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699 AHA Medical/Scient%~'tc Statement Position Statement Environmental Tobacco Smoke and Cardiovascular Disease A Position Paper From the Council on Cardiopulmonary and Critical Care, American Heart Association Aubrey E. Taylor, PhD, Chairman; Douglas C. Johnson, MD, and Homayoun Kazemi, MD, Members C tgarette smoking was identified by the Surgeon General in 1982 and 1983 as the most impor- tant modifiable risk factor for cancer and chronic heart disease in the United States.t-2 Recent studies have implicated exposure to environmental to- bacco smoke as a significant risk factor for the develop- ment of lung cancer and heart disease. Because more information on environmental tobacco smoke is now available, its health effects are reviewed in this report, with a major emphasis on the relation of environmental tobacco smoke to cardiovascular disease. Cigarette smoking has a significant effect on the health of Americans, and is a major cause of cardiovas- cular disease.' Cardiovascular disease attributable to voluntary cigarette smoking accounts for about as many deaths each year as chronic obstructive pulmonary disease and lung cancer deaths combined! In 1988 approximately 430,000 deaths in adults aged 35 and older were attributed to the intentional inhalation of tobacco smoke. This number included 201,000 deaths due to cardiovascular disease, 112,000 due to lung cancers, 83,000 due to chronic lung disease (including pneumonia, influenza, bronchitis, emphysema, chronic airway obstruction„and other respiratory diseases), and 31,000 due to other cancers.4 It has also been estimated that an additiona13,800 lung cancer deaths' and 37,000 cardiovascular deaths occurred in nonsmokers who had been exposed to environmental tobacco smoke.5 An additional 2,500 perinatal' deaths were estimated to have occurred because of tnaternal smoking, an& about 1,300 deaths resulted from burns related to smoking.4 Although the existing epidemiologiaal'studies on can- cer deaths associated with environmental tobacco smoke may be subject to questions about sample size, exposure, experimental design, and differing lifestyles of populations, sufficient information has been pub- lished to implicate environmental tobacco smoke as a definite health hazard. The 1986 Surgeon General's report concluded that involuntary smoking is a cause of "Environmental Tobacco Smoke and Cardiovascular Disease" was approved by the American Heart Association Steering Com- mittee on February 20, 1992. Requests for reprints should be sent to the Office of Scientific Atiaira„ American Heart Association, 7272 Greenville Avenue, DaUas, TX 75231-4596. disease, including lung cancer, in healthy nonsmokers, and it was postulated that approxdmately, 3;000-4,000 nonsmokers exposed to environmental tobacco smoke die of lung cancer each year.6 The report also concluded that children whose parents smoke have an increased frequency of respiratory infections, increased symptoms of respiratory problems,- . and slightly smaller rates of increase in lung function as the lung matures compared with children of nonsmoking parents. At the time of the report, environmental tobacco smoke could not be definitely linked to cardiovascular disease. However,, since 1986 several studies have been published docu- menting a link between environmental tobacco smoke, cancer,7 and heart disease s-3 The Environmental Pro- tection Agency has also done an extensive study of the effects of environmental tobacco smoke on lung cancer. Environmental Tobacco Smoke Burning cigarettes emit two types of smoke: main- stream smoke, which is the smoke directly inhaled into the smoker's lungs, and sidestream smoke, which is the smoke emitted into the air from the burning cigarette between puffs. Environmental tobacco smoke is about 85% sidestream an& 15% exhaled mainstream smoke. More than 4,000 chemicals, including at least 40 carcin- ogens, are contained in environmental tobacco smoke 9 Many toxic constituents are found in higher concentra- tions in sidestream than in mainstream smoke.3 For example, in sidestream smoke there is about five times as much carbon monoxide (which decreases the ability of hemoglobin to carry oxygen to the tissues), three times as much betuopyrene (a tumor- and plaque- producing compound), and 50 times as much ammonia (an eye and respiratory irritant) as is inhaled directly from a cigarette. The difference is because the cigarette burns at a higher temperature during inhalation, lead- ing to more complete combustion, and filters also screen some of these toxic compounds. Those in close proximity to someone smoking a cigarette are exposed to smoke not only while the cigarette is lit but continue to inhale smoke that has mixed with air long after the cigarette is extinguished. Environmental tobacco smoke can persist in indoor environments for many hours after cessation of smok- ing, the time depending on ventilation and the mixing of N 0 N W ~ ~ ~ X

t 700 Cht9lat3on Vol 84 No 2.4ugatt 1992 room air with uncontaminated air.1° To conserve en- ergy, building ventilation rates are sometimes de- creased, causing levels of smoke to increase in work- place environments, and in many homes ventilation of smoke to the outside is minimal. Ri'sk to Nonsmokers from Environmental Tobacco Smoke The relative risk of developing lung cancer has been estimated to be 1.3 for nonsmokers exposed to environ- mental tobacco smoke at home compared with non- amokets with no exposure to environmental tobacco smoke.'•70-1Q Active smoking has a relative risk factor for cancer of about 10.1 Average workplace exposures to environmental tobacco smoke are estimated to increase lung cancer risk twofold' because environmental tobacco smoke exposures are generally higher at the workplace than at home.12 Despite the difficulty of interpreting epidemiological studies of exposure levels in the home and workplace, several recent studies demonstrate a definite link between cardiovascular deaths in nonsmok- ers exposed to environmental tobacco smoke. Glantz and Parmley9 reviewed 10 of these studies, showing that men and women nonsmokers exposed to environmental tobacco smoke at home had an overall! cardiovascular relative risk factor of 1.3. This compares to a relative risk factor of 1.7 for smokers compared with nonsmok- ers.2 Kawachi et al13 predicted an even higher relative risk factor for workplace exposures of nonsmokers to environmental tobacco smoke. Repace and Lowrey" evaluated eight studies in which the number of lung cancer deaths of nonsmokers ez- posed to environmental tobacco smoke averaged 5,000_2 400 (mean = standard deviation) per year. As- suming that the ratio of lung cancer to heart disease deaths is the same with environmental tobacco smoke exposure as for voluntary smoking, approximately 10,000 deaths of nonsmokers exposed to environmental tobacco smoke would be expected to occur per year. However, this simple estimate does not include many aspects of environmental tobacco smoke exposure, such as the amount of environmental tobacco smoke ezpo- sure in the workplace and home, the number of persons exposed to environmental tobacco smoke, and the type and amount of smoke exposure. In fact, studies to evaluate these factors indicate that environmental to- bacco smoke causes a higher risk of heart disease than predicted by this simple estimate. Recently, Steenland' performed extensive analyses of the available literature on the cardiovascular effects of environmental tobacco smoke and predicted that isch- emic heart disease could cause as many as 15,000- 19,000 deaths yearly of nonsmokers due solely to envi- ronmental tobacco smoke from their spouses. Steenland also predicted an overall number of deaths due to environmental tobacco smoke-related cardiovascular disease of 35,000-40,000 yearly, a number similar to the number of deaths estimated by Glantz and Parmleys and Wells.1• Because the risk of coronary artery disease increases markedly with the number of risk factors,'-3•19 nonsmokers with hypertension or hypercholesterolemia and exposed to environmental tobacco smoke are likely to be at even greater risk of developing cardiovascular disease. It is well known that the risk of coronary beart disease caused by voluntary smoking decreases by about half after 1 year of smoking cessation and after several years approaches that of people who have never smoked.1° Similar health benefits should occur in pre- viously environmental tobacco smoke-exposed non- smoking individuals when environmental tobacco smoke is removed from the environment in which they work and live.' Exposure to Environmental Tobacco Smoke Although the proportion of smokers in the United States is decreasing, 32% of men and 27% of women aged 20 and older smoke cigarettes."' These smokers will'~ expose a vast number of nonsmokers to environ- mental tobacxo smoke, and it has been estimated that approximately 50 million nonsmoking adults over age 35 are regularly exposed to environmental tobacco smoke." Additionally, we estimate that 50% of all children live in families with one or more smokers. lin a survey conducted in 1979-1980, 63% of nonsmokers reported being exposed to environmental tobacco smoke for more than~ 1 hour per week, 35% were exposed to environmental tobacco smoke for more than 10 hours per week, and 16% were exposed to environ- mental tobacco smoke for at least 40 hours per week.," It is likely that exposure of nonsmokers to environmen- tal tobacco smoke has decreastd in recent years because of the increased public awareness of the hazards of environmental tobacco smoke, increased' restrictions on smoking areas, and better ventilation of the workplace. The public has now begun to understand the detrimen- tal health effects of environmental tobacco smoke ezpo- sure, but this increased awareness has not eliminated exposure to environmental tobacco smoke of spouses and children living in a smoker's home or that occurring in some workplaces and public buildings. Cardiovascular Effects of Environmental Tobacco Smoke Environmental tobacco smoke produces acute effects on cardiovascular function in human studies. In subjects with stable angina, environmental tobacco smoke in- creases resting heart rate, blood pressure, and blood carboxyhemoglobin, and reduces the duration of exer- cise that induces angina.1'= Environmental tobacco smoke also produces adverse effects on the exercise performance of healthy people.=1 Several studies have found increases in the incidence of nonfatal heart disease, including angina and myocardial infarction„ among nonsmokers enposed to environmental tobacco snaoke.= A few small sample cases show direct involvement between environmental tobacco smoke and peripheral' vascular disease. For example, Bocanegra and Es- pinozas' reported Raynaud's phenomenon in two suc- ocssive wives of a chain-smoker. The symptoms of both, nonsmokers, as would be expected, subsided after they were no lbnger exposed to environmental tobacco smoke. Cigarette smoking is a major, preventable risk factor that promotes atherosclerotic peripheral vascular disease,'s and it is likely that environmental tobacco smoke also increases the risk for peripheral vascular d'isease,, although the latter hypothesis remains to be studied.

AHA Sciatufic Council En.iroameatal Tob.m Smoke aad CVD 701 Meclmnisms of Inducing CardiovascWar Dlsease Nicotine, the drug in tobacco that causes addiction, produces acute increases in heart rate and blood pres- sure.ss Cigarette smoking has been shown to increase platelet aggregation and cause endothelial cell dam- age.7b-m Polycyclic aromatic hydrocarbons present in smoke (for example, benzo[a]pyrene) are capable of inducing and accelerating the development of athero- sclerosi's."a0 Exposure to environmental tobacco smoke will also increase carbon monoxide levels in red blood cells. Studies indicate that increased carbon monoxide levels in humans result in a more rapid onset of angina3t and increased arrhythmias'2 in exercising nonsmokers. A recent study indicates that environmental tobacco smoke sensitizes circulating neutrophils in humans and may cause their subsequent activation and oxidant- mediated tissue damage, leading to carcinogenesis and atherosclerosis.33 It is likely that these and more yct-to- be-identified mechanisms are involved in increasing the risk of heart disease in persons exposed to environmen- tal tobacco smoke. Potential for Prevention Although regulation of tobacco products is specifi- cally prohibited under the Federal Hazardous Sub- stances Act, many actions have been taken to protect the health of nonsmokers. For example, cigarette smok- ing has been banned from air flights in the 48 contiguous states; and as of March 1991, laws restrict smoking in public places in 46 states, in public-sector workplaces in 38 states, and in private-sector workplaces in 17 states.3' Many hospitals, health care facilities, and private and public workplaces are smoke-free. The benefit of re- stricting smoking in buildings and workplaces is obvious, but the effect of a greater awareness of the importance of reducing environmental' tobacco smoke in the home has not been evaluated. The final conclusion of the 1986 Surgeon General's Report was that separating the smokers and nonsmok- ers within the same air space may reduce but does not eliminate the exposure of nonsmokers to environmental tobacco smoke. Attempts to control tobacco smoke by increasing room ventilation can be futile, and the only sure way to protect nonsmokers from environmental tobacco smoke is to eliminate smoking from areas that they share with- nonsmokers. Environmental tobacco smoke must now be considered an envuonmental toxin from which the public and workers should be protected. Thus, it is the responsibility of the employer to protect workers, and of public building managers, to protect the public from environmental tobacco smoke exposure. It is the responsibility of parents to ensure that their children are not ezposed to environmental tobacco smoke in the home, and the responsibility of everyone to eliminate this health hazard from the environment.s' Summary Although the number of cardiovascular deaths asso- ciated with environmental tobacco smoke cannot be predicted with absolute certainty, the available evi- dence indicates that environmental tobacco smoke in- creases the risk of heart disease. The effects of environ- mental tobacco smoke on cardiovascular function, platelet function, neutrophil function, and plaque for- mation are the probable mechanisms leading to heart disease. The risk of death due to heart disease is increased by about 30% among those exposed to envi- ronmental tobacco smoke at home and could be much higher in those exposed at the workplace, where higher levels of environmental' tobacco smoke may be present. Even though considerable uncertainty is a part of any analysis on the health affects of environmental tobacco smoke because of the difficulty of conducting long-term studies and selecting sample populations, an estimated 35,000-40,000 cardiovascular disease-related deaths and 3,000-5,000 lung cancer deaths due to environmen- tal tobacco smoke exposure have been predicted to occui each year. The AHA's Council on Cardiopulmonary and Criti- cal Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. The council strongly supports efforts to eliminate all exposure of nonsmokers to envirotlmea tal tobacco smoke. This requires that environmental tobacco smoke be treated as an environmental toxin, and ways to protect workers and the public from this health hazard should be developed. According to a 1989 Gallup survey commissioned by the American Lung Association, 86% of non5mokers think that environ- mental'tobacco smoke is harmful and 77% believe that smokers should abstain in the presence of' nonsmokers. However, programs aimed at further educating the public about the cardiovascular effects on nonsmokers of exposure to environmental tobacco smoke must be strengthened and remain a major component of the AHA mission. A smoke-free environment in the home, public buildings, and workplace should be the goal of society.. References 1. The Heairk Coruequences of 5mokirg: Cancer. A report of the Surgeon General. Washington. DC. US Deparmtent of Health and Human Serviets. Public Health Service, Office on Smoking and Hsafth: 1982 DHHS (PHS);82•50179 2 The Heo4h Conseqt.encer of SnwkinW Caidiorarcular Direntt. A report of the Surgeon General. Wuhington, DC_ US Department of Health and Human Services, Office on Smoking and Health, 1983. DHHS (PHS);84-50204 3. HotbrookJH. Grundy SM. Henneketn CH, Kannel WB, Strong JP: Cigarette smolring and cardiovascular diseases: A statement for health professionals by a task force appointed' by the steering committee of the American Heart Association. Cir+rnlaaow 1964; 70:1114A-a 117A 4. StnolCing-atttibutabk mortality and years of potential life loar- United States, 1988. MbfWR 1991;40:62-63. 69-71 5. Glant: S.t, Parmley Ww: Passive smoking and heart disease: Epidemio{ogy, physiology, and biochemistry. CiirLlenot 1991:83: 1-12 6. The Hea(rh ' Con}LiQyp1CQ of /nMf)(yAfCrY SAlOking:. AA report of the Surgeon General. Wuhington. DC, US Depacuaent of Health and Human 5ervices, Public Health Service. Centers for Disease Con- trol. Center for Health Promotion andEduntion, Office on Stnok- ing and Health. 1986. DHNS (CDC):87-8398 7. Repace JL, l.owrcy AH: Risk astes.ent methodolopes for pas :ive smoking--induced lung cancer. Risk Anal 1990:10:22-37 8. Steenland 1C: Passive smoking and the risk of heart diaease.l.4Mi1 1992t267:94-•99 9. Reducin; dhe Heafrh Cor.scquences ojSnwkin;: 25 Yrarr oJPregrsrs. A report of the Surgeon General. Washington. DC, US Depart- ment of Health and Human Services. Public Health Service. Cen- ters for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Otbee of Smoking and Health. 1989. p 11. DHHS (CDC);89-8411 10. Repace JL, Izwey AH: Indoor air pouution. tobaeoo smoke. and public health. Science 1980;2D8:46t-472

702 CUeal.doe Yoi 84 No 2 Atgatt 1992 il. Esibea MP, IsMa'stre G, Newsb GR: Hwlth Eararde of passive smobo8. Anrui Rer Pudfic Healah 1968447-70 12. Repaoe 1L Lorrry AH: A qaaatitative esdmate af soaemaEms' Itmb caaoer risk from pasire moolrittb famm lu 19dS;13-22 13. Kawacbi l, Peara NE, Jasksoo RT: Deaths fiam luab taooer and schaemic beart disease due to passive amotinb ia Ner Tsaiaod. N Z .Ned J 1989;102:337-340 14. Wells A1: An eaaoate of adult moRelity from pt~sire solanb. Ewwot let 1988:14:2.9-263 15. Pooling project r neatrs BtwQ: Rdatiombip ot blood praettre. eerum cbolesterol, >moMob habit, relative weight and ECG aboor- tuaiities to ioddeace of major ooronary etienn: Final report of the pooling project. J Clirorrk Dir 19'78;31:7D1-306 16. The Heehh BarJFa of Sntakirq CsaaaoR A report ot tbe Sttrjeoc General. Waahinbtoo, DC, US Department of Health and Human Setvioea, Public Health Servfae. Ceoters for Disease C'oottol, Cea- tsr for Carooic Dieease Pte-nmioo and Health Promotioo, Offia on Smoking and Health. 1990. DHHS (CDC);90-84I6 17: Schoenborn G1, Boyd GM: Snrakins sf' Omtiar To6scco Uar: (laieed Srarv, 1987 Hyattaville, Md, US Department of Health aod Human Servioes, Public Health Service, Centers foc Disease Coo- tiot, PJatiooal Ceater for Health Stamtits, 1989, pp 1-78. DHHS (PHS);89-1597 18. Friedmao G0.Pertiti DB, BawN RD: Prer.knoe and ottrrelates of passive smotia8..4m J Pu!>L'c Healtk:1983;73:401-405 19. Arvoo.• WS: Effect of passive taotiob on angina petxoris. N Fr4f J Med 1978;299:21-24 20. KLalfeo ESL, Klochkov VA: (Edect of passive amokiab oo physical tolerance of ischemic heart disease patieats.j Ta Aridi 1987;19: 112-115 21. McMurray RG. Hicks LL Tbompsoo DL: 7be effects of passive iohalatioo of cigarette smoke on esetoie perfotmaoce.E+uJAyP1 Pkrtiot' 1985;54:196-200 , 22. Svendsen KH, Kuller 1K Martin MJ, Oekeoe 1K: Effects of passive smoking in the Muliiplr Risk Factor Intervention Trial. Am J Epidtmsot 1987;1'26:783-795 23. Hole DJ, Gillis CR. Cbopra C. HawtDorne VM: Passive smoking and cardioresQustory health in a general population in tLrwat of Scotland. J3r Med J/Clit Rrsj 1989;399:423-477 24. Bocanegra T3, Frpiooea LR: R,you,a's pbeoomeaoa m pasiye smokers (letter). N Eabi J Mcd 199Ir.303:1419 2S~ The Hadrh Gawquewo of Smo+tiW. Ni<aorr.dddiesbc A repott of the Surteoo General. Washington. DC. US Department of Health aad Human Services, Public Health Servia, Centers for D'neau Cootrol, Center for Health Promotion aod Educauom. Offioe on Smoking aod Heatlb, 1988. DHHS (CDC);88-8106 26.: D.vic JW, Sbeltoo L, F.igeoberb DA, Hipn+te CL WatanaDe 1'S: Fdectt of tobaceo and uoo-topaoro taprette zmotiob on endotDe- linm and platelets. Gtie PAonrocol The 1%5;37329-533 27:: Davs 1W, Hartman GR, Lewe HD Jr, Shelton L Eigeober= DA. Hawndn KM. Higtite CE, Ruttmber HA: Ciprette smoking- induced enhancement of platelet function: Le* of prevention bly nspirm in men with aorooarr arterX, direa+e. J Lb Gnt Md 1985; 105:479-483 28. Davis 1W, S6ehoo L EiBeoEerB DA. Hignite CF: Lct ot effect of npirip on cigarette smoke-uduoed increase m dttatlatiob endo- tDelial'mlls. H.emavarir 19%7;7:66-69 29. Albert RE, Vaoderlaao M., Burns F1', Niehiatmi Mc Effect of nrcinogeos on e8ickea atherosclerosis. C.mer Ra 1977;37: 22;32-2233 30. Penn A, Bataaini' G. Solomaa J. Burni F. Albert R: Dow- dependeat site uraeases of aortic ieeiont foilo.vg ahrenic aqo- twre to 7,12-dimetbylbens(a)aathracene. C&%cer Ra 1981;41: ssb-s42 31. Allred EN, Bleetter ER, Cbaittaao BR, Da!>ffi TE, Gottlieb SO. Hadmey JD, Pagano M. Sdvester RH, Walden SM, Warren J: Short-term eQecu of carbon monoxide exposure oo the eserciee performaoce of subjects with oorooary artery di.ease. N F.+tblJ' Med 1989 321:1426-1432 32. Sbepa DS, Herbst MC, Hinderliter AL, Adams KF, Ekelund LG: O'Nei! 1J, Goldstein GM, Brotaberb PA, Dalton 1L BaUbober MN', et al: Production of arrhytEmias by elevated arbarytiemo- blobia in patients with t:otvoary artery disease. Ann iwoern Med 1990;113:343-351 33. Anderson R. TDeron AJ, Rietiards GA. Myer MS. van Reneburbb Al: Passive smoking by Dumaos sensitizes oircvlating ueutroQhils. Am Rn• Rcrpv Dir 1991;144:S70-S74 34. World No-Tobaooo Day; 1991. MMWR 1991;4a.341-342 35. American Heart Asrxaatioa: 1992 Heert.ad SnaFs F.ca. Dallas. Tezv American Heart Association, 1991