CIGARETTE CONSUMPTION AND DEATHS FROM CORONARY HEART-DISEASE

1087

their tobacco consumption to an intermediate and that benefit of a similar order would be experilevel; enced by smokers of 21-40 cigarettes per day who cut down to less than one pack (20 cigarettes) daily.

reducing

Preventive Medicine CIGARETTE CONSUMPTION AND DEATHS FROM CORONARY HEART-DISEASE CHARLES H. HENNEKENS CHRISTOPHER BAIN FRANK E. SPEIZER BERNARD ROSNER MARY JANE JESSE

Channing Laboratory, Departments of Medicine and Preventive and Social Medicine, and Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts; and University

of Miami School of Medicine,

positive association between cigarette smoking and coronary heartdisease (C.H.D.). In non-fatal myocardial infarction a dose-response relation persists even after the effects of Summary

There is

U.S.A.

a

additional variables have been controlled for. The rela-

cigarette consumption and deaths from investigated in a matched-pair case/control The overall simple matched-pair risk ratio (R.R.) study. between current smokers and non-smokers was 1·9 (95% confidence limits 1·5-2·4). For smokers of fewer than 20 cigarettes per day, the R.R. was 1·2; at a level of 21-40 cigarettes per day the R.R. was 2·3; and for smokers of 41 + cigarettes per day, the R.R. was 4·0. A similar relation was found after adjustment for addi-

INTRODUCTION

THE positive relation between cigarette smoking and coronary heart-disease (C.H.D.), which persists after adjustment for age, sex, and other confounding variables, is well documented.1-6 A dose-response relation was described after age and sex had been controlled for .1,4,6 In a report of non-fatal myocardial infarction several additional variables were also controlled for and a dose-response relation with cigarette smoking was still found.7 In a case-control study we evaluated matchedpair risk ratio (R.R.) estimates, both simple and adjusted for effects of additional confounding variables, to explore the relation of various levels of cigarette smoking with fatal C.H.D.

tion between C.H.D. was

tional variables. These results suggest that the heaviest smokers could halve their risk of death from C.H.D. by

5. Bumpass, L. L. and Westoff, C. F. in The Later Years of Childbearing; p. 82. Princeton, 1970. 6. Economic Commission for Europe. Economic Survey of Europe in 1974, Part II. Post-War Demographic Trends in Europe and the Outlook Until the Year 2000; p. 74. New York, 1975. 7. Léridon, H. Institut National D’études Démographiques, Cahiers 65; p, 25.

Paris, 1973. 8. Registrar General’s Statistical Review of England and Wales for the Years 1968-70. Supplement on Cancer. H.M. Stationery Office. London. 1975. 9. Beral, V. Lancet, 1974, i, 1037. 10. Registrar General’s Statistical Review for England and Wales. Mortality Tables, 1971-1975. H.M. Stationery Office. London. 11. U.S. Public Health Service. Vital Statistics of the United States 1931-1973—Mortality. U.S. Government Printing Office. Washington D.C. 12. Farid, S. Personal Communication 1978. 13. U.S. Public Health Service. Fertility Tables for Birth Cohorts by Color— United States 1917-1973. U.S. Government Printing Office. Washington

D.C., 1976. 14. Census of England and Wales for 1951, 1961, and 1971. H.M. Stationery Office. London. 15. Ryder, N. B. in Recent Changes in Demographic Patterns in Developed Societies (edited by R. W. Hiorns); London. (in the press). 16. Institut National D’études Démographiques. Cahiers 76; p. 46. Paris, 1976. 17. International Union Against Cancer in Cancer Incidence in Five Continents (edited by R. Doll, P. Payne, and J. Waterhouse); Berlin, 1966. 18. Romaniuk, A. in The Population of Tropical Africa (edited by J. C. Caldwell and C. Okonjo); p. 241. London, 1968. 19. The Registrar-General’s Decennial Supplement, England and Wales. Occupational Mortality. 1931, 1949-53, 1970-72 (unpublished tabulations) H.M. Stationery Office. London. 20. The Registrar-General’s Decennial Supplement. England and Wales. Occupational Fertility, 1931 and 1939. H.M. Stationery Office. London, 1953. 21. MacMahon, B. Acta int. cancer congress. 1960, 16, 1716. 22. Buell, P. Dunn, J. E. Cancer, 1965, 18, 656. 23. King, H. Haenszel, W. J. chron. Dis. 1973, 26, 623. 24. Schenker, J. G., Polishuk, W. Z., Steinitz, R. Israel J. med. Sci. 1968, 4, 820. 25. Creagan, E. T., Fraumeni, J. F. J. Natn. Cancer Inst. 1972, 49, 959. 26. West, R. O. Cancer, 1966, 19, 1001. 27. Hoover, R., Gray, L. A. Sr., Fraumeni, J. F. Lancet, 1977, ii, 533. 28. Armstrong, B., Doll, R. Int. J. Cancer, 1975, 15, 617.

.

METHODS

Study population.-The study population of cases and controls was restricted to married White men aged thirty to seventy. Cases were identified by weekly reviews of death certificates during 1972-74. Only men whose deaths were attributed to C.H.D. within 24 h of the onset of symptoms were included. One living control, age-matched within the same decade (i.e., 30-39, 40—49, &c.) and neighbourhood of residence as the case was selected for each case by a systematic household survey. Of 1019 wives of eligible cases, 174 were non-respondents, and 196 refused to cooperate. 81 of the remaining pairs were excluded from the analyses because of missing data. Procedure.-Letters of introduction were sent to the wives of eligible cases. An interviewer telephoned the wives to obtain an interview, which was conducted in the home between two weeks and two months after the death of each case. For each wife of a case interviewed, a wife of a control was interviewed. The interviewer asked questions about the husband’s cigarette smoking during the three months before death for the case and the three months before interview for the control, as well as questions about other coronary risk factors. More detailed descriptions appear elsewhere.8 Data analysis.-Wives were asked whether cigarettes were smoked daily and, if so, how many. The matched-pair R.R. for current smokers versus current non-smokers was calculated to measure the degree of association between current cigarette smoking and coronary deaths. This association was explored further by controlling for additional relevant variables, by means of a recently developed method of analysis for matchedpair studies.9,lo To evaluate the dose-response relatibn, the analyses were repeated on subgroups of the discordant pairs (i.e., where one member smoked 1-20 or 21+ cigarettes daily and the other was not a current smoker). RESULTS

The accompanying table shows the various matchedpair and adjusted R.R. estimates. 308 of the 568 pairs were discordant for current smoking-in 201 the case was a current smoker and the control was not a current smoker and in 107 the control was a current smoker and the case was not a current smoker. The matched-pair R.R. for any vs. no current smoking is 1-9 (95% confidence limits from 1.5 to 2-4). The adjusted R.R. is 1-6

(12-21), indicating a 60% excess coronary mortality for current smokers compared with non-smokers. To evaluate whether there was a dose-response rela-

1088 SIMPLE AND

ADJUSTED

MATCHED-PAIR R.R. ESTIMATES AND

95%

CONFIDENCE LIMITS FOR VARIOUS LEVELS OF CURRENT CIGARETTE SMOKING IN

308

DISCORDANT PAIRS

as well as being a more realistic goal, than orders to stop the habit summarily. Any such reduction will, of course, lower the likelihood of other smoking caused or associated diseases from developing. Efforts to alter the smoking habit are likely to produce the greatest benefit to health in those who are relatively young, with low levels of other risk indicators,’ and possibly in women.6However, benefits have been noted even in those who have had a previous acute myocardial infarc-

ing patient,

tion."t

we repeated the analyses on two subgroups of the 308 (201+107) discordant pairs. The first consisted of 128 pairs where one smoked 1-20 cigarettes daily and the other none. The second consisted of 180 pairs where one smoked 21-40 cigarettes daily and the other none. For each of these levels of current cigarette consumption, the matched-pair R.R. and 95% confidence limits were 1.2 (0.8-1-7) and 2.7 (2.0-5.8), respectively. The corresponding adjusted R.R.S were 1-1(0-7-1-6) for smokers of 1-20 cigarettes daily and 2.2 (1.8-3-8) for smokers of 21 + cigarettes.

tion,

DISCUSSION

The results of this study are consistent with previous reports of a positive association between cigarette smoking and C.H.D. In addition, a dose-response relation was demonstrated between increasing levels of current smoking and fatal C.H.D. These R.R.S in married White men matched for age and neighbourhood are similar to those of previous studies in men, with or without adjustment for age.1,2,4 Compared with current non-smokers, smokers of 1-20 cigarettes daily had an R.R. of 1.2 (not significantly different from the null rate in these data); for those smoking 21+, the risk ratio climbed to 2.7. Subdividing the 21+ category further into smokers of 21-40 and 41+ cigarettes per day gave risk ratios oaf 2.3 and 4-0, respectively. The latter estimate is based on only 55 discordant pairs. The adjusted analysis also demonstrated an increasing effect of higher levels of current cigarette smoking. These findings for c.H.D. deaths resemble those described by Miettinen for non-fatal myocardial infarction, where increasing (though slightly smaller) R.R.S were observed, up to an exposure level of two packs per

day. The demonstration of a fourfold increase in the likelihood of death in the present series for smokers of more than 40 cigarettes per day compared with non-smokers and light smokers, with intermediate death-rates for smokers of 21-40 cigarettes per day, has a clear message. All data strongly support the benefits of stopping smoking completely, but these results and those of Miettinen suggest comparable advantages may be attained by reducing consumption to below one pack a day, with intermediate benefits from reductions to a point above this level. The current study suggests that White male smokers of over 40 cigarettes daily will reduce their risk of dying from C.H.D. by 50% if they reduce tobacco consumption to an intermediate level; and one to two pack per day smokers will achieve a similar order of benefit by smoking less than 20 cigarettes a day. Such a recommendation may well prove more acceptable to the smok-

About a third of the annual U.S.A. total of approximately 700 000 deaths from ischxmic heart-disease may be attributable to cigarette smoking.12 Effective intervention on smoking, hypertension, and raised serumcholesterol could reduce coronary events by up to 70%.12,13 Although in many Western countries (including the U.S.A. and the U.K.) lower cigarette consumption could reduce c.H.D., in some countries, both European14 and non-European,15,16 no association between cigarette smoking and coronary events is apparent. "Low tar" cigarettes with low nicotine yields seem to be slightly less strongly associated with C.H.D. death than do high tar and nicotine brands." Since most unventilated filter cigarettes also produce higher yields of carbon monoxide, the overall medical implications of their consumption remain uncertain.18,19 Further epidemiological studies are required to evaluate their association with ischxmic heart-disease in more detail. If switching brands proves to be as effective as reducing consumption, then this may be a preferred alternative for many smokers. We thank Dr D. B. Louria, Dr G. B. Hutchison, and Dr J. E. Davies for criticism and help, and Mr Martin Van Denburgh for performing the computer analyses.

This study was supported by research grant HL 14141 and training grant HL 03788 from the National Heart, Lung and Blood Institute. C.H.H. is the recipient of a Research Career Development Award (HL 00288) from the National Heart, Lung and Blood Institute.

Requests Laboratory,

for reprints should be addressed to C. B., Channing 180 Longwood Avenue, Boston, Massachusetts 02115,

U.S.A.

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G.B. New Engl.J.Med. 1976, 294, 633. 9. Prentice, R. Biometrics, 1976, 32, 599. 10. Rosner, B., Hennekens, C. H. Int. J. Epidem.

(in the press).

11. Wilhelmsson, C., Vedin, J. A., Elmfeldt, D., Tibblin, G., Wilhelmsen, L. Lancer, 1975, i, 415. 12. Miettinen, O. S. Hart Bull. 1973, 4, 64. 13. Louria, D. B., Kidwell, A. P., Lavenhar, M. A., Thind, I. S., Najem, R. G. Prev. Med. 1976, 5, 549. 14. Keys, A. (editor). Coronary Heart Disease in Seven Countries. American Heart Association Monograph no. 29, New York, 1970. 15. Gordon, T., Garcia-Palmieri, M., Kagan, A., Kannel, W. B., Schiffman, J. J. chron. Dis. 1974, 27, 329. 16. Robertson, T. L., Kato, H., Gordon, T., Kagan, A., Rhoads, G. G., Land, C. E., Worth, R. M., Belsky, J. L., Dock, D. S., Miyanishi, M., Kawamoto, S. Am. J. Cardiol. 1977, 39, 244. 17. Hammond, E. C., Garfinkel, L., Seidman, H., Lew, E. A. Environ. Res 1976, 12, 263. 18. Wald, N. J. Lancet, 1976, i, 136. 19. Wald, N., Idle, M., Smith, P. G., Bailey, A. ibid. 1977, i, 110.