Key Points
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The smoking of tobacco products increases the risk of cardiovascular diseases, including myocardial infarction, stroke, and peripheral artery disease.
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The continued smoking of tobacco products in patients with cardiovascular disease increases the risk of recurrent events, including sudden death, and smoking cessation reduces this risk.
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Environmental tobacco smoke (secondhand smoke) increases the risk for cardiovascular and other diseases in nonsmokers.
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Cigarette smoking rates among adults and youth have declined in the United States during several decades.
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Effective behavioral and pharmacologic methods are available to help smokers quit.
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Effective educational methods are available to prevent youth from starting to smoke.
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Policies and regulations including smoke-free spaces, limitations on advertising, enforcement of youth access laws, and increased cigarette excise taxes have contributed importantly to reductions in tobacco use.
There are approximately 43 million adult smokers in the United States. It is estimated that 443,000 deaths annually are attributable to cigarette smoking ( Fig. 20-1 ). These deaths are replenished by an estimated 3900 teenagers per day who begin the smoking habit. The economic costs are estimated to be more than $96 billion per year in medical expenses and $97 billion in lost productivity. Worldwide, tobacco is estimated to cause more than 5 million deaths per year. The costs in lost health and in human suffering are incalculable.
The causal links between cigarette smoking and human disease are incontrovertible. Smoking is linked to major cardiovascular diseases including sudden death, acute myocardial infarction, peripheral artery disease, and stroke. Cigarettes are also linked to many cancers and are the prime factor in lung cancer. Smoking is linked to acute and chronic pulmonary diseases including emphysema. There is growing evidence that environmental tobacco smoke, which results in exposure of nonsmokers, poses health risks to that group. Lung cancer, respiratory tract infections, and asthma attacks among those exposed to environmental tobacco smoke are well recognized. More recent evidence finds that environmental tobacco smoke causes heart disease and sudden infant death syndrome. These observations and others have resulted in a widespread call for prevention of tobacco uptake by teens, cessation among smoking adults, and restriction of smoking in the environment. This chapter discusses the scientific evidence relating active and passive tobacco smoking to cardiovascular risk and the benefits of quitting. It also describes the trends in cigarette use. Finally, individual and population intervention strategies for cessation among youth and adults are discussed.
Effects of Cigarette Smoking on Cardiovascular Disease
There is a wealth of evidence in the past five decades linking cigarette smoking to the major cardiovascular diseases, including myocardial infarction, sudden death, stroke, and peripheral vascular disease. These associations are found across all age, gender, and ethnic groups.
The relationship of coronary heart disease (CHD) mortality to smoking status from the 1959-1965 Cancer Prevention Study is shown in Figure 20-2 . CHD increases with age for both men and women; women have lower rates at all ages, and ever-smokers have significantly higher death rates than never-smokers. These differences are greatest in the younger age groups, in which the relative risk of CHD in smokers approaches 8. However, the differences remain into the older years, when relative risks are less but absolute risk is significantly greater. Smoking cessation among adults significantly reduces the risk of CHD and all cardiovascular disease as shown in many populations.
Data from the Multiple Risk Factor Intervention Trial (MRFIT) of 316,099 white men also find a graded relationship between number of cigarettes and CHD death. The relative risk for 1 to 25 cigarettes per day is 2.1, rising to 2.9 for daily smoking consumption above 25 cigarettes per day. Similarly, MRFIT found that quitting smoking reduces cardiovascular disease mortality.
In addition to age and gender effects, it is apparent that smoking-related disease also affects all the major ethnic and racial groups in the United States. The ill health effects of smoking cut across national boundaries as demonstrated in the Seven Countries Study of Keys and colleagues.
One of the most disturbing aspects of cigarette smoking is its strong association with sudden, unexpected death, particularly among younger individuals. Although sudden death is common among those with known cardiovascular disease, Escobedo and Caspersen found that only smoking predicted sudden death in those thought to be disease free. Similarly, in both men and women, acute myocardial infarction in younger individuals (younger than 50 years) is strongly associated with cigarette smoking.
The interaction of cigarette smoking with other known risk factors is well studied. Some suggest that the effect is additive, whereas others find a multiplicative effect. Cigarette smoking adds to cardiovascular risk associated with lipids, obesity, diabetes mellitus, hypertension, oral contraceptive use, and electrocardiographic abnormalities. The additive effects of smoking in relationship to other major risk factors are seen in Figures 20-3 and 20-4 for 10- and 30-year follow-up of men and women aged 25 years at study entry. It is apparent that smoking adds significantly to risk. Smokers who continue in the habit after an acute myocardial infarction have significantly higher rates of recurrent events and death. Individuals who quit smoking reduce that risk of a subsequent event. Smokers also suffer increased rates of peripheral arterial disease with a relative risk of two to three times and twice the risk of stroke.
The mechanisms by which cigarettes affect cardiovascular diseases have been studied in both animal and human models. Both acute and chronic mechanisms are postulated, and it is likely that both contribute. There is accumulating evidence that smoking plays an important role in the basic atherosclerotic process. This is elegantly confirmed in the PDAY (Pathobiological Determinants of Atherosclerosis in Youth) study. In this study, autopsies were performed on 1443 men and women aged 15 to 34 years who died of external causes, such as auto accidents. Smoking was associated with an excess of fatty streaks and raised lesions in the abdominal aorta in these otherwise healthy individuals. Injury of the arterial endothelium is suggested by some as the mechanism for the atherosclerotic lesions, but other mechanisms are also postulated. Acute effects of smoking are demonstrated by the known short-term vascular effects of nicotine and the rapid improvement in prognosis with smoking cessation.
There are also known associations and interactions of smoking with other recognized elements in the causal chain and biomarkers for cardiovascular disease. For example, many studies find smoking to be inversely associated with high-density lipoprotein cholesterol, the “good cholesterol,” whereas some report associations with elevated low-density and very-low-density lipoprotein cholesterol. Smoking has prothrombotic effects, including increasing platelet adhesion, increased fibrinogen, and decreased fibrinolytic activity. All are associated with increased clotting. As the interest in atherosclerosis as an inflammatory disease grows, increased leukocyte counts and elevated C-reactive protein support an association.
Environmental Tobacco Smoke
Recently, there is increased emphasis on exposure to environmental tobacco smoke among nonsmokers in the home, workplace, and public settings. This is more hotly debated than individual smoking because it affects those who may not have a choice about being exposed to tobacco smoke. In the 2006 Surgeon General’s report The Health Consequences of Involuntary Exposure to Tobacco Smoke, cardiovascular disease was clearly implicated along with the demonstrated cancer and respiratory disease effects of environmental tobacco smoke.
A meta-analysis incorporating more home-based studies along with workplace studies (total of 1699 cases) showed an overall increased risk associated with passive smoking (RR = 1.49; 95% CI, 1.29-1.72) and suggested relative risks from workplace exposure similar to those from home-based exposure. In addition, environmental tobacco smoke is associated with sudden infant death syndrome and respiratory diseases in exposed children.
The mechanism by which environmental tobacco smoke affects individuals is still debated, but considerable data are available. It is clear that mainstream smoke, that inhaled by the smoker, differs from sidestream smoke, which is released into the environment immediately. Sidestream smoke may be more toxic. It is apparent that nonsmokers who are exposed regularly to cigarette smoke develop a number of physiologic changes. Some studies find that nonsmokers are more sensitive to these changes than those regularly exposed. These include the chronic effects of cigarette smoke, such as lower high-density lipoprotein cholesterol, increased fibrinogen, and platelet abnormalities. It is also apparent that exposed nonsmokers have acute effects including endothelial dysfunction and lower exercise tolerance.
These observations are compatible with pathologic cardiovascular effects in nonsmokers exposed to environmental tobacco smoke. Recent estimates suggest that 23,000 to 70,000 deaths per year from acute myocardial infarction are associated with environmental tobacco smoke exposure. This effect is much larger than that observed for lung cancer. These observations underlie the recent efforts and successes in reducing environmental exposures or secondhand smoke.
Prevalence and Trends in Cigarette Smoking Among Youth
Cigarette smoking among youth is described in the 1994 Surgeon General’s report, and methods of prevention are expanded in the 2000 Surgeon General’s report. Most smokers begin this habit in their teenage years. It begins with social pressure based on friends, siblings, and parents who smoke. Youth believe that smoking makes you look more adult and is associated with social success, independence, and rebelliousness, common themes in the teenage years. The environment provides important support through advertising, which reinforces the “coolness” of smoking. The highly effective Joe Camel ads and other media approaches were clearly aimed at and successful with new-onset smokers. The basis of many tobacco lawsuits originated in this marketing practice. The most vulnerable period is in the sixth to eighth grades (ages 12 to 14 years), when much smoking initiation occurs.
Early surveys of national trends showed a steady rise in cigarette smoking among youth from 1968 to 1974. During that time, smoking of teenage girls began to exceed that of boys. However, from 1991 to 2007, a national sample of high-school students found a steady fall of smoking rates among this group until 2003, when it leveled ( Table 20-1 ). Importantly, the category never-smoked was increasing. There were also race and ethnicity differences, with non-Hispanic whites more likely to smoke than blacks or Hispanics in 2007 ( Table 20-2 ).
| Cigarette Use | 1991 (95% CI) | 1993 (95% CI) | 1995 (95% CI) | 1997 (95% CI) | 1999 (95% CI) | 2001 (95% CI) | 2003 (95% CI) | 2005 (95% CI) | 2007 (95% CI) |
|---|---|---|---|---|---|---|---|---|---|
| Lifetime || | 70.1 (67.8-72.3) | 69.5 (68.1-70.8) | 71.3 (69.5-73.0) | 70.2 (68.2-72.1) | 70.4 (67.3-73.3) | 63.9 (61.6-66.0) | 58.4 (55.1-61.6) | 54.3 (51.2-57.3) | 50.3 (47.2-53.5) |
| Current ¶ | 27.5 (24.8-30.3) | 30.5 (28.6-32.4) | 34.8 (32.5-37.2) | 36.4 (34.1-38.7) | 34.8 (32.3-37.4) | 28.5 (26.4-30.6) | 21.9 (19.8-24.2) | 23.0 (20.7-25.5) | 20.0 (17.6-22.6) |
| Current frequent || | 12.7 (10.6-15.3) | 13.8 (12.1-15.5) | 16.1 (13.6-19.1) | 16.7 (14.8-18.7) | 16.8 (14.3-19.6) | 13.8 (12.3-15.5) | 9.7 (8.3-11.3) | 9.4 (7.9-11.0) | 8.1 (6.7-9.8) |
* Ever tried cigarette smoking, even one or two puffs.
† Smoked cigarettes on at least 1 day during the 30 days before the survey.
‡ Smoked cigarettes on 20 or more days during the 30 days before the survey.
§ Linear, quadratic, and cubic trend analyses were conducted with a logistic regression model controlling for sex, race/ethnicity, and grade. These prevalence estimates are not standardized by demographic variables.
|| Significant linear and quadratic effects only ( P <0.06).
¶ Significant linear, quadratic, and cubic effects ( P <0.05).
| Characteristic | 1991 (95% CI) | 1993 (95% CI) | 1995 (95% CI) | 1997 (95% CI) | 1999 (95% CI) | 2001 (95% CI) | 2003 (95% CI) | 2005 (95% CI) | 2007 (95% CI) |
|---|---|---|---|---|---|---|---|---|---|
| Sex | |||||||||
| Female ‡ | 27.3 (23.9-31.0) | 31.2 (29.1-33.4) | 34.3 (31.0-37.7) | 34.7 (31.8-37.6) | 34.9 (32.3-37.7) | 27.7 (25.6-30.0) | 21.9 (19.2-24.9) | 23.0 (20.4-25.8) | 18.7 (16.5-21.1) |
| Male ‡ | 27.6 (24.6-30.9) | 29.8 (27.4-32.3) | 35.4 (32.9-37.9) | 37.7 (35.0-40.6) | 34.7 (31.8-37.7) | 29.2 (26.7-32.0) | 21.8 (19.8-24.1) | 22.9 (20.7-25.3) | 21.3 (18.3-24.6) |
| Race/Ethnicity § | |||||||||
| White, non-Hispanic ‡ | 30.9 (27.6-34.5) | 33.7 (31.4-36.0) | 38.3 (35.6-41.1) | 39.7 (37.3-42.2) | 38.6 (35.5-41.9) | 31.9 (29.6-34.4) | 24.9 (22.4-27.5) | 25.9 (22.9-29.2) | 23.2 (20.4-26.2) |
| Female ‡ | 31.7 (27.1-36.7) | 35.3 (32.6-38.0) | 39.8 (36.3-43.5) | 39.9 (36.6-43.2) | 39.1 (35.4-42.9) | 31.2 (28.7-33.7) | 26.6 (22.9-30.5) | 27.0 (23.4-31.0) | 22.5 (19.6-25.7) |
| Male ‡ | 30.2 (26.5-34.3) | 32.2 (29.4-35.0) | 37.0 (33.7-40.5) | 39.6 (35.8-43.5) | 38.2 (34.6-41.8) | 32.7 (29.7-35.9) | 23.3 (20.7-26.0) | 24.9 (22.2-27.7) | 23.8 (20.2-27.8) |
| Black, non-Hispanic || | 12.6 (10.2-15.5) | 15.4 (12.9-18.2) | 19.1 (16.1-22.6) | 22.7 (19.0-26.8) | 19.7 (15.8-24.3) | 14.7 (12.0-17.9) | 15.1 (12.4-18.2) | 12.9 (11.1-14.8) | 11.6 (9.5-14.1) |
| Female ¶ | 11.3 (9.2-13.9) | 14.4 (11.9-17.4) | 12.2 (9.3-15.7) | 17.4 (13.8-21.7) | 17.7 (14.4-21.7) | 13.3 (10.1-17.2) | 10.8 (8.2-14.2) | 11.9 (10.2-13.8) | 8.4 (6.6-10.6) |
| Male || | 14.1 (10.1-19.4) | 16.3 (12.4-21.1) | 27.8 (22.5-33.9) | 28.2 (23.0-34.1) | 21.8 (15.4-29.9) | 16.3 (13.2-19.8) | 19.3 (15.8-23.5) | 14.0 (11.5-16.9) | 14.9 (11.7-18.8) |
| Hispanic ‡ | 25.3 (22.5-28.2) | 28.7 (25.8-31.8) | 34.0 (28.7-39.6) | 34.0 (31.3-36.9) | 32.7 (29.0-38.6) | 26.6 (22.4-31.2) | 18.4 (16.1-20.9) | 22.0 (18.7-25.8) | 16.7 (13.5-20.4) |
| Female ‡ | 22.9 (19.2-27.1) | 27.3 (23.5-31.5) | 32.9 (27.4-39.0) | 32.3 (28.6-36.2) | 31.5 (26.8-36.5) | 26.0 (22.3-30.0) | 17.7 (15.6-19.9) | 19.2 (16.4-22.5) | 14.6 (11.3-18.8) |
| Male ‡ | 27.8 (24.3-31.8) | 30.2 (26.7-33.8) | 34.9 (26.6-44.3) | 35.5 (31.9-39.2) | 34.0 (29.7-38.7) | 27.2 (20.6-35.0) | 19.1 (15.8-23.0) | 24.8 (20.0-30.4) | 18.7 (15.0-23.2) |
* Smoked cigarettes on at least 1 day during the 30 days before the survey.
† Linear, quadratic, and cubic trend analyses were conducted with a logistic regression model controlling for sex, race/ethnicity, and grade in school. These prevalence estimates are not standardized by demographic variables.
‡ Significant linear, quadratic, and cubic effects ( P <0.05).
§ Numbers for other racial/ethnic groups were too small for meaningful analysis.
|| Significant quadratic and cubic effects only ( P <0.05).
If the long-term health of the nation is to be improved, prevention of cigarette smoking initiation among youth is an essential element.
Prevalence and Trends Among Adults
Cigarette consumption per capita for individuals aged 18 years and older rose steadily from 1900 to the late 1960s. Since that time, it steadily declined through 2007. This pattern is the result of complementary trends including increased levels of smoking cessation and increasing rates of never-smokers. The National Health Interview Survey found that 42.4% of adults smoked in 1965 and 19.8% in 2007 ( Fig. 20-5 ). The proportion of never-smokers in 2008 was 57.6%, with former smokers (21.5%) exceeding current smokers (20.8%) ( Fig. 20-6 ). These national rates confirm a declining number of adult smokers during the past 40 years. Although rates nationally have decreased, there still exists significant variation by region of the country. In 2004, the percentage of adults who smoked ranged from a high of 28.3% in Kentucky to 11.7% in Utah, with an average of 20%.
Whereas cigarette smoking among adults has substantially declined, a sizable portion of the population is still addicted. One of the national health objectives for 2010 is to reduce the prevalence of cigarette smoking among adults to 12% or less. With smoking rates of 19.8% in 2007, that goal may not be met. Prevalence was lowest among Asians (9.6%) and Hispanics (13.3%) and highest among American Indians/Alaska Natives (36.4%). Non-Hispanic whites (21.4%) and blacks (19.8%) were similar. Adults who lived below the poverty level were more likely to smoke (28.8%) than were those at or above this level (20.3%). Persons with graduate or professional post-college degrees were far less likely to smoke (6.2%) than were those with less than a high-school education (33%) or a GED diploma (44%). Smoking prevalence was far lower in those 65 years and older (8.3%) than in the younger age groups.
Prevention and Intervention among Youth
School-Based Prevention Programs
Much of the effort in preventing smoking among youth has focused on the school setting. School-based prevention programs generally have been targeted at junior-high or middle-school children, when the habit begins. Unfortunately, school-based programming alone may have limited impact in the absence of active parental and community involvement. At one time, it was assumed that simply educating youths about the harmful effects of smoking would be sufficient to prevent them from initiating cigarette use. However, it became apparent that information alone was not sufficient to deter adolescents from beginning to smoke.
Social influence approaches have identified the social environment as a critical determinant of smoking onset. Rather than focusing on long-term disease risk, these interventions have stressed more immediate consequences of smoking, including negative social consequences. Adolescents are seen as often lacking in skills needed to resist peer pressure and other influences that promote smoking. As described in the 1994 Surgeon General’s report, the principal messages of successful skills-based interventions focus on the negative short-term social consequences of smoking, on the techniques of tobacco advertising that may be falsely appealing to adolescents, and on the socially salient advantages of being a nonsmoker.
Meta-analyses of school-based smoking prevention programs have indicated that these programs do have an impact on preventing smoking onset. Furthermore, social influence approaches appear to be the most effective type of school-based program. On the basis of the results of a meta-analysis, Rooney concluded that the best results were obtained by social influence programs that were delivered to sixth-grade students, included booster sessions, concentrated the program within a short time, and used a peer to present the program.
Glynn listed essential elements of effective smoking prevention programs based on a consensus panel. These elements were summarized in the 1994 report of the Surgeon General as follows:
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Classroom sessions should be delivered at least five times per year in each of two years in the sixth through eighth grades.
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Programs should emphasize the social factors that influence smoking onset, short-term consequences, and refusal skills.
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Programs should be incorporated into the existing school curricula.
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Programs should be introduced during the transition from elementary school to junior high or middle school (sixth or seventh grade).
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Students should be involved in the presentation and delivery of the program (peer teaching).
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Parental involvement should be sought.
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Teachers should be adequately trained.
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Programs should be socially and culturally acceptable to each community.
Although some of these points might appear self-evident (e.g., adequate training of teachers, social and cultural acceptability of programs), they are often overlooked in practice. Furthermore, high-risk populations, including those of low socioeconomic status and some ethnic minorities, present unique challenges as described by Sherman and Primack. These groups require added attention.
Müller-Riemenschneider and colleagues evaluated the long-term effectiveness of smoking prevention programs published from 2001 to 2006. In 35 studies with a follow-up period of 1 to 10 years, they found that most studies reported long-term beneficial effects. They noted that school-based programs alone were least effective but that the addition of community-based and multisectorial approaches to school programs was most effective.
Community-Based Prevention Programs
Several model prevention programs have actively involved parents and the larger community in addition to schools. One example is described by Perry and colleagues in the context of the Minnesota Heart Health Program, a research and demonstration project designed to reduce cardiovascular disease at the community level. Perry and colleagues hypothesized that school-based smoking prevention would be more effective in communities in which multiple complementary school and community programs were established. Students participated in 5 years of school-based health education including peer-led prevention in a context in which adults were actively involved in community smoking cessation programs, and smoking restrictions were implemented both in schools and in the larger community. Results were very encouraging, with smoking initiation significantly lower among students in the intervention community compared with students in the control community. These differences persisted throughout junior and senior high school. At the end of the twelfth grade, students in the intervention community evidenced 40% lower smoking prevalence than did students in the comparison community; 14.6% of students were weekly smokers at the end of high school compared with 24.1% in the reference community.
Other successful community interventions affecting youth include parental involvement, smoking restrictions (e.g., schools, restaurants), and limitation of access to cigarettes through legal restrictions and increased taxes.
State and Federal Prevention Initiatives
After the successful tobacco lawsuits and increases in cigarette taxes, many states operated comprehensive anti-tobacco programs. A major emphasis of these programs is on prevention of tobacco use in youth. Many of these initiatives include anti-tobacco media campaigns. Florida launched an aggressive media campaign that directly targeted the tobacco industry. After 2 years, current cigarette use dropped from 18.5% to 11.1% among middle-school students and from 27.4% to 22.6% among high-school students.
Flynn and coworkers found that a combination of media intervention and school-based programming fared better than school-based intervention alone. The media campaign included both radio and television spots that were broadcast as paid advertisements over local media. Reported smoking in the past week was 35% less among youth in the school-and-media condition than in the school-only condition (12.8% versus 19.8%).
Restrictions on smoking in public places including schools and on tobacco availability to minors also may reduce smoking prevalence, although findings are inconsistent. All 50 states and the District of Columbia adopted a minimum age of 18 years for the purchase of tobacco, but these laws are variably enforced.
Increased taxation also has an impact on adolescent smoking. Adolescents are more price sensitive than adults are. The impact of significantly higher prices may be even greater in discouraging initiation than in reducing consumption among existing smokers. Furthermore, revenue from these taxes can be dedicated to comprehensive tobacco control programs that will further reduce the onset of smoking in youth.
The Centers for Disease Control published Best Practices for Comprehensive Tobacco Control Programs in 1999 and updated this report in 2007. This document provides recommendations to the states for establishment of initiatives that include local community programs, chronic disease programs to reduce the burden of tobacco-related diseases, school interventions, enforcement, statewide programs, countermarketing, cessation methods, surveillance and evaluation, and administration and management. Recommended funding levels are given for each of these components. Local community programs can engage young people; school-based interventions can be linked with local community coalitions and statewide counteradvertising; enforcement can reduce access of minors; and statewide initiatives can provide skill, resources, and information for coordinated strategic implementation of community programs.
Cessation Among Youth
Most of the work done with youth has focused on prevention rather than on cessation of smoking. Many of the interventions demonstrated to be effective among adults have not achieved comparable success in adolescent populations.
A review examined the literature on smoking cessation in adolescents. The authors evaluated 34 cessation studies. Program content for these studies was derived from a wide range of theoretical perspectives. Most studies were conducted in school settings that reach less than half of the potential population of adolescent smokers. End of treatment quit rates reported in 12 of the 17 studies averaged 20.7% (range, 0% to 36%); abstinence at follow-up declined to 13%. The most successful programs generally included some type of cognitive-behavioral intervention, such as instruction in coping skills and a focus on the immediate consequences of quitting.
A recently released handbook on cessation for youth, I Quit! What to Do When You’re Sick of Smoking, Chewing, or Dipping, from the Centers for Disease Control and Prevention, provides helpful tips on quitting tobacco in this group. Strategies for youth are summarized in Box 20-1 .
