Cigarette smoking and risk of coronary heart disease incidence among middle-aged Japanese men and women: the JPHC Study Cohort I (original) (raw)

Background

Few data have been available on the sex-specific magnitude of the smoking effect on the risk of coronary heart disease (CHD) in Asia.

Design and methods

A population-based prospective cohort study of 19 782 men and 21 500 women aged 40–59 years between 1990–1992 and 2001 was conducted to examine the relationship between smoking status and the risk of CHD.

Results

A total of 260 incidences of CHD were confirmed among men, including 174 myocardial infarctions (MI). The numbers among women were 66 and 43, respectively. The multivariate relative risk [95% confidence interval (CI)] for current smokers versus never-smokers in men after adjustment for cardiovascular risk factors, several life style factors and public health centre was 2.85 (1.98, 4.12) for total CHD and 3.64 (2.27, 5.83) for MI. These respective risks in women were 3.07 (1.48, 6.40) and 2.90 (1.18, 7.18). Among men, a dose-dependent relationship was observed between the number of cigarettes and the risk of MI. The population-attributable risk per cent (95% CI) of CHD was 46% (34, 55) in men and 9% (0, 18) in women. Smoking cessation, however, led to a rapid decline in the CHD risk within 2 years.

Conclusion

Smoking raises the risk of CHD significantly in both sexes of middle-aged Japanese, with large public health significance especially in men. Smoking cessation would have an immediate effect on risk reduction.

Introduction

Smoking is a well-established risk factor for coronary heart disease (CHD) for both men and women in western countries [1]. Evidence from prospective studies in Asian countries, however, has been limited. Several large cohort studies using mortality as an endpoint showed smoking caused a two to threefold higher mortality from CHD in men [2–5], but the magnitude of association among women was weaker and inconsistent [2, 4, 5].

A cohort study using the incidence as an endpoint showed that smoking raised the age-adjusted risk of CHD for both men and women, but in that study, other confounding variables were not taken into account [6]. Other cohort studies examined the smoking effect for men, but not for women, probably because of the low proportion of smokers in women and therefore the small number of incidences of CHD [7–9].

Compared with western countries, Japanese men had a high proportion of smokers (47%), whereas Japanese women had a low proportion (11%) in 1999 [10]. However, the proportion of smokers among Japanese women aged 20–49 years has been increasing from 11–12% in 1990 to 16–19% in 2003 [10]. Mortality from CHD in Japan was one-fifth to one-third of that in western countries [11]. A recent study has shown an increase in the incidence of CHD among middle-aged male workers [7]. Because of the high proportion of smokers among men and an increasing proportion among women, the investigation of smoking and CHD should be of value to formulate public health recommendations for the prevention of CHD. For this purpose, we used the data of the Japan Public Health Centre-based prospective study on cancer and cardiovascular diseases (JPHC Study) Cohort I [12] to determine the sex-specific relationships of smoking with the risk of CHD.

Materials and methods

Study cohort

To establish a population-based cohort, i.e. the JPHC Study Cohort I [12], we identified 27 063 men and 27 435 women who were born between 1930 and 1949 (40–59 years of age) and were registered in 14 administrative districts supervised by four public health centre (PHC) areas at 1 January 1990. The study cohort was a total of 20 666 men (76%) and 22 484 women (82%) who responded to the baseline lifestyle questionnaire between January 1990 and May 1992, mostly between February 1990 and October 1990.

Among them, 19 794 men and 21 513 women who reported their smoking habits and no histories of myocardial infarction (MI), angina pectoris, stroke, and cancer were entered into the present analysis. The study protocol was approved by the Human Ethics Review Committees of the National Cancer Centre.

Baseline survey

A self-administered questionnaire was distributed to all registered non-institutional residents in 1990. The questionnaire included anthropometric measures of height and weight, disease and medical history of the subject and his or her relatives, smoking and drinking habits, diet and other lifestyles, including leisure time sports and sleeping hours, occupation, personal histories including birthplace, education and living environments [13].

Smoking habit was categorized into three categories of never, ex and current smokers. For the current smokers, the daily number of cigarettes smoked was further ascertained. Drinking habit was also ascertained in the three categories of never, ex and current drinkers who drink more than once in a month. For the current drinkers, the frequency and kinds of alcoholic beverages were ascertained with the quantity in a usual drinking day.

Daily food intake was asked for rice, miso soup, and another nine types of foods. The frequency of weekly intake was asked for 27 food items in four categories of rarely, 1-2 days a week, 3-4 days a week and almost every day. The weekly intake of each food item, including fruit, green, yellow and other vegetables, fresh and dried fish, was calculated according to a score assigned to each frequency category of 0, 1.5, 3.5, and 6, respectively, corresponding to the category in the questionnaire.

Confirmation of coronary heart disease

In order to catch CHD cases, we asked to register MI cases and sudden deaths of unknown origin for a total of 30 hospitals with cardiology departments in the four PHC areas (number of hospitals: 10 in the Ninohe PHC area; four in the Yokote PHC area; three in the Saku PHC area; and 13 in the Ishikawa PHC area). They included all the major hospitals to which acute CHD cases would be admitted. In each hospital, medical records were reviewed by registered hospital physicians or PHC physicians who were blinded to the lifestyle data. Acute coronary events were registered if they occurred after the date the baseline questionnaire was administered, and before 1 January 2002.

MI was confirmed according to the criteria of the MONICA project [14], which requires evidence of electrocardiograms, cardiac enzymes, or autopsy; if such a work-up was not performed and there was a typical chest pain, a probable diagnosis was made.

Among the cases registered as sudden death of unknown origin, deaths occurring within 1 h of the onset of symptoms were regarded as sudden cardiac deaths. The cases registered in this registration system were 257 CHD (217 MI and 40 sudden deaths of unknown origin), and among them we confirmed 177 MI (169 definite, eight probable) and 10 sudden cardiac deaths (Table 1).

In addition, to complete the surveillance for non-fatal MI, we asked by letter or telephone for the onset of coronary events and for permission to review their medical records for 141 individuals who reported a history of MI on the 10-year follow-up questionnaire (88% followed) and had never been registered as a coronary event. Of these 141, 122 individuals (87%) could be contacted, and among them, 74 reported information for suspected MI. Of these, 63 (85%) provided written informed consent to review their medical records, and medical records were reviewed by hospital physicians, PHC physicians or research physicians. Among them, we confirmed 23 definite MI (Table 1).

Table 1

Confirmed incident cases of coronary heart disease from three information sources

Table 1

Confirmed incident cases of coronary heart disease from three information sources

For fatal MI and sudden cardiac deaths, we conducted a systematic search of death certificates. All death certificates were forwarded to the PHC in the area of residency, and mortality data are sent centrally to the Ministry of Health, Welfare and Labor, and coded for the national vital statistics. Registration of death is required by the Family Registration Law, and is believed to be complete in Japan. For all CHD and acute heart failure (International Classification of Diseases, 10th revision I21–I23, I46 and I50) listed on the death certificate, but not ever registered, medical records in registered hospitals were reviewed by hospital personnel, PHC physicians or research physician/epidemiologists. Other fatal coronary event was defined as a case in which the underlying cause of death was CHD on the death certificate, but for which the medical records were not obtained, or the information obtained did not meet our criteria for MI or sudden cardiac death. From the death certificate survey, we added 17 MI (two definite and 15 probable), 69 sudden cardiac deaths and 30 other fatal coronary events (Table 1). Finally, we confirmed 217 MI (194 definite and 23 probable), 79 sudden cardiac deaths and 30 other fatal coronary events in total.

Statistical analysis

Statistical analyses were based on incidence rates of CHD during 11.0 years of follow-up from 1990 to 2001. For each subject, person-months of follow-up were calculated from the date of collection of the baseline questionnaire to the first endpoint, death, or 1 January 2002, whichever was earlier. For the analyses of total MI, both definite and probable cases were used, and analyses were also performed for the subjects including total MI, sudden cardiac death and other fatal coronary events. The relative risk of CHD was defined as the incidence of acute coronary events among men and women in categories of smoking habits (never-smokers, ex-smokers, current smokers of 1–14, 15–34, and 35 per day or more for men, and never-smokers, ex-smokers, current smokers for women) divided by the corresponding rate among men and women of never smokers. The relative risk according to pack-years of cigarette smoking was also calculated.

The relative risk and 95% confidence intervals (CI) were calculated after adjusting for age and other potential confounding factors using the Cox proportional hazards model. Test for trend across the smoking categories among current male smokers was conducted by assigning median values for each category. Potential confounding factors for the adjustment were baseline values of age (5-year categories), alcohol intake [non-drinkers (less than 1 day per month), occasional drinkers (1–3 days per month), weekly alcohol intake of 1–149 g/week, 150–299 g/week, 300–449 g/week, and 450 g/week or more], histories of hypertension and diabetes (no and yes), sports at leisure time (less than 1 day/month, 1–3 days/month and 1 day/week or more), categories (less than 1 day/week, 1-2 days/week, 3-4 days/week and 5 days/week or more) of selected food intake of fruits, total vegetables (green, yellow and other vegetables) and fresh and dry fish, education (junior high school, high school, and college or more). Subjects were censored from the follow-up analysis at the date of death or movement out from a PHC area.

To examine an effect of smoking cessation on the risk of CHD, we used never-smokers as the reference category for the analyses of relative risk among current smokers, and current smokers as the reference category for the analysis of the relative risk among ex-smokers according to years since quitting (less than 2, 2–4, 5–9, 10–14 and 15 years or more). In that analysis, we adjusted for age at starting smoking (less than 20, 20–24, 25–29 and 30 years or more) as well as the above-mentioned confounding variables. For each Cox proportional hazards model, we examined the proportionality of risk and found it satisfactory.

The population attributable risk per cent was calculated by P × (1 – 1/RR), where P represented the prevalence of smokers among cases and RR represented the multivariate relative risk for current smokers compared with non-current smokers. The formula of Greenland [15] was used for calculation of the 95% CI.

Results

During the 461 761 person-year of follow-up, 260 CHD were determined among men, consisting of 174 total MI (155 definite type), 63 sudden cardiac deaths and 23 other fatal coronary events. The respective numbers of cases among women were 66, 43 (39), 16 and 7.

Compared with never-smokers, current-smokers were 0.6–1.0 years younger, and ex-smokers were 0.6 years older for men and 0.6 years younger for women (Table 2).

Table 2

Age-adjusted mean values or prevalence (%) of risk characteristics at baseline according to cigarette smoking categories, in a 11.0-year prospective study of 19 782 men and 21 500 women aged 40–59 years

Table 2

Age-adjusted mean values or prevalence (%) of risk characteristics at baseline according to cigarette smoking categories, in a 11.0-year prospective study of 19 782 men and 21 500 women aged 40–59 years

The mean alcohol intake was higher in ex-smokers and current smokers with an increased number of cigarettes smoked compared with never-smokers. The mean body mass index was lower in current smokers than in never-smokers. Hypertension was more prevalent in ex-smokers than in never and current smokers. Diabetes was more prevalent in ex and current smokers than in never-smokers. The percentage of high education and sport at leisure time and the frequency of fruit, green or yellow vegetable and other vegetable intakes were lower among current smokers than among never and ex-smokers. The frequency of fish intake or vitamin supplement did not vary among smoking categories.

Table 3 shows age-adjusted and multivariate relative risks of CHD according to smoking status as reference to never-smokers. For both men and women, current smoking was positively associated with the age-adjusted risk of total CHD, MI, but not sudden cardiac deaths. These associations remained statistically significant after adjustment for known cardiovascular risk factors, the frequency of selected food intake and PHC area. The multivariate relative risk (95% CI) for current smokers compared with never-smokers was 2.85 (1.98, 4.12) for total CHD, 3.64 (2.27, 5.83) for total MI, and 1.29 (0.68, 2.42) for sudden cardiac death. Similar relative risks were obtained for women. For women, past smokers had an excess risk of mortality from total MI. However, the number of cases was small (n = 3).

Table 3

Relative risk (RR) and 95% confidence interval (CI) of coronary heart disease according to cigarette smoking categories, in a 11.0-year prospective study of 19 782 men and 21 500 women aged 40–59 years

Table 3

Relative risk (RR) and 95% confidence interval (CI) of coronary heart disease according to cigarette smoking categories, in a 11.0-year prospective study of 19 782 men and 21 500 women aged 40–59 years

Among men there was a dose-response relationship between the number of cigarettes smoked and the risks of total CHD and total MI. For example, the multivariate relative risk of total MI was 3.19 (1.72, 5.92) for 1-14 cigarettes, 3.63 (2.23, 5.90) for 15–34 cigarettes and 4.38 (2.34, 8.19) for 35 or more cigarettes per day.

We examined the relationship of years since quitting smoking with the risk of CHD among men. We did not use the data for women because the number of ex-smokers was small. The multivariate relative risk (95% CI) of total CHD was 0.11 (0.02, 0.80) within 2 years since quitting (number of cases 1), 0.43 (0.20, 0.91) at 2-4 years (n = 7), 0.51 (0.28, 0.92) at 5–9 years (n = 12), 0.12 (0.03, 0.47) at 10–14 years (n = 2) and 0.48 (0.26, 0.89) at 15 years (n = 11) and more after smoking cessation, whereas the relative risk for never-smokers was 0.35 (0.24, 0.51; n = 36).

The multivariate relative risk (95% CI) of total CHD among current smokers versus non-smokers was 2.73 (2.06, 3.61) for men and 2.94 (1.42, 6.10) for women. Based on these estimates and the proportions of current smokers among cases with CHD (72% for men and 14% for women), the population attributable risk per cent (95% CI) for total CHD was 46 (34, 55) for men and 9 (0, 18) for women.

Discussion

The present large prospective study confirmed a positive relationship between smoking and the risk of total CHD, more specifically MI for both men and women after adjustment for known cardiovascular risk factors and selected lifestyles. The association of smoking and the risk of total MI was particularly strong: men had a fourfold excess risk and women had a threefold excess risk. There was, however, no significant relationship of smoking with the risk of sudden cardiac death.

A previous large Japanese cohort study of 122 261 men and 142 857 women showed that the age-adjusted relative risk of mortality from total CHD for current daily smokers compared with non-smokers was 1.13 (95% CI, 1.07, 1.20) in men and 1.21 (1.10, 1.34) in women [2]. A recent report from the follow-up study of NIPPON DATA 80, a cohort of national representative samples aged 30 years or over, showed that current smokers had a significant age-adjusted relative risk of mortality from CHD compared with non-smokers (relative risk was 2.2 for men and 1.8 for women) [4]. However, in these studies, no incident data were available. Most Japanese cohort studies, using the incidence as an endpoint, reported that the relative risks of CHD were approximately two or three for men [6–8]. However, only one cohort study showed a weak relationship between current smoking and the incidence of CHD among women, but in that study the multivariate-adjusted relative risk for a smoking habit was of borderline statistical significance [6].

We found a lack of association between smoking and the risk of sudden cardiac deaths in our cohort. Previous cohort studies in western countries showed a significant association between smoking and the risk of sudden cardiac deaths [16, 17]. The lack of association may be caused by the lower proportion of CHD among cases of sudden cardiac deaths in Japanese. Autopsy studies showed that this proportion is only 40% among Japanese [18], whereas it is 80% among Caucasians [19].

There are several plausible mechanisms for the relationship of smoking with the risk of CHD. First, smoking is associated with increased inflammatory indices such as fibrinogen concentration [20] or C-reactive protein concentration [21], increased platelet aggregability [22], increased haematocrit [23], reduced fibrinolytic activity [24] and reduced blood flow in the coronary artery as a result of vasoconstriction [25], all of which may contribute to accelerated thrombus formation. Second, smoking reduces high-density lipoprotein cholesterol [26], insulin sensitivity [27], and an anti-oxidative effect through lowering the vitamin C concentration [28], and causes direct injury to the endothelial cells [29], which contributes to atheroma formation. Combined together, the smoking-related biological effects may contribute to the increased risk of CHD.

No significant excess risk of CHD for ex-smokers compared with never-smokers corresponded to the previous epidemiological findings that smoking cessation led to a fall in the risk within 2 years [30]. In the present study, we found that the excess risk of total CHD fell substantially within 2 years after quitting smoking.

We also estimated that 46% of CHD for men and 9% of CHD for women were attributable to current smoking in individuals aged 40–59 years. In 1999, the estimated number of CHD patients according to the National Patient Survey was 564 000 for men and 507 000 for women, and the number of annual coronary deaths was 14 909 for men and 15 518 for women [31]. Therefore, if our data could be applied also to other ages, approximately 305 000 CHD patients (259 000 men and 46 000 women), 8300 coronary deaths (6900 men and 1400 women) could be preventable by smoking cessation or prevention in Japan.

In conclusion, the present large cohort study showed that smoking raises the risk of CHD with a strong effect of smoking on the risk of total MI for both men and women. CHD could be preventable through smoking cessation or prevention by nearly half for men and nearly one-tenth for women. Smoking cessation leads to the elimination of the excess risk of CHD within 2 years after quitting. Therefore, smoking cessation may have a large impact on the prevention of CHD in Japan.

The authors would like to thank all staff members in each study area and in the central office for their painstaking efforts to conduct the baseline survey and follow-up, and Dr Aaron R. Folsom, University of Minnesota, for his valuable comments on the manuscript.

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Appendix

The investigators and participating institutions in the Japan Public Health Centre-based prospective study on cancer and cardiovascular diseases (JPHC Study) Cohort I Group, a part of JPHC Study Group (principal investigator: S. Tsugane), were as follows: S. Tsugane, T. Hanaoka, M. Inoue and T. Sobue, Epidemiology and Prevention Division, National Cancer Centre, Tokyo; J. Ogata, S. Baba, T. Mannami, and A. Okayama, National Centre for Circulatory Diseases, Suita; K. Miyakawa, F. Saito, A. Koizumi, Y. Sano, and I. Hashimoto, Iwate Prefectural Ninohe Public Health Centre, Ninohe; Y. Miyajima, N. Suzuki, S. Nagasawa, and Y. Furusugi; Akita Prefectural Yokote Public Health Centre, Yokote; H. Sanada, Y. Hatayama, F. Kobayashi, H. Uchino, Y. Shirai, T. Kondo, R. Sasaki and Y. Watanabe, Nagano Prefectural Saku Public Health Centre, Saku; Y. Kishimoto, E. Takara, M. Kinjo, T. Fukuyama and M. Irei, Okinawa Prefectural Ishikawa Public Health Centre, Ishikawa; S. Matsushima and S. Natsukawa, Saku General Hospital, Usuda; S. Watanabe and M. Akabane, Tokyo University of Agriculture, Tokyo; M. Konishi and K. Okada, Ehime University, Matsuyama; S. Tominaga, Aichi Cancer Centre Research Institute, Nagoya; M. Iida and W. Ajiki, Osaka Medical Centre for Cancer and Cardiovascular Diseases, Osaka; S. Sato, Osaka Medical Centre for Health Science and Promotion, Osaka; the late M. Yamaguchi, Y. Matsumura and S. Sasaki, National Institute of Health and Nutrition, Tokyo; Y. Tsubono, Tohoku University, Sendai; H. Iso and Y. Honda, University of Tsukuba, Tsukuba; H. Sugimura, Hamamatsu University, Hamamatsu; M. Kabuto, National Institute for Environmental Studies, Tsukuba; N. Yasuda, Kochi Medical School, Kochi; S. Kono, Kyushu University, Kyushu; K. Suzuki, Research Institute for Brain and Blood Vessels, Akita; Y. Takashima, Kyorin University, Kyorin; E. Maruyama, Kobe University, Kobe.

Author notes

Sponsorship: This study was supported by grants-in-aid for Cancer Research and for the Third Term Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan.

© 2006 European Society of Cardiology