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SMIOlKE`COMP+ONENTS AN© CVfl 379 tar and niratine~cigarette consumption increases (41). However; despite this, car- boxyhemoglobin levels fall as a result of a change in smoking,pattern.Smoking behavior is evidently related to nicotine intake and achange to low tar and nico- tine. cigarettes generally results in an increased number of cigarettes smoked, a discouraging state of affairs. Fortunately, to maintain the!same nicotine intake, with some very low nicotine cigarettes requirestoo high a daily consumption for the smoker to achieve (41)i Carbon monoxide content can be reducediby dilutung the smoke, which is achieved by using more porous or perforated paper and tips. Unfortunately, smokers rate low tar and nicotine cigarettes unsatisfactory and evidently not many heavy smokers would voluntarily elect to use them. However„ cigarette manufacturers have in recent years been gradually reducing the tar and nicotine yield of cigarettes with little reduction in sales. This suggests that gradual changes in the :cigarettes' tar and nicotine may be acceptable.Similar gradual changes in the carbon monoxide content should be encouraged. Another alternative is a change toicigars: This is evidentdy not algood alter- native for the inveterate: cigarette smoker. J'udging from carboxyhemogiobin values, such converts continue to inhale and unfortunately the carbon monoxide concentration in the smoke from pipes and cigars is approximately twice that of cigarettes. The nicotine content is also higher. Thus there is little hope that the reformed' cigarette smoker diverted to pipes and l cigars will' acquire the Iow risk of'the non-inhaling inveterate pipe!or cigar smoker (4). Regarding the: nicotine: effects of cigarette smoking, it is possible that these may be controlled in the high risk cigarette smoker by counteracting,the sym+ pathomimetic effects with an1 agent such as propanalol. While the: acute effects cani be corrected in this~way, it remains to be shown whether the long-term car- diovascular consequences can likewise be uountered. Pharmacologic solutions to the cigarette problem in general, would seem less desirable tliani either altering the cigarette:to make it safer, or abstention. Because it is so much ~more common and so highly lethal, the most alarming cardiovascular consequence of smoking is an enhanced risk of lethal coronary at- tacks. It seems highly likely that coronary disease in particular can besubstantia!- Iy affected by deniccstizing, cigarettes, reducing their carbon monoxide or popu- lariaing non-inhaling practices. Since the impact of cigarettes is part~icularly per• nicious in persons already at high risk because of a bad cardiovascular risk profile: (Fig. 3) one might argue for efforts foeused especially on this segment of the population. However, the general risk is so high and so~many people.smoke thatt public health measures for the whole popuVation seem to be tequired. Substantial increases in mortality seem concentrated in those smoking more than one-half packagelday but this is about one-third of'the male smokers. The six year coro- nary mortality in these men 3'S-74 in Framingham is 17/1i000 in contrast to 5S/ 1000 in non-smokers (7). Perhaps when we have a "safe cigarette" (without much nicotine and'carbon •monoxide) we can iassess t'he mortality in those who use it againstthose who3on''t and'i in this way complete the fnall link in the chainiof evidenee in humans con- necting nicotine and carbon monoxide per se to cardiovascular mortality. •9

380 REFERENCES KANNEL AND:CASTELLI 1. Roya) ICollegp of Physicians. "Smoking and Health Now," London, 1971. 2. The Health Consequences of' Smoking, 1967-1973. U.S. Dept. Health Education and Welfare„Washington. D.C. 3. Fletcher, C.M. and Horn„D. Report to World Health Organization, 1970. 4. Kannel, W:B., Castelll, W.P., andl McNamara, P.M. Ciguetrte smoking and risk of coro- nary heart disease. Epidemiologic clues to pathogenesis. The Framingham Study. Nat. Cancer /est. Mnnogr. 28:9-20~ 1968. S. Intersociety Commission for Heart Disease Resources. Atherosclerosis' Study Group. Primary prevention of atherosclerotic diseases. Clrculation 42!(Suppl. A):5'Si,1970. 6, Hammond,, E.C. Smoking in relation to the death rates of one millionmen,and women. Nat. Cancer lnst. Monogr. 19:127-2p4,1966. 7. Gord oni T., Kannel, W.B., and IMcGee, D. Death and coronary attacks in men after giv ing,up cigarette smoking. A report from the Framingham Study: Lancet 1:L345-13'53, 1974. 8. Ball, K: and Turner, R. Smoking,and the heart. The:basis for action. Lancet 2:822-826, 1974. 9. Rose, G. Smoking andkardiovascular disese.,Anmotations:Amer. Heart/. 85r838-839, 1973. 10. Astrup, P. Carbon monoxide, smoking, and', atherosclerosis. Post-Grad Mtd./: 49C6'97- 706,19731 1'1. Hammond, E.C. and Garlfnkde; L Coronary heart disease, stroke andlaortic aneurysm., Alrch: Environ. Nealth, 119:167-1182, P969. 1'2. Kahni H.A. The Dorn Study of smoking,and mortality among US. veterans. Report on BAyearsof observation. Nat:,Cancerlnat Monogr. 19:1-1'25~ 1966. 13. James, G. and Rosenthal, T.'•Tobacco and Health;"'CharJes C. Thomas, Springfield, 111., 1962: 14. Wynder„E. and Hoffmann„D. Towards ailessharmful cig}rette.Not. Cancerlmrt Monogr , 2qi:a9'68. 1LS,. Keast, 0. and Hblt P. Smoking and the immunaresponse. New Scientdtt 61:806-807, 1974. 1i6i Pentecost, B. and Shiilingford, J. The acute effects of smoking on myocardial perfbrm- ancein patients with coronary, arterial disease. Brit. Xeart%: 26:4'22-4Z9;11964. 17. Mjoes,,O.D. and Ilbekk„A. Effects of nicotine on myocardial metabolism and perform- ance in dogs:Scand: J, C1ln. Lab. Invest. 32:75-810,1973. 18: Schievelbein, H., Londbng, V:, Londong, W., Grumbach, Hi, and Remplik, V. Nicotine and arteriosclerosis.,An experimental conudbution to the influence of'nicotineon fat metabolism. Z' klin: Ch'em. u. klin. Blochem. 8':190-196„ 1970. 19. Carlson, L.A. and Bottinger, L.E: Eschaemic heart disease in relation to fasting values of'plasma triglycerides and cholesterol. Stockholm ProspectivrStudy: Lancet 1':8I65* 8168, 1972. _ _ 20. Oliver„M.F. and Yates, P.A. Induction of ventricular arrhythmias by elevation of arterial free fatty acids ini experimentallmy,ocardiallinfarction. Cardiology 56:359,364', 197'1. • 21. Murphy, E.A. and Mustardl J.F. Smoking and thrombosis. Nat. Cancer Inst. Monogr., 28:47-55, 1'96i8. 22: Levine, P:H. An acute effect of cigarette smoking,on platelet function. A possible link between smoking and arterial thrombosis. Grculation 48:6'1!9-623, 1973. 23. Hawkins, R.i. Smoking platelets and thrombosis. Nature 236:450-4'S2; 1972. 24. Shinhj, E., Olesen, J., and'Paulson, 0:8. Influence of smoking and nicotine on cerebrall blood flow and metabolic rate of oxygen in men. f. Applied Physiol. 35:820422; 1973. 25: Astrup, P., Hellung-Larsen„P.,,Kieletsen, K.,,and Mellemgrard„ K. The effect of tobac+ co smoking on the dissociationi curve of oxyhemoglobin. Ihwestigations in patients with occlusive arterial' diseaae in nonmal'subjects. Scond. /. Clin: Lab. lhvest. 1I8:45'0- 4'57, 1966: -

SMOKE COMPONENTS ANIDCVD 38t' 26. Goldsmith, J.R. Carbon monoxide and coronary, heart disease. Ann. 1nt: Med. 7'1I:199- 201:,19i69. , 27. Ayres, S.M., Gianneili„ S., and Muller, Hl Carboxyhemoglobin and access to oxygen. Arch. Envlron. Health 26:8'-15, 1973., - 28. Coburn, R.F.Carbon monoxide body stress.Ann. M:Y:'Aud. Srl.' 174:1'1-22,1970. 29. Pauli, H1Gi, Ttuniger, Bi, Larsen„J.K:, et al: Renal functionAuring prolonged exposure to hypoxia and CO.Scand. /. CJIn. La6anvett, 22:(Suppl) 103:61-67„1968: 30. Sarma„ JS.M., Tilluranus, kl:, Ikeda, S~, et al. Lipid meubofism in perfused human,and dog,coronarry arteries.Amer. /. Cardiol. 35:579-587, 1975. 31.. Astrup, P., Kjeidsen,l.C:, and Wanstrup, J.The effects'ofexposureto carbon monoxide, hypoxia and hyperposia on the development of experimental atherosclerosis in rab- bits. In: "Atherosclerosis. Proc. 2nd Internat.Symp."'(James, RIJ. Ed.) pp. 1I08=1'11. Springer-V/erlag, Chicago,,1970: 32. Astrup, P. Some physiological and pathological effects of moderate carbon.monoxide exposure: Brit: Med /.,4:44'7+452; 1972. 33. Goldsmith, J,•R. Carbon monoxide:Scienct 15'7:842•844', 1967. 34. Eisen, M.Ec and Hammond, E.C. The effecrof smoking on packed cell volume, red cell' cour,ts„hemogiobin and platelet counts. Canad. Mtd. Assoc. /. 15:520423, 1956. 35. Isager, Hi and Hagerup, L. Relationship between•cigarette smoking and high packed cell volume and hemoglo;bin lev~e!s. Scond: J. Hoemetol.' 8':24'1•244, 1971. 36. Sagone, A.4., Jr., Lawrence, T., and Balcerzak, S.P. Effect of smoking;on tissue oxygen supply. B'lood 4T:845-831, 1'973. 37. Sagone. A.L., Jr. and Balcerzak, S.P. Smoking as a cause of erythrocytosis. Ann. Int. Med 82:512-S1S1 1975. 38. Kannel, W.B., Gordon, T:, Woif, P.A., and McNamara. P.MI Hamoglobin and'risk of cerebral infarction: The Framingham Study. Stroke 3:409-420, 1972. 39. Aronow„ W.S. and Isbell, M.W, Carbon monoxide effect on exercise-induced angina pectoru. Ann. lM. Med. 79:392-39S, 1973. 40. Waldl N.,Howard„S1,Smith,P:G:,andlKjelsden,K.Associationbetweenatherosclerotic diseases and carboxyhemoglobin levels in tobacco smokers. Brit. Med. /. 1i:761 165, ' 1973. 441. Turner, J.A. McM., Sillett„R.W.,;and Ball, K.P. Some effests of changing,tts lonvtarand low-nicotine cigarettes. Lancet 1:737-739, 1974.