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(Circulation. 1997;95:2374-2379.)
© 1997 American Heart Association, Inc.
Articles |
A Prospective Study of Passive Smoking and Coronary Heart Disease
the Channing Laboratory (I.K., G.A.C., F.E.S., J.E.M., M.J.S., W.C.W., C.H.H.) and Division of Preventive Medicine (J.E.M., C.H.H.), Departments of Medicine and Ambulatory Care and Prevention, Harvard Medical School and Brigham and Women's Hospital; and the Departments of Health and Social Behavior (I.K.), Nutrition (M.J.S., W.C.W.), Epidemiology (G.A.C., J.E.M., M.J.S., W.C.W., C.H.H.), and Environmental Health (F.E.S.), Harvard School of Public Health, Boston, Mass.
Correspondence to Dr Ichiro Kawachi, Channing Laboratory, 180 Longwood Ave, Boston, MA 02115. E-mail nhike{at}gauss.bwh.harvard.edu
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Abstract |
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Background Several epidemiological studies have suggested an association of passive smoking with coronary heart disease (CHD). However, few studies have taken account of exposure to passive smoking in the workplace. Additionally, several studies have been unable to control for the full range of potential confounding factors. We examined prospectively the relationship of passive smoking with risk of CHD in a cohort of women.
Methods and Results The study was carried out in an ongoing prospective cohort of US female nurses, in whom we assessed exposure to passive smoking at home and at work as well as duration of years spent living with someone who smoked regularly. We studied 32 046 women 36 to 61 years of age in 1982 who had never smoked and were free of diagnosed CHD, stroke, and cancer. During 10 years of follow-up (1982 to 1992), 152 incident cases of CHD (127 nonfatal myocardial infarction and 25 fatal CHD) occurred. Compared with women not exposed to passive smoking, the relative risks of total CHD—adjusted for a broad range of cardiovascular risk factors—were 1.58 (95% CI, 0.93 to 2.68) among those reporting occasional exposure and 1.91 (95% CI, 1.11 to 3.28) among women reporting regular exposure to passive smoking at home or work. There was no relation apparent between duration of living with a smoker and risk of CHD.
Conclusions Despite the fact that exposure to passive smoking was assessed by self-report and only at baseline (as well as other limitations), these data suggest that regular exposure to passive smoking at home or work increases the risk of CHD among nonsmoking women.
Key Words: smoking • coronary disease • women
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Introduction |
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Cigarette smoking is a well-established cause of coronary heart disease (CHD) in women, with current smokers showing a fourfold to fivefold increase in risk compared with never-smokers.1 Several, though not all, studies of passive smoking2 3 4 5 6 7 8 9 10 11 12 13 14 have reported a positive association with CHD. Although the American Heart Association has concluded that passive smoking is an important risk factor for CHD,15 some important issues remain unresolved. First, few epidemiological studies have assessed the impact of passive smoking in the workplace. With the exception of three case-control studies4 11 13 and one cohort study,14 all reports to date have assessed exposure only to spousal smoking. Yet, dosimetric studies suggest that exposure at work is comparable to and often greater than exposure at home because of the higher density of smokers at work.16 17 18 Failure to assess workplace exposure may therefore underestimate the risk of passive smoking.
Second, several previous studies have been unable to adjust for the full range of potential confounding factors. Evidence suggests that passive smokers may also be at increased risk of CHD for reasons such as diet in addition to their exposure to tobacco smoke pollution.19 20 21 In the present report, we carried out a prospective analysis of passive smoking and risk of CHD in a large cohort of women, taking into account both workplace and home exposures as well as adjusting for a broad range of cardiovascular risk factors.
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Methods |
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The Nurses' Health Study Cohort
The Nurses' Health Study cohort was established in 1976, when 121 700 female registered nurses 30 to 55 years of age completed mailed questionnaires requesting information about risk factors for CHD and cancer, including current and past smoking habits as well as past personal history of myocardial infarction (MI), angina, cancer, diabetes, hypertension, and high serum cholesterol levels. Since then, follow-up questionnaires have been mailed every 2 years to the cohort to update information on cardiovascular risk factors and the occurrence of major illnesses. Further details of the Nurses' Health Study have been described elsewhere.22
Exposure Data
On the 1982 questionnaires, we asked: "Are you currently exposed to cigarette smoke from other people?" We asked separately about two locations, home and workplace, and responses were categorized into three levels: no exposure, occasional exposure, and regular exposure. In addition to the question on current exposure to passive smoking, we also asked: "As an adult, how many years have you lived with someone who has smoked regularly?" Response categories were none or <1 year, 1 to 4, 5 to 9, 10 to 19, 20 to 29, 30 to 39, and 
40 years. On the basis of the distribution of person-years, these responses were recategorized a priori as none or <1 year, 1 to 9, 10 to 19, 20 to 29, and 30 years.
Ascertainment of CHD
The study end points comprised incident cases of nonfatal MI and fatal CHD occurring after the return of the 1982 questionnaire but before June 1, 1992. All women who reported having a nonfatal MI were asked for permission to review medical records. Cases were confirmed if they met the diagnostic criteria of the World Health Organization (ie, symptoms plus either cardiac enzyme level elevations or diagnostic ECG changes).23 Medical records were reviewed by physicians who were blinded to exposure status. An MI was defined as probable if medical records were not available, but hospitalization was required and confirmatory information was obtained by interview or letter. The present analyses included both definite and probable cases. Eighty-four percent of the total CHD cases included herein were "definite" by these criteria.
The ascertainment of death included systematic searches of the National Death Index to identify deaths among participants who did not respond during each questionnaire cycle. The searches were supplemented by reports from next of kin and postal authorities. More than 98% of deaths in the cohort were estimated to have been identified by this method.24 If death appeared to be from vascular causes, written permission was requested from the next of kin (subject to the regulations of vital records offices) to review medical records. Fatal CHD was defined as fatal MI confirmed by hospital records or at autopsy, or as CHD recorded on the death certificate if this was the underlying and most probable cause given and there was previous evidence of CHD. In no instance was the cause on the death certificate accepted without corroboration. Total CHD was defined as nonfatal MI plus fatal CHD.
Study Population
The study population comprised 32 046 women who had never smoked before baseline in 1982 and who remained nonsmokers during the follow-up period (1982 to 1992). We excluded all current or former smokers (n=63 130) as well as women who had died (n=1122) or had a past history of CHD (n=3452), stroke (n=318), or cancer (n=5332) before the beginning of follow-up. The study population was therefore free of diagnosed CHD, stroke, and cancer (except nonmelanoma skin cancer) at the beginning of follow-up. Because women who develop these major illnesses may alter their exposure to passive smoking, we excluded from the analysis all women who reported these diagnoses on subsequent questionnaires. Thus, at the start of each 2-year interval, the base population included no women reporting these diagnoses.
During the 10-year period from 1982 through June 1, 1992, the 32 046 women who comprised the study population accrued 300 325 person-years of follow-up. The follow-up rate, calculated as a percentage of the total potential person-years of follow-up, was 98% for nonfatal outcomes.
Data Analysis
The primary analysis of follow-up data from 1982 to 1992 used incidence rates with person-years of follow-up as the denominator. Exposure to passive smoking was assessed only in 1982. Other variables, such as personal history of hypertension, hypercholesterolemia, and diabetes, were updated every 2 years according to the information provided by the participants on the questionnaire.
The relative risk was defined as the CHD incidence rate among those exposed to second-hand tobacco smoke divided by the corresponding rate among women not exposed. Relative risks were adjusted for age, categorized in 5-year groups,25 and 95% CIs were calculated.26 In the analyses of duration of exposure to passive smoking, we also adjusted for age in single-year intervals. Proportional hazards models27 were used to adjust for multiple risk factors, including alcohol intake (0.0, 0.01 to 4.9, 5.0 to 14.9, 15.0 to 24.9, and 25.0 g/d); body mass index (in quintiles); history of hypertension, diabetes mellitus, and hypercholesterolemia; menopausal status; current use of postmenopausal hormones; past use of oral contraceptives; vigorous exercise (engaging in physical activity long enough to work up a sweat once/wk); quintiles of saturated fat intake; vitamin E intake (nonuser, <100, 100 to 250, 300 to 500, and 600 IU/d); average aspirin use (<1, 1 to 6, and 7 tablets/wk); parental history of MI before age 60 years; and father's occupation when the participant was 16 years of age (blue-collar worker, white-collar worker, farmer, deceased/unknown).
While we did not measure blood cholesterol, we did assess self-reported history of hypercholesterolemia, which predicted the incidence of total CHD in this cohort (relative risk of CHD in women with hypercholesterolemia versus women without hypercholesterolemia, 1.64; 95% CI, 1.18 to 2.33), and we adjusted for this variable in proportional hazards models.
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Results |
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Women exposed to passive smoking accounted for 80.8% of the total follow-up time of 300 325 person-years. Of the 25 959 women exposed to passive smoking, 15 407 (59%) reported occasional exposure at home or work, while 10 552 (41%) reported regular exposure at home or work.
Table 1
shows the age-standardized distributions of risk factors for cardiovascular disease and other characteristics according to the frequency of exposure to passive smoking. Women who reported being regularly exposed to second-hand tobacco smoke were more likely to have reported a diagnosis of hypertension, hypercholesterolemia, and diabetes mellitus compared with those not exposed. They were also less likely to engage in vigorous exercise, consumed more saturated fat, and had lower intake of vitamin E. These differences may partly reflect the lower socioeconomic backgrounds of women who were exposed to passive smoking: 26.2% of those exposed regularly to passive smoking had fathers who were blue-collar workers compared with 22.4% of women not exposed. Finally, the proportion of women reporting a parental history of MI before age 60 years was slightly higher (14.1%) in those reporting regular passive smoking exposure compared with women not exposed (12.6%). These findings provide clear evidence of the need to control for a broad range of cardiovascular risk factors in examining the association of passive smoking with risk of CHD.
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One hundred fifty-two incident cases of CHD (including 127 nonfatal MI and 25 CHD deaths) occurred during 10 years of follow-up. The age-adjusted relative risk of total incident CHD was 1.97 (95% CI, 1.20 to 3.24) in women reporting any exposure to passive smoking compared with none (Table 2). Adjustment for all of the risk factors shown in Table 1
resulted in a modest attenuation of the relative risk. There was no apparent difference in the magnitude of the association of passive smoking with nonfatal events compared with fatal end points (Table 2).
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We observed a dose-response gradient between self-reported frequency of passive smoking and risk of CHD. Compared with nonexposed women, those reporting occasional exposure to second-hand smoke had a multivariate adjusted relative risk for total CHD of 1.58, while those reporting regular exposure had a relative risk of 1.91 (P for trend, .002) (Table 3). We attempted to further refine the exposure categories by examining the effects of exposure at home and work, as distinct from exposure at home or work. The multivariate relative risks of total CHD were 1.81 (95% CI, 1.08 to 3.02) in women exposed at home or work and 1.36 (95% CI, 0.72 to 2.54) in women exposed in both settings. However, the data on women exposed in both settings was based on a small number of cases (n=24).
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Adjustment for a broad range of risk factors in proportional hazards models attenuated but did not eliminate the excess risks associated with passive smoking. Additionally, the strength of the association between passive smoking and CHD was similar for nonfatal and fatal events. Results were very similar when the coronary end points were confined to definite cases of CHD. Compared with women never exposed to passive smoking, the multivariate-adjusted relative risks of total CHD were 1.64 (95% CI, 0.92 to 2.93) in women occasionally exposed and 2.03 (95% CI, 1.11 to 3.68) in women regularly exposed.
To examine the separate effects of passive smoking at home and at work, we assessed the CHD risks among two groups of women: homemakers who were exposed only in the home environment and women in paid employment who were exposed only at work (but not at home). During 10 years of follow-up, 64 cases of incident CHD occurred among women in paid employment who were exposed to second-hand smoke only at work, while 53 cases of CHD occurred among homemakers exposed only at home. Among women exposed only at work, the multivariate relative risks of total CHD were 1.49 (95% CI, 0.71 to 3.14) among those occasionally exposed and 1.92 (95% CI, 0.88 to 4.18) among those regularly exposed to second-hand smoke. Among women exposed only at home, the multivariate adjusted relative risks of total CHD were 1.19 (95% CI, 0.63 to 2.23) among those occasionally exposed and 2.11 (95% CI, 1.03 to 4.33) among those regularly exposed. Thus, we found evidence of increased risks of CHD for both home and work exposure.
Finally, we examined the relationship of self-reported duration of living with someone who smoked regularly with risk of CHD (Table 4). During 10 years of follow-up, 176 cases of incident CHD occurred among 38 025 women who answered the question: "As an adult, how many years have you lived with someone who has smoked regularly?" No clear trend was evident between duration of exposure and CHD risk, although women reporting the longest duration (30+ years) had the highest relative risk. However, the relative risks were considerably attenuated after adjustment for potential confounding variables in multivariate analyses.
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Discussion |
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These data suggest that regular exposure to passive smoking at home or work may increase the risk of CHD among nonsmoking women. Unknown confounding factors may have contributed to the observed excess risk; however, a strength of the present study is that we controlled for a very broad range of behavioral and dietary factors that could account for the difference in CHD risk between passive smokers and nonsmokers.
The risks of CHD were similar among women exposed to second-hand smoke at home compared with those exposed only at work. Our finding of an increased risk of passive smoking at work is consistent with the results of a case-control study of Chinese women in full-time paid employment,13 which found an elevated though statistically nonsignificant risk of MI for passive smoking at work (adjusted RR, 1.85; 95% CI, 0.86 to 4.00). On the other hand, the American Cancer Society CPS-II Cohort study did not find increased risks of CHD mortality among men and women exposed to second-hand smoke at work.14 It is plausible that among full-time employed women, the workplace is a significant source of exposure to second-hand smoke.
The present study was carried out in a cohort of registered nurses. Few studies have been published on passive smoking in hospitals. Coultas et al28 reported a personal monitoring study of nonsmokers during their work shifts in 1987 and found median nicotine exposures of 10 µg/m3 among hospital workers, which was comparable to the levels of exposure in office workers (7.2 µg/m3) but lower than those among restaurant workers (45 µg/m3). Stillman et al29 carried out a nicotine vapor monitoring study at various locations within a large urban hospital in 1988. They reported nicotine concentrations of 2.43 µg/m3 in staff lounges, 2.05 µg/m3 in offices, 2.28 µg/m3 in corridors/elevators, and 7.06 µg/m3 in cafeterias. These concentrations were close to or exceeded the level of 2.3 µg/m3, which has been estimated to present a lung cancer risk of 3 in 10 000 over 40 years—the so-called "de manifestis" level of risk that usually prompts US regulatory agencies to take action.18 Thus, the limited available evidence suggests that passive smoking could occur in hospitals. Recently, however, the Joint Commission on Hospital Accreditation has required that all hospitals become smoke free, so that these intensities of exposure to second-hand smoke may no longer apply.
A limitation of the present study was its reliance on self-reported assessments of exposure to passive smoking. Self-reports of current exposure to passive smoking are correlated modestly (Pearson coefficients ranging between 0.2 and 0.5) with biochemical markers of tobacco smoke exposure, such as salivary30 and urinary cotinine.31 Part of the reason is that exposure to passive smoking is ubiquitous. For instance, in a study of 663 never-smokers and former smokers attending a cancer screening clinic, 91% of subjects had detectable levels of cotinine in their urine, even though only 76% of subjects reported exposure to passive smoking during the previous 4 days.31 In the same study, 84% of subjects who did not live with a smoker had detectable cotinine levels.31 The effect of this type of measurement error is usually conservative; that is, it pushes the relative risk estimates in the direction of the null.
When passive smoking has been assessed by questionnaire, self-reported duration has been found to be much less reliable than dichotomous responses (yes/no) to questions about exposure at home or work.32 33 34 Pron et al32 used a test-retest design to examine the reliability of passive smoking histories in 117 subjects enrolled in a lung cancer case-control study. When subjects were reinterviewed 6 months apart, good agreement was found for reports of occupational and residential exposure to second-hand smoke (
of 0.63 and 0.66, respectively, among female never-smokers). However, the reliability of reported duration of exposure to spousal smoking was substantially worse (product-moment correlation coefficient, 0.25; 95% CI, -0.01 to 0.48).32 The inability of several epidemiological studies to detect a dose-response relation between duration of passive smoking and lung cancer risk has been attributed to the low reliability of self-reported duration of passive smoking.32 35 If the duration of exposure was significantly misclassified, this could produce the type of pattern on Table 4, where passive smokers generally appear to be at increased risk of CHD but no dose-response relation is evident.
A further limitation of this study is that exposure to passive smoking was ascertained only at baseline. However, it is likely that exposure to passive smoking has been decreasing over time, since more people are stopping smoking, and more workplaces have been introducing smoking restriction policies.36 In other words, if there was misclassification of exposure to passive smoking, it is likely to have been in the conservative direction, ie, more passive smokers switching to become nonsmokers over time. We provided a test of this scenario by examining the risks of CHD among passive smokers over different follow-up periods. If substantial misclassification had occurred, then the relative risks of CHD might be expected to drift downward over time. However, we found no evidence of this type of drift. For example, the relative risks of CHD among women regularly exposed to second-hand smoke were 1.6 (95% CI, 0.8 to 3.6) after 4 years of follow-up (1982 to 1986), 2.0 (95% CI, 1.0 to 3.9) after 6 years of follow-up (1982 to 1988), and 2.3 (95% CI, 1.4 to 3.9) after 10 years of follow-up (1982 to 1992).
Several potential mechanisms have been identified through which passive smoking may increase the risk of CHD. These include carboxyhemoglobinemia, increased platelet aggregation, damage to the arterial endothelium, and reduced HDL cholesterol.37 38 In one experiment, the sensitivity of platelets to the antiaggregatory action of exogenous prostacyclin (PGI2) was compared in smokers and nonsmokers before and after they sat in a room for 20 minutes where cigarettes had been smoked just before the experimental subjects entered. No change in platelet sensitivity was detected among smokers; however, a significant change occurred among the platelets of nonsmokers such that their sensitivity to the antiaggregatory action of PGI2 was not discernibly different from the smokers.39 The effect of tobacco smoke on platelet activity may not be solely mediated by nicotine. Former smokers treated with nicotine patches show lower platelet activity compared with continuing smokers despite having similar nicotine levels.40 Thus, the effects of passive smoking on the cardiovascular system are not caused by any single component of tobacco smoke but rather are caused by the effects of many elements including carbon monoxide, nicotine, polycyclic aromatic hydrocarbons, and other not fully specified elements in the smoke.38
A recent study of 78 healthy teenagers and young adults found that those exposed to passive smoking for at least 1 hour daily exhibited early arterial damage, as assessed by endothelium-dependent brachial artery dilatation.41 Furthermore, a dose-response relation was found between intensity of exposure to passive smoking and the degree of endothelial dysfunction.41
The risk of CHD in passive smokers appears to be high compared with that among active smokers. However, risk estimates derived from studies of active and passive smoking are not directly comparable because they are calculated with the use of different reference categories. In studies of active smoking, the reference category includes all nonsmokers, including those with high levels of exposure to passive smoking, whereas the reference category in studies of passive smoking consists of those not exposed to second-hand smoke. In the Nurses' Health Study, we previously reported that women smoking just 1 to 4 cigarettes per day had a relative risk of total CHD of 1.94 (95% CI, 1.23 to 3.08) compared with never-smokers.42 When the reference category was set to never-smokers not exposed to passive smoking, the relative risk of CHD in women who used 1 to 4 cigarettes per day increased to 2.61 (95% CI, 1.24 to 5.51). Although based on a controversial methodology, the analysis of "cigarette equivalents" suggests that heavy passive smokers can inhale the equivalent of several cigarettes per day, depending on the constituent measured in the sidestream smoke.18 Thus, a relative risk of 1.9 among women regularly exposed to passive smoking is not biologically implausible in this cohort of women.
Further support for the association between passive smoking and CHD was provided by examining the risk among former smokers. Seventy-one cases of incident CHD occurred among 15 720 former smokers during the study period. Compared with former smokers not exposed to passive smoking, the multivariate-adjusted relative risks of CHD were 1.82 (95% CI, 0.76 to 4.34) among those occasionally exposed and 2.38 (95% CI, 0.98 to 5.79) among those regularly exposed to passive smoking.
Conclusions
Despite the fact that exposure to passive smoking was assessed by self-report and only at baseline, as well as other limitations, these data suggest that regular exposure to passive smoking at home or work increases the risk of CHD among nonsmoking women. The consistency of these findings with the existing totality of evidence increases the belief that the observed association represents cause and effect.
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Acknowledgments |
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This study was supported by research grants HL-34594 and CA-40356 from the National Institutes of Health. Dr Kawachi is the recipient of a National Heart, Lung, and Blood Institute Career Development Award. The authors are indebted to the participants in the Nurses' Health Study for their continuing cooperation.
Received October 1, 1996; revision received December 4, 1996; accepted December 14, 1996.
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 D. S. Celermajer Protecting Children From Passive Smoking Circulation, June 26, 2007; 115(25): 3143 - 3144. [Full Text] [PDF]
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 S. Stranges, M. R. Bonner, F. Fucci, K. M. Cummings, J. L. Freudenheim, J. M. Dorn, P. Muti, G. A. Giovino, A. Hyland, and M. Trevisan Lifetime cumulative exposure to secondhand smoke and risk of myocardial infarction in never smokers: results from the Western new york health study, 1995-2001. Arch Intern Med, October 9, 2006; 166(18): 1961 - 1967. [Abstract] [Full Text] [PDF]
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T M L Eagan, J Hetland, and L E Aaro Decline in respiratory symptoms in service workers five months after a public smoking ban Tob. Control, June 1, 2006; 15(3): 242 - 246. [Abstract] [Full Text] [PDF]
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J. Barnoya and S. A. Glantz Cardiovascular Effects of Secondhand Smoke: Nearly as Large as Smoking Circulation, May 24, 2005; 111(20): 2684 - 2698. [Abstract] [Full Text] [PDF]
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Z. Yang, C. A. Knight, M. M. Mamerow, K. Vickers, A. Penn, E. M. Postlethwait, and S. W. Ballinger Prenatal Environmental Tobacco Smoke Exposure Promotes Adult Atherogenesis and Mitochondrial Damage in Apolipoprotein E-/- Mice Fed a Chow Diet Circulation, December 14, 2004; 110(24): 3715 - 3720. [Abstract] [Full Text] [PDF]
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 P. H Whincup, J. A Gilg, J. R Emberson, M. J Jarvis, C. Feyerabend, A. Bryant, M. Walker, and D. G Cook Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement BMJ, July 24, 2004; 329(7459): 200 - 205. [Abstract] [Full Text] [PDF]
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 A. Nakata, T. Tanigawa, S. Araki, S. Sakurai, and H. Iso Lymphocyte Subpopulations Among Passive Smokers JAMA, April 14, 2004; 291(14): 1699 - 1700. [Full Text] [PDF]
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C Pitsavos, D B Panagiotakos, C Chrysohoou, J Skoumas, K Tzioumis, C Stefanadis, and P Toutouzas Association between exposure to environmental tobacco smoke and the development of acute coronary syndromes: the CARDIO2000 case-control study Tob. Control, September 1, 2002; 11(3): 220 - 225. [Abstract] [Full Text] [PDF]
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 C. Bolego, A. Poli, and R. Paoletti Smoking and gender Cardiovasc Res, February 15, 2002; 53(3): 568 - 576. [Abstract] [Full Text] [PDF]
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A. Woodward and M. Laugesen How many deaths are caused by second hand cigarette smoke? Tob. Control, December 1, 2001; 10(4): 383 - 388. [Abstract] [Full Text] [PDF]
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R. Otsuka, H. Watanabe, K. Hirata, K. Tokai, T. Muro, M. Yoshiyama, K. Takeuchi, and J. Yoshikawa Acute Effects of Passive Smoking on the Coronary Circulation in Healthy Young Adults JAMA, July 25, 2001; 286(4): 436 - 441. [Abstract] [Full Text] [PDF]
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 E. Nelson The miseries of passive smoiong Human and Experimental Toxicology, February 1, 2001; 20(2): 61 - 83. [Abstract] [PDF]
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 J. He, S. Vupputuri, K. Allen, M. R. Prerost, J. Hughes, and P. K. Whelton Passive Smoking and the Risk of Coronary Heart Disease -- A Meta-Analysis of Epidemiologic Studies N. Engl. J. Med., March 25, 1999; 340(12): 920 - 926. [Abstract] [Full Text] [PDF]
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 D. J. Berglund, D. E. Abbey, M. D. Lebowitz, S. F. Knutsen, and W. F. McDonnell Respiratory Symptoms and Pulmonary Function in an Elderly Nonsmoking Population Chest, January 1, 1999; 115(1): 49 - 59. [Abstract] [Full Text] [PDF]
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M. D. Eisner, A. K. Smith, and P. D. Blanc Bartenders' Respiratory Health After Establishment of Smoke-Free Bars and Taverns JAMA, December 9, 1998; 280(22): 1909 - 1914. [Abstract] [Full Text] [PDF]
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 Other Articles Noted Evid. Based Nurs., October 1, 1998; 1(4): 100 - 104. [Full Text]
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M. E LeVois, M. W Layard, P. Lee, R. Dempsey, K W E Denson, M R Law, J K Morris, and N J Wald Passive smoking and heart disease BMJ, August 1, 1998; 317(7154): 344 - 344. [Full Text]
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M. Valkonen and T. Kuusi Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein Circulation, May 26, 1998; 97(20): 2012 - 2016. [Abstract] [Full Text] [PDF]
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P. D. F. Adlkofer Passive Smoking and Coronary Heart Disease in Women Circulation, May 12, 1998; 97(18): 1870 - 1870. [Full Text] [PDF]
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F. J. Brennan Passive Smoking and Coronary Heart Disease Circulation, May 12, 1998; 97(18): 1871 - 1871. [Full Text]
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C. R. E. Coggins and C. R. E. DABT A Prospective Study of Passive Smoking and Coronary Heart Disease Circulation, May 12, 1998; 97 (18): 1870 - 1871. [Full Text]
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D. G. B. Gori and I. Kawachi Passive Smoking and Coronary Heart Disease • Response Circulation, May 12, 1998; 97 (18): 1871 - 1873. [Full Text]
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P. McElduff, A. J Dobson, R. Jackson, R. Beaglehole, R. F Heller, and R. Lay-Yee Coronary events and exposure to environmental tobacco smoke: a case-control study from Australia and New Zealand Tob. Control, March 1, 1998; 7(1): 41 - 46. [Abstract] [Full Text]
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R. M. Werner and T. A. Pearson What's So Passive About Passive Smoking?: Secondhand Smoke as a Cause of Atherosclerotic Disease JAMA, January 14, 1998; 279(2): 157 - 158. [Full Text] [PDF]
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M R Law, J K Morris, and N J Wald Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence BMJ, October 18, 1997; 315(7114): 973 - 980. [Abstract] [Full Text]
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 Second-Hand Smoke Increases CAD Risk Journal Watch Cardiology, June 13, 1997; 1997(613): 3 - 3. [Full Text]
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