure at' rest in our patients with angina pec- toris after exposure to passive smoking was presum- ably due to absorption of' nicotine. Russell and Feyerabend' sho%%ad'that after normal exposure to tobacco smoke, nicotine was present in urine colltcted during the early afternoon in 26 oFl27 nonsmokers (96'per cent). The mean urinary nicotine level of thcse 27 nonsmokers was 10.7ng per milliliter. Russell and' Feyerabcnd' also ha6 12'nonsmokers Table 3. Mean Heart Rate. Systolic and Diastolic Blood Pressure, Producfof Systolic Blood Pressure x Heart RaterJ0[7!,and Exercrse-lnduced ST-Segment Depression at Onset of Angina in the Control Periods and after Exposure to No' Smokmg, Smoking in, a Well Ventilated Room and Smoking in an Unventilated Room, (ti S.D.). Atk~)~It.fM~~T' t1M)Slalt'T'O No SYORING -CONT.OI ttlUSLaeTn 'tU SMULING E.t-l.ftn S.rr.l. t: IN. Wtl.l tsnsss.et ru. SMtI[aNe:IN WE~LI. tinssl,eero SVU)Rl't.l, U1tE.%TI{.NTt.D E.nlst:as ns S.1V\I'41, U-e4TiIANTrID eart rate 28.7 29:7 Vt'tn arED RtNS..- Cu.l/lue 128.9' YENT1lArfo Runr. 122:8 Rtlu4:- GoNr.oa. 128;4' RGUM 1199 (lycats/mm) f5.6 t'5.6 i44 tr.7t 25,3 s5.0tI SBPtmm H91 156.4 157.2. 156.1 150.1 1556 147 4 t7:6 t7.4 37,2' t7.8t t6.9 t7etj DBPfmm Hg) 80.2' 79 8 8U.0 8L5 81.3 81.8 ±3.3 t2:9 s2.2 t3.1 t3'1 t2.2 Heart rate 201.4 2019 2201.2 181.7~ 1998 .. 176:7~ x SBP!100 tI4J t.14:01 s1i':.8' 3~~ 12~.3t x I~1I .9 2 11 .9tj ST-segment-0c- 1.38 I'.35 1 _33 1 _40 1.33 1'.45 presstun(mm) 3014'. s0.24 x0~21~ iU:-'4 t'~0.26 to.26~ 'SBP denotes scssohe bloodpressureW & OBP dl.stohc bloodpreuure.. tP<0001i for exposure to smoerng in .elllrennlatedd room, mtnus respecu•e control ascompaned'lo e.pusure to nosmoarnit,mwuc rnpecu.e control at (or espusure ~ pared tocsposune tono smoalng minus rnptcu.e control. lo smoking In.un•enWated room minus respective control as com 1PtT1 D01I for esposure. to smokan` In un.enulated room: mrnus respeeu.e control ucompared to <sposure to smoking In .ed •cnndatedm room m.lnus rnpectsre: controd.

0 24 THE \EW ENCLANDJOC:RNAL OF SIEDICiVE Jj,lv r+, I9-v sit for an average of 78; rninutes among smokers in an unventilated~ smoke-Flled room with dimensionsof 4.37 by 3.66 by: 2.44 meters (13 bv 12 by 8 ft). The smoke was produced by smoking or burning ofi 80 cigarettes and two cigars and caused a mean carbon monoxide level ofl 38 ppm in the room air. Urine specimens collected 13 minutes alter the nonsmokers had left the smoke-fflled room, revealed a mean urinary nicotine level of 80 ng per milliliter. Smoking high-nicotine,s•° liow-nicotines or non- nicotine cigaretrtes'•s causes an incrcased carboxvhe- mugtotyin levcl, which reduces the amount of' oxygen available to the mvocardium. Numerous studies have d'ocumented the harmful effects of carbon monoxide in patients with coronary heart: disease."'a-'Q The decrease in product of systolic blood pressure times heart rate at the onset of angina pectoris after passive smoking in the study reported above indicates a probable decrease in, oxygen delivery to the myocar- dium. A number of' investigations have shown the ex- posure ofl passive smokers to carbon monoxide lev- eis"-" that may cause adverse effects im patients with coronary heart disease. The data from this study also indicate that passive smoking causes an increase in carboxyhemogtobin - more after passive smoking in an unventilated room than after passive smoking in a ventilated room. Premature ventricular beats occurred after exercise in: three of 110 patients exposed to passive smoking in an unventilated room. The increase in sudden death from coronary heart disease in cigarette smokers" may be related to lowering of the threshold for ven- tricular fibrillation by nicotine20'=t or carbon monox- idez2~" during an episode of' m,vucardial ischert,lia. Finally, in additiom, to carbon monoxide and'. nico- tine, other components of' tobacco smoke,: including oxides oflnitrogen.and hydrogen cyanide and possibly psychologic factors, may have contributed~ to the decrease in exercise performance observed in these patients with heart' disease after passive smoking through effects on the cardiovascular or respiratory systems. For example, do the oxides of nitrogen in. haled in tobacco smoke interfere with mvocardial ox- ygem delivery' This possibility needs to be in- vestigated. I am indebted to Clifford Kousseve and PaullTroop for techntcal' assistance. REFERENCES - I Public exposure to :ur pollution from lobacco smuke:: The Health Cuuscquences of Smoktn2,. A.A report of tFic Surveon Gcner¢I!. IN"-. 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Degueman uT:, Kustus 18, et ah The cffecu of inhalstton, of crl;are:te.smuke an ventncular:ftbnllatton threshold tn,normal dogs and dugs with, acute myocardial infarction. Am Heart 1 83 67.76. 147_ :2:. DeBras. DA. BanerJee CM. Birkhead NC... et alt Effects of carbon : monuxrde tnhal'rtton on ventneufar, libnllauon. ArchEnvtron Health, 31 . 42-t6.: 1976 _3! Arunuw WS. Stemmer, Ei9..Wood B, et.al: Carbon monoxide and .entnoular fibrillation threshold rn dogs with acute myocardial inlury. Am Heart J 95t754-156. 1978.