Reducing the Health Consequences of Smoking 25 YEARS OF PROGRESS a report of the Surgeon General 1989 Executive Summary ta, U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES a SERVIC ‘ > S- Public Health Service = 7 Centers for Disease Control = Center for Chronic Disease Prevention and Health Promotion “a, a: Office on Smoking and Health ervey. Rockville, Maryland 20857 Suggested Citation U.S. Department of Health and Human Services. Reducing the Health C. onsequen- ces of Smoking: 25 Years of Progress. A Report of the Surgeon General. US. Depart- ment of Health and Human Services, Public Health Service, Centers for Disease Con- trol, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. DHHS Publication No. (CDC) 89-8411, 1989. THE SECRETARY OF HEALTH AND HUMAN SERVICES WASHINGTON, D.C. 20201 DEC 29 1988 The Honorable Jim Wright Speaker of the House of Representatives Washington, D.C. 20515 Dear Mr. Speaker: It is my pleasure to transmit to the Congress the 1989 Surgeon General’s Report on the health consequences of smoking, as mandated by Section 8(a) of the Public Health Cigarette Smoking Act of 1969. The report was prepared by the Centers for Disease Control”s Office on Smoking and Health. This report, entitled Reducing the Health Consequences of Smoking: 25 Years of Progress, examines the fundamental developments over the past quarter century in smoking prevalence and in mortality caused by smoking. It highlights important gains in preventing smoking and smoking-related disease, reviews changes in programs and policies designed to reduce smoking, and emphasizes sources of continuing concern and remaining challenges. During the past 25 years, smoking behavior has changed dramatically. Nearly half of all living adults who ever smoked have quit. The prevalence of smoking has declined steadily, with a particularly impressive decline among men. Smoking prevalence among men decreased from 50 percent in 1965 to 32 percent in 1987. As a result, lung cancer mortality rates among men are now leveling off after many decades of consistent increase, Despite this progress, the prevalence of smoking remains higher among blacks, blue-collar workers, and less-educated persons, than in the overall population. Smoking among high school seniors leveled off from 1981 through 1987 after previous years of decline. In 1985, the last year for which estimates are available, approximately 390,000 Americans died as the result of past and current smoking. This represents more than one of every six deaths in the United States. Smoking remains the single most important preventable cause of death in our society. To maintain our momentum toward a smoke~free society, we must focus our efforts on preventing smoking initiation and encouraging smoking cessation among high-risk populations. Increased public information activities, smoking prevention and cessation programs, and policies that encourage nonsmoking behavior should be pursued. Unless we meet this challenge successfully, smoking-related mortality will remain high well into the 21st Century. Sincerely, Gee tee ee Otis R. Bowen, M.D. Secretary Enclosure THE SECRETARY OF HEALTH AND HUMAN SERVICES WASHINGTON, O.C. 20201 DFC 29 10RR The Honorable George Bush President of the Senate Washington, D.C. 20515 Dear Mr. President: It is my pleasure to transmit to the Congress the 1989 Surgeon General's Report on the health consequences of smoking, as mandated by Section 8(a) of the Public Health Cigarette Smoking Act of 1969. The report was prepared by the Centers for Disease Control's Office on Smoking and Health. This report, entitled Reducing the Health Consequences of Smoking: 25 Years of Progress, examines the fundamental developments over the past quarter century in smoking prevalence and in mortality caused by smoking. It highlights important gains in preventing smoking and smoking-related disease, reviews changes in programs and policies designed to reduce smoking, and emphasizes sources of continuing concern and remaining challenges. During the past 25 years, smoking behavior has changed dramatically. Nearly half of all living adults who ever smoked have quit. The prevalence of smoking has declined steadily, with a particularly impressive decline among men. Smoking prevalence among men decreased from 50 percent in 1965 to 32 percent in 1987. As a result, lung cancer mortality rates among men are now leveling off after many decades of consistent increase. Despite this progress, the prevalence of smoking remains higher among blacks, blue-collar workers, and less-educated persons, than in the overall population. Smoking among high school seniors leveled off from 1981 through 1987 after previous years of decline. In 1985, the last year for which estimates are available, approximately 390,000 Americans died as the result of past and current smoking. This represents more than one of every six deaths in the United States, Smoking remains the single most important preventable cause of death in our society. To maintain our momentum toward a smoke-free society, we must focus our efforts on preventing smoking initiation and encouraging smoking cessation among high-risk populations. Increased public information activities, smoking prevention and cessation programs, and policies that encourage nonsmoking behavior should be pursued. Unless we meet this challenge successfully, smoking-related mortality will remain high well into the 21st Century. Sincerely, | ee 4x Otis R. Bowen, M.D. Secretary Enclosure FOREWORD Twenty-five years have elapsed since publication of the landmark report of the Sur- geon General's Advisory Committee on Smoking and Health. By any measure, these 25 years have witnessed dramatic changes in attitudes toward and use of tobacco in the United States. The health consequences of tobacco use will be with us for many years to come, but those consequences have been greatly reduced by the social revolution that has occurred during this period with regard to smoking. Since 1964, substantial changes have occurred in scientific knowledge of the health hazards of smoking, in the impact of smoking on mortality, in public knowledge of the dangers of smoking, in the prevalence of smoking and using other forms of tobacco, in the availability of programs to help smokers quit, and in the number of policies that en- courage nonsmoking behavior and protect nonsmokers from exposure to environmen- tal tobacco smoke. These changes and other significant developments, as well as the overall impact of the Nation's antismoking activities, are reviewed in detail in the in- dividual chapters of this Report. Based on this review, five major conclusions of the entire Report were reached. The first two conclusions highlight important gains in preventing smoking and smoking-related disease in the United States. The last three conclusions emphasize sources of continuing concern and remaining challenges. The conclusions are: 1. The prevalence of smoking among adults decreased from 40 percent in 1965 to 29 percent in 1987. Nearly half of all living adults who ever smoked have quit. 2. Between 1964 and 1985, approximately three-quarters of a million smok- ing-related deaths were avoided or postponed as a result of decisions to quit smoking or not to start. Each of these avoided or postponed deaths repre- sented an average gain in life expectancy of two decades. 3. The prevalence of smoking remains higher among blacks, blue-collar workers, and less educated persons than in the overall population. The, decline in smoking has been substantially slower among women than among men. 4. Smoking begins primarily during childhood and adolescence. The age of initiation has fallen over time, particularly among females. Smoking among high school seniors leveled off from 1980 through 1987 after pre- vious years of decline. 5. Smoking is responsible for more than one of every six deaths in the United States. Smoking remains the single most important preventable cause of death in our society. The last 25 years have witnessed phenomenal changes in the way Americans think about tobacco use. More people now than ever before consider smoking to be outside the social norm. Antismoking programs and policies have contributed to this change. This shift in societal attitudes is almost certain to generate additional efforts to further limit the use of tobacco. Almost half of all living Americans who ever smoked have quit. This is especially remarkable when one takes into account the powerful media images enticing people to smoke and the powerfully addictive nature of nicotine. As the downward trends in smoking behavior continue, we can expect to see a decline in the number of premature deaths and avoidable morbidity due to smoking. For now, however, we must recognize that continued tobacco exposure in the popula- tion will cause a great deal of human suffering for many decades. Thus, we must not rest upon the laurels of the past quarter century. As long as children and adolescents continue to find reasons to use tobacco, replacements will be recruited for at least some of the smokers who quit or who die prematurely. If current trends continue, these re- placements will be found disproportionately among minority groups, among the less educated, among the most economically disadvantaged, and among women. We must look back on the last 25 years of change in order to look forward to our tasks for the future. Surely those tasks include expanding educational efforts for the young and old alike, restrictions against minors’ access to tobacco, support for cessa- tion activities, and restrictions against smoking in worksites, restaurants, transportation vehicles, and other public places. The Public Health Service is dedicated to continuing the legacy of the 1964 Report. We hope this 25th Anniversary Report will stimulate new commitment to action by public health officials, civic leaders, educators, scientists, and the public at large on the problem of tobacco use, especially among children, adolescents, and high-risk groups. Robert E. Windom, M.D. James O. Mason, M.D., Dr.P.H. Assistant Secretary for Health Director Public Health Service Centers for Disease Control PREFACE Exactly 25 years ago, on January 11, 1964, Luther L. Terry, M.D., Surgeon General of the U.S. Public Health Service, released the report of the Surgeon General’s Ad- visory Committee on Smoking and Health. That landmark document, now referred to as the first Surgeon General’s Report on Smoking and Health, was America’s first wide- ly publicized official recognition that cigarette smoking is a cause of cancer and other serious diseases. On the basis of more than 7,000 articles relating to smoking and disease already avail- able at that time in the biomedical literature, the Advisory Committee concluded that cigarette smoking is a cause of lung cancer and laryngeal cancer in men, a probable cause of lung cancer in women, and the most important cause of chronic bronchitis. The Committee stated that “Cigarette smoking is a health hazard of sufficient impor- tance in the United States to warrant appropriate remedial action.” What would constitute “appropriate remedial action” was left unspecified. But the release of the report was the first in a series of steps, still being taken 25 years later, to diminish the impact of tobacco use on the health of the American people. This 1989 Report, the 20th in a series of Surgeon General’s Reports on the Health Consequences of Smoking, spells out the dramatic progress that has been achieved in the past quarter century against one of our deadliest risks. The circumstances surrounding the release of the first report in 1964 are worth remembering. The date chosen was a Saturday morning, to guard against a precipitous Teaction on Wail Street. An auditorium in the State Department was selected because its security could be assured—it had been the site for press conferences of the late Presi- dent John F. Kennedy, whose assassination had occurred less than 2 months earlier. The first two copies of the 387-page, brown-covered Report were hand delivered to the West Wing of the White House at 7:30 on that Saturday moming. At 9:00, ac- credited press representatives were admitted to the auditorium and “locked in,” without access to telephones. Surgeon General Terry and his Advisory Committee took their seats on the platform. The Report was distributed and reporters were allowed 90 minutes to read it. Questions were answered by Dr. Terry and his Committee mem- bers. Finally, the doors were opened and the news was spread. For several days, the Report furnished newspaper headlines across the country and lead stories on television newscasts. Later it was ranked among the top news stories of 1964. During the quarter century that has elapsed since that Report, individual citizens, private organizations, public agencies, and elected officials have tirelessly pursued the Advisory Committee’s call for “appropriate remedial action.” Early on, the U.S. Con- gress adopted the Federal Cigarette Labeling and Advertising Act of 1965 and the ill Public Health Cigarette Smoking Act of 1969. These laws required a health warning on cigarette packages, banned cigarette advertising in the broadcast media, and called for an annual report on the health consequences of smoking. In 1964, the Public Health Service established a smail unit called the National Clearinghouse for Smoking and Health (NCSH). Through the years, the Clearinghouse and its successor organization, the Office on Smoking and Health, have been respon- sible for the 20 reports on the health consequences of smoking previously mentioned, eight of which have been issued during my tenure as Surgeon General. In close coopera- tion with voluntary health organizations, the Public Health Service has supported high- ly successful school and community programs on smoking and health, has disseminated research findings related to tobacco use, and has ensured the continued public visibility of antismoking messages. Throughout this period, tremendous changes have occurred. As detailed in this Report, we have witnessed expansion in scientific knowledge of the health hazards of smoking, growing public knowledge of the dangers of smoking, increased availability of programs to prevent young people from starting to smoke and to help smokers quit, and widespread adoption of policies that discourage the use of tobacco. Most important, these developments have changed the way in which our society views smoking. In the 1940s and 1950s, smoking was chic; now, increasingly, it is shunned. Movie stars, sports heroes, and other celebrities used to appear in cigarette advertisements. Today, actors, athletes, public figures, and political candidates are rarely seen smoking. The ashtray is following the spittoon into oblivion. Within this evolving social milieu, the population has been giving up smoking in in- creasing numbers. Nearly half of all living adults who ever smoked have quit. The most impressive decline in smoking has occurred among men. Smoking prevalence among men has fallen from SO percent in 1965 to 32 percent in 1987. These changes represent nothing less than a revolution in behavior. The antismoking campaign has been a major public health success. Those who have participated in this campaign can take tremendous pride in the progress that has been made. The analysis in this Report shows that in the absence of the campaign, there would have been 91 million American smokers (15 to 84 years of age) in 1985 instead of 56 million. As a result of decisions to quit smoking or not to start, an estimated 789,000 smoking-related deaths were avoided or postponed between 1964 and 1985. Further- more, these decisions will result in the avoidance or postponement of an estimated 2.1 million smoking-related deaths between 1986 and the year 2000. This achievement has few parallels in the history of public health. It was ac- complished despite the addictive nature of tobacco and the powerful economic forces promoting its use. The Remaining Challenges Despite this achievement, smoking will continue as the leading cause of preventable, premature death for many years to come, even if all smokers were to quit today. Smok- ing cessation is clearly beneficial in reducing the risk of dying from smoking-related iv diseases. However, for some diseases, such as lung cancer and emphysema, quitting may not reduce the risk to the level of a lifetime nonsmoker even after many years of abstinence. This residual health risk is one reason why approximately 390,000 Americans died in 1985 as the result of smoking, even after two decades of declining smoking rates. The critical message here is that progress in curtailing smoking must continue, and ideally accelerate, to enable us to turn smoking-related mortality around. Otherwise, the disease impact of smoking will remain high well into the 21st century. Just maintaining the current rate of progress is a challenge. Compared with non- smokers, smokers are disproportionately found in groups that are harder to reach, and this disparity may increase over time. Greater effort and resources will need to be devoted to achieve equivalent reductions in smoking among those whose behavior has survived strong, countervailing social pressures. Today, thanks to the remarkable progress of the past 25 years, we can dare to en- vision a smoke-free society. Indeed it can be said that the social tide is flowing toward that bold objective. To maintain momentum, we need to direct special attention to the following groups within our society: Children and Adolescents As a pediatric surgeon, and now as Surgeon General, I have dedicated my career to protecting the health of children. In the case of smoking, children and adolescents hold the key to progress toward curbing tobacco use in future generations. If the adult rate of smoking were to continue at the present level, the impact of smok- ing on the future health and welfare of today’s children would be enormous. Research has shown that one-fourth or more of all regular cigarette smokers die of smoking-re- lated diseases. If 20 million of the 70 million children now living in the United States smoke cigarettes as adults (about 29 percent), then at least 5 million of them wiil die of smoking-related diseases. This figure should alarm anyone who is concerned with the future health of today’s children. Two additional factors make smoking among young people a preeminent public health concern: (1) the age of initiation of smoking, and (2) nicotine addiction. As this Report shows, four-fifths of smokers born since 1935 started smoking before age 21. The proportion of smokers who begin smoking during adolescence has been increas- ing over time, particularly among women. In the Teenage Smoking Survey conducted by the Department of Health, Education, and Welfare in 1979, respondents were asked, “What would you say is the possibility that five years from now you will be a cigarette smoker?” Among smokers, half answered “definitely not” or “probably not.” This response suggests that many children and adolescents are unaware of, or underestimate, the addictive nature of smoking. The predecessor to this volume, The Health Consequences of Smoking: Nicotine Addiction, Provided a comprehensive review of the evidence that cigarettes and other forms of tobacco are addicting and that nicotine is the drug in tobacco that causes addiction. These two factors refute the argument that smoking is a matter of free choice. Most smokers start smoking as teenagers and then become addicted. By the time smokers become adults, when they would be expected to have greater appreciation of the health effects of smoking, many have difficulty quitting. Today, 80 percent of smokers say they would like to quit; two-thirds of smokers have made at least one serious attempt to quit. Characteristically, people quit smoking several times before becoming per- manent ex-smokers. The prevalence of daily smoking among high school seniors leveled off from 1981] through 1987, at about 20 percent, after previous years of decline. Each day, more than 3,000 American teenagers start smoking. If we can substantially reduce this number, we will soon achieve a major impact on smoking prevalence among adults. Although research efforts in prevention are increasing, prevention programs are not yet reaching large numbers of young people. The public health community should pay at least as much attention to the prevention of smoking among teenagers as it now pays to smok- ing cessation among adults. Comprehensive school health education, incorporating tobacco use prevention, should be provided in every school throughout the country. Women Since release of the first Surgeon General’s Report, the prevalence of smoking among women has declined much more slowly than among men. If current trends continue, smoking rates will be about equal among men and women in the mid- 1990s, after which women may smoke at a higher rate than men. The public health impact of this trend is already being seen. Lung cancer mortality rates are increasing steadily among women, and estimates by the American Cancer Society indicate that this disease has now overtaken breast cancer as the number one cause of cancer death among women. Smoking during pregnancy poses special risks to the developing fetus and is an important cause of low birthweight and infant mor- tality. Smoking and oral contraceptive use interact to increase dramatically the risk of cardiovascular disease. Women’s organizations and women’s magazines have paid scant attention to these issues. The key to addressing this problem is the prevention of smoking among female adolescents. The disparity in smoking prevalence between men and women is primari- ly a reflection of differences in smoking initiation. Smoking initiation has declined much more slowly among females than among males. This difference is due, in large part, to increasing initiation rates among less educated young women. Among high school seniors, the prevalence of daily smoking has been higher among females than among males each year since 1977. In summary, women, and especially female adolescents not planning higher educa- tion, are an important target group for prevention activities. Minorities Smoking rates are higher in certain racial and ethnic minority groups, many of which already suffer from a disproportionate share of risk factors and illness. In particular, smoking prevalence has been consistently higher among black men than among white vi men (41 and 31 percent, respectively, in 1987). In addition, the limited data available show higher rates of smoking among Hispanic men than among white men. Trends in smoking initiation, prevalence, and quitting among blacks and whites show similar rates of change from 1974 to 1985. Thus, the gap in smoking prevalence be- tween blacks and whites is not widening. However, to reduce the gap in smoking be- tween blacks and whites, prevention efforts must focus on blacks more successfully. The public health community is only now beginning to address this problem. The ur- gency of the situation is greater because cigarette companies are increasingly targeting their marketing efforts at blacks and Hispanics. Blue-Collar Workers The prevalence of smoking has been consistently higher among blue-collar workers than among white-collar workers. In 1985, 40 percent of blue-collar workers smoked compared with 28 percent of white-collar workers. Again, blue-collar workers are a major target of cigarette company advertising and promotional campaigns. Worksite smoking cessation programs, employee incentive programs, and policies banning or restricting smoking at the workplace are effective strategies to reach this group. Toward a Smoke-Free Future Because the genera! health risks of smoking are well known, because smoking is banned or restricted in a growing number of public places and worksites, and because smoking is losing its social acceptability, the overall prevalence of smoking in our society is likely to continue to decline. The progress we have achieved during the past quarter century is impressive. Equally impressive, however, are the challenges we face. During the next quarter century and beyond, progress will be slow, and smoking-related mortality will remain high, unless the health community more effectively reaches children and adolescents, women, minorities, and blue-collar workers. Organizations that represent these groups can contribute substantially to the antismoking movement. In large part, the future health of these populations will depend on the degree to which schools, educators, parents’ organizations, women’s groups, minority organizations, employers, and employee unions join the campaign for a smoke-free society. Here in the United States, such a society is an attainable long-term goal. Unfortunately, the looming epidemic of smoking and smoking-related disease in developing countries does not encourage similar optimism. According to the World Health Organization, increases in cigarette consumption between 1971 and 1981 ex- ceeded population growth in all developing regions: by 77 percent in Africa, and by 30 percent in Asia and Latin America. The topic of tobacco and health internationally, although critically important, espe- cially for developing nations, is beyond the scope of this Report. I can only hope that vii the lessons we have leamed in the United States, as detailed in this Report, will help other countries take the necessary steps to avoid the devastation caused by use of tobacco. C. Everett Koop, M.D., Sc.D. Surgeon General vill ACKNOWLEDGMENTS This Report was prepared by the Department of Health and Human Services under the general editorship of the Office on Smoking and Health, Ronald M. Davis, M.D., Director. The Managing Editors were Susan A. Hawk, Ed.M., M.S., and Thomas E. Novotny, M.D., Office on Smoking and Health. The scientific editors of the Report were: Kenneth E. Warner, Ph.D. (Senior Scientific Editor), Professor, Department of Public Health Policy and Administration, School of Public Health, University of Michigan, Ann Arbor, Michigan Ronald M. Davis, M.D., Director, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland John H. Holbrook, M.D., Professor of Internal Medicine, Department of Internal Medicine, University Hospital, Salt Lake City, Utah Thomas E. Novotny, M.D., Medical Epidemiologist, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland Judith K. Ockene, Ph.D., Associate Professor of Medicine, and Director, Division of Preventive and Behavioral Medicine, Department of Medicine, University of Mas- sachusetts Medical School, Worcester, Massachusetts Nancy A. Rigotti, M.D., Associate Director, Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts, Instructor in Medicine, Harvard Medical School, Bos- ton, Massachusetts The following individuals prepared draft chapters or portions of the Report. Elvin E. Adams, M.D., M.P.H., Associate Director, Health Department, General Con- ference of Seventh-Day Adventists, Washington, D.C. Gregory N. Connolly, D.M.D., M.P.H., Director, Office for Nonsmoking and Health, Massachusetts Department of Public Health, Boston, Massachusetts K. Michael Cummings, Ph.D., M.P.H., Director, Smoking Control Program, Roswell Park Memorial Institute, Buffalo, New York ix Ronald M. Davis, M.D., Director, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland Joseph R. DiFranza, M.D., Director of Research, Fitchburg Family Practice Residen- cy Program, University of Massachusetts Medical Center, Fitchburg, Massachusetts Michael P. Eriksen, Sc.D., Director, Behavioral Research Program, Department of Can- cer Prevention and Control, The University of Texas M.D. Anderson Cancer Center, Houston, Texas David P. Fan, Ph.D., Professor of Genetics and Cell Biology, University of Minnesota, St. Paul, Minnesota Michael C. Fiore, M.D., M.P.H., Assistant Professor, Department of Medicine, Center for Health Sciences, University of Wisconsin, Madison, Wisconsin Edwin B. Fisher, Jr., Ph.D., Associate Professor of Psychology, Director, Center for Health Behavior Research, Washington University, St. Louis, Missouri Jeffrey E. Harris, M.D., Ph.D., Visiting Associate Professor, Department of Biostatis- tics, Harvard School of Public Health, Boston, Massachusetts; Clinical Associate, Medical Services, Massachusetts General Hospital, Boston, Massachusetts; As- sociate Professor of Economics, Massachusetts Institute of Technology, Cambridge, Massachusetts Jan L. Hitchcock, Ph.D., Associate Director, Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Thomas A. Hodgson, Ph.D., Chief Economist, Office of Analysis and Epidemiology, National Center for Health Statistics, Hyattsville, Maryland Dietrich Hoffmann, Ph.D., Associate Director, Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, New York Ilse Hoffmann, Research Coordinator, Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, New York Juliette S. Kendrick, M.D., Deputy Chief, Pregnancy Epidemiology Branch, Division of Reproductive Health, Center for Chronic Disease Prevention and Health Promo- tion, Centers for Disease Control, Atlanta, Georgia Lewis H. Kuller, M.D., Dr.P.H., Professor and Chairperson, Department of Epidemiol- ogy, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsyl- vania Eugene M. Lewit, Ph.D., Associate Professor, Departments of Medicine and Preven- tive Medicine and Community Health, Office of Primary Health Care Education, UMDNJ—New Jersey Medical School, Newark, New Jersey Edward Lichtenstein, Ph.D., Research Scientist, Oregon Research Institute; Professor of Psychology, University of Oregon, Eugene, Oregon Thomas E. Novotny, M.D., Medical Epidemiologist, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland Judith K. Ockene, Ph.D., Associate Professor of Medicine, and Director, Division of Preventive and Behavioral Medicine, Department of Medicine, University of Mas- sachusetts Medical School, Worcester, Massachusetts Chris Leo Pashos, M.P.P., Project Coordinator, Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Richard Peto, M.A., M.Sc., ICRF Cancer Studies Unit, Radcliffe Infirmary, Oxford, England John P. Pierce, M.Sc., Ph.D., Chief, Epidemiology Branch, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland John M. Pinney, Executive Director, Institute for the Study of Smoking Behavior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Edward T. Popper, M.B.A., D.B.A., Associate Professor of Marketing, Bryant College, Smithfield, Rhode Island Patrick L. Remington, M.D., M.P.H., Medical Epidemiologist, Bureau of Community Health and Prevention, Wisconsin Division of Health, Madison, Wisconsin Nancy A. Rigotti, M.D., Associate Director, Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts, and Instructor in Medicine, Harvard Medical School, Boston, Massachusetts Jonathan M. Samet, M.D., Professor of Medicine, Department of Medicine, Chief, Pul- monary Division, University of New Mexico, Albuquerque, New Mexico Russell C. Sciandra, M.A., Associate Director, Smoking Control Program, Roswell Park Memorial Institute, Buffalo, New York Carol Anne Soltanek, M.D., Resident, Southwestem Michigan Area Health Education Center, Kalamazoo, Michigan Michael A. Stoto, Ph.D., Senior Staff Officer, Institute of Medicine, National Academy of Sciences, Washington, D.C. Owen T. Thornberry, Ph.D., Director, Division of Health Interview Statistics, Nation- al Center for Health Statistics, Centers for Disease Control, Hyattsville, Maryland Kenneth E. Warner, Ph.D., Professor, Department of Public Health Policy and Ad- ministration, School of Public Health, University of Michigan, Ann Arbor, Michigan The editors acknowledge with gratitude the following distinguished scientists, physicians, and others who lent their support in the development of this Report by coor- dinating manuscript preparation, contributing critical reviews, or assisting in other ways. Elvin E. Adams, M.D., M.P.H., Associate Director, Health Department, General Con- ference of Seventh-Day Adventists, Washington, D.C. Charles Althafer, M.P.H., Assistant Director for Health Promotion and Risk Appraisal, Office of Program Planning and Evaluation, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia Lynn M. Artz, M.D., M.P.H., Senior Policy Advisor, Office of Disease Prevention and Health Promotion, Office of the Assistant Secretary for Health, Washington, D.C. xi Donald A. Berreth, Director, Office of Public Affairs, Centers for Disease Control, At- lanta, Georgia Gayle M. Boyd, Ph.D., Program Director, Smoking, Tobacco and Cancer Program, Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland Allan Brandt, Ph.D., Department of Social Medicine and Health Policy, Harvard Medi- cal School, Boston, Massachusetts Lester Breslow, M.D., M.P.H., Professor, School of Public Health, and Director, Health Services Research, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, California Clarice Brown, M.S., Data Analyst, Office of Prevention, Education, and Control, Na- tional Heart, Lung, and Blood Institute, Bethesda, Maryland David P. Brown, M.D., Deputy Director, Division of Surveillance, Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia Martin Brown, Ph.D., Surveillance and Operations Research Branch, Division of Can- cer Prevention and Control, National Cancer Institute, Bethesda, Maryland David M. Burns, M.D., Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, San Diego Medical Center, San Diego, California Dee Burton, Ph.D., Assistant Professor, Prevention Research Center, School of Public Health, University of Illinois at Chicago, Chicago, Illinois Frank J. Chaloupka, Ph.D., Assistant Professor, Department of Economics, College of Business Administration, University of Illinois at Chicago, Chicago, Illinois Paul D. Cleary, Ph.D., Department of Health Care Policy and The Division on Aging, Harvard Medical School, Boston, Massachusetts Alexander Cohen, Ph.D., Deputy Director, Division of Biomedical and Behavioral Science, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia Joel B. Cohen, Ph.D., Distinguished Service Professor and Director, Center for Con- sumer Research, University of Florida, Gainesville, Florida Michael J. Cowell, F.S.A., Vice President and Corporate Actuary, UNUM Life In- surance Company, Portland, Maine Joseph W. Cullen, Ph.D., Deputy Director, Division of Cancer Prevention and Control, National Cancer Institute, Coordinator for the National Cancer Institute’s Smoking, Tobacco and Cancer Program, Bethesda, Maryland Sir Richard Doll, Emeritus Professor of Medicine, University of Oxford, Acting Direc- tor, Imperial Cancer Research Fund, Cancer Epidemiology and Clinical Trials Unit, Oxford, England J. David Erickson, D.D.S., Ph.D., Chief, Birth Defects and Genetic Diseases Branch, Division of Birth Defects and Developmental Disabilities, Center for Environmental Health and Injury Control, Centers for Disease Control, Atlanta, Georgia Michael P. Eriksen, Sc.D., Director, Behavioral Research Program, Department of Can- cer Prevention and Control, University of Texas M.D. Anderson Cancer Center, Houston, Texas xii Virginia L. Ernster, Ph.D., Professor of Epidemiology, Department of Epidemiology and International Health, School of Medicine, University of California, San Francis- co, California Roberta G. Ferrence, Ph.D., Prevention Studies Department, Addiction Research Foun- dation, Toronto, Ontario, Canada Jonathan E. Fielding, M.D., M.P.H., Professor of Public Health and Pediatrics, Univer- sity of California at Los Angeles, Los Angeles, California, Vice President and Health Director, Johnson and Johnson Health Management, Inc., Santa Monica, California John R. Finnegan, Jr., Ph.D., Assistant Professor, School of Public Health, University of Minnesota, Minneapolis, Minnesota Martin Fishbein, Ph.D., Professor of Psychology and Research Professor, Institute of Communications Research, University of Illinois, Champaign—Urbana, Illinois Brian R. Flay, D.Phil., Associate Professor and Director, Prevention Research Center, School of Public Health, University of Illinois at Chicago, Chicago, Illinois William H. Foege, M.D., M.P.H., Executive Director, The Carter Center, Emory University, Atlanta, Georgia Peter L. Frommer, M.D., Deputy Director, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland Lawrence Garfinkel, M.A., Vice President for Epidemiology and Statistics, Director, Cancer Prevention, American Cancer Society, New York, New York Donald W. Gamer, J.D., Professor of Law, Souther Illinois University School of Law, Carbondale, Illinois Russell E. Glasgow, Ph.D., Research Scientist, Oregon Research Institute, Eugene, Oregon Thomas J. Glynn, Ph.D., Program Director for Smoking Research, Smoking, Tobacco, and Cancer Program, National Cancer Institute, Bethesda, Maryland Frederick K. Goodwin, M.D., Administrator, Alcohol, Drug Abuse, and Mental Health Administration, Rockville, Maryland Nancy P. Gordon, Sc.D., Behavioral Scientist, Division of Research, Northern Califor- nia Kaiser Permanente Medical Care Program Leonard Green, Ph.D., Professor of Psychology, Department of Psychology, Washington University, St. Louis, Missouri Ellen R. Gritz, Ph.D., Director, Division of Cancer Control, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles, California Neil E. Grunberg, Ph.D., Associate Professor, Department of Medical Psychology, Uniformed Services University of the Health Sciences, Bethesda, Maryland Dudley H. Hafner, Executive Vice President, American Heart Association, Dallas, Texas James A. Harrell, M.A., Acting Director, Office of Disease Prevention and Health Promotion, Office of the Assistant Secretary for Health, Washington, D.C. Jeffrey E. Harris, M.D., Ph.D., Visiting Associate Professor, Department of Biostatis- tics, Harvard School of Public Health, Boston, Massachusetts; Clinical Associate, Medical Services, Massachusetts General Hospital, Boston, Massachusetts; As- sociate Professor of Economics, Massachusetts Institute of Technology, Cambridge, Massachusetts xiii Jack E. Henningfield, Ph.D., Chief, Biology of Dependence and Abuse Potential As- sessment Laboratory, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland Carol J. Hogue, Ph.D., Director, Division of Reproductive Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Elvin Hilyer, Associate Director for Policy Coordination, Centers for Disease Control, Atlanta, Georgia Richard Jessor, Ph.D., Professor of Psychology, Director of the Institute of Behavioral Science, University of Colorado at Boulder, Boulder, Colorado Lloyd D. Johnston, Ph.D., Program Director, Institute for Social Research, University of Michigan, Ann Arbor, Michigan John T. Kalberer, Jr., Ph.D., Deputy Director, Division of Disease Prevention, Office of Disease Prevention, Office of the Director, National Institutes of Health, Bethes- da, Maryland Martha F. Katz, M.P.A., Director, Office‘of Program Planning and Evaluation, Centers for Disease Control, Atlanta, Georgia John H. Kelso, Acting Administrator, Health Resources and Services Administration, Rockville, Maryland Larry Kessler, Sc.D., Surveillance and Operations Research Branch, National Cancer Institute, Bethesda, Maryland A. Joan Klebba, M.A., Statistician, Division of Vital Statistics, National Center for Health Statistics, Centers for Disease Control, Hyattsville, Maryland Lloyd J. Kolbe, Ph.D., Acting Director, Division of Adolescent and School Health, Cen- ter for Chronic Disease Prevention and Health Promotion, Centers for Disease Con- trol, Atlanta, Georgia Jeffrey P. Koplan, M.D., M.P.H., Director, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Lynn T. Kozlowski, Ph.D., Head, Behavioral Research on Tobacco Use, Addiction Re- search Foundation, Toronto, Ontario, Canada Marshall W. Kreuter, Ph.D., Director, Division of Chronic Disease Control and Com- munity Intervention, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Harry A. Lando, Ph.D., Associate Professor, Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota Charles A. LeMaistre, M.D., President, University of Texas M.D. Anderson Cancer Center, Houston, Texas Claude Lenfant, M.D., Director, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland Eugene M. Lewit, Ph.D., Associate Professor, Departments of Medicine and Preven- tive Medicine and Community Health, Office of Primary Health Care Education, UMDNJ—New Jersey Medical School, Newark, New Jersey Bryan R. Luce, M.B.A., Ph.D., Battelle Human Affairs Research Center, Washington, D.C. xiv Dolores M. Malvitz, Dr.P.H., Dental Disease Prevention Activity, Center for Preven- tion Services, Centers for Disease Control, Atlanta, Georgia Alfred C. Marcus, Ph.D., Associate Director, Division of Cancer Control, Jonsson Com- prehensive Cancer Center, University of California at Los Angeles, Los Angeles, California James S. Marks, M.D., M.P.H., Deputy Director for Public Health Practice, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, At- lanta, Georgia James O. Mason, M.D., Dr.P.H., Director, Centers for Disease Control, Atlanta, Geor- gia Robin J. Mermelstein, Ph.D., Assistant Professor, Prevention Research Center, School of Public Health, University of Illinois at Chicago, Chicago, Illinois Dannie C. Middleton, M.D., Medical Officer, Document Development Branch, Division of Standards Development and Technology Transfer, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia Gregory J. Morosco, Ph.D., M.P.H., Coordinator, National Heart, Lung, and Blood Institute’s Smoking Education Program, National Institutes of Health, Bethesda, Maryland Joseph P. Mulholland, Ph.D., Bureau of Economics, Federal Trade Commission, Washington, D.C. Hillary Murt, M.P.H., Research Associate, Department of Health Services Management and Policy, School of Public Health, University of Michigan, Ann Arbor, Michigan Herbert W. Nickens, M.D., M.A., Director, Office of Minority Health, Public Health Service, Washington, D.C. Richard W. Niemeier, Ph.D., Acting Director, Division of Standards Development and Technology Transfer, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia Stuart L. Nightingale, M.D., Associate Commissioner for Health Affairs, Food and Drug Administration, Rockville, Maryland Ira S. Ockene, M.D., Professor of Medicine; Director, Preventive Cardiology, Division of Cardiovascular Medicine, University of Massachusetts Medical School, Wor- cester, Massachusetts Horace G. Ogden, Consultant, Gaithersburg, Maryland Patrick M. O’Malley, Ph.D., Associate Research Scientist, Institute for Social Research, University of Michigan, Ann Arbor, Michigan Mario A. Orlandi, Ph.D., M.P.H., Chief, Division of Health Promotion Research, American Health Foundation, New York, New York Carole Tracy Orleans, Ph.D., Senior Investigator, Behavioral Medicine and Director of Smoking Cessation Services, Fox Chase Cancer Center, Philadelphia, Pennsylvania Gerry Oster, Ph.D., Vice President, Policy Analysis, Inc., Brookline, Massachusetts Clifford H. Patrick, Ph.D., Senior Public Health Advisor, Office of Minority Health, Washington, D.C. Cheryl L. Perry, Ph.D., Associate Professor, Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota Michael Pertschuck, J.D., Co-director, Advocacy Institute, Washington, D.C. XV Edward L. Petsonk, M.D., Senior Medical Officer, Clinical Investigations Branch, Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control, Atlanta, Georgia John P. Pierce, M.Sc., Ph.D., Chief, Epidemiology Branch, Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland John M. Pinney, Executive Director, Institute for the Study of Smoking Behavior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Edward T. Popper, M.B.A., D.B.A., Associate Professor of Marketing, Bryant College, Smithfield, Rhode Island William F. Raub, M.D., Deputy Director, National Institutes of Health, Bethesda, Maryland Dorothy P. Rice, B.A., Sc.D.(Hon.), Professor in Residence, Department of Social and Behavioral Sciences, School of Nursing, University of California, San Francisco, San Francisco, California ; Lynn Gloeckler Ries, M.S., Division of Cancer Prevention and Control, Surveillance and Operations Research Branch, National Cancer Institute, Bethesda, Maryland Ruth Roemer, J.D., Adjunct Professor of Health Law, School of Public Health, Univer- sity of California at Los Angeles, Los Angeles, California; Past President, American Public Health Association Kenneth J. Rothman, Dr.P.H., Professor of Family and Community Health, University of Massachusetts Medical School, Worcester, Massachusetts Jonathan M. Samet, M.D., Professor of Medicine, Department of Medicine; Chief, Pul- monary Division, University of New Mexico, Albuquerque, New Mexico Thomas C. Schelling, Ph.D., Lucius N. Littauer Professor of Political Economy, Direc- tor, Institute for the Study of Smoking Behavior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Marvin A. Schneiderman, Ph.D., National Academy of Sciences, National Research Council, Board on Environmental Studies and Toxicology, Washington, D.C. David Schottenfeld, M.D., M.Sc., John G. Searle Professor and Chairman, Department of Epidemiology, School of Public Health, Professor of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, Michigan Lowell E. Sever, Ph.D., Assistant Director for Science, Division of Birth Defects and Developmental Disabilities, Center for Environmental Health and Injury Control, Centers for Disease Control, Atlanta, Georgia Saul Shiffman, Ph.D., Associate Professor, Department of Psychology; Director, Psychology Clinic, University of Pittsburgh, Pittsburgh, Pennsylvania Donald R. Shopland, Public Health Advisor, Smoking, Tobacco, and Cancer Program, Office of the Director, Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland John Slade, M.D., Department of Medicine, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey Jesse L. Steinfeld, M.D., former Surgeon General, Public Health Service, San Diego, California xvi Steven D. Stellman, Ph.D., Assistant Commissioner for Biostatistics and Epidemiologic Research, New York City Department of Health, New York, New York Michael A. Stoto, Ph.D., Senior Staff Officer, Institute of Medicine, National Academy of Sciences, Washington, D.C. James A. Swomley, Managing Director, American Lung Association, New York, New York Owen T. Thormberry, Ph.D., Director, Division of Health Interview Statistics, Nation- al Center for Health Statistics, Centers for Disease Control, Hyattsville, Maryland William M. Tipping, Executive Vice President and Chief Executive Officer, American Cancer Society, Atlanta, Georgia Dennis D. Tolsma, M.P.H., Assistant Director for Public Health Practice, Centers for Disease Control, Atlanta, Georgia Frederick L. Trowbridge, M.D., Director, Division of Nutrition, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Diana Chapman Walsh, Ph.D., University Professor, Professor of Public Health and Associate Director of the Health Policy Institute, Boston University, Boston, Mas- sachusetts Judith P. Wilkenfeld, J.D., Program Advisor, Cigarette Advertising and Testing, Federal Trade Commission, Washington, D.C. Ronald W. Wilson, M.A., Director, Division of Epidemiology and Health Promotion, National Center for Health Statistics, Centers for Disease Control, Hyattsville, Maryland Deborah M. Winn, Ph.D., Deputy Director, Division of Health Interview Statistics, Na- tional Center for Health Statistics, Hyattsville, Maryland Ernst L. Wynder, M.D., President, American Health Foundation, New York, New York James B. Wyngaarden, M.D., Director, National Institutes of Health, Bethesda, Maryland The editors also acknowledge the contributions of the following staff members and others who assisted in the preparation of this Report. Margaret Anglin, Secretary, Office on Smoking and Health, Rockville, Maryland Charles Appiah, Project Clerk, The Circle, Inc., McLean, Virginia John Artis, Courier, The Circle, Inc., McLean, Virginia John L. Bagrosky, Associate Director for Program Operations, Office on Smoking and Health, Rockville, Maryland Sonia Balakirsky, Secretary, Office on Smoking and Health, Rockville, Maryland Carol A. Bean, Ph.D., Project Director, The Circle, Inc., McLean, Virginia Marissa Bernstein, Editorial Assistant, The Circle, Inc., McLean, Virginia Doreen M. Bonnett, Senior Editor, The Circle, Inc., McLean, Virginia Catherine E. Burckhardt, Editorial Assistant, Office on Smoking and Health, Rockville, Maryland Gayle A. Christman, Administrative Assistant, The Circle, Inc., McLean, Virginia Carol K. Cummings, Secretary, Office on Smoking and Health, Rockville, Maryland xvii Karen M. Deasy, Assistant to the Director for Special Projects, Office on Smoking and Health, Rockville, Maryland Joanna Ebling, Word Processing Specialist, The Circle, Inc., McLean, Virginia David Fry, Editor, The Circle, Inc., McLean, Virginia Lynn Funkhauser, Word Processing Specialist, The Circle, Inc., McLean, Virginia Amy Garson, Student Intern, Office on Smoking and Health, Rockville, Maryland Gary A. Giovino, Ph.D., Epidemiologist, Office on Smoking and Heaith, Rockville, Maryland Ametta G. Glover, Secretary, Office on Smoking and Health, Rockville, Maryland Victoria M. Grier, Conference Coordinator, The Circle, Inc., McLean, Virginia Andree C. Harris, Program Analyst, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Evridiki Hatziandreu, M.D., Dr.P.H., Epidemic Intelligence Service Officer, Office on Smoking and Health, Rockville, Maryland Patricia E. Healy, Technical Information Specialist, Office on Smoking and Health, Rockville, Maryland Timothy K. Hensley, Technical Publications Writer, Office on Smoking and Health, Rockville, Maryland Robert S. Hutchings, Associate Director for Information and Program Development, Office on Smoking and Health, Rockville, Maryland Karen Jacob, Senior Editor, The Circle, Inc., McLean, Virginia Beth Jacobsen, Student Intern, Office on Smoking and Health, Rockville, Maryland Sheila M. Jones, Word Processing Specialist, The Circle, Inc., McLean, Virginia Kathleen M. Keever, Secretary, Department of Public Health Policy and Administra- tion, School of Public Health, University of Michigan, Ann Arbor, Michigan Rick Keir, Senior Editor, The Circle, Inc., McLean, Virginia Jennifer L. Kirscht, M.P.H., Statistics Consultant, Department of Public Health Policy and Administration, School of Public Health, University of Michigan, Ann Arbor, Michigan Laura Y. Martin, Program Analyst, Office of Program Planning and Evaluation, Centers for Disease Control, Atlanta, Georgia Daniel F. McLaughlin, Editor, The Circle, Inc., McLean, Virginia Sherry L. Mills, M.D., M.P.H., Epidemic Intelligence Service Officer, Office on Smok- ing and Health, Rockville, Maryland Nancy A. Miltenberger, M.A., Senior Editor, The Circle, Inc., McLean, Virginia Elizabeth Mugge, Special Assistant, Office of the Deputy Director, Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland Millie R. Naquin, M.Ed., Research Assistant, Office on Smoking and Health, Rock- ville, Maryland Regina Nwankwo, Editor, The Circle, Inc., McLean, Virginia Ruth C. Palmer, Secretary, Office on Smoking and Health, Rockville, Maryland Lida Peterson, Computer Systems Manager, The Circle, Inc., McLean, Virginia Renate Phillips, Desktop Publishing/Graphic Artist, The Circle, Inc., McLean, Virginia Margaret E. Pickerel, Public Information and Publications Specialist, Office on Smok- ing and Health, Rockville, Maryland XVill Rose Mary Romano, Chief, Public Information Branch, Office on Smoking and Health, Rockville, Maryland Tamara Shipp, Publications Assistant, The Circle, Inc., McLean, Virginia Edwin Silverberg, Supervisor, Statistical Information Service, American Cancer Society Linda R. Spiegelman, Administrative Officer, Office on Smoking and Health, Rock- ville, Maryland Traion Stallings, Word Processing Specialist, The Circle, Inc., McLean, Virginia Daniel R. Tisch, Senior Project Manager, The Circle, Inc., McLean, Virginia Pamela Wilson, Editor, The Circle, Inc., McLean, Virginia Louise G. Wiseman, Technical Information Specialist, Office on Smoking and Health, Rockville, Maryland XIX TABLE OF CONTENTS Foreword 2.0.00. e ete e etn n nee teens i Preface 2... cn nee e ttn e etn n eee nes iil Acknowledgments 2.0.2.0... 0... c cece cee etn tne e nee nn tenes IX 1. Historical Perspective, Overview, and Conclusions ..................005. 1 2. Advances in Knowledge of the Health Consequences of Smoking .......... 33 3. Changes in Smoking-Attributable Mortality ....................000005 117 4. Trends in Public Beliefs, Attitudes, and Opinions About Smoking ........ 171 5. Changes in Smoking Behavior and Knowledge About Determinants ....... 259 6. Smoking Prevention, Cessation, and Advocacy Activities ............... 379 7. Smoking Control Policies 0.0.0.0... 00 cette enn 465 8. Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences ..............2-.-..405: pet eee eet ess esses 645 Glossary .. 0. eee teen tenet een nee tees 685 Index oc cee ett e enn e cent teen ee enenes 689 xxi CHAPTER 1 HISTORICAL PERSPECTIVE, OVERVIEW, AND CONCLUSIONS CONTENTS Historical Perspective ...... 0... ccc cc teens 5 Highlights of Conclusions and Findings ........-..-. eee e eee eee eee ees 1] Major Conclusions 02.0.2... cece eens 11 Key New Findings ........ 0.00. e ccc ene nent eees 11 OVEFVIEW 26 ee en en een enn ee eee nee n teas 13 Coverage of the Report 2.2.00... ce eee teenies 13 1990 Health Objectives for the Nation .......... 0... cece eee eee eee 16 Limitations of Coverage 2... 6.0... ee tte tenes 19 Development of the Report . 0.6.0... 6.666 19 Chapter Conclusions ©... 000... e cece eee eee eee es 20 Chapter 2: Advances in Knowledge of the Health Consequences of Smoking. 20 Part I. Health Consequences .......... 00.6 c cece eee etna 20 Part I]. The Physicochemical Nature of Tobacco .........--...+--5: 21 Chapter 3: Changes in Smoking-Attributable Mortality ...........-...5055 21 Chapter 4: Trends in Public Beliefs, Attitudes, and Opinions About Smoking . 22 Chapter 5: Changes in Smoking Behavior and Knowledge About Determinants 0.0.0... 0. ccc eee ee ee eens 23 Part I. Changes in Smoking Behavior ......... 50.0. s eee ee neers 23 Part il. Changes in Knowledge About the Determinants of Smoking Behavior 10.2.0... 0000 c eect ene ete ees 24 Chapter 6: Smoking Prevention, Cessation, and Advocacy Activities ........ 25 Part I. Smoking Prevention Activities . 0.0.00... 0... - eee e ee eee es 25 Part II. Smoking Education and Cessation Activities .........-...--- 25 Part III. Antismoking Advocacy and Lobbying ..............--+545- 26 Chapter 7: Smoking Control Policies ... 6... 2.6.0 beeen eee nee 26 Part I. Policies Pertaining to Information and Education ............. 26 Part II. Economic Incentives ... 0.0.0.0 0c e eee eee eee eee 27 Part III. Direct Restrictions on Smoking .......... 0. ee eee eee eee 28 Chapter 8: Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences ........ 0.00 e cece tte nee 28 References 2.00... ccc ee ent ee eee eee e teens 30 Historical Perspective Each of the last five Surgeons General of the U.S. Public Health Service (PHS) has identified cigarette smoking as one of this Nation's most significant sources of death and disease. Today, more than one of every six American deaths is the result of cigarette smoking. Smoking is responsible for an estimated 30 percent of all cancer deaths, in- cluding 87 percent of lung cancer, the leading cause of cancer mortality; 21 percent of deaths from coronary heart disease; 18 percent of stroke deaths; and 82 percent of deaths from chronic obstructive pulmonary disease. Other forms of tobacco use, including pipe and cigar smoking and use of smokeless tobacco, are also associated with sig- nificantly elevated risks of disease and death (US DHEW 1979a; US DHHS 1986b). Although the health hazards of tobacco use have been suspected for almost 400 years, the first reported clinical impressions of a relationship between tobacco and disease date from the 18th century, when tobacco use was associated with lip cancer (US DHEW 1979a) and nasal cancer (US DHHS 1986b). However, true scientific under- standing of the health effects of tobacco has been achieved only in the present century. Broders (1920) published an article in the Journal of the American Medical Associa- tion linking tobacco use to lip cancer, and 8 years later, Lombard and Doering (1928) published an article in the New England Journal of Medicine noting that heavy smok- ing was more common among cancer patients than among control groups. Later, Pearl (1938) observed in the journal Science that heavy smokers had a shorter life expectan- cy than nonsmokers. During the 1930s, the Nation’s increasing rate of lung cancer and other diseases prompted the initiation of epidemiologic and laboratory studies of the relationship be- tween tobacco use and disease. In the late 1940s and early 1950s, a number of retrospec- tive epidemiologic studies, published by Wynder and Graham (1950) and by other in- vestigators, provided scientific evidence strongly linking smoking to lung cancer. This association was soon thereafter supported by the emerging early findings of major prospective (cohort) mortality studies, including the work of Doll and Hill (1954, 1956) in Great Britain and Hammond and Horn (1958a, 1958b) in the United States. The strength and consistency of these results, combined with evidence from laboratory and autopsy studies, led a national scientific study group to conclude in 1957 that the relationship between smoking and tung cancer was causal (Study Group on Smoking and Health 1957). On July 12 of that year, U.S. Surgeon General Leroy Burney issued a statement declaring that “The Public Health Service feels the weight of the evidence is increas- ingly pointing in one direction; that excessive smoking is one of the causative factors in lung cancer” (US PHS 1964). Two years later, in 1959, Surgeon General Burney said that “The weight of evidence at present implicates smoking as the principal factor in the increased incidence of lung cancer” (Burney 1959). Increases in chronic diseases in other parts of the world led health authorities in other countries to examine the relationship between tobacco and disease, particularly in Europe and Scandinavia. In 1957, the British Medical Research Council reported that a major part of the increase in lung cancer was attributable to smoking (British Medi- cal Research Council 1957). Later, the Royal College of Physicians (1962) issued a landmark document on smoking and health that concluded that “Cigarette smoking is the most likely cause of the recent world-wide increase in deaths from lung cancer . . . is an important predisposing cause of the development of chronic bronchitis . . . probab- ly increases the risk of dying from coronary heart disease...has an adverse effect on healing of [gastric and duodenal] ulcers . . . [and] may be a contributing factor in can- cer of the mouth, pharynx, oesophagus, and bladder.” On June 1, 1961, the presidents of the American Cancer Society, the American Public Health Association, the American Heart Association, and the National Tuberculosis Association (now the American Lung Association) urged President John F. Kennedy to establish a commission to study the health consequences of smoking. Repre- sentatives of these organizations met with Surgeon General Luther L. Terry in January 1962 to reiterate their call for action. In April, the Surgeon General presented a detailed proposal for an advisory group to reevaluate the position adopted by the Public Health Service in 1959. In calling for the advisory group, Dr. Terry cited new research on the adverse health effects of tobacco, a request from the Federal Trade Commission for guidance on policy regarding the labeling and advertising of tobacco products, and the findings in the new report of the Royal College of Physicians. On July 27, 1962, following consultations between the White House and the Public Health Service, the Surgeon General held a meeting to define the work of an expert advisory group and to identify candidates for the committee. Meeting with the Sur- geon General were representatives of the American Cancer Society, the American Col- lege of Chest Physicians, the American Heart Association, the American Medical As- sociation, the Tobacco Institute, the Food and Drug Administration, the National Tuberculosis Association, the Federal Trade Commission, and the President’s Office of Science and Technology. The group agreed on a list of more than 150 scientists and physicians. Each of the organizations had the right to veto any of the names on the list for any reason. Persons who had taken a public position on smoking and health were not considered for inclusion on the advisory committee. Dr. Terry selected 10 individuals from the list to serve on the Surgeon General’s Ad- visory Committee on Smoking and Health: Stanhope Bayne-Jones, M.D., LL.D., former Dean, Yale School of Medicine; Walter J. Burdette, M.D., Ph.D., University of Utah; William G. Cochrane, M.A., Harvard University; Emmanuel Farber, M.D., Ph.D., University of Pittsburgh; Louis F. Fieser, Ph.D., Harvard University; Jacob Furth, M.D., Columbia University; John B. Hickam, M.D., Indiana University; Charles LeMaistre, M.D., University of Texas, Leonard M. Schuman, M.D., University of Minnesota; and Maurice H. Seevers, M.D., Ph.D., University of Michigan. The Advisory Committee held nine meetings from November 1962 through Decem- ber 1963, during which they reviewed all the available data from animal laboratory ex- periments, clinical and autopsy studies, and retrospective and prospective epi- demiologic studies. The Committee had access to over 7,000 publications pertaining to smoking and health, including more than 3,000 articles reporting research findings published after 1950. In evaluating evidence linking smoking to disease, the Commit- tee restricted judgments of a causal relationship to those associations for which the evidence was (1) consistent, (2) strong, (3) specific, (4) supportive of appropriate tem- poral relationships, and (5) coherent (US PHS 1964). The final Report of the Advisory Committee was released on January 11, 1964 (US PHS 1964). It concluded that “Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction... . The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking.” The Report also concluded that pipe smoking is causally related to lip cancer, that cigarette smoking is causally related to laryngeal cancer in men, and that “Cigarette smoking is the most important of the causes of chronic bronchitis.” The Advisory Com- mittee identified significant associations between smoking and cancer of the esophagus, cancer of the urinary bladder. coronary artery disease, emphysema, peptic ulcer dis- ease, and low-birthweight babies, but it did not consider the available data to be suf- ficient to label these associations causal. The Committee found that male cigarette smokers had a 70-percent excess mortality rate over men who had never smoked and that female smokers also had an elevated mortality rate, although less than that of males. The Advisory Committee concluded that “Cigarette smoking is a health hazard of sufficient importance in the United States to warrant appropriate remedial action.” “Remedial action” was initiated immediately after publication of the Advisory Committee’s Report, when the Federal Trade Commission (FTC) proposed that cigarette packs and advertisements bear warning labels and that strict limitations be placed on the content of cigarette advertising. With passage of the Federal Cigarette Labeling and Advertising Act of 1965 (Public Law 89-92; amended in April 1970 by Public Law 91-222), Congress preempted the FTC's recommendation: beginning in 1966, a congressionally mandated health warning appeared on all cigarette packs but not on advertisements. The Act also required the Secretary of Health, Education, and Welfare to submit an- nual reports to Congress on the health consequences of smoking, together with legis- lative recommendations, beginning no later than mid-1967. New reports of the Sur- geon General on smoking and health were issued in each calendar year beginning in 1967, except for 1970, 1976, 1977, and 1987. (In 1976, a volume of selected chapters from the 1971-75 Reports was published. The report issued in 1978 was a joint Report for the years 1977 and 1978.) Thus, the present volume, commemorating the 25th an- niversary of the 1964 Report, is the 20th Report in the series. In addition, in 1986, PHS issued a report on the health consequences of using smokeless tobacco (US DHHS 1986b). Table | identifies the previous reports and highlights their coverage. The reports published since the 1964 Report have confirmed the scientific judgment of the Advisory Committee and have extended its findings. The evidence available today has reinforced the Advisory Committee’s judgments of causality; converted most of its “significant associations” into causal relationships, adhering to the strict criteria described in the first Report; confirmed causal associations for relationships not con- templated in the 1964 Report (e.g., the health hazards of involuntary smoking (US DHHS 1986a)); and identified additional disease associations. Accompanying the growth and dissemination of scientific knowledge has been in- creased public understanding of the hazards of smoking. reflected in decreases in smok- TABLE 1.—Surgeon General’s Reports on smoking and health, 1964~88 Year Subject/Highlights 1964 1967 1968 1969 1971 1972 1973 First official report of the Federal Government on smoking and health. Concluded that “Cigarette smoking is a health hazard of sufficient importance in the United States to warrant appropriate remedial action.” Concluded that Cigarette smoking is a cause of Jung cancer in men and a suspected cause of lung cancer in women. Identified many other causal relationships and smoking—disease associations (US PHS 1964). Confirmed and strengthened conclusions of 1964 Report. Stated that “The case for cigarette smoking as the principal cause of lung cancer is overwhelming.” Found that evidence “strongly suggests that cigarette smoking can cause death from coronary heart disease.” 1964 Report had described this relationship as an “association.” Also concluded that “Cigarette smoking is the Most important of the causes of chronic non-neoplastic bronchiopulmonary diseases in the United States.” Identified measures of morbidity associated with smoking (US PHS 1968a). Updated information presented in 1967 Report. Estimated smoking-related loss of life expectancy among young men as 8 years for “heavy” smokers (over 2 packs per day) and 4 years for “light” smokers (less than 1/2 pack per day) (US PHS 1968b). Also supplemented 1967 Report. Confirmed association between maternal smoking and infant low birthweight. Identified evidence of increased incidence of prematurity, spontaneous abortion, stillbirth, and neonatal death (US PHS 1969). Reviewed entire field of smoking and health. with emphasis on most recent literature. Discussed new data indicating associations between smoking and peripheral vascular disease, atherosclerosis of the aorta and coronary arteries, increased incidence and severity of respiratory infections, and increased mortality from cerebrovascular disease and nonsyphilitic aortic aneurysm. Concluded that smoking is associated with cancers of the oral cavity and esophagus. Found that “Maternal smoking during pregnancy exerts a retarding influence on fetal growth” (US DHEW 1971). Examined evidence on immunological effects of tobacco and tobacco smoke, harmful constituents of tobacco smoke, and “public exposure to air pollution from tobacco smoke.” Found tobacco and tobacco smoke antigenic in humans and animals, tobacco may impair protective mechanisms of immune system; nonsmokers’ exposure to tobacco smoke may exacerbate allergic symptoms; carbon monoxide in smoke-filled rooms may harm health of persons with chronic lung or heart disease; tobacco smoke contains hundreds of compounds, several of which have been shown to act as carcinogens, tumor initiators, and tumor promoters. Identified carbon monoxide. nicotine, and tar as smoke constituents most likely to produce health hazards of smoking (US DHEW 1972). Presented evidence on health effects of smoking pipes, cigars, and “little cigars.” Found mortality rates of pipe and cigar smokers higher than those of nonsmokers but lower than those of cigarette smokers. Found that cigarette smoking impairs exercise performance in heaithy young men. Presented additional evidence on smoking as risk factor in peripheral vascular disease and problems of pregnancy (US DHEW 1973). TABLE 1.—Continued Year Subject/Highlights 1974 1975 1976? 1977-78 1979 1980 1981 1982 1983 Tenth Anniversary Report. Reviewed and strengthened evidence on major hazards of smoking. Reviewed evidence on association between smoking and atherosclerotic brain infarction and on synergistic effect of smoking and asbestos exposure in causing lung cancer (US DHEW, 1974). Updated information on health effects of involuntary (passive) smoking. Noted evidence linking parental smoking to bronchitis and pneumonia in children during the first year of life (US DHEW 1975). Compiled selected chapters from 1971-75 Reports (US DHEW 1976). Combined 2-year Report focused on smoking-related health problems unique to women. Cited studies showing that use of oral contraceptives potentiates harmful effects of smoking on the cardiovascular system (US DHEW 1978). Fifteenth Anniversary Report. Presented most comprehensive review of health effects of smoking ever published, and first Surgeon General’s Report to carefully examine behavioral, pharmacologic, and social factors influencing smoking. Also first Report to consider role of adult and youth education in promoting nonsmoking. First Report to review health consequences of smokeless tobacco. Many new sections, including one identifying smoking as “one of the primary causes of drug interactions in humans” (US DHEW 1979a). Devoted to health consequences of smoking for women. Reviewed evidence that strengthened previous findings and permitted new ones. Noted projections that lung cancer would surpass breast cancer as leading cause of cancer mortality in women. Identified trend toward increased smoking by adolescent females (US DHHS 1980a). Examined health consequences of “the changing cigarette,” i.e., lower tar and nicotine cigarettes. Concluded that lower yield cigarettes reduced risk of lung cancer but found no conclusive evidence that they reduced risk of cardiovascular disease, chronic obstructive pulmonary disease, and fetal damage. Noted possible risks from additives and their products of combustion. Discussed compensatory smoking behaviors that might reduce potential risk reductions of lower yield cigarettes. Emphasized that there is no safe cigarette and that any risk reduction associated with lower yield cigarettes would be smali compared with benefits of quitting smoking (US DHHS 1981). Reviewed and extended understanding of the health consequences of smoking as a cause or contributory factor of numerous cancers. Included first Surgeon General's Report consideration of emerging epidemiologic evidence of increased lung cancer risk in nonsmoking wives of smoking husbands. Did not find evidence at that time sufficient to conclude that relationship was causal, but labeled it “a possible serious public health problem.” Discussed potential for low-cost smoking cessation interventions (US DHHS 1982). Examined health consequences of smoking for cardiovascular disease. Concluded that cigarette smoking is one of three major independent causes of coronary heart disease (CHD) and, given its prevalence, “should be considered the most important of the known modifiable risk factors for CHD.” Discussed relationships between smoking and other forms of cardiovascular disease (US DHHS 1983). TABLE 1.—Continued Year Subject/Highlights 1984 Reviewed evidence on smoking and chronic obstructive lung disease (COLD). Concluded that smoking is the major cause of COLD, accounting for 80 to 90 percent of COLD deaths in the United States. Noted that COLD morbidity has greater social impact than COLD mortality because of extended disability periods of COLD victims (US DHHS 1984). 1985 Examined relationship between smoking and hazardous substances in the workplace. Found that for the majority of smokers, smoking is a greater cause of death and disability than their workplace environment. Risk of lung cancer from asbestos exposure characterized as multiplicative with smoking exposure. Observed special importance of smoking prevention among blue-collar workers because of their greater exposure to workplace hazards and their higher prevalence of smoking (US DHHS 1985). 1986 Focused on involuntary smoking, concluding that “Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers.” Also found that, compared with children of nonsmokers, children of smokers have higher incidence of respiratory infections and symptoms and reduced rates of increase in lung function. Presented detailed examination of growth in restrictions on smoking in public places and workplaces. Concluded that simple separation of smokers and nonsmokers within same airspace reduces but does not eliminate exposure to environmental tobacco smoke (US DHHS 1986a). 1986° Special Report of advisory committee appointed by the Surgeon General to study the health consequences of smokeless tobacco. Concluded that use of smokeless tobacco can cause cancer in humans and can lead to nicotine addiction (US DHHS 1986b). 1988 Established nicotine as a highly addictive substance, comparable in its physiological and psychological properties to other addictive substances of abuse (US DHHS 1988). “Excluded from count of series volumes in text because no new evidence was reviewed. Excluded from count of series volumes in text because it was a Special Report, not in the series of reports on smoking and health. ing prevalence and, in recent years, the intensification of public and private measures to discourage smoking. A quarter century after publication of the first Report, smok- ing remains the leading cause of preventable premature death in our society, but per capita cigarette consumption is declining annually, and analyses of consumption and disease trends augur eventual decreases in smoking’s toll. Given these changes, the remaining toll of tobacco-related disease, and the Surgeon General’s objective of a smoke-free society by the year 2000 (Koop 1984), Surgeon General C. Everett Koop devotes this 25th anniversary edition of the Surgeon General’s Report to an assessment of progress against smoking in the quarter century since the first Report was published. 10 Highlights of Conclusions and Findings Major Conclusions As the present Report documents, knowledge of the health consequences of smok- ing has expanded dramatically since 1964, and programs and policies to combat the hazards of smoking have proliferated. The essential chapter-specific conclusions relat- ing to these and other topics of this Report are presented at the end of each chapter and are reproduced in the final Section of this introductory Chapter. The major conclusions of the entire Report, immediately following, address fundamental developments over the past quarter century in smoking prevalence and in mortality caused by smoking. The first two conclusions highlight important gains in preventing smoking and smok- ing-related disease in the United States. The last three conclusions emphasize sources of continuing concern and remaining challenges. 1. The prevalence of smoking among adults decreased from 40 percent in 1965 to 29 percent in 1987. Nearly half of all living adults who ever smoked have quit. 2. Between 1964 and 1985, approximately three-quarters of a million smok- ing-related deaths were avoided or postponed as a result of decisions to quit smoking or not to start. Each of these avoided or postponed deaths repre- sented an average gain in life expectancy of two decades. 3. The prevalence of smoking remains higher among blacks, blue-collar workers, and less educated persons than in the overall population. The decline in smoking has been substantially slower among women than among men. 4. Smoking begins primarily during childhood and adolescence. The age of initiation has fallen over time, particularly among females. Smoking among high school seniors leveled off from 1980 through 1987 after pre- vious years of decline. 5. Smoking is responsible for more than one of every six deaths in the United States. Smoking remains the single most important preventable cause of death in our society. Key New Findings While this Report is designed to provide a retrospective view of smoking and health over the past 25 years, several findings never previously documented in a report of the Surgeon General emerged during the process of reviewing and analyzing the voluminous materials consulted for the study. Discussed in detail throughout the Report, key new findings include the following: 11 12 Cigarette smoking is a major cause of cerebrovascular disease (stroke), the third leading cause of death in the United States. By 1986, lung cancer caught up with breast cancer as the leading cause of can- cer death in women. Women smokers’ relative risk of lung cancer has increased by a factor of more than four since the early 1960s and is now comparable to the relative risk identified for men in that earlier period. Gender differences in smok- ing behavior are disappearing; consistent with this, gender differences in the rela- tive risks of and mortality from smoking-related diseases are narrowing. Cigarette smoking is associated with cancer of the uterine cervix. To date, 43 chemicals in tobacco smoke have been determined to be car- cinogenic. In 1985, approximately 390,000 deaths were attributable to cigarette smoking. This figure is greater than other recent estimates of smoking-attributable mor- tality, reflecting the use of higher relative risks of smoking-related diseases for women and, especially in the case of lung cancer, for men. These higher rela- tive risks were derived from the largest and most recent prospective study of smoking and disease, conducted by the American Cancer Society. Disparities in smoking prevalence, quitting, and initiation between groups with the highest and lowest levels of educational attainment are substantial and have been increasing. Educational attainment appears to be the best single sociodemographic predictor of smoking. There is growing recognition that prevention and cessation interventions need to target specific populations with a high smoking prevalence or at high risk of smoking-related disease. These populations include minority groups, pregnant women, military personnel, high school dropouts, blue-collar workers, un- employed persons, and heavy smokers. One-quarter of high school seniors who have ever smoked had their first cigarette by sixth grade, one-half by eighth grade. Associated with knowledge of this fact is a growing consensus that smoking prevention education needs to begin in elementary school. Whereas past smoking control efforts targeting children and adolescents focused exclusively on prevention of smoking, the smoking control community has iden- tified the need to develop cessation programs for children and adolescents ad- dicted to nicotine. As of mid-1988, more than 320 local communities had adopted laws or regula- tions restricting smoking in public places. This compares with a total of about 90 as of the end of 1985, a more than threefold increase in 3 years. The number of new State laws restricting smoking in public places in 1987 exceeded the num- ber passed in any preceding year. * A growing body of evidence on the role of economic incentives in influencing health behavior has contributed to increased interest in and use of such incen- tives to discourage use of tobacco products. These include excise taxation of tobacco products, workplace financial incentives, and insurance premium dif- ferentials for smokers and nonsmokers. « In marked contrast to the trends in virtually all other areas of smoking control policy, the number of legal restrictions on children’s access to tobacco products has decreased over the past quarter century. Studies indicate that vendor com- pliance with minimum-age-of-purchase laws is the exception rather than the rule. * The marketing of a variety of alternative nicotine delivery systems has heightened concern within the public health community about the future of nicotine addiction. The most prominent development in this regard was the 1988 test marketing by a major cigarette producer of a nicotine delivery device having the external appearance of a cigarette and being promoted as “the cleaner smoke.” * While over 50 million Americans continue to smoke, more than 90 million would be smoking in the absence of the changes in the smoking-and-health environ- ment that have occurred since 1964. * Quitting and noninitiation of smoking between 1964 and 1985, encouraged by changes in that environment, have been or wiil be associated with the postpone- ment or avoidance of almost 3 million smoking-related deaths. That figure reflects the three-quarters of a million deaths noted in conclusion 2 above, and an additional 2.1 million deaths estimated to be postponed or avoided between 1986 and the year 2000. Overview Coverage of the Report As the major conclusions and new findings suggest, progress against smoking is necessarily measured in several dimensions. Ultimately, the most important measure is the burden of mortality, morbidity, and disability associated with smoking. Secon- darily, changes in the prevalence of smoking and its distribution among sociodemographic groups foretell the future course of smoking-related disease. Be- havioral changes in turn reflect a myriad of social and psychological influences that have evolved over the past 25 years. These include public knowledge of smoking hazards and attitudes toward the behavior; availability and effectiveness of smoking prevention and cessation programs; and adoption of smoking-related social policies, often reflections of public attitudes and opinions. At the heart of all these phenomena is the substantial and expanding body of scientific knowledge about the health conse- quences of smoking. The 1989 Report examines changes in each of these dimensions over the past quarter century. The Report includes a Foreword by the Assistant Secretary for Health and the Director of the Centers for Disease Control, a Preface by the Surgeon General of the U.S. Public Health Service, and the following chapters: Chapter |. Historical Perspective, Overview, and Conclusions Chapter 2. Advances in Knowledge of the Health Consequences of Smoking Chapter 3. Changes in Smoking-Attributable Mortality Chapter 4. Trends in Public Beliefs, Attitudes, and Opinions About Smoking Chapter 5. Changes in Smoking Behavior and Knowledge About Determinants Chapter 6. Smoking Prevention, Cessation, and Advocacy Activities Chapier 7. Smoking Control Policies Chapter 8. Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences A key to abbreviations used throughout the Report is found at the end of the volume. Analysis of changes in scientificmedical understanding follows the core tradition of the Surgeon General’s Report series. Chapter 2 summarizes current knowledge of the health consequences of smoking and examines how it has advanced, both qualita- tively and quantitatively, beyond that reflected in the original Surgeon General’s Report. The Chapter also summarizes knowledge of the physicochemical nature of tobacco smoke. Chapter 3 examines the ultimate population impact of smoking-disease relationships in its review of changes in smoking-attributable mortality. The patterns of mortality have changed in predictable ways, reflecting variations in the rates and sociodemographic distribution of smoking prevalence (the subject of much of Chapter 5). In particular, smoking-attributable mortality in women has increased dramatically, the predictable consequence of the rapid growth in smoking by women in the middle decades of the century. Shifts in sociodemographic patterns of smoking, with greater prevalence now found among blue-collar workers and some minorities than among the white-collar population, presage a continuing disproportionate burden of illness for the Nation’s poor and minority populations. One element of the decision of whether or not to smoke is personal understanding of the dangers involved. Chapter 4 reviews changes in public knowledge since 1964. The most basic findings from scientific research on the health consequences of smoking have been conveyed to and accepted by the American public, at least at a generalized level. Nevertheless, survey research reveals important gaps in public understanding of the hazards of smoking. Smokers report less understanding of the basic consequences of smoking than do nonsmokers; furthermore, smokers often do not internalize, or per- sonalize, the hazards they acknowledge as applying to smokers in general. In addition, knowledge of smoking-and-health facts beyond the most basic information is not pos- sessed by significant numbers of Americans. Thus, a substantial educational task remains. Although significant gaps remain, it is also clear that the public has a much better ap- preciation of the hazards of smoking than it did 25 years ago. Associated with the grow- ing acceptance of smoking as a health hazard for the smoker, and more recently as a hazard for nonsmokers, is a growing public desire to restrict smoking in public places 14 to protect the rights of nonsmokers to breathe clean air. Opinions about smoking and the appropriate role of smoking control are also considered in Chapter 4. The relationship between knowledge and opinion change, on the one hand, and sub- sequent behavior change, on the other, is quite complex. Nevertheless, substantial smoking behavior change has occurred since issuance of the first Surgeon General’s Report and has often followed shifts in beliefs and opinions about smoking. The many dimensions of such behavior change are explored in Chapter 5. Part ! of the Chapter examines empirical evidence on behavior change across a number of smoking behaviors and across the major sociodemographic groups. Several previous reports of the Sur- geon General have included consideration of these trends (US DHEW1979a;US DHHS 1980a,1983, 1985, 1988). Part II of Chapter 5 reviews the evolution of understanding of smoking behaviors and their determinants. The 1979 Surgeon General's Report devoted several chapters to the psychological and social determinants of smoking (US DHEW 1979a). Most recently, the phenomenon of nicotine addiction was reviewed thoroughly by the Surgeon General (US DHHS 1988). Changes in public attitudes toward smoking and in the prevalence of smoking are reflected in the rapid expansion in the 1980s of State and local laws and workplace policies restricting smoking. The Nation’s growing nonsmoking ethos is also reflected in more attention to both voluntary and regulatory measures intended to prevent the in- itiation of tobacco use or to assist smokers to quit. The number of smoking-cessation techniques and programs has expanded. Smoking policy discussions today concern such diverse activities as excise taxation, restriction of advertising and promotion of tobacco products, limitation of children’s access to tobacco products, and regulation of the newly emerging nicotine-based products collectively referred to as “alternative nicotine delivery systems.” Chapters 6 and 7 examine developments over the past quarter century in voluntary programmatic efforts and public policies directed at smoking control, respectively. Chapter 6 describes separately programs directed at smoking prevention and cessation, and highlights the work of the major voluntary health associations. The Chapter reviews such diverse efforts as comprehensive school health education curricula and antismoking public service announcements on the broadcast media. Chapter 6 con- cludes with a brief overview of advocacy and lobbying activities related to smoking and health. Advocacy activities are purely voluntary in nature, yet most have been directed at promoting smoking control policies, particularly in recent years. As such, a discussion of advocacy serves as a logical transition between the focus of Chapter 6 on voluntary efforts to combat smoking and concentration in Chapter 7 on policy measures. Coverage of developments in smoking control policies in Chapter 7 has few precedents in prior reports of the Surgeon General, despite the first Report’s call for “appropriate remedial action” a quarter of a century ago (US PHS 1964). The major exception was the substantial attention accorded workplace and Government smoking restriction policies in the 1986 Report (US DHHS 1986a). Otherwise, the report series’ principal references to policy have come in the form of legislative recommen- dations to the Congress. Yet, as noted above, policies intended to diminish smoking and its disease burden have become increasingly common in both the public and 15 private sectors. Thus, as part of the history of smoking and health, and as a determinant of progress against smoking, smoking-related policy is examined in detail in this 25th anniversary Report. Coverage of policy in Chapter 7 includes documentation of trends in specific policies, analogous to the coverage afforded smoking restrictions in the 1986 Report. Policies are grouped into three categories: policies pertaining to information and education (Part I), economic incentives (Part II), and direct restrictions (Part IID. Where possible, discussion includes examination of scientific understanding of specific policy effects. Such understanding derives from a growing and increasingly sophisti- cated body of empirical social science research. Collectively, the program and policy efforts discussed in Chapters 6 and 7, combined with changing public knowledge and social norms, have encouraged tens of millions of Americans not to smoke. As examined in Chapter 8, this behavioral change can be credited with the avoidance of many hundreds of thousands of premature deaths and the associated saving of millions of life-years. Chapter 8 reviews these and other find- ings on the behavioral and health consequences of changes in the Nation’s smoking- and-health environment. Conclusions pertaining to the findings of each of the Report’s chapters are reviewed in the final Section of this introductory Chapter. By all accounts, the 1964 Report of the Surgeon General’s Advisory Committee is a landmark document in the history of public health and a seminal contribution to the Nation’s efforts to understand and combat tobacco-related morbidity and mortality. The present Report chronicles progress against smoking in the intervening 25 years, demonstrating an extraordinary array of advances in knowledge, changes in norms and behavior, and effects on the health of the American people. By any reasonable measure, the burden of smoking remains enormous; but the legacy of the 1964 Report is a society that has made impressive strides toward ridding itself of this most prevent- able source of disease, disability, and death. 1990 Health Objectives for the Nation In 1979, PHS released the first Surgeon General’s Report on Health Promotion and Disease Prevention (US DHEW 1979b). The Report identified 15 priority areas, in- cluding smoking, in which significant health gains could be expected in the 1980s, with appropriate actions. Subsequently, working with health experts from both the private and public sectors, the PHS established 226 specific health objectives for the Nation (US DHHS 1980b). Seventeen of these pertain directly to cigarette smoking (Table 2). Many others relate to smoking as well, because they address the prevention of heart disease, cancer, burn injuries, and other smoking-related disease problems. In 1986, the PHS published a midcourse assessment of progress toward achieving the 226 ob- jectives (US DHHS 1986c). One of the goals of the present Report is to offer addition- al insight in this assessment as it relates to the 17 smoking objectives. This is discussed in the relevant chapters. PHS is currently developing national health goals for the year 2000, again working with organizations and individuals in the private and public sectors. The reduction of I TABLE 2.—1990 health objectives for the nation pertaining to smoking Reduced risk factors _ 1. By 1990, the proportion of adults who smoke should be reduced to below 25 percent. 2. By 1990, the proportion of women who smoke during pregnancy should be no greater than one-half the proportion of women overall who smoke. 3. By 1990, the proportion of children and youth aged 12 to 18 years who smoke should be reduced to below 6 percent. 4, By 1990, the sales-weighted average tar yield of cigarettes should be reduced to below 10 mg. The other components of cigarette smoke known to cause disease should also be reduced proportionately. Increased public/professional awareness 5. By 1990, the share of the adult population aware that smoking is one of the major risk factors for heart disease should be increased to at least 85 percent. 6. By 1990, at least 90 percent of the adult population should be aware that smoking is a major cause of lung cancer, as well as multiple other cancers including laryngeal, esophageal, bladder, and other types. 7. By 1990, at least 85 percent of the adult population should be aware of the special risk of developing and worsening chronic obstructive pulmonary disease, including bronchitis and emphysema, among smokers. 8. By 1990, at least 85 percent of women should be aware of the special health risks for women who smoke, including the effect on outcomes of pregnancy and the excess risk of cardiovascular disease with oral contraceptive use. 9. By 1990, at least 65 percent of 12-year-olds should be able to identify smoking cigarettes with increased risk of serious disease of the heart and lungs. 81 TABLE 2.—Continued Improved services/protection Improved surveillance/evaluation 10. By 1990, at least 35 percent of all workers should be offered employer/employee-sponsored or -supported smoking cessation programs either at the worksite or in the community. 11. By 1985, tar, nicotine, and carbon monoxide yields should be prominently displayed on each cigarette package and promotional material. 12. By 1985, the present cigarette warning should be strengthened to increase its visibility and impact, and to give the consumer additional needed information on the specific multiple health risks of smoking. Special consideration should be given to rotational warnings and to identification of special vulnerable groups. 15. By 1985, insurance companies should have collected, reviewed, and made public their actuarial experience on the differential life experience and hospital utilization by specific cause among smokers and nonsmokers, by sex. 16. By 1990, continuing epidemiologic research should have delineated the unanswered research questions regarding low-yield cigarettes, and preliminary partial answers to these should have been generated by research efforts. 13. By 1990, laws should exist in all SO States and all jurisdictions prohibiting smoking in enclosed public places, and establishing separate smoking areas at work and in dining establishments. 14. By 1990, major health and life insurers should be offering differential insurance premiums to smokers and nonsmokers. 17. By 1990, in addition to biomedical hazard surveillance, continuing examination of the changing tobacco product and the sociological phenomena resulting from those changes should have been accomplished. SOURCE: US DHHS (1980b). tobacco use is one of 21 priority areas in which objectives are being formulated. PHS intends to publish the objectives in 1990. Limitations of Coverage Despite the broad scope of this Report, certain limitations have had to be placed on coverage. Two in particular are worthy of mention here: (1) The Report focuses primarily, but not exclusively, on cigarette smoking, reflect- ing its dominance among forms of tobacco use, in terms of both prevalence and disease impact. This focus also reflects the desire to represent the principal interest of the 1964 Advisory Committee in this 25th anniversary Report. Pipe and cigar smoking are much less prevalent than cigarette smoking but also carry significant health risks (US DHEW 1979a). Growing use of smokeless tobacco products (snuff and chewing tobacco), primarily by adolescent males, has focused national attention on the prevalence and health consequences of using these tobacco products (Connolly et al. 1986). This sub- ject was recently reviewed thoroughly by an advisory committee to the Surgeon General (US DHHS 1986b) and in a National Cancer Institute monograph (Boyd and Darbey, in press). (2) The Report concentrates on smoking in the United States. Both within the United States and around the world, there is growing concern about the spread of smoking, particularly in the world’s poorer countries. While per capita cigarette consumption is stable or falling in most developed nations, it is rising in Third World countries. Rates of smoking-related chronic diseases are also increasing rapidly, to the point that tobac- co is expected to soon become the leading cause of premature, preventable mortality in the Third World, as it is at present in the developed world (Aoki, Hisamichi, Tominaga 1988). Concentration of this Report on smoking in the United States is no reflection on the telative importance of the international situation, Rather, it results from the principal objective of reviewing where this Nation has come in its efforts to control smoking-re- lated disease since the 1964 report of the Surgeon General’s Advisory Committee. The Public Health Service hopes that this review, like its predecessors, will prove to be of value to scientists, health professionals, and public health officials in countries throughout the world. Development of the Report This Report was developed by the Office on Smoking and Health (OSH), Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Public Health Service of the U.S. Department of Health and Human Services, as part of the Department’s responsibility, under Public Law 91-222, to report new and current in- formation on smoking and health to the U.S. Congress. The scientific content of this Report was produced through the efforts of more than 130 scientists in the fields of medicine, the biological and social sciences, public health, and policy analysis. Manuscripts for the Report, constituting drafts of chapters or sec- tions of chapters, were prepared by 33 scientists selected for their expertise in the 19 specific content areas. An editorial team including the Director of OSH, a medical epidemiologist from OSH, and four non-Federal experts edited and consolidated the individual manuscripts into chapters. These draft chapters were subjected to an inten- sive outside peer review, with each chapter reviewed by 5 to 12 individuals knowledge- able about the chapter’s subject matter. Incorporating the reviewers’ comments, the editors revised the chapters and assembled a draft of the complete Report. The draft Report was then submitted to 25 distinguished scientists for their review and comment on the entirety of its contents. Simultaneously, the draft Report was submitted to 9 in- stitutes and agencies within the U.S. Public Health Service for their review. Comments from the senior scientific reviewers and the agencies were then used to prepare the final draft of the Report, which was then reviewed by the Offices of the Assistant Secretary for Health and the Secretary, Department of Health and Human Services. Chapter Conclusions Chapter 2: Advances in Knowledge of the Health Consequences of Smoking Part I. Health Consequences 1. The 1964 Surgeon General’s Report concluded that cigarette smoking increases overall mortality in men, causes lung and laryngeal cancer in men, and causes chronic bronchitis. The Report also found significant associations between smok- ing and numerous other diseases. 2. Reports of the Surgeon General since 1964 have concluded that smoking increases mortality and morbidity in both men and women. Disease associations identified as causal since 1964 include coronary heart disease, atherosclerotic peripheral vascular disease, lung and laryngeal cancer in women, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, intrauterine growth retardation, and low-birthweight babies. 3. Cigarette smoking is now considered to be a probable cause of unsuccessful preg- nancies, increased infant mortality, and peptic ulcer disease; to be a contributing factor for cancer of the bladder, pancreas, and kidney; and to be associated with cancer of the stomach. 4. Accumulating research has elucidated the interaction effects of cigarette smoking with certain occupational exposures to increase the risk of cancer, with alcohol ingestion to increase the risk of cancer, and with selected medications to produce adverse effects. 5. A decade ago, the 1979 Report of the Surgeon General found smokeless tobacco to be associated with oral cancer. In 1986, the Surgeon General concluded that smokeless tobacco was a cause of this disease. 6. Research in the present decade has established that involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers, and that the children of parents who smoke have an increased frequency of respiratory infections and symptoms. 20 7. In 1964, tobacco use was considered habituating. A substantial body of evidence accumulated since then, and summarized in the 1988 Surgeon General's Report. has established that cigarettes and other forms of tobacco are addicting. Given the prevalence of smoking, tobacco use is the Nation’s most widespread form of drug dependency. Studies dating from the 1950s have consistently documented the benefits of smok- ing cessation for smokers in all age groups. Recent evidence, including that presented in this 1989 Report of the Surgeon General, documents that cigarette smoking is a cause of cerebrovascular disease (stroke) and is associated with cancer of the uterine cervix. Part I]. The Physicochemical Nature of Tobacco 1. The estimated number of compounds in tobacco smoke exceeds 4,000, including many that are pharmacologically active, toxic, mutagenic, and carcinogenic. Forty-three carcinogens have been identified in tobacco smoke. Carcinogenic tobacco-specific nitrosamines are found in high concentrations in smokeless tobacco. Chapter 3: Changes in Smoking-Attributable Mortality 1. Lung cancer death rates increased two- to fourfold among older male smokers over the two decades between the American Cancer Society's two Cancer Preven- tion Studies (CPS-I, 1959-65, and CPS-II, 1982-86). Lung cancer death rates for younger male smokers fell about 30 to 40 percent during this period. Lung cancer death rates increased four- to sevenfold among female smokers aged 45 years or older in CPS-II compared with CPS-I, while lung cancer death rates among younger women declined 35 to 55 percent. The two-decade interval witnessed a two- to threefold increase in death rates from chronic obstructive pulmonary disease (COPD) in female smokers aged 55 years or older. There was no change in the age-adjusted death rates for lung cancer and COPD between CPS-I and CPS-II among men and women who never smoked regularly. Overall death rates from coronary heart disease (CHD) declined substantially be- tween CPS-I and CPS-IL. The decline in CHD mortality among nonsmokers, however, was notably greater than among current cigarette smokers. In CPS-II, the relative risks of death from cerebrovascular lesions were 3.7 and 4.8 for men and women smokers under age 65. Increased risks of stroke were also observed among older smokers and former smokers. Along with the recently reported results of other studies, these findings strongly support a causal role for cigarette smoking in thromboembolic and hemorrhagic stroke. In 1985, smoking accounted for 87 percent of lung cancer deaths, 82 percent of COPD deaths, 21 percent of CHD deaths, and 18 percent of stroke deaths. Among men and women less than 65 years of age, smoking accounted for more than 40 percent of CHD deaths. 8. 10. The large increase in smoking-attributable mortality among American women be- tween 1965 and 1985 was a direct consequence of their adoption of lifelong cigarette smoking, especially from their teenage years onward. In 1985, 99 percent of smoking-attributable deaths occurred among people who started smoking before the 1964 Surgeon General’s Report. For this group, the annual smoking-attributable fatality rate is about 7,000 deaths per 1 million per- sons at risk. For 10 causes of death, a total of 337,000 deaths were attributable to smoking in 1985. These represented 22 percent of all deaths among men and 11 percent among women. If other cardiovascular, neoplastic, and respiratory causes of death were included—as well as deaths among newborns and infants resulting from maternal smoking, deaths from cigarette-caused residential fires, and lung cancer deaths among nonsmokers due to environmental tobacco smoke—the total smoking-attributable mortality was about 390,000 in 1985. Chapter 4: Trends in Public Beliefs, Attitudes, and Opinions About Smoking I. 22 In the 1950s, 40 to 50 percent of adults believed that cigarette smoking is a cause of lung cancer. By 1986, this proportion had increased to 92 percent (including 85 percent of current smokers). Between 1964 and 1986, the proportion of adults who believed that cigarette smoking increases the risk of heart disease rose from 40 to 78 percent. A similar increase occurred among smokers, from 32 to 71 percent. The proportion of adults who believed that cigarette smoking increases the risk of emphysema and chronic bronchitis rose from 50 percent in 1964 to 81 percent (chronic bronchitis) and 89 percent (emphysema) in 1986. These proportions in- creased among current smokers from 42 percent in 1964 to 73 percent (chronic bronchitis) and 85 percent (emphysema) in 1986. Despite these impressive gains in public knowledge, substantial numbers of smokers are still unaware of or do not accept important health risks of smoking. For example, the proportions of smokers in 1986 who did not believe that smok- ing increases the risk of developing lung cancer, heart disease, chronic bronchitis, and emphysema were 15 percent, 29 percent, 27 percent, and 15 percent, respec- tively. These percentages correspond to between 8 and 15 million adult smokers in the United States. In 1985, substantial percentages of women of childbearing age did not believe that smoking during pregnancy increases the risk of stillbirth (32 percent), mis- carriage (25 percent), premature birth (24 percent), and havinga low-birthweight baby (15 percent). Of women in this age group, 28 percent did not believe that women taking birth control pills have a higher risk of stroke if they smoke. Some smokers today do not recognize their own personal risk from smoking or they minimize it. In 1986, only 18 percent of smokers were “very concerned” about the effects of smoking on their health, and 24 percent were not at all con- cerned. 10. M1. 12. 13. In 1986, about half of current smokers and 40 percent of never smokers incorrect- ly believed that a person would have to smoke 10 or more cigarettes per day before it would affect his or her health. A national survey conducted in 1983 by Louis Harris and Associates found that the public underestimates the health risks of smoking compared with many other health risks. Many smokers underestimate the population impact of smoking. In 1987, 28 per- cent of smokers (and 16 percent of the general population) disagreed with the statement, “Most deaths from lung cancer are caused by cigarette smoking.” The proportion of high school seniors who believe that smoking a pack or more of cigarettes per day causes great risk of harm increased from 51 percent in 1975 to 66 percent in 1986. In 1986, about three-quarters of adults believed that using chewing tobacco or snuff is harmful to health. The social acceptability of smoking in public is declining, as measured by the proportion of adults who find it annoying to be near a person smoking cigarettes. This proportion increased from 46 percent in 1964 to 69 percent in 1986. A majority of the public favors policies restricting smoking in public places and worksites, prohibiting the sale of cigarettes to minors, and increasing the cigarette tax to fund the medicare program. Recent surveys indicate that about half the public supports a ban on cigarette advertising. Chapter 5: Changes in Smoking Behavior and Knowledge About Determinants Part I. Changes in Smoking Behavior 1. Prevalence of cigarette smoking has declined substantially among men, slightly among women, and hardly at all among those without a high school diploma. From 1965-87, the prevalence of smoking among men 20 years of age and older decreased from 50.2 to 31.7 percent. Among women, the prevalence of smoking decreased from 31.9 to 26.8 percent. Smoking prevalence among whites fell steadily. Among blacks, the prevalence of smoking changed very little between 1965 and 1974; subsequently, prevalence declined at a rate similar to that of whites during the same period. Smoking prevalence has consistently been higher among blue-collar workers than among white-collar workers. Annual per capita (18 years of age and older) sales of manufactured cigarettes decreased from 4,345 cigarettes in 1963 to 3,196 in 1987, a 26-percent reduction. Total cigarette sales increased gradually to 640 billion cigarettes in 1981 and then fell to 574 billion in 1987. , In 1965, 29.6 percent of adults who had ever smoked cigarettes had quit. This proportion (quit ratio) increased to 44.8 percent in 1987. The rate of increase in the quit ratio from 1965-85 was similar for men and women. The rate of change in quitting activity in recent years is similar for whites and blacks. From 1965- 85, the quit ratio increased more rapidly among college graduates than among adults without a high school diploma. 23 10. Li. 12. Of all adults who smoked at any time during the year 1985-86, 70 percent had made at least one serious attempt to quit during their lifetime and one-third stopped smoking for at least 1 day during that year. The age of initiation of smoking has declined over time, particularly among females. Among smokers born since 1935, more than four-fifths started smoking before the age of 21. Trends in prevalence of cigarette smoking among those aged 20 to 24 years are an indicator of trends in initiation. By this measure, initiation has declined be- tween 1965 and 1987 from 47.8 to 29.5 percent. Initiation has fallen four times more rapidly among males than among females. The rate of decline has been similar among whites and blacks. Initiation has decreased three times more rapid- ly among those with 13 or more years of education than among those with less education. The prevalence of daily cigarette smoking among high school seniors decreased from 29 percent in 1976 to 21 percent in 1980, after which prevalence leveled off at 18 to 21 percent. Prevalence among females has consistently exceeded that among males since 1977. Prevalence was lower for students with plans to pursue higher education than for those without such plans. The difference in prevalence by educational plans widened throughout this period; in 1987, smoking rates were 14 percent and 30 percent in these two groups, respectively. The best sociodemographic predictor of smoking patterns appears to be level of educational attainment. Marked differences in smoking prevalence, quitting, and initiation have occurred and have increased over time between more and less edu- cated people. The domestic market share of filtered cigarettes increased from 1 percent in 1952 to 94 percent in 1986. The market share of low-tar cigarettes (15 mg or less) in- creased from 2 percent in 1967 to 56 percent in 1981, after which this proportion feli slightly and then stabilized at 51 to 53 percent. The market share of longer cigarettes (94 to 121 mm) increased from 9 percent in 1967 to 40 percent in 1986. Between 1964 and 1986, use of smokeless tobacco (snuff and chewing tobacco) declined among men and women 21 years of age and older. However, among males aged 17 to 19, snuff use increased fifteenfold and use of chewing tobacco increased more than fourfold from 1970-86. Differences in prevalence of cigarette smoking and smokeless tobacco use be- tween young males and young females suggest that the prevalence of any tobac- co use is similar in these two groups. From 1964 to 1986, the prevalence of pipe and cigar smoking declined by 80 per- cent among men. Part IT. Changes in Knowledge About the Determinants of Smoking Behavior 1. 24 Smoking was viewed as a habit in 1964 and is now understood to be an addiction influenced by a wide range of interacting factors, including pharmacologic effects of nicotine; conditioning of those effects to numerous activities, emotions, and settings; socioeconomic factors; personal factors such as coping resources; and social influence factors. Since 1964, there has been a gradual evolution of understanding of the progres- sion of smoking behavior through the broad stages of development, regular use, and cessation. Each of these stages is differentially affected by multiple and in- teracting determinants. Views of determinants of smoking are affected by the predominating theoretical and methodological perspectives. In smoking, the earlier focus on broad, disposi- tional variables (e.g., extraversion) has given way to an emphasis on situation- specific and interactional variables; a focus ona search for a single cause has given way to a focus on multiple and interacting causes. Chapter 6: Smoking Prevention, Cessation, and Advocacy Activities Part I. Smoking Prevention Activities 1. Diverse program approaches to the prevention of smoking among youth grew out of antismoking education efforts in the 1960s. These approaches include media- based programs and resources; smoking prevention as part of multicomponent school health education; psychosocial prevention curricula; and a variety of other resources developed and sponsored by professional and voluntary health or- ganizations, Federal and State agencies, and schools and community groups. Psychosocial curricula addressing youths’ motivations for smoking and the skills they need to resist influences to smoke have emerged as the program approach with the most positive outcomes. Evolution in program content has been accom- panied by a shift since the 1960s in prevention program focus from youths in high school and college to adolescents in grades 6 through 8. Existing prevention programs vary greatly in the extent to which they have been evaluated and used. Psychosocial prevention curricula have been intensively developed over the last decade and have been the most thoroughly evaluated and best documented; however, they are generally not part of a dissemination system. More widely disseminated smoking prevention materials and programs, such as those using mass media and brochures, have not always been as thoroughly evaluated; however, they have achieved wider use in the field. The model of stages of smoking behavior acquisition underlies current smoking prevention programs and suggests new intervention opportunities, ranging from prevention activities aimed at young children to cessation programs for adoles- cent smokers. There has been and continues to be a lack of smoking prevention programs that target youth at higher risk for smoking, such as those from lower socioeconomic backgrounds or school dropouts. Part II. Smoking Education and Cessation Activities 1. During the past 25 years, national voluntary health agencies, especially the American Cancer Society, the American Heart Association, and the American 25 Lung Association, have played a significant role in educating the public about the hazards of tobacco use. Individual and group smoking cessation programs evolved from an emphasis on conditioning-based approaches in the 1960s, to the cognitively based self- management procedures of the 1970s, to the relapse prevention and pharmacologi- cally based components of the 1980s. There has recently been an increased emphasis on targeting specific groups of smokers for cessation activities (e.g., pregnant women, Hispanics, blacks). Packaging and marketing of self-help smoking cessation materials have become more sophisticated and there is more of an emphasis on relapse prevention, while much of the content has changed relatively little over the years. Mass-mediated quit-smoking programs have become an increasingly popular strategy for influencing the smoking behavior of a large number of smokers. The 1980s have seen an increase in the promotion of smoking control efforts in the workplace in response to increasing demand and opportunity for worksite wellness programs and smoking control policies. In the last decade there has been an increasing interest in involving physicians and other health care professionals in smoking control efforts. Medical organizations have played a more prominent role in smoking and health during the 1980s than they had in the past. Part III. Antismoking Advocacy and Lobbying I. Lobbying and advocacy efforts have expanded through the increasing commit- ment of the national voluntary health agencies to political action and the forma- tion of coalitions at the local, State, and national levels. Antismoking advocacy and lobbying have evolved over the past 25 years and now focus on a growing number of local, State, and national legislative and regulatory initiatives designed to reduce smoking, regulate the cigarette product, and prevent the uptake of smoking by children and adolescents. Chapter 7: Smoking Control Policies Part I. Policies Pertaining to Information and Education 1. 26 The Federal Government’s efforts to reduce the health consequences of cigarette smoking have consisted primarily of providing the public with information and education about the hazards of tobacco use. Two of the most well-known mechanisms are the publication of Surgeon General’s Reports and the require- ment of warning labels on cigarette packages. A system of rotating health warn- ing labels is now required for all cigarette and smokeless tobacco packaging and advertisements. Current laws do not require health warning labels on all tobacco products and do not require monitoring of the communications effectiveness of the warnings. Fur- thermore, existing laws do not provide administrative mechanisms to update the contents of labels to prevent the overexposure of current messages or to reflect advances in scientific knowledge, such as new information about the addictive nature of tobacco use. There is insufficient evidence to determine the independent effect of cigarette warming labels, particularly the rotating warning labels required since 1985, on’ public knowledge about the health effects of smoking or on smoking behavior. Information about tar and nicotine yields appears on all cigarette advertisements but not on all cigarette packages. Levels of other hazardous constituents of tobac- co smoke, such as carbon monoxide, hydrogen cyanide, and ammonia, are not dis- closed on packages or advertisements. Little information is available to the public about the identity or health consequences of the additives in tobacco products. Declines in adult per capita cigarette consumption have occurred in years of major dissemination of information on the health hazards of smoking. These include 1964, the year of the first Surgeon General's Report on smoking and health, and 1967-70, when antismoking public service announcements were widely broad- cast on radio and television, as mandated by the Federal Communications Commission’s Fairness Doctrine. In 1985, when cigarette advertising and promotion totaled 2.5 billion dollars, cigarettes were the most heavily advertised product category in the outdoor media (e.g., billboards), second in magazines, and third in newspapers. Over the past decade, the majority of cigarette marketing expenditures has shifted from tradi- tional print advertising to promotional activities (e.g., free samples, coupons, sponsorship of sporting events). An estimated | percent of the budget allocated to disease prevention by the U.S. Department of Health and Human Services is devoted specifically to tobacco con- trol. These expenditures totaled 39.5 million dollars in 1986. Part II. Economic Incentives 1. Cigarette excise taxes are imposed by the Federal Government (16 cents per pack), all State governments, and nearly 400 cities and counties. On average, Federal and State excise taxes add 34 cents per pack to the price of cigarettes. Cigarette excise tax rates have fallen since 1964 in real terms because the rate and mag- nitude of periodic tax increases have not kept pace with inflation. Studies demonstrate that increases in the price of cigarettes decrease smoking, particularly by adolescents. It has been estimated that an additional 100,000 or more persons will live to age 65 as a result of the price increases induced by the 1983 doubling of the Federal excise tax on cigarettes. In 1964, smoking status was not considered in the determination of insurance premiums. Currently, nearly all life insurers but only a few health, disability, and property and casualty insurers offer premium discounts for nonsmokers. Few health insurers reimburse for the costs of smoking cessation programs or treat- ment. 27 Part III. Direct Restrictions on Smoking 1. Restrictions on smoking in public places and at work are growing in number and comprehensiveness, as a result of both Government actions and private initiatives. Forty-two States and more than 320 communities have passed laws restricting smoking in public, and an estimated one-half of large businesses have a smoking policy for their employees. The goal of these smoking restrictions is to protect individuals from the conse- quences of involuntary tobacco smoke exposure, but they may also contribute to reductions in smoking prevalence by changing the attitudes and behavior of cur- rent and potential smokers. Insufficient research has been undertaken to deter- mine the extent, if any, of these effects. There are fewer legal restrictions on children’s access to tobacco products now than in 1964, despite what has been learned since then about the dangers of tobac- co use, its addictive nature, and the early age of initiation of smoking. As of January 1, 1988, laws in 43 States and the District of Columbia restricted the sale of cigarettes to minors. Nevertheless, tobacco products are relatively easy for children to obtain through vending machines and over-the-counter purchases because of low levels of compliance with and enforcement of current laws. Tobacco products have been exempted by law or administrative decision from the jurisdiction of Federal regulatory agencies under whose authority they might otherwise fall. Chapter 8: Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences 1. 28 All birth cohorts born between 1901 and 1960 experienced reductions in the prevalence of smoking relative to the rates that would have been expected in the absence of the antismoking campaign. By 1985, the gap between actual (reported) prevalence and that which would have been expected ranged from 6 percentage points for the eldest female cohort to 28 percentage points for the youngest male cohort. In 1985, an estimated 56 million Americans 15 to 84 years of age were smokers. In the absence of the antismoking campaign, an estimated 91 million would have been smokers. Adult per capita cigarette consumption has fallen 3 to 8 percent in years of major smoking-and-health events, such as publication of the first Surgeon General’s Report on smoking and health in 1964. Per capita consumption fell each of the years the Fairness Doctrine antismoking messages were presented on television and radio (1967-70). By 1987, adult per capita cigarette consumption would have exceeded its actual level by an estimated 79 to 89 percent had the antismoking campaign never oc- curred. One of the most substantial behavioral responses to concerns about smoking and health has been the shift toward filtered cigarettes in the 1950s and low-tar and low-nicotine cigarettes in the 1970s. The net health impact of these product chan- ges is unknown. As a result of the antismoking campaign, an estimated 789,000 deaths were postponed during the period 1964 through 1985, 112,000 in 1985 alone. The average life expectancy gained per postponed death was 21 years. . The avoidance of smoking-related mortality associated with the antismoking cam- paign will represent a growing percentage of smoking-related mortality over time, as the principal beneficiaries of the campaign, younger men and women, reach the ages at which smoking-related disease is most common. Campaign-induced quitting and noninitiation through 1985 will result in the postponement or avoidance of an estimated 2.1 million smoking-related deaths between 1986 and the year 2000. 29 References AOKI, M., HISAMICHI, S., TOMINAGA, S. (eds.) Smoking and Health 1987. Proceedings of the 6th World Conference on Smoking and Health, Tokyo, November, 9-12, 1987. Amster- dam: Excerpta Medica, 1988. BOYD, G., DARBEY, C.M. (eds.) Smokeless Tobacco Use in the United States, NCI Monograph. National Cancer Institute, in press. BRITISH MEDICAL RESEARCH COUNCIL. Tobacco smoking and cancer of the lung. Statement by the Medical Research Council. British Medical Journal 1:1523-1524, 1957. BRODERS, A.C. 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Tobacco smoking as a possible etiologic factor in bronchiogenic carcinoma: A study of 684 proved cases. Journal of the American Medical Association 143:329-396, May 27, 1950. 32 CHAPTER 2 ADVANCES IN KNOWLEDGE OF THE HEALTH CONSEQUENCES OF SMOKING 33 CONTENTS Introduction 2.0... ene enn eee nee 37 Part [: Health Consequences ©... 0... eee eee eee ees 38 Smoking and Overall Mortality .. 0.6... 00. cee eee 38 Lung Cancer 20066. eens 43 Introduction .. 6. ee eee tenes 43 Dose-Response Relationships .......... 02-0 s eee eee e eee eee 43 Women and Lung Cancer 1.1.0... 0 06.0 c eee tenes 46 Type of Lung Cancer and Smoking ........ 6.5.02 e eee eee eee eee 50 Pipe and Cigar Smoking ......... 0.00. c eee eens 50 Determinants of Susceptibility ©0000... 06. ee eee 50 Familial Factors .......00. 0022 cece tee eee nents 52 Other Host Factors 2.0.0.2... 0 cece eee tee eens 52 Occupational Exposures... 6.6... ee eee eee ee 52 Ambient Air Pollution ...........0. 000 cece eee eee 53 Indoor Air Pollution ..........0. 002 cece teens 53 Diet o.oo teen ene ete 54 Smoking Cessation 02... 6.00.0 cece teens 55 Laryngeal, Oral, and Esophageal Cancer ...... 0.06... cee eee eee eee eens 56 Bladder and Kidney Cancer 0.0.0.0. cee eee eee eee 56 Pancreatic Cancer 0... ee teen ene e nets 56 Stomach Cancer 0... 0... ccc eee ee ete ene ent eee 57 Cervical Cancer... 0... ee nen eet een e ees 57 Endometrial Cancer 2.6... cee tenet nents 58 Coronary Heart Disease 2.0... ee eee eee 58 Epidemiology ........ 006 et eee eens 58 Coronary Heart Disease Risk Factors 1... 6.60. ee eee ee eee ees 59 Pathophysiological Mechanisms .........6 206 eee eee e ee eee eens 60 Clinical Correlations ....... 00.0.2 cee eect ees 61 Smoking Cessation 0.2.0.0... 0. ete eee ee 61 Cerebrovascular Disease (Stroke) 2.0.0.2... eee eee ee eee 61 Atherosclerotic Peripheral Vascular Disease ....... 00-00 eee ee eee eee 63 Atherosclerotic Aortic Aneurysm .... 0.6 ee eee eee eens 65 Chronic Obstructive Pulmonary Disease ......... 220.00 e eee 66 Pathogenesis 0.0.6... ccc eee eee e eens 67 Pathophysiology 2.0.0.0... 0. cece eee eee eee eee nent ees 67 Natural History of COPD and the Role of Cigarette Smoking ......... 68 Pregnancy and Infant Health .... 0.2.2... eee ee teens 71 Infant Birthweight: 2.2.0... 0 eee eee ees 72 Fetal and Perinatal Mortality 22.2.0... 0.00 cece eee ee eee eee 73 Congenital Malformations 2.0.2.6... 60. e eee eee eens 73 Fertility 0.00... c ec n nee eee 75 Long-Term Effects on the Child 2.6.00... eee e eee eee 75 Peptic Ulcer 2... cc ene eens 716 Osteoporosis 6... ence cent cece eee eeeneeennnee 76 Involuntary Smoking . 1.0.0.0... ccc cece ence cence eecevues 77 Smokeless Tobacco... 0... 0. ec ccc c cece cee enteevreennes 78 Addiction to Smoking 22.00... 0... ccc ccc ccc cece neces eeeeneeeees 78 Part Hl: The Physicochemical Nature of Tobacco ........0....cccceeseeeeee 79 The Changing Cigarette 20.0.0. c cece ene een aeeeneeeees 85 Environmental Tobacco Smoke ..... 2.0.00... c cece cece cee eeeeeuces 88 Smokeless Tobacco «0.0.0.2... ccc ec c nce nce e en eeeeeeetneens 90 Toxicity and Carcinogenicity of Tobacco Smoke ...........-..000cc0eeee 92 Nicotine 2.0.0... c cence eens eee eeeneeennns 93 Biological Markers 2.00.06... cle cece cece nce eeeeeaeneenenns 94 Summary 2.0... cnn eee e tee eeeteeuebnenbnens 97 Conclusions 0.0... ce cee teen teen teen tevucreenes 100 References 2.0.0.0. cece ccc nce eect ee eeuneneenens 102 36 INTRODUCTION The purpose of this Chapter is to summarize and compare the state of biomedical knowledge concerning tobacco and health in 1989 with that presented in the 1964 Sur- geon General's Report (see Table 13). The Chapter addresses major tobacco-related disorders that are well documented in the medical literature; it does not consider many areas of current research that may prove to be important but are in an early or provisional state of investigation. The 1964 Surgeon General’s Report was a landmark publication that included a sur- vey of more than 7,000 available scientific articles on smoking and health. The Ad- visory Committee that prepared the 1964 Report reviewed and assessed epidemiologic, clinical, pathological, and experimental data for evidence linking smoking to disease. To reach conclusions concerning the causality of associations between smoking and disease, the Committee constructed a framework for evaluating the evidence. With regard to causality, the Committee concluded: The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability. To judge or evaluate the causal significance of the as- sociation between attribute or agent and the disease, or effect upon health, a number of criteria must be utilized, no one of which is an all-sufficient basis for judgment. These criteria include: a) the consistency of the association b) the strength of the association c) the specificity of the association d) the temporal relationships of the association e) the coherence of the association (US PHS 1964). These criteria were applied throughout the 1964 Report. When the word “cause” was used in the 1964 Report, it was felt to convey “the notion of a significant, effectual relationship between an agent and an associated disorder or disease in the host.” Use of the word “cause” in relation to cigarette smoking did not exclude other agents as causes; rather, the members of the Advisory Committee shared “a common conception of the multiple etiology of biological processes.” The principal findings on the health effects of smoking were summarized in the Sur- geon General’s 1964 Report as follows: 1. Cigarette smoking is associated with a 70-percent increase in the age-specific death rates of men. 2. Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction. 3. Cigarette smoking is the most important of the causes of chronic bronchitis in the United States and increases the risk of dying from chronic bronchitis and 37 emphysema. A relationship exists between cigarette smoking and emphysema, but it has not been established that the relationship is causal. 4. It is established that male cigarette smokers have a higher death rate from coronary artery disease than nonsmoking males. Although the causative role of cigarette smoking in deaths from coronary disease is not proven, the Commit- tee considers it more prudent from the public health viewpoint to assume that the established association has causative meaning than to suspend judgment until no uncertainty remains. 5. Pipe smoking appears to be causally related to lip cancer. Cigarette smoking is a significant factor in the causation of cancer of the larynx inmen. The evidence supports the belief that an association exists between tobacco use and cancer of the esophagus, and between cigarette smoking and cancer of the urinary blad- der in men, but the data are not adequate to decide whether these relationships are causal. 6. Women who smoke cigarettes during pregnancy tend to have babies of lower birthweight. It is not known whether this decrease in birthweight has any in- fluence on the biological fitness of the newborn. 7. Epidemiologic studies indicate an association between cigarette smoking and peptic ulcer that is greater for gastric than for duodenal ulcer. 8. The habitual use of tobacco is related primarily to psychological and social drives, reinforced and perpetuated by the pharmacologic actions of nicotine. Since 1967, the U.S. Department of Health and Human Services has transmitted to the U.S. Congress mandated reports on the health consequences of smoking. Some of the reports have been encyclopedic reviews similar to the 1964 Report, whereas others have focused on the relationship between smoking and a specific topic. The Federal unit charged with preparing these annual reports. the Office on Smoking and Health, now has more than 57,000 documents on smoking and health in its Technical Informa- tion Center database. Research performed during the subsequent 25 years has substantiated and strengthened the conclusions of the 1964 Advisory Committee. Studies published since 1964 have also established associations between smoking and disease in areas for which data did not exist in 1964, shed light on pathogenetic mechanisms of tobacco-related disease, and added scientific depth to areas mentioned only briefly in the 1964 Report. PART I: HEALTH CONSEQUENCES Smoking and Overall Mortality [See Chapter 3 for more detailed discussion) The major prospective studies of the disease risks associated with smoking completed in the 1960s and 1970s contributed substantially to an understanding of the relation- ship between smoking and disease (US DHEW 1979). These studies provided es- timates of both the relative and attributable risks related to cigarette and other types of smoking (Table 1) (US DHEW 1979). Male cigarette smokers had approximately 70 percent higher overall death rates than nonsmokers: the excess mortality of female 38 6f TABLE 1.—Mortality ratios of current cigarette-only smokers, by cause of death in eight prospective epidemiologic studies British Males in 25 States” US. Japanese Canadian = Males in 9 Swedish’ Califomia Cause of death doctors! 45-64 65-79 veterans" study* veterans” States® Males Females occupations® All cancers’ (140-205) 2.14 1.76 2.21 1.62 1.97 Cancer of lung and bronchus (162-163) 14.0 7.84 11.59 12.14 3.64 14.2 10.73 7.0 45 15.9 Cancer of larynx (161) 6.09 8.99 9.96 13.59 13.10 Cancer of buccal cavity (140-141) 13.0° 4.09 7.04 3.9° 2.80 Cancer of pharynx (145-148) 9.90° 2.93° 12.54 2.81 1.0 Cancer of esophagus (150) 47 4.17 1.74 6.17 2.57 3.3 6.60 Cancer of bladder and other (181) 2.1 2.20 2.96 2.15 0.98 13 2.40 18 1.6 0.7 Cancer of pancreas (157) 1.6 2.69 2.47 1.84 1.83 2.1 3.1 2.5 6.0 Cancer of kidney (180) 1.42 1.57 1.45 Lil 1.4 1.50 Cancer of stomach (151) 1.42 1.26 1.60 151 1.9 2.30 0.9 2.3 Cancer of intestines (152—153) 1.27 1.27 1.4 0.50 0.8 Cancer of rectum (154) 2.7 1.01° 1.175 0.98 0.91 0.6 0.80 0.9 All cardiovascular disease (330-334, 1.90 131 1.75 1.57 400-468) CHD (420) 1.6 2.08 1.36 1.74 1.96 1.6 1.70 17 1.3 2.0 Cerebrovascular lesions (330-334) 13 1.38 1.06 1.52 1.14 0.9 1.30 1.0 Ll 1.8 Aortic aneurysm (nonsyphilitic) (451) 6.6 2.62 4.92 5.24 1.8 1.6 Hypertension (440-447) 1.40 1.42 1.67 2.51 1.6 1.20 1.3 1.4 1.0 General arteriosclerosis (450) 1.4 1.86 3.3 2.00 2.0 2.0 OP TABLE 1.—Continued British Males in 25 States” US. Japanese Canadian = Males in 9 Swedish’ California Cause of death doctors! 45-64 65-79 veterans* study* veterans” States® Males Females occupations® All respiratory disease (nonneoplastic) 2.85 Emphysema and/or bronchitis 24.7 10.08 2.30 1.6 2.24 43 Emphysema without bronchitis (527.1) 6.55 11.41 14.17 77 Bronchitis (500-502) 4.49 11.3 Respiratory tuberculosis (001-008) 5.0 2.12 1.27 Asthma (241) 3.47 Influenza and pneumonia (480-498) 1.4 1.86 1.72 1.87 1.4 2.60 2.4 Certain other conditions Stomach ulcer (540) 25° 4.06 4.13 4.13 2.06° Duodenal ulcer (541) 2.86 1.50 2,98 6.9 2.16 0.5 Cirthosis (581) 3.0 2.06 1.97 3.38 1.35 2.3 1.93 2.4 0.8 4.0 Parkinsonism (350) 0.4 0.26 All causes 1.64 1.88 1.43 1.84 1.22 1.52 1.70 14 1.2 1.78 “Numbers in parentheses represent International Classification of Diseases (ICD) codes. "Includes cancers of larynx, buccal cavity, and pharynx. “Includes cancers of buccal cavily and pharynx. “Includes cancers of intestines and rectum. “Includes stomach ulcer and duodenal ulcer. ‘Includes emphysema, bronchitis, and asthma. SOURCE: Studies cited are as follows: 'Doll and Hill (1956); “Hammond (1966); Kahn (1966): “Hirayama (1967); “Best, Josie, Walker (1961): (1975); ’Dunn, Linden, Breslow (1960). US DHEW (1979). * Hammond and Horm (1958); "Cederlof et.al. cigarette smokers was somewhat less than that of men, but it increased over the fol- lowup intervals. A strong dose-response relationship was found between exposure to cigarette smoke and excess mortality, cessation of cigarette smoking was associated with a decrease in this excess mortality. The relative risks were greater for smoking- related cancers and chronic obstructive pulmonary disease (COPD) than for coronary heart disease (CHD). however. because of the higher mortality rates for CHD the smok- ing-attributable mortality associated with CHD accounted for over one-third of the ex- cess mortality due to smoking-related diseases. There have been relatively few long-term longitudinal studies that have measured the overall effects of cigarette smoking since these earlier reports. Results from a new American Cancer Society (ACS) prospective study (Cancer Prevention Study II, CPS-II) and a detailed discussion of total smoking-related mortality are presented in Chapter 3. Based on this study, cigarette smoking is currently estimated to account for 21 percent of all CHD deaths, 30 percent of all cancer deaths, and 82 percent of all COPD deaths. The Multiple Risk Factor Intervention Trial (MRFIT) is a recent prospective study that screened 361,662 men aged 35 to 57 years between 1972 and 1974 and has been following them since then, both through the Social Security Administration and the Na- tional Death Index files. To gauge smoking status, only the number of cigarettes smoked per day at enrollment was reported. Because former smokers were included in the nonsmoker category, the risk comparisons in this study between nonsmokers and smokers are conservative in estimating the effects of smoking. Findings for the 6 years of followup for the MRFIT enrollees screened from 1972-73 are consistent with the studies reported in the 1960s, despite changes in the type of cigarettes in terms of tar and nicotine yield and the increased use of filters (see later section of this Chapter and Chapter 5). The MRFIT study shows that smoking status and number of cigarettes smoked per day have remained powerful predictors for total mortality and the develop- ment of CHD, stroke. cancer, and COPD. In the study population, there were an es- timated 2.249 (29 percent) excess deaths due to smoking, of which 35 percent were from CHD and 21 percent from lung cancer. The nonsmoker—former smoker group had 30 percent fewer total cancers than the smoking group over the 6-year followup. A study of a random sample of 25,129 Swedish men between 1964 and 1979 evaluated the relationship between cigarette smoking (prevalence of 32 percent), pipe smoking (27 percent), cigar smoking (5 percent), and subsequent ‘mortality (Table 2, Carstensen, Pershagen, Eklund 1987). The all-cause relative death rate was 1.7-fold higher for those smoking greater than 15 g of tobacco per day (estimated as 16 to 25 cigarettes equaling 20 g or a package of pipe tobacco lasting | to 4 days equaling 16 g). The relative risks associated with cigarette smoking were consistent both with those of the current MRFIT sample and the earlier cohorts from the 1950s and 1960s. The risks were also increased for pipe and cigar smokers for many of the causes of death. Epidemiologic studies have shown that cigarette smoking exerts an adverse effect on mortality in older as well as younger age groups. The 17-year followup of the Alameda County Study (Kaplan et al. 1987) demonstrates an increased risk of death even among older cigarette smokers. The adjusted relative risk of death among smokers at entry was 1.46 (age 60 to 69) and 1.43 at age 70 or more. Smoking remained the strongest 4l predictor of mortality even in this older age group. Other studies have also substan- tiated that smoking remains an important risk factor in the older age groups (Jajich, Ostfeld, Freeman 1984). TABLE 2.— Mortality ratios for selected causes in Swedish males, 1964-1979, by type of smoking Type of smoking* Cigarettes Pipe Cigars Cause of death only only only Cancer of oral cavity and larynx 2.9 (8) 1.4(3) 0.6 (Lt) (140-146, 148, 161) Cancer of esophagus (150) 3.7 (9) 3.6 (6) 6.5 (2) Cancer of liver and biliary 3.0 (13) 1.7 (S) 7.2 (4) passages (155-156) Cancer of pancreas (157) 3.3 (28) 2.8 (19) 1.01) Cancer of trachea, bronchus, and 7.4 (77) 7.2 (59) 7.6(11) lung (162) Cancer of bladder (188) 4.2 (17) 4.0 (16) 1.9 (1) Ischemic heart disease (410-414) 1.48 (399) 1.39 (366) 1.16 (42) Aortic aneurysm (nonsyphilitic) 2.111) 2.1 (11) 5.1 (4) (441) Bronchitis and emphysema 3.3 (18) 3.6 (16) 1.3) (490-492) Peptic ulcer (531-534) 2.0 (11) 2.8 (13) 4.0 (3) Cirrhosis of liver (571) 1.8 @Q1) 0.7 (4) 2.7 (3) Suicide, accidents, and violence 1.7 (90) 0.9 (35) 2.5 (10) (E800-E999) All causes 1.45 (1,063) 1.29 (866) 1.39 (131) NOTE: Death rates standardized for age and residence. Never smokers constitute the reference group. Number of deaths are given in parentheses. *The mean grams of tobacco smoked per day in 1963, standardized for age and residence, was estimated to be 10.7 in cigarette smokers, 8.4 in pipe smokers, and 13.5 in cigar smokers. Numbers in parentheses are ICD-8 codes. SOURCE: Carstensen, Pershagen, Eklund (1987). 42 Lung Cancer Introduction One of the most prominent conclusions of the 1964 Report was the determination that “Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect far outweighs all other factors. The data for women, though less extensive. point in the same direction.” The epidemiologic evidence available in 1964 on smoking and lung cancer was already extensive. Sharply increasing lung cancer mortality rates in the United States across the 20th century provided indisputable documentation of anew epidemic. Clinical observations and early epidemiologic findings suggested that tobac- co smoking was associated with lung cancer, but hypotheses related to air pollution, occupation, and other factors were also extant. By 1964, however, the epidemiologic data. derived from 29 retrospective and 7 prospective studies, were conclusive: smok- ing was causally related to cancer of the lung. Further support for this conclusion was obtained from animal studies showing that condensates of tobacco smoke were car- cinogenic and from the demonstration that tobacco smoke contained carcinogens (US DHHS 1982). The evidence compiled through 1964 also provided additional insight into quantitative aspects of respiratory carcinogenesis by tobacco smoke. The risk of lung cancer was shown to increase with the amount and duration of smoking and to decline with cessation of smoking. In the 25 years since the 1964 Report, voluminous evidence has continued to support the causal relationship between smoking and lung cancer. The new evidence has been sufficient to establish that smoking also causes lung cancer in women, more com- prehensive epidemiologic data have provided expanded descriptions of dose-response relationships between smoking and lung cancer risk. Research has also been directed at environmental and host factors determining susceptibility to tobacco smoke. New investigative techniques in molecular and cellular biology are now providing insight into the molecular mechanisms of carcinogenesis by tobacco smoke. Dose-Response Relationships The 1964 Report reviewed evidence from retrospective and prospective epidemiologic investigations that documented dose-response relationships between lung cancer risk and measures of exposure to tobacco smoke. This evidence was cited by the 1964 Report in relation to the criterion of strength of association for determin- ing causality. Investigation of dose-response relationships for lung cancer has sub- sequently been extended. Mathematical models have been applied to the epidemiologic data to gain biological insight into respiratory carcinogenesis. The cigarette has evolved substantially since 1964 with modifications designed to reduce tar and nicotine yields. Recent research has addressed the risks of smoking the newer products. Studies of lung cancer and involuntary smoking have examined lung cancer risks at low dose levels (US DHHS 1986a). Abundant epidemiologic evidence has shown dose-response relationships of lung cancer risk with cigarettes smoked per day, degree of inhalation, and age at initiation 43 of regular smoking. For the purpose of illustration, selected examples of dose-response relationships from two of the early. large prospective epidemiologic studies are reviewed here. Figure | shows lung cancer mortality ratios for males by the number of cigarettes smoked per day. For those who smoked more than 40 cigarettes per day, the risk of dying of lung cancer was 23 times greater than the risk experienced by non- smokers. Figure 2 illustrates the lung cancer mortality ratios for males by self-reported degree of inhalation of cigarette smoke. These data confirm that even those who reported “just puifing™ on cigarettes still had a significantly increased risk of lung cancer. Those who reported inhaling “none” or “slightly” experienced a risk of developing lung cancer that was eight times greater than that of nonsmokers. The relative risk increased to 17 for those who inhaled deeply. Figure 3 shows lung cancer mortality ratios for males by the age they began smok- ing. The risk of developing lung cancer was greatest for those who began smoking at an early age. Mathematical modeling of dose-response relationships, in the biological framework of a multistage model of carcinogenesis, has provided further insight into the nature of dose-response relationships for smoking and lung cancer. Using data from the prospec- tive study of British doctors. Doll and Peto (1978) have performed the most widely cited analysis. They compared regular smokers and lifelong nonsmokers and showed that lung cancer incidence increased with the square of the amount smoked daily, but with the duration of smoking raised to a power of 4to 5. This finding implies that dura- tion of smoking is the stronger determinant of lung cancer risk and that initiation of smoking during the teenage years will have serious consequences for lung cancer risk (Peto 1986). Commercial cigarettes have continuously evolved through the addition of filters and other modifications designed to reduce tar and nicotine yields (US DHHS 1981). Since extensive modification of the cigarette began in the 1950s, it has only recently become possible to investigate smokers with predominant use of the newer products. Evidence from prospective and case-control studies and assessment of temporal trends of lung cancer mortality indicate somewhat lower risks for cigarettes with reduced tar and nicotine yield. although the risks remain markedly higher than for nonsmokers (US DHHS 1982). Doil and Peto (1981) examined trends of lung cancer mortality in males in the United States, Britain. and other European countries. They concluded that the international differences and the temporal trends were generally consistent with the tar yields and tar intakes across time and across countries. Relevant information is also available trom case-control and prospective studies. In the United States, investigations spanning the 1960s and 1970s have shown somewhat reduced lung cancer risks in smokers who switched from nonfilter to filter cigarettes (Bross and Gibson 1968: Wynder, Mabuchi, Beattie 1970; Hammond et al. 1976: Wynder and Stellman 1979). More recent studies continue to document lower risks in smokers of filter cigarettes compared with smokers of nonfilter cigarettes. In a case— control study conducted in Western Europe, the relative risk for lifelong nonfilter Cigarette smokers was approximately twice that for smokers of filter cigarettes alone 44 ° Mortality Ratio 23.7 Nonsmoker 1-9 10-20 21-39 404 Cigarettes Smoked Per Day FIGURE 1!.—Lung cancer mortality ratio for males by cigarettes smoked per day SOURCE: USS. Veterans (Kahn 1966). 7 Mortality Ratio Nonsmoker None Slight Moderate Deep Degree of Inhalation FIGURE 2.—Lung cancer mortality ratio for males by degree of inhalation SOURCE: CPS-I (Hammond 1966). 5 Mortality Ratio Nonsmoker 25+ 20-24 15-19 Under 15 Age Began Smoking FIGURE 3.—Lung cancer mortality ratio for males by age began smoking SOURCE: U.S. Veterans (Kahn 1966). (Lubin et al. 1984a: Lubin et al. 1984b). However, dose-response relationships could not be demonstrated between relative risk and the proportion of years nonfilter brands were smoked or with a cigarette tar index. Among sustained smokers, switching from nonfilter to filter cigarettes was associated with a small reduction in risk (Lubin et al. 1984a). The results from another recent case-control study conducted tn Cuba also did not show a convincing association between tar intake and relative risk of lung cancer (Joly, Lubin, Caraballoso 1983). In New Mexico, a case-control study found that lifelong filter cigarette smokers and smokers of both filter and nonfilter cigarettes were at lower risk than lifelong smokers of nonfilter cigarettes only (Pathak et al. 1986). However, there was no evidence of decreasing risk as the extent of filter smoking in- creased. In addition, few data are available on the reduced risk of smoking low-tar or filter cigarettes for any other smoking-related disease (see Chapter 3). Women and Lung Cancer In 1964, at the time of the first Surgeon General’s Report, lung cancer was the lead- ing cause of cancer mortality in males, but was only the fifth leading cause of cancer mortality among women. In 1964, the male—female ratio of death rates from lung can- cer was 6.7. The 1964 Report did not determine that smoking was causally related to lung cancer in women, although the suggestive nature of the evidence was cited in the Report’s conclusion on lung cancer. The consistency of the male-female differences in lung cancer mortality with temporal trends of smoking was noted. In the 25 years that have elapsed since the 1964 Report, lung cancer mortality has in- creased dramatically in women. In 1986, lung cancer and breast cancer were the lead- ing causes of cancer death in U.S. women, accounting for approximately equal num- bers of cancer deaths (Figure 4): lung cancer deaths are now projected to have surpassed breast cancer deaths (American Cancer Society 1988). Lung cancer mortality for women now equals that observed for men three decades earlier and the male-female ratio of death rates has now fallen to 2.0. Since the late 1970s, the rise in the age-adjusted death rates of lung cancer among men began to level off (Horm and Kessler 1986). In contrast, lung cancer death rates among women continue to climb (Figure 4). As Figures 4 and 5 demonstrate, lung cancer is the only major cancer whose death rates have increased substantially and steadily since the 1930s. The dramatic increase among women began approximately 30 years after the increase for men, consistent with the later adoption of smoking by women; the slope of the curve for women appears to be nearly identical to that of men 30 years earlier. Figure 4 also demonstrates that amon g women, the lung cancer death rate closely approximated the breast cancer death rate in the mid-1980s. Illustrative of the importance of lung cancer in overall cancer mortality is the fact that, excluding lung cancer, the Nation's age-adjusted cancer death rate fell by 13 percent from 1950 through 1982. Including lung cancer, the rate increased by 8 percent (Bailar and Smith 1986). The mounting evidence on smoking and lung cancer in women led to a strengthen- ing of the tentative conclusion in the 1964 Report. The 1971 Report concluded that “Cigarette smoking is a cause of lung cancer in women but accounts for a smaller 46 Rate per 100,000 female population eT tT oy Td Age-Adjusted Cancer Death Rates* for 70 — Selected Sites, Females, United States, 1930-1986 60 50 40 0 1930 1940 1950 1960 1970 1980 1990 Lung = Ovary —-—-—Colon & Rectum — a Breast — om =: Uterus — ++ —— Leukemia sass aes e Pancreas —---— Stomach ----~-~~— Liver FIGURE 4.—Age-adjusted cancer death rates. for selected sites, females, United States, 1930-86 Adjusted to the age distribution of the 1970 U.S. Census poputation. SOURCES OF DATA: National Center for Health Statistics: U.S. Bureau of the Census. proportion of cases than in men” (US DHEW 1971). The conclusion of the 1979 Report was similar (US DHEW 1979). The 1980 Report (US DHHS 1980), concerned with smoking and women, and the 1982 Report (US DHHS 1982), concerned with smoking and cancer, comprehensively reviewed the epidemiologic data and reaffirmed the ear- lier conclusions concerning the causal association of smoking and lung cancer in 47 Rate per 100,000 male population i Age-Adjusted Cancer Death Rates* for — 70 +~ Selected Sites, Males, a United States, 1930-1986 J 60 / 50 7 40 ~ | o N 30 x ™.. ee. ae \ afin a NIA, . / C sd _ Ns -- |e . Leo 20 L c “\_A . . JT J aN L-” eA oN Pe ope 0 1930 1940 1950 1960 1970 1980 1990 "—"—+—-Esophagus —- ~—Prostate — ---—Colon & Rectum Lung cose, Bladder — --—-Leukemia ttre Pancreas 9 —---——Stomach -------Liver FIGURE 5.—Age-adjusted cancer death rates for selected sites, males, United States, 1930-86 Adjusted to the age distribution of the 1970 LS. Census population, SOURCES OF DATA: National Center for Health Statistics: U.S. Bureau of the Census. women, the evidence also provided comprehensive descriptions of dose-response relationships with findings similar to those reported previously for men. Recently teported dose-response relationships from the American Cancer Society Cancer Prevention Study II for lung cancer and women extend these observations (Figure 6). 48 These data also dramatically illustrate that the current lung cancer epidemic in women is confined to those who smoke cigarettes (Figure 7). Mortality Ratios 26 None All SM < 10 11-19 20 2-30 31+ No. of cigarettes daily FIGURE 6.—Lung cancer mortality ratios of female cigarette smokers, compared to never smokers, by daily cigarette consumption SOURCE: CPS-II 1982-86, ACS. Age-standardized death rates per 100,000 women 160 SE Nonsmokers Smokers 130.4 100 50 FIGURE 7.—Lung cancer death rates among females over time SOURCE: CPS-l and CPS-II, ACS. 49 Type of Lung Cancer and Smoking At the time of the 1964 Surgeon General's Report. the Kreyberg classification of tung tumors was being investigated. Group | Kreyberg tumors included the epidermoid and small-cell histology types: Group 2 Kreyberg tumors included adenocarcinoma and bronchioalveolar cell types. It was felt at that time that the Group I tumors, but probab- ly not the Group 2 tumors, were associated with smoking. The 1982 Surgeon General’s Report noted that smoking was related to all four major types of lung cancer: epider- moid, small cell, large cell, and adenocarcinoma. A detailed study of trends in type of lung cancer has been reported from Olmsted County, MN. a region where a large percentage of medical care is provided through the Mayo Clinic. The investigators measured the incidence by type of lung cancer over a 45-year period. The incidence rates for squamous (epidermoid), adenocarcinoma, small-cell, and large-cell lung cancer all increased during this time (Figure 8) (Beard et al. 1985). Adenocarcinomas are more common than other cell types among nonsmokers, in whom lung cancer is rare. Pipe and Cigar Smoking Mortality ratios for lung cancer in those who have always smoked only cigars or pipes are significantly higher than in nonsmokers (US DHHS 1982). The mortality ratios are lower, however, than among those who have always smoked cigarettes. The risk of lung cancer increases in relation to the number of cigars smoked per day, the number of pipesful smoked per day, and the degree of smoke inhalation. The lower risk of lung cancer among pipe and cigar smokers compared with cigarette smokers is due to the lesser amount of tobacco smoked and the lower degree of inhalation. Chemical analysis of the smoke from pipes. cigars, and cigarettes indicates that car- cinogens are found in similar levels in the smoke of all these tobacco products. Addi- tionally, experimental studies have shown that in a variety of animal models, smoke condensates from pipes and cigars are equally, if not more, carcinogenic than conden- sates from cigarettes (US DHEW 1979). Determinants of Susceptibility Since the 1964 Report, substantial epidemiologic and experimental investigation has been directed at the determinants of susceptibility to tobacco smoke; both environmen- tal exposures and host characteristics have been investigated. The identification of determinants of susceptibility not only would further understanding of the mechanisms of carcinogenesis by tobacco smoking, but would offer new approaches for prevention of lung cancer by identification of smokers at higher risk. Synergistic interactions among risk factors may place persons with particular combinations of exposures at higher risk for lung cancer. Interactions among risk factors, such as cigarette smoking and occupational ex- posures, may be either synergistic or antagonistic; synergism refers to an increased ef- fect of the independent exposures when both are present, whereas antagonism refers to 50 20 Adenocarcinoma Large cell Small cet Squamous cell 16 > ew 4+ 0 14 12 10 Hate per 100,000 population 1935-44 1945-54 1955-64 1965-74 1975-79 FIGURE 8.—Mean annual incidence rates per 100,000 population for males of bronchogenic carcinoma by cell type, Olmsted County, MN, 1935- 79, by decade SOURCE: Beard etal. (1985). a reduced effect, Statistical methods are used with epidemiologic data to describe in- teractions. Either an additive or a multiplicative scale may be used to measure interac- tion statistically (Saracci 1987). For two exposures, on an additive scale, the sum of the two independent relative risks reduced by one is compared with the relative risk ob- served when both exposures are present. Ona multiplicative scale. the comparison rela- tive risk value is the product of the two independent relative risks. For public health purposes, a positive departure from additivity is considered to represent synergism (Saracci 1987). As the extent of interaction increases, the proportion of the excess Cases attributable to the interaction also increases (Saracci 1987). This Section briefly reviews the current evidence on host characteristics and environ- mental agents that may modify the risk of cigarette smoking. S| Familial Factors The 1964 Report considered and dismissed the “constitutional hypothesis” that predilections to cigarette smoking and to lung cancer share a common genetic origin. The Report did consider that genetic factors might determine susceptibility for a minority of cases. Subsequent epidemiologic studies have provided empirical evidence of possible genetic or familial determinints of suscepttbility (Tokuhata and Lilienfeld 1963a, 1963b: Samet. Humble, Pathak 1986: Ooi et al. 1986). For example, ina recent case-control study in New Mexico (Samet, Humble, Pathak 1986). a parental history of lung cancer was associated with a fivefold increase in lung cancer risk, after adjust- ment for cigarette smoking. Clinical studies of selected families have also indicated familial aggregation (Brisman et al. 1967; Lynch et al. 1982: Goffman et al. 1982). Research has not yet identified the mechanisms underlying the familial aggregation of lung cancer. In 1973, Kellermann, Shaw, and Luyten-Kellerman (1973) reported the promising observation that patients with lung cancer had a higher degree of in- ducibility of aryl hydrocarbon hydroxylase than did control subjects. Because this en- zyme converts polycyclic aromatic hydrocarbons to more active carcinogens and be- Cause enzyme concentrations are under genetic control, this observation suggested a possible genetic determinant of lung cancer risk. However, not all subsequent studies have been confirmatory. and the inheritance of inducibility in humans has not yet been fully described (Mulvihill and Bale 1984). Other Host Factors Acquired host characteristics have also been examined as determinants of lung can- cer risk including pulmonary tuberculosis. chronic bronchitis, COPD, disorders as- sociated with interstitial fibrosis of the lung, and peripheral pulmonary scars. However, the evidence related to these disorders is incomplete and frequently is derived from case series rather than from epidemiologic investigations. Recent epidemiologic evidence, however, has indicated increased lung cancer risk for smokers with COPD compared with unaffected smokers (Peto et al. 1983: Samet, Humble. Pathak 1986: Skillrud, Of- ford, Miller 1986). Occupational Exposures Diverse agents inhaled in the workplace have been shown to cause lung cancer. In- teraction between occupational exposures and smoking was the focus of the 1985 Report of the Surgeon General (US DHHS 1985). That Report concluded that “For the majority of American workers who smoke. cigarette smoking represents a greater cause of death and disability than their workplace environment.” The Report also highlighted the limitations of the evidence on interactions between smoking and occupational ex- posures. Little new information has become available since the 1985 Report. The evidence remains strongest for interactions of smoking with exposure to radon decay products and with exposure to asbestos (Saracci 1987). For both exposures, the preponderance s2 of the evidence indicates synergism (Doll and Peto 1985, National Research Council 1988), although the results of some individual investigations are inconsistent with synergism. Ambient Air Pollution The 1964 Report noted that lung cancer mortality rates tended to be higher in urban than in rural locations. Air pollution was considered a plausible explanation for these differences. The association of lung cancer with atmospheric pollution derives biologi- cal plausibility from the presence of carcinogens in polluted air and has some support trom epidemiologic data. However. epidemiologic investigation of ambient air pollu- tion as a risk factor for lung cancer has been hampered by methodological problems, including the necessity of considering cigarette smoking and the difficulty of assessing pollution exposure (NIH 1986). Recent epidemiologic investigations have not shown strong effects of air pollution (Samet et al. 1987: Buffler et al. 1988): and Doll and Peto (1981), in their review of the causes of cancer, estimated that only | to 2 percent of jung cancer was related to air pollution. Indoor Air Pollution As the hazards posed by ambient air pollution from conventional fossil fuels have diminished in some countries, the relevance of indoor air quality for health has become increasingly apparent. Studies of time—activity patterns demonstrate that residents of more developed countries, including the United States. spend on average little time out- doors (Spengler and Sexton 1983: Samet, Marbury. Spengler 1987}. Indoor spaces may be polluted by entry of contaminants from outdoor air and by indoor sources including those related to human activity, such as tobacco smoking. building materials, combus- tion devices, personal care and other household products. and other sources. A trend of reduced building ventilation in the aftermath of the energy problems of the 1970s may have worsened indoor air quality. Two pollutants in indoor air have been causally linked to lung cancer: environmen- tal tobacco smoke (ETS) (US DHHS 1986a) and radon (National Research Council 1988). The evidence on ETS and cancer was comprehensively reviewed in the 1986 Report (see Section on Involuntary Smoking in this Chapter). Radon is an inert gas that is formed from radium during the natural decay of uranium. The predominant source of radon in indoor air is the soil beneath structures. Radon dif- fuses through the ground into basement and crawl spaces. and then throughout the air ina home. or crosses cracks and other penetrations in homes on concrete slabs to enter the indoor environment. Radon daughters are invariably present in indoor air and a wide range of concentrations has been observed in homes (Samet et al. 1988). Some homes have levels comparable to those measured in uranium mines, but the majority of homes probably have levels that are currently considered acceptable. Radon decays into short-lived particulate decay products. Two of the decay products emit alpha particles, which are highly effective in damaging cells because of their high energy and high mass. When these alpha emissions take place within the lung. the S3 epithelial lining of the tracheobronchia! tree may be damaged and lung cancer may ul- timately result. Extensive epidemiologic data from studies of uranium and other un- derground miners have established a causal association between exposure to radon daughters and lung cancer (National Research Council 1988). The committee on the Biological Effects of lonizing Radiation (BEIR) IV concluded that the studies of miners indicated synergism between cigarette smoking and radon decay products (National Research Council 1988), The evidence, however, was not considered adequate to deter- mine if the interaction was multiplicative or submultiplicative. To date, epidemiologic investigations of domestic radon daughters as a risk factor for lung cancer have been limited and preliminary (Samet et al. 1988). However, it is assumed that radon decay products are carcinogenic in the indoor environment as they are in the mining environment. Dosimetric analyses indicate equivalent car- cinogenicity in the domestic and mining environments (National Research Council 1988). Thus, radon must be considered one of the most important factors interacting with cigarette smoking. All smokers are exposed to radon, some at unacceptable levels. Quantitative estimates of the contribution of radon to lung cancer are variable. The es- timates vary with the underlying assumptions and the risk model employed (Samet et al. 1988). Although cigarette smoking is by far the major cause of lung cancer, radon must also be considered a cause of the disease. The public health burden of radon-related lung cancer is substantially increased by the synergism between cigarette smoking and radon exposure. Diet Diet has recently been considered as potentially influencing the risk of lung cancer in smokers. Nutrients of particular interest include preformed vitamin A, carotene, vitamin E, and vitamin C (Colditz, Stampfer, Willett 1987). An enlarging body of experimental and epidemiologic evidence supports the hypothesis that the risk for certain cancers varies inversely with consumption of preformed vitamin A or beta-carotene, its precursor (Peto et al. 1981; National Academy of Sciences 1982; Colditz, Stampfer, Willett 1987). The biological plausibility of this hypothesis derives from the known effects of vitamin A deficiency on the differentiation of epithelial surfaces, from in vitro and in vivo models, which show that retinoids can suppress the development of malignancy, and from possible an- ticarcinogenic activity of beta-carotene. the principal dietary precursor of vitamin A (Peto et al. 1981; National Academy of Sciences 1982). The epidemiologic evidence indicates a protective effect of dietary vitamin A intake from vegetable sources, but not of preformed vitamin A, which is derived from meat and dairy sources, and vitamin supplements. Clinical trials on vitamin A and lung cancer risk are in progress. Vitamins E and C are antioxidants, which might have anticancer effects. To date, the epidemiologic data on these vitamins are sparse and inconclusive (Colditz, Stampfer, Willett 1987). Smoking Cessation Cessation of cigarette smoking results in a gradual decrease in lung cancer risk. Several of the prospective and retrospective epidemiologic studies have demonstrated a reduction in lung cancer risk over time following smoking cessation. One example is provided from the U.S. Veterans study (Kahn 1966) (Figure 9). Other recent studies have continued to confirm the benefit of smoking cessation for jung cancer risk (Lubin et al. 1984b: Alderson, Lee. Wang 1985: Pathak et al. 1986; Higgins, Mahan, Wynder 1988). For example. Lubin and colleagues (1984b) described the pattern of reduction in risk following smoking cessation in a case-control study that Mortality Ratio 25, 207 18.83 1-4 5-9 10-14 15-19 20+ Nonsmoker Number of Years Stopped Smoking FIGURE 9.—Lung cancer mortality ratio for male former smokers SOURCE: U.S. Veterans (Kahn 1966). involved 7,181 lung cancer patients and 11,006 controls. For men and women in this study who had smoked for less than 20 years and had not smoked for 10 years. the risks of lung cancer were approximately the same as those of lifelong nonsmokers. On the basis of the study of British physicians, Peto and Doll (1984) have suggested that the effect of cigarette smoking cessation is to fix the age-specific risk of lung cancer at the rate achieved at the time of cessation, based on the smoking history up to that time. Ac- cording to this analysis, the former smoker’s relative risk of lung cancer declines as the background rate for lung cancer rises with age. Therefore, smoking cessation is clearly beneficial in reducing the risk of lung cancer compared with continued smoking; but cessation may not reduce the risk to the levels of a lifetime nonsmoker even after many years of cessation. (See Table 2. Chapter 3.) 55 Laryngeal, Oral. and Esophageal Cancer The 1964 Surgeon General's Report concluded that cigarette smoking was causally related to laryngeal cancer in men and that pipe smoking was causally related to lip cancer (US PHS 1964). Subsequent reports reviewed the accumulating epidemiologic evidence that established that cancers of the larynx. oral cavity, and esophagus are caused by smoking in both men and women. The mortality ratios for these cancers are similar for smokers whether they smoke cigars. pipes, or cigarettes. A strong dose— response relationship exists, and the risk decreases with cessation, compared with con- tinued smoking. Recent studies have confirmed these findings (Blot et al. 1988: El- wood et al. 1984: Schottenfeld 1984). (See Chapter 3.) Alcohol consumption is also a risk factor for oral, pharyngeal, laryngeal. and esophageal cancer. The combination of alcohol and smoking produces a synergistic increase in risk. In one study (Schottenfeld 1984), for all upper airway cancers com- bined, the risk was 8.6 tor those smoking 30 or more cigarettes per day in combination with 20 oz of alcohol consumed per week. Bladder and Kidney Cancer A relationship between smoking and bladder cancer was noted in the 1964 Surgeon General’s Report. The 1979 Report concluded that cigarette smoking acts inde- pendently and probably acts synergistically with other risk factors to increase the risk ot bladder cancer. The 1982 Surgeon General's Report concluded that cigarette smok- ing is a contributory factor for both bladder and kidney cancer. Cigarette smoking is estimated to account for 30 to 40 percent of bladder cancer (US DHHS 1982). Recent studies have confirmed earlie: findings. For bladder cancer, in both men and women, cigarette smokers have a relative risk of 2 to 3. A dose-response relationship has been demonstrated, and the risk of bladder cancer decreases following smoking ces- sation (McLaughlin et al. 1984: Hartge et al. 1987; Zahm, Hartge, Hoover 1987). There is a positive association between smoking and kidney cancer. with relative risks ranging from | to more than 5. The increased risk of kidney cancer due to cigarette smoking is found for both males and females, and there is a dose-response relation- ship, as measured by the number of cigarettes smoked per day. Pancreatic Cancer The first Surgeon General's Report did not examine the relationship between smok- ing and cancer of the pancreas. Several subsequent reports of the Surgeon General have noted that cigarette smoking is a contributory factor for pancreatic cancer. The major prospective epidemiologic studies have consistently shown an increased risk of pancreatic cancer among both male and female cigarette smokers. The mortality ratio for cigarette smokers compared with nonsmokers is generally in the range of 2 to 56 Laryngeal, Oral, and Esophageal Cancer The 1964 Surgeon General's Report concluded that cigarette smoking was causally related to laryngeal cancer in men and that pipe smoking was causally related to lip cancer (US PHS 1964). Subsequent reports reviewed the accumulating epidemiologic evidence that established that cancers of the larynx, oral cavity, and esophagus are caused by smoking in both men and wornen. The mortality ratios for these cancers are similar for smokers whether they smoke cigars, pipes. or cigarettes. A strong dose— response relationship exists, and the risk decreases with cessation, compared with con- tinued smoking. Recent studies have confirmed these findings (Blot et al. 988; El- wood et al. 1984; Schottenfeld 1984). (See Chapter 3.) Alcohol consumption is also a risk factor for oral, pharyngeal, laryngeal, and esophageal cancer. The combination of alcohol and smoking produces a synergistic increase in risk. In one study (Schottenfeld 1984), for all upper airway cancers com- bined. the risk was 8.6 for those smoking 30 or more cigarettes per day in combination with 20 oz of alcohol consumed per week. Bladder and Kidney Cancer A relationship between smoking and bladder cancer was noted in the 1964 Surgeon General’s Report. The 1979 Report concluded that cigarette smoking acts inde- pendently and probably acts synergistically with other risk factors to increase the risk of bladder cancer. The 1982 Surgeon General's Report concluded that cigarette smok- ing is a contributory factor for both bladder and kidney cancer. Cigarette smoking ts estimated to account for 30 to 40 percent of bladder cancer (US DHHS 1982). Recent studies have confirmed earlier findings. For bladder cancer, in both men and women, cigarette smokers have a relative risk of 2 to 3. A dose-response relationship has been demonstrated. and the risk of bladder cancer decreases following smoking ces- sation (McLaughlin et al. 1984; Hartge et al. 1987; Zahm, Hartge, Hoover 1987). There is a positive association between smoking and kidney cancer, with relative risks ranging from | to more than 5. The increased risk of kidney cancer due to cigarette smoking is found for both males and females, and there ts a dose-response relation- ship, as measured by the number of cigarettes smoked per day. Pancreatic Cancer The first Surgeon General's Report did not examine the relationship between smok- ing and cancer of the pancreas. Several subsequent reports of the Surgeon General have noted that cigarette smoking is a contributory factor for pancreatic cancer. The major prospective epidemiologic studies have consistently shown an increased risk of pancreatic cancer among both male and female cigarette smokers. The mortality ratio for cigarette smokers compared with nonsmokers is generally in the range of 2 to 56 3. A detailed review of the epidemiology of pancreatic cancer was written by Gordis and Gold (1984). For those in the MRFIT Study who smoked 40 or more cigarettes a day, the mortality ratio for pancreatic cancer was 2.3 compared with nonsmokers. Other recent studies (Mack et al. 1986; Whittemore et al. 1985) report that cigarette smoking is strongly and consistently related to pancreatic cancer. Most epidemiologic studies show a dose— response relationship between cigarette smoking and pancreatic cancer for both men and women and a gradual decline in the risk of developing pancreatic cancer follow- ing smoking cessation (US DHHS 1982; Mack et al. 1986). Autopsy studies report hyperplastic changes in the pancreatic duct cells and atypical changes in their nuclei among cigarette smokers compared with nonsmokers. The pancreas is probably exposed to tobacco carcinogens or carcinogenic metabolites present in bile or blood (US DHHS 1982). Stomach Cancer The 1964 Surgeon General's Report reviewed smoking and stomach cancer and, on the basis of the limited evidence available at that time, concluded that there was no relationship between smoking and stomach cancer. Evidence from prospective and retrospective studies available more recently has shown a small but consistent increase in mortality ratios, averaging approximately 1.5 for smokers compared with non- smokers. Dose-response relationships have been demonstrated for the number of cigarettes smoked per day. The 1982 Surgeon General's Report concluded that cancer of the stomach is associated with cigarette smoking. Cervical Cancer Cancer of the uterine cervix was not reviewed in the 1964 Surgeon General's Report. The 1982 Report of the Surgeon General reviewed the studies published up to that time and concluded that further research was necessary to define whether there was an as- sociation between cigarette smoking and cervical cancer. There are several risk factors for cervical cancer including early and frequent coitus, multiple sexual partners, pregnancy at an early age, and the presence of sexually trans- mitted diseases. Some of these risk factors may also be associated with smoking. Winkelstein and coworkers (1984) reviewed 12 studies dealing with smoking and cervical cancer, and in most studies there was a positive relationship that could not be explained by other risk factors. Two studies published in 1985 confirmed these tind- ings (Clarke et al. 1985; Greenberg et al. 1985). Baron and coworkers (1986) reported on a case-control study of 1,174 patients with cervical cancer. Cigarette smoking was associated with a statistically significant in- crease in risk for cervical cancer. LaVecchia and associates (1986) in Italy studied the relationship between cigarette smoking and the risk of cervical neoplasia in a case—con- trol study of 183 women with intraepithelial neoplasia. Cigarette smoking was as- sociated with an increased risk of intraepithelial neoplasia and invasive cancer. This association could not be totally explained by potential confounding factors. In a case— 57 control study of 480 patients with cervical cancer, there was a 50-percent excess risk of cancer among cigarette smokers (Brinton et al. 1986). This excess risk persisted after adjustment for sexual practices associated with smoking such as age at first inter- course and number of sexual partners. There was a twofold excess risk of cervical can- cer for women who smoked more than 40 cigarettes per day. The dose-response relationship persisted after adjusting for several variables. There was no increased risk of cervical cancer among former smokers. The finding of nicotine and cotinine in the cervical secretions of cigarette smokers (Sasson et al. 1985) and of mutagenic mucus in the cervix of smokers (Holly et al. 1986) complements the epidemiologic findings. In summary, more than 15 epidemiologic studies have consistently shown an in- creased risk for cervical carcinoma in cigarette smokers compared with nonsmokers. Supportive clinical studies provide a plausible biological basis for the relationship. The available data confirm an association between cigarette smoking and carcinoma of the uterine cervix. Endometrial Cancer Several studies have reported that endometrial cancer is less frequent among women who smoke cigarettes than among nonsmokers (Baron et al. 1986). Ci garette smoking exerts an antiestrogenic effect that may explain this inverse association. The public health significance of this association is limited because of the overall adverse impact of cigarette smoking on morbidity and mortality. Coronary Heart Disease The 1964 Surgeon General's Report (US PHS 1964) noted that male cigarette smokers have higher death rates from CHD than nonsmokers. Subsequent reports con- cluded that cigarette smoking can cause death from CHD and that smoking is one of the major independent risk factors for heart attack, manifested as fatal and nonfatal myocardial infarction and sudden cardiac death. Smoking also increases the risk of heart attack recurrence among survivors of a myocardial infarction (US DHEW 1979). The 1980 Report (US DHHS 1980) noted the increased risk of CHD among women who smoke. It also described the synergistic interaction between smoking and oral con- traceptive use that substantially increases CHD risk. The 1983 Report (US DHHS 1983) stated that cigarette smoking is 4 major cause of CHD and noted the decreased risk of CHD among former smokers compared with current smokers. Epidemiology The findings from several prospective studies involving more than 20 million per- son-years of observation in North America, Northern Europe, and Japan have been remarkably similar: cigarette smokers are at increased risk for fatal and nonfatal myocardial infarction and for sudden death. Overall, smokers have a 70 percent greater 58 CHD death rate, a two- to fourfold greater incidence of CHD, and a two- to fourfold greater risk for sudden death than nonsmokers (US DHHS 1983). Although women experience lower CHD rates than men, cigarette smoking 1s a major determinant of CHD in women. Ina recent prospective study of 119,404 female nur- ses, smoking accounted for approximately one-half of the coronary events (Willett et al. 1987). Cigarette smoking produces a greater relative CHD risk in men and women under 50 years of age than in those over 50 years of age (Glover, Kuber et al. 1982; Rosenberg, Miller et al. 1983). Dose-response relationships between cigarette smoking and CHD mortality have been demonstrated for several measures of exposure to cigarettes, including the num- ber of cigarettes smoked per day, the depth of inhalation, the age at which smoking began, and the number of years of smoking (US DHHS 1983). Smoking cigarettes with reduced yields of tar and nicotine has not been found to reduce CHD risk (Kaufman et al. 1983). Coronary Heart Disease Risk Factors The risk of experiencing a heart attack is multifactorial (US DHHS 1983). The presence of one or more of the major CHD risk factors, cigarette smoking, hyper- cholesterolemia, and hypertension, identifies individuals at high or very high risk. These risk factors interact synergistically to greatly increase CHD risk (Figure 10). The risk of CHD associated with cigarette smoking is comparable to that associated with the other major CHD risk factors. The risk of CHD is greatly increased among diabetic men and women who smoke cigarettes (Suarez and Barrett-Connor 1984; Stamler, Wentworth, Neaton 1986), and the sex differences in CHD are substantially reduced among diabetics. Among the MRFIT screenees free of a history of heart attack, there were 5,245 diabetics and 350.977 nondiabetic men aged 35 to 57 years at the time of enrollment (Suarez and Barrett-Connor 1984). The CHD death rate was much higher among diabetics than among nondiabetics. Smokers had higher CHD death rates than nonsmokers among both diabetics and nondiabetics. Six-year CHD mortality was 4.0/1,000 for non- smokers who were nondiabetic and 23.2/1,000 for diabetics who smoked at least 36 Cigarettes per day. Hyperlipoproteinemia is a primary cause of premature coronary atherosclerosis and heart attacks. Cigarette smoking substantially increases the risk of CHD among in- dividuals with genetic familial hyperlipidemias. Williams and coworkers (Williams et al. 1986; Hopkins, Williams, Hunt 1984) studied four large Utah pedigrees with familial hypercholesterolemia. They noted a substantially increased risk of CHD within the high-risk pedigrees in relation to cigarette smoking. Miettinen and Gylling (1988) have recently completed a long-term followup of 96 patients with familial hypercholesterolemia. Cigarette smoking was a significant predictor of coronary mortality after adjustment for disease history, sex, and various metabolic parameters. 59 189 180 oJ 170 160 150 1 140 J 130 _] 120 _] 110 100 J 90 80 70 J 60] 50 40] 30 20] 10 103 92 RATE PER 1,000 54 54 None SM only CorH SM&C C&H Aul3 of 3 only or (no SM) SM &H RISK FACTOR STATUS AT ENTRY *® FIGURE 10.—Major risk factor combinations, 10-year incidence of first major coronary events, males aged 30 to 59 years at entry, Pooling Project Definitions of the three major risk factors and their symbols: hy percholesterolemia (C), 2250 my/dh: elevated blood pres- sure (H). diastolic pressure 290 mm Hy: cigarette smokirg (SM any current use of cigaretles at entry. NOTE: All rates were age-adjusted by 10-sear age groups to the U.S. white male population, 1980, SOURCE: Pooling Project Research Group (1978). Pathophysiological Mechanisms Autopsy studies indicate that cigarette smoking has a significant positive association with atherosclerosis (US DHHS 1983). Studies have noted the strongest relationship of cigarette smoking with aortic atherosclerosis. but smokers also show increased coronary atherosclerosis compared with nonsmokers (US DHHS 1983). Smokers un- dergoing coronary angiography have more coronary urtery disease than nonsmokers (Peurson 1984). Cigarette smokers who continue to smoke following transluminal coronary angioplasty may be more likelv to require repeat angioplasty than nonsmokers (Galan et al. 1988) Cigarette smoking exerts both acute and chronic adverse coronary effects (US DHHS 1983: Holbrook et al. 1984). It contributes to acute ischemic and occlusive events through several possible mechanisms: an imbalance between myocardial oxygen sup- ply and demand. coronary artery spasm. a hypercoagulable state. increased platelet ad- hesiveness and aggregation, and a decreased ventricular fibrillation threshold (US 60 DHHS 1983: Martin et al. 1984: Fitzgerald, Oates, Nowak 1988). Cigarette smoking also contributes to the development of coronary atherosclerosis. Possible mechanisms for this chronic effect include: repetitive endothelial injury, a decreased high-density lipoprotein (HDL )/low-density lipoprotein (LDL) cholesterol ratio. abnormalities in the synthesis of thromboxane A2 and prostacyclin, and increased neutrophil elastase ac- tivity (Holbrook, in press: Nowak et al. 1987: Weitz et al. 1987). Clinical Correlations Cigarette smoking has an adverse effect on individuals with symptomatic or asymptomatic CHD. Compared with nonsmokers, smokers having a positive exercise test (Rautaharju et al. 1986; Gordon et al. 1986) or a history of coronary bypass surgery (Viietstra et al. 1986; Kemp et al. 1986) face a worse prognosis. Smokers who have an- gina pectoris have a higher risk of death than nonsmokers (Hubert, Holford, Kannel 1982) and have a poorer long-term prognosis after a myocardial infarction (Ronnevik,. Gundersen, Abrahamsen 1985: Kuller et al. 1982). Continuing to smoke increases the likelihood of recurrent acute myocardial infarction and sudden death (Hallstrom, Cobb. Ray 1986). Smoking may also cause silent ischemic disturbances in patients with stable angina pectoris (Deanfield et al. 1986). Cigarette smoking interferes with the efficacy of medication used to treat CHD such as propranolol, atenolol, and nifedipine (Deanfield et al. 1984). Smoking Cessation Prospective epidemiologic studies have documented a substantial reduction in CHD death rates following smoking cessation (US DHHS 1983). While some studies have shown a benefit within 2 years after quitting, other studies have suggested that the former smoker’s CHD risk gradually decreases over a period of several years (Cook et al. 1986), For heavier smokers, the residual CHD risk is proportional to the total lifetime exposure to cigarettes. Cerebrovascular Disease (Stroke) In the United States stroke is the third leading cause of death. It is also a major cause of morbidity, with more than 400.000 Americans suffering nonfatal strokes each year (Harrison’s Principles of Internal Medicine 1987). . There are two major types of cerebrovascular disease: (1) cerebral infarction due to occlusion of a vessel by an embolus or thrombosis, and (2) cerebral hemorrhage. in- cluding subarachnoid and parenchymal. The terms cerebrovascular accident and stroke are nonspecific and usually refer to clinical syndromes. A stroke may be caused by disease of the extra- or intracranial blood vessels. Em- bolization from the heart or extracranial arteries is also an important cause of stroke. The stroke can result from hemorrhage from a blood vessel or from occlusion of an artery because of atherosclerosis. thrombosis, or embolization. In the Framingham study, atherothrombotic brain infarction accounted for the majority of strokes (Wolf. 61 Dawber et al. 1978). Improved diagnostic methods have provided a better categoriza- tion of the causes of stroke. Epidemiologic studies have shown that hypertension is the most important risk factor for stroke (US DHHS 1983). The 1964 Report of the Surgeon General stated that the large epidemiologic studies of Hammond and Horn (1958) and Dorn (1958) had found a moderate increase in the mortality rate from cerebrovascular disease in cigarette smokers compared with non- smokers. The 1971 Report (US DHEW 1971) reviewed six major prospective epidemiologic studies. Cigarette smokers in these studies experienced increased stroke mortality com- pared with nonsmokers. The 1980 Report (US DHHS 1980) noted that women who smoke have an increased risk of subarachnoid hemorrhage. The 1983 Report (US DHHS 1983) reviewed the data associating cigarette smoking with stroke and found an increased risk for stroke among smokers that was most evident in younger age groups. It also noted that women cigarette smokers experience an increased risk for subarach- noid hemorrhage and that the concurrent use of both cigarettes and oral contraceptives greatly increased this risk. Since the release of the 1983 Surgeon General's Report the relationship between cigarette smoking and stroke has been clarified in several large studies involving men and women. The risk of stroke was evaluated in a prospective study of 8,006 Japanese-American men living in Hawaii (Abbottet al. 1986). After 12 years of followup. cigarette smokers had two to three times the risk of thromboembolic or hemorrhagic stroke compared with nonsmokers. The increased risk was independent of other risk factors such as hy- pertension and CHD. Those smokers who stopped smoking during the course of the study experienced more than a 50-percent reduction in the risk of stroke compared with continuing smokers, The impact of cigarette smoking on stroke incidence was assessed prospectively in the Framingham Study of 4.255 men and women (Wolf et al. 1988). This cohort was followed for 26 years, and the diagnoses were confirmed by clinical examination. Cigarette smoking made a significant. independent contribution to the risk of stroke. The risk increased as the number of cigarettes smoked increased. Smoking cessation resulted in a significant decrease in stroke risk so that 5 years after stopping smoking the risk was at the level of nonsmokers. The relationship between cigarette smoking and the risk of stroke was evaluated in a prospective study of 118,539 middle-aged women who were followed for 8 years (Colditz, Bonita, Stampfer 1988). Compared with nonsmoking women, those who smoked | to 14 cigarettes per day had a relative risk of fatal and nonfatal stroke of 2.2. Those who smoked 25 or more cigarettes per day had a relative risk of fatal and non- fatal stroke of 3.7. In this latter group of women, the relative risk of subarachnoid hemorrhage was 9.8. The contribution of cigarette smoking to increased stroke risk was independent of other risk factors. Smoking cessation resulted in a prompt decrease in stroke risk; the relative risk of stroke in women who had stopped smoking for 2 years was 1.4, compared with women who had never smoked. The authors of this study also reviewed eight prospective cohort studies and seven case—control studies involving 62 women, and concluded that most of these studies had shown a positive association be- tween cigarette smoking and stroke (Table 3). Inthe ongoing study of approximately 1.2 million persons (CPS-II), cigarette smokers under the age of 65 years experienced increased risks of death from stroke. For men and women (current smokers), the relative risks of death from stroke were 3.7 and 4.9, respectively. The relative risks for those over age 65 years were 1.9 and 1.5 for men and women, respectively (Chapter 3). Cigarette smoking was associated with decreased cerebral blood flow in a recent clinical study involving 192 normal volunteers (Rogers, Meyer et al. 1983). Ina sub- sequent study of 268 normal volunteers, abstention from cigarette smoking improved cerebral perfusion (Rogers, Meyer et al. 1985). As already noted in this Chapter, cigarette smoking increases the risk for CHD, and consequently for congestive heart failure, both of which increase the risk for stroke. Data from the Medical Research Council study on the treatment of mild hypertension illustrate the impact of cigarette smoking on the efficacy of drug therapy and stroke in- cidence (Medical Research Council Working Party 1985). Nonsmokers receiving propranolol to control hypertension experienced a reduction in stroke incidence, while cigarette smokers did not. Wolf and coworkers (1988) recently reviewed the association between cigarette smoking and stroke and concluded that it is causal. These investigators noted that the causal connection is supported by all of the traditional epidemiologic criteria; these include an increased risk for stroke among smokers compared with nonsmokers that is independent of other risk factors, a dose-response relationship, and a decrease in stroke risk with smoking cessation (Abbott et al. 1986; Wolf et al. 1988; Colditz, Bonita, Stampfer 1988). The aforementioned recent clinical studies also confirm that cigarette smoking increases the risk for stroke. Thus, current evidence indicates that cigarette smoking is a cause of stroke and that smoking cessation reduces the risk for stroke. Atherosclerotic Peripheral Vascular Disease Lower extremity arterial vascular disease causes substantial mortality and morbidity; the complications may include intermittent claudication, tissue ischemia and gangrene, and ultimately, loss of the limb. The 1964 Surgeon General’s Report commented that little is known about the relationship of smoking to peripheral arteriosclerosis. Subsequent reports have described the evidence establishing that cigarette smoking is a cause of and the most powerful risk factor for atherosclerotic peripheral vascular disease and that smoking cessation is the most important intervention in the management of this problem (US DHEW 1971, 1979; US DHHS 1983). Cigarette smoking is directly related to the extent of atherosclerotic disease involv- ing large and small arteries in the lower extremity (Criqui et al. 1985). Cigarette smok- ing also causes peripheral vasoconstriction. Epidemiologic and clinical studies have clearly demonstrated that cigarette smokers have a higher prevalence than nonsmokers 63 TABLE 3.—Summary of studies of cigarette smoking and stroke in women No. First author Cohort size Type of stroke of cases Relative risk Comments Prospective cohort studies Colditz 118,539 All 274 2.2 (95% CI, 1.5-3.3) 1-14 cigarettes/day 2.7 (95% CI, 1.9-3.7) 15-24 cigarettes/day 3.7 (95% CI, 2.7-5.1) 225 cigarettes/day Salonen 4,334 = Infarction 21 1.4 (90% CI, 0.4~5.0) Other 38 0.8 (90% CI, 0.3-2.2) Tanaka 1,681 Hemorrhage 30 2.1 (NS) Included 780 men Infarction 81 1.0 (NS) Sacco 2,421 Subarachnoid 22 1.6 Relative risk was 2.9 hemorrhage for heavy smokers Vessey 17,000 Subarachnoid 13 3.0 hemorrhage Nonhemorrhagic 33 L.4 Doll 6,194 Cerebralthrom- 68 0.5 for 15-24 ciga- Risk tended to bosis Tettes/day decrease with amount smoked Layde 46,000 Subarachnoid 20 Smokers had higher hemorrhage risk of fatal subarachnoid hemorrhage Petitti 16.759 Subarachnoid 11 5.7 (90% CI, 1.8-17.8) hemorrhage Other 23 4.8 (90% CI, 2.3-9.8) Wolf 2.421 All 238 1.6 (p<0.025) Case—control studies Taha Subarachnoid 124 2.6 for aneurysm Based on 68 female hemorrhage cases Bell Subarachnoid 134 3.7(90% Cl, 2.3-5.9) hemorrhage Collaborative study Hemorrhage 192 Smoking doubled risk Thrombosis 140 No increased risk Abu-Zeid Hemorrhage 137 {.4 (NS) Included men Thrombosis 410 2.4 (p<0.001) Bonita Subarachnoid 70 4.7 (95% CI, 2.9-7.6) Dose-response hemorrhage relationship not significant Bonita Not subarach- 53 2.6 (95% Cl, 1.4.4.6) noid hemorrhage Herman Stroke 25 1.2 (95% Cl, 0.7-2.3) Included 78 men NOTE: Cl, confidence interval: NS, not significant. SOURCE: Colditz, Bonita, Stampfer (1988). 64 of both symptomatic and asymptomatic lower extremity arterial disease (US DHHS 1983). In the Lipid Research Clinic prevalence study (Pomrehn et al. 1986), 48 percent of individuals with claudication were current cigarette smokers compared with 30 percent of the controls. Smoking was twice as frequent among individuals developing leg pain, compared with those not developing leg pain, during the exercise test. In the Framingham Study, the risk of developing intermittent claudication was directly and strongly related to cigarette smoking (Kannel and Shurtleff 1973). Diabetes mellitus and cigarette smoking are the key risk factors for lower extremity arterial disease and subsequent amputation. Peripheral neuropathy and lower extremity arterial disease and infection predispose individuals with diabetes to gangrene and am- putation (Herman, Teutsch, Geiss 1987). Diabetics have a sixteenfold increased risk of lower extremity amputation compared with nondiabetics, about 50 percent of the lower extremity amputations in the United States are performed on diabetics. Ap- proximately 31,000 American diabetics undergo such surgery each year. The disease tends to be more progressive and occurs at younger ages in diabetic smokers than in nonsmokers. In a study in Sweden, practically all diabetic patients under the age of 60 years with gangrene were cigarette smokers (Lithner 1983). The prevalence of lower extremity arterial disease was evaluated for diabetic subjects. One-third of the smokers had evidence of peripheral vascular disease compared with only 16 percent of the non- smokers. Diabetics who stopped smoking for at least 2 years had a 30 percent lower prevalence of lower extremity arterial disease than those who continued to smoke. Epidemiologic studies in a Rochester, MN, population (Zimmerman et al. 1981) demonstrated that for 1,073 residents over the age of 30 who were diagnosed with diabetes mellitus between 1945 and 1969, about 8 percent of men and 7 percent of women had clinical evidence of peripheral vascular disease at the time that diabetes was diagnosed. The annual incidence of lower extremity arterial disease among the diabetics was 21/1,000 for men and 17.6/1,000 for women; about 20 percent had gangrene and 36 percent had intermittent claudication. Among diabetics with lower extremity arterial disease, 77 percent of men and 43 percent of women had been cigarette smokers compared with 55 percent of normal control men and 36 percent of normal control women. Effective treatment of diabetes mellitus and smoking cessation are the two most im- portant interventions to prevent the development of atherosclerotic peripheral vascular disease. Atherosclerotic Aortic Aneurysm The 1964 Report of the Surgeon General commented on the increased mortality rates for aortic aneurysm in cigarette smokers compared with nonsmokers. The 1969 Report concluded that there is a close association between cigarette smoking and death caused by aortic aneurysm. The 1983 Report summarized the epidemiologic data and noted that the mortality rate for abdominal aortic aneurysm was 2 to 8 times greater in cigarette smokers than in nonsmokers. As already noted, pathology studies have showna sig- 65 nificant association between cigarette srnoking and atherosclerosis that is most striking in the aorta (US DHHS 1983). Chronic Obstructive Pulmonary Disease In the 1950s, increasing morbidity and mortality from chronic respiratory conditions prompted clinical and epidemiologic investigations of the etiology of chronic bronchitis, emphysema, and related disorders. A variety of terms have subsequently been applied to permanent airflow obstruction in cigarette smokers. In the 1984 Sur- geon General's Report, chronic obstructive lung disease (COLD) referred to chronic mucus hypersecretion, airways abnormalities, and emphysema. In this Report, the term COPD is used for the permanent airflow obstruction that develops in cigarette smokers. Thirty years ago, the most widely advanced hypothesis on the etiology of COPD linked progressive lung damage to recurrent respiratory infection and atmos- pheric pollution (Stuart-Harris 1954). Hlowever, epidemiologic investigations, largely carried out in the United Kingdom, quickly indicated the predominant role of cigarette smoking in causing COPD (Stuart-Harris 1968a,b). By 1964, the evidence was sufficiently compelling to support the conclusion by the Advisory Committee to the Surgeon General that “Cigarette smoking is the most im- portant of the causes of chronic bronchitis in the United States, and increases the risk of dying from chronic bronchitis and emphysema” (US PHS 1964). The Report stopped short of classifying the relationship between cigarette smoking and emphysema as causal, however. The Report also noted the increased prevalence of respiratory symptoms and the reduction of lung function in smokers. The epidemiologic data cited in support of these conclusions were drawn from seven prospective studies of mortality in relation to cigarette smoking and about a dozen surveys of respiratory morbidity; only one prospective study on lung function had been reported at that time. In the 25 years that have elapsed since the release of the 1964 Surgeon General’s Report, the findings of numerous laboratory, clinical, and epidemiologic studies have continued to reaffirm the predominant role of cigarette smoking in causing COPD and have extended understanding of the pathogenesis, pathophysiology, and natural history of this disorder. As the evidence has accumulated, the conclusions of the Surgeon General’s Reports on cigarette smoking and COPD have been strengthened. The 1967 Surgeon General's Report labeled cigarette smoking as the most important of the causes of COPD (US PHS 1968). In the 1971 and 1979 Reports, the conclusions of the 1964 and 1967 Reports were strengthened (US DHEW 1979). Increased morbidity and mor- tality from chronic bronchitis and emphysema were documented in cigarette smokers compared with nonsmokers. Additionally, autopsy evidence confirmed that the lungs of smokers were widely damaged, and the evolving protease—antiprotease hypothesis provided a framework for understanding mechanisms through which cigarette smoke causes emphysema. The 1984 Surgeon General's Report focused on COLD (US DHHS 1984). The over- all conclusion of the Report was: “Cigarette smoking is the major cause of chronic obstructive lung disease in the United States for both men and women. The contribu- tion of cigarette smoking to chronic obstructive lung disease morbidity and mortality 66 far outweighs all other factors.” In contrast to the sparse evidence in the 1964 Report, the 1984 Report reviewed numerous cross-sectional and longitudinal studies of mor- bidity and mortality. The longitudinal studies described the evolution of the cigarette- related decline in Jung function that leads to impairment sufficient to result in a clini- cal diagnosis of COPD. This Section provides an overview of the evidence on COPD that has accumulated since the 1964 Report in the areas of pathogenesis, pathophysiology. and natural his- tory of COPD and the role of cigarette smoking. Pathogenesis The 1964 Report described the deposition of cigarette-smoke particles and gases in the lungs and the effects of cigarette smoke on lung defenses but did not address the mechanisms by which cigarette smoking causes COPD (US PHS 1964). Much of the subsequent investigation of the mechanism of lung injury by cigarette smoke was sparked by the observation that homozygous deficiency of alpha) -antitrypsin, the major protease inhibitor, is associated with familial panlobular emphysema (Laurell and Eriksson 1963; Eriksson 1964), This observation led to the hypothesis. generally referred to as the protease—antiprotease hypothesis, that the development of emphysema results from an imbalance between proteolytic enzymes and their inhibitors (Janoff 1985: Niewoehner 1988). Cigarette smoking is postulated to produce unchecked proteolytic activity by increasing proteolytic enzyme activity in the lung while decreas- ing antiprotease activity. Experimental and clinical observations have been consistent with the protease—an- tiprotease hypothesis (US DHHS 1984). Observations that smokers, compared with nonsmokers, have an increased number of neutrophils in peripheral blood (Yeung and dy Buncio 1984), in bronchoalveolar lavage fluid. and in lung biopsy specimens (Hunninghake and Crystal 1983) provide indirect evidence for an increased elastase burden in smokers’ lungs, since neutrophils are the primary source of elastase (Janoff 1985). Furthermore. elastase levels are elevated in bronchial lavage fluid immediate- ly after smoking cigarettes (Fera et al. 1986). Cigarette smoking has also been shown to decrease the levels and activity of antiproteases, an effect attributed to oxidants in cigarette smoke and the pulmonary macrophages of smokers (Janoff 1985, US DHHS 1984). Animal models confirm that unchecked proteolytic activity can cause em- physema (US DHHS 1984). The lungs of patients with COPD generally display both emphysema and abnor- malities of the small airways. Mechanisms by which cigarette smoke damages small airways have not been so extensively investigated as the factors determining the development of emphysema. Pathophysiology The lungs of smokers with COPD generally have both thickening and narrowing of airways and emphysema, although the extent of these two processes is variable (US DHHS 1984). Both the airways changes and emphysema produce airflow obstruction. 67 The 1964 Report noted that smokers’ lungs displayed airways changes and emphysema: however. the pathophysiological correlates of these changes were not explored. Subsequent investigations, correlating structural changes with function. have described the relationship between smoking-caused changes in lung structure and airflow obstruction. Emphysema and smill-airway injury contribute to the phystologi- cal impairment found in COPD: in individuals with symptomatic airflow obstruction, either type of injury may be predominant. but both are probably important (US DHHS 1984), While the 1964 Report described effects of cigarette smoking on the airways, the importance of the small airways as a site of airflow obstruction was not recognized until the late 1960s (Hogg. Macklem. Thurlbeck 1968). More recent investigations have confirmed that measures of small-airway injury are correlated with the degree of airflow obstruction (US DHHS 1984: Hale et al. 1984: Nagai, West, Thurlbeck 1985), Autopsy studies have shown that changes in the small airways develop in the lungs of young smokers and antedate the development of symptomatic airflow obstruction {Niewoehner. Kleinerman, Rice 1974) The importance of emphysema in producing chronic airflow obstruction has also been amply documented since the 1964 Report. Emphysema reduces the driving pressure for expiratory flow and contributes to increased airways resistance by reducing tether- ing of small airways. In patients with symptomatic airflow obstruction. the extent of anatomic emphysema is correlated with the severity of airflow obstruction, as are small-airway abnormalities (US DHHS 1984: Hale et al. 1984: Nagai, West, Thurlbeck 1985). Thus. the smoking-caused lung. changes in the airways and parenchyma have both been unequivocally linked to airflow obstruction. Natural History of COPD and the Role of Cigarette Smoking Nearly all the epidemiologic evidence reviewed in the 1964 Report was cross-sec- tional in nature. These data established that cigarette smoking increased respiratory symptoms and reduced the level of ventilatory function, but they did not provide in- sight into the temporal evolution of COPD. Subsequent cross-sectional studies have provided more complete quantitative descriptions of the effects of cigarette smoking on Jung function, and new longitudinal studies have partially described the evolution of lung function changes in smokers and the factors determining the rate of change over time. The numerous cross-sectional studies published since the 1964 Surgeon General's Report have shown that cigarette smoking is a strong determinant of the level of ven- Hlatory function, which is most often assessed by the measurement of the I-sec forced expiratory volume (FEV;). The level of FEV, declines as the amount of smoking in- creases (US DHHS 1984). Multiple rezression techniques have been applied to data from several different populations to describe the quantitative relationship between the amount smoked and loss of ventilatory function. These analyses indicate that ven- tilatory function declines ina linear fashion with cumulative consumption of cigarettes, usually expressed as pack-years (Burrows et al. 1977: Dockery et al. 1988). For ex- ample. based on analysis of data from 8.191 men and women trom six U.S. cities, Dock- ery and others (1988) reported that male smokers of average height lose 7.4 mL of FEV, 68 on average for each pack-year and that women lose 4.4 mL per pack-year. Although the decline in mean level of FEV) appears small, the distributions of lung function level in smokers and in nonsmokers are different: the distribution for smokers is skewed toward lower levels so that a much greater proportion of smokers than nonsmokers have levels below the usual limit of normal (Figure 11) (US DHHS 1984; Burrows et al. 1977: Dockery et al. 1988). 30 O PRK-YAS ~ 20 N=3303 10 1OR=.512 0 r S r - "3.0. -2.0 -1-0 06.0 0.0 2.0 3.0 1-20 PK-YRS ~ 20 N=2477 10 1QR=.560 0 T T ir - T _ "3,0 -2.0 -1.0 0.0 1.0 2.0 3.0 30 21-40 PK-YRS we 20 N=1539 0 10R=.638 03 titel, , "3.0 -2.0 -1.0 OO 1.0 2.0 3.0 30 i 20 N i I 0 ee 0 ‘ Ati : 3.0 -2.0 -).0 0.0 1.0 20 3.0 30 61-90 PRK-YRS ~ 20 None 881 of aottiinn 0 , i . . r . -3.0 -2.0 -1.0 0.0 1.0 2.9 3.0 30 PRK-TRS 20 82108 N=] ~ Re. 0 eth. “ ™ Or i °30 2.0 10 OCt«iaCSS*‘i CSC HEIGHT ADJUSTED FEV, RESIOUAL (LITERS) FIGURE 11.—Percent distribution of predicted values of forced expiratory volume in l-sec (FEV |) in subjects with varying pack - years of smok- ing. NOTE: Triangle indicates mean. IQR is interquartile range. SOURCE: Dockery et al. (1988). The longitudinal studies published since the 1964 Report have partially described the natural history of lung function changes in COPD (Fletcher et al. 1976: US DHHS 1984). Ventilatory function, as measured by FEV1, for example, increases during 69 childhood and reaches a peak level during early adulthood (Figure 12). From the peak level. ventilatory function declines with increasing age. In cigarette smokers who develop symptomatic airflow obstruction, a similar loss of function takes place, but at a more rapid rate than in nonsmokers and in smokers who do not develop disease. A physician is likely to diagnose COPD when continued excessive loss of ventilatory function results in sufficient impairment to cause dyspnea and limitation of activity. 5s FEV, (hters) 25 35 “5 ss 65 75 Years FIGURE 12.—Decline of FEV; at normal rate (solid line) and at an accelerated rate (dashed line) NOTE: A. person who has attained a “normal” maximal FEV; during lung growth and development: B. person whose maximal FEV) has been reduced by childhood respiratory infection, CAO, chronic airflow obstruction. SOURCE: Samet et al. (19823), The factors influencing rate of lung function decline in cigarette smokers have not yet been fully characterized. The rate of decline tends to increase with the amount smoked, and former smokers generally revert to the rate of loss of nonsmokers. In fact, the excessive decline observed in some smokers may represent a common physiologi- cal consequence of different pathophysiological mechanisms. Habib and coworkers (1987) carefully characterized 13 subjects from a longitudinal study in Tucson with a mean annual decline in FEV, greater than 60 mL per year. Clinically, these subjects were not unique and none had alphaj-antitrypsin deficiency. Physiological assessment 70 suggested that some were developing emphysema, whereas others appeared to have disease of the large and/or small airways. The studies of longitudinal change in lung function have spanned only segments of the full natural history of COPD, and many questions remain unanswered. It is unclear, for example, whether the excessive decline takes place at a constant rate in continuous smokers, as suggested by much of the epidemiologic evidence, or whether the exces- sive decline occurs intermittently after some triggering event. The factors determining the susceptibility of individuals to cigarette smoking are also unclear. Current hypotheses emphasize determinants of protease—antiprotease imbalance, level of non- specific airways reactivity, and severe respiratory ilIness during early childhood. Since the release of the 1964 Surgeon General's Report, abundant evidence has in- dicated the overwhelming importance of cigarette smoking in causing COPD: in fact, COPD would be an uncommon condition in the United States without cigarette smok- ing. Unfortunately, death rates due to COPD have paralleled those for lung cancer and have increased progressively over the last 25 years (National Center for Health Statis- tics 1986). The trends are consistent with cohort changes in smoking; in this regard, while age-specific rates for males have been increasing at older ages, a recent decline in COPD mortality has been observed at younger ages (US DHHS 1984). While im- portant scientific questions remain unanswered concerning the pathogenesis of COPD, the available evidence provides sufficient rationale for preventing COPD through smoking prevention and cessation. Pregnancy and Infant Health Several endpoints have been studied to evaluate the adverse effects of smoking on pregnancy, including (1) infant birthweight, (2) fetal and infant mortality; (3) congeni- tal malformations: (4) fertility; and (5) long-term effects on the child. The 1964 Report indicated an association between smoking and low-birthweight babies (US PHS 1964), but it did not consider the evidence sufficient to establish a causal relationship. The 1969 Report (US PHS 1969) confirmed the association between maternal smok- ing and low-birthweight babies, an increased incidence of prematurity, spontaneous abortions, stillbirths, and neonatal deaths. The 1971 Report (US DHEW 1971) con- cluded that maternal smoking during pregnancy exerts a retarding influence on fetal growth. The 1973 Report (US DHEW 1973) noted that cigarette smoking is a prob- able cause of increased late fetal mortality and infant mortality. The 1977-78 Report (US DHEW 1978) noted a dose-response relationship between smoking and abruptio placentae, placenta previa, bleeding during pregnancy, and prolonged premature rup- ture of membranes, as well as the association of smoking during pregnancy with im- paired physical and intellectual development of the offspring. The 1979 Report (US DHEW 1979) linked smoking with sudden infant death syndrome. The 1980 Report (US DHHS 1980) noted that up to 14 percent of preterm deliveries in the United States may be attributed to maternal smoking. It also surveyed studies of men and women suggesting that cigarette smoking may impair fertility. 71 In 1985, the Center for Health Promotion and Education of the Centers for Disease Control. Atlanta, GA. defined the fetal tobacco syndrome as follows. (1) The mother smoked 5 or more cigarettes a day throughout the pregnancy. (2) The mother had no evidence of hypertension during pregnancy, specifically no preeclampsia and documentation of normal blood pressure at least once after the first trimester. (3) The newborn has symmetrical growth retardation at term, 37 weeks, defined as birthweight less than 2,500 g. and a ponderal index (weight in grams divided by length) greater than 2.32. (4) There is no obvious cause of intrauterine growth retardation, that is, congeni- tal malformation or infection (Nieburg et al. 1985). Infant Birthweight A clear dose-response relationship exists between the number of cigarettes smoked during pregnancy and the birthweight deficit (US DHHS 1980; Committee to Study the Prevention of Low Birthweight 1985). Compared with nonsmokers, light and heavy smokers have a 54- and 130-percent increase, respectively, in the prevalence of new- bors weighing less than 2,500 g. A review of five studies including 113,000 births in the United States, Canada, and Wales found that from 21 to 39 percent of the incidence of low birthweight was attributed to maternal cigarette smoking (Committee to Study the Prevention of Low Birthweight 1985). Also, cigarette smoking seems to be a more significant determinant of birthweight than the mother’s prepregnancy height, weight, parity, payment status, or history of previous pregnancy outcome, or the infant's sex. The reduction in birthweight associated with maternal tobacco use seems to be a direct effect of smoking on tetal growth. Mothers who smoke also have increased rates of premature delivery. The newborns are also smaller at every gestational age. The infants display symmetrical fetal growth retardation with deficits in measurements of crown—heel length, chest and head circum- ferences, and birthweight. A recent study in Boston (Lieberman et al. 1985) attempted to evaluate the reasons for differences in rates of prematurity between blacks and whites. Of the 1,365 black women, 34.7 percent were cigarette smokers compared with only 23.4 percent of the white women. Cigarette smoking and low hematocrit levels were two of the most im- portant risk factors accounting for the differences in prematurity rates between blacks and whites. Finally, a number of careful studies have found that the effect of cigarette smoking on birthweight is not mediated through decreased maternal appetite or weight gain (US DHHS 1980). The most widely accepted hypothesis relating maternal smoking and the effects on the fetus and newborn is intrauterine hypoxia (Rush and Cassano 1983). The hypoxia could occur as a result of factors associated with smoking, such as increased levels of carbon monoxide (CQ) in the blood. reduction of blood flow, or inhibition of respiratory enzymes, There is strong experimental evidence that maternal smoking causes fetal hypoxia. Several studies have demonstrated that smoking cessation prior to or during pregnan- cy can partly reverse the reduction in the child's birthweight (Rush and Cassano 1983; Hebel, Fox. Sexton 1988). Ina large study using the 1970 British Birth Cohort (Lieber- man et al. 1987), an inverse relationship between measures of social class and the prevalence of smoking was demonstrated that was similar to that seen in the United States. In all social class groups. babies of the nonsmokers weighed more than those whose mothers had smoked during pregnancy. and the women who had stopped smok- ing either before or during pregnancy had babies with higher birthweights than women who continued to smoke throughout pregnancy. Fetal and Perinatal Mortality Kleinman and colleagues (1988) from the National Center for Health Statistics used Missouri birth records from 1979-83 (Table 4) to study the relationship between cigarette smoking in mothers and infant mortality. Among the [34.429 primiparas, the infant mortality rates (adjusted for age. parity. education. and marital status) were (per 1,000 subjects) 15.1 for white nonsmokers. 18.8 for whites who smoked less than | pack of cigarettes per day, and 23.3 for whites who smoked more than | pack of ciga- rettes per day. For black nonsmoking women, the infant mortality rate (per 1,000 women) was 26.0: for blacks who smoked less than | pack per day. 32.4: and for blacks who smoked greater than | pack per day, 39.9. Mortality was increased during the fetal, neonatal, and postneonatal periods. It was estimated that if all pregnant women stopped smoking, the number of fetal and infant deaths would be reduced by approximately 10 percent. In the United States this would result in about 4,000 fewer infant deaths each year. A study conducted by the Office on Smoking and Health attributed approximate- ly 2.500 infant deaths to maternal smoking in 1984 (CDC 1987). Stein and associates (1981) have studied the causes of spontaneous abortion in three New York City hospitals. They compared women with spontaneous abortion to con- trols (women who carried their pregnancy to 28 weeks or more). Within the spon- taneous abortion groups, they then compared those with evidence of chromosomal ab- normalities and those with apparently normal chromosomes. The odds of a spontaneous abortion increased by 46 percent for the first 10 cigarettes smoked per day and by 61 percent for the first 20 cigarettes smoked. Smoking was not associated with the spon- taneous abortion of chromosomally abnormal conceptions. but only with those in which the chromosomes were normal. These results were not confounded by such factors as maternal age or race. Congenital Malformations Evidence that exposure to tobacco and cigarette smoking could be related to congeni- tal malformations is less clear. About 3 percent of all live births have major congeni- tal malformations (Behrman and Vaughn 1987). Maternal smoking has not been demonstrated to be a major risk factor for the induction of congenital malformations, although elevated risks have been reported in some studies. Kelsey and coworkers (1978) reported an increased risk of 1.6 for congenital malformations among the 73 PL TABLE 4.— Infant mortality rates and odds ratios (95% confidence intervals), by maternal race, among 134,429 primiparas, based on multiple logistic regression, Missouri, 1979-83 Crude rates Adjusted rates (per 1,000) (per 1,000) Adjusted odds ratios Whites Blacks Whites Blacks Whites Blacks Marital status Married 14.5 25.4 15.9 29.5 1.00 1.00 Unmarried 24.0 28.6 21.0 27.2 1,33 (1.18-1.50) 0.92 (0.73-1.16) Education (years) <12 22.9 33.2 19.8 34.1 1.36 (1.16-1.59) 12 15.2 25.9 16.7 28.8 1.14 (1.02-1,28) >12 12.8 21.5 14.6 25.3 1.00 Age (years) 100 Hg/cigarette), is absorbed upon in- halation and is detoxified in the liver, yielding SCN~. Since SCN~ can also originate from dietary intake, only values above 100 mol of SCN~ per L of serum as measured for cigarette smokers are meaningful for dosimetry of uptake. In general, the average cigarette smoker has SCN” levels between 100 and 250 uUmol/L of serum (US DHHS 1987). A number of studies have clearly demonstrated that the mutagenic activity of the urine of cigarette smokers is higher than that of nonsmokers (IARC 1986). The most widely applied method for determining mutagenic activity of urine samples was developed by Yamasaki and Ames (1977), using a resin to concentrate the body fluid and, upon metabolic activation, measuring the mutagenic activity on bacterial tester strains TA98 and TA1538. In general, the urine of cigarette smokers exhibits at least twice the mutagenic activity of that measured in nonsmokers’ urine. In summary. there are several biochemical indicators that enable investigators to assay the uptake of tobacco smoke by individuals or by groups of individuals. Whereas analyses of exhaled CO, of COHb, and of SCN” and nicotine-cotinine in saliva, serum, and urine are well suited for determining the smoking intensity of an active smoker, 96 only nicotine and cotinine determinations in serum and urine can also serve as indicators for the exposure of nonsmokers to ETS. Summary The 1964 Surgeon General's Report was a landmark study that reviewed and assessed the available epidemiologic. clinical, pathological, and experimental literature for evidence linking cigarette smoking to disease. The principal findings of that Report are summarized in Table 13. In men, cigarette smoking was found to increase overall mortality and to cause lung and laryngeal cancer. Several other important conclusions were also drawn (Table 13). Since 1964, 20 reports of the Surgeon General (including this Report) have been released on tobacco and health that substantiate and strengthen the original conclusions of the 1964 Report. These reports have also established associations between smoking and disease in areas for which data did not exist, shed light on pathogenetic mechanisms of tobacco-related disease, and added scientific depth to areas mentioned only briefly in the 1964 Report. A review of Table 13 allows the reader to survey quickly the state of knowledge on cigarette smoking and health in 1989 and to compare it with what was known in 1964. Of the 27 principal effects presented in Table 13. 13 were first noted in 1964, among those 13 effects, many have been strengthened since 1964. Recent reports of the Sur- geon General have also covered important topics not even mentioned in the 1964 Report. For example, these reports have concluded that involuntary smoking can cause disease, including lung cancer. in healthy nonsmokers and that smokeless tobacco can cause oral cancer. The most recent Surgeon General's Report also concluded that the use of cigarettes and other forms of tobacco is addicting (US DHHS 1988). Much progress has been made in understanding the physicochemical nature of tobac- co smoke. Today, the estimated number of compounds in tobacco smoke exceeds 4,000, including some that are pharmacologically active, toxic, mutagenic, or car- cinogenic. The diverse biological effects of tobacco smoke constituents provide a framework for understanding the multiple adverse consequences of smoking. For ex- ample, the identification of 43 different carcinogenic substances in tobacco smoke helps explain why cigarette smoking can cause cancer at different sites including the lung, larynx, oral cavity. and esophagus: why cigarette smoking is a contributory factor for the development of cancer at different sites including the bladder, kidney, and pancreas, and why cigarette smoking is associated with cancer of the stomach and uterine cervix. The central role of cigarette smoking as a massive. preventable personal and public health problem can now be better appreciated. In the United States, it is a major cause of CHD. this country’s most common cause of death; cigarette smoking is estimated to account for 2] percent of all CHD deaths. Cigarette smoking is the major cause of lung cancer, the most common cause of cancer death in the United States: smoking ts es- timated to account for 87 percent of lung cancer deaths and 30 percent of all cancer deaths. While lung cancer death rates for women who are nonsmokers have not in- creased since the early 1960s, comparable death rates for women who smoke cigarettes have increased more than fourfold. In 1986, lung cancer and breast cancer were the 97 86 TABLE 13.—Summary of the principal effects of cigarette smoking Effect first discussed in Surgeon General's Reports Mortality and morbidity Overall mortality, increased in men Overall morbidity, increased Cardiovascular CHD, mortality increased in men Cerebrovascular disease (stroke), mortality increased Atherosclerotic aortic aneurysm, mortality increased Atherosclerotic peripheral vascular disease, risk factor Cancer Lung cancer, the major cause in men Laryngeal cancer, a cause in men Oral cancer (lip), a cause (pipe smoking) Esophageal cancer, associated with Bladder cancer, associated with Pancreatic cancer, increased mortality Renal cancer, increased mortality Gastric cancer, associated with Cervical cancer, possible association with Year first discussed in a Surgeon General’s Report 1964 1967 1964 1964 1967 1971 1964 1964 1964 1964 1964 1967 1968 1982 1982 Current knowledge in 1989 Overall mortality increased in men and women Overall morbidity increased A major cause of coronary heart disease in men and women A cause of cerebrovascular disease (stroke) Increased mortality from atherosclerotic aortic aneurysm A cause and most important risk factor for atherosclerotic peripheral vascular disease The major cause of lung cancer in men and women The major cause of laryngeal cancer in men and women A major cause of cancer of the oral cavity (lip, tongue, mouth, pharynx) A major cause of esophageal cancer A contributory factor for bladder cancer A contributory factor for pancreatic cancer A contributory factor for renal cancer An association with gastric cancer An association with cervical cancer 66 TABLE 13.—Continued Effect first discussed in Surgeon General’s Reports Year first discussed in a Surgeon General's Report Current knowledge in 1989 Pulmonary Chronic bronchitis, the major cause Emphysema, increased mortality Women Low-birthweight babies, associated with Unsuccessful pregnancy, associated with Other effects Tobacco habit, related to psychological and social drives Involuntary smoking, irritant effect Peptic ulcer disease, associated with Occupational interactions, adverse Alcohol interactions, adverse Drug interactions, adverse Nonmalignant oral disease, associated with Smokeless tobacco, associated with oral cancer 1964 1964 1964 1980 1964 1972 1964 1971 1971 1979 1969 1979 The major cause of chronic bronchitis The major cause of emphysema A cause of intrauterine growth retardation A probable cause of unsuccessful pregnancies Cigarette smoking and other forms of tobacco use are addicting A cause of disease, including lung cancer, in healthy nonsmokers A probable cause of peptic ulcer disease - Adverse occupational interactions that increase the risk of cancer Adverse interactions with alcohol that increase the risk of cancer Adverse drug interactions An association with nonmalignant oral disease Smokeless tobacco is a cause of oral cancer leading causes of cancer death in U.S. women, accounting for approximately equal numbers of cancer deaths. Cigarette smoking is the major cause of COPD, an effect that far outweighs all other factors: smoking is estimated to account for 82 percent of COPD deaths. (See Chapter 3.) The 1964 Report of the Surgeon General stated that death rates from cerebrovascular disease (stroke) were increased in cigarette smokers compared with nonsmokers, but it drew no conclusions concerning causality. In the current 1989 Report, for the first time, cigarette smoking is cited as a cause of stroke. the third most common cause of death in the United States. Stopping smoking reduces the risk of stroke, The effect of smoking on pregnancy was briefly mentioned in the 1964 Report. Many studies have subsequently shown that cigarette smoking causes fetal growth retarda- tion and is a probable cause of unsuccessful pregnancies. Table 13 summarizes other important smoking associations with several diseases, in- cluding atherosclerotic aortic aneurysm, atherosclerotic peripheral vascular disease, and peptic ulcer disease: it also includes occupational and alcohol-related interactions with smoking that increase the risk of cancer. Finally, the reports of the Surgeon General have emphasized the benefits of quitting tor smokers of all ages. CONCLUSIONS Part I. Health Consequences 1. The 1964 Surgeon General's Report concluded that cigarette smoking increases overall mortality in men, causes lung and laryngeal cancer in men, and causes chronic bronchitis. The Report also found significant associations between smok- ing and numerous other diseases. 2. Reports of the Surgeon General since 1964 have concluded that smoking increases mortality and morbidity in both men and women. Disease associations identified as causal since 1964 include coronary heart disease, atherosclerotic peripheral vascular disease, lung and laryngeal cancer in women, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, intrauterine growth retardation, and low-birthweight babies. 3. Cigarette smoking is now considered to be a probable cause of unsuccessful preg- nancies, increased infant mortality, and peptic ulcer disease; to be a contributing factor for cancer of the bladder. pancreas, and kidney: and to be associated with cancer of the stomach. 4. Accumulating research has elucidated the interaction effects of cigarette smoking with certain occupational exposures to increase the risk of cancer, with alcohol ingestion to increase the risk of cancer, and with selected medications to produce adverse effects. 5. A decade ago, the 1979 Report of the Surgeon General found smokeless tobacco to be associated with oral cancer, In 1986, the Surgeon General concluded that smokeless tobacco was a cause of this disease. 6. Research in the present decade has established that involuntary smoking is a cause of disease, including lung cancer. in healthy nonsmokers, and that the children of parents who smoke have an increased frequency of respiratory infections and symptoms. 7. In 1964, tobacco use was considered habituating. A substantial body of evidence accumulated since then, and summarized in the 1988 Surgeon General's Report, has established that cigarettes and other forms of tobacco are addicting. Given the prevalence of smoking, tobacco use is the Nation's most widespread form of drug dependency. 8. Studies dating from the 1950s have consistently documented the benefits of smok- ing cessation for smokers in all age groups. 9. 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Mayo Clinic Proceedings 56:217-222, April 1981. onal Bladder Cancer Study: Employment of the National Cancer Institute 79(2):217-222, August CHAPTER 3 CHANGES IN SMOKING-ATTRIBUTABLE MORTALITY 117 CONTENTS Introduction 0.0.0.0... 0 cece een eee beet tent eeee 121 A Twenty-Year Perspective: 1965-85 .. 020. eens 122 The Concept of Attributable Risk 2.0.0.0. 0.0 ee ee eens 122 Mathematics of Attributable Risk ........ 000.0 c ee eee 123 Illustrative Calculation: Smoking and Lung Cancer in Women ...........- 125 Uncertainties in Attributable Risk ... 2.0.2.0... ec eee ene 127 Aggregation Bias Versus Statistical Precision .............+----005 127 Age-Standardization 2.0... 0... c cece eens 127 Potential Biases in Applying the Results of Prospective Studies to the General Population ............. 00.020. e eee 128 Uncertainties in Exposure 2.0... eee ee 129 Errors in the Classification of Causes of Death ................00-- 130 Previous Estimates of Attributable Risk from Cigarette Smoking .......... 130 Populations at Risk: 1965 and 1985) 0.1... 6. eee ees 132 Cigarette Smoking and Other Forms of Tobacco Use ............-2200055 133 Older Cohorts of Cigarette Smokers .......... 0... cece eee eee eens 134 Overlapping Populations at Risk ........... 0.0. nes 136 Changes in the Cigarette Product ........ 0... ccc cece eee 138 Other Changes in the Cigarette Smoking Population ...................5. 139 Those Smokers Most at Risk in 1985 Were Also Smokers in 1965 .......... 140 Cancer Prevention Study I and Cancer Prevention Study I] .........--+.---- 140 Nonsmokers’ Death Rates ....... 0.0... c cece eee eet e ene 141 Current Cigarette Smokers’ Death Rates: Lung Cancer ..............---- 143 Current Cigarette Smokers’ Death Rates: Coronary Heart Disease ......... 144 Current Cigarette Smokers’ Death Rates: Chronic Obstructive Pulmonary Disease ... 1.22.0... 0. c cece ee een e tenes 146 Estimated Relative Risks from CPS-I and CPS-II «1.2... 0.0.2... eee ee eee 146 Endocrine and Sex-Related Cancers in Women ............0 00 seer ee eeee 152 Summary ......0.0..0 0.00 eee teeter enn es 152 Smoking-Attributable Mortality in the United States, 1965 and 1985 ........- 153 Conclusions 0.0.0... cc cece ee ence eee teens 161 References 2.0.00... cece cece ene teen eee eee eee nena 162 119 Introduction In 1938, Raymond Pearl reported elevated death rates among white males who smoked tobacco, especially those aged 30 to 60 years (Pearl 1938). Pearl's study of 6,800 subjects revealed the increase in mortality risk to be highest among heavy smokers. In 1954, Hammond and Horn reported on the 20-month followup of their prospective study of 188,000 white men, aged 50 to 69 years (Hammond and Horn 1954). Death rates were highest among men who smoked cigarettes but not other tobac- co products, and increased with the amount of cigarette use. Overall, the number of deaths among cigarette smokers was 52 percent greater than would be expected from nonsmokers’ mortality rates. Most of the increased mortality could be attributed to deaths from cancer and especially from coronary heart disease (CHD). In 1964, the Advisory Committee to the Surgeon General reviewed seven prospec- tive studies of smoking and mortality, encompassing over 1.7 million entrants. For the 1.1 million male enrollees, the overall mortality ratio, defined as the observed number of deaths in current cigarette smokers divided by the number expected from nonsmokers’ rates, was 1.68. “For all seven studies,” the Committee stated, “coronary artery disease is the chief contributor to the excess number of deaths of cigarette smokers over nonsmokers, with lung cancer uniformly in second place. For all seven studies combined, coronary artery disease (with a mortality ratio of 1.7) accounts for 45 percent of the excess deaths among cigarette smokers, whereas lung cancer (with a ratio of 10.8) accounts for 16 percent” (US PHS 1964, p. 30). In 1979, the Surgeon General described cigarette smoking as “the single most impor- tant preventable environmental factor contributing to illness, disability and death in the United States” (US DHEW 1979, p. vii). The 1982 Surgeon General’s Report, citing ananalysis by Doll and Peto (1981), estimated that for the year 1978, tobacco use caused 122,000 cancer deaths in men and women (US DHHS 1982). For 1982, the estimate for smoking-caused cancers was 129,000 (US DHHS 1982). The 1983 Surgeon General’s Report estimated that 170,000 Americans died annually from CHD caused by cigarette smoking (US DHHS 1983). “During 1965-1977,” the Report noted, “there were an estimated 2.8 million premature deaths from heart disease, primarily CHD, in American men and women attributable to the use of tobacco” (US DHHS 1983, p. 66). The 1984 Report estimated that 80 to 90 percent of the 62,000 deaths from chronic obstructive lung disease (COLD), referred to later in this discussion as chronic obstruc- tive pulmonary disease (COPD), in the United States in 1983 were attributable to cigarette smoking (US DHHS 1984). “Over 50,000 of the COLD deaths can therefore be considered preventable and premature since these individuals would not have died of COLD if they had not smoked” (US DHHS 1984, p. ii). In 1987, the Economic Report of the President stated, “Smoking presents the largest single source of health risk in America” (U.S. President 1987, p. 184). This Chapter further delineates the mortality consequences of cigarette smoking in the United States. Deaths attributable to cigarette smoking are reported for two benchmark years—1965 and 1985. The Chapter focuses on the health consequences of smoking for current and former cigarette smokers. Deaths of nonsmokers caused by environmental tobacco smoke (National Research Council 1986;US DHHS1988a) and 121 deaths from cigarette-related fires (Consumer Product Safety Commission 1987; Bot- kin 1988) are not discussed, nor are the morbidity consequences of cigarette smoking (US DHEW 1979; Rice et al. 1986). A Twenty-Year Perspective: 1965-85 The two-decade interval, 1965-1985, was selected primarily for reasons of data availability. The year 1985 was the most recent one for which complete, nationwide, cause-specific mortality statistics were available from the National Center for Health Statistics (NCHS). Moreover, in both 1965 and 1985, questions on cigarette use were appended to the National Health Interview Survey (NHIS), a nationally representative, face-to-face interview survey that has been conducted annually by NCHS (Massey et al., 1987; NCHS 1986). In particular, 1985 was the most recent full year for which complete population-weighted data from the NHIS were available (see Chapter 5). In addition, the years 1965 and 1985 represented the approximate midpoints of two large-scale prospective surveys of smoking and mortality among men and women in the United States, both sponsored by the American Cancer Society. In the first of these two prospective studies (Garfinkel 1980a,b, 1981; Hammond 1961, 1964a,b, 1966, 1968, 1969, 1972; Hammond and Garfinkel 1961, 1964, 1966, 1968, 1969, 1975; Ham- mond et al. 1976; Hammond and Seidman 1980; Lew and Garfinkel 1984, 1988), about 1 million persons were followed from 1959 through 1972. In the second study (Gar- finkel 1985; Stellman and Garfinkel 1986; Stellman, Boffetta, Garfinkel 1988), about 1,2 million participants were followed from 1982 through 1988. The two studies will be referred to, respectively, as “Cancer Prevention Study I (CPS-D” and “Cancer Prevention Study II (CPS-II).” In particular, this Chapter will present unpublished, preliminary results from the 4-year followup (1982-86) of CPS-II. The theory, mathematics, limitations, and other methodological issues concerning the calculations of smoking-attributable mortality are described in the next section. The results of the analysis follow thereafter. Readers interested primarily in those results may proceed directly to the Section entitled “Populations at Risk: 1965 and 1985.” The Concept of Attributable Risk In 1953, Levin estimated that 62 to 92 percent of all male lung cancers were “at- tributable to cigarette smoking” (Levin 1953). Levin’s computations addressed the general problem: How many cases of a disease in a given population can be explained by the presence of a particular hazardous agent or a particular personal trait? Put dif- ferently, how many cases would have been avoided but for the presence of the agent or the trait (Doll and Peto 1981)? In principle, the answer requires an experiment whereby disease rates are measured before and after the complete elimination of the hazardous agent or particular trait from the population of interest. Since this type of experiment is usually impractical, the most widely used approach is to estimate disease rates in representative sample populations of exposed and unexposed persons. The results are then extrapolated to the population of interest. 122 The phrase “cases attributable to agent A” is often used interchangeably with “cases caused by agent A.” The latter term is meaningful so long as it is recognized that “caused” refers to an entire population rather than to any single, predetermined mem- ber of the population. Thus, the scientific validity of an estimate that 1,000 lives would be saved by the removal of some hazardous agent does not hinge upon naming the names of the people to be saved. The population-based notion of causation is especially important for chronic diseases with multiple causes. Agent A, forexample, may promote or enhance the disease-caus- ing effect of agent B. A case-by-case analysis of afflicted individuals may never iden- tify agent A as the primary cause in a single instance. Yet its elimination might sub- stantially reduce disease incidence in the population under study. Moreover, the concept of attributable risk generally requires a timeframe. In an as- sessment of the effects of removing a hazardous agent, a researcher could ask how many cases of a specific disease could be avoided in a specified time period, such as | year. When the disease has multiple causes, this quantity may differ from the number of cases of the disease that may eventually be avoided. By specifying a timeframe, the re- searcher inquires not whether such cases could be completely prevented, but whether their premature occurrence could be avoided. For many diseases, death rates are more accessible and reliable than disease rates. Accordingly, computations of “attributable deaths” from a disease have been used in place of “attributable cases” of the disease. Because death from one cause or another is inevitable, such computations necessarily refer to a specific time period during which premature mortality may have been prevented. Mathematics of Attributable Risk Let d1 and do, respectively, denote the incidence rates (in terms of new cases per unit time) of a particular disease among two sample cohorts—one exposed to a hazardous agent, the other unexposed. The two samples are assumed not to differ materially in any other respect, so that both would experience disease incidence do in the absence of exposure. Accordingly, the difference di—do measures the increase in disease in- cidence, or absolute risk, due to the agent. Moreover, the unitless ratio r =d 1/do, termed the relative risk, measures the degree to which the hazardous exposure multiplies the baseline incidence rate. It is often employed as a measure of the epidemiologic and biological significance of an observed association between an agent and a particular disease (Lilienfeld and Lilienfeld 1980; US DHEW 1979). In the exposed cohort, the proportion of disease cases attributable to the hazardous agent is thus equal to s=(d}-do)d1 (which equals (r—1)/r). This quantity has been variously termed the assigned share or probability of causation or attributable propor- tion of risk among the exposed (Bond 1981; Oftedal, Magnus, Hvinden 1968; Black and Lilienfeld 1984; National Research Council 1984; Cox 1987). For some hazardous agents, such as cigarette smoke, the disease incidence rates d} and do and the relative risk r have been estimated directly from prospective longitudinal studies of exposed and unexposed cohorts. Alternatively, retrospective case-control studies do not provide estimates of di and do but yield a close approximation to the rela- 123 tive risk when incidence of the disease is low (Cornfield 1951). Both types of studies provide estimates of the assigned share s. The estimate of relative risk r, derived from epidemiologic studies, is then applied to the population of interest. Let p denote the proportion of exposed persons in the sub- Ject population, estimated independently from survey data. Then the quantity f = pri{p(r—l)+1] is the fraction of all cases of the disease (in a given time interval) that occurs among exposed persons in the subject population. This is sometimes called the “case fraction” (Miettinen 1974). Moreover, if fraction fot all cases occurs among ex- posed persons, and if fraction s of such exposed cases is attributable to the hazardous agent, then the fraction of all cases attributable to the agent is a= fs. From the defini- tions of f and s, the quantity @ can be expressed as a= p(r-l) W) pa-l+l This is Levin’s measure of attributable risk, also termed etiologic fraction (Miettinen 1974), attributable fraction (CDC 1987b), and population-attributable risk (MacMahon and Pugh 1970). When a is expressed in percentage terms, it is often termed percent attributable risk or population-attributable risk percentage. Equation (1) shows how the attributable risk a depends upon both the relative risk r and the proportion exposed p. Thus, an agent may be significant in the causation of disease among exposed persons so that its relative tisk r greatly exceeds 1. Yet that agent may Cause a small proportion of all cases of the disease because exposure rates p are low. Conversely, an agent that is widely prevalent (with large p) may contribute substantially to the total number of cases, even when its relative risk r ts Close to unity. As a consequence of equation (1), the logistic transformation of a is a log (oa) = log p + log (r-1) (2) where log denotes the natural logarithm. Equation (2) provides a convenient method of decomposing the uncertainty in the attributable risk a into two components—uncer- tainty in the proportion exposed p and uncertainty in the relative risk r. Levin's measure of attributable risk can be generalized to cases where there are mul- tiple levels of exposure, multiple causative agents, or confounding or stratifying vari- ables, or when an agent can prevent a disease (Walter 1976; Miettinen 1974). In the case of multiple levels of exposure, it is convenient to let dx denote the incidence rate and rx = dk/do denote the relative risk for the k-th exposure level. Similarly, let px denote the proportion of the subject population exposed at the k-th level. Then Sk = (rk-1)/rk is the assigned share among cases exposed at the k-th level. Likewise, the quantity fr=pkrk/[Zkpk (7kK-1) +1],where Ly denotes summation over exposure levels, is the fraction of all cases occurring among persons exposed at the k-th level. The generalized formula for attributable risk becomes 2k fk 5k, Which can be expressed as x | ; ax kPk (rk-1) (3) Xkpk (Tk~] y+] Let D denote the total number of cases of disease in the population of interest in a given time interval. Then A = aZ is the estimated number of cases in the interval that 124 are attributable to the agent. The quantity A is sometimes called “attributable cases.” When relative risks or exposure rates vary by age, sex, or other stratifying variables, then separate estimates of A can be made for each combination of variables. When there are multiple causative agents, attributable risks can be computed for each agent separately and for combined exposures. Thus, if agents X and Y both have a causal role in the development of a particular disease, then the relative risk for agent X may depend upon the presence or absence of exposure to agent Y. When X and Y act synergistically, some portion of the total risk attributable to X will reflect the combined contribution of X and Y. For example, indoor exposure to radon has recently been es- timated to account for about 13,300 lung cancer deaths annually in the United States (Lubin and Boice 1988). Radon exposure and cigarette smoking interact synergistical- ly in causing lung cancer (National Research Council 1988). Of the estimated 13,000 deaths attributable to radon exposure, about | 1,000 would be due to the combined ef- fect of smoking and radon, while about 2,000 would reflect radon exposure in non- smokers (Lubin and Boice 1988). Illustrative Calculation: Smoking and Lung Cancer in Women Table | provides a detailed illustrative application of Levin’s method to female deaths from lung cancer in the United States during 1985. The population of female smokers has been divided into ten exposure levels: five categories of current cigarette smokers based on the number consumed per day; and five categories of former cigarette smokers based on the length of time since quitting. For each exposure category, the upper panel shows the estimated prevalence px, derived from the 1985 NHIS. Also given are es- timates of relative risk rk derived from the 4-year followup (1982-86) of the second American Cancer Society prospective study (Garfinkel and Stellman 1988). At each exposure level, the upper panel also shows the assigned share sk and the case fraction tk The computations are summarized in the lower panel of Table 1. For both current and former smokers, as well as for all females at risk, the estimated prevalences p rep- resent the corresponding sums Zk px over the prevalence rates px in the individual sub- categories. The case fractions f likewise represent sums of individual fractions fx, while the attributable risks @ are derived from the corresponding sums Zk skfk. Attributable deaths A are derived from the products aD, where D = 38,687 lung cancer deaths among adult females in 1985. Table 1 shows that almost two-thirds of all female lung cancer deaths occurred among women who currently smoke one pack or more daily or who have quit smoking within the last 5 years. Nine out of ten lung cancer deaths occurred in women with any his- tory of regular cigarette use. Cigarette smoking accounted for an estimated 82 percent of lung cancer deaths in women, or 31,600 deaths in 1985. About 9,300 (or 29 percent) of the 31,600 female lung cancer deaths that were caused by smoking occurred among former smokers. Both the prevalence rates and the relative risks in Table 1 are subject to sampling variability. By a formula analogous to equation (2), a standard error for the logistic transformation of a can be derived. Under the assumption that D has no sampling 125 TABLE 1.—Detailed computation of smoking-attributable lung cancer deaths among females, United States, 1985 Exposure Prevalence Relative risk* Assigned share Case fraction category p(%) r 5(%) f(%) Current smokers 1-10 per day® 9.3 5.5 81.9 9.4 11-19 per day 3.3 11.3 91.1 6.7 20 per day 9.3 14.2 93.0 24.0 21-30 per day 3.2 20.4 95.1 11.8 231 per day 27 22.3 95.5 10.8 Former smokers 0-2 years® 5.0 18.2 94.1 16.7 3-5 years 2.5 11.2 91. 5.0 6-10 years 3.4 4.9 79.5 3.0 11-15 years 2.0 3.2 68.5 1.2 216 years 4.0 1.8 43.4 1.3 Exposure Prevalence Case fractions Auributable Aa unaple category P(%) R%®) a(%) A Current smokers 27.8 62.7 57.7 22,300 Former smokers 16.9 27.2 24.1 9,300 Current and former smokers 44.7 89.9 81.8 31,600 “Ratio of age-adjusted death rates, where age adjustment was performed by direct standardization to the age distribution of woman-years of exposure among nonsmokers. "Number of cigarettes smoked per day, as of the dale of enrollment (September 1982). “Number of years elapsed since last smoked regularly, as of the date of enrollment (September 1982). “Auributable deaths A equal aD, where ais attributable risk and D equals 38,687 lung cancer deaths among adult females in 1985. SOURCE: Garfinkel and Stellman (1988); NHIS 1985, unpublished tabulations; NCHS, Division of Vital Statistics, 1985, unpublished. variability, statistical confidence bounds for A can also be calculated. For the calcula- tion shown in Table 1, the estimated 95-percent confidence interval on a for all smokers was 72.1 to 88.6 percent. The corresponding confidence interval for D was 27,900 to 34,300 deaths. Only 2.6 percent of the variance of the logistic transformation of a was due to sampling variability of prevalence rates. 126 Uncertainties in Attributable Risk Aggregation Bias Versus Statistical Precision Sampling variation is not the sole source of uncertainty in estimates of attributable risk. The computations of Table | entail the assumption that the relative risks rk depend only upon the specified indices of current and former smoke exposure. Thus, for former cigarette smokers in Table 1, the degree of risk after cessation of smoking is shown as depending only upon the length of cessation. Yet the magnitude of the residual risk also depends upon the extent of prior cigarette smoke exposure (Hammond 1968; Lubin et al. 1984) and the reason for stopping (Kahn 1966). Also, some persons may have quit smoking after lung cancer had been diagnosed. As Table 1 shows, women who had stopped smoking for 16 or more years at the time of enroll- ment into CPS-II had a subsequent 4-year relative risk of lung cancer equal to 1.8. Within this group of long-term quitters, however, those women who had previously smoked 21 or more cigarettes daily had an estimated relative risk of 4.0 (Garfinkel and Stellman 1988). Likewise, for current smokers in Table 1, the degree of lung cancer risk is shown as depending only upon the current number of cigarettes smoked per day. Yet the risk depends critically upon the lifetime dosage of cigarette smoking, especially the dura- tion of cigarette use and the age of initiation of regular smoking (Brown and Kessler 1988: Doll and Peto 1978, 1981; Peto 1986; US DHHS 1982). While the relative risk + was 22.3 for all women currently smoking 31 or more cigarettes daily (Table 1), it was 18.9 for heavy smokers of 18 to 30 years’ duration and 38.8 for heavy smokers of more than 40 years (Garfinkel and Stellman 1988). A more detailed, multidimensional breakdown of exposure levels may minimize er- rors of classification, but such disaggregation also increases the sampling variability of the estimates. Conversely, increased aggregation of exposure levels will reduce sam- pling variability. Thus, if relative risk were assumed to depend only upon present smok- ing status (current versus former), then the estimated attributable risk for female lung cancer deaths in 1985 would be 80 percent, with a confidence range of 77 to 83 per- cent. The confidence range of attributable deaths A would be narrowed to 29,700 to 32,000. Age-Standardization The relative risks in Table 1 were estimated as a ratio of age-adjusted death rates, where the age adjustment was performed by direct standardization to the age distribu- tion of nonsmokers’ person-years at risk. In principle, if the relative risk is in fact age independent, then the estimate of relative risk in large samples should not be very sen- sitive to the choice of the standard population (Anderson et al. 1980). In practice, however, the estimates can depend strongly upon the standard population. For the il- lustrative calculation in Table 1, the use of the entire population of CPS-II woman-years at risk (rather than nonsmokers only) resulted in an attributable risk for lung cancer of 79 percent, with a confidence range of 75 to 82 percent (see Table 11). 127 Potential Biases in Applying the Results of Prospective Studies to the General Population Subjects enrolled in the CPS-II prospective study constituted over 1.5 percent of all American adults age 45 and over (Stellman, Boffetta, Garfinkel 1988). Still, they dif- fered from the U.S. population in a number of ways (Garfinkel 1985; Stellman and Gar- finkel 1986). CPS-II entrants were more highly educated. The black and Hispanic populations were underrepresented, though less so than in CPS-I (Garfinkel 1985). As in CPS-I, institutionalized and seriously ill persons, as well as illiterate people who could not complete a questionnaire, were excluded (Lew and Garfinkel 1984). In both CPS-I and CPS-H, the overall mortality rates of the enrollees fell substantially below those of the general U.S. population (Hammond 1969; Lew and Garfinkel 1988). These considerations do not by themselves invalidate the use of CPS-II to estimate smoking-attributable risks for the entire American population. The critical assumption in Table 1 above is whether the estimated relative risks r,—not the absolute death rates d\—are representative of the general population. For CHD and for all-cause mortality, CPS-I subjects who were reportedly well at the time of enrollment showed higher estimated relative risks of cigarette smoking than those subjects who said they were sick or who gave a recent history of cancer, heart disease, or stroke (Hammond and Garfinkel 1969: Lew and Garfinkel 1988). A similar elevation of relative risk in well subjects has been found for lung cancer in CPS-II (Gar- finkel and Stellman 1988). Since initially well persons had lower disease rates, the proportional effect of cigarette smoking appeared to be larger. While CPS-I and CPS- II excluded seriously ill and institutionalized persons, the magnitude of the resulting bias is unclear. In the 1980 U.S. Census, about 1.5 percent of the U.S. adult popula- tion was institutionalized. Among persons aged 65 years and over, the proportion was 5.3 percent (U.S. Bureau of the Census 1986). Cigarette smoking has been found to act synergistically with certain workplace ex- posures (such as asbestos and ionizing radiation) in the development of lung cancer (US DHHS 1985; Saracci 1987; National Research Council 1988). Such interactions may also be present in the etiology of nonneoplastic lung disease. Alcohol and tobacco likewise interact synergistically in the etiology of oral and esophageal cancer (US DHEW 1979). Moreover, cigarette smoking has been found to interact synergistical- ly with elevated serum cholesterol! and elevated blood pressure in enhancing the risk of CHD (US DHHS 1983). Persons of lower socioeconomic status (SES) may be more likely to receive such workplace exposures, to consume alcohol heavily, or to have un- favorable CHD risk factors. However, if the effects of cigarette smoking are multi- plicative, then exclusion of such persons from CPS-I and CPS-I] would not bias the es- timated relative risks of disease due to cigarette smoking. Conversely, if the effects of cigarette smoking are purely additive, rather than synergistic, then the exclusion of per- sons with elevated baseline disease rates would bias upward the estimated relative risks of disease due to smoking. The estimated relative risks in Table | are specific to women and have been stand- ardized for age. Standardization for other stratifying or confounding variables was not performed. In principle, failure to control for such variables could bias upward or 128 downward the estimated relative risks due to cigarette use. As discussed in Chapter 2, numerous attempts to control statistically for confounding and stratifying variables have not materially altered the estimated relative risks for cigarette-related diseases. In the illustrative computation of Table 1, no distinction among the races has been drawn. For both sexes, the prevalence of current cigarette use is higher for blacks than for whites. Conversely, smaller fractions of black men and women are former cigarette smokers (US DHHS 1988b). Black persons were underrepresented in CPS-II, con- stituting only 4 percent of entrants (Stellman and Garfinkel 1986). Hence, the relative risks reported in Table 1 may not be accurate for black women. Among the 38,687 adult female lung cancer deaths in 1985, a total of 4892 (8.8 percent) occurred in black women. Hypothetically, if the attributable risks a among black women had been only half those of whites, then the smoking-attributable lung cancer deaths in Table 1 would be reduced from 31,600 to 30,300. In prospective cohort studies, mortality rates tend to be reduced in the initial year or. two of followup. This phenomenon of lower initial mortality results from a tendency to exclude persons who are sick at the outset of the study. In particular, the relative risks in Table 1 were derived from the 4-year followup (1982-86) of CPS-II subjects. Accordingly, it is possible that the planned 6-year followup of CPS-II (1982-88) will reveal somewhat lower relative risks than those reported for the first 4 years. Conversely, measurements of exposure and other personal characteristics, typically obtained at the start of a prospective study, become less accurate as the duration of fol- lowup increases. The relative risks reported in Table 1, for example, have been clas- sified according to the subjects’ cigarette smoking practices upon enrollment in 1982. If many women who were current smokers in 1982 had in fact quit smoking by 1986, then the reported relative risks for “current” smokers are actually those of a mixture of current and former smokers. In the analysis reported below, the 4-year followup of CPS-II is to be compared with the 6-year followup of CPS-I. Such a comparison needs to be interpreted in light of potential biases arising from short- and long-duration followup in prospective studies. Uncertainties in Exposure Potential errors in estimated exposure rates pk are a further source of uncertainty in the computation of attributable risk a. In the illustrative calculation of Table 1, such exposure rates were derived from the 1985 NHIS, a large-scale, stratified, face-to-face household interview survey of the noninstitutionalized civilian population of the United States. Among the possible errors in NHIS estimates are: underreporting or misreport- ing of current cigarette use; inaccurate recall of past cigarette smoking; nonresponse biases due to exclusion of some persons not available for interview; and underrepresen- tation of certain population segments. These sources of uncertainty are discussed in Chapter 5. On the whole, NHIS-derived estimates of population smoking rates have been consistent with other face-to-face interview surveys (CDC 1987a). 129 Errors in the Classification of Causes of Death The estimation of attributable deaths A requires information on total deaths D. For the computation in Table 1, the latter quantity was defined as deaths in 1985 whose un- derlying cause was primary lung cancer (International Classification of Diseases, Ninth Revision [ICD-9], Code 162). Deaths from the larger class of Respiratory Cancers (ICD-9 Codes 162-165) were not used because they include pleural mesotheliomas and secondary lung cancers. Still, the use of ICD-9 Code 162 alone may not eliminate all errors of death certification. In a review of over 1,300 thoracic cancer deaths in Min- nesota between 1979 and 1981, Lilienfeld and Gunderson (1986) identified four cases of pleural malignant mesothelioma that had been classified as Code 162.9. Moreover, it is at least arguable that physicians in recent years have been reluctant to diagnose primary lung cancer in the absence of a history of cigarette smoking (McFarlane et al. 1986). While errors in disease classification and death certification of lung cancer in 1985 may be relatively minor, the same cannot be said with assurance about other diseases caused by cigarette use. Thus, deaths certified as being caused by CHD (ICD-9 Codes 410-414) may not adequately reflect the lethal consequences of cigarette use on the cardiovascular system. Many deaths from Hypertensive Diseases (Codes 401-404, in- cluding Hypertensive Heart Disease, 402, and Hypertensive Disease, 404) may have been aggravated by cigarette use. Similarly, deaths certified as being caused by COPD (ICD-9 Codes 490-492 and 496) may incompletely reflect the numbers of deaths from nonneoplastic respiratory disease due to smoking. Many cases of Influenza and Pneumonia (ICD-9 Codes 480-487) may not have been lethal but for the coexistence of cigarette-induced lung damage. The major prospective studies of cigarette smoking and mortality that were initiated in the 1950s relied upon the International Classification of Diseases, Seventh Revision (ICD-7) (Hammond 1966; Dorn 1959; Kahn 1966; Rogot 1974; Rogot and Murray 1980; Doll and Hill 1956, 1964, 1966; Doll et al. 1980: Doll and Peto 1976). Coding conventions have changed considerably since ICD-7 was adopted in 1955 (Klebba 1975, 1982; Klebba and Scott 1980). While ICD-7 Code 162 was reserved for lung cancer that was “specified as primary,” a separate code 163 was allocated to lung can- cers “not specified as primary or secondary.” In practice, however, epidemiologists and vital statisticians recognized that the great fraction of lung cancer deaths certified under ICD-7 Code 163 were primary and that deaths certified under the two codes were in fact indistinguishable. Accordingly, it was standard procedure to report combined deaths for Codes 162 and 163—a practice adhered to in the analysis below. Still, the use of the combined category 162-163 in ICD-7 may have introduced greater diagnos- tic uncertainty than the current use of Code 162 in ICD-9. Previous Estimates of Attributable Risk from Cigarette Smoking Many authors have estimated the number or proportion of deaths attributable to cigarette use, either from a single cause, a group of causes, or all causes (Ravenholt 1964, 1984; Rice et al. 1986; McIntosh 1984; Whyte 1976; Hammond and Seidman 130 1980: Doll and Peto 1981; Garfinkel 1980a; U.S. Office of Technology Assessment (US OTA) 1985; Schultz 1986; Goldbaum et al. 1987; CDC 1987b). Doll and Peto (1981) estimated 83,000 smoking-attributable deaths from lung cancer in 1978. Rice and colleagues (1986, Table 5) estimated 270,000 smoking-attributable deaths among USS. adults in 1980, including 86,000 from CHD, 75,000 from lung cancer, and 14,000 from “emphysema, chronic bronchitis.” The Centers for Disease Control (1987b) es- timated 315,000 smoking-attributable deaths for 1984, including 77,000 from CHD, 93,000 from lung cancer, and 51,000 from “chronic bronchitis, emphysema” combined with “chronic airways obstruction.” These studies differ with respect to specific causes of disease, the time period under consideration, the populations at risk, the sources of epidemiologic data, and the specific methodology for estimation of risk. Thus, some researchers have directly applied Levin's measure of attributable risk, as defined in equations (1) and (3) (Rice et al. 1986; McIntosh 1984; CDC 1987b; Goldbaum et al. 1987; Whyte 1976). In doing so, they assumed that estimates of relative risk r, derived from particular epidemiologic studies, could be extrapolated to the population under consideration. By contrast, Ham- mond and Seidman (1980) and Garfinkel (1980a) computed attributable risks directly for the CPS-I study population. In an analysis of avoidable deaths from cancer, Doll and Peto (1981) employed a dif- ferent model. Let N denote the size of the population at risk, while D denotes the total number of deaths from a specific cause. If do denotes the cause-specific death rate among unexposed persons, then D-doN is an estimate of the number of deaths at- tributable to the exposure. To estimate attributable cancer risks for the United States in 1978, Doll and Peto (1981) then assumed that the age- and sex-specific cancer mor- tality rates for nonsmokers do observed in CPS-I during 1959-72 could be applied to nonsmokers in the general population in 1978. In support of such an assumption, they note that for men, nonsmokers’ cancer rates in other prospective studies (Kahn 1966; Doll and Peto 1976) closely matched those observed in CPS-I (Doll and Peto 1981). Moreover, CPS-I lung cancer rates of nonsmoking women were similar to those of U.S. women in 1950, before their lung cancer rates began to increase. Doll and Peto’s method was employed by OTA (1985) to estimate attributable deaths from CHD (US OTA 1985). For cancer, nonsmoker death rates in CPS-I may well ap- proximate do for the U.S. population. But the same conclusion does not appear to be warranted for CHD (Sterling and Weinkam 1987). In fact, the use of CPS-I nonsmoker death rates yielded an estimate of 142,000 smoking-attributable deaths from CHD in 1982. By contrast, application of the Levin method gave an estimate of 91,000 deaths (US OTA 1985). Doll and Peto (1981) rejected the application of relative risks derived from CPS-I to the U.S. population in 1978. Their central concern was that such relative risks had in- creased in the two decades since the start of CPS-I in 1959. Among smokers aged 60 years or more in 1965, a much smaller fraction had smoked regularly during early life. For older women smokers, in particular, only one in eight had begun to smoke regular- ly as a teenager. This proportion increased markedly in subsequent decades (Chapter 5). In view of the importance of quantity and duration of smoking in determining lung cancer risk—and especially in view of the critical role of early-life smoking in the etiol- 131 ogy of smoking-induced cancers (Peto 1986)—it was highly likely that the relative risks for smoking-induced cancers would have increased since the early 1960s. (See also Doll et al. 1980.) Accordingly, there may be serious biases in the application of relative risks from 1960s prospective epidemiologic studies to 1980s populations. Such potential biases constitute the most serious criticism of prior studies of smoking-attributable deaths. Updated epidemiologic evidence for the 1980s is needed to address this criticism. Populations At Risk: 1965 and 1985 Table 2 and Figures | through 5 describe the populations at risk in 1965 and 1985. While Table 2 reports the percentages of smokers, the figures show the absolute num- bers of U.S. resident adults in each smoking category for each year. Children and young adults under age 18, who may also suffer adverse effects from cigarette use, are ex- cluded from Table 2 and the figures. In both 1965 and 1985, respondents to the NHIS were asked, “Have you smoked at least 100 cigarettes in your entire life?” Those who answered affirmatively were then asked how much they smoked currently or, if they were not current smokers, when they TABLE 2.—Prevalence of cigarette smoking, persons aged 18 years or more, United States, 1965 and 1985 1965° 1988" (%) (%) Males Current smokers‘ 53.4 32.7 Former smokers 20.8 29 Never smoked regularly® 25.8 3 Females Current smokers® 34.1 27.5 Former smokers 8.1 (7.1 Never smoked regularly? 57.8 55.4 NOTE: Prevalence estimates for 1965 and 1985 have been directly standardized to the age distributions of the U.S. tesident populations in each year, respectively (U.S. Bureau of the Census 1974, 1986). “Based upon 52,873 self-responses to the Cigarette Smoking Supplement to the 1965 National Health Interview Survey. Standard errors 0.3 to 0.4 percent for males, 0.1 to 0.2 percent for females. Inclusion of 33,422 additional proxy responses resulted in the following estimates: male current smokers, 51.9 percent, male former smokers, 19.0 percent: female current smokers, 33.6 percent: and female former smokers, 7.7 percent. "Based upon 32,859 self-responses to the Cigarette Smoking Supplement to the 1988 National Health Interview Survey. Standard errors 0.4 percent for males. 0.3 percent for females. “In 1965, current smokers included all respondents who reported a current number smoked per day. including “less than | per day.” In 1985, current smokers included all respondents who answered affirmatively to the question "Do you smoke now?” ‘In both 1965 and 1985, the category “never smoked regularly” included two groups of respondents: (1) those who answered negatively to the question “Have you ever smoked at least 100 cigarettes in your life?"; and (2) those who answered affirmatively but denied ever smoking cigarettes regularly, In 1965 and 1985. respectively, group 1 accounted for 99 percent and 97 percent of all respondents in the category “never smoked regularly.” 132 last smoked regularly. While the NHIS for 1965 permitted proxy respondents, the es- timates in both years have been derived from self-respondents only (see Note b of Table 2). Table 2 shows the percentage distribution among adult men and women in three categories: current smokers, former smokers, and those who never smoked regularly. Between 1965 and 1985, the proportions of current smokers declined and the propor- tions of former smokers increased. The most marked change was the decline in the prevalence of current cigarette use among adult men. In Figure 1, the responses have been further divided into four categories: current smokers of fewer than 25 cigarettes daily: current smokers of 25 or more cigarettes daily: former smokers who quit within the last 5 years: and former smokers who stopped for more than 5 years. The weighted proportions in each category, tabulated by age and sex, were then multiplied by the corresponding estimates of the U.S. resident population (U.S. Bureau of the Census 1974. 1986). In 1965, there were an estimated 53.7 million adult current cigarette smokers (stand- ard error, 0.2 million), which represented about 43 percent of all U.S. residents aged 18 years or more. By 1985, there were an estimated 53.5 million adult current smokers, composing 30 percent of U.S, adults. While the total number of current smokers stayed about the same. there was a shift in their distribution by sex. The number of adult male current smokers declined from 31.7 million (53.4 percent) in 1965 to 28.2 million (32.7 percent) in 1985, while adult female smokers increased from 22.0 million (34.1 per- cent) to 25.3 million (27.5 percent) (Figure 1). In 1965, about 28 percent of adult male smokers who were nonproxy respondents to the NHIS consumed 25 or more cigarettes per day (Figure 1). By 1985, this proportion had risen to 32 percent. For women, the proportions of heavier current smokers rose from 14 percent of nonproxy respondents in 1965 to 21 percent of smokers in 1985. The true population prevalence of smoking 25 or more cigarettes per day in 1965 is somewhat uncertain because the elimination of proxy respondents may make the sample nonrepresentative. As shown in Chapter 5. however, there was no significant change in the proportion of heavy smokers between 1974 and 1985. By contrast, the numbers of former smokers increased substantially between 1965 and 1985. Thus, in 1965, there were about 17.6 million adult former smokers (12.4 million men and 5.2 million women). By 1985, this number had risen to 40.9 million (25,2 million men and 15.7 million women). There was an increase in the proportion of former smokers who had stopped for more than 5 years (from 49 to 63 percent of male former smokers, and from 41 to 57 percent of female former smokers) (Figure 1). Cigarette Smoking and Other Forms of Tobacco Use Figure 2 shows the 1965 and 1985 adult populations broken down according to the type of tobacco used. In 1965, the NHIS included questions on cigar and pipe smok- ing as well as cigarette use. The 1985 questionnaire inquired only about cigarette smok- ing. However, questions about all forms of tobacco use, including smokeless tobacco, were included on a supplement to the 1985 Current Population Survey, performed by the U.S. Bureau of the Census (see Chapter 5). 133 60 FEMALES 50 40 30 MILLIONS AGED 18 YEARS OR MORE 0 1985 1985 1965 1985 = Current smokers, less than 25 per day NJ Current smokers, 25 or more per day ill Former smokers, 5 years or less A A Former smokers, more than 5 years FIGURE 1.—Populations of current and former cigarette smokers, adult men and women, United States, 1965 and 1985 SOURCE: Estimated from unpublished tabulations, NHISs 1965 and 1985; and estimates of the resident populations of the United States by age and sex. 1965 and 1985 (US Bureau of the Census 1974, 1986). Figure 2 shows a marked change over two decades in the forms of tobacco used by men. In 1965, 5.2 million men (9 percent) hada history of ever smoking pipes or cigars, but not cigarettes. In 1985, the number using noncigarette tobacco dropped to 2.7 mil- lion or 3 percent of the men. In 1965, 29 million men had a history of ever smoking cigarettes and other forms of tobacco, about two-thirds of all cigarette smokers. By 1985, the number had dropped to 5.6 million, only 1 in 10 of all cigarette smokers. Older Cohorts of Cigarette Smokers Figures 3 and 4 focus on persons aged 60 years and over, who suffer the highest in- cidence rates of smoking-related diseases. For 1965 and 1985, respectively, these groups of older persons were born before 1906 and before 1926. Among older men, as shown in Figure 3, the two-decade interval witnessed a 136-percent increase in the num- ber of former cigarette smokers. Among older women, the number of current smokers 134 MILLIONS AGED 18 YEARS OR MORE 0 {965 . 1985 1965 1985 Never smoked regularly Noncigarette tobacco only Cigarettes only NB 4 Cigarettes and other tobacco FIGURE 2.—Populations of adult men and women classified by history of tobac- co use, United States, 1965 and 1985 SOURCE: Estimated from unpublished tabulations, NHISs 1965 and 1985, unpublished tabulations, CPS 1985, and es- timates of the resident populations of the United States by age and sex, 1965 and 1985 (US Bureau of the Census 1974, 1986). doubled, while the number of former smokers increased sixfold. Between 1965 and 1985, the population of older women with a history of regular cigarette use, past or present, increased over threefold. The NHISs for 1965 and 1985 did not ask about the age of initiation of cigarette use. However, this information is available from other sources. For 1985, tabulations of the age of onset of regular cigarette use were made from the Current Population Survey. About 69 percent of older men with a history of cigarette use, past or present, began to smoke before age 20 (Figure 4). Among older women, the proportion was 39 percent. For 1965, three sources of information provide the age of smoking initiation among cohorts born before 1906: the NHISs of 1978-80 (Harris 1983), the Current Popula- tion Survey of 1955 (Haenszel et al. 1956), and the initial 1959 questionnaire to CPS- 1 (Hammond 1966, Appendix tables). For older men with a history of cigarette use, about 60 percent started smoking before age 20 (range, 56 to 62 percent). For older women smokers, about 12 percent started in their teenage years (range, 9 to 15 percent). 135 14 FEMALES MILLIONS AGED 60 YEARS OR MORE 9-NMWOnRA TAN wMWOET 1 EB Current smokers NJ Former smokers FIGURE 3.—Populations of current and former cigarette smokers, men and women aged 60 years or more, United States, 1965 and 1985 SOURCE: Estimated from unpublished tabulations, NHISs 1965 and 1985; and estimates of the resident populations of the United States by age and sex, 1965 and 1985 (US Bureau of the Census 1974, 1986). Accordingly, the period between 1965 and 1985 saw a marked increase in the num- ber of women smokers who reached the age of 60 years (Figures 3 and 4). Moreover, the number of such women who started smoking in their teens increased by about ten- fold (Figure 4). Additional data on age of initiation are presented in Chapter 5. Overlapping Populations at Risk In 1965, a total of 71.3 million adults had a history of regular cigarette smoking, past or present. By 1985, this count had increased to 94.4 million. These two populations overlapped. Among the adult population at risk in 1985, about 54.8 million were born before 1948, and therefore they were also aged 18 years or more in 1965. About 95 percent of the latter group began to smoke during 1965 or earlier (Harris 1983: un- published tabulations from the Current Population Survey 1985). This means that about 51.8 million adults, who had ever smoked in 1985, had also been at risk in 1965. The overlap is depicted graphically in Figure 5, where the diagonal lines show the populations common to both years. Among 44.1 million adult men with a history of 136 o-~nNoskG MILLIONS AGED 60 YEARS OR MORE Oo- NW F&F A An OO 1 i & Began smoking before age 20 NJ NS Began smoking age 20 or older FIGURE 4.—Populations of men and women aged 60 years or more with a history of regular cigarette smoking, classified by age started to smoke regularly, United States, 1965 and 1985 SOURCE: Estimated from Harris (1983); Haenszel et al. (1956); Hammond (1966); unpublished tabulations, NHISs 1965 and 1985; unpublished tabulations, CPS 1985; and estimates of the resident populations of the United States by age and sex, 1965 and 1985 (US Bureau of the Census 1974, 1986). cigarette smoking in 1965, about 30.8 million survived to 1985. The vertical lines show the remaining 13.3 million men who died before 1985 (standard error, 0.4 million). Likewise, among 27.2 million adult women with a smoking history in 1965 (diagonal lines and vertical lines combined), about 6.2 million died before 1985 (vertical lines). Not all of the decedents, however, died as a consequence of their cigarette use. The horizontal lines in Figure 5 show the populations of adults at risk in 1985 who were not also at risk in 1965. The estimates are 22.6 million men and 20.0 million women. These counts do not include persons who may have taken up smoking after 1965 but died before 1985. Nor do they include smokers under age 18 in 1965 and 1985. Still, it appears that in the two-decade period following the 1964 Surgeon General’s Report and the 1965 Federal Cigarette Labeling and Advertising Act, some 43 million Americans took up regular cigarette smoking, either temporarily or per- manently. About two-thirds of them began to smoke by age 18. 137 70 FEMALES 60 50 40 30 20 10 MILLIONS AGED 18 YEARS OR MORE 0 1965 1985 1965 1985 = 1985 smokers born after 1947 ‘J N Populations common to both 1965 and 1985 Mm Decedents by 1985 FIGURE 5.—Populations of adult men and women with a history of regular cigarette smoking, United States, 1965 and 1985 SOURCE: Estimated from Harris (1983): unpublished tabulations, NHISs 1965 and 1985: unpublished tabulations, CPS 1985, and estimates of the resident populations of the United States by age and sex, 1965 and 1985 (US Bureau of the Cen- sus 1974, 1986). Changes in the Cigarette Product The 1965 and 1985 population surveys did not elicit information on the type of cigarette smoked. However, there was a decline in the average tar and nicotine yield of cigarettes, at least as measured by the U.S. Federal Trade Commission (FTC) using smoking machines under standardized conditions (Chapters 2 and 5). Data on ag- gregate cigarette sales and other population surveys (US DHEW 1979; US DHHS 1980, 1981; Chapter 5) also show that the Proportion of persons smoking filter-tipped ciga- rettes increased substantially. Among entrants into CPS-II in 1982, more than 90 per- cent were filter-tipped-cigarette smokers. In this group, there was an average of 18 years of filter-tipped-cigarette smoking prior to enrollment (Stellman and Garfinkel 1986). The majority of these persons had smoked nonfilter cigarettes earlier in life. 138 It remains problematic whether such changes in cigarette manufacture and patterns of cigarette smoking have substantially reduced risks to cigarette smokers. There is considerable evidence that the actual reduction in the dangerous chemicals in cigarette smoke is much smaller than implied by the FTC machine measurements (US DHHS 1988a). While there is evidence that the long-term use of filter cigarettes and low-tar cigarettes may somewhat reduce the risk of lung cancers, there are considerably fewer data on a protective effect for other smoking-induced diseases (Alderson et al. 1985; Castelli et al. 1981; Hawthorne and Fry 1978; Kaufman et al. 1983; Lee and Garfinkel 1981; Lubin et al. 1984; Hammond et al. 1976; Wynder and Stellman 1979, US DHHS 1981; Wilcox et al. 1988; Stellman 1986a,b). During the 1965—85 period, numerous chemical treatments and additives have been applied to cigarettes during tobacco curing and storage, sheet reconstitution, puffing, casing, and cigarette assembly. The chemicals include humectants, pesticides, flavor- ings, plasticizers, ash adhesives, and other agents. Cigarette filters, plug wraps, and tipping papers have evolved. The mix of domestic tobaccos has also changed, and oriental varieties have been added increasingly to American cigarette blends. The details of these product changes remain proprietary (US DHHS 1981). Other Changes in the Cigarette Smoking Population The present comparison of populations at risk in 1965 and 1985 has been confined to sex, age, and history of tobacco use. Still, there may have been other changes in the characteristics of persons who smoke cigarettes. Surveys such as the NHIS have consistently shown a socioeconomic gradient in cur- rent cigarette use, as measured by education, occupation, and other characteristics (US DHEW 1979; US DHHS 1980; Novotny et al. 1988; US DHHS 1988a; Brackbill, Frazier, Shilling 1988; Chapter 5). There is some evidence that socioeconomic dif- ferentials in smoking rates have widened. The proportionate decline in adult smoking rates between 1965 and 1985 was highest for people who had graduated from college and lowest for those who had not completed high school (Chapter 5). Between 1970 and 1980, white-collar men and women showed proportionately greater declines in smoking rates than their blue-collar counterparts (US DHHS 1985). Among the factors that may influence the risks of cigarette smoking are: the coexis- tence of untreated hypertension; elevated serum cholesterol; consumption of oral con- traceptives; alcohol use; diabetes mellitus; and workplace exposure to other toxic and carcinogenic agents such as asbestos and radon daughters. With respect to these fac- tors, it needs to be determined whether the typical cigarette user of the 1980s differs from his or her counterpart of the 1960s. Cigarette smokers have higher rates of alcohol use, are more sedentary, and are less likely to wear seat belts (Schoenborn and Benson 1988; Williamson et al. 1986). It is unknown whether these relationships have strengthened or weakened over the years. There is evidence in the American population of declines in dietary cholesterol, in dietary saturated fat as a percentage of total calories, and in serum cholesterol levels (Havlik and Feinbeib 1979). The prevalence of untreated and inadequately treated hy- pertension has also declined (Havlik and Feinleib 1979). However, detailed studies of 139 the clustering of cigarette smoking with other risk factors for CHD are unavailable. It remains unclear whether the observed long-term declines in hypercholesterolemia and hypertension have been more or less pronounced in cigarette smokers than in non- smokers. There is some evidence that ci garette smoking reduces therapeutic effective- ness of new pharmacologic and invasive treatments of CHD (Deanfield et al. 1984; Galan et al. 1988), Finally, in 1965, oral contraceptives were just coming into widespread use. By 1985, oral contraceptive use was prevalent among both smokers and nonsmokers (Goldbaum et al. 1987), Those Smokers Most at Risk in 1985 Were Also Smokers in 1965 In sum, between 1965 and 1985, there have been major changes in the populations of smokers at risk for cigarette-related injury. In 1965, most men who smoked ciga- rettes had also used cigars and pipes. However, by 1985 the great majority smoked cigarettes exclusively. In 1965, about 40 percent of current smokers were women. By 1985, women numbered almost half of current smokers. Moreover, the numbers of former smokers increased substantially in both sexes— especially in men. In 1965, about one-quarter of all living men (self-respondents to NHIS, age 18 or older) with a history of regular cigarette use were former smokers. By 1985, former smokers made up almost half of all living men age 18 or older who ever smoked. Finally, the two-decade interval witnessed a substantial increase in the number of women smokers reaching the age of 60 years, with a tenfold rise in the population of older women who had begun to smoke as teenagers. These changes in the population at risk have also been observed in other, nonrandom samples of the U.S. smoking population, including a recent comparison of the 1959 entrants into CPS-I with the 1982 entrants into CPS-II (Stellman and Garfinkel 1986). The percentage of male smokers who smoked 20 or more cigarettes per day in CPS II (76 percent) was higher than in CPS-I (69 percent), the percentage of female smokers who smoked 20 or more cigarettes per day increased even more from CPS-I to CPS-I] (43 percent to 61 percent). Among the 94.4 million adults in 1985 witha history of cigarette use, about 51.8 mil- lion smoked cigarettes as adults before 1966. The youngest of these persons is now in his or her late thirties. This group represents the vast majority of persons who are now at risk for the fatal and nonfatal consequences of cigarette smoking. Cancer Prevention Study I and Cancer Prevention Study II CPS-I, formerly termed the American Cancer Society 25-State study, began in Oc- tober 1959 and ended in October 1972. Over | million men and women, representing 3 percent of the population over the age of 45 years, were recruited in 1,121 counties (Hammond 1964a,b, 1966: Garfinkel 1985). Illiterate persons, institutionalized populations, itinerant workers, and illegal aliens were not recruited. More than 97 per- cent of enrollees were white. Enrollment was by family; an eligible family had to have one member over age 45. Once a family was eligible, every family member over the age of 35 was asked to participate. As a result of family-based recruitment, more than 140 three-quarters of CPS-I subjects were married. As a consequence of the eligibility rules, the age distribution of entrants peaked at 45-49 years. More than one-third of par- ticipants had at least some college education. CPS-II was instituted in September 1982. The study, conducted in all 50 States, had the same enrollment plan and organizational structure as CPS-I. Over 1.2 million per- sons were enrolled. As in CPS-I, subjects were predominantly white and more edu- cated than the general population. While 2 percent of CPS-I participants were black, the proportion increased to 4 percent in CPS-II. Still, black persons were under- represented. Like CPS-I participants, CPS-II enrollees were predominantly over 40 years of age. Unlike CPS-I, the mode of their age distribution was 50 to 59 years (Gar- finkel 1985; Stellman and Garfinkel 1986). CPS-II is planned to continue through 1988. Preliminary results of the first 4 years of followup (1982-86) are available. For these 4 years, ascertainment of the fact of death among enrollees is thought to be virtually complete. However, as of July 1988, the cause of death had not been ascertained for about 9 percent of male deaths and 13 percent of female deaths. Comparison of the 6-year followup (1959-65) of CPS-I and the 4-year followup of CPS-II is reported below. For computation of relative risks, cause-specific death rates for CPS-I males and females have been standardized to the age distributions of man- years and woman-years of exposure during 1965-69. Relative risks in CPS-II were likewise computed as the ratios of age-adjusted death rates, where standardization was performed with respect to the age distributions of man- and woman-years of exposure during 1982-86. For comparison of absolute death rates (as opposed to relative risks), the age-specific rates in both studies were standardized to the age distribution of U.S. resident white males and females in 1965. For CPS-Il, absolute death rates have been corrected for underascertainment of causes of death. No such correction was made for CPS-I, where death certificate retrieval is virtually complete. No attempt has been made to correct for possible noncomparability between ICD-7 (CPS-I) and ICD-9 (CPS-II). Studies of the transition between the Seventh and Eighth Revisions of the International Classification of Diseases have shown significant non- comparability (Klebba 1975, 1982). Similar results have been reported for the transi- tion between the Eighth and Ninth Revisions (Klebba and Scott 1980). Comparison of the Seventh and Ninth Revisions, however, suggests that the combined changes have been self-cancelling (Personal communication, J. Klebba to J. Harris, June 1988). Both CPS-I and CPS-II are more representative of middle-class white Americans than the U.S. population as a whole. Still, the two cohorts were derived from virtually iden- tical sampling schemes, and analysis of the entrants has shown similar demographic characteristics (Stellman and Garfinkel 1986). These considerations enhance the validity of comparisons between the American Cancer Society studies. Nonsmokers’ Death Rates Table 3 reports a comparison of the age-adjusted death rates for the three leading causes of death from cigarette smoking: CHD; chronic obstructive pulmonary disease 141 (COPD); and lung cancer. For COPD and lung cancer, in particular, there has been no discernible change in nonsmokers’ death rates. The relatively small changes—less than 15 percent up or down—are all Statistically insignificant. The absence of significant change in nonsmokers’ lung cancer rates confirms and extends the findings of Doll and Peto (1981) and Garfinkel (1981). For COPD, the table presents the first information on trends in nonsmokers’ death rates. It needs to be emphasized, however, that the Statistical test for a change in lung can- cer or COPD rates is of relatively low power. For COPD, there are sufficient data to have detected an increase of 53 percent or more in males and an increase of 42 percent or more in females at the 0.05 level of significance. For lung cancer, increases of more than 37 and 24 percent for males and females, respectively, were detectable as statisti- cally significant. In contrast to lung cancer and COPD, Table 3 shows a very marked decline in CHD death rates in nonsmokers. Over an approximate 20-year period, nonsmokers’ age- adjusted death rates dropped by 64 percent in men and 69 percent in women. The ob- served decline in nonsmokers’ CHD death rates is in keeping with the CHD decline in the general population. However, the magnitude of the decline is larger in the American Cancer Society subjects. Among U.S. white males, the age-adjusted death rate from CHD (standardized to the 1965 population distribution) declined by 41 percent during 1965-85. For U.S. white females, the decline was 40 percent (NCHS 1967 and unpublished; U.S. Bureau of the Census 1974, 1986). TABLE 3.—Age-adjusted annual death rates per 100,000 for CHD, COPD, and lung cancer among males and females, aged 35 years or more, who never smoked regularly, 6-year followup (1959-65) of CPS-I compared with 4-year followup (1982-86) of CPS-II Males Females Disease CPS-I cps-1? CPS-I CPS-IF > CHD 745 270 479 153 420°; 410-414° (726-775)4 (256-284) (467-491) (146-159) COPD 9.5 87 4.0 56 $00-502, 527.1°: (7.0-12.9) (6.5-11.7) (3.1-5.3) (4.5-7.0) 490-492, 496° Lung cancer 15.5 13.6 10.3 11.4 162-163"; 162° (12,5~19.3) (10.8-17.0) (8.9-11.9) (9.8-13.3) “For both CPS-] and CPS-II, age adjustment of rates was performed by direct standardization to the age distributions of U.S. resident white males and females, respectively, in 1965 (U.S. Bureau of the Census 1974). For CPS-II, death rates were corrected for delayed ascertainment of causes of death. Among 4,959 known deaths during 1982-86 in male nonsmokers. death certificates had not been received for 439 by June 1988. Among 10,161 known deaths in female nonsmokers, 1,411 had not been received. “CPS-I coding, International Classification of Diseases, Seventh Revision. Numbers in parentheses are 95-percent confidence intervals. “CPS-I] coding, International Classification of Diseases. Ninth Revision. SOURCE: Unpublished tabulations. American Cancer Society. 142 Current Cigarette Smokers’ Death Rates: Lung Cancer Figures 6 and 7, respectively, show changes in the age-specific lung cancer death rates of men and women who described themselves as regular cigarette smokers on the original questionnaire for each prospective study. The death rates, depicted in each figure on a logarithmic scale, apply to all such current smokers. No adjustment has been made for differences in the number of cigarettes smoked or duration of cigarette use. The age—incidence curves in both figures show a striking crossover effect. Among older male smokers, especially those aged 70 years or more, lung cancer death rates in CPS-II exceed those in CPS-I twofold to fourfold. By contrast, among younger male smokers, especially those less than 50 years old, CPS-II death rates are about 30 to 40 percent lower. The observed crossover phenomenon appears to be consistent with long- term changes in cigarette smoke exposure among successive cohorts. The increase in lung cancer among older male smokers reflects their increased frequency of cigarette use and increased cigarette smoking in early life. The decline in lung cancer among MALES 8 ~ 1000 f aa A a 2 i ao o— oh a Ww = 100+ a & wa = eo “ th L— vo a a g 10 za c { 1 i 1 4 Lk 1 1 L 35-30 40-44 46-40 50-64 50-69 60-64 66-60 70-74 75-70 80-84 AGE AT ENROLLMENT O oPs-| A CPS-ll FIGURE 6.—Age-specific death rates (log scale) for lung cancer, male current cigarette smokers aged 35-84 years; 6-year followup of CPS-I (1959- 65), compared with 4-year followup of CPS-II (1982-86) SOURCE: Unpublished tabulations, American Cancer Society. Estimates for CPS-I] are preliminary. 143 younger men may reflect their increased use of filter-tipped and low-tar cigarettes. Most currently smoking men aged 35 to 39 years in CPS-II, for example, were likely to have been lifelong filter-tipped cigarette smokers. An even more striking crossover is shown for female current cigarette smokers in Figure 7. In particular, the age of crossover comes somewhat earlier, Among women smokers aged 45 years or more, lung cancer death rates have increased fourfold to sevenfold. (There were no deaths and a small number of person-years of exposure at ages 75 or more in CPS-I.) By contrast, lung cancer death rates in the very youngest cohorts, aged 35 to 44 years, have declined by 35 to 55 percent. As in the case of men, the crossover appears to reflect differential trends in cigarette smoking amon g succes- sive cohorts of women. FEMALES 8 cy |}000 9 i a4 j ao ao yu a c 100 + A a = ao oa oo Oo Oy z 10 7 5 = = 1 i L 1 i J 1 i i 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 AGE AT ENROLLMENT QO CPS-1 4 CPS-Il FIGURE 7.—Age-specific death rates (log scale) for lung cancer, female current cigarette smokers aged 35-84 years; 6-year followup of CPS-I (1959- 65), compared with 4-year followup of CPS-II (1982-86) SOURCE: Unpublished tabulations, American Cancer Society. Estimates for CPS-II are preliminary. Current Cigarette Smokers’ Death Rates: Coronary Heart Disease Figure 8 shows the proportional decline from CPS-I to CPS-II in the age-adjusted CHD death rates of current smokers and nonsmokers. The relative declines are depicted 144 separately for men and women, and for persons younger than 65, and 65 and older. CHD death rates have declined in both cigarette smokers and nonsmokers. For the predominantly white, middle-class populations under study in CPS-I and CPS-II, the overall decline among smokers and nonsmokers was greater than observed for the U.S. white population. Still, the declines in CHD mortality rates among nonsmokers were notably greater than among current cigarette smokers. The disparity is seen at all ages, but appears somewhat greater among younger persons. In contrast to lung cancer (Figures 6 and 7), no crossover in age—incidence curves is observed. The increasing smoker—non- smoker disparity at younger ages argues against a significant salutary effect of lifelong filter-tipped cigarette use. The possibility that changes in other coronary risk factors among cigarette smokers may explain their reduced decline in CHD rates needs further investigation. 100 got MALES = FEMALES MALES FEMALES 80 70 80 50 40 30 20 10 PERCENT DECLINE IN CHO DEATH RATE 0 AGED 35-64 AGED 65+ m Nonsmokers i Smokers FIGURE 8.—Percentage decline in age-adjusted death rates for CHD; 6-year fol- lowup of CPS-I (1959-65), compared with 4-year followup of CPS- II (1982-86) SOURCE: Unpublished tabulations, American Cancer Society. Estimates for CPS-I] are preliminary. 145 1000 100 t—_—_b-9—o-— ANNUAL DEATH RATE PER 100,000 3 \\ 1 45-54 55-64 65-74 78-B4 © Females, CPS-I 4 Females, CPS-li © Males, CPS-II © Males, CPS-! FIGURE 9.—Age-specific death rates for COPD, male and female current cigarette smokers aged 45-84 years; 6-year followup of CPS-I (1959- 65), compared with 4-year followup of CPS-II (1982-86) SOURCE: Unpublished tabulations, American Cancer Society. Estimates for CPS-II are preliminary. Current Cigarette Smokers’ Death Rates: Chronic Obstructive Pulmonary Disease Figure 9 gives corresponding changes in age-specific death rates for COPD. In this figure, the ages are grouped into 10-year rather than 5-year age ranges as in Figures 6 and 7. For male smokers, there has been a reduction in COPD death rates for ages 45 to 74 years. For female smokers over 55 years old, there has been about a twofold to threefold increase in COPD rates. Estimated Relative Risks from CPS-I and CPS-II For men and women, respectively, Tables 4 and 5 depict estimated relative risks in the 6-year followup of CPS-I for all-cause mortality and for 14 specific causes of death (15 causes for women, including cervical cancer). For men in Table 4, the estimated 146 relative risks for current and former cigarette smokers are given separately. For women in Table 5, the numbers of deaths and person-years of exposure among former smokers were too small to give reliable death rates for many causes. Accordingly, in conformity with earlier reports of CPS-I mortality, the death rates for current smokers are compared with those of women with any history of regular cigarette use, past or present. For both men and women, the estimates in Tables 4 and 5 are in accord with earlier reports on CPS-I mortality (Garfinkel 1980b; Hammond 1964a,b, 1966, 1972; Ham- mond and Garfinkel 1969; Hammond and Seidman 1980). Among men, former smokers have lower mortality ratios. In both sexes, relative risks for CHD are higher at younger ages. Both sexes, but to a greater extent, men, show elevated risks of other cardiovascular diseases including stroke, hypertensive heart disease, and aortic aneurysm. In both sexes, smokers’ death rates are higher for bronchitis and emphysema and for seven cancers including lung cancer. The relative risk of Jung cancer among current smokers in CPS-I is about 11.3 for men and 2.7 for women. The results for CPS-II, given in Tables 6 and 7, show substantial changes in the mor- tality risk of cigarette smoking over two decades. The all-cause relative risk for men has increased from 1.8 in CPS-I to 2.3 in CPS-II. For women, it has risen from 1.2 to 1.9. These increases in overall mortality are not an artifact of the method of age adjust- ment, because CPS-II contained proportionately fewer person-years of exposure at the youngest ages than CPS-I. As reflected in Table 6 and Table 7, the relative risks for CHD death have increased for both men and women. The relative risks for men, in particular, are consistent with those reported from recent case-control studies (Kaufman et al. 1983, Rosenberg et al. 1985) and from the followup of the Multiple Risk Factor Intervention Trial (MRFIT) cohort, as described in Chapter 2. The markedly elevated relative risks for younger women in Table 7 are consistent with those reported in a recent case-control study (Slone et al. 1978) and in a prospective study of 120,000 female nurses (Willett et al. 1987). Such consistencies across epidemiologic studies—especially cohort and case— control studies reported during the 1980s—argue against any appreciable bias in the 4- year preliminary results of CPS-II given in Tables 6 and 7. Tables 6 and 7 show consistently increased relative risks for cerebrovascular lesions among both men and women, particularly in the younger age groups. Among women under 65 years old, the estimated relative risk of death from stroke is 4.8, with a 95- percent confidence range of 3.5 to 6.5. The observed increases in risk for current smokers are reduced in former smokers. The finding of an elevated risk of cerebrovascular disease among cigarette smokers is not new. Elevated death rates from stroke were reported in CPS-I (Hammond 1966; Hammond and Garfinkel 1969) and are reproduced in Tables 4 and 5. The 1983 Sur- geon General’s Report noted the association between stroke and cigarette use, no data on the effect of smoking cessation were available (US DHHS 1983). A recent prospec- tive study of 8,000 men of Japanese origin (Abbott et al. 1986) showed an elevated risk of thromboembolic and hemorrhagic strokes among cigarette smokers. While there was no clear trend of increasing risk with higher daily smoking rates, subjects who quit smoking had reduced risks compared with continuing smokers. Inthe prospective study of 120,000 female nurses, Colditz et al. (1988) found a dose-response relationship be- 147 TABLE 4.—Estimated relative risks for current and former smokers of cigarettes, males aged 35 years or more, 6-year (1959-65) followup of American Cancer Society 25-State study (CPS-I) Underlying cause Current. Former, of deat smokers* smokers* All causes 1.80 b 1.38 b (1.75-1.85) (1.33—1.42) CHD, age 235 (420)° 1.83 1.42 (1.76-1.91) (1.34~-1.49) CHD, age 35-644 (420) 2.25 1.56 (2.13~2.39) (1.45-1.68) CHD, age 265 (420) 1.39 1.27 (1.30-1.48) (1.17-1.37) Hypertensive Heart Disease (440-443) 1,63 1.19 (1.36-1.96) (0.94-1.51) Cerebrovascular Lesions, age 235 (330-334) 1.37 0.96 (1,25-1.49) (0.85-1.08) Cerebrovascular Lesions, age 35-64 (330-334) 1.79 1.02 (1.55-2.08) (0.83-1.25) Cerebrovascular Lesions, age 265 (330-334) 1.15 0.93 (1.02-1.30) (0.80-1.08) Aortic Aneurysm. Non-Syphilitic (451) 4.11 2.40 (3.13-5.40) (1.73-3.34) Ulcer, Duodenal. Gastric, and Jejunal (540-542) 3.06 1.49 - (2.24-4.18) (0.98-2.27) Influenza and Pneumonia (480-481, 490-493) 1.82 1.62 (1.45-2.27) (1.24-2.12) Bronchitis and Emphysema (500-502, 527.1) 8.81 10.20 (6.40-12.13) (7.34-14.17) . Cancer, Lip. Oral Cavity. and Pharynx (140-148) 6.33 2.73 (3.60-11.13) (1.36-5.49) Cancer, Esophagus (150) 3.62. 1.28 (2.02-6.48) (0.53-3.08) Cancer, Pancreas (157) 2.34 1.30 (1.81-3.02) (0.92-1.84) Cancer, Larynx (161) 10.00 8.60 (3.51-28.51) (2,87-25.74) Cancer, Lung (162-163) 11.35 4.96 (9.10-14.15) (3.866. 38) Cancer, Kidney (180) 1.84 1.79 (1.23-2.76) (1.11-2.87) Cancer, Bladder, Other Urinary Organs (181) 2.90 1.75 : (2.01-4.18) (1.07-2.87) NOTE: Based upon 1.692.652 man-years of exposure among male subjects who never smoked regularly, or who smoked only cigarettes, present or past. Relative risks, estimated with respect to men who never smoked regularly, have been directly standardized to the age distribution of all man-years of exposure. “Refers to cigarette smoking status at enrollment (October 1959-March 1960). Numbers in parentheses are 95-percent confidence intervals, computed on the assumption that the logarithm of telative risk was normally distributed. ~ “All disease codes refer to International Classification of Diseases, Seventh Revision. When an age range is given, it refers to the age at enrollment in 1959, SOURCE: Unpublished tabulations, American Cancer Society. 148 TABLE 5.—Estimated relative risks for current cigarette smokers and for all subjects with a history of regular cigarette smoking, females aged 35 years or more, 6-year (1959-65) followup of American Cancer Society 25-State study (CPS-D) Underlying cause Current Current and former of death smokers" smokers All causes 1.23 b 1,24 b (1.18-1.28) (1.20-1.28) CHD, age 235 (420) 1.40 1.38 (1.29-1.51) (1.29-1.74) CHD, age 35-644 (420) 1.8] 1.74 (1.67-1.97) (1.61-1.89) CHD, age 265 (420) 1.24 1.25 (1.11-1.39) (1.14-1.37) Hypertensive Heart Disease (440-443) 1.31 1.27 (1.04—-1.66) (1.04-1.55) Cerebrovascular Lesions, age 235 (330-334) 1.19 1.26 (1.06-1.35) (1.13-1.80) Cerebrovascular Lesions, age 35-64 (330-334) 1.92 1.80 (1.69-2.18) (1.59-2.03) Cerebrovascular Lesions, age 265 (330-334) 0.97 1.09 (0.81-1.16) (0.95—1.26) Aortic Aneurysm, Non-Syphilitic (451) 4.64 3.67 (3.00-7.20) (2.46-5.48) Ulcer, Duodenal, Gastric, and Jejunal (540-542) 1.37 1.52 (0.81~-2.31) (0.96-2.41) Influenza and Pneumonia (480-481, 490-493) 0.91 0.96 . (0.59-1.41) (0.69-1.33) Bronchitis and Emphysema (500-502, 527.1) $.89 5.85 (3.97-8.76) (4.02-8.53) Cancer, Lip, Oral Cavity, and Pharynx (140-148) 1.96 1.89 (1.14-3.39) (1.16-3.08) Cancer, Esophagus (150) 1.94 2.15 (1.02-3.69) (1.09-4.23) Cancer, Pancreas (157) 1.39 1,38 (1.04-1.86) (1.07-1.78) Cancer, Larynx (161) 3.81 3.10 (0.78-18.52) (0.65-14.99) Cancer, Lung (162-163) 2.69 2.59 (2.14-3.37) (2.04—-3.30) Cancer, Cervix Uteri (171) 1.10 1.32 (0.83-1.47) (1.02-1.71) Cancer, Kidney (180) 1.43 1.47 (0.89-2.31) (0.97~2.23) Cancer, Bladder, Other Urinary Organs (181) 2.87 2.31 (1.74-4.74) (1.45~3.67) NOTE: Based upon 3,325,989 woman-years of exposure among subjects who never smoked regularly, or who smoked only cigarettes, present or past. Relative risks, estimated with respect to women who never smoked regularly, have been directly standardized to the age distribution of all woman-years of exposure. Refers to cigarette smoking status at enrollment (October 1959-March 1960). Numbers in parentheses are 95-percent confidence intervals, computed on the assumption that the Jogarithm of relative risk was normally distributed. All disease codes refer to Internationa! Classification of Diseases, Seventh Revision. ‘When an age range is given, it refers to the age at enrollment in 1959. SOURCE: Unpublished tabulations, American Cancer Society. 149 TABLE 6.—Estimated relative risks for current and former smokers of cigarettes , males aged 35 years or more, 4-year (1982-86) followup of American Cancer Society 50-State study (CPS-II) Underlying cause Current Former of death smokers" smokers” All causes 2.34 b 1.58 b (2.26-2.43) (1.53-1.64) CHD, age >35 (410-414)° 1.94 1.41 (1.80—2.08) (1.33-—1.50) CHD, age 35-647 (410-414) 2.81 L.75 (2.49-3.18) (1.55-1.99) CHD, age 265 (410-414) 1.62 1.29 (1.48-1.77) (1.20+-1.38) Other Heart Disease* (390-398, 401-405, 1.85 1.32 415-417, 420-429) (1.63-2.10) (1.18-1.48) Cerebrovascular Lesions, age >35 (430-438) 2.24 1.29 (1.88-2.67) (1.10-1.51) Cerebrovascular Lesions, age 35-64 (430-438) 3.67 1.38 (2.51-5.36) (0,.91-2.07) Cerebrovascular Lesions, age >65 (430-438) 1.94 1.27 (1.58-2.38) (1.07-1.50) Other Circulatory Disease’ (440-448) 4.06 2.33 (3.08-5.35) (1.81-3.01) COPD (490-492,496) 9.65 8.75 (7.00-13.30) (6.48-1 1.80) Other Respiratory Disease®(010-012, 1.99 1.56 480-489,493) (1.52-2.61) (1.25-1.95) Cancer, Lip, Oral Cavity, Pharynx (140-149) 27.48 8.80 (9.96-75.83) (3.15-24.59) Cancer, Esophagus (150) 7.60 5.83 (3.81-15.17) (3.02-11.25) Cancer, Pancreas (157) 2.14 1.12 (1.62-2.82) (0.86-1.45) Cancer, Larynx (161) 10.48 5.24 (3.61-30.43) (1.83-14.99) Cancer, Lung (162) 22.36 9.36 (17.77-28.13) (7.43-11.77) Cancer, Kidney (189) 2.95 1,95 (1.92-4.54) (1.31-2.90) Cancer, Bladder, Other Urinary Organs (188) 2.86 1.90 (1.85-4.44) (1.28-2.82) NOTE: Preliminary estimates, based upon 1,491,791 man-years of exposure among male subjects who never smoked tegularly, or who smoked only cigarettes, present or past. Relative risks, estimated with respect to men who never smoked regularly, have been directly standardized to the age distribution of all man-years of exposure. “Refers to cigarette smoking status at enrollment (September 1982). Numbers in parentheses are 95-percent confidence intervals, computed on the assumption that the logarithm of relative risk was normally distributed. “All disease codes refer to International Classification of Diseases, Ninth Revision. When an age range is given, it refers to the age at enrollment in 1982. “Includes Hypertensive Heart Disease (401-404). ‘Includes Aortic Aneurysm, Non-Syphilitic, and Genera! Arteriosclerosis (440-44 1). ®Inctudes Influenza and Pneumonia (480-487). SOURCE: Unpublished tabulations, American Cancer Society. 150 TABLE 7.—Estimated relative risks for current and former cigarette smokers, females aged 35 years or more, 4-year (1982-86) followup of American Cancer Society 50-State study (CPS-II) Underlying cause Current Former of death smokers" smokers" All causes 1.90 b 1,32 b (1.82-1.98) (1.27-1.37) CHD, age 235 (410-414)° 1.78 1,31 (1.62-1.97) (1.19-1.44) CHD, age 35-649 (410-414) 3.00 1.43 (2.50-3.59) (1.15-1.77) CHD, age 265 (410-414) 1.60 1.29 (1.42-1.80) (1.16-1.43) Other Heart Disease* (390-398, 1.69 1.16 401-405, 415-417, 420-429) (1.44-1.99) (1.00-1.34) Cerebrosvascular Lesions, age 235 1.84 1.06 (430-438) (1.56-2.16) (0.88-1.27) Cerebrovascular Lesions, age 35-64 4.80 1.41 (430-438) (3.52-6.54) (0.94—2.13) Cerebrovascular Lesions, age 265 1.47 1.01 (430-438) (1.19-1.81) (0.83-1.24) Other Circulatory Disease’ (440-448) 3.00 1,34 (2.20-4.08) (0.95-1.90) COPD (490-492,496) 10.47 7.04 (7.78-14.09) (5.33-9.30) Other Respiratory Disease® 2.18 1.38 (010-012,480-489 493) (1.60-2.97) (1.04-1.84) Cancer, Lip, Oral Cavity, Pharynx 5.59 2.88 (140-149) (3.15~9.91) (1.57-5.26) Cancer, Esophagus (150) 10.25 3.16 (4.94-21.27) (1.45-6.85) Cancer, Pancreas (157) 2.33 1.78 (1.77-3.08) (1.37-2.30) Cancer, Larynx (161) 17.78 11.88 (3.45-91.74) (2.46-57.34) Cancer, Lung (162) 11,94 4.69 (9.99-14.26) (3.86-5.70) Cancer, Cervix Uteri (180) 2.14 1.94 (1.06-4.30) (0.97-3.87) Cancer, Kidney (189) 1.41 1.16 (0.86—2.30) (0.72-1.87) Cancer, Bladder, Other Urinary Organs (188) 2.58 1,85 (1.31-5.08) (1.00-3.42) NOTE: Preliminary estimates, based upon 2,418,909 woman-years of exposure among female subjects who never smoked regularly, or who smoked only cigarettes, present or past. Relative risks, estimated with respect to women who never smoked regularly, have been directly standardized to the age distribution of all woman-years of exposure. sRefers to cigarette smoking status at enrollment (September 1982). ‘Numbers in parentheses are 95-percent confidence intervals, computed on the assumption that the logarithm of relative risk was normally distributed. All disease codes refer to International Classification of Diseases, Ninth Revision. When an age range is given, it refers to the age at enrollment in 1982. includes Hypertensive Heart Disease (401-404). Includes Aortic Aneurysm, Non-Syphilitic, and General Arteriosclerosis (440-441). "Includes Influenza and Pneumonia (480-487). SOURCE: Unpublished tabulations, American Cancer Society. 151 tween Cigarette use and risk of stroke. They also noted a slight increase in risk among former cigarette smokers, especially for the first 2 years after cessation. The prelimi- nary results from CPS-II, reported in Tables 6 and 7, further support a causal role for cigarette smoking in stroke. The preliminary results of CPS-II also show significantly higher relative risks for cancers of the lip, oral cavity and pharynx, esophagus, and lung, as compared with CPS- I. The computed relative risk for lung cancer death has increased to 22 in men and 12 in women. While the relative risks for COPD death have not changed significantly among men, there is a trend toward increasing risk among women. The available data from CPS-II do not permit identification of specific mortality risks for hypertensive heart disease, aortic aneurysm, and influenza and pneumonia, as in CPS-I. However, among broader categories of cardiovascular and nonneoplastic respiratory disease, in- creased risks are likewise found in CPS-II. Endocrine and Sex-Related Cancers in Women A protective effect of smoking on cancer of the endometrium has been suggested in a recent case-control study (Lesko et al. 1985). For CPS-I, the relative risk for cancers of the uterine corpus (ICD-7 Codes 172-174) among current smokers was 0.94 (95-per- cent confidence interval, 0.57 to 1.53). Preliminary results for CPS-II suggest a reduced relative risk for endometrial cancer (ICD-9 Code 182). Recent data on a possible protective effect of smoking for breast cancer have been contradictory (See Chapter 2; Rosenberg et al. 1984). For CPS-I, the relative risk for breast cancer (ICD-7 Code 170) among current smokers was 0.88 (95-percent con- fidence interval, 0.77 to 1.01), while the relative risk among former smokers was 1.20 (95-percent confidence interval, 1.15 to 1.35). Preliminary data from CPS-II have likewise been contradictory. An increased risk of cervical cancer among cigarette smokers has been reported in case-control studies (LaVecchia et al. 1986; Nischan, Ebeling, Schindler 1988). For CPS-I, the relative risk for cervical cancer (ICD-7 Code 171) was 1.10 (95-percent con- fidence interval, 0.83 to 1.47). Data from CPS-II show a twofold increase in cervical cancer mortality among current smokers (relative risk 2.14, 95-percent confidence in- terval 1.06 to 4.30). Summary The relative risks for current smokers for selected comparable disease categories causally related to smoking in CPS-I and CPS-II are summarized and listed side by side in Table 8. These comparisons show substantial increases in the risk of death due to smoking for most of the disease categories listed between the years 1959 and 1965 and 1982 and 1986. Statistically significant increases in relative risks occurred in those dis- ease categories for which 95-percent confidence limits around the estimated relative risks do not overlap between CPS-I and CPS-II. Compared with men during this period, women experienced greater increases in the relative risks of cerebrovascular lesions (ages 35 to 64 years), COPD, laryngeal cancer, and lung cancer. 152 TABLE 8.—Summary of estimated relative risks for current cigarette smokers, major disease categories causally related to cigarettes, males and females aged 35 years and older, CPS-I (1959-65) and CPS-II (1982-86) Underlying cause : Males Females of death” CPS-I CPS-II CPS-I CPS-II CHD, age 235 1.83 1.94 1.40 1.78° CHD, age 35-64 2.25 2.81° 1.81 3.00° Cerebrovascular Lesions, 1.37 2.24° 1.19 1.84° age 235 Cerebrovascular Lesions, 1.79 - 3.67° 1.92 430° age 35-64 COPD 8.81 9.65 5.89 10.47 Cancer, Lip, Oral Cavity, 6.33 27.48 1.96 5.59 and Pharynx Cancer, Esophagus 3.62 7.60 1.94 10.25° Cancer, Pancreas 2.34 2.14 , 1.39 2.33 Cancer, Larynx 10.00 _ 10.48 3.81 17.78 Cancer, Lung 11.35 22.36 2.69 11.94? "See Tables 4-7 for International Classification of Disease codes. *95-percent confidence intervals do not overlap between CPS-I and CPS-IL SOURCE: Tables 4-7. Smoking-Attributable Mortality in the United States, 1965 and 1985 Table 9 reports the attributable risks a from cigarette smoking during the year 1965. Ten causes of death are considered: CHD, COPD, cerebrovascular disease, and can- cers of seven sites. The computations are based upon the age-adjusted relative risks reported in CPS-I and the prevalence rates reported in the 1965 NHIS. For men, the age-adjusted relative risks among present and past cigarette smokers with a history of pipe or cigar use were slightly lower than those for present and past smokers of ciga- rettes exclusively. While the latter are reported for comparison in Table 4, the former were used in the attributable risk computations. In 1965, as shown in Figure 2, about two-thirds of men with a history of regular cigarette smoking were also exposed to pipe or cigar smoke. (As noted in Note b of Table 10 below, the use of relative risks derived from the death rates of men who smoked cigarettes exclusively resulted in about a 5- percent increase in attributable deaths for 1965.) For women, the computation of at- tributable risks in 1965 did not distinguish between current and former smokers. 153 TABLE 9.—Estimated attributable risks for 10 selected causes of death from cigarette smoking, males and females, United States, 1965 Males" b Cause of death (Se) ar CHD, age 35-64 42 26 (40-45)° (23-30) CHD, age 265 ll 3.3 (9-14) (2.1-5.1) COPD 84 67 (79-88) (57-76) Cancer of lip, oral cavity, and pharynx 74 27 (59-85) (12-51) Cancer of larynx 84 47 (61-94) (8-90) Cancer of esophagus 57 14 (36-76) (6-29) Cancer of lung 86 40 (82-88) (31-50) Cancer of pancreas 41 14 (30-53) (6-30) Cancer of bladder 53 36 (39-66) (20-56) Cancer of kidney 36 17 (19-56) (5-42) Cerebrovascular disease, age 35-64 28 28 (21-36) (22-33) Cerebrovascular disease, age 265 2.0 1.3 (0.6-6.6) (0.2-6.5) “For males, computations based on prevalence rates in Table 2 and relative risks for male current and former cigarette smokers, with or without a history of pipe and cigar smoking, derived from CPS-1. "For females, attributable risks computed from prevalence rates in Table 2 and relative risks for all female smokers, past and present, in Table 5, “Numbers in parentheses are 95-percent confidence intervals. In 1965, as Table 9 reveals, cigarette smoking was responsible for 42 percent of CHD deaths among younger men and 26 percent of deaths among younger women. For COPD deaths at all ages, the smoking-attributable risks were 84 percent for men and 67 percent for women. For lung cancer, the respective attributable risks were 86 per- cent and 40 percent for men and women. With the exception of deaths from stroke among younger persons, attributable risks were markedly higher for men. Table 10 reports the corresponding smoking-attributable deaths, A, during the year 1965. Attributable deaths were computed by multiplying the attributable risk percent- ages in Table 9 by the corresponding cause-specific death rates among persons aged 20 154 TABLE 10.—Estimated deaths (in thousands) attributable to cigarette smoking, 10 selected causes, males and females, United States, 1965 Cause of death Males Females CHD, age <65 51 9.5 (48-54)? (8.2-10.8) CHD, age 265 25 6.0 (20-30) (3.9-9.4) COPD 16 2.3 (15-17) (2.0-2.7) Cancer of lip, oral cavity, and pharynx 3.6 0.4 (2.9-4.2) (0.2-0.8) Cancer of larynx 1.9 O14 (1.42.2) (0.02-0.3) Cancer of esophagus 2.4 0.1 (1.5-3.2) (0.2-0.8) Cancer of lung 35 3.1 (34-36) (2.4-3.8) Cancer of pancreas 3.8 0.9 (2.8-4.9) (0.4—2.0) Cancer of bladder 3.0 1.0 (2.2-3.7) (0.5-1.5) Cancer of kidney 1.2 0.3 (0.7-1.9) (0.1-1.8) Cerebrovascular disease, age <65 5.5 AT (4.2-7.2) (3.8-5.6) Cerebrovascular disease, age 265 1.5 1.0 (0.4-4.8) (0.2-5.9) Ten causes 150° 30 (143-157) (26-34) NOTE: Computed from Table 9 and tabulations of deaths at ages 20 years or more by cause for 1965 (NCHS 1967). Sums may not equal totals because of rounding. *Numbers in parentheses are 95-percent confidence intervals. >When the attributable risk estimates given in Note a of Table 9 were used, the total attributable deaths for males were 158,000 (95-percent confidence interval, 151,000 to 166,000). Approximately two-thirds of the 8,000 additional deaths were from CHD. years or more. For the 10 causes combined, cigarette smoking was responsible for 150,000 deaths among men and 30,000 deaths among women in 1965. Among men, CHD deaths made up 51 percent of smoking-attributable mortality for the 10 causes combined. This proportion is consistent with the estimate of 45 percent reported by the 1964 Advisory Committee to the Surgeon General for excess mortality from all causes (US PHS 1964). Similarly, lung cancer accounted for 23 percent of the smoking-attributable mortality for the 10 causes combined—again consistent with the 155 1964 Report’s estimate of 16 percent of deaths from all causes. Among women, CHD deaths made up 52 percent and lung cancer 10 percent of the smoking-attributable mor- tality from the 10 causes combined. Table 11 shows the estimated attributable risks a from cigarette smoking for the year 1985. For comparability with the 1965 calculations, the same 10 causes of death are considered. The computations are based upon the relative risks reported in CPS-II and the prevalence rates reported in the 1985 NHIS. For men, the computations employed the relative risks for past and present smokers of cigarettes exclusively, as shown in Table 6. As Figure 2 indicates, the proportion of male smokers who used other forms TABLE 11.—Estimated attributable risks for 10 selected causes of death from cigarette smoking, males and females, United States, 1985 Males Females Cause of death (%) (%) CHD, age <65 45 ; 4) (40-50) (34-48) CHD, age 265 21 12 (17-26) (9-15) COPD 84 79 (78-88) © (73-83) Cancer of lip, oral cavity, and pharynx 92 61 (79-97) (45-76) Cancer of larynx 81 87 (57-93) (56-97) Cancer of esophagus 78 75 (62-89) (57-87) Cancer of lung 90 79 (88-92) (75-82) Cancer of pancreas 29 34 (18-43) (25-44) Cancer of bladder 47 37 (31-63) (18-61) Cancer of kidney 48 12 (32-64) (3-43) Cerebrovascular disease, age <65 51 Rp) (36-65) (45-65) Cerebrovascular disease, age 265 24 6 (16-35) (2-14) NOTE: Computed from Tables 2, 6, and 7. For adult men under 65, the proportions of current and former cigarette smokers in 1985 were, respectively, 34.7 and 25.8 percent. For men 65 or older, the prevalences of current and former cigarette smoking were, respectively, 19.4 and 51.1 percent. For adult women under 65, the corresponding proportions were 30.1 and 16.5 percent; for adult women 65 or older, 12.6 and 19.6 percent. “Numbers in parentheses are 95-percent confidence intervals. 156 of tobacco was too small to affect significantly the results for 1985. For women, rela- tive risks for current and former cigarette smokers were employed (Table 7). Comparison of Tables 9 and 11 reveals significant increases in attributable risk from 1965-85. In 1985, smoking accounted for 21 percent of CHD deaths in older men, compared with 11 percent in 1965. The attributable risks for cancers of the lip, oral cavity and pharynx, esophagus, and lung increased significantly. Changes in the attributable risk estimates for women are even more striking. Among younger women, smoking now accounts for an estimated 41 percent of CHD deaths and an estimated 55 percent of lethal strokes, compared with 26 and 28 percent, respec- tively, in 1965. Among women of all ages, 79 percent of lung cancers are attributable to cigarette use (see Table 11). Overall, smoking accounted for 86.7 percent of all lung cancer deaths (95-percent confidence interval 84.9 to 88.4), 81.8 percent of all COPD deaths (95-percent con- fidence interval 78.3 to 85.3), and 21.5 percent of all CHD deaths (95-percent con- fidence interval 19.4 to 23.4). In addition, smoking accounted for 18.0 percent of all stroke deaths (95-percent confidence interval 14.2 to 22.9). Table 12 reports estimated smoking-attributable deaths for the 10 causes during 1985. Total deaths have increased to 231,000 for men and 106,000 for women. As op- posed to 1965, CHD in men now accounts for only one-third of the smoking-attributable mortality from the 10 causes combined. The proportion of these attributable deaths due to lung cancer has increased to one-third. Likewise, among women, smoking-at- tributable CHD fatalities now account for one-third of the 10-cause total; the relative importance of smoking-induced cancer fatalities has also increased. The total 10-cause smoking-attributable mortality for 1985 was 337,000 deaths, com- pared with 183,000 in 1965. A portion of the observed 1965-85 increase, however, was the result of population growth. In addition, there were increases in the proportion of elderly persons who would be more at risk for smoking-induced death. For men and women, respectively, Figures 10 and 11 show the results of a correction for population increase and population aging. In each figure, three quantities are shown for each of four categories of smoking-attributable mortality: CHD deaths under age 65; CHD deaths age 65 years or more: COPD deaths; and lung cancer deaths. The first quan- lity is the estimated smoking-attributable deaths for 1965. The second bar shows smok- ing-attributable deaths for 1985. The third bar shows the estimated 1985 smoking-at- tributable deaths if the U.S. populations at each age had remained at 1965 levels. The latter quantities were computed as aD, where a is the attributable risk given in Table li and D’ isa population-corrected estimate of 1985 U.S. deaths. The latter quantity was computed by multiplying 1985 age-specific death rates by the populations at risk in 1965. Figures 10 and 11 show that population growth and aging cannot explain the chan- ges in smoking-attributable mortality between 1965 and 1985. In particular, the marked increases in smoking-attributable deaths from lung cancer and COPD in women are systematic consequences of the American woman's adoption of lifelong cigarette smoking, from teenage years onward. For men, population-corrected deaths due to smoking in 1985 were 165,000, com- pared with 150,000 in 1965. For women, population-corrected deaths due to smoking 157 TABLE 12.—Estimated deaths (in thousands) attributable to cigarette smoking, 10 selected causes, males and females, United States, 1985 Cause of death Males Females CHD, age <65 34 11 (30-38)" (9-12) CHD, age 265 44 26 (36-54) (20-34) COPD , 37 20 (35-39) (18-21) Cancer of lip, oral cavity, and pharynx S.1 1.6 (4.4.5.4) (1.2-2.0) Cancer of larynx 2.3 0.6 (1.6-2.7) (0.4-0.7) Cancer of esophagus 5.0 1.6 (4.0-5.7) (1.3-1.9) Cancer of lung 76 30 (74-77) (29-32) Cancer of pancreas 3.3 3.4 (2.1-5.0) (2.8-5.1) Cancer of bladder : 3410 Ld (2.1-4.2) (0.6-1.9) Cancer of kidney 2.6 0.4 (1.8-3.5) (0.1-1.5) Cerebrovascular disease, age <65 5.5 5.2 (3.9-7.0) (4.3-6.2) Cerebrovascular disease, age 265 12 48 . (8-17) (1.9-11.4) Ten causes 231 106 (220-242) (98-115) NOTE: Computed from Table 11 and unpublished tabulations of deaths at ages 20 years or more by cause from NCHS, 1985. Sum of individual causes may not equal totals because of rounding. “Numbers in parentheses are 95-percent confidence intervals. in 1985 were 67,000, compared with 30,000 in 1965. Even if the population had remained entirely stable during 1965 through 1985, the lethality of cigarette use in American women would have doubled. Among men, the total of 231,000 smoking-induced deaths in 1985 represented 41 percent of total deaths from the 10 causes combined and 22 percent of all deaths among persons aged 20 years or more. Among women, the total of 106,000 smoking-induced deaths represented 25 percent of deaths from the 10 causes combined and 11 percent of deaths from all deaths among persons aged 20 years or more. The computations in Tables 10 and 12 have omitted other causes of death that are likely to be attributable to cigarette use. If the relative risks given in Tables 6 and 7 for 158 8s 8 6 8 8 38 8 SMOKING ATTRIBUTABLE DEATHS (1000s) 0 CHO 85+ COLD Ca Lung FIGURE 10.—Estimated cigarette-smoking-attributable deaths from CHD, COPD, and lung cancer, males aged 20 years or more, United States, 1965 and 1985 NOTE: For the bars marked 1985", the estimated smoking-attributable deaths in 1985 have been corrected for population increases during 1965-85. FEMALES SRRBBSRE 4 T3 SMOKING ATTRIBUTABLE DEATHS ¢ 1000s) @ CHO <85 CHD 65+ COLD Ca Lung FIGURE 11.—Estimated cigarette-smoking-attributable deaths from CHD, COPD, and lung cancer, females aged 20 years or more, United States, 1965 and 1985 NOTE: For the bars marked 1985”, the estimated smoking-attributable deaths in 1985 have been corrected for population increases during 1965-85. 159 the broader categories of cardiovascular and nonneoplastic respiratory disease are ap- plied to deaths from hypertensive heart disease, arteriosclerosis, aortic aneurysm, and influenza and pneumonia, then smoking-attributable deaths would increase to 256,000 among men and 126,000 among women. Inclusion of deaths among newborns and in- fants due to smoking during pregnancy would add an additional 2,500 to the total (CDC 1987b; McIntosh 1984; Kleinman et al. 1988); this does not include fetal loss due to smoking (Stein et al. 1981). Inclusion of lung cancer deaths among nonsmokers due to environmental tobacco smoke (NRC 1986) would add 3,800 and inclusion of deaths from cigarette-caused fires (Hall 1987) would add 1,700 to total attributable deaths. In- clusion of deaths due to cervical cancer caused by smoking would add 1,500. Includ- ing these additional causes of death, the smoking-attributable mortality in 1985 is then estimated to be approximately 390,000. Recent studies have also noted increased risks among smokers for hepatic cancer (Trichopoulos et al. 1987), penile cancer (Hellberg et al. 1987), leukemia (Kinlen and Rogot 1988), and anal cancer (Daling et al. 1987), Among all persons at risk during 1985, an estimated 52 million were also cigarette smokers in 1965. The remaining 42 million were new cigarette smokers. In 1985, only about 4,400 deaths occurred among the latter group, which consists of persons in their teens, twenties, and thirties. Thus, 99 percent of deaths attributable to cigarette use in 1985 occurred among people who started smoking in 1965 or earlier. The vast majority of these people started smoking before the release of the 1964 Surgeon General’s Report TABLE 13.—Estimated risks of various activities Annual fatalities per | million Activity or cause exposed persons Active smoking 7,000" Alcohol 541 Accident 275 Disease 266 Motor vehicles 187 Alcohol-involved 95 Non-alcohol-involved 92 Work 113 Swimming 22 Passive smoking? 19 All other air pollutants? 6 Football 6 Electrocution 2 Lightning 0.5 DES in cattlefeed 0.3 Bee sting 0:2 Basketball 0.02 NOTE: Activities are not mutually exclusive: there are overlaps between categories. Differences in fatalities do not imply proportionate differences in years of life lost. “Number of deaths per million smokers who began smoking before 1965. °Cancer deaths only. SOURCE: Active smoking, CPS-II; NHISs 1965, 1985: U.S. Bureau of the Census (1974, 1986). Other activities or causes, U.S. President (1987). 160 and before the 1965 Federal Cigarette Labeling and Advertising Act. For this group, the annual smoking-attributable fatality rate is about 7 deaths per 1,000 at risk, or about 7,000 deaths per 1 million persons. As shown in the Economic Report of the President (U.S. President 1987), this rate far exceeds the rates for other risks of death (Table 13). 10. Conclusions Lung cancer death rates increased two- to fourfold among older male smokers over the two decades between the American Cancer Society’s two Cancer Preven- tion Studies (CPS-I, 1959-65, and CPS-II, 1982-86). Lung cancer death rates for younger male smokers fell about 30 to 40 percent during this period. Lung cancer death rates increased four- to sevenfold among female smokers aged 45 years or older in CPS-II compared with CPS-I, while lung cancer death rates among younger women declined 35 to 55 percent. The two-decade interval witnessed a two- to threefold increase in death rates from chronic obstructive pulmonary disease (COPD) in female smokers aged 55 years or older. There was no change in the age-adjusted death rates for lung cancer and COPD between CPS-I and CPS-II among men and women who never smoked regularly. Overall death rates from coronary heart disease (CHD) declined substantially be- tween CPS-I and CPS-II. The decline in CHD mortality among nonsmokers, however, was notably greater than among current cigarette smokers. In CPS-II, the relative risks of death from cerebrovascular lesions were 3.7 and 4.8 for men and women smokers under age 65. Increased risks of stroke were also observed among older smokers and former smokers. Along with the recently reported results of other studies, these findings strongly support a causal role for cigarette smoking in thromboembolic and hemorrhagic stroke. In 1985, smoking accounted for 87 percent of lung cancer deaths, 82 percent of COPD deaths, 21 percent of CHD deaths, and 18 percent of stroke deaths. Among men and women less than 65 years of age, smoking accounted for more than 40 percent of CHD deaths. The large increase in smoking-attributable mortality among American women be- tween 1965 and 1985 was a direct consequence of their adoption of lifelong cigarette smoking, especially from their teenage years onward. In 1985, 99 percent of smoking-attributable deaths occurred among people who started smoking before the 1964 Surgeon General’s Report. For this group, the annual smoking-attributable fatality rate is about 7,000 deaths per | million per- sons at risk. For 10 causes of death, a total of 337,000 deaths were attributable to smoking in 1985. These represented 22 percent of al] deaths among men and 11 percent among women. 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Journal of the National Cancer Institute 62(3):471- 477, March 1979. 169 CHAPTER 4 TRENDS IN PUBLIC BELIEFS, ATTITUDES, AND OPINIONS ABOUT SMOKING 171 CONTENTS Introduction .. 0... cece ee teen eee beet enna een nes 175 Data SOUrceS 0... 0 cece ee eee teen eee entrees 175 Issues in Comparing Surveys... 6.0.62 cece eee teen eens 177 Trends in Public Beliefs About the Health Effects of Smoking ..........----- 179 OVErVIEW 2. cece ee eee teen ence teense nent etn 179 Is Cigarette Smoking Harmful to Smokers in General? ............ ae 179 Heavy Versus Light Smoking .......:-..++-- ene ene e eens 181 Tar Yield 0.0.20... cee cece cece eee err rere Le. 183 Duration of Smoking ......... 0. 0c eee c ee teeters 185 Does Cigarette Smoking Cause: .... 0.0... 000s eee eee Deke eee 185 Lung Cancer? 6.6... cee cece eet nen enn ns 185 Heart Disease? ....... 0.0 cece eee ee eee eens 188 Chronic Obstructive Pulmonary Disease? ......-. Lecce cease 188 . Other Cancers? 20... cc ccc ee ee eee e ene 195 What Are the Special Health Risks for Women? .......---++-+++5+5 195 Effects of Smoking on Pregnancy Outcome .........- toes 197 Risk of Cardiovascular Disease Among Smokers Who Use Oral Contraceptives ©. ..-- 6 eee e eee cere nee 197 Other Health Risks Related to Tobacco Use ........--+ see eee veees 200 Involuntary (Passive) Smoking «2... 06... 0+ eee e ete e eens 200 Is Smoking an Addiction? ...:.. cece tence nee eee eeeeee 200 Interaction Between Smoking and Other Exposures ......-....-- 202 Smokeless Tobacco .........-+-+-0055 Lecce eet ee teens 202 Personal Health Risks for Smokers .........0 0200 e ee tee tee eee tees 202 How Harmful Is Smoking? 2.0.0... 6 60 eee eee eet eter e eens 204 Absolute Risk 2.0.0.0... 0c cece eee cee ee teen tenn nenes 206 Relative Risk ... 0.00.0 ccc eee cee tent e enn nneees 206 Attributable Risk and Smoking- Attributable Mortality ...........+-- 206 Comparative Risk ....... 0000s cece terete ene tent en nes 207 Knowledge Among Adolescents About the Health Risks of Smoking .......- 212 General Health Effects ......... 002 cee cece e eee ene een e renee 212 Personalized Risk 22.0... 00. c ee cece tee tee eet ee enn ee eens 215 Comparative Risk 22.02... 6-000 e cece ete eee teeter ents 215 Addiction .... cece cece cece eee tenet eee nent nee 216 Smokeless Tobacco Use ....... 00 ce eee eee teen teen eres 217 Constituents of Tobacco Smoke... 0.0... 0 eee eee ete tenets 217 Health Benefits of Smoking Cessation .......--.-. see e eee e eee e eens 219 DiscusSiON .... ccc ccc tee eeeee ee ee ee eee eee ee eee ene rena 219 Current Gaps in Public Beliefs About the Health Effects of Smoking .. 219 Factors Interfering With Changes in Knowledge ......---+--+-+++: 222 The 1990 Health Objectives for the Nation .......... +--+ sees reese 223 173 Trends in Public Attitudes About Smoking and Smokers ................... 224 Involuntary Smoking as an Ammoyance ....... 00... cece eee cee eee. 224 Nonsmokers’ Rights... 0... eee eeeeeeeee cece 224 Actions When Smokers Light UP occ cece e cece eee. 227 Opinions of Teenagers 2.0.2... eee eee eee! 227 Trends in Public Opinion About Smoking Policies ........................ 230 Overview ooo eee cee etter entree! 230 Background ...... 2.00... e cece cece cece. 230 Limitations of the Surveys in Assessing Public Opinion About Smoking Policies ©... 0.2... cece eee ee. 230 Restrictions on Smoking ...... 20.00... o kee e ce ceee cece 230 General... cece cee eee! 230 Public Places... 02. ceee eee. 232 Workplace... 6.6 ee cece cence. 232 Airplanes 2.0.2.0 cece eee ee cece 232 Restaurants... eee cece eee! 235 Other Places 62. cece cece. 235 Restrictions on the Sale and Distribution of Cigarettes 2......0.00.0....., 235 Complete Ban on Sales... 000.0... ce cece cece. 235 Limiting Sales to Minors 2.2.0.2... 235 Banning Free Samples ....... 0.00.00... cece eee eee 239 Policies Pertaining to Information and Education........................ 239 Restricting or Prohibiting Tobacco Advertising ................0.. 239 Waming Labels for Cigarettes... 2.2.2.0... ooo cece cee. 241 Economic Policies... 2... cece cee eee cee el 241 Taxation 0c ccc ce cece cece 241 Hiring 2... cece cece cece 241 Conclusions ..... 6... eiceeeer se pre eeT 244 Appendix 2... ii eeeeessssre ers re enn 246 References... 0. esses eres serene 254 174 Introduction This Chapter analyzes trends in public beliefs, attitudes, and opinions about smok- ing. It is divided into three sections. The first describes trends in public beliefs regard- ing the health effects of smoking, the second describes trends in public attitudes about smokers and smoking, and the third describes trends in public opinion about smoking policies. At the outset, it is important to define and clarify the important terms used in this Chapter. Terms such as knowledge, awareness, opinions, beliefs, and attitudes have commonsense meanings to the lay person, but more complex meanings to the social scientist. For example, Allport (1935) reviewed many definitions of attitude and con- structed his own comprehensive definition: “An attitude is a mental or neural state of readiness, organized through experience, exerting a directive or dynamic influence upon the individual’s response to all objects and situations with which it is related.” Entire books have been devoted to the science of defining and measuring public at- titudes, opinions, and beliefs (e.g., Oskamp 1977). For sections two and three of this Chapter, which deal with attitudes and opinions, the commonplace understanding of these terms will suffice. For the first section, however, which covers beliefs about health effects, a more careful approach is war- ranted. This Section generally follows the construct described by Fishbein (1977), which embraces three levels of belief: 1. Level 1 (awareness): A person may believe that “the Surgeon General has deter- mined that cigarette smoking is dangerous to health.” 2. Level 2 (general acceptance): A person may believe that “cigarette smoking is dangerous to health.” 3. Level 3 (personalized acceptance): A person may believe that “my cigarette smoking is dangerous to my health.” Most of the survey data presented in the first section address Level 2 beliefs. At times, the term public knowledge is used to refer to public beliefs (Level 2 beliefs at the population level). There are few data regarding Level 1 beliefs; consequently, use of the terms awareness and public awareness is generally avoided. Data pertinent to Level 3 beliefs are available from a few surveys in three forms: (1) questions asking whether smoking “is harmful to your health”; (2) questions asking whether respondents are “concerned” about the effects of smoking on their health; and (3) questions asking whether respondents believe that they are less likely, as likely, or more likely than other people to be adversely affected by smoking. These levels of beliefs are discussed in more depth later in this Chapter. Data Sources The information presented in this Chapter is derived from three principal sources: 1. Nationally representative surveys conducted by the U.S. Public Health Service from 1964-87, including the Adult Use of Tobacco Surveys (AUTSs) (1964, 1966, 1970, 1975, 1986) and the National Health Interview Surveys (NHISs) (1985, 1987). The NHIS questions were part of the Health Promotion and Dis- 175 ease Prevention Supplement in 1985 and the Cancer Control Supplement in 1987. The surveys for 1964-75 used, for the most part, the same methods and questionnaire wording. Different methods and questionnaires were used in sub- sequent surveys. 2. Nationally representative surveys conducted by private organizations, such as Gallup and Roper, and sponsored by various organizations. 3. National surveys of population subgroups or local surveys. These surveys were used, for the most part, only when nationally representative data were unavail- able. Data from these surveys are presented in several tables throughout this Chapter, each of which addresses beliefs or opinions about a particular smoking-related scientific fact or policy. When one of the primary data sources (e.g., the AUTS) is not included in a table, it is because the relevant question was not asked in the survey or survey year or because the data were not available. Preliminary first-quarter estimates from the Cancer Control Supplement to the 1987 NHIS are provided in some tables (unpublished data, National Cancer Institute). These data are unweighted. When available, year-end weighted data are cited; in all cases, these figures are very similar to the first-quarter estimates. The surveys used in this Chapter and in Chapter 5 are described in the Appendix to this Chapter. Table 1 provides basic information about the survey methodology. The amounts of information provided for the different surveys vary because certain TABLE 1.—Methodology of surveys Sample Age Response a Survey Survey firm size (years) rate (%) Mode AUTS 1964 Nationa] Analysts 5,794 221 76 AUTS 1966 National Analysts 5,768 72 Opinion Research T AUTS 1970 Chilton 5,200 221 P(9%") T(91%) AUTS 1975 Chilton 12,000 T(96%) P(4%°) Roper 1978 Roper 2,511 P NHIS 1985 Census Bureau 33,630 218 90 P AUTS 1986 Westat 13,031 217 74 T AMA 1986 Kane, Parsons 1,500 T AMA 1987 Kane, Parsons 1,500 T MTF* 1975-87 University of Michigan 18 Q *P, personal interview: T, telephone interview; Q, self-administered questionnaire. "Nonrespondents to personal interviews. “Nontelephone households. “Monitoring the Future Project, survey of high school seniors. 176 methodological details were available for some surveys but not for others. Additional information on the methodology of these surveys has been published elsewhere (Mas- sey et al. 1987). Issues in Comparing Surveys When assessing trends from different surveys conducted at different times by dif- ferent organizations, it is important to consider the following caveats. The response to each specific question depends upon multiple factors, including the mode of data col- lection (e.g., in person versus telephone), the sociodemographic representativeness of the sample, the exact wording of the question (€.g., bold, direct-sounding questions ver- sus conservative-sounding statements), the type of response allowed or requested (e.g., open- versus closed-ended questions), the order of questions within the survey, and the content and nature of the rest of the survey (e.g., a survey specifically addressing smok- ing versus another of a general topic). Even minor changes in the survey methods or questionnaire wording may lead to markedly discrepant results for a specific question. Additional precautions exist when interpreting surveys that assess public knowledge. When asked a knowledge question, respondents may attempt to answer it “correctly” in order to please the interviewer. The Health Promotion and Disease Prevention Sup- plement to the 1985 NHIS sheds light on this question. In this survey (NCHS 1986), respondents were asked whether smoking increases the risk of developing cataracts and gall bladder disease-two conditions not associated with smoking. The extent to which these types of questions (sometimes called “red herrings”) are answered in the affirm- ative (and thus incorrectly) may reflect the respondents’ general tendency to respond in the affirmative. More than 85 percent of respondents reported that smoking causes emphysema, chronic bronchitis, and laryngeal, esophageal, and lung cancer, however, 11 percent and 16 percent reported that smoking causes gallstones and cataracts, respec- tively. The responses indicating a connection between smoking and cataracts or gall bladder disease may represent misinformed beliefs or a bias from attempting to answer knowledge questions “correctly.” There are other possible explanations, however. For instance, these responses (as well as other “correct” responses) may represent inferen- ces that respondents have made, in some cases regarding questions they have never thought about. In these cases, some persons may be inclined to infer a connection be- tween a known risk behavior and any disease outcome. In the case of questions about public knowledge (€.g., “Do you think that smoking is or is not a cause of lung cancer?”), the “don’t know” response should be included in the denominator when calculating the proportion of the population that believes a par- ticular fact. This process was used for calculating unpublished data presented below. When two surveys produce unexpected or discrepant results, a close inspection of the methods often explains the findings. Two examples involve surveys of public opinion about smoking policies. In one case, two separate national surveys conducted in 1986 regarding support for a ban on cigarette advertising provided apparently dis- crepant results (American Medical Association (AMA) 1986). A careful review of the questionnaire wording revealed marked differences in the remarks made just prior to each question. Ina survey conducted for AMA, respondents were first informed about 177 the AMA’s support of a policy to ban advertising —67 percent subsequently responded that they were in favor of sucha ban. In contrast, in a survey conducted for the American Cancer Society (ACS), the American Heart Association (AHA), and the American Lung Association (ALA), respondents were first informed that “some people feel that as long as cigarettes are legal, cigarette advertising should be permitted. Others feel that cigarette advertising should not be permitted.” Thirty-three percent subsequently responded that cigarette companies should not be permitted to advertise in newspapers and magazines. There are at least three reasons these questions might be expected to evoke different responses. First, the wording prior to each question may have biased the respondents— one to align with the sponsoring agency’s policy and the other to consider the legal im- plications of such a ban. Second, the first survey asked whether cigarette advertising should be banned while the second asked whether cigarette advertising should be per- mitted. To the extent that some respondents may have a general inclination to answer in the affirmative, such wording differences could influence the results. Third, the word “ban” may have negative connotations for some respondents. Two national surveys (including one sponsored by AMA) conducted 1 year later, which provided no intro- ductory comments, found that 49 percent of adults (Gallup 1987a) and 55 percent of adults (Harvey and Shubat 1987) were in favor of a ban on tobacco advertising (see Table 31). A second example involves two surveys conducted in Michigan in 1986 regarding public opinion on smoking in public places (Perlstadt and Holmes 1987). A survey sponsored by the affiliates of ALA and AHA in Michigan revealed that 82 percent of adults favored restrictions on smoking in public places. In contrast, a survey conducted 2 months later and sponsored by the Michigan Tobacco and Candy Distributors and Vendors Association indicated that 82 percent of the public thought the legislature Should refrain from further legislation restricting smoking. After assessing the survey methods and questionnaires, the Michigan Department of Public Health concluded that markedly different questionnaire wording and survey methods accounted for the dis- crepant results. To assist in the interpretation of the data presented in this Report, data sources are described in Table ! and in the Appendix to this Chapter, and the exact (or approximate) question wording and response choices are provided as a footnote to each table when available. Response choices, when obvious, are often omitted (e.g., simple yes—no questions). Although the same question wording may be used in different surveys, other factors may have important effects on the responses. The reader should therefore in- terpret with caution observed differences and trends presented in this Chapter because many of the potential factors that may affect responses are not known. 178 Trends in Public Beliefs About the Health Effects of Smoking Overview The health consequences of smoking are well documented and widely acknowledged in the scientific literature (see Chapter 2 in this Report). In 1964, the Surgeon General’s Advisory Committee on Smoking and Health, after an extensive review of the litera- ture, reported that cigarette smoking was causally associated with lung and laryngeal cancer in men, was the most important cause of chronic bronchitis, and was associated with esophageal cancer, bladder cancer, coronary artery disease, emphysema, peptic ulcer, and low-birthweight babies (US PHS 1964). During the 25-year period since 1964, subsequent reports of the Surgeon General have updated and extended the findings of the Advisory Committee. The purpose of this Section is to determine the extent to which this information has been disseminated to and accepted by the U.S. public. Public knowledge of the health risks of smoking can be considered under three broad categories: whether smoking is harmful to health in general and whether smokers perceive themselves to be at risk from smoking, as well as the magnitude of risk from smoking and how this compares to other health risks. Be- cause health concerns and risks among adolescents differ from those of adults, we have addressed surveys of their knowledge under a separate heading. For each specific known health risk noted, the section below includes: (1) a descrip- tion of the known medical or scientific facts; that is, a brief summary of the informa- tion known about the health risk (see Chapter 2 for a more detailed description of the information about health risks), (2) a report on the trends in the public’s knowledge of this fact (if available), and (3) a brief description of the current status of knowledge with respect to smoking status. This Section concludes with a summary of the impor- tant gains in knowledge, the gaps that remain, the factors that may promote or interfere with change, and the relationship between these trends and the 1990 Health Objectives for the Nation. In a few cases, published studies have analyzed public knowledge or beliefs by sociodemographic groupings (NCHS 1988; Folsom et al. 1988; Fox et al. 1987; Shopland and Brown 1987; Dolecek et al. 1986). Because these analyses were avail- able only occasionally, and because some of these studies did not control for smoking status, sociodemographic correlation data are not presented below. Because smoking tates and socioeconomic status are inversely correlated (Chapter 5), differences in public knowledge or beliefs according to smoking status may reflect differences in socioeconomic status. Is Cigarette Smoking Harmful to Smokers in General? In 1964, 81 percent of adults strongly or mildly agreed that smoking is harmful to health (Table 2). An identical series of questions asked in the AUTSs from 1964-75 demonstrated an increase in this belief to 90 percent of adults. Public knowledge on this question increased during this period among current smokers (70 to 81 percent), as well as among never smokers (89 to 95 percent). 179 O8T TABLE 2.—Trends in public knowledge about smoking and health Cigarette smoking is harmful to health (percentage who agree by smoking status) Current Former Never All non- Survey Year Reference smokers smokers smokers smokers All aduits 1. AUTS® 1964 US DHEW 1969 70 91 89 89 8 2. AUTS® 1966 US DHEW 1969 78 89 89 89 85 3. AUTS* 1970 US DHEW 1973 79 92 92 92 87 4. AUTS? 1975 US DHEW 1976a 81 95 95 95 90 “Percentages include those who “strongly agree” or “mildly agree.” NOTE: Actual questions: 1. Smoking cigarettes is harmful to health (strongly agree, mildly agree, no opinion, mildly disagree, strongly disagree), 2. Cigarette smoking is harmful to health (strongly agree, mildly agree, no opinion, mildly disagree, strongly disagree). 3-4. Smoking cigarettes is harmful to health (strongly agree, mildly agree, no opinion/don't know, mildly disagree, strongly disagree). TABLE 3.—Trends in public beliefs regarding the relative hazards of different cigarette brands, 1970, 1975, 1986 Percentage of current smokers 1970 1975 1986 Some kinds of cigarettes are probably more hazardous to health than others Kind I smoke probably more hazardous than others* (6) (10) (8) Kind I smoke probably less hazardous than others* (25) (25) (21) Kind I smoke probably about the same as others* (14) (14) (13) Don’t know (2) (2) (2) Subtotal 47 51 45 All cigarettes are probably about equally hazardous* 43 4} 50 Cigarettes are probably not hazardous to health at all 4 5 2 Don’t know or not stated if some are hazardous 6 4 3 Total 100 100 100 “The word “probably” was not used in the 1986 AUTS. The wording in the three surveys was otherwise similar. SOURCE: AUTSs 1970, 1975, 1986 (US DHEW 1973, 1976a; US DHHS, in press). Although smokers and nonsmokers acknowledge the health risks from smoking, cer- tain types of smoking (such as light smoking or smoking low-tar cigarettes) or smok- ing for a limited period of time may be perceived as less hazardous. In general, there are few data to assess the degree to which these beliefs are held. According to the AUTSs in 1970, 1975, and 1986, 45 to 50 percent of current smokers believed that “some kinds of cigarettes are probably more hazardous than others,” 40 to 50 percent believed that “all cigarettes are probably about equally hazardous,” and 5 percent or less believed that “cigarettes are probably not hazardous to health at all” (Table 3). More specific data are reviewed below. Heavy Versus Light Smoking A large body of evidence has shown that light smoking, that is, 1 to 9 cigarettes per day, is associated with a significantly increased risk of overall morbidity and mortality from lung cancer, chronic obstructive pulmonary disease (COPD), heart disease, and other smoking-related diseases compared with never smoking (US DHEW 1979a; US DHHS 1982, 1983, 1984). Between 1970 and 1978, national surveys conducted by the Roper Organization ad- dressed beliefs regarding the health risks of heavy versus light smoking (FTC 1981). Respondents were asked how hazardous smoking is and were given three possible responses: any amount, only heavy smoking, and not hazardous. In 1970, 45 percent of respondents considered only heavy smoking to be hazardous (Table 4); by 1978, 31 181 csi TABLE 4.—Trends in public knowledge about the health hazards of smoking What amount of smoking is hazardous to health?*?- (percentage who responded for each amount) Any Only heavy Not Don’t Survey Year Reference amount smoking hazardous know : 1. Roper 1970 Roper 1978 47 45 5 3 2. Roper 1972 Roper 1978 48 42 6 4 3. Roper 1974 Roper 1978 54 39 4 3 4. Roper 1976 Roper 1978 54 38 4 4 5. Roper 1978 Roper 1978 61 31 5 4 6. AUTS 1986 US DHHS, in press 72 20 5 (current smokers) 81 13 4 (former smokers) 85 1 4 (never smokers) “Respondents were allowed to choose only one answer. The “not hazardous” response was not available for the AUTS. *Percentages of responses in Roper surveys refer to all respondents; in AUTS 1986, percentages represent current, former, and never smokers, respectively, NOTE: Actual questions: 1~5. How hazardous is smoking ? (any amount, only heavy smoking, not hazardous, don’t know), 6. Do you think that only heavy smoking is hazardous or that any smoking is hazardous | (only heavy smoking, any smoking, don’t know} percent considered only heavy smoking to be hazardous. Corresponding increases oc- curred in those responding “any amount.” The 1986 AUTS posed a similar question but did not offer “not hazardous” as a pos- sible response (Table 4). It showed that most respondents, given the two choices of “any amount” or “only heavy smoking,” chose the former (85, 81, and 72 percent of never, former, and current smokers, respectively). When asked, “How many cigarettes a day do you think a person would have to smoke before it would affect their (sic) health?” 49 percent of current smokers and 40 percent of never smokers cited 10 or more (Table 5), thus failing to recognize light smoking as ahealth risk. Twenty percent of current smokers cited 25 or more cigarettes as the min- imum number necessary for adverse health effects (Table 5), which is identical to the proportion of current smokers who indicated, in response to the prior question, that only heavy smoking is hazardous to health (Table 4). Tar Yield Studies have shown that smoking filtered lower tar cigarettes reduces the risk of lung cancer compared with smoking unfiltered higher tar cigarettes. However, there is no conclusive evidence that the lower yield cigarettes are associated with reduced risk of overall mortality, cancers other than lung, COPD, or heart disease. Moreover, com- pensatory smoking behavior in response to lower nicotine intake might actually increase the intake of tobacco smoke toxins in some individuals (US DHHS 1981). Very few surveys have assessed the perceived harmfulness of low-tar cigarettes ver- sus high-tar cigarettes or never smoking. In the 1980 Roper Survey (FTC 1981), respondents were presented with the following false statement: “Tt has been proven that smoking low-tar, low-nicotine cigarettes does not significantly increase a person’s risk of disease over that of a nonsmoker.” Nine percent of smokers said they “know it’s true,” 27 percent said they “think it’s true,” and 32 percent said they did not know if it was true or not. The complicated wording of this question and use of the word “proven” make interpretation of these results difficult. Different results may have been obtained using a question such as, “Do you believe that smoking low-tar cigarettes is or is not harmful to health?” The 1980 Roper survey also asked respondents their beliefs about the following state- ment: “Even if a woman smokes low tar, low nicotine cigarettes during pregnancy, she still significantly increases her risk of losing the baby before or during birth.” Forty- three percent of all respondents and 37 percent of smokers said they “know it’s true” or “think it’s true” (unpublished data, FTC). The 1987 NHIS asked respondents if they believed that “People who smoke low tar and nicotine cigarettes are less likely to get cancer than people who smoke high tar and nicotine cigarettes.” A total of 30 percent agreed with the statement whereas 50 percent disagreed (year-end data). Folsom and associates (1988) surveyed 1,252 blacks (aged 35 to 74 years) and 1,870 whites in the metropolitan Minneapolis/St. Paul area during 1985-86. Respondents were presented with the following statement: “If ‘tar’ and nicotine were removed from cigarettes, there would be no other chemicals in tobacco smoke that cause disease.” 183 P8I TABLE 5.—Public knowledge about the health hazards of smoking in relation to daily cigarette consumption, 1986 How many cigarettes a day you think a person would have to smoke before it would affect their health?* (percentage indicating the following number of cigarettes per day) Don’t 1 2-4 5-9 10-14 15-24 25-39 240 know Current smokers 14 4 8 12 7 3 17 25 Former smokers 17 6 10 13 19 2 9 22 Never smokers 21 9 10 11 19 I 9 20 “The question was open ended. Responses were grouped in the categories 1-9, 10-24, and 225 cigarettes per day to conform to the common definitions of light, moderate, and heavy smoking. SOURCE: AUTS 1986 (US DHHS, in press). The percentages of those correctly identifying this statement as false were 59 percent of black men, 76 percent of white men, 42 percent of black women, and 60 percent of white women. Those who considered the statement to be true may believe low-tar and -nicotine cigarettes to be less hazardous. Duration of Smoking Overall mortality ratios for smokers compared with nonsmokers increase with the duration of smoking. Overall mortality rates among smokers are slightly above the rates of nonsmokers for the first 5 to 15 years of smoking but then increase more rapid- ly as the years of smoking increase (US DHEW 1979a). Mortality ratios for lung can- cer, coronary heart disease (CHD), and COPD increase with decreasing age of initia- tion (US DHHS 1982, 1983, 1984). An increased risk of morbidity (e.g., as measured by days of hospitalization, bed disability, and work lost) among smokers may occur much earlier than increases in mortality ratios. The 1964 AUTS asked respondents, “How many cigarettes a day for how many years might make a cigarette smoker more likely to get lung cancer?” Most of those who considered smoking to be a cause of lung cancer believed that smoking would increase the risk of lung cancer only after at least 10 years of smoking (regardless of the num- ber of cigarettes smoked per day) (Table 6). The 1986 AUTS asked respondents, “How long would a person have to smoke (num- ber) of cigarettes each day before it would affect their (sic) health?” The number of cigarettes used in this question was the number identified by the respondent (in the pre- vious question) as that which “‘a person would have to smoke before it would affect their (sic) health” (see Table 5). A majority of respondents in ail smoking categories believed that smoking 10 or fewer years would affect a person’s health. A higher per- centage of never smokers (36 percent) than current smokers (23 percent) believed that smoking less than 1 year would affect a person’s health. Correspondingly, a slightly higher percentage of current smokers (10 percent) than never smokers (5 percent) believed that health effects would occur only after at least 15 years of smoking (Table 7). The wording in these two questions from the 1964 and 1986 AUTSs is substantially different, making any comparison difficult. In particular, the 1986 question may have favored responses indicating a shorter duration of smoking by referring to general ef- fects on health (which could be interpreted as nothing more than a cough) whereas the 1964 question asked about the risk of lung cancer. Does Cigarette Smoking Cause: Lung Cancer? Lung cancer, first correlated with smoking more than 50 years ago, is the single largest contributor to the total cancer death rate (US DHHS 1982). Lung cancer alone accounted for an estimated 139,000 (28 percent) of the estimated 494,000 total cancer deaths in the United States in 1988 (ACS 1988a). It is estimated that cigarette smoking 185 981 TABLE 6.—Public beliefs about the health effects of smoking in relation to duration of smoking, 1964 How many cigarettes a day for how many years might make a cigarette smoker more likely to get lung cancer?* (percentage indicating the following number of years’) Smokers not more Don’t know/ likely to get lung <9 10-19 20-29 230 no answer cancer Current smokers 10 12 12 I! 10 43 Former smokers 17 {7 16 14 14 22 Never smokers 17 16 10 13 19 24 “Asked only of those who indicated in the previous survey question that smokers are more likely than nonsmokers to develop lung cancer. The denominators for these percentages include all respondents. *Regardless of number of cigarettes per day. SOURCE: AUTS 1964 (US DHEW 1969). L81 TABLE 7.—Public beliefs about the health effects of smoking in relation to duration of smoking, 1986 How long would a person have to smoke (number) cigarettes" each day before it would affect their health? (percentage indicating the following years of smoking) 15 Never Don't Current smokers 23 15 10 8 3 10 0.6 30 Former smokers 24 13 13 10 3 9 0.4 29 Never smokers 36 16 10 6 2 5 0.1 25 "The number of cigarettes used in this question was the number identified by the respondent (in the previous survey question) as that which “a person would have to smoke before it would affect their health.” (See Table 6). SOURCE: AUTS 1986 (US DHHS, in press). causes approximately 90 percent of lung cancer deaths in men and 80 percent in women (see Chapter 3). Surveys have addressed public knowledge about the relationship between smoking and lung cancer since 1954. In 1954, fewer than half of adults (41 percent) thought that smoking is one of the causes of lung cancer (Table 8). Since that time, public knowledge of the association between smoking and lung cancer has increased steadi- ly. By 1964, a majority of adults (66 percent) believed that smoking causes lung can- cer; surveys in 1985, 1986, and 1987 showed that this proportion had increased to be- tween 87 and 95 percent. Heart Disease? The 1964 Report of the Surgeon General’s Advisory Committee identified an associa- tion between smoking and CHD, although it did not consider the available data to be sufficient to establish a causal relationship (US PHS 1964). Since that time, evidence from numerous investigations has established cigarette smoking as the most important modifiable risk factor for CHD in the United States (US DHHS 1983). Cigarette smok- ing increases the risk of death from CHD approximately threefold in persons less than 65 years old and is responsible for 40 to 45 percent of CHD deaths in this age group (Chapter 3). Public beliefs that smoking is associated with the risk of CHD have steadily increased since 1964, when fewer than half of adults (40 percent) thought that smokers were more likely than nonsmokers to develop heart disease (Table 9). Surveys in 1985, 1986, and 1987 showed that 77 to 90 percent of adults believed that smoking increases the risk of developing heart disease. Each of these recent surveys showed that current smokers were less likely to have this belief than former and never smokers. In 1986, current smokers were less likely to acknowledge a relationship between smoking and heart disease (71 percent) than were former smokers (84 percent) and never smokers (80 percent). Chronic Obstructive Pulmonary Disease? The 1964 Report of the Surgeon General’s Advisory Committee identified cigarette smoking as the most important cause of chronic bronchitis (US PHS 1964). Today, cigarette smoking has been identified as the major cause of chronic bronchitis and em- physema in the United States. Eighty to eighty-five percent of deaths from COPD are attributed to cigarette smoking (Chapter 3; also see US DHHS 1984), Since 1964, the public belief that smoking is associated with an increased risk of COPD has increased. In 1964, half of adults (50 percent) thought that smokers were more likely to get chronic bronchitis and emphysema (Table 10). By 1986, most adults thought that cigarette smokers were more likely than nonsmokers to develop chronic bronchitis (81 percent) and emphysema (89 percent). The preliminary first-quarter 1987 NHIS estimates were similar. In three surveys that asked identical questions regarding emphysema and chronic bronchitis (NHISs 1985 and 1987, AUTS 1986), there were consistent slightly higher Proportions who believed that smoking is associated with emphysema compared with chronic bronchitis. In 1986, smokers were less likely to acknowledge an association between smoking and chronic bronchitis (73 percent) than were former smokers (84 percent) and never 188 681 TABLE 8.—Trends in public knowledge about smoking and lung cancer Cigarette smoking causes lung cancer (percentage who agree by smoking status) Current Former Never All All Survey Year Reference smokers smokers smokers nonsmokers adults 1. Gallup 1954 Gallup 1981 41 2. Gallup 1957 Gallup 1981 50 3. Gallup 1958 Gallup 1981 44 4. AUTS 1964 US DHEW 1969 53 75 75 75 66 5. AUTS 1966 US DHEW 1969 57 79 70 72 66 6. Gallup 1969 Gallup 1981 I 7. Gallup 1971 Gallup 1981 7) 8. Gallup 1977 Gallup 1981 81 9. Gallup 1978 Gallup 1978 72 87 81 10. Gallup 1981 Gallup 1981 69 91 83 061 TABLE 8.—Continued Cigarette smoking causes lung cancer (percentage who agree by smoking status) Current Former Never All All Survey Year Reference smokers smokers smokers nonsmokers adults 11. NHIS 1985 NCHS 1986" 92 96 96 96 95 12. AUTS 1986 US DHHS, in press 85 94 95 95 92 13. Gallup 1987 ALA 1987 75 90 94 87 14. NHIS® 1987 83 92 92 89 “And unpublished data. »Preliminary first-quarter data (unpublished). Year-end percentage for all adults is 89 percent. NOTE: Actual questions: . 1-3. Do you think that cigarette smoking is or is not one of the causes of lung cancer? (yes, is a cause; no, is not a cause: no opinion) 4-5. Would you say that cigarette smoking is definitely, probably, probably not, or definitely not a major cause of lung cancer, or that you have no opinion either way?" 6-10. Do you think that cigarette smoking is or is not one of the causes of lung cancer? (yes, is a cause; no, is not a cause: no opinion) It. Tell me if you think cigarette smoking definitely increases, probably increases, probably does not, or definitely does not increase a person’s chances of getting the following problems .. . lung cancer. 12. Do you think a person who smokes is any more likely to get lung cancer than a person who doesn’t smoke? (much more likely, somewhat more likely, no, don’t know) 13. Do you think smoking is a cause of lung cancer? (yes, no, don’t know) 14. People have differing beliefs about the relationship between smoking and health. Do you believe cigarette smoking is related to . . . lung cancer? “Percentages include those who say smoking is “definitely” or “probably” a major cause of lung cancer. **Percentages include those who believe smoking “definitely” or “probably” increases the risk. *Percentages include those who believe smokers are “much more likely” or “somewhat more likely” to get lung cancer. 161 TABLE 9.—Trends in public knowledge about smoking and heart disease Smoking cigarettes causes heart disease (percentage who agree by smoking status) Current Former Never All All Survey Year Reference smokers smokers smokers nonsmokers adults 1. AUTS 1964 US DHEW 1969 32 Si 44 46 40 2. AUTS 1966 US DHEW 1969 33 53 43 47 42 3. AUTS 1966 US DHEW 1969 46 65 58 60 54 4. Gallup 1969 Gallup 1981 60 5. Gallup 1977 Gallup 1981 68 6. Gallup 1978 Gallup 1978 63 72 68 7. Gallup 1981 Gallup 1981 59 82 74 8. NHIS 1985 NCHS 1988 88 93 92 92 90 9. AUTS 1986 US DHHS, in press 71 84 80 81 78 761 TABLE 9.—Continued Smoking cigarettes causes heart disease (percentage who agree by smoking status) Current Former Never All All Survey Year Reference smokers smokers smokers nonsmokers adults 10. NHIS? 1987 73 82 77 77 “Preliminary first-quarter data (unpublished). Year-end percentage for all adults is 76 percent. NOTE: Actual questions: 1-2. Do you think the chances of getting coronary heart disease are the same for people who don't smoke cigarettes as they are for people who do smoke cigarettes? Who would be more likely to get it, people who don’t smoke cigarettes or people who do smoke cigarettes’ 3. Cigarette smokers are more likely to die from heart disease than people who don’t smoke cigarettes. (strongly agree, mildly agree, no opinion, mildly disagree, strongly disagree)" 4-7. Do you think that cigarette smoking is or is not one of the causes of heart disease? 8. Do you think cigarette smoking definitely increases, probably increases, probably does not, or definitely does not increase a person's chances of getting heart disease?” 9. Do you think a person who smokes is any more likely to get heart disease than a person who doesn't smoke? (much more likely, somewhat more likely, no, don’t know)” 10. People have differing beliefs about the relationship between smoking and health. Do you believe cigarette smoking is related to . . . heart disease? 7 : as, ” Mee ” Percentages include those who “strongly agree” or “mildly agree. *Percentages include those who believe that smoking “definitely” or “probably” increases the risk. “ . . earn ae : Percentages include those who believe smokers are “much more likely” or “somewhat more likely” to get heart disease. c6l TABLE 10.—Trends in public knowledge about smoking and emphysema or chronic bronchitis Percentage who agree by smoking status Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults Smoking is a cause of emphysema/chronic bronchitis 1. AUTS 1964 US DHEW 1969 42 60 55 56 50 2. AUTS 1966 US DHEW 1969 46 60 52 54 51 Smoking is a cause of emphysema 3. NHIS 1985 NCHS 1986? 89 94 91 92 91 4. AUTS 1986 US DHHS, in press 85 92 90 91 89 5. Gallup 1987 ALA 1987 75 91 90 85 6. NHIS* 1987 79 87 84 84 Smoking is a cause of chronic bronchitis 7. AUTS 1966 US DHEW 1969 50 56 65 56 59 8. NHIS 1985 NCHS 1986? 82 89 88 88 86 rel TABLE 10.—Continued Percentage who agree by smoking status Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults 9. AUTS 1986 US DHHS, in press 73 84 83 84 81 10. NHIS? 1987 71 81 79 77 “Preliminary first-quarter data (unpublished). Year-end percentages for all adults are 75 percent (chronic bronchitis) and 82 percent (emphysema). ‘And unpublished data. NOTE: Actual questions: 1-2. Do you think the chances of getting emphysema and chronic bronchitis are the same for people who don't smoke cigarettes as they are for people who do smoke cigarettes? Who would be more likely to get it, people who don’t smoke cigarettes or people who do smoke cigarettes?” 3. Tell me if you think cigarette smoking definitely increases, probably increases, probably does not, or definitely does not increase a person’s chances of getting the following problems . . . emphysema. 4. Do you think a person who smokes is any more likely to get emphysema than a person who doesn’t smoke? (much more likely, somewhat more likely, no, don’t know)"” 5. Do you think that smoking is a cause of emphysema? (yes, no, don’t know) 6. Do you believe cigarette smoking is related to emphysema? : 7. Cigarette smoking causes chronic bronchitis. (strongly agree, mildly agree, no opinion, mildly disagree, strongly disagree)’ 8. Tell me if you think cigarette smoking definitely increases, probably increases, probably does not, or definitely does not increase a person's chances of getting the following problems . . . chronic bronchitis. 9. Do you think a person who smokes is any more likely to get chronic bronchitis than a person who doesn’t smoke? (much more likely, somewhat more likely, no, don’t know)"” 10. People have differing beliefs about the relationship between smoking and health. Do you believe cigarette smoking is related to... . chronic bronchitis? “Percentages are those who believe that smokers are more likely to get emphysema and chronic bronchitis. Percentages include those who “strongly agree” or “mildly agree.” **Percentages include those who believe smokers are “much more likely” or “somewhat more likely” to get the disease. *Percentages include those who believe that smoking “definitely” or “probably” increases the risk. smokers (83 percent). Similarly, smokers were less likely to acknowledge an associa- tion between smoking and emphysema (85 percent) than were former smokers (92 per- cent) and never smokers (90 percent). Similar patterns were seen in the earlier surveys. Other Cancers? Laryngeal and esophageal cancer: By 1964, smoking was identified as a cause of laryngeal cancer in men; an association between smoking and cancer of the esophagus was also noted, although the data were not considered sufficient to establish a causal relationship at that time (US PHS 1964). An estimated 75 to 90 percent of laryngeal and esophageal cancer deaths are attributed to smoking, and smokers have mortality rates from these diseases that are approximately 8 to 18 times higher than those of never smokers (Chapter 3). Since 1977, public beliefs that smoking increases the risk of developing cancer of the larynx and esophagus have not changed substantially (Table 11). In 1977, 79 percent of adults reported that smoking is one of the causes of throat cancer. In 1985, 80 per- cent of adults thought that smoking increases a person’s risk of developing esophageal cancer and 88 percent thought that smoking increases the risk of acquiring laryngeal cancer. Use of different wording to describe the cancer site (throat, laryngeal, esophageal, “mouth and throat”) makes comparisons among these surveys difficult. In 1986, current smokers were less likely to acknowledge a relationship between smoking and laryngeal cancer (82 percent) than were former smokers (91 percent) or never smokers (91 percent). Similar patterns were seen in the earlier surveys and in the preliminary 1987 NHIS data (Table 11). Bladder cancer: The 1964 Report of the Surgeon General’s Advisory Committee identified an association between smoking and cancer of the bladder, although the evidence was not considered sufficient to establish a causal relationship (US PHS 1964). Thirty-seven to forty-seven percent of bladder cancer deaths are now attributable to smoking (Chapter 3). Few data are available on public knowledge about the association between smoking and cancer of the bladder. The 1979 Chilton Survey (Chilton 1980) showed that 25 percent of adult respondents (29 to 31 years of age) believed that “cancer of the blad- der (has) been found to be associated with cigarette smoking.” In the 1985 NHIS, 36 percent of adults thought that cigarette smoking definitely or probably increases a person’s risk of developing bladder cancer. In the 1986 AUTS, 33 percent of adults thought that smokers are more likely than nonsmokers to develop bladder cancer. Cur- rent smokers were less likely to acknowledge this relationship (25 percent) than were former smokers (32 percent) and never smokers (38 percent). What Are the Special Health Risks for Women? The special health risks for women include effects of smoking on pregnancy out- come, increased risk of cardiovascular disease (CVD) among smokers who use oral contraceptives, and increased risk of cervical cancer in women who smoke (Chapters 2 and 3). Data exist on public beliefs regarding the first two of these three categories of risk. 195 961 TABLE 11.—Trends in public knowledge about smoking and cancer of the mouth/throat/larynx/esophagus Smoking causes cancer of the mouth/throat/larynx/esophagus (percentage who agree by smoking status) Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults 1. Gallup 1977 Gallup 1981 79 2. Gallup * 1978 Gallup 1978 73 82 79 3. Gallup 1981 Gallup 1981 69 87 81 4. NHIS 1985 NCHS 1986° 83 90 90 90 88 5. NHIS 1985 NCHS 1986? 75 83 82 82 80 6. AUTS 1986 US DHHS, in press 82 91 91 91 88 7. NHIS* 1987 73 85 83 80 *Preliminary first-quarter data (unpublished), Year-end percentage for all adults is 80 percent. ®And unpublished data. NOTE: Actual questions: 1-3. Do you think that cigarette smoking is or is not one of the causes of cancer of the throat? 4-5. Tell me if you think cigarette smoking definitely increases, probably increases, probably does not, or definitely does not increase a person's chances of getting the following problems .. . cancer of the larynx or voice box (question 4). . . cancer of the esophagus (question 5). 6. Do you think a person who smokes is any more likely to get cancer of the larynx or voice box than a person who doesn't smoke? 7. People have differing beliefs about the relationship between smoking and health. Do you believe cigarette smoking is related to . . . cancer of the mouth and throat? “Percentages include those who believe that smoking “definitely” or “probably” increases the risk. Effects of Smoking on Pregnancy Outcome In 1964, knowledge of the health consequences of smoking during pregnancy most- ly concerned the increased risk of low-birthweight babies (US PHS 1964). Con- siderable evidence has accumulated since that time. In the 1980 Surgeon General’s Report, smoking was identified as an important cause of premature births, miscarriages, and stillbirths, as well as low-birthweight babies (US DHHS 1980). From the data available, it appears that the public has become more knowledgeable about the effects of smoking on premature births. In 1966, 34 percent of adults of all ages thought that women who smoke during pregnancy are more likely to have prema- ture babies than women who do not smoke (Table 12). Fox and coworkers (1987) published data on beliefs about the risks of smoking during pregnancy among persons 18 to 44 years of age. By 1985, 70 percent of adults aged /8 to 44 vears thought that smoking during pregnancy definitely or probably increases the chances of premature birth. Only recent data are available on public knowledge of the effects of smoking on spon- taneous abortion (miscarriage), stillbirth, and low birthweight (Table 12). In 1985, 80 percent of adults (aged 18 to 44 years) thought that smoking during pregnancy definite- ly or probably increases the risk of having a low-birthweight baby; 74 percent of adults thought that smoking definitely or probably increases the risk of miscarriage; and 66 percent of adults thought that smoking during pregnancy definitely or probably in- creases the risk of stillbirth. The 1987 NHIS showed that 89 percent of respondents believed that smoking during pregnancy “may” harm the baby. The 1966, 1985, and 1987 surveys each showed that current smokers were less likely than nonsmokers to believe that smoking increases the risk of adverse pregnancy outcomes. The Federal Trade Commission (FTC) (1981) reviewed data from a 1979 Chilton survey and a 1980 Roper survey on public beliefs concerning the effects of smoking during pregnancy. Risk of Cardiovascular Disease Among Smokers Who Use Oral Contraceptives In 1964, the interactive effect of smoking and oral contraceptive use on the risk of CVD had not been established. The 1977/1978 Surgeon General’s Report cited recent studies showing that oral contraceptive use potentiates the harmful effects of smoking on the cardiovascular system (US DHEW 1978). Since 1978, the package inserts for oral contraceptives have described this risk for users (see Chapter 7). It is now known that oral contraceptives or cigarettes, when used alone, increase the risk of heart attacks twofold; however, when used in combination, the increased risk is tenfold (US DHHS 1980). Smoking and oral contraceptive use also appear to interact synergistically to greatly increase the risk of subarachnoid hemorrhage (US DHHS 1983). No trend data are available on the knowledge of health risks from the combined use of cigarettes and oral contraceptives. In 1985, 62 percent of adults aged 18 to 44 years believed that a woman who both takes oral contraceptives and smokes is more likely to have a stroke (Table 12). Nonsmokers were only slightly more likely than smokers to believe this (65 vs. 59 percent). Women were much more likely to believe this than were men (72 vs. 52 percent). In 1980, 64 percent of women believed that a woman who takes birth control pills further increases her risk of getting a heart attack if she also smokes. 197 861 TABLE 12.—Trends in public knowledge about the special health risks for women who smoke Percentage who agree by smoking status” Current Former Never All All Survey Year smokers smokers smokers nonsmokers adults Smoking during pregnancy increases the chances of premature birth 1, AUTS 1966 25 43 34 2. NHIS 1985 (all) 64 71 75 70 2. NHIS 1985 (men) 64 2. NHIS 1985 (women) 716 Smoking during pregnancy increases the chances of stillbirth 3. NHIS 1985 (all) 57 67 72 66 3. NHIS 1985 (men) 63 3. NHIS 1985 (women) 68 Smoking during pregnancy increases the chances of miscarriage 4, NHIS 1985 (all) 6 75 79 74 4. NHIS 1985 (men) 72 4. NHIS 1985 (women) 75 Smoking during pregnancy increases the chances of having a low-birthweight baby 5. NHIS 1985 (all) 74 82 83 80 5. NHIS 1985 (men) 74 5. NHIS 1985 (women) 85 A woman taking birth control pills is more likely to have a stroke if she smokes 6. NHIS 1985 (all) 59 67 64 65 62 6. NHIS 1985 (men) _ 48 57 54 55 52 6. NHIS 1985 (women) 70 80 72 714 72 661 TABLE 12.—Continued Percentage who agree by smoking status Current Former Never All All Survey Year smokers smokers smokers nonsmokers adults A woman who takes birth control pills further increases her risk of getting a heart attack if she also smokes 7. Roper 1980 (women) 64 Smoking by a pregnant woman may harm the baby 8. NHIS 1987 83 90 93 89 “Data for 1966 include all adults (US DHEW 1969). Data for 1985 are from Fox et al. (1987) and NCHS (1986) and include only those people 18 to 44 years of age. Roper data for 1980 are from the FFC (1981). Preliminary first-quarter data (unpublished). Year-end percentage for all adults is 89 percent. NOTE: Actual questions: 1. Women who smoke during pregnancy are more likely to have premature babies than women who do not smoke (strongly agree, mildly agree, no opinion, mildly disagree, strongly disagree)” 2. Does cigarette smoking during pregnancy definitely increase, probably increase, probably not or definitely not increase the chances of premature birth?’ _... of stillbirth?® 3 4... 0f miscarriage?’ 5. ... of low birthweight of the newborn?" 6. If a woman takes birth control pills, is she more likely to have a stroke if she smokes than if she does not smoke? 7. A woman who takes birth control pills further increases her risk of getting a heart attack if she also smokes (know it's true, don’t know if it’s true, think it’s true, think it's not true, know it’s not true).* 8. Smoking by a pregnant woman may harm the baby. (strongly agree, agree, disagree, strongly disagree)” *Percentages include those who “strongly agree” or “mildly agree.” ‘Percentages include those who believe that smoking “definitely” or “probably” increases the risk. *Percentage includes those who “know it's true” or “think it’s true.” **Percentages include those who “strongly agree” or “agree.” Other Health Risks Related to Tobacco Use Involuntary (Passive) Smoking In 1964, the health effects of environmental tobacco smoke (ETS) exposure were not established. Today, ETS has been identified as a cause of disease, including lung can- cer, in healthy nonsmokers. In addition, compared with the children of nonsmoking parents, children of parents who smoke have an increased frequency of respiratory in- fections and slightly lower rates of increase in lung function as the lungs mature (US DHHS 1986a). From the available data, it appears that the public is more likely to believe that there are health risks from ETS exposure. The percentage of adults who thought that smok- ing is hazardous to nonsmokers’ health increased from 46 percent to 58 percent be- tween 1974 and 1978 (Table 13). By 1986 (AUTS), 81 percent of adults thought that tobacco smoke is harmful for nonsmokers who live or work with smokers. Similarly, in 1987 (ACS 1988b), 81 percent thought that people’s smoke is harmful to others near- by. The 1986 and 1987 surveys used wording corresponding to Level 2 (general ac- ceptance) beliefs. The 1987 NHIS used wording corresponding to Level 3 (personal- ized acceptance) beliefs, but nevertheless obtained the same proportion (81 percent) (Table 13). In the 1986 AUTS, former and never smokers were more likely to consider ETS to be generally harmful to health (82 and 87 percent; respectively), compared with cur- rent smokers (69 percent). Similar patterns were seen in the 1987 NHIS and 1988 Gal- lup survey. In the 1986 AUTS, when nonsmokers were asked whether they considered ETS to be harmful to their health, 69 percent responded that they thought so (62 per- cent of former smokers and 74 percent of never smokers). Is Smoking an Addiction? In 1964, the Surgeon General’s Advisory Committee came to the following con- clusion, based on the evidence available at that time: “The tobacco habit should be characterized as an habituation rather than an addiction.” The Advisory Committee’s Report, however, did note that tobacco use is “reinforced and perpetuated by the phar- macologic actions of nicotine on the central nervous system” (US PHS 1964). The 1979 Surgeon General’s Report called smoking “the prototypical substance-abuse de- pendency” (US DHEW 1979a). The 1988 Surgeon General's Report reaffirmed that conclusion and provided a detailed review of the evidence (US DHHS 1988). Only limited data are available to assess public knowledge of the addictive nature of tobacco use. In a 1978 survey conducted by the Roper Organization, 50 percent of adults (57 percent of smokers) considered smoking a habit, 29 percent (22 percent of smokers) thought it an addiction, and 17 percent (15 percent of smokers) believed it to be both (Roper 1978). In a 1986 Gallup poll of 1,046 adults 18 years and older conducted in Canada by household interviews, 76.5 percent of respondents considered “cigarette smoking to be 200 102 TABLE 13.—Trends in public knowledge about the health risks of passive smoking Smoking is hazardous to nonsmokers’ health (percentage who agree by smoking status) Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults 1. Roper 1974 Roper 1978 30 57 46 2. Roper 1976 Roper 1978 38 61 52 3. Roper 1978 Roper 1978 40 69 58 4. AUTS? 1986 US DHHS, in press 69 82 87 85 81 5. NHIS? 1987 68 85 88 81 6. Gallup 1987 ACS 1988b 64 86 89 81 *Percentages presented here are slightly |ower than those previously published (CDC 1988) because the latter did not include “don't know” responses in the denominator. >Preliminary first-quarter data (unpublished). Year-end percentage for all adults is 81 percent. NOTE: Actual questions: 1-3. Is smoking hazardous to nonsmokers’ health? (probably is hazardous, probably doesn’t have any real effect, don’t know) 4. Think now for a moment about a nonsmoker who lives or works with smokers .... Do you think that exposure to tobacco smoke is harmful or not harmful to the nonsmoker’s health? 5. The smoke from someone else's cigarette is harmful to you. (strongly agree, agree, disagree, strongly disagree)” 6. If people smoke, do you think that it is harmful or is not harmful to people who are near them? (yes, harmful; no, not harmful; can’t say/no opinion) “Percentages include those who “strongly agree” or “agree.” like a drug addiction.” Of current smokers, 79.6 answered “yes” to the question, “Do you think you are addicted to cigarettes?” (Canadian Gallup 1986) Interaction Between Smoking and Other Exposures The 1985 Surgeons General’s Report (US DHHS 1985) reviewed evidence regard- ing the interaction between smoking and a variety of occupational exposures in caus- ing disease. With respect to the interaction between smoking and asbestos, the Report concluded that these two exposures act synergistically to increase the risk of lung can- cer. The risk of lung cancer in cigarette-smoking asbestos workers is more than fif- tyfold the risk in nonsmokers who have not been exposed to asbestos. Few data are available on public knowledge of these interactions. The 1980 Roper survey (unpublished data, FTC) asked respondents about their belief conceming the following statement: “If you smoke and have worked with asbestos you are at least 50 times more likely to get lung cancer than if you have done neither.” Seventy-four per- cent of respondents (and 69 percent of smokers) said that they “know it’s true” or “think it’s true.” Smokeless Tobacco Smokeless tobacco (ST) use leads to increased risk of oral cancer and nicotine ad- diction (US DHHS 1986c). No data are available to assess trends in public knowledge of the health risks of ST use. In the 1986 AUTS, 78 percent of adults thought that the use of chewing tobacco is harmful in any way to a person’s health. Similarly, 73 percent thought that the use of snuff is harmful to a person’s health. Current smokers were less likely to know about the health effects of using chewing tobacco and snuff (71 and 66 percent, respective- ly) compared with former smokers (79 and 75 percent, respectively) and never smokers (81 and 76 percent, respectively). According to the 1987 NHIS (preliminary first-quarter estimates), 82 percent of adults thought that a relationship exists between chewing tobacco use and mouth and throat cancers. Seventy-seven percent thought that snuff use is related to these cancers (unpublished data, National Cancer Institute). , Personal Health Risks for Smokers There have been few attempts to determine smokers’ beliefs Tegarding their own per- sonal risk. Several Gallup surveys conducted between 1977 and 1987 asked respon- dents, “Do you think cigarette smoking is or is not harmful to your health?” (Table 14). Data are available for current smokers for the years 1981 and 1985. The proportion of current smokers answering in the affirmative increased from 80 percent in 1981 to 90 percent in 1985. These data, at first glance, suggest that a high percentage of smokers 202 £07 TABLE 14.—Trends in public beliefs about one’s personal risk from smoking Cigarette smoking is harmful to YOUR health (percentage who agree by smoking status) Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults 1. Gallup 1977 Gallup 1985 90 2. Gallup 1978 Gallup 1978 83 95 90 3, Gallup 1981 Gallup 1985 80 96 90 4, Gallup 1983 Gallup 1985 92 5. Gallup 1985 Gallup 1985 90 96 96 94 6. Gallup 1987 ALA 1987 94 7. NHIS* 1987 55 *Preliminary first-quarter data (unpublished). Year-end percentage is 55 percent. NOTE: Actual questions: 1-6. Do you think cigarette smoking is or is not harmful to your health? 7. Do you believe your smoking has affected your health in any way? perceive a personalized risk from smoking. However, nonsmokers were asked to respond to the question, implying that the wording may not be understood by some respondents as referring to truly personalized health risks. Wording such as, “Do you think that your cigarette smoking is or is not harmful to your health?” might elicit dif- ferent responses. The 1987 NHIS (unpublished data. National Cancer Institute) showed that 55 per- cent of current smokers answered “yes” to the question, “Do you believe your smok- ing has affected your health in any way?” The principal reason this percentage is sub- stantially lower than that obtained by the 1985 Gallup survey (90 percent) is probably that the former was likely to be understood as referring to overt symptoms or disease, while the latter was likely to be understood as referring to the risk of harm. Another approach to measure perceptions of personalized risk has been to ask smokers whether they are “concerned” about the effects of smoking on their health. It appears that smokers are more likely today to be concerned that smoking is harmful to their own health. In 1964, 50 percent of current smokers were concerned about the pos- sible effects of smoking on their own health (Table 15); this proportion increased to 75 percent by 1986. However, in 1986, only 18 percent of smokers were very concerned about the effects of smoking on their health: 56 percent of smokers were only fairly or slightly concerned; and 24 percent were not at all concerned. From 1970-86, the percentage of smokers who were very concemed about the pos- sible effects of smoking on their health decreased from 29 to 18 percent, while the per- centage who were only slightly concerned increased from 19 to 34 percent. This redistribution within the population of smokers having any concern may have occurred because a much greater proportion of those who were very concerned may have quit smoking during this period; therefore, they would not have been included in subsequent surveys. A third approach to assess personalized risk, or more correctly, the absence of per- sonalized risk, is to ask smokers if they believe themselves to be at lower risk than other smokers. In 1986, 21 percent of adults thought that the cigarettes they smoked were less hazardous than other cigarettes (Table 3). Other data pertaining to perceptions of personalized risk from ETS and from smok- ing among adolescents appear in the sections on Involuntary Smoking (above) and Adolescent Knowledge (below). How Harmful Is Smoking? The data presented above reveal that a vast majority of adults agree that smoking is hazardous to health and correctly recognize the conditions that are associated with smoking. However, these data do not address the depth of the public’s understanding regarding the absolute risk of smoking, the relative risks of smoking, the population- attributable risk of smoking, and the risk of smoking in comparison with other risks. A more in-depth understanding of the risks of smoking may be much more important in promoting behavioral change than the more superficial beliefs measured by the data presented above. Unfortunately, only limited data are available to address the public’s in-depth understanding of the risks of smoking. 204 soz TABLE 15.—Trends in smokers’ concern about the effects of smoking on their own health Concem about the possible effects of cigarette smoking on your health (percentage who responded by level of concern) Very Fairly Only slightly Not Any a Survey Year concerned concered concerned concerned concem! 1. AUTS 1964 13 18 19 50 50 2. AUTS 1966 12 7 18 53 47 3. AUTS 1970 29 22 19 31 69 4. AUTS 1975 25 23 19 32 68 5. AUTS 1986 18 22 34 24 75 Very, fairly, or only slightly concerned. NOTE: Actual questions: 1-5. Are you in any way concerned about the possible effects of cigarette smoking on your health? SOURCE: US DHEW (1969, 1973, 19764); US DHHS, in press. Absolute Risk Absolute risks can be described by the proportion of those exposed to a given risk factor who will actually die or develop the particular condition, or by the reduction in life expectancy caused by exposure. As many as one-third of heavy smokers aged 35 years will die before age 85 of diseases caused by their smoking (Mattson, Pollack, Cul- len 1987), and 30-year-old smokers will shorten their lives an average of 6 to 8 years if they smoke a pack a day (US DHEW 1979a). From 1970-78, the proportion of adults who believed that smoking a pack of ciga- rettes a day made a great deal of difference in longevity increased slightly from 42 to 50 percent (FTC 1981). However, most adults underestimate the impact of smoking on longevity, according to a 1980 Roper survey. In this survey, 30 percent of the population and 41 percent of smokers did not know that a typical 30-year-old smoker shortened his life expectancy at all by smoking (FTC 1981). Among those who did know that smoking reduces one’s life expectancy, many underestimated the degree to which this is true. On average, nonsmokers underestimated the loss in life expectancy by about 2 years and smokers underestimated it by more than 4 years. Relative Risk Relative risk describes the risk of dying or developing disease for a person exposed to a particular risk factor compared with someone not exposed. For example, male smokers are 22 times more likely and female smokers are 12 times more likely to develop lung cancer compared with nonsmokers of the same sex (Chapter 3). In the 1980 Roper study, respondents were asked if smokers were specifically 10 times more likely to die from lung cancer (the estimated relative risk derived from the data available at that time); 23 percent of the general population and 39 percent of smokers did not believe this statement. Some of this lack of belief may be due to the use of a specific figure. However, using more general terms, 16 percent of adults and 25 percent of smokers did not think that smokers were “many times” more likely than nonsmokers to develop lung cancer (FTC 1981). Attributable Risk and Smoking-Attributable Mortality Attributable risk refers to that proportion of a disease that can be “attributed” to (or is caused by) a particular risk factor, such as smoking. For example, smoking accounts for about 80 to 90 percent of lung cancer deaths and 80 to 85 percent of deaths from COPD (Chapter 3). Much of the information regarding the public’s understanding of the magnitude of the risks of smoking comes from the Roper survey conducted in 1980. In this survey, 43 percent of adults and 49 percent of smokers did not know that smoking causes most of the cases of lung cancer and 22 percent of adults and 27 percent of smokers did not know that smoking even causes many cases of lung cancer (FTC 1981). In the 1987 NHIS (unpublished data, National Cancer Institute), 28 percent (preliminary first- quarter estimate) of smokers and 16 percent (year-end figure) of the general population 206 disagreed with the statement, “Most deaths from lung cancer are caused by cigarette smoking.” Attributable risk figures can be used to calculate smoking-attributable mortality. The 1979 Surgeon General’s Report (US DHEW 1979a, p. ii) attributed approximately 350,000 deaths each year to cigarette smoking. In 1985, an estimated 390,000 deaths in the United States were attributable to smoking (Chapter 3). In the 1979 Chilton sur- vey, adults aged 29 to 31 years were asked: “In the United States, two million people die each year. About how many of these deaths are probably related to cigarette smok- ing?” The responses offered by the interviewer, along with the percentages chosen, were: 10,000 deaths, 22 percent; 50,000, 16 percent; 100,000, 16 percent; 300,000, 17 percent; don’t know, 31 percent (Chilton 1980). Comparative Risk The risk of dying from smoking can be compared with the risk of dying from other behavioral risk factors, such as living under stress, eating high-cholesterol foods, or drinking heavily. The public’s perception of these comparative risks was assessed by Roper surveys from 1970-78 (Table 16). In 1970, living under a lot of tension and stress and not getting regular exercise were considered by more adults to make a great deal of difference in longevity than was smoking a pack of cigarettes daily. In contrast, fewer adults considered regularly eating food high in cholesterol, consuming three or four drinks of liquor a day, or being 20 Ib overweight to have an effect on longevity. In 1978, only stress was considered by more adults to make a great deal of difference on longevity. In 1983, Louis Harris and Associates conducted a national telephone survey of 1,254 randomly selected adults for Prevention magazine (Harris 1983). Respondents were asked to rank 24 health and safety factors on a 1-to-10 (low-to-high) scale of impor- tance. A sample of 103 health experts (medical school chairmen of preventive medicine, public health school deans, government officials, journal editors, and others) was also interviewed and was asked to make the same rankings. All of the public’s mean rankings were in the top half of the scale; thus, none of the factors were seen as trivial in importance. “Not smoking” was ranked near the middle, below “keeping water quality acceptable,” “having smoke detectors in the home,” “taking steps to con- trol stress,” and “getting enough vitamins and minerals” (Figure 1). In contrast, the panel of experts ranked “not smoking” at the top of the list (Figure 2). The 1986 AUTS asked five questions comparing the perceived risk of cigarette smok- ing with the perceived risk of drinking alcoholic beverages, smoking marijuana, being exposed to air pollution, driving without a seat belt, and being 20 Ib overweight (Table 17). In each of the comparisons, never smokers were more likely to disagree than to agree that cigarette smoking is less harmful than the other risks. Only in the case of marijuana smoking are the percentages of those agreeing and disagreeing similar. On the other hand, current smokers were more likely to agree than to disagree that cigarette smoking is less dangerous than marijuana smoking and air pollution. Dolecek and coworkers (1986) surveyed 973 adults in Chicago from a sample of family members of students who participated in AHA’s Chicago Heart Health Cur- 207 807 TABLE 16.—Trends in public knowledge about the health risks of smoking compared to other risks, 1970-78 It makes a great deal of difference in longevity if a person... (percentage who agree by year) Question 1970 1972 1974 1976 1978 lives under a lot of tension and stress 69 72 74 76 74 doesn’t get regular exercise 49 38 38 33 34 smokes a pack of cigarettes a day 42 42 44 45 50 regularly eats a lot of food with high cholesterol 3h 34 38 39 43 drinks 3 or 4 highballs a day 29 34 35 37 39 is 20 pounds overweight 23 26 25 24 24 SOURCE: Roper (1978). 607 Q.: In helping people in general to lve a tong ano neaitny Hie, Now would you rate the importance of. . . Keeping air quality acceptable 9.11 (.05) re Keeping water quality acceptable 8.95 (.05) eH Having smoke detectors in home 8.89 (.06) eH Keeping close to recommended weight 8.54 (.05) Fe Having blood pressure reading annually 8.51 (.06) pe Taking steps to contro! stress 8.38 (.06) re Getting enough vitamins, minerals 8.37 (.06) b-e-| Exercising regularly 8.32 (.06) re Not smoking 8.25 (.08) e414 Having friends, relatives, neighbors 8.18 (.06) re Inheriting genes from parents for long life 8.16 (.06) re Receiving advice from doctor on health habits 8.13 (.06) het Not eating too much sodium 8.10 (.06) red Getting 7-8 hours sleep 8.04 (.06) rH Eating enough fiber 7.98 (.06) eH Wearing seatbelts all the time in front seat 7.89 (.07) t-e+4 Not eating too much fat 7.88 (.07} Fei = Getting enough calcium 97.84 (.06) feo Not eating too much sugar 7.81 (.07) Fee Eating breakfast daily 7.61 (.08) e+ — Not getting too much cholesterol 7.42 (.07) te-4 Drinking alcohol moderately 6.53 (.09) F-e4H{_ Drinking no alcohol 6.42 (.09) FIGURE 1.—Adult public’s rating of 24 health and safety factors NOTE: Shown above is the mean importance rating for each factor given by 1,254 adults using a | to 10 scale. Given in parentheses is the standard error of the mean. The 95-percent confidence interval around each mean is graphically displayed as a band or range consisting of + two standard error values. SOURCE: Harris (1983). Of Utmost Of Low Importance Importance 10 9 8 7 6 3 1 1 q q q | q V1 ee Never driving after drinking 9.25 (.05) eH O17 Q.: Thinking about the overall health of the general population, how important is it for adults to... Of Utmost Of Low 10 Importance 9 8 7 6 5 4 3 importance f T T T T T T IV eH Not smoke 9.78 (.09) --—+i Wear seatbelts all the time in front seat 9.16 (.12) -—oe—_j Never drive after drinking 9.03 (.18) -—oe—+4| Have smoke detectors in home 8.53 (.17) -—_e—_} Live where drinking water is of acceptable quality 8.41 (.17) —o—_{ Have friends, relatives, neighbors 8.31 (.16) -e—+ Exercise regularly 8.20 (.16) --—_—e—_ Drink alcohol moderately 8.15 (.19) '—e—_+{ Not eat too much fat 7.82 (.15) '-e—1 Keep close to recommended weight 7.71 ( .15) -—e— Receive advice from doctor on health habits j 74.67 (.22) -—_—e—-—+4 Have blood pressure reading annually 7.62 (.21) -———_o—___ Inherit genes from parents for long life 7.62 (.28) -—e—_ Take steps to control stress 7.58 (.18) -—e— Eat enough fiber 7.41 (.17) -—_e—_ Get enough calcium (for women) 7.28 (.19) -——e-— Not get too much cholesterol 7.15 (.19) ——_e—-———_} Live where air is acceptable 7.12 (.22) —e-—_} Get enough vitamins and minerals 7.12 (.22) -—o—_{ Not eat too much sodium 7.04 (.19) -——e-—+4 Not eat too much sugar 6.90 (.19) -—e——{_ Get 7-8 hours sleep 6.71 (.20) /———e-——} _ Eat breakfast daily 6.16 (.25) Drink no aicohot 3.15 (.23) -——«—_—} FIGURE 2.—Experts’ rating of 24 health and safety factors NOTE: Shown above is the mean importance rating for each factor given by 103 experts using a! to 10 scale. Given in Parentheses is the standard error of the mean. An indicator of the variability of individual ratings around each mean is graphi- cally displayed as a band or range consisting of + two standard error values. SOURCE: Harris (1983). lz TABLE 17.—Public knowledge about the harmfulness of cigarette smoking compared with other risks, 1986 Percentage who agree Percentage who disagree Curent Former Never Current Former Never smokers smokers smokers smokers smokers smokers Moderate use of cigarettes is less harmful to health than 32 21 20 54 63 63 moderate use of alcoholic beverages. Smoking cigarettes is less harmful to health than smoking 48 38 37 33 34 40 marijuana. Air pollution is a greater health risk than cigarettes. 48 30 28 41 54 57 Smoking cigarettes is less dangerous than driving without a 36 25 26 $2 58 68 seat belt. Smoking is less harmful than being 20 pounds overweight. 31 19 18 59 69 71 NOTE: Percentages of those who agree include those who “strongly agree” or “somewhat agree.” Percentages of those who disagree include those who SOURCE: AUTS 1986 (US DHHS, in press). “strongly disagree” or “somewhat disagree.” ely 2 g riculum Program during the 1980-81 school year, Respondents were asked to select the three major risk factors for CVD from a list of nine. The percentage responses for these risk factors were: high blood Pressure, 25 percent; overweight, 22 percent; stress/tension/worry, 14 percent; cigarette smoking, 13 percent; heredity/family history, 7 percent; eating too much cholesterol (fat), 7 percent; not enough rest/working too hard, 6 percent; not enough exercise, 4 percent; and diabetes, 2 percent. From 1982-86, Becker and Levine (1987) surveyed 90 adults with no known CHD who were siblings of patients hospitalized for recently documented CHD. Patients and siblings were all less than 60 years old. The siblings were randomized into an assess- ment group (interviewed within 2 weeks of the index patients’ discharge and again 4 months later) and a control group (received only one interview at 4-month followup). Participants were asked in an open-ended question to name factors thought to cause or be associated with CHD. Smoking was identified by 81 percent of the control group (after stress, 91 percent) and was the risk factor most often cited by the assessment group (97 percent). Folsom and others (1988) conducted two surveys in the metropolitan Minneapolis/St. Paul area during 1985-86. One survey sampled blacks aged 35 to 74 years, while the other sampled a primarily white population. Subjects were asked the open-ended ques- tion, “What do you think are the most important causes of cardiovascular diseases (heart attack or stroke)?” The percentage of blacks (total sample size=1,252) who identified smoking as one of the most important causes of CVD was 32 percent; stress/worry (54 percent) and improper diet (45 percent) ranked higher. Among whites (total sample size= 1,870), smoking and improper diet were both ranked highest (54 percent). In a survey conducted in 1987 by the Gallup Organization for ACS, 90 percent of adults reported that smoking cigarettes contributes to a higher risk of cancer. Lower percentages reported that a higher cancer risk is associated with suntan and sunburn (73 percent), alcohol (34 percent), high-fat diet (33 percent), and smoked and nitrite-cured meats (31 percent) (ACS 1988b). For the studies reviewed above on comparative risk, data stratified by smoking status were available only from the 1986 AUTS. Knowledge Among Adolescents About the Health Risks of Smoking Because most regular cigarette smokers begin to smoke before age 21 (Chapter 5), it is important to consider teenagers” knowledge about the health effects of smoking. This knowledge can be addressed in the following categories: (1) general health effects of smoking, (2) personalized risk of smoking-related diseases, (3) risks of smoking com- pared with other health risks, (4) beliefs about addiction, and (5) health effects of ST use. General Health Effects Since 1975, beliefs among adolescents that cigarette smoking is harmful have in- creased. National data on knowledge of high school seniors about the health risks of smoking are available from the Monitoring the Future Project (sponsored by the Na- 212 £12 4 ' TABLE 18.—Knowledge about the health risks of smoking among high school seniors, 1975-86, Monitoring the Future Project, National Institute on Drug Abuse How much do you think people risk harming themselves (physically or in other ways), if they smoke one or more packs of cigarettes per day? (percentage responding in each category) Survey year Don’t know No risk Slight risk Moderate risk Great risk Any risk * 1975 2 3 9 35 51 95 1976 2 2 9 31 56 96 1977 2 2 9 29 58 96 1978 2 2 8 30 59 97 1979 1 2 7 27 63 97 1980 1 I 7 27 64 98 1981 1 1 6 28 63 98 1982 2 2 7 30 61 97 1983 1 2 7 29 61 97 1984 1 2 6 27 64 97 1985 2 2 6 24 67 97 1986 l i 5 26 66 97 “Slight, moderate, or great risk of harm combined. SOURCE: Bachman, Johnston, O’Malley (1980a,b, 1981, 1984, 1985, 1987); Johnston and Bachman (1980); Johnston, Bachman, O'Malley (1980a.b, 1982, 1984, 1986). TABLE 19.—Perceived harmfulness of drugs among high school seniors, 1986; Monitoring the Future Project, National Institute on Drug Abuse How much do you think people risk harming themselves (physically or in other ways), if they... (percentage of people responding) Great risk try one or two drinks of an alcoholic beverage (beer, wine, liquor)? 5 try marijuana (pot, grass) once or twice? 15 take one or two drinks nearly every day? 25 smoke marijuana occasionally? 25 try amphetamines (uppers, pep pills, bennies, speed) once or twice? 25 try barbiturates (downers, goofballs, reds, yellows, etc.) once or twice? 25 use smokeless tobacco regularly (chewing tobacco, plug, dipping tobacco, snuff)? 26 try cocaine once or twice? 34 have five or more drinks once or twice each weekend? 39 try LSD once or twice? 42 try heroin (smack, horse) once or twice? 46 take cocaine occasionally 54 smoke one or more packs of cigarettes per day? 66 take amphetamines regularly? 67 take barbiturates regularly? 67 take four or five drinks nearly every day? 67 take heroin occasionally? 68 smoke marijuana regularly? 71 take cocaine regularly? 82 take LSD regularly? . 83 take heroin regularly? 87 NOTE: Possible responses included great risk, moderate risk, slight risk, no risk, don’t know. SOURCE: Bachman, Johnston, O'Malley (1987). tional Institute on Drug Abuse) for every year since 1975. Although nearly all teenagers recognize some risk of harm from smoking, the proportion who think that smoking a pack or more a day causes great risk of harm increased from 51 percent in 1975 to 67 percent by 1985 (Table 18). A 1975 survey (US DHEW 1975a) of teenagers who smoked revealed that many thought that the dangers of smoking were exaggerated for their age group (52 percent of girls; 54 percent of boys); that there was too much talk about things that were bad for them (43 percent of girls; 48 percent of boys); and that air pollution was just as im- portant a cause of lung cancer as cigarettes (67 percent of girls; 51 percent of boys). In 1986, only 16 percent of high school seniors agreed with the statement, “The harmful 214 effects of cigarettes have been exaggerated” (see Table 24; Bachman, Johnston, O’Malley 1987) (data stratified by smoking status were not published). Personalized Risk Inasurvey of 895 students in grades 2 through 12 in 134 public schools in Milwaukee, WI, during the 1979-80 academic year, Leventhal, Glynn, and Fleming (1987) assessed the degree to which the students personalized the health risk from smoking. When asked, “Do you think that smoking can injure or hurt the body?” 98 percent answered affirmatively and were able to accurately name one or more body parts that are adversely affected by smoking. A subsample of 622 subjects (smokers and non- smokers) was asked whether they “would be less tikely, about as likely, or more like- ly to get sick from smoking than other people.” Those answering “less likely” ac- counted for 47 percent of the smokers but only 36 percent of the nonsmokers, 47 percent of those who intended to become adult smokers versus 36 percent of those who did not intend to become adult smokers, and 41 percent of those from smoking families versus 28 percent of those from nonsmoking families. These findings suggest that although children and adolescents recognize smoking as harmful, they may not personalize the tisk. This failure to personalize the perception of risk may play a role in the initiation of smoking. Some teenagers may minimize or deny their personal risk because of a belief that cer- tain smoking patterns are safe. In the 1974 and 1979 Teenage Smoking Surveys con- ducted by the Department of Health, Education, and Welfare (US DHEW 1976b, 1979b), about one-quarter of teenagers agreed with the statement, “There’s nothing wrong with smoking cigarettes if you don’t smoke too many.” About one-third agreed with the statement, “Cigarette smoking is harmful only if a person inhales.” Comparative Risk In the 1979 Chilton Survey (Chilton 1980), teenagers were asked which of the fol- lowing caused the most deaths during the past year: traffic accidents, fires, cigarette smoking, or drug overdose. Traffic accidents were cited by 44 percent of teenagers, followed by drug overdose (21 percent), cigarette smoking (19 percent), and fires (6 percent). The High School Seniors Survey includes questions about the risks associated with using a variety of licit and illicit drugs at different levels of intake. In 1986, 66 percent of high school seniors thought that smoking one or more packs of cigarettes per day causes great risk of harming oneself. More students saw great risk in the regular use of marijuana, cocaine, LSD, and heroin (Table 19). In contrast, more teenagers saw great risk in regular smoking compared with trying amphetamines, barbiturates, cocaine, or LSD; in trying or using occasionally marijuana or cocaine; or in trying al- cohol, having one to two drinks per day, or having five or more drinks one or two times per week. The Weekly Reader magazine includes a survey twice a year in the periodical, which is distributed throughout the country to more than 10 million children in grades 2 215 through 9. Surveys are filled out in class by students under a teacher’s supervision. The topics addressed are rotated so that the same survey is repeated every 4 years. The Spring 1986 survey covered safety and health (Weekly Reader 1986). Of an estimated 400,000 student responses for grades 2 through 6, 128,000 were randomly chosen for analysis. Although the respondents do not represent a randomly selected sample, results pertaining to tobacco are presented here because of the large sample size and the paucity of data available for young children. The survey included the following question: “Many people say the following things are harmful for kids to do. How harmful do you think each is for kids your age? (very harmful, somewhat harmful, not harmful) . . . overeating, eating junk food, listening to very loud music, smoking, chewing tobacco, staying up late, failing to get enough ex- ercise.” Grade-specific results for students in grades 4 through 6 showed that smoking (90 to 95 percent) and chewing tobacco (80 to 90 percent) were much more likely to be perceived as “very harmful” compared with the other choices, all of which were con- sidered to be “very harmful” by less than 40 percent of respondents (except for loud music, among fourth graders—70 percent). However, these results should be inter- preted with caution because of the possibility of sampling bias and the leading nature of the question. Addiction Of particular concern are teenagers who are unaware of the addictive nature of cigarette smoking, and who, therefore, may be tempted to “experiment” with smoking. In the 1974 and 1979 DHEW Teenage Smoking Surveys (US DHEW 1976b, 1979b), about one-quarter of the teenagers agreed with the statement, “Teenagers who smoke regularly can quit for good any time they like.” About 60 percent agreed that “It’s okay for teenagers to experiment with cigarettes if they quit before it becomes a habit.” In the 1979 survey, teenagers were asked, “What would you say is the possibility that 5 years from now you will be a cigarette smoker?” Fifty percent of the current regular smokers (48 percent of boys and 52 percent of girls) answered “definitely not” or “probably not.” These findings suggest that a large proportion of new smokers are un- aware of or underestimate the addictive nature of smoking. In 1975, 56 percent of girls aged 13 to 17 years and 62 percent of young women aged 18 to 35 years thought that smoking was as addictive as illegal drugs (US DHEW 1975a). In the study by Leventhal, Glynn, and Fleming (1987) of 895 students in grades 2 through 12 in Milwaukee, WI, subjects were asked how hard it is for heavy smokers and for light smokers to quit smoking, and how heavy and light smokers feel when they quit. Answers were used to construct a “knowledge of addiction” scale. The inves- tigators found that young people who smoke or who have smoking family members have lower “knowledge of addiction” scores. The authors speculate that these in- dividuals may be “defending against the thought that either they or a parent has an un- controllable problem.” Information on teenage beliefs concerning the addictiveness of ST use is discussed below. 216 Smokeless Tobacco Use In 1985, the Office of the Inspector General, Department of Health and Human Ser- vices, surveyed a nonrandom sample of 399 students in 1 | junior high or middle schools and 20 high schools in 16 States regarding ST use (US DHHS 1986d). ST users were oversampled based on identification of users and nonusers by school officials. The sample was composed of 290 current ST users (73 percent) and 109 nonusers (27 per- cent). Eighty percent of junior high school users and 92 percent of high school users acknowledged that dipping snuff and chewing tobacco can be harmful to a person’s health (Table 20). When asked about the extent of physical harm that may result from ST use, however, about half of users believed that there is no risk or only slight risk from regular use. One-third of junior high school users and only 5 percent of high school users thought that ST use may lead to mouth cancer. There was poor under- standing of the effects of ST use on gum and dental conditions. One-quarter of junior high school users believed that regular ST use is not addictive, and more than one-third did not know that snuff contains nicotine. In summary, these findings suggest that users are substantially uninformed about the health effects and addictiveness of smokeless tobacco use. However, the degree to which these results can be generalized national- ly is limited by the nonrepresentative nature of the sample. Data from the Monitoring the Future Project showed that in 1986, a total of 59 per- cent of high school seniors believed that regular ST use poses a great (26 percent) or moderate (33 percent) risk of harm, compared with 36 percent who believed that ST use poses slight (28 percent) or no (8 percent) risk (Bachman, Johnston, O’Malley 1987). Constituents of Tobacco Smoke - The estimated number of known compounds in tobacco smoke exceeds 4,000, in- cluding some that are pharmacologically active, toxic, mutagenic, carcinogenic, and antigenic (Chapter 2). One of these is carbon monoxide, whose presence in cigarette smoke is cited in one of the four health warnings rotated on cigarette packages and ad- vertisements since 1985 (Chapter 7). Ina 1979 survey conducted by Chilton Research Services for the Federal Trade Com- mission (FTC 1981), respondents were asked, ‘Does cigarette smoke contain carbon monoxide?” Fifty-one percent of teenagers (aged 13-18) either did not know (21 per- cent) or said ‘‘no” (29 percent); 45 percent of adults (aged 29-31) either did not know (26 percent) or said “no” (19 percent). In a 1980 Roper survey (FTC 1981), 53 percent of all respondents and 56 percent of smokers did not know or believe that “Cigarette smoke contains carbon monoxide, which is a dangerous gas.” In the 1986 AUTS, 62 percent of current smokers answered “yes” to the question, “As far as you know, does cigarette smoke contain carbon monoxide?” Thirteen per- cent said “no,” and 25 percent did not know. Former and never smokers were not asked this question. 217 TABLE 20.—Beliefs about the health effects of smokeless tobacco (ST) use among 399 junior and senior high school students (percentage who agree) in 16 States, 1986 Users Nonusers Junior high school High school _ : (N = 76) (N = 214) (N = 109) ST use can be harmful 80 92 97 Risk from ST use None or slight 57 . 42 32 Moderate to great 43 58 68 Regular ST use may lead to 33 5 5 mouth cancer Gum and mouth problems among 64 41 33 users are very rare ST use increases risk of tooth 24 11 16 Stains, wear, and loss Snuff does not contain nicotine 38 20 32 Regular ST use is not addictive 25 15 10 ST use is much more safe than 81 81 59 cigarettes NOTE: ST user defined as follows: has dipped or chewed more than 100 times, currently uses daily or at least 3 days per week, dipping at least three times on days of use. Nonuser defined as follows: has never dipped or chewed, or has only tried it a few times or more than a few times but fewer than 100 times. SOURCE: US DHHS (1986d). 218 Health Benefits of Smoking Cessation The overall mortality ratio of former smokers (compared with never smokers) declines with increasing years of abstinence. According to data reviewed in the 1979 Surgeon General’s Report (US DHEW 1979a) from the U.S. Veterans Study and the British Doctors Study, overall mortality rates of former smokers are similar to those of never smokers 15 years after quitting (US DHEW 1979a). With respect to lung cancer mortality, the increased risk diminishes substantially by 5 to 9 years after quitting, but remains above the risk of never smokers for many more years except for those with fewer than 30 years of cigarette smoking (Chapter 2). A reduction in CHD mortality occurs within the first few years after cessation (US DHHS 1983). The risk of COPD mortality decreases eventually after smoking cessation but does not decline to equal that of never smokers, even after 20 years of cessation (US DHHS 1984). In the 1986 AUTS, respondents were asked how long it takes before former smokers’ chances of developing a disease return to normal. Slightly more than half believed that the risks return to normal within 5 years (Table 21). Results were similar when stratified by smoking status. The 1987 NHIS included questions regarding the health benefits of quitting in terms of specific disease risks. These data were not available for inclusion in this Report. Discussion It has been 25 years since the release of the first Surgeon General’s Report on smok- ing and health. During that time, a major public health effort has been made to educate the public regarding the health consequences of smoking (see Chapters 6-8). Public knowledge of the health risks of smoking has improved as a result of this mas- sive public health education campaign. The belief that smoking is harmful to health has increased since 1964. In 1964, a majority of adults acknowledged the general health risk of smoking and believed that smoking is a major cause of lung cancer, but a minority believed that smoking increases the risk of COPD, heart disease, and premature birth. By the mid-1980s, a substantial majority of adults (including nonsmokers and smokers) recognized the general health risks of smoking and believed that smoking increases the risk of lung cancer, COPD, and heart disease, and prematurity, low birthweight, mis- carriage, and stillbirths. Knowledge of the risks of exposure to ETS has also increased markedly since 1974; in fact, this high level of belief preceded the release of the 1986 Surgeon General’s Report on the health consequences of involuntary smoking. Current Gaps in Public Beliefs About the Health Effects of Smoking Despite the growing level of public knowledge noted above, a substantial number of Americans are still uninformed about or do not believe the health risks of smoking. These gaps in knowledge or beliefs are more evident when one considers the propor- tion of adults who do not acknowledge certain health risks rather than the proportion who do. For example, among smokers—for whom this information is particularly 219 Ot TABLE 21.—Public knowledge about the health benefits of smoking cessation in relation to years of abstinence, 1986 If someone gives up smoking completely, how long do you think it will take before their chances of developing a disease return to normal? (percentage indicating the following number of years) Provisional data only. “In percentage points. “The slope of the regression line was not significantly different from zero, making the R? computation inappropriate. SOURCE: NHISs 1965-87; unpublished data, Office on Smoking and Health. 1985 age distribution, whereas the previously published figures were adjusted to the 1970 age distribution. For each group, observed smoking prevalence for each survey year is reported. Ad- ditionally, to assess time trends from 1965-85, weighted least-squares regression analyses have been applied to these data. The 1987 data were not included in the regres- sion analyses because these data are preliminary estimates. These estimates can be used to provide a measure of predictive validity of the model; in general, the preliminary 1987 estimates are similar to Projections from the model (Pierce, Fiore et al. 1989a). The R? statistic was used for each trend analysis and is a measure of how well the linear model fits the observed data values. R* values may range from 0 (no linear trend) to 1.0 (a perfect fit between the observed values and a linear model). The data on overall smoking prevalence, as well as for each sex and racial group presented in Table 3, demonstrate linear trends with R? values ranging from 0.74 to 0.98; thus, the models fit the data very well. Trends for three of the four educational categories are also fitted well by a linear model. For one category, less than high school graduation, no R? value is reported because the rate of change is very close to zero (making the R? statistic inappropriate as an index of the amount of variation explained by the model). The change (in percentage points) per year is the slope of the line of best fit calculated by the model. The standard error of the slope allows confidence limits to be placed around the estimate of change per year. Ninety-five-percent con- fidence limits around the estimate of a Slope are approximately equal to the slope plus Or minus two times the standard error. Overall smoking prevalence declined from 40.4 percent in 1965 to 29.1 percent in 1987. The trend from 1965-85 is fitted almost exactly by a linear model (R*=0.97), Smoking prevalence in the United States adult population is decreasing at a rate of 0.50 Percentage points per year with a standard error of 0.03. Thus, the 95-percent con- fidence interval for the change per year is 0.44 to 0.56. There is no evidence of any sudden deviations from the identified trend such as that seen in the per capita consump- tion data in 1983 (Table 2). The prevalence of smoking among men has decreased steadily from 50.2 percent in 1965 to 31.7 percent in 1987. The rate of decline between 1965 and 1985 was 0.84 per- centage points per year (95-percent confidence limits, 0.76, 0.92). Female smoking prevalence remained stable at 31 to 32 percent from 1965-77. Subsequently, prevalence began to decline slowly and reached 26.8 percent in 1987. The overall rate of decline from 1965-85 was 0.2] percentage points per year (95-percent confidence limits, 0.15, 0.27). Fiore and coworkers (1989) have examined more recent trends in smoking by gender in greater detail. This analysis showed a rate of decline in prevalence among women of 0.33 percentage points per year between 1974 and 1985 (95-percent confidence limits, 0,21, 0.45) (R7=0.88). Although there has been a difference in smoking prevalence between blacks and whites, it may be explained by socioeconomic status (Novotny, Warner et al. 1988), and the rate of change in smoking prevalence in recent years has been similar between the races (Fiore et al..1989). Smoking among whites decreased from 40.0 percent in 1965 to 28.8 percent in 1987. The rate of decline from 1965-85 was 0.50 percent- age points per year (95-percent confidence limits, 0.44, 0.56; R?=0.97), 270 For blacks the R’ value for the simple linear model is 0.74, suggesting that the data should be reviewed more carefully. In 1965, 43.0 percent of blacks smoked. This number had changed little by 1977 when 41.8 percent smoked. From 1977-87, there was a considerable drop in smoking prevalence to 34.0 percent. Thus, the data suggest that there may be two trends among blacks. Fiore et al. (1989) fitted a linear model to the data for 1974-85 and reported a rate of change among blacks of —0.67 percent- age points per year with 95-percent confidence limits of 0.37 and 0.97 (R?=0.80). This rate of change was not significantly higher than that among whites for the same period (-0.57 percentage points per year). However, smoking prevalence among black men was decreasing at a faster rate than among white men (1.15 percentage points per year compared with 0.87, p=0.03). There were no significant differences noted in the rates of decrease among women of either race (blacks, 0.26 percentage points per year, whites, 0.32). Trends in smoking among the various educational groups have differed markedly since 1966 (Pierce, Fiore et al. 1989b). College graduates have decreased their smoking level from 33.7 percent in 1966 to 16.3 percent in 1987. The rate of decline from 1966-85 was 0.76 percentage points per year (95-percent confidence limits, 0.60 to 0.92). Smoking prevalence in respondents who reported having attended some col- lege decreased from 42.5 percent in 1966 to 26.1 percent in 1987 at a slightly lower rate of change (-0.70 percentage points per year) than that of college graduates. High school graduates who did not attend college reduced their smoking from 41.1 percent in 1966 to 33.1 percent in 1987 at a rate (0.32 percentage points per year) less than half that for respondents who had attended college. Smoking prevalence in those respondents without a high school diploma did not change appreciably from 1966 (36.5 percent) to 1987 (35.7 percent); the rate of decline between 1966 and 1985 was only 0.06 percentage points per year. Thus, there is a twelvefold difference in rate of decline in smoking prevalence between the most and least educated groups in our society. The increasing gap in smoking prevalence by educational attainment is particularly evident when comparing the difference in smoking prevalence between the most and least edu- cated groups in 1966 with the difference in 1987. In 1966, the prevalence rates were similar (33.7 and 36.5 percent, respectively); in 1987, prevalence in the most educated group (16.3 percent) was less than half that in the least educated group (35.7 percent). Adult Use of Tobacco Surveys: 1964-86 In 1964, 1966, 1970, 1975, and 1986, the Office on Smoking and Health (formerly the National Clearinghouse for Smoking and Health) conducted detailed surveys of a representative sample of the U.S. adult population. The purpose of these surveys has been to study the population’s knowledge, attitudes, and practices regarding the use of tobacco. The first two surveys primarily used in-person household interviews while the last three used telephone interviews. Prevalence of cigarette smoking in the United States as measured by the AUTSs has declined from 40.3 percent in 1964 to 26.5 per- cent in 1986 (Table 4). This decrease represents an overall decline in smoking of more than 34 percent during this 22-year period. 271 TABLE 4.—Trends in smoking prevalence (%), AUTS versus NHIS Estimated Difference Survey year AUTS* NHIs° (NHIS-AUTS) 1964 40.3 40.4 0.1 1966 42.2 39.4 -2.8 1970 36.2 37.4 1.2 1975 33.8 34.9 Ll 1986 26.5 29.4 2.9 *For all survey years, includes respondents aged 21 years and older except 1986, which includes respondents aged 17 years and older. All data weighted. "Includes respondents aged 20 years and older. Values for each year are determined by extrapolating expected prevalence values based on regression analysis from Table 3. SOURCE: Office on Smoking and Health (US DHEW 1969, 1973a, 1976; CDC 1987a). Unlike the NHIS, for which data are collected during an in-person household inter- view, AUTSs collected data via telephone interviews in 1970, 1975, and 1986. The three AUTSs conducted since 1970 all produced prevalence estimates below those es- timated (by regression analysis) from the NHISs (Table 4). The largest difference be- tween the two surveys was 2.9 percentage points in 1986. The 95-percent confidence limits around the NHIS projection for 1986 are 27.8 to 31.7 compared with limits of 25.8 to 27.3 from the 1986 AUTS; thus, the difference in estimates between the two Surveys is statistically significant. A difference in sampling modalities is among the most likely explanations for this discrepancy in prevalence estimates. A similar find- ing has been noted in State-specific prevalence estimates (see below). Telephone sur- veys have a small sampling bias by excluding households lacking telephones and may have a greater nonresponse bias because of generally lower response rates compared with household surveys (CDC 1987a). Cigarette Smoking Among Different Occupational Groups NHIS data have been published on smoking prevalence by occupation for the years 1970, 1978-80 combined, and 1985 (Table 5). There is a consistent pattern of higher smoking rates among blue-collar and service workers than among white-collar workers for all these survey years. For example, in 1985, the prevalence of smoking among blue-collar and white-collar workers was 40 and 28 percent, respectively. This dif- ference was greater among males (14 percentage points) than among females (6 per- centage points). Detailed data on smoking prevalence, percentage of former smokers, quitting attempts, and age of initiation within specific occupational categories for 1978~ 80 were published in the 1985 Surgeon General’s Report (US DHHS 1985). Weinkam and Sterling (1987) also provided a detailed analysis of smoking by occupation using the 1970 and 1979-80 NHIS data. Novotny, Warner, and colleagues (1988) performed multivariate logistic regression analyses on data from the 1985 NHIS (ages 25 to 64 years) to examine the independent 272 tLe TABLE 5.—Prevalence of smoking (%) by occupation, 1970, 1978-80, and 1985 1970 1978-80" 1985" Occupation Males Females Males Females Males Females Total Currently employed 47.9 36.5 39.9 33.3 33.8 30.0 32.1 White collar 40.8 36.1 33.0 31.9 26.4 28.0 27.5 Blue collar 55.0 37.7 47.1 38.1 40.1 33.9 39.7 Service $3.3 39.4 475 37.4 40.3 35.4 37.2 Unemployed 55.9 42.3 53.1 39.6 44.3 28.0 36.4 “Aged 20 to 64 years. "Aged 20 years and older. SOURCE: NHISs 1970, 1978-80 (combined), and 1985, NCHS (US DHHS 1985, 1988). effects of socioeconomic status (SES) and selected demographic factors on the odds of ever smoking (versus never smoking) and current smoking (versus former smoking), The SES/demographic factors included in the models were: sex, employment status, occupation, education, marital status, and poverty status. The investigators found that when they simultaneously controlled for the effects of these factors, unemployed per- sons were more likely than employed persons to be ever smokers or current smokers. However, blue-collar and service workers were not found to have significantly in- creased odds of ever or current smoking compared with white-collar workers, Employed persons were more likely to have quit smoking than unemployed persons. Special Populations: Hispanics Information on smoking among Hispanics was collected as part of the Hispanic Health and Nutrition Examination Survey (HHANES) between 1982 and 1984. This was a geographically based sample of Hispanics from three areas of the United States designed to represent three large Hispanic groups (Puerto Ricans in the New York City area; Cuban-Americans in Dade County, Florida; and Mexican-Americans in the South- west). Sample sizes were 9,000 Mexican-Americans, 4,000 Puerto Ricans, and 1,500 Cuban-Americans. According to the HHANES, the age-adjusted smoking rates for males aged 20 to 74 years were 43 percent for Mexican-Americans, 42 percent for Cuban-Americans, and 40 percent for Puerto Ricans. Among females, the smoking prevalence was 24 percent for Mexican-Americans and Cuban Americans and 30 percent for Puerto Rican Americans (Haynes 1987). A birth-cohort analysis of these data showed that smoking rates have decreased among successive cohorts of men, but increased among succes- sive cohorts of women (Escobedo and Remington 1989). These rates are higher than those obtained from the NHISs for the years 1979 and 1980 (Marcus and Crane 1985; Rogers and Crank 1988) and 1985 (Marcus and Crane 1987). However, the number of Hispanics in these NHIS samples was small, making prevalence estimates less reliable. Haynes (1987) suggests that NHIS data may under- estimate smoking prevalence among Hispanics because questions about smoking were not asked in Spanish. The first estimates of smoking behavior among Hispanics that are both national and statistically reliable will be available from the 1987 NHIS, which oversampled for this population group. Special Populations: American Indians and Alaskan Natives There are no reliable national estimates of smoking prevalence among American In- dians. Several surveys have assessed smoking rates among specific Indian tribes or on certain Indian reservations (CDC 1987b). Smoking prevalence is highest among North- ern Plains Indians (42 to 70 percent) and Alaskan Natives (56 percent), where rates greatly exceed the rate in the general U.S. population. Much lower rates have been reported for Indians from the Southwest (13 to 28 percent). High rates of smokeless tobacco use have also been reported among some American Indian groups, especially in Indian youth. According to a survey of approximately 5,000 children 5 to 18 years of age in rural Alaska conducted by the Indian Health Service, 28 percent of girls and 34 percent of boys reported using smokeless tobacco products (CDC 1987c). Similar findings were obtained in other surveys of Native Americans (Schinke et al. 1987; CDC 1988; Hall and Dexter 1988). 274 Special Populations: Asian Americans There are no reliable national estimates of smoking prevalence among Asian Americans. A few local surveys provide estimates of smoking prevalence among Asian Americans in specific geographic regions. The State of Hawaii has a population composed of 29 percent Caucasian, 26 percent Japanese, 15 percent Hawaiian, and 15 percent Filipino. The State conducted a Be- havioral Risk Factor Survey (see below) of 1,002 people by telephone in 1984. Smok- ing prevalence estimates were 28 percent for Caucasians, 27 percent for both Hawaiians and Filipinos, and 23 percent for Japanese (Hawaii State Department of Health 1984). A similar survey of 1,557 residents of the State was completed in 1986. Prevalence es- timates from this second survey were 29.3 percent for Caucasians, 28.8 percent for Hawaiians, 25.1 percent for Filipinos, and 20.6 percent for Japanese (Chung 1986). Special Populations: Pregnant Women National data on smoking during pregnancy are scarce, especially prior to 1980. Since 1980, several national surveys have directed smoking questions to previously pregnant women, but survey methodologies vary widely and it is not possible to study secular changes in behavior. Probably the best source of national data on smoking among pregnant women has been the National Natality Surveys (NNSs), which were conducted among national samples of married mothers of live infants born in 1967 and 1980. Data from these sur- veys were used by Kleinman and Kopstein (1987) to document changes in smoking be- havior during pregnancy over that period of time. Among teenagers, smoking rates remained fairly constant over time at about 38 percent among whites and 27 percent among blacks. Among women over age 20, there were decreases in smoking prevalence that varied markedly by race and by educational attainment of the mother. Smoking prevalence among white women over age 20 declined from 40 percent in 1967 to 25 percent in 1980; among black women over age 20, it declined from 33 percent to 23 percent. Among white women over age 20, there was an increase in the proportion quitting smoking during pregnancy (11 percent to 16 percent), while among blacks the proportion quitting actually decreased (17 percent to 11 percent). Among white women with less than 12 years of education, the prevalence of smoking during pregnancy declined from 48 percent to 43 percent, while for women with 16 or more years of education, it declined from 34 percent to 11 percent. Among white smokers with less than 12 years of education, there was relatively little change in the proportion quitting during pregnancy (11 percent to 9 percent), but among smokers with 16 years or more of education, the proportion more than doubled (12 percent to 27 percent). Insufficient numbers of black women were sampled to study trends by education among blacks. A study similar to the NNS, the National Maternal and Infant Health Survey, was begun in 1988. Data from that study will provide the best estimates of smoking during pregnancy for the late 1980s. At this time, however, no comparable national data exist to study women after 1980. Studies that have asked about smoking behavior during pregnancy have not asked about behavior during specific years, so it is not possible to 275 calculate estimates of the prevalence of smoking in any particular time period. However, it is possible to use these data sources to examine general patterns of smok- ing during pregnancy. In general, women in the lowest age and socioeconomic categories have the highest likelihood of smoking during pregnancy. The earliest data available to examine these patterns are from the Collaborative Perinatal Study (Niswander and Gordon 1972), which included women who obtained prenatal care at selected university centers in the early 1960s. White women were more likely to smoke than black women (53 percent versus 43 percent), and among smokers, whites smoked more cigarettes per day than blacks. By comparison, the national prevalence of smoking among women 25 to 44 years of age was 44 percent in 1965 (NCHS 1988c). The National Survey of Family Growth (NSFG) collected data in 1982 on the smok- ing behavior of women, 15 to 44 years of age, during their most recent pregnancy, regardless of when the pregnancy occurred (NCHS 1988a). Of these women, 32 per- cent smoked during the pregnancy. Women who were aged 15 to 19 years when preg- nant, who had less than 12 years of education, who were at 149 percent or less of pover- ty level, or who were unmarried had the highest smoking rates. In the 1985 NHIS, questions related to smoking were asked of women aged 18 to 44 years who had given birth within the past 5 years (NCHS 1988b). Of these women, 32 percent reported having smoked during the 12 months preceding the birth; 21 percent of smokers reported quitting smoking and 36 percent reported reducing the number of cigarettes smoked after learning they were pregnant. Women under 25 years of age, with low income, of black race, unmarried, or unemployed were more likely to smoke than others. These same groups of women were less likely to quit smoking or to reduce the number of cigarettes smoked. The 1990 Health Objectives for the Nation (US DHHS 1980a) state that “The propor- tion of women who smoke during pregnancy should be no greater than one-half the Proportion of women overall who smoke.” At the time of the midcourse review of the objectives (US DHHS1986c), no data were available to evaluate progress directly. Ac- cording to the 1985 NHIS, approximately 31 percent of women aged 18 to 44 years smoked cigarettes in 1985 (31.7 percent of 18- to 29-year-olds and 31.2 percent of 30- to 44-year-olds) (NCHS 1988c). In the same survey, as mentioned above, 32 percent of women who had given birth in the preceding 5 years reported smoking in the 12 months preceding the birth, 21 percent of whom reportedly quit after learning they were pregnant. This indirect evidence seems to indicate that the smoking prevalence among pregnant women was much more than half the prevalence among nonpregnant women in the early 1980s. Unless major changes in smoking behavior have occurred in the latter half of the decade, the 1990 objective will not be met. Analysis of data from the Behavioral Risk Factor Surveillance System supports this conclusion (Williamson et al. 1989). Special Populations: Military Personnel In 1980, 1982, 1985, and 1988, the Department of Defense (DOD) performed worldwide surveys of alcohol and nonmedical drug use among military personnel. 276 These surveys assessed cigarette smoking among personnel by asking, “During the past 30 days, how many packs of cigarettes did you usually smoke during a typical day?” (The 1980 survey question used the phrase “‘in one day.”) There were five possible responses: 3 or more packs; 2 or more, but less than 3 packs, | or more, but less than 2 packs: less than 1 pack, but smoked some; did not smoke in the past 30 days. Sample sizes ranged from 15,000 to 21,000. The number of military installations participating in the surveys ranged from 58 to 81. The surveyed population was proportionally rep- resentative of all DOD active duty members for sex, race/ethnicity, marital status, education, and age (Herbold 1987; US DOD 1987, 1988). Overall smoking prevalence among military personnel declined steadily from 53 per- cent in 1982 to 46 percent in 1985 to 42 percent in 1988 (Table 6). These prevalence figures, although declining, are considerably higher than among all males or young males in the general population (Tables 3 and 18). This disparity may reflect socioeconomic differences between military personnel and the general population, al- though one study suggests that smoking initiation may often occur among recruits after entering the military (see below). The 1988 estimates for the individual military branches were: Air Force, 37 percent; Marine Corps, 42 percent; Army, 44 percent; and Navy, 45 percent (US DOD 1988). TABLE 6.—Prevalence of cigarette smoking among U.S. military personnel, 1980, 1982, 1985, and 1988 Percentage of current smokers" 1980 1982 1985 1988° Rank” (N=15,016) - (N=21,412) (N=17,328) (N=18,673) El-3 55 56 47 47 E46 55 55 52 45 E7-9 56 61 56 48 Wwi-4 40 34 01-03 19 O1-02 24 25 7 03 23 24 18 04-010 21 20 04-06 27 28 Total 52 53 46 42 *Persons who had smoked cigarettes during the past 30 days. *In ascending rank, from enlisted personnel (E]-9) to warrant officers (W 1-4) to commissioned officers (01-010). “Preliminary data (not adjusted for nonrespondents). SOURCE: Herbold (1987); US DOD (1986, 1987, 1988). 277 Smoking prevalence rates among enlisted personnel (ranks E1-9) are at least twice the rates among commissioned officers in each survey year (Table 6). In 1988, for in- stance, smoking prevalence estimates ranged from 47 percent for the lowest ranks of enlisted personnel (E1~3) to 20 percent for the higher ranks of commissioned officers (04-010). The proportion of smokers smoking a pack or more a day was 55 percent; there was no consistent association between this proportion and military rank (US DOD 1988). Cronan and Conway (1987) collected smoking information from 687 recruits enter- ing the Navy and from 1,357 Navy servicemen stationed aboard ships in the San Diego area. The prevalence of smoking was 27.6 percent among recruits and 49.8 percent among shipboard men. The investigators concluded that the Navy is not attracting a higher than expected percentage of smokers from the U.S. population, but that many men start to smoke after they enter the Navy. Reasons for higher smoking rates among military personnel include the inexpensive price of cigarettes in military facilities, peer pressure heightened by conditions of group living, stress, boredom, and lack of other forms of recreation (Cronan and Conway 1987; Blake 1985). In addition, there has been a historical connection between ciga- rettes and the military: cigarettes have been a part of the K-rations and C-rations provided to soldiers and sailors, and cigarette advertisements on radio and in the print media during World War II commonly featured military themes (Blake 1985). Cigarette advertising continues to appear in military-oriented publications (Davis 1987). In September 1988, Philip Morris Tobacco Company began to publish a month- ly newsletter, “Military Smoker,” which features articles Opposing restrictions on smok- ing and on cigarette sales in military facilities; readers are urged to call a toll-free “Military Smoker” hotline telephone number (Philip Morris 1988), Recent DOD initiatives to reduce smoking among military personnel are described in Chapter 6, State-Specific Smoking Prevalence Behavioral Risk Factor Surveillance System: 1982-87 The Behavioral Risk Factor Surveillance System (BRFS) has provided State-specific smoking prevalence estimates for adults 18 years of age and older for about half of the States since 1982 (Table 7). Data are collected through random-digit-dialed telephone interviews. Since 1984, the number of States participating in this surveillance system has increased steadily. For reporting States, median prevalence declined from 37 per- cent in 1982 to 24 percent in 1987. This decline exceeded the decline in national prevalence in the NHIS (Table 3), probably because of the nonrepresentative mix of States included in the BRFS in different years. In 1987, prevalence ranged from 15 percent in Utah to 32 percent in Kentucky. Current Population Survey: 1985 In 1985, the Current Population Survey (CPS), a population-based, in-person household survey of more than 114,000 adult Americans, conducted by the U.S. Bureau of the Census, collected information about smoking and smokeless tobacco use. About 45 percent of interviews were conducted with proxy respondents. The survey estimated adult smoking prevalence (20 years of age and older) at 29.5 percent. Table 8 presents estimates of prevalence of cigarette smoking according to region of the country, cen- sus division, and State. Among the nine census divisions, prevalence was lowest in the Pacific (26.3 percent) and Mountain (27.2 percent) divisions and was highest in the East South Central (31.8 percent) and South Atlantic (31.3 percent) divisions. Overall gender-specific prevalence was reported as 32.9 percent for males and 26.5 percent for females. Prevalence of smoking among males exceeded that among females in all States except Oregon and Wyoming (where the prevalence rates among men and women were either very similar or the same). Overall education-specific prevalence was 35.4 percent for persons with 12 years orless education (high school diploma or less) and 22.2 percent for persons with 13 or more years of education (some college or more education). Persons with 13 or more years of education reported lower smok- ing prevalence rates than those with 12 years or less education in all 50 States by a range of 20.2 percentage points in Tennessee to 5.7 percentage points in Hawaii. 279 TABLE 7.—State-specific smoking prevalence (%), Behavioral Risk Factor Surveillance System, adults aged 18 years and older, 1982-87 State 1982 1984 1985 1986 1987 Alabama 31 25 27 Alaska 36 34 Arizona 32 28 26 24 26 Arkansas 27 California 28 26 26 25 21 Colorado 34 Connecticut 27 Delaware 31 District of Columbia 33 38 26 27 24 Florida 32 27 28 28 Georgia 29 37 29 27 25 Hawaii 25 23 Idaho 25 24 23 21 lilinois 34 26 28 26 Indiana 33 28 32 27 29 Iowa 30 Kansas 22 Kentucky 37 29 35 32 Maine 28 Maryland 25 Massachusetts 27 25 Michigan 31 Minnesota 27 28 25 24 Missouri 26 29 Montana 26 29 25 23 22 Nebraska 23 New Hampshire 29 New Jersey 32 New Mexico 29 26 21 New York 31 27 23 North Carolina 38 31 27 27 26 North Dakota 28 26 26 24 Ohio 30 29 29 28 27 280 TABLE 7.—Continued State 1982 1984 1985 1986 1987 Pennsylvania 34 Rhode Island 3] 29 39 South Carolina 26 29 27 25 South Dakota 25 Tennessee 32 32 28 28 28 Texas 30 Utah 16 16 18 15 Virginia 34 Washington 24 West Virginia 32 33 27 29 29 Wisconsin 27 25 26 26 Minimum 22 16 16 18 15 Maximum 38 38 32 35 32 Median 37 29 27 26 24 Number of States" 27 19 22 26 29 “Includes the District of Columbia. NOTE: No data were available for the following States: LA, MS, NV, OK, OR, VT, and WY. SOURCE: CDC (1986a,b, 1987f, unpublished data). BRFS and CPS Comparison In 1985, both the BRFS and the CPS collected State-specific information on adult smoking prevalence. Among the 22 States (including the District of Columbia) where comparisons can be made, the CPS (an in-person household survey) estimated higher smoking prevalence in 13 States and lower prevalence in 8 States than the BRFS (a telephone survey) The median difference in smoking nrevalence hetween the CPS and the BRFS was +1.8 percentage points. This pattern is similar to that observed in com- parisons between the in-person NHIS and the telephone AUTS (see above). 281 TABLE 8.—Smoking prevalence rates according to region of the country, census division, and State, adults aged 20 years and older, by gender and education, United States, CPS, 1985 Education “siI2 OI Overall Males Females years years United States 29.5 32.9 26.5 35.4 22.2 Northeast Region 28.9 31.3 26.8 34.5 22.1 New England Division 29.5 30.6 28.6 36.3 22.5 Maine 30.3 31.8 29.1 37.0 17.3 New Hampshire 30.7 35.2 26.7 37.4 21.0 Vermont 30.7 31.8 29.7 37.7 21.4 Massachusetts 28.2 28.4 28.1 35.0 22.9 Rhode Island 34.4 35.8 33.3 39.9 26.3 Connecticut 29.6 30.9 28.5 36.3 23.1 Mid-Atlantic Division 28.7 31.6 26.2 34.0 22.0 New York 28.7 31.4 26.3 34.1 22.3 New Jersey 27.9 31.0 25.2 33.6 21.7 Pennsylvania 29.3 32.3 26.6 34.0 21.7 North Central Region 30.2 32.4 28.1 36.2 22.2 East North Central Division 31.0 33.0 29.3 37.5 22.5 Ohio 32.2 34.4 30.3 38.6 22.0 Indiana 32.8 35.7 30.1 38.4 23.8 Illinois 28.7 31.5 26.3 35.0 22.7 Michigan 34.0 34.4 33.7 40.9 24,7 Wisconsin 26.3 27.6 25.2 32.6 17.9 West North Central Division 28.1 31.1 25.4 33.1 21.7 Minnesota 28.7 30.0 27.4 34.6 21.6 Iowa 28.1 33.0 23.7 31.8 22.2 Missouri 27.7 31.1 24.6 32.0 21.4 North Dakota 26.4 28.3 24,7 31.3 21.8 South Dakota 28.6 30.7 26.8 34.5 21.0 Nebraska 24.9 26.6 23.6 29.2 19.4 Kansas 30.2 34.6 26.6 37.1 23.1 South Region 31.2 36.4 26.8 36.5 23.3 South Atlantic Division 31.3 36.3 27.1 36.6 24.0 Delaware 31.8 34.9 29.1 39.1 19.0 Maryland 29.7 31.5 28.1 36.3 20.1 282 TABLE 8.—Continued Education <12 >12 Overall Males Females years years District of Columbia 31.4 34.2 29.3 38.5 24.2 Virginia 32.7 37.8 28.5 38.5 26.3 West Virginia 34.0 38.6 30.0 38.1 22.9 North Carolina 31.6 39.7 24.6 37.0 24.0 South Carolina 27.1 34.2 21.5 31.7 18.4 Georgia 31.8 38.5 26.5 36.4 25.1 Florida 31.7 35.5 28.4 36.8 25.4 East South Central Division 31.8 37.6 26.9 37.3 21.8 Kentucky 35.3 37.8 33.4 40.2 22.5 Tennessee 30.8 36.6 26.0 38.6 18.4 Alabama 30.6 38.5 23.5 35.3 23.6 Mississippi 31.1 38.8 24.8 34.9 25.3 West South Central Division 30.6 35.5 26.3 35.9 22.8 Arkansas 31.3 37.2 26.5 34.8 25.0 Louisiana 29.1 35.4 23.8 34.1 21.1 Oklahoma 33.0 35.7 30.4 41.5 22.7 Texas 30.6 35.5 26.3 35.9 22.8 West Region 26.5 29.3 23.9 32.8 20.9 Mountain Division 27.2 30.1 24.6 34.7 20.2 Montana 25.9 26.1 25.9 32.2 19.3 Idaho , 24.1 26.6 21.7 29.6 17.8 Wyoming 31.7 31.9 31.9 40.9 21.0 Colorado 28.6 30.6 26.9 37.9 21.9 New Mexico 28.5 32.6 24.3 32.8 24.4 Arizona 29.5 34.3 25.3 37.4 21.5 Utah 14.1 18.2 10.2 22.5 8.0 Nevada 35.7 37.6 33.9 39.0 31.4 Pacific Division 26.3 29.0 22.7 32.0 21.1 Washington 28.6 29.9 27.4 36.1 21.8 Oregon 27.1 26.8 27.5 34.7 21.2 California 25.6 28.9 22.5 28.3 20.8 Alaska 34.3 40.9 28.0 41.1 27.2 Hawaii 27.6 30.7 24.7 30.6 24.9 NOTE: Percentages are age adjusted to the total U.S. population. SOURCE: Office on Smoking and Health, unpublished data. 283 Summary A number of national and State-based surveys provide information on cigarette smok- ing. These surveys have varying methodologies and response rates. The data of highest quality (large sample size, high response rate) are from the NHIS, and this source also has the best series of data for analyzing trends in smoking prevalence since 1965. Trend analysis demonstrates that smoking prevalence among adults overall is declining by 0.50 percentage points per year and this rate of decline has been consistent since 1965, If this rate of change continues for the next few years, overall prevalence will be 27 to 28 percent in 1990, which is higher than the 1990 Health Objective for the Nation (less than 25 percent) (US DHHS 1980a; see Chapter 1). Although there are differences be- tween whites and blacks in smoking prevalence, the rate of change within each race has been similar in recent years. The decline has been much higher in men than in women and much higher in the more educated than in the less educated. The consistency of the trends in these smoking prevalence data contrasts with the lack of year-to-year consistency in the consumption (excise tax) data presented in an earlier section. Given that both data sets report cigarette usage in the population, reasons for this difference need to be addressed. Each data set has its advantages. Ex- cise tax data have the advantage of being an objective measure of manufactured- cigarette sales and are not subject to questions of validity that must be addressed with self-reported smoking from survey data. On the other hand, survey data provide infor- mation on smoking behavior in specific subpopulations within society. Cigarette sales data, and trend analyses of these data, reflect both the number of people who smoke and the number of cigarettes each smoker consumes (plus a wastage and stock error term). On the other hand, trend analyses of self-reported smoking prevalence reflect only the number of people who smoke. Antismoking interventions may affect an individual’s smoking status or daily cigarette consumption. For example, worksite smoking restrictions may induce some smokers to quit, whereas others who continue to smoke may smoke fewer cigarettes per day because of fewer opportunities to smoke. Similarly, increases in cigarette price (e.g., mediated by increased excise taxation) may induce price-sensitive smokers to quit or to reduce daily consumption. While consumption data are often used as a more sensitive index of the relative im- pact of differing antismoking strategies, the primary goal of these strategies is a change in smoking prevalence. Smokers who reduce their daily cigarette consumption will reduce their health risks, but to a lesser extent compared with quitting entirely (see Chapters 2 and 3). 284 Trends in Quitting Introduction As the 1988 Surgeon General’s Report documented (US DHHS 1988), cigarettes and other forms of tobacco are addicting. This addiction, including both pharmacologic and behavioral components, helps to explain the difficulty that most smokers ex- perience in quitting and then maintaining abstinence. Smokers can be on a quitting cycle in which they are abstinent for a while, followed by a relapse to smoking for a period of time, after which they may quit again, and so on. Given this pattern, no single statistic can fully describe trends in quitting activity. Three interrelated statistics are: 1. Percentage of former smokers. The percentage of the population who are former smokers has been used as one indicator of quitting activity. For example, the total number of living persons who have quit smoking is often cited and is cal- culated by multiplying the proportion of the population who are former smokers by the size of the population. This figure, as calculated from the 1986 AUTS, is 43.2 million adults 17 years of age and older. However, the prevalence of former smokers is of limited value in assessing quitting activity because it does not take into account the number of people in the population who have ever smoked, because it does not include former smokers who have died, and be- cause of marked differences in the initiation of smoking between males and females in different birth cohorts (Harris 1983; Warner and Murt 1982). Quit ratio. This statistic is defined as the proportion of people who have ever smoked who are former smokers at a specific point in time; that is, the number of former smokers divided by the number of ever smokers (Pierce et al.1987a). Thus, this statistic is to quitting activity what smoking prevalence is to smoking activity. Both statistics consider the size of the population undertaking a be- havior as a proportion of those who could undertake that behavior. However, the quit ratio does not provide all the information needed when describing quitting activity. It does not distinguish between a person who has been a former smoker for 3 days and a person who has been off cigarettes for 10 years. It does not distinguish between a current smoker who has just relapsed after 6 years of abstinence and a current smoker who has never tried to quit. In addition, the quit ratio does not reflect the magnitude of smoking prevalence; for example, a group in which 10 percent are current smokers and 10 percent are former smokers has the same quit ratio as a group in which 30 percent are current smokers and 30 percent are former smokers. The smoking continuum. This is a 10-category index of the total population derived from the smoking status variable (current, former, or never smoker) and timing and duration of quit attempts. This index is particularly relevant for describing which segments of the population are trying to quit. Trends in the quit ratio using NHIS data and an analysis of the smoking continuum using data from the 1986 AUTS are presented below. 285 Trends in the Proportion of Smokers Quitting (Quit Ratio) (NHIS) Quit ratios for the total U.S. adult population and stratified by sex, race, and educa- tion, as derived from the 1965-87 NHISs, are presented in Table 9. Linear regression analyses of the weighted data from those surveys conducted between 1965 and 1985 are also provided to assess time trends. The 1987 data are not used in the regression analyses because they are preliminary. The linear models for the observed data in the subpopulations defined by sex, race, and education had R values all between 0.78 and 0.95. In 1965, 29.6 percent of ever smokers had quit. By 1987, this proportion had increased to 44.8 percent. The rate of increase in the quit ratio between 1965 and 1985 is 0.68 percentage points per year. Almost half (48.7 percent) of male smokers had quit by 1987 compared with 40.1 percent of female smokers. The rate of increase in the quit ratio is the same among men and women. Regarding racial differences, 46.4 percent of whites who had been smokers had quit by 1987 compared with 31.5 percent of blacks. For whites, the rate of change in the quit ratio from 1965-85 was 0.72 percentage points per year, and the linear model fits the data exceedingly well. For blacks, the rate of change during this period was 0.43 percentage points per year. As with smoking prevalence, the quit ratio for blacks did not change between 1965 and 1974 but did change between 1974 and 1985. Fiore and colleagues (1989) have reported trends from 1974-85; during this period the rate of increase in the quit ratio among blacks (0.75 percentage points per year) was similar to that among whites (0.77). However, this similarity masks a difference between the sexes. The change in the quit ratio among blacks from 1974-85 was mainly seen in males, where the rate increased at 1.04 percentage points per year (compared with 0.67 in white males). Among black females, the quit ratio increased at 0.46 percentage points per year from 1974-85 (compared with 0.95 in white females). Thus, in recent years, black males have been quitting smoking at a significantly higher rate of change than white males (p=0.01). The difference in the rate of change between black and white females is in the opposite direction but is not statistically significant (p=0.3 1) be- cause of the reduced linearity of the trends and smaller sample sizes of ever smokers among females than among males. In 1966, about 40 percent of college graduates who had ever been smokers had quit. This proportion was 20 to 40 percent higher than the other educational groups. By 1987, the quit ratio among college graduates had risen to 61 percent, and the rate of change from 1966-85 (+0.85 percentage points per year) was greater than in any other educational category. Quitting has been increasing in all the other educational categories, with the slowest rate of change (0.41 percentage points per year) among per- sons without a high school diploma. Smoking Continuum (AUTS) The process of quitting smoking has been categorized by Prochaska and DiClemente (1983) according to smokers’ intention to quit and the status of their most recent quit attempt. They labeled five stages of the quitting process as follows: precontemplation, 286 L8Z TABLE 9.—Trends in smoking quit ratio (%), NHISs, United States, 1965-87, adults aged 20 years and older Sex Race Educational level Overall Less than High Year population Males Females Whites Blacks high school school Some College graduate graduate college graduate 1965" 29.6 31.4 24.6 30.5 22.8 1966 29.5 31.4 24.2 30.4 22.6 33.3 28.0 28.7 39.7 1970 35.3 37.9 29.2 36.7 23.2 38.1 33.6 34.9 48.2 1974 36.3 39.3 30.8 38.0 21.8 38.0 35.2 36.6 47.9 1976 37.1 39.9 32.1 38.4 26.3 39.5 35.0 37.2 46.1 1977 36.8 40.3 31.3 38.2 24.8 38.3 34.0 36.8 48.6 1978 38.5 41.3 33.8 39.9 27.5 38.7 36.3 41.0 49.7 1979 39.0 41.5 34.0 40.3 28.0 40.8 36.7 37.5 50.6 1980 39.0 41.5 34.0 40.4 27.7 39.4 36.5 40.6 48.7 1983 41.8 44.1 37.6 43.3 29.3 42.1 38.7 41.2 54.9 1985 45.0 49.0 40.0 46.7 31.8 41.3 40.5 46.0 61.1 1987° 44.8 48.7 40.1 46.4 31.5 39.7 40.9 46.9 61.4 Trend information (1965~—85) Change‘/ year +0.68 +0.73 +0.73 +0.72 +0.43 +0.41 +0.57 +0.73 +0.85 Standard error (+) 0.05 0.06 0.05 0.06 0.07 0.06 0.07 0.10 0.16 R? 0.95 0.94 0.96 0.94 0.82 0.85 0.89 0.88 0.78 NOTE: Quit ratio = (Former Smokers/Current + Former Smokers) *For 1965, data stratified by education were not available. >Provisional data only. “In percentage points. SOURCE: NHISs 1965-87; unpublished data, Office on Smoking and Health. contemplation, action, maintenance, and relapse. This categorization has proven use- ful in longitudinal research studies (see Part II of this Chapter and also Chapter 6); however, for cross-sectional population studies, this process of quitting can be analyzed according to current smoking status and the timing and duration of previous quit at- tempts. Thus, everyone can be classified on a smoking continuum. This continuum is presented in Table 10. It is based on questions from the AUTS (see Appendix to this Chapter). Ten different categories are presented as percentages of the total population and as percentages of ever smokers. Categories of current smokers can also be described as percentages of all current smokers. These percent- ages are not provided below because of the possibility of misinterpretation.In particular, the percentage of those attempting to quit during the past year should not be calculated using current smokers as the denominator because this percentage excludes those who successfully quit during the past year. Instead, a more appropriate denominator (used below) would be those who were smokers at any time during the past year (including former smokers who quit during the past 12 months). TABLE 10.—Smoking continuum, adults aged 17 years and older, United States, 1986 Percentage of Percentage of population ever smokers Category 1 Never smokers _ . 47.3 Category 2 Former smokers who had quit 5 14.7 27.9 or more years ago Category 3 Former smokers who had been 5.7 10.8 abstinent for | to 5 years : - Category 4 Former smokers who had been 2.0 : 3.8 abstinent for 3 to 12 months : Category 5 Former smokers who had quit 3.2 6.1 within the last 3 months Category 6 Current smokers who had quit . 3.9 TA for 7 or more days in the past year . Category 7 Current smokers who had quit ‘ 2.0 3.8 for 1-6 days in the past year Category 8 Current smokers who had quit 11.6 22.0 previously but not in the last year Category 9 Current smokers who had never 5.4 10.2 tried to quit but who had thought about it or would quit if there was an easy way to do so Category 10 Current smokers who had never 4.5 8.5 tried to quit, had not thought about it, and would not try to quit even if there was an easy way to do so SOURCE: AUTS 1986 (US DHHS. in press, a). 288 The first category on this continuum includes those who have never smoked ciga- rettes. In 1986, 47.3 percent of the U.S. population 17 years of age and older was in this category. Former smokers who had quit smoking 5 or more years previously made up 14.7 percent of the population and 27.9 percent of ever smokers. Those in this category can be considered to be confirmed ex-smokers who are unlikely to relapse. Former smokers who had been abstinent for | to 5 years represented 10.8 percent of ever smokers. Former smokers who had been abstinent for less than a year represented 9.9 percent of ever smokers (categories 4 and 5 combined). Current smokers who had quit smoking for 7 or more days during the past year made up 7.4 percent of ever smokers. Another 3.8 percent of ever smokers had quit during the past year but were not able to stay off cigarettes for a week or more. Combining categories 4 through 7, 21.1 percent of ever smokers stopped smoking for at least 1 day during the year prior to the 1986 survey. This is 34 percent of all those who smoked that year. Of ever smokers, 22.0 percent were current smokers who had previously made a serious quit attempt but not during the past year. Approximately 19 percent of ever smokers were current smokers who had never tried to quit; 45 percent of these have never thought about quitting and say that they would not quit even if there was an easy way to do so. Of those who had smoked during the past year, 70 percent had made at least one quit attempt (categories 4 through 8 divided by categories 4 through 10). For the sake of convenience, category 10 is referred to below as the “hard-core smokers” category. However, it should be noted that others might also use this term to describe smokers who have failed to quit despite repeated attempts. Tables 11 and 12 give the distribution for this smoking continuum by gender, educa- tion, race, and age. There are large differences between the subgroups in the propor- tion of ever smokers who are long-term abstainers (category 2). Males are more like- ly to be in this category than females, whites more than blacks, older people more than younger people, and the most highly educated more than the less well educated. The percentages of ever smokers in the categories reflecting recent quitting activity (4 through 7) and no recent quitting activity (8 through 10) were slightly higher for women than for men, probably resulting from the higher percentage of men in the combined categories 2 and 3 (abstinence for a year or more). Educational differences in the smoking continuum are generally consistent with educational differences in smoking prevalence and quit ratio mentioned above. The proportion of ever smokers who have not tried to quit during the past year (categories 8 through 10) is 43.5 percent for the least educated group compared with 29.1 percent for the most educated group. The proportion in the hard-core smokers category is 9.8 percent for the least educated group compared with only 5.7 percent for the most edu- cated group. However, the proportion of those who have made a quit attempt during the past year (categories 4 through 7) is also higher for the least educated group than for the most educated group (21.8 percent and 17.2 percent, respectively); this latter difference may reflect a lower success rate for quitting attempts among the least edu- cated group. The differences between the least and most educated in these categories (4 through 7) become progressively smaller and then disappear as one moves from failed quit attempts during the past year (categories 6 and 7) to successful quit attempts 289 067 TABLE 11.—Smoking continuum by sex and education, percentage of ever smokers, United States, 1986 Sex Education Males Females S11 years 12 years 13-15 years 216 years (%) (%) (%) (%) (%) (%) Smoking continuum Smokers who never tried to 8.3 (8.3)? 9.1 (9.1) 9.8 (9.8) 9.5 (9.5) 7.7 = «((7.7) 5.7 (5.7) quit (10)" Smokers who never tried to 9.1 (17.4) 9.6 (18.7) 9.8 (19.6) 9.5 (19.0) 10.9 (18.6) 5.7 (11.4) quit (9) Smokers not quitting in the last 21.5 (38.9) 23.9 (41.7) 23.9 (43.5) 22.5 (41.5) 22.5 (41.1) 17.7 (29.1) year (8) Smokers quitting 1-6 days in 3.4 (42.3) 4.6 (46.3) 4.4 (47.9) 4.9 (46.4) 2.6 (43.7) 1.5 (30.6) the last year (7) Smokers quitting 7 or more 6.5 (48.8) 8.6 (54.9) 7.4 (55.3) 7,9 (54,3) 8.6 (52.3) 5.0 (35.6) days in the last year (6) Ex-smokers 0-3 months (5) 6.8 (55.6) 5.2 (60.1) 6.6 (61.9) 5.4 (59.7) 6.0 (58.3) 7.0 (42.6) Ex-smokers 3-12 months (4) 3.6 (59.2) 4.3 (64.4) 3.4 (65.3) 4.1 (63.8) 4.7 (63.0) 3.7 (46.3) Ex-smokers |-5 years (3) 10.9 (70.1) 10.7 (75.1) 7.8 (73.1) 10.7 (74.5) 12.8 (75.8) 14.0 (60.3) Ex-smokers 25 years (2) 30.1 (100) 25.1 (100) 27.2 (100) 25.3 (100) 24.4 (100) 39.2 (100) *Category on the smoking continuum (see Table 10 for definitions). "Numbers in parentheses are cumulative percentages. i SOURCE: AUTS 1986 (US DHHS, in press, a). 16z TABLE 12.—Smoking continuum by race and age, percentage of ever smokers, United States, 1986 Race Age Whites Blacks 18-24 years 25-44 years 45-64 years 265 years (%) (%) (%) (%) (%) (%) Smoking continuum Smokers who never tried 8.7 (8.7)? 8.6 (8.6). 9.1 (9.1) 6.9 (6.9) 8.3 (8.3) 74 (7.4) to quit (10)* Smokers who never tried 8.9 (17.6) 12.3 (20.9) 18.4 (27.5) 10.6 (17.5) 7.5 (15.8) 3.6 (11.0) to quit (9) Smokers not quitting in the last 22.2 (39.8) 22.2 (43.1) 16.3 (43.8) 26.4 (43.9) 21.6 (37.4) 14.5 (25.5) year (8) Smokers quitting 1-6 days in 3.6 (43.4) 6.9 (50.0) 7.2 (51.0) 4.4 (48.3) 3.2 (40.6) 2.1 (27.6) the last year (7) Smokers quitting 7 or more 7.0 (50.4) 10.7 (60.7) 19.3 (70.3) 8.6 (56.9) 4.7 (45.3) 2.0 (29.6) days in the last year (6) Ex-smokers 0-3 months (5) 5.9 (56.3) 7.5 (68.2) 7.2 77.5) 5.8 (62.7) 6.2 (51.5) 8.2 (37.8) Ex-smokers 3—12 months (4) 4.0 (60.3) 3.3 (71.5) 9.0 (86.5) 4,3 (67.0) 3.2 (54.7) 2.5 (40.3) Ex-smokers 1-5 years (3) 10.8 (71.1) 9.4 (80.9) 10.3 (96.8) 11.4 (78.9) 9.9 (64.6) 10.1 (50.4) Ex-smokers 25 years (2) 28.8 (100) 19.0 (100) 3.0 (100) 20.6 (100) 35.6 (100) 49.7 (100) “Category on the smoking continuum (see Table 10 for definitions). >Numbers in parentheses are cumulative percentages. SOURCE: AUTS 1986 (US DHHS, in press, a). during the past year (categories 4 and 5). For prolonged abstinence (1 or more years) (categories 2 and 3), the proportions then become greater for the more educated. Among ever smokers, about two-fifths of both blacks and whites have not tried to quit during the past year, with 9 percent in the hard-core smokers category. Twenty- one percent of white ever smokers have made a quit attempt during the past year com- pared with 28 percent of blacks. A person’s likelihood of being in different categories of the smoking continuum dif- fers considerably with age. About 44 percent of ever smokers between the ages of 25 and 44 years are smokers who have not made an attempt to quit during the past year, compared with 26 percent of those 65 years of age and older. However, there are rough- ly equal proportions of each age group in the hard-core smokers category. The propor- tion of ever smokers who made a quit attempt in the last year was highest (42.7 per- cent) in the youngest age group (18 to 24 years old) and is progressively smaller for each older age group (23.1 percent, 17.3 percent, and 14.8 percent, respectively, in those aged 25 to 44 years, 45 to 64 years, and 65 years and older). Summary As with trends in smoking status, trends in quitting activity have exhibited a consis- tent pattern since 1965. Almost half of the population who have ever been smokers have quit. Although the proportion of males who have quit is higher than that of females and the proportion of whites who have quit is higher than that of blacks, the rate of in- crease in the quit ratio is similar between these categories. The only diverging trend over time is the quitting activity for the less educated compared with the more educated. One-third of those who smoked during the year prior to the 1986 AUTS quit smok- ing for at least 1 day during that year. Health education and motivational campaigns targeted at these individuals could help maintain them in “contemplation” and “action” stages (Prochaska and DiClemente 1983) and move them toward repeated quit attempts (see Part II). Trends in the Proportion of Smokers Who Are Heavy Smokers Although all the NHISs have included information on the number of cigarettes smoked per day, respondent rules on this question changed in 1974. Prior to that date, smoking information was obtained from either the sampled individual or a proxy adult living in the same household. For each survey since the 1974 NHIS, smoking informa- tion has been accepted only from the sampled individual. Proxy respondents have been shown to be less accurate in reporting daily cigarette consumption than self-respon- dents (US DHEW 1969, p. 794; Rogot and Reid 1975; National Research Council 1986, pp. 110-112). Proxy responses can be eliminated from analyses of the pre-1974 data to examine long-term trends in daily cigarette consumption. However, excluding proxy responses may make the sample nonrepresentative (see Chapter 3). Accordingly, in considering trends in the proportion of the smoking population who smoke 25 or more cigarettes per day, only NHIS data from 1974-85 are used here. 292 The proportion of smokers who smoked 25 or more cigarettes per day in each survey is presented in Table 13 and is shown in Figure 1. This proportion ranged from 25.5 to 29.8 percent and did not change significantly from 1974 through 1985 (p=0.4). In ad- dition, this proportion did not change among sex- and race-specific subgroups of the smoking population (Figure 2) or in different age groups (NCHS 1988c). Heavy smok- ing has been consistently more common among whites compared with blacks, and among men compared with women; the differential by race has been greater than the differential by sex (Figure 2). TABLE 13.—Self-reported cigarettes smoked per day (percentage of current smokers), United States, aged 20 years and older, 1974-85 Number of cigarettes smoked per day Year 1-14 15-24 225 1974 30.8 43.2 26.0 1976 30.1 44.4 25.5 1977 30.3 43.2 26.5 1978 28.1 42.8 29.1 1979 28.2 43.0 28.8 1980 27.6 42.6 29.8 1983 28.5 44.9 26.6 1985 31.0 41.9 27.1 SOURCE: NHISs 1974-85; unpublished data, Office on Smoking and Health. It is theoretically possible that the proportion of the “heaviest” smokers is increasing even though the proportion of “heavy” smokers (25 or more cigarettes per day) has not changed. However, no major increase occurred from 1974-85 in the proportion of smokers smoking 40 or more cigarettes per day (Table 14). The overall proportion smoking 40 or more cigarettes per day was 12.6 percent in 1974 and 13.2 percent in 1985. Table 14 also demonstrates respondents’ inclination to report their daily cigarette consumption in round numbers related to the size of a cigarette pack (€.g., 10 or 20 cigarettes per day) (see Kozlowski 1986). Because the sales-weighted average nicotine yield declined from 1974-83 (see Figure 14 in Chapter 2), one might expect to have observed an increase in average daily cigarette consumption. Compensatory changes in smoking behavior to maintain rela- tively constant nicotine intake have been shown to occur when smokers switch from high-yield to lower yield cigarettes (US DHHS 1988). Although daily cigarette con- sumption did not increase from 1974-85, other compensatory changes may have oc- curred (e.g., increased frequency of puffing or depth of inhalation) as the smoking population moved toward lower yield brands. 293 Percentage —_ —_ ND a oa Oo 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 1985 YEAR FIGURE 1.—Percentage of current smokers smoking 225 cigarettes per day, adults aged 20 years and older, United States, 1974-85 SOURCE: NHISs 1974-85; unpublished data, Office on Smoking and Health. Percentage i i 1 am L 0 i 1 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 1985 YEARS “~~ White Males —— Black Males —*— White Females —s~ Black Females FIGURE 2.—Percentage of current smokers smoking 225 cigarettes per day, by race and gender, adults aged 20 years and older, United States, 1974- 85 SOURCE: NHISs 1974-85; unpublished data, Office on Smoking and Health. 294 G67 TABLE 14.—Self-reported cigarettes smoked per day (percentage of current smokers) by sex and race, United States, aged 20 years and older, 1974 and 1985 Females Cigarettes per day 1974 1985 1974 1985 1974 1985 1974 1985 1974 1985 1-9 15.0 15.0 12.0 12.5 18.3 17.7 30.0 28.1 12.7 12.8 10 12.6 12.6 99 10.2 15.6 15.1 21.9 21.3 11.4 11.2 11-19 10.9 11.3 10.0 10.9 12.0 11.7 14.8 14.1 10.3 10.9 20 35.1 32.9 35.5 32.4 34.5 33.5 23.9 26.1 36.7 33.9 21-39 13.8 15.0 16.8 17.2 10.7 12.6 $.1 5.8 15.1 16.6 40 10.1 9.5 12.3 11.9 15 7.0 3.7 3.0 11.0 10.6 241 2.5 3.7 3.5 4.9 1.4 2.4 0.6 1.6 2.8 40 SOURCE: NHISs 1974, 1985 (unpublished data, Office on Smoking and Health). Trends in the Initiation of Smoking Information on smoking patterns during adolescence is important because smoking initiation usually occurs during this age. Presented below are data concerning three measures of smoking behavior during adolescence: (1) age of smoking initiation; (2) trends in smoking prevalence among persons 20 to 24 years of age, used as an indicator of smoking initiation; and (3) smoking prevalence among adolescents. Data on age of initiation provide information on the ages during which initiation usually occurs, but provide no information on the extent of tobacco use within the adolescent population. The prevalence of smoking among those 20 to 24 years of age serves as an indicator of smoking initiation among adolescents during the several years preceding a particular survey. This measure offers the advantages that smoking initia- tion is relatively complete by the time one enters this age group, and a survey sample representative of the total age-specific population can be obtained readily. However, these data offer no information on the ages during which smoking initiation actually occurred and do not necessarily reflect the most current initiation patterns among adolescents. Data on smoking prevalence among adolescents provide direct and cur- rent information on smoking behavior in the population of concern. However, inter- pretation of adolescent survey data is complicated by the use of different definitions of regular and experimental smoking in different surveys and by the failure of some sur- veys (e.g., school surveys of high school seniors) to include groups known to smoke at higher rates (e.g., high school dropouts). Age of Initiation Age of smoking initiation is a critical variable in targeting prevention efforts. Infor- mation on self-reported age of initiation is available from surveys of adolescents and adults. Adolescent surveys offer the advantage of providing current information on age of initiation without concerns of recall bias. However, these surveys cannot provide complete information on age of initiation because the samples exclude those who may Start smoking at older ages. Adult surveys provide complete information on age of in- itiation, but recall bias may occur because adults are asked about an event (smoking in- itiation) that typically occurred decades earlier. A major value of an adult survey is that, by using birth cohorts, one can assess whether smoking initiation has changed over time. In the 1986 High School Seniors Survey sponsored by NIDA (see below), seniors who had ever smoked were asked the grade in which they had smoked their first cigarette. About one-quarter of seniors smoked their first cigarette by grade 6, one-half by grade 8, three-fourths by grade 9, and 94 percent by grade 11 (Table 15). Males and whites were more likely to smoke their first cigarette at earlier grades than females and blacks, respectively. The pattern of smoking initiation was similar for those with and without plans for higher education. In addition, the 1987 National Adolescent Student Health Survey (NASHS) (see below) collected information on the grade in which 8th and 10th grade students had smoked their first cigarette. Data are presented in Table 16 for 10th graders only. Ap- 296 TABLE 15.—Grade by which ever smokers smoked their first cigarette (%), reported by high school seniors, United States, 1986 Higher education plans Grade Total Males Females Whites Blacks Yes No 6 25.8 31.1 20.7 26.8 23.3 25.3 25.7 8 57.3 59.5 55.3 59.0 50.2 56.5 58.0 9 725 724 72.5 74.0 65.8 70.8 75.3 10 84.2 83.8 84.7 85.0 78.4 83.0 86.7 11 94.3 93.8 95.0 95.3 89.9 93.5 95.9 12 100.0 100.0 100.0 100.0 100.0 100.0 100.0 Sample size 3,079 1,423 1,526 2,308 302 1,791 972 SOURCE: Institute for Social Research, University of Michigan (Bachman, Johnston, O'Malley 1987). proximately one-quarter of smokers reported that they had started smoking by grade 6 and approximately one-half of smokers had started by grade 7 or 8. Males were some- what more likely than females to start smoking prior to grade 7, but females caught up by grade 9 due to their higher initiation rates in grades 7 to 9. TABLE 16.—Recall of grade at smoking initiation by 10th-grade students, United States, 1987 Males Females % Cumulative % % Cumulative % By grade 4 11.0 11.0 8.5 8.5 Grades 5 or 6 17.9 28.9 14.0 22.5 Grades 7 or 8 24.1 53.0 26.1 48.6 Grade 9 6.9 59.9 10.9 59.5 Grade 10 2.1 62.0 46 64.1 Not smoking by grade 10 38.1 100.0 35.9 100.0 SOURCE: National Adolescent Student Health Survey 1987 (US DHHS, in press, b). Information on age of initiation is available for adults from NHISs conducted in 1978, 1979, 1980, and 1987. The 1987 data were not available for inclusion in the data presented below. The 1978-80 data are derived from responses to the question, “About how old were you when you first started smoking cigarettes fairly regularly?” These data have been used in previously published analyses of age of smoking initiation(US DHHS 1985; Harris 1983; McGinnis, Shopland, Brown 1987) and are again used below. The populations from the three NHISs were combined and grouped by 5-year birth cohorts. In the total sample, the average age of initiation among ever smokers (aged 20 to 64 years) was 17.2 for men and 19.1 for women (US DHHS 1985). The proportion of ever smokers (20 years of age and older) within each birth cohort who 297 had started smoking before different ages is presented separately for males and females in Table 17 and Figures 3 and 4. Among smokers born since 1935, more than four-fifths started smoking before age 21 and almost half started before age 18. The data reveal few differences across birth cohorts in age of initiation before age 16. However, for more recent birth cohorts, there has been a tendency for a higher percentage of ever smokers to have initiated smoking before age 18 or 21. The proportion starting before age 18 has increased from 38 per- cent of ever smokers born from 1910-14 to approximately half of ever smokers born between 1950 and 1954. The proportion starting before age 21 has increased between these two birth cohorts from 66 to 87 percent (Table 17). Stratifying by sex shows that this tendency for more recent birth cohorts to initiate smoking at a younger age has oc- curred among both sexes but has been more striking among females (Figures 3 and 4). The data from the earliest birth cohorts may be biased somewhat by differential mor- tality among smokers with different ages of initiation. Mortality rates for smoking-re- lated diseases are higher for smokers with younger ages of initiation (US DHHS 1982, 1983, 1984). Thus, the age of initiation data may be biased upward among, for ex- ample, the 1910-19 birth cohort, whose members were 61 to 70 years old in the last survey year included in these data (1980). However, the trend noted above toward declining age of initiation, especially among females, is still apparent when consider- ing only those born since 1930. As pointed out above, the decline in age of initiation among males is only seen in the proportion of ever smokers starting before age 21. In summary, these data indicate that uptake of smoking is now a phenomenon that occurs almost entirely during the teenage years and that the initiation of smoking is oc- curring at younger ages among more recent birth cohorts, especially among females. Data from the 1986 AUTS on age of initiation of smokeless tobacco use are presented in the Section on Smokeless Tobacco later inthis Chapter. Prevalence in 20- to 24-Year Age Group The most complete ascertainment of smoking initiation would involve the collection of longitudinal data on children from the ages of about 9 to 21 years. Such complete population-based information for the United States is not available. However, trends in smoking prevalence in the 20- to 24-year age group (Table 18), as determined by the NHIS, provide an indirect measure of trends in smoking initiation. Using this measure has the advantage that smoking initiation is relatively complete by age 20. However, there is a lag of several years between actual initiation during adolescence and prevalence in this group. The R? values for the regression lines derived from these data are above 0.70 for sex-, race-, and education-specific groups, except for females over- all, among whom initiation rates varied considerably. From 1965-87, smoking initiation, as measured by prevalence among those aged 20 to 24 years, decreased from 47.8 percent to 29.5 percent, at a rate of decline from 1965— 85 of 0.69 percentage points per year. There are marked gender differences in this measure of initiation. Smoking prevalence among young males has fallen from 56.3 percent in 1965 to 31.1 percent in 1987 at arate of change (1965-85) of ~1.19 percent- age points per year. In contrast, smoking prevalence among young females has fallen 298 667 TABLE 17.—Proportion of ever smokers (%) who started smoking before various ages, by gender, birth cohorts from NHISs Age at smoking LS liidhiala initiation 1910-14 1915-19 1920-24 1925-29 1930-34 1935-39 1940-44 1945-49 1950-54 <14 Overall 8.9 11.0 9.2 8.1 8.8 8.3 8.5 8.5 8.6 Male 13.0 16.3 12.5 11.7 12.8 11.1 1 10.1 10.3 Female 2.6 3.4 4.2 2.7 3.7 4.7 5.1 6.1 6.6 <16 Overall 20.0 21.6 19.5 19.1 22.2 21.3 23.0 23.7 23.8 Male 28.4 30.3 25.7 25.5 30.1 25.9 27,7 28.2 26.8 Female 7.2 9.5 97 98 11.9 15.6 17.1 17.9 20.2 <18 Overall 38.3 42.1 40.0 42.9 45.0 46.0 48.5 47.2 §2.0 Maile 49.9 53.1 48.7 54.0 56.9 53.8 55.6 $2.2 56.6 Female 20.6 26.7 26.2 26.8 29.8 35.6 40.1 40.9 46.7 <2 Overall 66.2 70.8 70.7 76.5 75.6 81.7 83.1 83.8 87.3 Male 76.5 78.8 79.9 85.4 83.1 85.9 86.1 87.3 90.3 Female 50.3 59.5 56.0 63.5 66.3 75.9 79.5 79.1 83.8 <25 Overall 78.0 83.2 86.9 88.8 90.0 92.7 93.8 95.5 97.7 Male 88.7 90.4 93.8 95.2 95.0 95.0 96.3 97.8 98.5 Female 61.9 72.6 75.8 79.5 83.7 89.5 90.9 92.7 96.7 SOURCE: NHISs 1978, 1979, 1980 combined (unpublished data, Office on Smoking and Health). PERCENTAGE OF EVER SMOKERS 0 80 60 40 20 BEFORE AGE 21 L BEFORE AGE 18 pe BEFORE AGE 14 0 1910-— 1915— 1920— 1925— 1930— 1935-—- 1940— 1945— 1950— 1914 1919 1924 1929 1934 1939 1944 1949 1954 YEAR OF BIRTH FIGURE 3.—Age by which males started smoking, by birth cohort SOURCE: NHISs 1978-80, combined (unpublished data, Office on Smoking and Health). 100 80 60 40 PERCENTAGE OF EVER SMOKERS BEFORE AGE 21 BEFORE AGE 18 BEFORE AGE 16 207 BEFORE AGE 14 J er ee >_< 0 1910— 1915- 1920~- 1925- 1930— 1935—- 1940- 1945- 1950— 1914 1919 1924 1929 1934 1939 1944 1949 1954 YEAR OF BIRTH FIGURE 4.—Age by which females started smoking, by birth cohort SOURCE: NHISs 1978-80, combined (unpublished data, Office on Smoking and Health). 300 l0¢ TABLE 18.—Trends in smoking initiation, NHISs, United States, 1965-87 Smoking prevalence (%), ages 20-24 Education level Overall Sex Race High school graduate or less Some college or more Year population Males Females Whites Blacks Males Females Males Females 1965 478 56.3 40.5 47.5 50.8 63.6 42.6 42.7 34.5 1966 477 51.7 39.5 48.2 45.5 65.1 41.3 43.5 34.7 1970 415 48.5 35.8 41.2 45.2 60.0 40.2 33.2 26.8 1974 39.5 44.3 35.4 38.6 47.1 $2.7 40.1 34.7 26.4 1976 39.6 45.9 34.2 39.5 42.3 54.1 41.0 34.4 23.0 1977 38.8 40.4 37.4 38.5 41.5 52.2 43.0 24.0 27.5 1978 35.4 38.5 32.5 35.7 34.8 46.8 39.3 25.9 21.1 1979 35.8 37.7 34.0 35.6 36.7 47.1 41.9 23.8 22.1 1980 36.1 40.0 32.5 35.9 37.9 50.1 40.3 20.1 19.4 1983 36.9 36.9 37.0 36.8 38.7 49.1 45.5 16.2 22.9 1985 31.8 31.0 32.5 32.5 28.2 43.0 43.6 15.5 17.2 1987" 29.5 31.1 28.1 30.5 25.6 43.8 37.6 16.3 15.1 Trend information (1965-85) Change” /year 0.69 -1.19 0.28 0.68 0.79 ~1.00 0.10 -1.51 0.72 Standard error 0.09 0.10 0.12 0.09 0.17 0.13 0.10 0.13 0.15 R? 0.86 0.94 0.40 0.85 0.71 0.87 NA‘ 0.95 0.75 Provisional data only. In percentage points. “The slope of the regression line was not significantly different from zero, making the R? computation inappropriate. SOURCE: NHISs 1965-87; unpublished data, Office on Smoking and Health. only from 40.5 percent in 1965 to 28.1 percent in 1987 at a rate of change (1965-85) one-quarter that of young males (—0.28 percentage points per year). The slower rate of decline among women is due, in large part, to the increase in initiation rates in less edu- cated young women (Pierce, Fiore et al. 1989b). Smoking initiation patterns among whites and blacks have been similar during the past 20 years. From 1965-87, smoking prevalence among whites aged 20 to 24 years has decreased from 47.5 percent to 30.5 percent, while for blacks the decline has been from 50.8 percent to 25.6 percent. The rates of change between 1965 and 1985 among whites and blacks were similar (-0.68 and -0.79 percentage points per year, respective- ly). The prevalence of smoking had been higher among young blacks than among young whites for most survey years between 1965 and 1983, but whites had a higher prevalence in 1985 and 1987, Marked differences in smoking initiation rates based on educational level have oc- curred. From 1965-87, the smoking initiation rate as measured by prevalence, ages 20 to 24, fell among males with 12 or fewer years of schooling (high school graduate or less) from 63.6 percent to 43.8 percent (1.00 percentage point per year from 1965~ 85). In contrast, for males with 13 or more years of schooling (some college or more), prevalence has fallen from 42.7 percent to 16.3 percent, at a rate of decline (1965-85) of 1.51 percentage points per year. A similar difference in initiation rates by education was seen among women, although the rate of decline between 1965 and 1985 was less among women than among men of equivalent education. In the overall sample (men and women combined), the rate of decrease in initiation among persons with 13 or more years of education (1.10 percentage points per year) was three times that among per- sons with 12 or fewer years of education (0.35). Trends in Adolescent Smoking Several surveys have provided national estimates of smoking prevalence among adolescents. Because these surveys differ in terms of the definitions of smoking, ages of respondents, sample size, method of data collection (household versus school ver- sus telephone interview), years in which the surveys were conducted, and overall results, the findings of the major surveys are presented below. NIDA High School Seniors Surveys on Drug Use, 1976-87 Data from the NIDA-sponsored High School Seniors Surveys have been collected annually since 1975 and are presented in Table 19. These surveys have been carried out by the University of Michigan Institute for Social Research (Johnston, O'Malley, Bachman 1987). This data set is most useful for examining trends in smoking. In- dividual prevalence figures probably underestimate actual adolescent smoking prevalence because the survey does not include high school dropouts, who are known to have much higher smoking rates (Pirie et al. 1988; Yates et al. 1988), Reported daily smoking of cigarettes has decreased among high school seniors from a peak prevalence of 29 percent in 1976 to 19 percent in 1987. However, the trend has not been linear. The majority of the change occurred between 1978 and 1980, after 302 TABLE 19.—Smoking status (%) of high school seniors, United States, 1975-87 Daily Less than Previous smokers, Never Year smokers daily smokers not in last month smokers 1975 27 10 37 26 1976 29 10 36 25 1977 29 10 38 24 1978 28 9 38 25 1979 26 9 40 26 1980 2k 9 41 29 1981 20 9 42 29 1982 21 9 40 30 1983 20 9 4i 29 1984 18 i 41 30 1985 19 il 39 31 1986 18 11 38 32 1987 19 11 38 33 SOURCE: Institute for Social Research, University of Michigan (Bachman, Johnston, O’ Malley 1980a,b, 1981, 1984, 1985, 1987: Johnston and Bachman 1980; Johnston, Bachman, O'Malley 1980a,b, 1982, 1984, 1986, and unpublished data, 1987). which prevalence has remained relatively stable. The proportion of high school seniors who have smoked within the last month, although not on a daily basis, has not changed substantially during this period. There is also rather little change in the proportion of this population who has previously smoked but not in the last 30 days. The proportion of high school seniors who have never smoked increased from 26 percent to 33 percent between 1975 and 1987. Trends in smoking status by sex, race, and educational plans are presented in Table 20. The prevalence of daily smoking decreased in all major subcategories of high school seniors between 1976 and 1987. Daily smoking among males decreased from a peak prevalence of 28 percent in 1976 to 16 percent in 1987; most of this drop oc- curred between 1977 and 1980. Daily smoking among females decreased from a peak prevalence of 30 percent in 1977 to 20 percent in 1987, with the largest decrease oc- curring from 1979-81. Since 1981, the prevalence of daily smoking among high school students has remained fairly constant for both males and females. In each year since 1977, the prevalence of daily smoking has been higher in females than in males (median difference=4 percentage points). The prevalence of daily smoking fell substantially among blacks, from 26 percent in 1976 to 8 percent in 1987. During the same period, prevalence declined among whites from 29 percent to 20 percent. The reasons for the dramatic decline among blacks are unclear. It does not appear to be due to increasing sampling bias over time—survey methods and sample sizes by race have been consistent. A substantial decrease in smok- ing initiation among blacks also occurred, as measured in the NHIS by prevalence in persons 20 to 24 years of age, between 1983 (38.7 percent) and 1985 (28.2 percent) (Table 18). This figure declined further to a preliminary estimate of 25.6 percent in 1987. Students with plans to pursue higher education were much less likely to be daily smokers in 1976 than those without such plans (21 percent versus 37 percent). The ab- 303 POE TABLE 20.—Smoking status (%) of high school seniors by sex, race, and educational plans, United States, 1975-87 Daily smokers Less than daily smokers Sex Race Plans for higher education Sex Race Plans for higher education Year M F Ww B Yes No M F Ww B Yes No 1975 27 26 10 10 1976 28 28 29 26 21 37 10 10 10 13 10 10 1977 28 30 28 25 20 38 10 10 9 I 10 9 1978 26 29 27 22 18 36 9 10 9 9 9 9 1979 22 28 26 19 17 35 9 9 9 9 9 9 1980 18 24 22 16 14 31 8 10 9 10 9 10 1981 18 22 20 13 13 30 8 10 9 9 9 9 1982 18 24 23 12 13 30 9 9 9 9 9 9 1983 19 23 22 12 14 30 9 10 9 9 10 9 1984 16 21 20 8 11 29 10 iB 11 9 1] It 1985 17 21 20 I 13 31 10 i U1 8 10 ll 1986 17 20 21 8 12 29 P| iM 12 7 It 10 1987 16 20 20 8 14 30 Ul I 12 6 ll 11 coc TABLE 20.—Continued Previous smokers, not in last month Never smokers Sex Race Plans for higher education Sex Race Plans for higher education Year M F wW B Yes No M F WwW B Yes No 1975 38 36 24 28 1976 38 36 37 36 39 35 24 25 25 24 31 19 1977 39 35 37 49 41 35 24 25 25 26 30 19 1978 40 38 38 40 42 35 26 24 25 29 31 20 1979 42 38 39 4l 42 37 27 25 26 30 32 20 1980 43 39 40 45 44 37 30 28 29 30 34 23 1981 43 41 41 45 45 38 31 27 29 33 33 24 1982 4l 39 40 43 43 37 32 28 29 36 35 24 1983 41 40 40 45 43 38 3h 28 29 34 34 24 1984 4l 39 40 42 42 38 33 29 29 40 35 24 1985 39 39 38 42 41 36 33 30 30 39 36 24 1986 38 38 38 41 39 37 34 31 30 44 37 25 1987 38 38 38 41 39 35 35 31 30 45 37 25 SOURCE: Institute for Social Research, University of Michigan (See Table 19 for citations). solute difference (in percentage points) between the two groups remained constant be- tween 1976 and 1987. In 1987, the prevalence of daily smokers among those with plans for higher education was less than half the prevalence among those without such plans (14 percent versus 30 percent). The percentage of blacks who smoke on less than a daily basis exceeded the percent- age of whites in 1976 (13 and 10 percent, respectively) but was lower than the percent- age of whites in 1987 (6 and 12 percent, respectively). The percentage who have pre- viously smoked but not in the past month has consistently been slightly higher among blacks than among whites and among those with plans for higher education than among those without college plans. Besides these findings, there have been few differences between subgroups and few changes between 1976 and 1987 in the proportion of high school seniors who are in these categories. As mentioned above, the decrease in the proportion of high school seniors who smoke on a daily basis is reflected by a complementary increase in the proportion of high school seniors who have never smoked. This increase has been more marked among males compared with females and among blacks compared with whites. 1987 National Adolescent Student Health Survey The 1987 NASHS collected data on prevalence of smoking within the last 30 days (US DHHS, in press,b). Respondents to this survey Composed a random sample of the Nation’s students in 8th and 10th grades. Sixty-three percent of the 8th graders were 13 years old and 27 percent were 14 years old. Sixty-two percent of the 10th graders were 15 years old and 28 percent were 16 years old. For each grade, 68 percent were white, 17 percent were black, and 9 percent were Hispanic. Prevalence data are presented in Table 21. Eighty-four percent of the eighth graders reported that they had not even puffed on a cigarette in the last 30 days, with little dif- ference between the sexes. Forty-nine percent of all eighth graders reported never having smoked a cigarette, with no difference between the sexes. Among 10th graders, the proportion not having puffed on a cigarette in the last 30 days was slightly lower: 76 percent among males and 71 percent among females. Thirty-eight percent of males and 36 percent of females in this grade reported that they had never had a cigarette. TABLE 21.—30-day prevalence of smoking (%), United States, 1987, 8th and 10th grades 8th grade 10th grade Males Females Males Females Not even a puff 84.9 83.0 75.9 71.3 | cigarettes 7A 8.2 7.8 10.4 5—19 cigarettes 2.7 3.4 48 S.1 1-5 packs 2.4 3.5 5.6 74 More than 5 packs 2.9 19 6.0 5.8 SOURCE: National Adolescent Student Health Survey 1987 (US DHHS, in press, b). 306 Approximately equal proportions (7 to 8 percent) of males and females in the eighth grade reported smoking a pack or more in the last month. Among 10th graders, this proportion was more than twice as high, with 17 percent of males and 19 percent of females reporting that they smoked a pack or more in the last month. US DHEW Teenage Smoking Surveys, 1968-79 Detailed questions on smoking were asked in five national telephone surveys of adolescents (ages 12 to 18 years) conducted by Chilton Research Services for the U.S. Department of Health, Education, and Welfare from 1968 through 1979 (US DHEW 1979b). Adolescents were classified by smoking status as follows: never smokers, had not taken even a few puffs of a cigarette; experimental smokers, had had a few puffs but had not smoked as many as 100 cigarettes; ex-smokers, had smoked at least 100 cigarettes but no longer smoked; current occasional smokers, smoked less than one cigarette per week; and current regular smokers, smoked at least one cigarette per week. In published results for these surveys, data for never smokers and experimental smokers were generally aggregated. Summary data from each of the surveys are presented in Table 22 (males) and Table 23 (females). The proportion of both males and females of each age group who are classified as either never smokers or experimental smokers is substantially higher than the proportion of never smokers reported by other surveys. For example, the 1979 Teenage Smoking Survey showed that 75 percent of males and 82 percent of females aged 15 to 16 years had never smoked or had only experimented with cigarettes; in con- trast, the 1987 NASHS (above) showed that only 38 percent of males and 36 percent of females in the 10th grade (15 to 16 years old) had never had a cigarette. Similarly, the 1979 Teenage Smoking Survey showed that 68 percent of males and 64 percent of females aged 17 to 18 years were either never smokers or experimental smokers; in contrast, the 1979 High School Seniors Survey showed that 27 percent of males and 25 percent of females were never smokers. There are at least two possible explanations for the consistently and surprisingly high proportion of teenagers in the categories of never smokers and experimental smokers. First, 100 cigarettes may be too high a cutoff to use for classifying teenagers as never smokers or experimenters. Second, telephone interviewing may lead to more under- reporting of cigarette smoking behavior than other survey modalities. Underreporting may be more important for some smoking categories than others—for instance, oc- casional smokers might be particularly sensitive about their smoking behavior and might be more likely to underreport the total number of cigarettes they have ever smoked. Current smoking rates can also be compared between the Teenage Smoking Surveys and the High School Seniors Surveys. In the 1979 telephone survey, teenagers were classified on their reported smoking on a weekly basis. Of males aged 17 to 18 years, 19.3 percent were classified as current regular smokers (one or more cigarettes per week) and another 0.3 percent were classified as current occasional smokers (less than one cigarette per week). For females aged 17 to 18 years, these figures were 26.2 per- cent and 0.8 percent, respectively. In the High School Seniors Survey, students are 307 80€ TABLE 22.—Cigarette smoking among teenage males, United States, 1968-79 Age 12-14 years 15-16 years 17-18 years Total Smoking status Year N % N % N % N % Never smoked or 1968 876 93.1 465 75.2 344 54.7 1,685 770 experimented only 1970 S12 90.5 268 70.5 178 48.1 958 72.8 1972 533 91.1 273 68.3 211 54.4 1,017 74.1 1974 496 90.7 253 69.5 202 55.3 951 74.5 1979 $27 92.8 284 75.3 254 68.1 1,065 80.8 Former smoker 1968 25 2.7 34 5.5 71 11.3 130 5.9 1970 21 3.7 35 9.2 52 14.1 108 8.2 1972 20 3.4 50 12.5 56 14.4 126 9.2 1974 28 5.1 45 12.4 44 12.1 117 9.2 1979 23 40 38 10.1 46 12.3 107 8.1 Current occasional 1968 13 1.4 14 2.3 24 3.8 31 2.3 smoker 1970 1 0.2 3 0.8 2 0.5 6 0.5 1972 5 0.9 6 LS 4 1.0 1) Ll 1974 0 0.0 0 0.0 6 1.6 0.5 1979 0 0.0 4 1.1 1 0.3 0.4 60£ TABLE 22.—Continued Age 12-14 years 15-16 years 17-18 years Total Smoking status Year N % N % N % N % Current regular 1968 27 2.9 105 17.0 190 30.2 322 14.7 smoker 1970 32 5.7 74 19.5 138 37.3 244 18.5 1972 27 4.6 71 17.8 117 30.2 215 15.7 1974 23 4.2 66 18.1 113 31.0 202 15.8 1979 18 3.2 51 13.5 72 19.3 141 10.7 Total 1968 941 100 618 100 629 100 2,188 100 1970 566 100 380 100 370 100 1,316 100 1972 585 100 400 100 388 100 1,373 100 1974 547 100 364 100 365 100 1,276 100 1979 568 100 377 100 373 100 1,318 100 SOURCE: US DHEW Teenage Smoking Surveys, 1968, 1970, 1972, 1974, 1979 (US DHEW 1979b). Ole TABLE 23.—Cigarette smoking among teenage females, United States, 1968-79 Age 12-14 years 15-16 years 17-18 years Total Smoking status Year N % N % N % N % Never smoked or 1968 919 97.9 552 84.4 462 73.0 1,933 86.8 experimented only 1970 536 95.0 312 81.5 264 70.0 1,112 84.0 1972 569 95.3 312 77.0 277 66.7 1,158 81.7 1974 495 90.2 250 69.3 228 62.1 973 76.2 1979 $14 92.3 319 81.8 239 63.9 1,072 81.2 Former smoker 1968 7 0.7 25 3.8 38 6.0 70 3.1 1970 8 1.4 15 3.9 22 5.8 45 3.4 1972 1 1.8 26 6.4 30 7.2 67 47 1974 26 4.7 33 9.1 42 11.4 101 7.9 1979 19 3.4 23 5.9 34 9.1 76 5.8 Current occasional 1968 7 0.7 14 2.1 15 2.4 36 1.6 smoker 1970 3 0.5 I 0.3 5 13 9 0.7 1972 0 0.0 0.2 3 0.7 4 0.3 1974 1 0.2 1.4 2 0.5 8 0.6 1979 0 0.0 0.5 3 0.8 5 0.4 Il¢ TABLE 23.—Continued Age 12-14 years 15-16 years 17-18 years Total Smoking status Year N % N % N % N % Current regular 1968 6 0.6 63 9.6 118 18.6 187 8.4 smoker 1970 17 3.0 55 14.4 86 22.8 158 11.9 1972 17 2.8 66 16.3 105 25.3 188 13.3 1974 27 49 73 20.2 95 25.9 195 15.3 1979 24 43 46 11.8 98 26.2 168 12.7 Total 1968 939 100 654 100 633 100 2,226 100 1970 564 100 383 100 377 100 1,324 100 1972 597 100 405 100 415 100 1,417 100 1974 549 100 361 100 367 100 1,277 100 1979 557 100 390 100 374 100 1,321 100 SOURCE: US DHEW Teenage Smoking Surveys, 1968, 1970, 1972, 1974, 1979 (US DHEW 1979b). classified based on their reported smoking during the past 30 days. In the 1979 High School Seniors Survey (Table 22), 22 percent of males were classified as daily smokers and another 9 percent reported having smoked in the last month but not on a daily basis. In the same year, 29 percent of females were daily smokers and 9 percent smoked on less than a daily basis. Comparing these two data sets shows that the telephone survey obtained lower es- timates for weekly smoking than the school survey obtained for daily smoking (19 vs. 22 percent for males, 26 vs. 28 percent for females). The remaining current smokers (defined as less than one cigarette per week in the telephone survey and less than one per day in the school survey) were also estimated at lower rates in the telephone sur- vey (0.3 vs. 9 percent for males, 0.8 vs. 9 percent for females). This suggests that the telephone survey underestimated both the number of daily smokers and the number of less-than-daily smokers. Most of the discrepancy appears to be due to a failure to iden- tify the latter. It is unclear whether this difference is related to the system of classifying smokers or the telephone survey methodology. NIDA National Household Surveys on Drug Abuse, 1979-85 NIDA conducted household surveys on drug abuse in 1979, 1982, and 1985. For each of these surveys, data were obtained from a stratified random sample of 8,000 U.S. households; approximately 2,000 in-person interviews were conducted with respon- dents in the 12- to 17-year-old age group. Questions included whether any cigarettes were smoked within 30 days as well as within the previous year. These surveys indi- cated that approximately 26 percent of the teenage population surveyed smoked at least one cigarette at some time during 1985 (Table 24). In 1985, 15.6 percent of this popula- tion had smoked within the previous month. Comparisons between data from the 1979 household survey and data from the more recent surveys are not appropriate, because in 1979 prevalence of use within the past year or past month was reported only for those who had smoked 100 cigarettes in their lifetime; this lifetime cutoff was not used in the later surveys. , TABLE 24.—Prevalence (%) of cigarette use among youth 12 to 17 years of age, 1979, 1982, and 1985, United States Any use in Used in last Survey year last year 30 days 1979* : 13.3 12.1 1982 24.8 14.7 1985 : 26.0 15.6 *The 1979 estimates are not necessarily comparable to later estimates because the 1979 survey asked questions only of those who had smoked 100 cigarettes in their lifetime. SOURCE: NIDA National Household Surveys on Drug Abuse 1979, 1982, 1985 (US DHHS 1988). 312 Summary Several national surveys provide information on adolescent smoking. These surveys vary substantially in sample size, methodology, definitions of smoking, ages of respon- dents, and other factors that may appreciably affect prevalence estimates. The best trend data are available from the annual high school seniors survey. This survey shows that prevalence of daily cigarette consumption declined from 29 percent of seniors in 1976 to 21 percent in 1980, after which prevalence leveled off at 18 to 21 percent. Smoking prevalence among females has consistently exceeded that among males since 1977. The leveling off of smoking prevalence among high school seniors raises concern that the steadily declining initiation rates as determined by prevalence among adults aged 20 to 24 (NHIS) may soon level off as well. Smoking prevalence has been consistently lower for high school seniors with plans to pursue higher education than for those without such plans. In 1987, smoking rates were 14 and 30 percent in these two groups, respectively. Differences in prevalence of smoking and smokeless tobacco use (see below) be- tween young males and young females suggest that the prevalence of any tobacco use is similar in these two groups. Whereas the prevalence of smoking is higher among female high school seniors than among males, the prevalence of smokeless tobacco use is higher among young males than among young females. Changes in the Types of Cigarettes Smoked Data on the market share of filter and nonfilter cigarettes, cigarettes of different machine-determined “tar” and nicotine yields, menthol and nonmenthol cigarettes, and cigarettes of different length have been published by the Federal Trade Commission (FTC) from information supplied to the agency by the major cigarette companies. Filtered Cigarettes Filters are the design characteristic of commercial cigarettes that most affects their machine-measured yield of harmful constituents (US DHHS 1981). Filters selectively remove nitrosamines and semivolatile phenols from smoke. Thus, filters affect not only the absolute amounts of these constituents delivered in smoke but also their relative concentrations in cigarette “tar. ” Since the early 1950s, the proportion of cigarettes in the United States sold as filtered cigarettes has increased steadily. In 1950, less than 1 percent of cigarettes sold in the United States were filtered. That proportion rose to 19 percent in 1955, 51 percent in 1960, and 94 percent in 1986 (Table 25). Low-Tar, Low-Nicotine Cigarettes Trends in the sales-weighted average yield of tar and nicotine for cigarettes sold in the United States are shown in Figure 14 of Chapter 2. The sales-weighted average is based on the tar and nicotine yield of specific brands (as measured by the FTC machine- 313 TABLE 25.—Domestic market share of filter cigarettes as a proportion of total cigarettes sold, United States, 1950-86 Year Market share (%) Year Market share (%) 1950 0.6 1969 77 _ 1951 0.7 1970 80 1952 1 1971 82 1953 3 1972 84 1954 9 1973 85 1955 19 1974 86 1956 28 1975 87 1957 38 1976 88 1958 45 1977 90 1959 49 1978 90 1960 51 1979 91 1961 52 1980 92 1962 55 1981 92 1963 58 1982 93 1964 61 1983 93 1965 64 1984 93 1966 68 1985 94 1967 72 1986 94 1968 74 SOURCE: FTC (1988). testing method) multiplied by the quantity of sales for those brands. The sales-weighted average yield of tar fell from 35 mg in 1957 to 13 mg in 1987. For nicotine, the sales- weighted average fell from 1.3 mg in 1968 to 1.0 mg in 1985. However, the sales- weighted average yield of tar and nicotine leveled off between 1981 and 1987. As pointed out in Chapter 2, modifications in the makeup of commercial cigarettes have profoundly influenced these yields; for example, the steepest declines occurred in the late 1950s after introduction of filter tips. Trends in the percentage of domestic sales of cigarettes yielding lower tar levels are shown in Table 26. The domestic market share of cigarettes yielding 15 mg or less tar increased from 2.0 percent in 1967 to 56.0 percent in 1981. Since 1981, this propor- tion has fallen slightly and has stabilized at 51 to 53 percent. About two-thirds of these cigarettes have tar yields between 9 and 15 mg. It should be noted that the parameters used in the FTC machine-testing method (developed in the 1960s) do not necessarily reflect current smoking patterns. For ex- ample, the FTC methad uses one puff per minute (Pillsbury et al. 1969), whereas human 314 TABLE 26.—Domestic market share of cigarettes with reduced tar, percentage of total cigarettes sold, United States, 1967-86 Tar Yield Year <15 mg S12 mg <9 mg <6 mg <3 mg 1967 2.0 1968 2.5 1969 3.0 1970 3.6 1971 3.8 1972 6.6 1973 8.9 1974 8.9 1975 13.5 1976 15.9 1977 22.7 1978 27.5 1979 40.9 10.6 5.8 2.7 1980 44.8 16.8 73 3.3 1981 56.0 24.6 9.6 3.7 1982 $2.2 43.8 27.8 8.9 2.9 1983 53.1 44.9 27.9 9.4 3.1 1984 51.0 43.4 26.3 9.4 2.9 1985 51.9 43.1 25.3 8.4 2.3 1986 52.6 44.5 22.3 9.9 2.6 SOURCE: FTC (1988); Kozlowski (1989). studies of smoking patterns show an average interpuff interval of 34 seconds (that is, about two puffs per minute) (US DHHS 1988, Chapter 4, Table 2). According to the 1986 AUTS, 41 percent of smokers smoke cigarettes yielding 15 mg or less tar (Table 27). The proportion of smokers smoking cigarettes yielding more than 15 mg tar is higher among males, blacks, and persons with less ‘education com- pared with females, whites, and more educated persons, respectively. This proportion decreases with age; the higher proportion among those 17 to 19 years of age probably reflects the popularity of the higher tar Marlboro brand among adolescents (Hunter et al. 1986; Goldstein et al. 1987; Glantz 1985). Increased consumer demand for lower yield cigarettes during the past two decades is probably attributed to consumer beliefs that lower yield brands are less hazardous. This impression may have resulted in part from cigarette advertising implying that low- yield brands are less hazardous or are safe (Davis 1987). According to the 1986 AUTS, 45 percent of current smokers believe that some kinds of cigarettes are probably more hazardous than others (see Chapter 4). 315 TABLE 27.—Percentage of current smokers, aged 17 years and older, who use cigarettes of varying tar yields and who use menthol cigarettes, by sex, race, and education, 1986 Percentage of current smokers Tar yield (mg/cigarette) Menthol a cigarette s10 >10~-15 >15 : Total smokers Total 29.6 11.6 58.8 100 29.2 Sex Males 26.8 8.0 65.2 100 29.9 Females 32.7 15.6 $1.7 100 34.0 Age 17-19 31.7 2.7 65.6 100 29.3 20-24 30.4 49 64.8 100 24.1 25-44 31.5 8.8 59.7 100 34.4 45-64 26.3 17.8 55.9 100 23.7 265 26.3 22.6 $1.1 100 21.1 Race White 31.8 12.3 55.9 100 23.1 Black 14.5 7.6 78.0 100 75.5 Other 26.2 5.3 68.5 100 24.9 Education S11 years 23.5 11.6 64.8 100 27.6 12 years 29.4 11.9 358.7 100 29.7 13-15 years 36.8 9.7 53.5 100 32.0 216 years 36.4 13.2 50.4 100 27.1 SOURCE: Self-reported data on cigarette brand use, AUTS 1986 (US DHHS, in press, a). Sample sizes for each Stratum are shown in Table 34. The 1981 Surgeon General’s Report (US DHHS 1981) concluded that although smoking lower yield cigarettes appears to reduce the risk of lung cancer, the benefits are minimal compared with giving up cigarettes entirely. Moreover, there is no defini- tive evidence that smoking lower yield cigarettes is associated with reduced risks of other cancers, cardiovascular disease, and fetal damage. Switching to low-yield brands may even increase the health risk for smokers who compensate for reduced nicotine in- take by increasing the number of cigarettes smoked per day, the frequency of puffing, and the depth and duration of inhalation (US DHHS 1988). 316 The leveling off of sales-weighted tar and nicotine yields may be related to one or a combination of the following factors (US DHHS 1988): (1) a persistent brand loyalty of some smokers to moderate- or high-yield brands because of brand image; (2) a diminishing perception that low-yield brands are less hazardous (see Chapter 4); and (3) atendency of some smokers to smoke cigarettes of such low tar and nicotine yields that further reductions in those yields may be unacceptable; that is, the “lower bound- ary” of comfortable cigarette use has been reached (Kozlowski 1987, 1989). Menthol Cigarettes From 1963~76, the domestic market share of menthol cigarettes increased gradually from 16 percent to 28 percent. Since 1976, this proportion has remained at 28 percent (FTC 1988). According to the 1986 AUTS, 29 percent of current smokers smoke men- thol cigarettes. Seventy-six percent of black smokers smoke menthol cigarettes com- pared with 23 percent of whites (Table 27). Similar findings were reported by Cum- mings and colleagues (1987). Menthol in cigarettes provides a sensation of cooling, which may promote deeper, prolonged inhalation of cigarette smoke. This may help to explain why blacks (who are much more likely to smoke menthol cigarettes) have higher mortality rates from certain smoking-related diseases (e.g., lung cancer, heart disease, and cerebrovascular disease) than whites despite smoking fewer cigarettes per day (Novotny, Warner et al. 1988). Increased lung cancer mortality rates among blacks may also relate to increased occupational or environmental exposures among blacks that promote the carcinogenic effects of smoking, or to the fact that blacks are more likely to smoke higher tar brands (Table 27), which are associated with higher lung cancer mortality rates (US DHHS 1981). There does not appear to be a positive correlation between the presence of men- thol and higher tar yields in cigarette brands: in the FTC’s 1985 list of 207 brands (FTC 1985), 67 percent (51/76) of menthol brands had tar yields of less than 13 mg, com- pared with 56 percent (73/131) of nonmenthol brands. Cigarette Length From 1967-86, the domestic market share of cigarettes 68 to 88 mm in length decreased from 91 percent to 60 percent. During the same time, the domestic market share of cigarettes 94 to 101 mm in length increased from 9 to 37 percent (Table 28). Because of the dose-response relationship between smoking and risk of disease (see Chapter 2), this increase in the average length of cigarettes has potentially important public health implications. However, smokers tend to compensate for changes in cigarette length by changing the number of cigarettes smoked per day, puffing frequen- cy, and other measures of smoking behavior so as to minimize the change in overall nicotine intake (US DHHS 1988). 317 TABLE 28.—Domestic market share of cigarettes (%), by cigarette length, percentage of total cigarettes sold, United States, 1967-86 Year 68-72 mm 79-88 mm 94-101 mm 110-121 mm 1967 i4 77 9 1968 12 74 13 1969 I 74 16 1970 9 73 18 1971 8 72 20 1972 8 71 21 1973 7 71 22 1974 6 7] 23" 1975 6 69 24 1 1976 5 69 24 2 1977 5 67 26 2 1978 5 65 27 2 1979 4 65 30 2 1980 3 63 32 2 1981 3 62 33 2 1982 3 61 34 2 1983 3 60 34 2 1984 3 59 36 2 1985 3 58 37 2 1986 2 58 37 3 NOTE: Because of rounding, the total of the individual percentages may not equal 100 percent in some instances. “The 110- to 12t-mm length was combined with the 94- to 10]-mm length. SOURCE: FTC (1988). Summary and Comment During the past 40 years, filtered cigarettes have virtually replaced nonfiltered cigarettes in the United States. The domestic market shares of lower (15 mg or less) tar cigarettes and menthol cigarettes have increased during the past two decades but have leveled off in recent years. The domestic market share of longer (94-101 mm) cigarettes has increased substantially since the mid-1960s and still appears to be rising slowly. Continued health concerns among smokers are likely to encourage the cigarette in- dustry to continue to design new cigarettes that are perceived as less hazardous. Be- sides filtered, low-yield cigarettes, other “high-tech” cigarettes have been marketed that may appear to smokers to be less hazardous. These include one brand with a recessed filter and another with a “flavor-control filter” that apparently aliows the smoker to regulate the tar yield of individual cigarettes (Davis 1987). The R.J. Reynolds Tobac- co Company announced in September 1987 plans to market a new product that heats rather than burns tobacco. R.J. Reynolds asserts that the product is a cigarette, and it 318 has commonly been referred to in the press as a “smokeless cigarette.” In a press release, the company’s chief executive officer stated that “a majority of the compounds produced by burning tobacco are eliminated or greatly reduced, including most com- pounds that are often associated with the smoking and health controversy” (R.J. Reynolds 1987). The American Medical Association (1988) and the Coalition on Smoking OR Health (1988) have filed petitions with the U.S. Food and Drug Ad- ministration (FDA) seeking FDA regulation of this new product as a drug or medical device based on implicit health claims, among other reasons. As of November 1988, these petitions were under review by the FDA. In October 1988, R.J. Reynolds began test marketing the product, named Premier, in three cities (Phoenix and Tucson, AZ, and St. Louis, MO). (See Chapter 7.) Other Types of Tobacco Use Smokeless Tobacco Use Smokeless tobacco (ST) use, including snuff and chewing tobacco, became a subject of concern in the United States during the 1980s (US DHHS 1986). Cross-sectional national surveys and various regional surveys have identified several demographic categories at high risk for the use of these products, including young white males, per- sons living in the Southern and North Central United States, American Indians, and Alaskan Natives (Rouse, in press; Boyd et al. 1987; CDC 1987c, 1988; Schinke et al. 1986). Trend data on ST use are available primarily through the AUTSs, which included persons aged 21 years or older in 1964, 1966, 1970, and 1975 (US DHEW 1969, 1973a, 1976), and persons aged 17 years and older in 1986 (Novotny, Pierce et al., in press). In addition, the 1970 and 1987 NHISs included data on ST use among persons aged 17 years and older and aged 18 years and older, respectively. The Behavioral Risk Factor Surveillance System of the Centers for Disease Control collected State-specific data on ST use among persons aged 18 years and older beginning in 1986 (CDC 1987d). The 1985 CPS of the U.S. Bureau of the Census included questions about ST use among persons aged 17 years and older (Marcus et al., in press). This survey also produced State-specific estimates for prevalence of use of these products. Definitions of ST use and questions asked about ST use in these surveys are listed in the Appendix to this Chapter. Figure 5 compares age-specific data for men from the 1970 NHIS and the 1986 AUTS. Between 1970 and 1986, snuff use increased fifteenfold and chewing tobacco use more than fourfold among males aged 17 to 19 years. Smailer increases were ob- served among the middle-aged groups, and a decrease in the use of both products was noted for older men (age 50 and above). The NHIS used household interviews, and the AUTS used telephone interviews as their primary mode of data collection; however, this difference in methodology is unlikely to account for the substantial increase in ST use among teenage males. Data on ST use among persons aged 21 years or older are presented below from the 1964-86 AUTSs. These surveys were based on in-person interviews in 1964 and 1966 and telephone interviews in 1970, 1975, and 1986. State-specific data from the 1985 319 1970 CT] Chewing tobacco 6.5 Percentage Percentage w l 1 — 20-29 30-39 40-49 2 50 Age FIGURE 5.—Prevalence of chewing tobacco and snuff use among men, 1970 (NHIS) and 1986 (AUTS) SOURCE: US DHHS (1986a); Novotny, Pierce et al. , in press. CPS are reported. Finally, data from a more detailed analysis of ST use from the 1986 AUTS for men aged 17 years and older (Novotny, Pierceet al., in press) are described. The prevalence of current ST use from 1964-86 among persons aged 21 years and older, stratified by product and sex, is shown in Figure 6. For both products, there has been a steady overall decline in use by both men and women. It is possible that this decline is due in part to the change in the AUTS interview technique from in-person 320 Prevalence (%) 1 27374 75 76 77 78 79 80 81 82 83 84 85 86 Year L i Oo i. 1 64 65 66 67 68 69 70 71 7 j —— Snuff, Men ~*~ Chew, Men ~-* Snuff, Women —= Chew, Women FIGURE 6.—Smokeless tobacco use among adults 21 years of age and older, United States, 1964-86 SOURCE: AUTSs (Novotny, Pierce et al., in press). interview (1964 and 1966) to telephone interview (1970, 1975, 1986); telephone sur- veys generally provide slightly lower smoking prevalence estimates than in-person sur- veys (see above). The prevalence of ST use among women has consistently been very low. However, the use of snuff by older black women in the South is much more com- mon than among women in the general population (Rouse, in press). In 1986, the weighted prevalence of snuff use was 2.2 percent for men and 0.5 per- cent for women, and of chewing tobacco use, 3.1 percent for men and 0.1 percent for women among adults aged 21 years and older. For 1986, overall prevalence of ever and current use of ST among males, aged 17 years and older, is shown in Table 29. More than 10 percent of male respondents had ever used ST products; chewing tobac- TABLE 29.—Prevalence (%) of ever use and current use of smokeless tobacco, males aged 17 years and older, United States, 1986 Product used Ever use Current use Any smokeless tobacco 12.6 5.2 Snuff* 5.8 2.4 Chewing tobacco” 9.9 3.3 Both 34 0.5 "Includes those who also use chewing tobacco. includes those who also use snuff. SOURCE: AUTS 1986 (Novotny, Pierce et al. , in press). 321 co appears to be used slightly more commonly than snuff. Few men (0.5 percent) use both products. The prevalence of ever use and current use of any ST product by males, stratified by selected sociodemographic variables, is shown in Table 30. The prevalence of both current and ever use was highest among younger men, whites, men living in the Southeast, less educated men, men below the poverty level, unemployed men, and lower income men. Among males 17 to 19 years of age, 8.2 percent were current ST users. In a multivariate model using the sociodemographic variables as predictors of ST use (Table 31), white men were more than twice as likely to use ST as black men; men employed in blue-collar or service/laborer jobs or who were unemployed were 3 times more likely to use ST than white-collar workers; and men in the Southeast and West were more likely to use ST than men in other regions. Two-thirds of men who ever used ST began use before age 21; more than one-third began before age 16 (Table 32). The median age of initiation of ST use for both snuff and chewing tobacco is 19 years (Novotny, Pierce et al., in press). The State- and region-specific prevalence of current snuff and chewing tobacco use among men aged 16 years and older is shown in Table 33. These data are from the 1985 CPS. As mentioned earlier, 45 percent of interviews in the CPS were with proxy respondents. Proxy responses are known to affect the accuracy of information on smok- ing behavior, especially daily cigarette consumption (see above). The effect of proxy responses on data relating to ST use is unknown. Overall prevalence for males in the 1985 CPS was 1.9 percent for snuff and 3.9 per- cent for chewing tobacco. Use of ST was lowest in the Northeast and highest in the South, with intermediate values reported for the North Central and Western regions. Among women, the overall prevalence of snuff use was only 0.5 percent, with all regions having prevalence rates of 0.5 percent or less except the South (1.4 percent). Prevalence of chewing tobacco use among women was 0.2 percent overall. In summary, ST use is increasing among adolescent males and is decreasing slight- ly overall among men aged 21 years and older in the United States. It continues to be arare behavior among women. According to national surveys, sociodemographic cor- relates of use include blue-collar and service/laborer employment, unemployment, and residence in the South. Local surveys have also shown high usage rates among American Indian youth (CDC 1987c, 1988; Schinke et al. 1987; Hall and Dexter 1988). Because ST use is more common among young males than among young femaies, while the prevalence of smoking among high school seniors is higher among females than among males (see above), the prevalence of any tobacco use may be similar among young males and young females. Cigar and Pipe Smoking Table 34 presents data from the 1986 AUTS for cigar and pipe smoking. Cigar and/or pipe smoking mainly occurs among men, in whom prevalence of use is 8.7 percent. The highest proportion of users are between the ages of 45 and 64 years. Usage is slight- ly higher in the most and least educated groups than in the intermediate education categories. 322 TABLE 30.—Prevalence (%) of smokeless tobacco use by sociodemographic categories, males aged 17 years and older, United States, 1986 Category Ever use Current use Age group 17-19 12.3 8.2 20-29 11.4 5.9 30-39 73 4] 40-49 9.7 5.0 250 11.5 4.8 Race White W1 5.6 Black 6.6 3.0 Other 77 2.9 Geographic area Southeast 14.5 75 West 9.6 45 Midwest 9.5 43 Northeast 5.5 3.0 Completed years of school sll 14.6 73 12 11.1 5.6 13-15 9.1 3.8 216 48 2.9 Poverty level Below 16.1 8.5 Above 9.9 49 Employment Unemployed 13.0 8.3 Service/laborer 12.3 6.4 Blue collar 7.0 3.6 White collar 2.3 ‘1.0 Household income (dollars per year) <10,000 16.1 8.6 10,000-29,999 4.7 2.2 230,000 3.0 1.6 SOURCE: AUTS 1986 (Novotny, Pierce et al., in press). 323 TABLE 31.—Significant sociodemographic correlates of current use of any smokeless tobacco, males aged 17 years and older, United States, 1986 Parameter Odds ratio 95% confidence limits Region Southeast 3.0 1.8, 4.8 West 19 1.1, 3.3 Midwest 14 0.8, 2.5 Northeast Referent Race White 2.4 1.3,4.3 Black Referent Employment Unemployed 3.8 1.9, 7.6 Service/laborer 2.9 1.8, 4.6 Blue collar 3.0 2.1,4.3 White collar Referent SOURCE: AUTS 1986 (Novotny, Pierce et al., in press). TABLE 32.—Reported age of initiation and median age of initiation of smokeless tobacco use among ever users, males aged 17 years and older, United States, 1986 Age group at initiation (percentage reporting) Product SOURCE: US DHHS (1988, pp. 194, 250-253). other effect. Prolonged use also leads to physical dependence, as indexed by various psychological and physical withdrawal symptoms following cessation of smoking. The inclusion of tobacco dependence as a disorder in the Diagnostic and Statistical Manual of Mental Disorders III, the official diagnostic reference for the American Psychiatric Association (1980), was another major marker in the shift of scientific opinion about the addictive nature of cigarette smoking. Central to the 1964 view was the distinction between compulsive use (addiction) and the less compulsive “desire” (habituation). The difference was noted to rest primarily on the source of the desire or compulsion. The 1964 Report emphasized “serious per- sonality defects from underlying psychologic or psychiatric disorders” (US PHS 1964, p. 351) as a defining factor in compulsive use and therefore in addiction. Evidence gathered since the early 1960s contradicts the assumptions that underlying pathology drives the compulsive use seen in addiction. Drugs commonly viewed as addictive, e.g., heroin, may be abandoned with little apparent effort as with many Vietnam veterans addicted to heroin who gave it up after their return to the United States (Robins, Helzer, Davis 1975: US DHHS 1988). On the other hand, the extent to which smok- ing can be highly compulsive is suggested by its continuance in the face of substantial awareness of its harm, as by cardiac patients (Baile et al. 1982; Burling et al. 1984: Ockene et al. 1985; US DHHS 1984). The generality of nicotine’s effects argues against its compulsive use resting on individual psychopathology; the basis for nicotine addic- tion rests on the interaction of conditioning processes and nicotine action in the brain. Mechanisms of Nicotine Action Much research in the 1970s on the behavioral effects of nicotine has been guided by the nicotine regulation (or titration) model put forth over the years by Jarvik (1977), Jarvik, Glick, and Nakamura (1970), Russell (1976), and Schachter, Silverstein and col- leagues (1977). According to this model, smokers regulate their smoking to maintain a certain level of blood nicotine within a range of upper and lower limits (Herman and Kozlowski 1979; Kozlowski and Herman 1984). This includes the avoidance of withdrawal symptoms or anticipated withdrawal by maintaining a nicotine level above a lower limit and avoidance of toxicity by maintaining it below an upper limit. This formulation has been criticized as failing to explain the self-perceived Positive effects or benefits of smoking that may promote use (Pomerleau and Pomerleau 1984: Leventhal and Cleary 1980). Interestingly, the 1964 Surgeon General’s Report devoted only | 1/2 pages to such effects. In the last few years, several investigators (e.g., Ock- ene et al. 1988; Pomerleau and Pomerleau 1984) have proposed that smoking, by vir- tue of the varied actions of nicotine, provides several positively perceived effects and is employed by many smokers as a responsive and effective coping strategy. This im- plies that smokers can be reinforced for continued smoking without maintaining a min- imum blood nicotine level. The 1988 Report devoted an entire chapter to this topic. An influential and historically important model of perceived positive effects of smok- ing stressed the psychological effects of nicotine and other pharmacologic aspects of smoking (Pomerieau and Pomerleau 1984). This model holds that nicotine increases the release of anumber of neuroregulatory hormones, conferring on smoking the ability 342 to act as stimulant or sedative depending on level of ingestion, background hormone levels, and the like. Nicotine thus can serve to reduce anxiety or produce euphoria (US DHHS 1988) and enhance vigilance for certain cognitive tasks (e.g., Warburton et al. 1986). The work of Grunberg (1986; US DHHS 1988) also suggests that nicotine may aid smokers in maintaining lower body weight. Although objective judgment indicates that the health effects of smoking are more important than the weight maintenance ef- fects (Abrams et al. 1987), the latter seem to be of particular importance to some women (Klesges and Klesges, in press, US DHHS 1988). This growing recognition that smokers may value several effects of cigarettes can be used not so much to justify the behavior but rather to direct intervention strategies (e.g., physical activity) that might help people meet needs previously served by cigarettes. Interventions also are likely to be seen as more credible to smokers if the coping value of cigarettes is recognized (Ockene et al. 1988). Conditioning and Smoking What most distinguishes recent analyses of the conditioning of smoking from earlier views (e.g., Hunt 1970) is their emphasis on the conditioning of the biological effects of nicotine. The occurrence of stimuli previously associated with the effects of nicotine will tend to evoke responses related to those effects or cues for further consumption (e.g., Abrams et al., in press; Herman 1974; Niaura et al. 1988; Rickard-Figueroa and Zeichner 1985). Such conditioned effects may link smoking to aversive states al- leviated by nicotine. For example, investigations described earlier (e.g., Schachter, Sil- verstein et al. 1977) suggested that smoking covaries with stress, which is hypothesized to deplete nicotine. Leventhal and Cleary (1980) suggested that stress as well as other emotions may be alleviated by nicotine and would then come to serve as cues for smok- ing. Pomerleau and Pomerleau (1984, 1987) identified neurohumoral effects of nicotine as the paths of its impact and elaborated on the ways such effects might be con- ditioned to circumstances surrounding smoking so as to regulate it in the future. Two influential theories of addiction emphasize the role of relief of withdrawal or anticipated withdrawal in smoking. As suggested by Wikler’s classic work with opioids (Wikler 1973; Wikler and Pescor 1967), withdrawal symptoms may be conditioned to the circumstances in which they occur. This would set the stage for stimuli associated with prior drug taking to elicit withdrawal symptoms and urges. With smoking, greater withdrawal symptoms have been noted when cessation occurs in natural rather than ar- tificial environments, presumably because those natural environments contain numerous cues associated with prior smoking (Hatsukami, Hughes, Pickens 1985). Within this model, return to smoking after brief or extended abstinence is reinforced by the reduction in such conditioned withdrawal symptoms. Opponent-process theory (Solomon and Corbit 1973) suggests that the reduction of aversive withdrawal symptoms may be the result of the interaction of the immediate response to a drug, called the “A” state, and the delayed response, the “B” state. The B state is “opposed” to or opposite the A—hence “opponent process”; if the A is pleasurable, the B will be aversive. Initially, the A state is stronger. While initial, pleasurable responses to nicotine may encourage increased smoking, regular smoking 343 leads the aversive B state to become stronger, which in tum may be reduced or avoided by the A-state consequences of further smoking. After regular smoking has been es- tablished, the A state serves only to avoid or reduce the aversive B state. That is, regular smoking is pursued to reduce displeasure rather than to bring about the pleasure that may have been its initial appeal. It is important to note that there is little evidence on the validity of the Wikler theory or Opponent-process theory as applied to smoking. In contrast to models emphasizing relief of withdrawal, a recent review (Niaura et al. 1988) proposes an “‘appetitive” model of responses to cues associated with smoking. Evidence indicates that cues surrounding smoking are more strongly conditioned to its positively perceived effects than to withdrawal symptoms. That is, cues associated with intake of nicotine (e.g., holding a cigarette or inhaling) come to elicit conditioned responses similar to the effects of nicotine (e.g., relaxation, heightened arousal). These effects are strong reinforcers and encourage continued efforts to obtain or ingest the drug. These reinforcing effects may be more critical than the reduction of withdrawal symptoms after periods of abstinence. Critical to understanding the appetitive model is the idea that negative emotions are not necessarily withdrawal symptoms. However, negative emotions previously al- leviated by nicotine may serve as cues for seeking repetition of smoking’s reinforcing effects (Stewart, DeWit, Eikelboom 1984). For example, social anxiety may be the oc- casion for smoking, which is then reinforced by nicotine’s ability to reduce anxiety. The anxiety, however, is a response toa stressful situation, nota symptom of withdrawal from cigarettes. Smoking is reinforced by the anxiety reduction, not by reduction of withdrawal symptoms. The many ways smoking is conditioned to circumstances around it may explain “the thorough interweaving of the smoking habit in the fabric of daily life” (Pomerleau and Pomerleau 1987, p. 119). The sheer repetition of smoking also strengthens such inter- weaving. It is estimated that the average pack-a-day smoker of 20 years’ duration has inhaled cigarette smoke over 1 million times (Fisher and Rost 1986; Pomerleau and Pomerleau 1984), each inhalation providing an opportunity for conditioning smoking to numerous circumstances of daily life. Moreover, with years of smoking, the emo- tional states and daily circumstances conditioned to it may continue to increase, result- ing in urges to smoke being conditioned to almost every circumstance encountered and complicating the task of maintaining abstinence. Cognition and Decisionmaking Cognitive and decisionmaking processes play a lesser role in the maintenance of regular smoking relative to the other factors discussed here. Smokers have long believed that they derive positive effects from smoking. The “pros” of smoking have been embodied in the instruments used in decisionmaking studies (Mausner and Platt 1971; Velicer et al. 1985) and in the Horn and Waingrow (1966) Reasons-for-Smok- ing Scale. As documented in Chapter 4 of this Report, public knowledge of the health conse- quences of smoking has increased steadily over the past 25 years. Eighty-seven per- cent of current smokers now report that they understand that smoking is harmful to their 344 health (ALA 1985) and two-thirds of high school seniors report “great risk” being as- sociated with pack-a-day smoking (Johnston, O’Malley, Bachman 1987). Why, then, do so many persist in regular smoking? One reason may be that they do not appreciate just how dangerous smoking is. For example, 75 percent of current smokers agreed that smoking is a cause of lung cancer (ALA 1985), while 94 percent of nonsmokers and 90 percent of former smokers agreed to this. For emphysema, the parallel figures were 75 percent of current smokers compared with 91 percent and 90 percent of former smokers and nonsmokers, respectively (ALA 1985). Surveys indicate a general insen- sitivity to the relative level of risk associated with smoking. Health professionals rated nonsmoking as the first priority among things Americans can do to protect their health. The public rated nonsmoking as 10th, behind such worthy but, for most Americans, less critical behaviors as consuming adequate vitamins and minerals and drinking water of acceptable quality (Fisher and Rost 1986). As discussed below, the health belief model (Rosenstock 1974) requires that smokers believe they are personally vulnerable to a threat before they will be motivated to attempt change. It has been suggested that personalized acceptance (“Cigarette smoking is dangerous to my health”) always lags behind general acceptance (“Cigarette smoking is dangerous to health”) (Fishbein 1977; Lichtenstein and Bernstein 1980; Shiffman 1987) (See Chapter 4). These con- siderations suggest that many smokers still find it possible to discount the riskiness of their behavior. Another possible reason for some smokers’ insensitivity to smoking risks is that they have not always been given the full message, or they have been given mixed messages, including prosmoking messages (advertising) from the cigarette industry. Factors that impede public awareness and acceptance of the health hazards of smoking include cigarette advertising and promotion and cigarette companies’ public relations and lob- bying activities, which are also reviewed in Chapters 6 and 7. Other issues related to persistence of smoking will be covered in the Section on Quit- ting and Relapse. Personal Characteristics and Social Context Personal Characteristics The 1964 Surgeon General’s Report linked smoking in adulthood and adolescence to extraversion, or as it defined it, a tendency “to live faster and more intensely” (US PHS 1964, p. 366), and this relationship has been confirmed in later studies (e.g., Ash- ton and Stepney 1982). However, reviews indicate that there is no consistent evidence relating smoking to neuroticism or emotional instability (Smith 1970; US DHEW 1979a). More recent studies have continued to find relationships with smoking and be- haviors linked to extraversion: coffee and alcohol consumption (Istvan and Mataraz- zo 1984); circadian phase differences, being an “evening type” as opposed to a “mormn- ing type” (Ishihara et al. 1985); alcohol consumption, driving accidents, divorce, frequent job changes, low levels of vocational success, and impulsivity (Eysenck 1980). 345 Another personality construct that received a great deal of attention earlier in the smoking literature was Rotter’s (1966) internal versus external locus-of-control dimen- sion (e.g., Foss 1973; Best and Steffy 1975; Best 1975; Straits and Sechrest 1963). Two general hypotheses characterized work in this area. The first noted that smokers tended to have a more external locus of control, that is, perceive that things occur because of fate, not because of one’s own actions, compared with nonsmokers. The second held that smokers with a greater internal locus of control, that is, a perception that things happen because of one’s own actions, would be more successful in quitting. A review of this literature revealed inconsistent support for both hypotheses (Baer and Lich- tenstein 1988b). The multidimensional health locus of control scale (Wallston, Wallston, DeVellis 1978) was an attempt to anchor the locus of control construct specifically to health be- havior consistent with the trend away from broad, dispositional traits (Mischel 1973). Most studies using this scale examined the effect of health locus of control on cessa- tion attempts. Three investigations reported small but significant prospective relation- ships between subscales of the Health Locus of Control Scale and maintenance of abstinence (Kaplan and Cowles 1978; Rosen and Shipley 1983; Shipley 1981). A popular approach to understanding social or psychological problems has been through typologies. Tomkin’s typology of smoking and affect regulation was very in- fluential in the 1960s and early 1970s (Ikard and Tomkins 1973; Tomkins 1966, 1968). Tomkins originally proposed a fourfold typology including positive affect, negative af- fect, habitual, and addictive smoking. This model gave rise to the Reasons-for-Smok- ing Scale (Horn and Waingrow 1966), which continues to be used widely in public education and cessation programs despite receiving little empirical support (Shiffman 1988). Validity studies have yielded the most consistent support for the negative af- fect smoking construct (Ikard and Tomkins 1973: Pomerleau, Adkins, Pertschuk 1978; Joffe, Lowe, Fisher 1981). The support demonstrated for negative affect smoking is also consistent with recent reviews’ emphasis on stress reduction as being among those biological effects of nicotine that maintain regular smoking (e.g., Leventhal and Cleary 1980, Pomerleau and Pomerleau 1987). Much evidence for such effects comes from the retrospective reports of relapsers and smokers attempting to stop, which are reviewed later in this Chapter. However, relatively few data demonstrate that heightened stress leads to greater smoking. Among them are Ikard and Tomkin’s observations (1973) of greater incidence among race track spectators during horse races—presumed to be times of stress—than in the periods before and after races, and Silverman’s observations of nicotine-induced reductions in aggression among rats (1971). A number of other studies reviewed in the 1988 Surgeon General’s Report link smoking and negative af- fect but, as noted in that review, are not conclusive as to whether reduction of negative affect makes a substantial contribution to regular smoking. Design problems include comparisons of smokers smoking with smokers who are deprived, leaving unclear, for instance, whether smoking reduces negative affect or whether, for regular smokers, not smoking merely causes an aversive, deprivation state. As concluded in the 1988 Report, “.. caution must be exercised in generalizing about smoking and nicotine’s effects on stress and mood . . .” (US DHHS 1988, p. 405). 346 Less direct support for effects of stress on smoking lies in studies of smoking prevalence among groups who are disadvantaged in our society, including psychiatric outpatients (Hughes et al. 1986) and male users of soup kitchens (McDade and Keil 1988). Of the 38 subgroups defined by gender and economic, educational, vocational, or marital status listed in the 1988 Report, divorced or separated men had the highest prevalence of smoking, 48.2 percent (US DHHS 1988). Other social problems such as alcoholism and suicide are also more prevalent in this group (Kaplan and Sadock 1985). Beyond those groups with significant disadvantages such as psychopathology and very low income, the more general effects of income and education are quite substan- tial. For instance, preliminary data from the 1987 NHIS indicate a 35-percent smok- ing prevalence among adults with less than a high school education, more than twice the 16.3 percent prevalence among those with postgraduate college training (see Part I). Prevalence among both women and men declines with increases in income range. Among unemployed men, the prevalence is 44.3 percent (US DHHS 1988). Such trends indicate that the social and economic context affects the relationship of personal charac- teristics with smoking. Consistent with this, trends presented in Part I of this Chapter indicate that observed differences of race and sex are attributable to effects of income and education (see also Novotny, Warner et al. 1988). Social Context Influences The arrival at regular use roughly corresponds to the period of transition from adoles- cence to adulthood. At least until very recently, the social changes that accompany this passage—entering a university, the military, or the workforce—have been associated with a marked change in the acceptability of smoking. For high school students, smok- ing is often prohibited on school property, even if the prohibition is poorly enforced. In the workforce, community college, and university setting, smoking has been wide- ly accepted. The military until recently had supported smoking among its men and women, as reflected in low prices for cigarettes at military exchanges and commissaries and by the announcement of breaks with “The smoking lamp is lit.” The extent to which smoking is a part of the role of the serviceman was shown in a survey of Navy enlisted men with a mean age of 22.6 years and a mean of 3.9 years’ service. Seventy-two per- cent were self-reported smokers (Burr 1984). That the military has an effect on creat- ing rather than attracting smokers is suggested by a comparison of prevalence among naval recruits, 27.6 percent, and shipboard men, 49.8 percent (Cronan and Conway 1988). The military has recently recognized the enormous costs attendant to the high prevalence of smokers within its ranks and has begun efforts directed at reducing the percentage of smokers among its personnel (See Chapters 6 and 7). Cigarette marketing, discussed above and in Chapter 7, continues to be an important influence encouraging adult smoking, with several possible direct and indirect influen- ces on smoking patterns (Warner 1985). 347 Summary The past 25 years have seen a deepening appreciation of the importance of nicotine in maintaining regular smoking. In contrast to the 1964 Surgeon General’s Report, cigarette smoking is now defined as an addiction (US DHHS 1988). Earlier emphasis on the maintenance of blood nicotine levels as a means to avoid withdrawal has been balanced by the awareness that nicotine’s varied effects make smoking an efficient coping strategy for affect regulation and perhaps weight regulation. Conditioning models of smoking have become more sophisticated and firmly integrated with the pharmacologic actions of nicotine to explain addiction. While the public is now better informed about the health consequences of smoking, many smokers still minimize their perception of their vulnerability amid extensive marketing of tobacco products. Broad, dispositional traits or motives are now seen to be of limited value in understanding smoking. The role of social settings and social influence in encouraging regular smok- ing is also better understood. Cessation and Relapse A large body of literature on determinants of cessation has evolved, driven by the need to provide empirical and theoretical guidelines for intervention programs. All three sets of determinants—pharmacologic processes and conditioning, cognition and decisionmaking, and personality and social context—play an important role in the ces- sation stage (Table 39). It is with respect to cessation, especially, that the concept of stages—treating stopping as a process over time—has evolved (Figure 8) and now guides research and interventions (e.g., Marlatt 1985). The influential and well-articu- lated cessation stage model of Prochaska and DiClemente (1983) defines four stages of cessation. Precontemplation is the stage in which the smoker is neither considering stopping nor actively processing smoking-and-health information. During the con- templation stage, smokers are thinking about stopping and are processing information about the effects of smoking and ways to stop. In the action or cessation stage, the smoker is no longer smoking and has been without cigarettes for less than 6 months. The maintenance phase involves establishment of long-term abstinence, while relapse is the resumption of smoking. When relapse occurs, the smoker recycles to any one of the three previous stages. Specific cognitive and behavioral processes are employed during the different stages of cessation (Prochaska and DiClemente 1983). Determinants of each stage are also different. Thus, factors that affect an initial decision to stop smoking may not predict success in stopping or sustained maintenance after stopping. Working from a related but different stage mode!—initial decision, initial control, maintenance—Rosen and Shipley (1983) used health locus of control, desire to stop, and self-esteem to predict self-initiated smoking reduction. Using regression analysis, a different set of predic- tors was demonstrated at each stage, suggesting the possible need for different inter- vention techniques at each stage of the smoking reduction process. An important implication of a stage model is that interventions may need to address cessation’s several stages. The precontemplator’s tendency to ignore quitting strategies 348 may need to be met with continued personalized information on smoking and health; the contemplator may need social support to attempt cessation; and the abstainer may need help that emphasizes the development of relapse prevention skills. There are as yet no data available to demonstrate the effect of interventions tailored to specific stages of cessation. Thus, a model like the Prochaska and DiClemente stage model is best viewed as a tentative conceptualization, useful for guiding research and interventions. The next section considers changes in our understanding of the determinants of cessa- tion in relation to the stages in the cessation process. Pharmacologic Processes and Conditioning Pharmacologic processes and conditioning exert a strong influence on the process of quitting. One indicator of the role of addiction is that heavier, more dependent smokers in intervention programs are less likely to quit than are lighter, less dependent smokers (e.g., Hall et al. 1984;Ockene et al. 1982b), especially when smokers with much variability in baseline smoking are studied, as in the Multiple Risk Factor Intervention Trial (MRFIT) (Hughes et al. 1981). As is noted in the 1988 Surgeon General’s Report, “Withdrawal symptoms, whether elicited by acute deprivation or by conditioned stimuli, are hypothesized to be the link between dependence and relapse” (p. 523), al- though some analyses (e.g., Niaura et al. 1988) place greater emphasis on positive ef- fects of smoking in motivating relapse. Further evidence of the influence of addiction comes from intervention studies evaluating nicotine-containing gum. Several studies have found that nicotine polacrilex gum is more effective when used with nicotine-de- pendent smokers (as measured by the Fagerstrom (1978) addiction questionnaire) than with less dependent smokers (Hall et al. 1985; Killen et al. 1984; Schneider et al. 1983). Nicotine polacrilex gum most likely is effective because it reduces withdrawal symptoms frequently noticed in the first days and weeks of abstinence (Hughes et al. 1984; West et al. 1984). Recently, more work has focused on nicotine replacement strategies or other pharmacologic treatment adjuncts reflecting the importance of biological factors in smoking and cessation (Grabowski and Hall 1985; US DHHS 1986b; US DHHS 1988). Conditioning mediates the role of the pharmacologic effects of nicotine in cessation. As noted in the discussion of regular smoking, numerous conditioned environmental stimuli are likely to evoke urges or cues to smoke. Recent work by Abrams and col- leagues demonstrates that former smokers manifest psychophysiological reactivity to smoking cues long after they have quit (Abrams et al., in press; Abrams 1986). Con- ditioned reactivity to environmental cues, then, may be more decisive in the later stage of maintenance after withdrawal symptoms have subsided. Research on relapse triggers reflects current interest in specific, situational vari- ables. Primary triggers include stress, interpersonal conflict, dysphoria, presence of other smokers, and alcohol consumption (Marlatt and Gordon 1980; Shiffman 1982). Although the data are primarily retrospective reports from relapsed or tempted subjects, there is convincing consistency on the importance of stress and negative affect in deter- mining maintenance or relapse (Baer and Lichtenstein 1988a; Marlatt and Gordon 1980; Ockene etal. 1982a; Shiffman 1982; US DHHS 1988). The mechanism whereby 349 a lapse becomes a full return to smoking has also recently been analyzed as a series of stages (Marlatt 1985). These include a hi gh-risk occasion that triggers a smoking lapse (that is, a brief return to smoking) and a subsequent interpretation of the lapse that may lead to abandoning the cessation effort and a return to regular smoking. Much recent attention has been paid to the importance of coping responses in dealing with both high-risk situations and lapses (e.g., Shiffman 1984; Shiffman and Wills 1985). The available data suggest that the absence of any coping response is predictive of relapse but there are few differences that relate to the use of specific coping strategies used (Shiffman 1984). Cognition and Decisionmaking The role of cognitions in smoking cessation is evident in the relapse model noted above (Marlatt 1985). In this model, a lapse diminishes self-efficacy or self-confidence and expectations for long-term success. These diminished efficacy expectations then become the basis for an individual to abandon the effort and return to regular smoking (Marlatt 1985). In fact, lapses are highly predictive of subsequent relapse (Brandon, Tiffany, Baker 1986; Baer et al. 1988). Researchers have long noted the relationship of knowledge about the health conse- quences of smoking, beliefs about personal susceptibility, attitudes toward smoking, and expectations about the benefits of quitting to cessation efforts and their long-term success or failure. Cognitive-behavioral models of smoking cessation emphasize the importance of an individual’s interpretation of health risks and perceived self-efficacy for refraining from smoking (Pechacek and Danaher 1 979), as well as attributions about addiction and lapses during the maintenance stage (Marlatt 1985), Expectancy-Value Models Expectancy-value models have guided approaches to smoking cessation for many years (e.g., Kirscht 1983; Mausner and Platt 1971; Sutton 1987). Outcome expecta- tions refer to expected consequences that would occur if one continued smoking or quit smoking (Bandura 1977). Their value refers to the personal importance or weight given to the various possible outcomes and can be extended to perceptions about what sig- nificant others wish one to do (Fishbein 1982). Expectations include the positive (e.g., enjoyment) and negative (e.g., disease) consequences of smoking and the positive (e.g., enhanced lung capacity) and negative consequences (e.g., loss of enjoyment, withdrawal symptoms) of quitting. Expectancy-value models tend to assume that human behavior is rationally guided by logical or at least internally consistent thought processes (Henderson, Hall, Linton 1979). Decisionmaking models represent one variant of the expectancy-value approach and have been (e.g., Mausner and Platt 1971) and continue to be (Velicer et al. 1985) ap- plied to smoking cessation. The more recent applications (Velicer et al. 1985) may prove more useful because they take into account stage of change (Prochaska and Di- Clemente 1983). Changes in the relative level of pro and con views of smoking, for example, appear related to stages of quitting. Smokers not contemplating quitting report substantially higher levels of pro thancon views, while those contemplating quit- 350 ting report equal pro and con views. For quitters, con views were higher than pro views. These relative pro and con views also predicted subsequent change in smoking (Velicer et al. 1985). Since the 1960s, the health-belief model (Kirscht 1983; Rosenstock 1974; Swinehart and Kirscht 1966) has been a popular approach to understanding expectancy-value con- cepts applied to smoking cessation. According to this model, attempting to stop smok- ing is a function of three factors: beliefs about the health consequences of smoking and perceived susceptibility to the disease consequences, perceptions of available actions that can reduce one’s risk, and perceptions of the costs and benefits of accomplishing these actions (Kirscht and Rosenstock 1979). Johnston (1985) and his colleagues (Bachman, Johnston, O’Malley, and Humphrey 1988), for example, have shown that changes in perceived risk have accounted for a considerable reduction in adolescent marijuana use—particularly regular use. They suggest that effects of such beliefs may be more limited in the case of cigarettes because of the addictive properties of nicotine. As described in the next section, some recent models have addressed individuals’ belief in their ability to change behaviors, or self-efficacy (Bandura 1977; Eiser 1983, Eiser and Sutton 1977; Sutton and Eiser 1984). Self-Efficacy and Smoking Bandura (1977, 1982) defines self-efficacy as an individual’s belief in his or her ability to perform a specific behavior and proposes that efficacy beliefs represent a final common pathway mediating behavior change. Information from past behavior, model- ing, affective states, and instruction combine to produce a performance expectation, which then predicts future behavior. This behavior would, in turn, influence subsequent efficacy; behavior and efficacy are reciprocally related (Bandura 1982). The belief in one’s ability to stop smoking has been implicated in the health-belief model and in Eiser’s (1983) analysis of decisionmaking about stopping smoking. Self- efficacy theory, then, can be viewed as a historical descendant of the health-belief model and recently has had a major impact on models of smoking cessation. It is a major con- struct in Marlatt’s (1985) influential relapse prevention model, which has spawned several intervention studies (e.g., Brown et al. 1984; Curry et al., in press). In Marlatt’s model, self-efficacy is the key variable in the stage of maintenance (or relapse). It helps determine how well the individual will deal with high-risk situations or urges and is, in turn, influenced by successful or unsuccessful coping (Marlatt 1985). Consistent with Marlatt’s (1985) model, significant results with self-efficacy primari- ly pertain to client ratings after intervention, and thus predict smoking during followup periods. When all clients in treatment are considered, posttreatment self-efficacy ratings correlate strongly with short-term maintenance (Condiotte and Lichtenstein 1981; Coelho 1984; McIntyre-Kingsolver, Lichtenstein, Mermelstein 1983). For the most part, efficacy scores seem to correlate with outcome most highly when the fol- lowup interval is shorter (e.g., 3 months) and diminish over time (Coelho 1984; Mc- Intyre-Kingsolver, Lichtenstein, Mermelstein 1983). In order to view efficacy as a determinant of maintenance of cessation, it is neces- sary to demonstrate that it influences the latter independent of performance (level of 351 smoking) at the time efficacy is assessed. Results using partial correlations suggest that efficacy scores do provide limited information above and beyond that of current smok- ing behavior (Baer, Holt, Lichtenstein 1986). A second approach is to correlate self. efficacy measured postintervention with subsequent followup status only for those clients who initially quit. Studies using this paradigm have found significant but modest correlation with 3-month followup (McIntyre-Kingsolver, Lichtenstein, Mermelstein 1983; Coelho 1984), Self-efficacy also can be assessed during the maintenance phase, in order to predict longer term followup. Two studies have examined these relation- ships and both found significant prospective relationships (DiClemente 1981; Baer, Holt, Lichtenstein 1986). While intervention studies have usually found pretreatment efficacy unrelated to outcome, one study of unaided quitters found that baseline efficacy correlated with continuous abstinence at 1 year (Gritz, Carr, Marcus, in press). Another intervention study found that participants’ attribution of stopping to their own skill and effort, gathered 3 months after stopping, was correlated with abstinence at 6-month followup (Fisher, Levenkron et al. 1982). National survey data reviewed by Shiffman (1986) suggest that lack of confidence in the ability to stop deters many smokers from attempting cessation. Outcome Expectations From a stage perspective, outcome expectations (perceived consequences of smok- ing or stopping) are more likely to be related to the decision to stop smoking or the in- itiation of quit attempts than to success in the stopping process. The effects of brief ad- vice from a physician offer indirect support for the role of outcome expectations (Russell et al. 1979). Patients recciving brief advice to stop smoking were more like- ly to stop relative to control subjects. The physicians’advice probably enhanced the salience of the perceived positive consequences of stopping or the negative consequen- ces of continuing to smoke and thus prompted the decision to attempt to stop. Nega- tive consequences of smoking are potentiated by dramatic illness such as myocardial infarction, which is often the occasion for cessation efforts; however, relapse is often considerable (e.g., Baile et al. 1982), although less than with nondiseased smokers (Ockene et al. 1987). Cognitions concerning the health risks of smoking and the posi- tive benefits of stopping remain very important from a public health perspective (see Chapter 4) and the health-belief model may be useful for guiding interventions aimed at smokers in the precontemplation or contemplation stages of change. The role of disease in smoking cessation is substantial but not well understood. Cer- tain environmental changes following a serious illness may aid cessation and/or the in- formation and fear arousal provided by serious illness may motivate serious quit at- tempts, but continued maintenance is problematic (Ockene et al. 1985; Perkins 1988). . Approximately one-quarter to one-half of survivors. of myocardial infarctions are "abstinent from smoking at. extended followups (Ockene et al. 1985; Perkins 1988: Rigotti and Tesar 1985). While rates of cessation are impressive in some studies of car- diac and other patients, results of smoking cessation interventions produce inconsistent intervention effects (Perkins 1988: US DHHS 1986b). Research needs to evaluate the 352 impact of diseases and of dimensions of diseases including chronic and acute events, severity, and symptom mitigation following cessation, all of which vary across different diseases. Information about negative effects on the fetus may trigger cessation among preg- nant women, perhaps by potentiating a more general awareness of smoking’s dangers. Pregnancy does prompt some cessation or reduction relative to the “natural” popula- tion; however, relapse after delivery is high (US DHHS 1980b). Prevalence of smok- ing among pregnant women and historical shifts are documented in the first part of this Chapter. Personal Characteristics and Social Context Personal Characteristics Less educated smokers who do stop tend to have higher rates of relapse and shorter periods of abstinence than do more educated persons. Stopping smoking is more com- mon among those smokers with greater personal skills or socioeconomic resources (US DHHS 1982). Prospective studies indicate that education level, income, and skills in self-management or personal coping are significantly related to success in self-initiated efforts to stop (Blair et al. 1980; Gritz, Carr, Marcus, in press; Perri, Richards, Schul- theis 1977). Ina multivariate logistic regression analysis of 1985 NHIS data, blacks were significantly less likely than whites to quit smoking, regardless of SES or demographic factors (Novotny et al. 1988). Currently there are several research projects funded by NCI aimed at better understanding SES and ethnic differences in smoking that may eventually provide information to explain these differences. The sections on the initiation of smoking and regular smoking discussed the roles of several personality variables such as extraversion and neuroticism. While associations between extraversion and smoking have been replicated over the years (Eysenck 1980), it and other broad personality variables have not shown strong effects in smoking ces- sation (Lichtenstein 1982). Some evidence indicates that persons high in extraversion and low in neuroticism are more able to stop smoking (US DHEW 1979a). Internal— external locus of control has been hypothesized to be related to cessation (internals more successful) but the evidence is inconclusive (US DHEW 1979a). Research on personal characteristics is now focusing on more situation-specific or interactional variables such as self-efficacy, stress, and social support (Cohen et al. 1988; Condiotte and Lichtenstein 1981; Shiffman 1982). Stress has been shown to affect initiation of smoking and smoking rate, as well as relapse following smoking cessation (US DHHS 1988). It appears to be a factor espe- cially influencing women’s cessation (Abrams et al. 1987; Sorensen and Pechacek 1987), as well as their initiation of smoking (Mitic, McGuire, Neumann 1985). High levels of anxiety (Schwartz and Dubitzky 1968) and self-reported tendencies to smoke to relieve negative affect (Pomerleau, Adkins, and Pertschuk 1978) have been as- sociated with reduced success in stopping. The link of smoking to stress and research demonstrating the role of social support in buffering stress (Cohen and Syme 1985) 353 suggest that women’s cessation efforts may benefit from interpersonal support more than those of men (Fisher, Bishop 1986; Gritz 1982). Gender differences in cessation have been a major focus in recent years (US DHHS 1980b). Sex differences in onset and prevalence and historical shifts in these differen- ces are well documented in the first section of this Chapter. These differences and shifts have prompted a search for physiological (e.g., Silverstein, Feld, Kozlowski 1980) and especially psychosocial variables (US DHHS 1980b) that might account for them. No compelling factors have yet emerged to account for the historical shifts although chan- ges in social acceptability and the women’s rights movement seem likely candidates (US DHHS 1980b). It has also been suggested, on the basis of survey data, that women have lower rates of quitting smoking than do men (Remington et al. 1985). This inter- pretation has been criticized for failing to adjust male quit rates to reflect the propor- tion of men who switch to other tobacco products (Jarvis 1984). Women’s concern about weight gain associated with smoking cessation has received much recent attention (US DHEW 1980b; US DHHS 1988). The likelihood of women gaining weight following smoking cessation and the role of weight gain in precipitat- ing relapse deserve further investigation (US DHHS 1988) as does the hypothesis that women prefer and are more successful in cessation programs that provide social sup- port (e.g., from a group or counselor) (Fisher and Bishop 1986; Gritz 1982). Studies of sex differences in cigarette cessation programs yield equivocal results, and the issue of gender differences in cessation remains unresolved (US DHHS 1988). Social Context Influences Although findings published as early as 1971 indicated the importance of peer smok- ing in adult smoking and cessation (Eisinger 1971; Graham and Gibson 1971), these factors did not receive the attention they were given in discussions of smoking among adolescents. This difference reflected, perhaps, popular notions that adolescents are especially influenced by social forces such as peer pressure but that adults are more tied to psychological and physiological needs (US DHHS 1988). The popularity of self- management procedures (Fisher 1986) was manifest in smoking cessation programs of the 1970s that stressed the individual's control over smoking by manipulating its trig- gers or antecedents. Unfortunately, research directed at such procedures failed to yield appreciable improvements in program impacts (Lichtenstein 1982). This led to a search for important variables that had not been well researched. The 1980 and 1982 Surgeon General’s Reports (US DHHS 1980b, 1982) identified social support as possibly im- portant in mediating cessation among adults. A number of recent papers have sought to explore empirically the effects of social support on smoking cessation (e.g., Cop- potelli and Orleans 1985; Fisher, Lowe etal. 1982: Mermelstein, Lichtenstein, McIntyre 1983; Morgan, Ashenberg, Fisher 1988). As recently reviewed by Lichtenstein, Glasgow, and Abrams (1986), social support measures have been repeatedly correlated with abstinence, but the addition of social Support Components to standard behavioral cessation programs has not yielded in- cremental gains on outcome. For instance, an emphasis on group cohesion to enhance social support led to initial but not long-term advantages over a control group receiv- 354 ing standard intervention (Etringer, Gregory, Lando 1984). Similarly, efforts to mobi- lize spouse support have been disappointing (McIntyre-Kingsolver, Lichtenstein, Mer- melstein 1986). An understanding of the lack of a relationship between intervention strategies that promote interpersonal support and long-term smoking cessation may be advanced by considering the nature of support and its functions in different stages of smoking ces- sation (Cohen et al. 1988). Interpersonal emotional support seems especially related to maintained abstinence in the first several months after cessation (Coppotelli and Or- leans 1985; Mermelstein, Lichtenstein, McIntyre 1983; Morgan, Ashenberg, Fisher 1988: Ockene et al. 1982a). On the other hand, long-term abstinence of a year or more may be more closely tied to the number of smoking friends and relatives in the social network (Eisinger 1971; Graham and Gibson 1971; Mermelstein et al. 1986; Cohen et al. 1988; Smith 1988). The parallel between the importance of social network smoking status for long-term abstinence and for development of smoking in adolescence is noteworthy. Just as the adolescent progressing toward regular use will tend to have friends who also are smokers, so the long-term abstainer may benefit from friends who also are nonusers. At the stages of the transition to regular smoking and of long-term maintenance of cessation, the importance of peers’ behavior, either smoking or nonsmoking, seems greatest. It may be more effective to intervene to change norms and smoking behavior of networks than to teach supportive strategies to a few significant others. One way to have an effect on smoking by changing norms and the smoking of social networks is through the workplace, and worksite programs are attracting considerable attention (See Chapters 6 and 7). Worksites differ in smoking prevalence and cessa- tion rates as well as in norms for supporting cessation attempts (Sorensen and Pechacek 1986; Sorensen, Pechacek, Pallonen 1986). Programs aimed at worksite norms and general support for nonsmoking have reported substantial quit rates, even among smokers who did not join cessation clinics. Employees’ ratings of management sup- port for such programs were associated with cessation attempts and with ratings of so- cial support for nonsmoking (Fisher, Bishop et al. 1988b; Fisher, Bishop et al. 1988c). Summary Cross-sectional data reviewed earlier in this Chapter demonstrate that smokers with lower levels of education are less likely to stop. Stopping smoking seems more com- mon among smokers who have greater personal and socioeconomic resources. Educa- tional level, income, and skills in self-management or personal coping are related to success in self-initiated efforts to quit. Less educated smokers who stop tend to have higher rates of relapse and shorter periods of abstinence than more educated persons. Conditioned responses to smoking cues and alternative coping skills are important in maintenance and avoidance of relapse. The relationship of cognitive and decisionmaking determinants to smoking cessation has received increasing attention over the past 25 years. Cognitions about outcome ex- pectations—the pros and cons of smoking and quitting—relate primarily to decisions 355 to attempt cessation; efficacy cognitions about perceived ability to manage temptations or urges are related primarily to maintenance or relapse. Prospective studies indicate that the presence of acute disease, which is likely to affect cognitions about the pros and cons of smoking, is related to cessation. Consistent with an overall] increasing ap- preciation of the importance of nicotine in all Stages of smoking, more dependent smokers are less likely to succeed in quitting. Interpersonal support helps smokers in the early stages of quitting, but current evidence indicates that a low density of smokers in the social network is decisive for long-term abstinence. Summary of Changes in Knowledge About Determinants of Smoking Behavior There has been a dramatic increase in research on the determinants of smoking over the past 25 years. In 1964, there were few studies: by 1979 the number had expanded to a few hundred studies; now there are probably thousands. This increase in research reflects both specific Federal initiatives to support smoking research and larger trends toward recognizing the important relationship of behavioral factors to disease and the effect of preventive strategies in reducing morbidity and mortality. Several historical trends are predominant in considering all three major Stages together—development, regular smoking, and cessation. A strong consensus has evolved on the critical role of nicotine in smoking. The pharmacologic effects of nicotine and the role of conditioning are now understood as integrated processes that combine to produce the addictive nature of cigarette smoking. Cigarette smoking is now recognized to develop over a series of stages with multiple and different deter- minants at each stage (Figure 8; Table 35). The interaction of determinants (e.g., con- ditioning and the pharmacologic effects of nicotine with social influences) has become more clearly articulated. Recognition of these Stages and their multiple interacting Causes currently guides the development of intervention and educational programs. Smoking onset is associated with social influences, educational and economic disad- vantage, alcohol and other drug use, and antisocial behavior. Our increased knowledge of pharmacologic and psychosocial determinants has facilitated the development of interventions—behavioral or combined behavioral and pharmacologic—to aid cessation of regular smoking. Continued increases in our un- derstanding of the stages of cessation combined with better validated interventions of various levels of intensity or cost will help to offer smokers more choices to meet their needs. There continues to be a gap in our knowledge of how to target intervention programs for the educationally and economically disadvantaged. As described in the next two chapters, the knowledge gained about the determinants of smoking has guided interventions and campai gns to reduce the prevalence of smok- ing in adults from 40 percent in 1965 to 29 percent in 1987. It has led to promising prevention and cessation programs, which use existing community channels—media, worksites, schools, physicians’ offices, and hospitals—to deliver low-cost but effective interventions (Chapter 6). 356 CONCLUSIONS Part I. Changes in Smoking Behavior 1. Prevalence of cigarette smoking has declined substantially among men, slightly among women, and hardly at all among those without a high school diploma. From 1965-87, the prevalence of smoking among men 20 years of age and older decreased from 50.2 to 31.7 percent. Among women, the prevalence of smoking decreased from 31.9 to 26.8 percent. Smoking prevalence among whites fell steadily. Among blacks, the prevalence of smoking changed very little between 1965 and 1974; subsequently, prevalence declined at a rate similar to that of whites during the same period. Smoking prevalence has consistently been higher among blue-collar workers than among white-collar workers. Annual per capita(18 years of age and older) sales of manufactured cigarettes decreased from 4,345 cigarettes in 1963 to 3,196 in 1987, a 26-percent reduction. Total cigarette sales increased gradually to 640 billion cigarettes in 1981 and then fell to 574 billion in 1987. In 1965, 29.6 percent of adults who had ever smoked cigarettes had quit. This proportion (quit ratio) increased to 44.8 percent in 1987. The rate of increase in the quit ratio from 1965—85 was similar for men and women. The rate of change in quitting activity in recent years is similar for whites and blacks. From 1965— 85, the quit ratio increased more rapidly among college graduates than among adults without a high school diploma. Of all adults who smoked at any time during the year 1985-86, 70 percent had made at least one serious attempt to quit during their lifetime and one-third stopped smoking for at least 1 day during that year. The age of initiation of smoking has declined over time, particularly among females. Among smokers born since 1935, more than four-fifths started smoking before the age of 21. Trends in prevalence of cigarette smoking among those aged 20 to 24 years are an indicator of trends in initiation. By this measure, initiation has declined be- tween 1965 and 1987 from 47.8 to 29.5 percent. Initiation has fallen four times more rapidly among males than among females. The rate of decline has been similar among whites and blacks. Initiation has decreased three times more rapid- ly among those with 13 or more years of education than among those with less education. The prevalence of daily cigarette smoking among high school seniors decreased from 29 percent in 1976 to 21 percent in 1980, after which prevalence leveled off at 18 to 21 percent. Prevalence among females has consistently exceeded that among males since 1977. Prevalence was lower for students with plans to pursue higher education than for those without such plans. The difference in prevalence by educational plans widened throughout this period; in 1987, smoking rates were 14 percent and 30 percent in these two groups, respectively. The best sociodemographic predictor of smoking patterns appears to be level of educational attainment. Marked differences in smoking prevalence, quitting, and 357 10. 11. 12. initiation have occurred and have increased over time between more and less edu- cated people. The domestic market share of filtered cigarettes increased from | percent in 1952 to 94 percent in 1986. The market share of low-tar cigarettes (15 mg or less) in- creased from 2 percent in 1967 to 56 percent in 1981, after which this proportion fell slightly and then stabilized at 51 to 53 percent. The market share of longer cigarettes (94 to 121 mm) increased from 9 percent in 1967 to 40 percent in 1986. Between 1964 and 1986, use of smokeless tobacco (snuff and chewing tobacco) declined among men and women 21 years of age and older. However, among males aged 17 to 19, snuff use increased fifteenfold and use of chewing tobacco increased more than fourfold from 1970-86. Differences in prevalence of cigarette smoking and smokeless tobacco use be- tween young males and young females suggest that the prevalence of any tobac- co use is similar in these two groups. From 1964-86, the prevalence of pipe and cigar smoking declined by 80 percent among men. Part II. Changes in Knowledge About Determinants of Smoking Behavior 1. 358 Smoking was viewed as a habit in 1964 and is now understood to be an addiction influenced by a wide range of interacting factors, including pharmacologic effects of nicotine; conditioning of those effects to numerous activities, emotions, and settings; socioeconomic factors; personal factors such as coping resources; and social influence factors. Since 1964, there has been a gradual evolution of understanding of the progres- sion of smoking behavior through the broad stages of development, regular use, and cessation. Each of these stages is differentially affected by multiple and in- teracting determinants. Views of determinants of smoking are affected by the predominating theoretical and methodological perspectives. In smoking, the earlier focus on broad, disposi- tional variables (e.g., extraversion) has given way to an emphasis on situation- specific and interactional variables; a focus ona search fora single cause has given way to a focus on multiple and interacting causes. Appendix Questions Regarding Smoking Status and Quitting from the 1986 AUTS Smoking status (current, former, never) is decided from responses to the following two questions: “Have you ever smoked at least 100 cigarettes in your life?” “Do you smoke cigarettes now?” Current smokers were then asked: “Have you ever made a serious attempt to stop smoking cigarettes entirely?” “Thinking of your last serious attempt to quit, how long did you stay off ciga- rettes?” “How long ago did that attempt to quit begin?” Current smokers who reported that they had never made a serious attempt were asked: “Have you ever thought about quitting?” “Would you try to quit if there was an easy way to do so?” Questions Regarding Smokeless Tobacco Use 1986 AUTS Ever use: “Have you ever used (snuff and chewing tobacco asked separately) on a fair- ly regular basis?” Current use: “Do you use (snuff, chewing tobacco) now?” 1964, 1966, 1970, and 1975 AUTS Ever use: “Have you ever used snuff at all regularly?” “Have you ever chewed tobacco regularly?” Current use: “Do you now use (snuff, chewing tobacco)?” 1985 NIDA National Household Survey on Drug Abuse Ever and current use: “On the average, in the past 12 months, how often, if ever, have you used chewing tobacco or snuff or other smokeless tobacco?” Responses included “never,” “almost daily,” “less than daily,” and “not in past year.” 359 1985 CPS Current other tobacco use: “Does (name) presently use any other form of tobacco, such as snuff or chew- ing tobacco?” Current smokeless tobacco use: “What other form(s) of tobacco does (name) presently use?” The categories “snuff,” “chewing tobacco,” “cigars,” “pipe tobacco,” or “other” were coded in response to this followup question. 1986, 1987, and 1988 BRFS Ever use: “Have you ever used or tried any smokeless tobacco products such as chew- ing tobacco or snuff?” Current use: “Do you currently use any smokeless tobacco products such as chewing tobacco or snuff?” 1987 NHIS Ever Use: “Have you ever used chewing tobacco, such as Redman, Levi Garrett, or Beechnut?” “Have you ever used snuff, such as Skoal, Skoal Bandits, or Copenhagen?” In addition, those who answered “yes” to the above questions were asked, “Have you used chewing tobacco at least 20 times?” Current use: “Do you use (chewing tobacco, snuff} now?” 1970 NHIS Current use: “Do you use any other form of tobacco?” Respondents could answer yes or no to “snuff,” “chewing tobacco,” or “other.” 360 References ABRAMS, D.B. 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American Journal of Public Health 74(3):261-263, March 1984. 378 CHAPTER 6 SMOKING PREVENTION, CESSATION, AND ADVOCACY ACTIVITIES 379 CONTENTS Introduction 0.0... ce ee eee e eee teens 383 Integrating Educational and Behavioral Interventions With Policy Initiatives . . 383 Part 1. Smoking Prevention Activities . 0.0... 6.0.0.6 e cece ree eee teenies 384 Overview of Major Approaches to Smoking Prevention ................-, 384 Prevention Opportunities Associated With Stages in the Acquisition of Smoking .......... 000.0 e eee eee eee eens 385 Prevention Program Approaches ..........6 0 cece cence renee eee 386 Media-Based Prevention Programs .......... 0.0.0 eee eee eee 387 Smoking Prevention Programs in the Context of Multicomponent School Health Education Curricula ... 0.6.0.0... cece ete 388 Psychosocial Curricula 2.0... 0.6... e eee eens 389 Youth Smoking Cessation Programs .... 22.66.00 cece eee eee teens 392 History of Agency and Organizational Prevention Activities .........-...-- 394 National Voluntary Health Organizations ..........--.--2 ee eeeee 394 National Interagency Council on Smoking and Health ............-. 395 Federal Government Prevention Support .............0 60s eee ee eee 396 Office on Smoking and Health ............6 2-02 eee eee nee 397 National Cancer Institute ©... 0.2. c ee ee eee eee 398 National Heart, Lung, and Blood Institute ...........--....4455 399 National Institute on Drug Abuse ......... 0.000 e eee ee nes 399 National Institute for Child Health and Human Development ..... 399 Office of Disease Prevention and Health Promotion...........-. 400 Surgeon General’s Reports 0.0... 6... c eee eee eee eee ees 400 State Health Departments ........... 006 cece eee eee teens 401 Other Organizations and Agencies ........... 0. see e eee teens 402 Problems in Dissemination of Smoking Prevention Programs .............. 403 Problems in Evaluation of Smoking Prevention Programs .............-+-- 405 Need For Long-Term Followup ......... 00: e seer reece eee eens 406 Construct Validity ....... 00... cece cece tee eens 406 Failure to Reach Dropouts and Other Youth at Higher Risk for Smoking .......... 60 e eee e eee eee tee eee 407 Population Factors Related to Diversification of Smoking Prevention Programs ......... 0.0 cece cece ee eee eee tees 408 Part I]. Smoking Education and Cessation Activities ........6.....0 00 eee eee 409 Changes in Cessation Activities Over Time ......... 0... 0 eee eee rece eee 409 National Voluntary Health Organizations ............--5 0-050 - sees 413 Health Professional Associations .......... 00.6 e eee eee eee teens 418 Federal Government Cessation Support .........-. 2: ee ere erences 421 Office on Smoking and Health ..........-- 0s eee ee eee eee 421 National Cancer Institute: Smoking, Tobacco, and Cancer Program 421 National Heart, Lung, and Blood Institute ..............5 50006: 423 Office of Disease Prevention and Health Promotion ............ 425 381 State Health Departments ....00.0. 00. cece eee, 427 Commercial Ventures in Smoking Control........................ 427 Pharmacologic Cessation Aids .............000...0000c000. 428 Nonpharmacologic Cessation Aids ...............00000000... 430 Stop-Smoking Programs ............. 0.000. 00c cece cece. 43} Worksite and Hospital Wellness Programs .................... 432 Summary... cece cece cece e tee eeeneeee. 434 Part III. Antismoking Advocacy and Lobbying ...............0..000....0,., 436 Nature and Objectives of Advocacy and Lobbying ............0...0....0.., 436 Objectives ccc cece cence ec ee eee. 437 Organizational Characteristics ..... 0.0.0... 0000... cee ee cece eee. 439 The Tobacco Lobby ...... 0.6... c cc cee cece ce eeeeeeeee ce. 440 Antismoking Advocacy and Lobbying: 1964 to the Present ............... 44] Early Efforts 2.202... oe cece ccc ee ees e eee eeee eee. 44) Nonsmokers’ Rights ........ 060... c ccc ec eee teeeceeceeeeeeee. 442 Coalition Building and the Growth of Advocacy ..............0.004, 443 Conclusions ....... 0.0.0... e ee ceeeeneeeeevenssiepeeeln 444 References .... 0.0... e tests seveeetessens sree 446 382 INTRODUCTION The tobacco control movement in the United States has involved the efforts of many diverse groups. Voluntary health agencies, State and local health departments, the Federal Government, medical organizations, private industry, and grassroots organiza- tions have all contributed. This Chapter reviews the nonpolicy activities of these groups in the areas of smoking prevention and cessation, and advocacy over the past 25 years. It will not provide a complete review of the efficacy of different prevention and cessa- tion methods; this has been done by others (e.g., Lichtenstein and Brown 1980; Pechacek 1979; Schwartz 1969, 1987; Schwartz and Rider 1978; Flay 1985a,b; Best et al. 1988; Biglan and Ary 1985; McCaul and Glasgow 1985; Snow, Gilchrist, and Schinke 1985, US DHEW 1979b: US DHHS 1986a). A selective review of the broader trends in these activities will provide a basis for understanding the current status of the smoking con- trol movement and its possible future directions. A review of advocacy activities in- tended to lead to changes in smoking control policies over the last 25 years will serve as a bridge between this Chapter and Chapter 7, Smoking Control Policies. The smoking prevention and cessation activities discussed in this Chapter were designed as direct antismoking messages incorporating advice and instruction on how to remain or become a nonsmoker. Smoking prevention programs include school cur- ricula, both those specific to smoking and those integrated within a multicomponent health education approach; media-based efforts; and an array of other materials, events, and campaigns. Smoking cessation programs include a broad variety of activities rang- ing from self-help cessation materials to special smoking groups to the use of medica- tion. The programs occur in various channels in the community including worksites, physician offices, hospitals, schools, and media. Integrating Educational! and Behavioral Interventions With Policy Initiatives The integration of educational and behavioral programs with policy initiatives, in- cluding those that affect the price of cigarettes, the information printed on the packag- ing, the manner in which cigarettes can be advertised, the conditions of their sale, and the circumstances under which they may be smoked, has been one of the most impor- tant recent trends in smoking prevention, as well as in cessation-oriented interventions. Projects such as “Tobacco-Free America Project” (Bailey 1987) work on both fronts, advocating nonsmoking policies in schools along with providing more traditional smok- ing prevention materials and programs to reduce the number of new smokers. Ad- vocacy activities and lobbying leading to policy changes were almost nonexistent at the time of the 1964 Surgeon General’s Report, but became progressively more evident during the 1970s and expanded significantly during the 1980s, setting the stage for many of the changes in prevention and cessation policies and activities. Even when explicit policy components are lacking in prevention or cessation programs, the content and impact of these programs should be considered in the con- text of the social and policy climate prevailing at the time of their design and implemen- tation (see Best et al. 1988; Chassin, Presson, Sherman 1985; Chassin et al. 1987; Perry and Murray 1982). For example, the effects of a prevention or cessation activity might 383 be moderated by whether it was conducted during the era of television cigarette com- mercials alone (pre-1967), the era of both commercials and antismoking public service announcements (PSAs) mandated by the Government (1967-70) (see Chapter 7), or during the subsequent era of no televised cigarette commercials and the end of the man- dated PSAs (post-1970). Other potentially relevant policy contexts include school regulation of student smoking and the level of public debate and restrictions on smok- ing in other settings at the time of the smoking prevention or cessation program. Both the smoking prevention and cessation programs and the public policy context remain in a continuous process of evolution and interaction. PART I. SMOKING PREVENTION ACTIVITIES Overview of Major Approaches to Smoking Prevention In the years since the release of the first Surgeon General’s Report (US PHS 1964), both the basic design of prevention efforts and their designated targets have changed. Generally, there has been a shift in the target group from high school and college stu- dents (US PHS 1964) to middle school and junior high school students, and a shift away from information-oriented antismoking education to psychosocial curricula designed not only to address youth’s motivations to smoke but also to impart skills for resisting influences to smoke (Botvin, Eng, Williams 1980; Flay 1985a; McAlister, Perry, Mac- coby 1979). The changes in focus and design and the proliferation of prevention programs since the early 1960s have resulted in such a variety of approaches that they are now rarely considered together in reviews of smoking prevention programs. These differing ap- proaches include (1) media-based prevention programs and resources, (2) smoking prevention as a component of multicomponent school health education curricula, and (3) smoking prevention through the psychosocial approaches of social influence and generic life skills curricula. Other smoking prevention resources and activities such as physician presentations to school assemblies, brochures, community campaigns, and educational resources have been sponsored by voluntary, professional, and community groups. While the prevention approaches overlap considerably, both in form and content, this differentiation of program types can serve as a framework for tracing the prevention initiatives and directions taken by various organizations, as well as for highlighting the evolution of smoking prevention programs over the years. The following outline of the major prevention approaches will be expanded upon in a later section. Media-based messages and campaigns were part of the earliest smoking prevention activities. The National Clearinghouse for Smoking and Health (later reorganized as the Office on Smoking and Health (OSH)) and the voluntary health organizations were among the early and continuing sponsors of newspaper and broadcast antismoking cam- paigns. These smoking prevention campaigns have continued with varying intensity over the decades, continuing into the present era of controlled research in the develop- ment and evaluation of media-based smoking prevention programs (e.g., Bauman et 384 al. 1988; Flay et al. 1988; NCI 1986a; Ramirez and McAlister 1988; Sussman et al. 1986; Worden et al. 1988). The integration of smoking prevention curricula into comprehensive and multicom- ponent school health education curricula was one response to the findings of limited impact from early smoking-specific prevention efforts (see Davis 1977). The develop- ment of psychosocial approaches including social-influence and life skills programs in the 1970s was another response to the limited impact of early prevention efforts (Evans 1976; US DHEW 1979b). The integration of smoking prevention into general health education represented an important shift in the vehicle for antismoking messages, and the psychosocial approaches were based on a fundamental revision of the model under- lying prevention strategies for smoking by youth. The psychosocial approaches deviated from traditional antismoking education models by deemphasizing communication of the long-term health risks of smoking. In- stead, these new curricula focused on young people’s susceptibility to social pressures to smoke—influences inferred from consistent findings relating smoking by youth to smoking by their parents, siblings, and peers (Flay et al. 1983; US DHEW 1979c; US PHS 1964). In their various forms, social influence and life skills curricula have been designed to raise young people’s awareness of the influences to smoke; to highlight the more immediate, and especially socially based, negative effects of smoking; and to “in- oculate” youth against the effects of continued pressure and examples of others who smoke. The new approaches were bolstered by the literature on communication theory and on the psychosocial development of adolescents (US DHEW 1979b). This Section covers the course of smoking prevention activities over the past 25 years. The first part presents a model of developmental stages of smoking acquisition as a framework for describing trends and options for prevention programs. This is followed by further description of the three major categories of current prevention programs and of cessation programs for youth. The next part describes in more detail the history of prevention activities of the major national voluntary health agencies, Federal support with emphasis on their early responses in the campaign to prevent smoking, and the ac- tivities of State and other organizations and agencies with emphasis on their recent ac- tivities. Considered next are problems in program dissemination and the gaps that fre- quently exist between the scientific literature and widespread program application in the field. Problems in program evaluation are reviewed in the next section. The review closes with a consideration of population factors such as changing attitudes toward smoking and secular trends in smoking prevalence as they relate to program diversifica- tion. Prevention Opportunities Associated With Stages in the Acquisition of Smoking As noted in the preceding chapter, several researchers (e.g., Flay et al. 1983; Leven- thal and Cleary 1980) have proposed models of developmental stages in the acquisi- tion of smoking. These models provide one dimension for describing and evaluating prevention opportunities and trends. The stages—for example, “preparation and an- ticipation,” “initiation,” “experimentation,” “transition (becoming), and “regular smoking” (Flay et al. 1983)—suggest a continuum of associated prevention oppor- 385 tunities. Spanning this developmental continuum are approaches to keep children from experimenting with tobacco, efforts to disrupt the evolution from experimentation to regular smoking, and early interventions aimed at influencing the young smoker to stop before the behavior and nicotine dependence become more firmly entrenched. Stage models of smoking acquisition posit that different influences are at play at various ages; for instance, parents have a greater influence than peers in determining smoking intentions and behavior among young adolescents, while peers are more im- portant for older adolescents. Social factors are viewed as more influential for begin- ning smokers, and physiological dependence and coping patterns as more important for the older, more established smokers (Flay et al. 1983; Leventhal and Cleary 1980; Chas- sin, Presson, Sherman 1985). (See Chapter 5, Part II.) Prevention programs designed to reduce the number of young adolescents who in- itiate smoking reflect the dominant model for current smoking prevention. However, early antismoking education efforts addressed smoking by high school and college students (US PHS 1964), age groups encompassing several stages in smoking acquisition. The majority of current prevention programs focus on adolescents in grades 6 through 8, the age groups now at maximal risk for cigarette experimentation (Flay et al. 1983; Flay 1985a; Chapter 5). The shift of interest to smoking prevention programs aimed at younger adolescents is related to four considerations: (1) the find- ings of greater program impact among younger children (Jason, Mollica, Ferrone 1982; Johnson et al. 1986; Merki et al. 1968), (2) the general ineffectiveness of previous prevention approaches (Thompson 1978), (3) the recognition of secular trends toward earlier initiation of smoking (Evans et al. 1979; Flay et al. 1983; Chapter 5), and (4) the appeal of prevention versus the challenge of adult cessation (Evans et al. 1979). A stage model of smoking acquisition and associated prevention opportunities sug- gests the potential for prevention programs aimed at even younger children in the preparation stage of smoking acquisition, the period during which early attitudes toward smoking are formed. The stage model also suggests cessation programs among older adolescents at the other end of the prevention continuum. Thus, some smoking prevention programs are directed at very young children in preschool or early elemen- tary grades (ACS described in US DHHS 1986a; Peterson described in NCI 1986a; Pigg et al. 1985), and there are cessation programs directed at adolescents (e.g., ACS 1980, 1986; Weissmann et al. 1987). A call for continued development of programs addressing “pre-onset” issues and youth cessation was included in the National Cancer Institute (NCI) expert advisory panel’s recommendations (Glynn, in press). Youth smoking cessation approaches are described in a later section in this Chapter. Prevention Program Approaches As outlined above, the evolution of prevention programs since the 1960s can be clas- sified into three major approaches: media-based programs, smoking prevention in the context of multicomponent school health education, and psychosocial curricula. The three major approaches will be more fully described in this Section. Other resources and activities in the field will be described in a subsequent section. 386 Media-Based Prevention Programs Media-based prevention approaches have included antismoking messages delivered through newspapers and television and radio broadcasts. Most often these have taken the form of brief announcements, but more extended special programs and curricula have also been developed and distributed. The American Lung Association (ALA), American Heart Association (AHA), American Cancer Society (ACS), and National Heart, Lung, and Blood Institute (NHLBI) sponsored one such extended prevention program, first aired in November 1984, a 1-hr Public Broadcasting System special, “Breathing Easy,” aimed at young people (Bailey 1985; US DHHS 1986a). Mass-media-based messages and programs were included among the earliest smok- ing prevention efforts of the Federal agencies and voluntary health associations. Flay (1986 and 1987b) has provided comprehensive reviews of these and later media-based smoking control efforts. Early evaluations of mass media in health promotion were not encouraging, leading to Flay’s (1986) appraisal that mass media programs alone are not effective. Review- ing studies of media campaigns that were used either as the sole intervention or in con- junction with other material and programming, Flay concluded that the most effective use of mass media in substance abuse prevention lies in furthering the dissemination of other prevention resources, such as school-based programs. Parents, for example, may become more supportive of the efforts of school-based prevention programs brought to their attention through the mass media (Flay 1986). In reviews of mass media cam- paigns specifically focused on smoking, Flay (1987a,b) found some basis for optimism about their potential impact on adult smoking cessation. He recommended, however, further evaluation of mass media campaigns for the prevention of adolescent smoking; only 3 of the 56 evaluations reviewed included specific reference to smoking by children (Flay 1987b). There have been several controlled studies of mass-media-based prevention programs in recent years (Bauman et al. 1988; Sussman et al. 1986; Flay et al. 1988; Worden et al. 1988; Ramirez and McAlister 1988). A University of Southern California study demonstrated that effects on student smoking correlated with amount of attention to the television segments and amount of discussion of the program with others (Sussman et al. 1986; Flay 1987b; Flay and Sobel 1983; Flay, Hansen et al. 1987). The program, which parents were encouraged to watch with their children, also had a cessation effect on the adults’ smoking (Flay 1986). Mass media interventions can also augment other prevention programs, generating prevention effects that occur more broadly, acting over time in the aggregate to affect the level of public awareness and the social acceptability of smoking. The potential for this level of public health impact is described by Leventhal and Cleary (1980) and Warner and Murt (1982) in their consideration of factors inhibiting the rise of smoking rates in the late 1960s and 1970s. Even small program effects can have a large public health impact, given the very large audiences of mass media (Flay 1987b), making the actual distribution and broad- casting of these programs critical. Dissemination of media materials has been depend- ent on the good will and interest of publishers and broadcast managers, or on funds for 387 purchase of air time and print space. In recent years, video news releases (essentially press releases on videotape) have been used increasingly by private health organiza- tions and Federal agencies (including the Office on Smoking and Health) to motivate television news coverage of tobacco-related “events” (Davis 1988a). Smoking Prevention Programs in the Context of Multicomponent School Health Education Curricula Smoking prevention components have long been incorporated in more general school health programs. This represents an alternative approach to programs focused ex- clusively on smoking prevention. The development and evaluation of the 8- to 10-week curriculum of “Growing Healthy” have involved a partnership between Federal agen- cies and national voluntary organizations spanning three decades, with ALA serving as a lead agency in these endeavors. “Growing Healthy” is the combined Primary Grades Health Curriculum Project aimed at students in kindergarten through grade 3, and the School Health Curriculum Project (SHCP) aimed at students in grades 4 through 7, Both are designed to integrate smoking and health into a comprehensive school health education curriculum. An evaluation of the original SHCP component between 1982 and 1985 demonstrated a delay in onset of smoking among the seventh grade students who had been in the program. Among the intervention students, 7.7 percent had started smoking by grade 7, compared with 12.7 percent among the control group (US DHHS 1986a). The School Health Education Evaluation Project (Connell and Turner 1985; Connell, Turner, Mason 1985) also included a review of “Growing Healthy,” as well as of three other school health programs with various dimensions of program implementation and impact. “Growing Healthy” has been validated by the Department of Education and included in the National Diffusion Network (NDN), an organization that includes data on the extent of diffusion of curricula that have been evaluated and validated by the Department of Education (US DHHS 1986a). As part of NDN, dissemination of “Growing Healthy” is facilitated and monitored. The Teenage Health Teaching Modules, a comprehensive health education program for junior and senior high school students, were developed by the Centers for Disease Control (CDC) Center for Chronic Disease Prevention and Health Promotion through a contract with Education Development Center, Inc., and are also currently being evaluated (US DHHS 1986a). They are also now being promoted as part of ALA’s “Growing Healthy” activities. The American Health Foundation “Know Your Body” program is a multicomponent school health education curriculum aimed at reducing smoking and risk factors for coronary heart disease. A recent study of program impact after 6 years of intervention found significantly lower rates of initiation of smoking among subjects in the intervention schools (Walter, Vaughan, Wynder 1988). Another study comparing the effectiveness of this program’s smoking prevention component when offered alone or as part of the multicomponent package is currently under way. Although many substance abuse prevention programs have adopted social influence and life skills training approaches (Bell and Battjes 1985; Polich et al. 1984), prevention of tobacco use is not consistently part of, let alone prominent in, the derivative 388 programs. One rationale for integrating tobacco use prevention with prevention programs for other forms of substance abuse is provided by the recently increasing ap- preciation of the common nature of licit and illicit drug addictions (US DHHS 1988). In addition to comprehensive school health education curricula developed and evaluated by Federal agencies and national voluntary organizations, curriculum guidelines designed by individual school systems and commercial textbook writers sometimes include antismoking components. No systematic review of this category of smoking prevention programs in comprehensive health education curricula exists. The degree of emphasis on and implementation of smoking-specific prevention cur- ricula can be obscured within more general health education curricula. Evaluation of the impact of these programs on smoking behavior has been far less detailed than in smoking-specific curricula. In addition, the integration of tobacco prevention programs into a basic health education curricula presents substantive questions of program im- pact: Will the same basic prevention material be more effective if presented inde- pendently, as a special program? Will its impact be augmented or decreased by an on- going context of basic health education? Drawing on the currently available research and on preliminary findings from ongoing studies, an expert advisory panel convened by NCI in December 1987 concluded that school-based smoking prevention conducted within a multicomponent health focus appeared as effective as programs with an ex- clusive emphasis on smoking, provided the smoking component received a minimum level of attention. One criterion for this minimum level of attention was five classroom sessions in each of 2 years (Glynn, in press). More focused evaluations of smoking prevention in the context of school health education are needed to answer these ques- tions. While a unified multicomponent health education curriculum may be attractive to schools faced with a multitude of health education requirements, this approach to smok- ing prevention depends on the state of health education at the State and national levels and faces all the obstacles and challenges experienced by such larger enterprises (Iver- son and Kolbe 1983; Kolbe and Gilbert 1984; Kolbe and Iverson 1984; Lohrmann, Gold, Jubb 1987). Psychosocial Curricula Increased funding of smoking prevention research in the 1980s (Bell and Levy 1984; NCI 1984, 1986a; Stone 1985), as well as the advocacy of using psychosocial ap- proaches developed for smoking prevention for other substance abuse prevention ef- forts (Bell and Battjes 1985; Polich et al. 1984), has brought psychosocial approaches to the forefront of attention. From a research perspective, they represent the dominant strategy in smoking prevention, the culmination of the preceding 25 years of investiga- tion. Reviewing the literature on the psychosocial prevention curricula, Bell and Battjes (1985) identified two main types of programs: (1) the social influence curricula that foster youths’ awareness of and ability to resist peer and other social pressures and in- fluences to smoke (Dielman et al. 1985; Flay et al. 1985; Hurd et al. 1980; Johnson et al. 1986; Killen 1985; Luepker et al. 1983; Perry, Killen, Telch et al. 1980; Shaffer, 389 Beck, Boothroyd 1983), and (2) those more broadly structured to also strengthen more general social skills and competencies underlying initial vulnerability to these pressures to smoke, referred to as life skills training approaches or generic life skills approaches (Botvin, Eng, Williams 1980; Botvin and Wills 1985; Gilchrist and Schinke 1985; Schinke et al. 1985). Both varieties include programs that have been originally designed or expanded to include substance abuse prevention of other kinds. Com- ponents of psychosocial approaches have also been integrated into the more general health education curricula. The social influence approach growing out of work by Evans and his colleagues (Evans 1976; Evans et al. 1981) shifted the smoking preven- tion agenda from issues in the development and dissemination of antismoking educa- tional messages to questions about ways to affect the psychosocial processes underly- ing children’s responses to social influences to smoke. The social influence and generic life skills curricula for smoking prevention are the best documented and most thoroughly evaluated among the smoking prevention programs. The field has reached the point that some general statements can be made conceming components of programs and the general extent of their effect (e.g. Glynn, in press). Common features of programs that have been found to have positive prevention ef- fects include a focus on students in the middle and junior high grades; multiple ses- sions; intervention components designed to correct young people’s misimpressions of the social significance and prevalence of smoking among peers; emphasis on the short- term reasons not to smoke (both physiological and social); education regarding the variety of social factors (parental, peer, and media) influencing smoking; practice with skills used to resist offers to smoke and examples of smoking; involvement of peers, either as peer leaders or as videotaped role models; and public commitment procedures (Flay 1985a,b). In addition, life skills training curricula are likely to include program components to enhance decisionmaking, self-esteem, and social competencies (Botvin and Wills 1985). Three minimum program components were recommended by the 1987 NCI expert advisory panel: information about the social consequences and short-term physiologi- cal effects of tobacco use; information about social influences on tobacco use, especial- ly peer, parent, and media influences; and training in refusal skills, including modeling and practice of resistance skills (Glynn, in press). The panel added the caveat that the quality of the delivery of these components would be critical to their success. Teacher training and adoption of existing smoking prevention programs, as designed, were recommended as two assurances of better quality program delivery. Although use of peer leaders or models has been a frequent component of these programs, evaluations comparing the role of peer versus adult leaders have been mixed regarding the importance of peer leaders to program success (Arkin et al. 1981; Clarke et al. 1986; Murray et al. 1984; Perry, Killen, Slinkard et al. 1980; Perry et al. 1983). The logistic challenges entailed in implementing a peer-led program also must be con- sidered. Arkin and colleagues (1981) found, for instance, that “Teachers, principals and students generally had more trouble adjusting to peer-led programs than to the health educator led programs” (p. 614). The recent NCI panel concluded that the most effec- tive use of peer leaders was as assistants to a trained teacher, with responsiblity for car- 390 rying out specified program components (Glynn, in press). The findings of Perry and colleagues (1983) suggest that peer leaders may be most effective in delivering cur- ricula focused on social pressures, as opposed to more traditional health effects cur- ricula. Within social influence and life skills curricula there has been a marked refinement of research methods and a better scientific and theoretical basis for program design and evaluation. Flay (1985a,b) described in detail the evolution of psychosocial smoking prevention programs and their evaluations, in which methodological progress has been made. This progress includes greater numbers of schools per condition, use of ran- domization, and greater emphasis on internal validity of programs. The use of proce- dures to validate reports of smoking status (Evans 1976) has also reflected the increas- ing methodological rigor of the psychosocial curricula research. Validated behavioral outcomes of prevention programs have progressively replaced earlier reliance on chan- ges in measures of attitudes and intentions and on self-reported smoking, thus provid- ing a firmer ground for comparison of program impact. After more than one decade of this research, however, the findings are characterized as tentative and subject to further evidence. No single study unequivocally establishes the effectiveness of the psychosocial approaches, but reviewers, taking the sum of the research, see support for the potential of these programs. The social influence and life skills training approaches programs have been characterized as capable of a 50-percent reduction of smoking onset that has been shown to persist for up to 2 years (Flay 1985a; Botvin, Renick, Baker 1983). The promise of these programs is tempered by such fac- tors as the complexity of the natural history of smoking acquisition (Cleary et al. 1988) and the continued need for long-term followup. (See subsequent sections for further discussion of these factors.) Two other variations in smoking prevention programs also have been considered and, pending their further development, are best classified along with the social influence approaches. One is the parent-oriented approach to social influences, whereby parents and their communication skills and influences are the direct object of intervention (Wor- den et al. 1987; Oei and Fea 1987). Parental support and involvement in school-based smoking prevention programs, especially for pre- to grade 6 programs, is recommended in Glynn (in press). Worden and colleagues (1987) tested the smoking prevention ef- fects of communication skills workshops for parents. While not presented to parents as a smoking prevention program, smoking was a focal topic and example throughout. Six months after the program was offered, significantly lower levels of self-reports of smoking among the fifth and sixth grade students in the communities that received high- intensity workshop coverage were demonstrated. Based on Oei and Fea’s (1987) review of data and rationale from studies bearing on youth smoking and on parents as educators, they recommend further utilization of parents in smoking prevention programs with young children. Another variation of smoking prevention programs using a cognitive development approach also builds on a developmental perspective on smoking acquisition. However, it considers social influences as but one set of factors bearing on the initia- tion of smoking among the young. Understanding processes of addiction, mechanisms for controlling emotions, and the relationship between smoking-induced sensations and 391 health threats is also seen as bearing on smoking by youth (Glynn, Leventhal, Hirschman 1985). A prevention program based on this model has been developed for students in the early stages of contemplating and experimenting with smoking. This cognitive development program significantly deviates from the social influence cur- ricula in its inclusion of both young nonsmokers and smokers and in its examination of nonsocial influences on their experience of smoking. However, the age groups targeted are the same, social influences are also part of the curricula, and, more fundamentally, the program shares with the social influence curricula a theory-based approach to direct- ly intervening in the processes and needs thought to underlie the development of smok- ing among young people. An 18-month followup of program and control students in grades 6 through 8 revealed significant differences in attitudes toward smoking and in students’ self-reports of smoking (Glynn, Leventhal, Hirschman 1985). Youth Smoking Cessation Programs Youth smoking cessation programs are properly viewed as part of smoking preven- tion efforts to the extent that their ultimate goal is the prevention of the establishment of dependent, regular smoking. The limited research in this area cannot yet suggest the optimal balance of traditional “prevention” and cessation strategies for programs tar- geting young smokers. Some young smokers may exhibit much variability in their smoking; others show a pattern of consumption very closely resembling older, addicted smokers. (See Chapter 5.) Recent interest in teenage cessation has been heightened by increasing social disap- proval of smoking and acceptance of its restriction on the part of adolescents and society more broadly (Johnston, O’Malley, Bachman 1987; US DHHS 1986b), as well as voluntary health association and public health agency commitments to promoting non- smoking environments in the schools (National School Boards Association 1987; US DHHS 1986a). Data on naturally occurring rates of quit attempts and cessation among young smokers support interest in teenage cessation. These rates range from 18 to over 50 percent cessation with varying followup periods and suggest considerable flux in the natural history of smoking, as well as opportunities for intervention with young smokers after they begin experimenting with cigarettes (Alexander et al. 1983; Chassin, Pres- son, Sherman 1984; Ershleret al., in press; Hansen 1983; Hansen et al. 1985; O’Rourke, Nolte, Smith 1985; Skinner et al. 1985; US DHHS 1982). Many of the early antismoking education programs incorporated cessation functions by virtue of their inclusion of older youth. Description of these early teenage smoking cessation programs, including those among the prototypes of antismoking education for youth, is included in the 1979 Surgeon General’s Report (US DHEW 1979b) and in Seffrin and Bailey (1985). Smoking cessation programs specifically for youth have been developed by researchers (Weissman et al. 1987; St. Pierre, Shute, Jaycox 1983), voluntary associations (ACS 1980, 1986; Bennett, Austin, Janizewski 1986), and school personnel (Hulbert 1978). Program effects on cessation rates among young smokers have also been examined in studies that emphasize prevention of initiation (Best et al. 1984; Botvin, Renick, Baker 1983; Johnson et al. 1986; Perry, Killen, Telch 392 et al. 1980). Cessation programs addressing young people’s use of smokeless tobacco have also been designed (e.g., Glover 1986; Severson et al. 1987). NCI is currently funding research on both prevention and cessation interventions for smokeless tobacco use, though no outcomes have been reported as yet (NIH 1986). Teenage cessation programs have met with mixed success, in terms of both recruit- ment and retention of program participants, and of program impact. Study of teenage cessation programs has also generally suffered from very small numbers of participants (in part, a reflection of difficulty in recruitment) and from a dearth of formal outcome evaluations. Subject characteristics, including baseline smoking levels, vary greatly from study to study, as do length of followup periods and outcome criteria considered. Although these limitations to the research are substantial and restrict conclusions that can be made conceming the efficacy of teen smoking cessation programs, the emer- gence of new demands for and research on such programs warrants the following review in comparatively more detail than for other larger and more controlled smoking preven- tion studies. St. Pierre, Shute, and Jaycox (1983) found reductions in self-reported rates of con- sumption among 10 of the 1] teen smokers who regularly participated in their program of peer-designed and peer-led “stop smoking” clinics. In evaluating AHA’s “Save a Sweet Heart” program’s no-smoking pledge day component, Bennett, Austin, and Janizewski (1986) found that the pledging was related to cessation at a I-year posttest in their sample of 194 10th-grade male smokers only, but not in the sample of 315 10th- grade female smokers. Overall, female students, including nonsmokers and smokers, were more apt than males to participate in the pledge component of the program. Weissman and colleagues’ teen cessation program (1987) used a contingency-based system of monetary rewards for reduction of expired carbon monoxide levels. The study suggested some promise among the males; four of the six male participants main- tained abstinence during the 5-month followup period, with only limited “slips.” However, all of the five females dropped out of the program before completion. Perry, Killen, Telch, and colleagues (1980) compared the effects of a four-session program emphasizing the immediate physiological effects of smoking and the role of social influences with outcomes from a more traditional curriculum emphasizing the long-term health effects of smoking. Statistically significant differences in self-reports of smoking 5 months later were found within the treatment group of 498 10th-grade students, pre-and posttest for daily and monthly smoking; and between treatment and control (399 10th-grade students) groups posttest only for weekly and monthly smok- ing. Significant differences in corresponding measures of expired carbon monoxide were also found. Taken in sum, there is some evidence that adolescent smoking cessation programs are efficacious, although the data and analyses are limited and difficult to interpret, and results are, therefore, far from conclusive. Further research and continued program development in this area are greatly needed. 393 History of Agency and Organizational Prevention Activities Although the concept of disease prevention did not gain its widest currency and im- pact in antismoking efforts or in health promotion and medicine as a whole until the late 1970s (US DHEW 1979a), young smokers always have been an important focus of antismoking efforts. Prevention activities were under way during the 1950s and early 1960s, even as the data on the health consequences of smoking were being reviewed by the scientific community (US DHEW 1979b). This Section on the history of preven- tion programs covers the national organizations’ initial antismoking efforts and State departments’ more current responses to the smoking problem, and the activities of a range of other organizations and agencies. The emphasis is on the major directions of their efforts, as opposed to comprehensive cataloging of all programs and initiatives. National Voluntary Health Organizations The three major national voluntary health organizations involved in the antismoking campaign, ACS, AHA, and ALA (previously called the National Tuberculosis Associa- tion and later the National Tuberculosis and Respiratory Diseases Association), developed their own curricular materials and resources for use in schools, as well as mass-distributed brochures, posters, films, and PSAs. In addition, they have funded smoking prevention research conducted by outside investigators (Bell and Levy 1984) and have contributed to the development of comprehensive school health education curricula that include smoking. In the late 1960s, in conjunction with CDC and other agencies, ALA began funding the development of the School Health Curriculum Project and the Primary Grades Health Curriculum Project, now jointly referred to as ‘Growing Healthy” (see descrip- tion in earlier section). In addition to promoting the adoption of “Growing Healthy” in schools nationwide, ALA has developed smoking education modules and curriculum materials, and a variety of films and posters. More recently, ALA developed the Biofeedback Smoking Education Project (BIOSEP) for students in grades 7 through 12, using student smokers and laboratory equipment, as a firsthand demonstration of the immediate negative physiological ef- fects of smoking (Mitchell 1978; Young, Chen, Cemada 1982). Two studies have evaluated the effect of BIOSEP on the smoking behavior of adolescents, Mitchell (1978) and Young, Chen, and Cernada (1982). However, the outcomes from these two studies are not consistent and offer only modest support for BIOSEP’s effects on smok- ing behavior. An alternative approach for younger students aged 9 to 13 years is ALA’s “Smoking Deserves a Smart Answer” (Bailey 1985). This kit uses a social influence approach centered on specific responses to direct peer pressure to smoke and includes humorous posters, stickers, a teacher resource guide, student worksheets, and sample role-play- ing Situations. Having issued a policy statement in 1963 to discourage smoking among both children and adults, AHA in 1967 developed sets of materials including a kit with a brochure for children to help their parents quit, a program that again may have had both cessa- 394 tion and prevention impact. Similarly, AHA’s “Like Father, Like Son” campaign tapped both cessation and prevention themes. AHA also has developed educational modules to prevent smoking among youth. Both the “Save a Sweet Heart” program and “Let’s Talk About Smoking” are based on social influence approaches, the former involving parodies of cigarette advertisements and the use of a pledging procedure, the latter teaching skills to resist peer pressure to smoke (US DHHS 1986a). Brochures have also been aimed at smoking in the context of the family (Children and Smoking: Message to Parents (AHA 1987)). In 1964, a National Conference on Cigarette Smoking and Youth was held under the auspices of ACS. Forty-four national organizations with a mission concerning young people participated. ACS developed numerous antismoking PSAs with prevention messages, including a 1967 television spot focused on the influence of parental smok- ing on children’s acquisition of smoking. Other early campaigns used popular cartoon and children’s story characters such as “The Three Little Pigs” to convey antismoking messages. ACS has developed a series of health and smoking prevention programs for students in kindergarten through the intermediate grades. “An Early Start to Good Health,” “ACS Health Network,” “Healthy Decisions,” and “Health Myself” are among the most widely disseminated ACS youth health education programs (US DHHS 1986a). The last of these programs, geared to students in the intermediate grades, emphasizes the role of societal influences on smoking. Referred to earlier in this Section, ACS has also developed teen cessation programs (ACS 1980, 1986). In 1987, ACS, AHA, and ALA began a collaborative campaign for a “Tobacco-Free America.” The project involves multiple goals and strategies, including smoke-free schools, mass media and advertising campaigns, a smoke-free class of 2000 promotion, and legislative initiatives (Bailey 1987). State-level coalitions of the three voluntary organizations also have developed programs of their own in support of this effort (US DHHS 1986a). The prevention program efforts of the voluntary associations were fairly quick responses to the accumulating data on the health risks of smoking. Their materials have used several channels of potential influence on young people’s smoking, primarily in- cluding family, media, and the school system. Compared with other prevention ap- proaches, the family and parental influences have been emphasized—specifically, the influence of parental smoking on the initiation of smoking by children. Antismoking messages in the context of the family thus could have both prevention and cessation ef- fects; parental nonsmoking was advocated as a powerful preventive influence. Wide distribution of materials was possible. The comprehensive school health education cur- ricula were evaluated while the other programs incorporated only limited evaluation. The extent of actual utilization and impact of the specific distributed materials is not known. National Interagency Council on Smoking and Health The National Interagency Council on Smoking and Health, created shortly after the first Surgeon General’s Report, fostered the early development of a variety of innova- 395 tive smoking prevention programs, many of which went on to receive continued major support from other Federal agencies. The “Youth Leadership in Smoking Controls Program,” begun in 1976 with funds from CDC and renewed through 1979, was not in- tended as a study of adolescent smoking education programs per se. Rather, its primary goal was “to identify new approaches for involving youth in smoking control activities” (National Interagency Council on Smoking and Health 1979, p. 12.). Anticipating later prevention programs’ orientation to the psychosocial factors affecting youth smoking, the program required that projects “show sensitivity to the needs, lifestyles and feel- ings of the 12-18-year-old adolescent,” and involve youth in the design and delivery of the material (p. 12). Thirteen smoking prevention projects were supported through these contract funds, none receiving more than 10,000 dollars in any one award. Ex- tent of program evaluation varied greatly. Projects resulting from this program were described in the program’s final report (National Interagency Council on Smoking and Health 1979) and in Cookbook for a Smokeless Diet, a humorous manual written for teachers and community members (National Interagency Council on Smoking and Health 1977). (See next section for further discussion of the National Interagency Council.) Federal Government Prevention Support The late 1970s were a key time for Federal Government involvement in and funding of prevention programs. Until that time, federally funded research emphasized biomedical mechanisms of smoking-related disease, as opposed to research on smok- ing behavior and interventions to reduce its prevalence (Bell and Levy 1984). Secretary of Health, Education, and Welfare Joseph A. Califano’s 1978 initiative to combat smok- ing led to appropriations for Federal agencies to support biobehavioral research into the factors affecting smoking and for the development of prevention and cessation programs (Bell and Levy 1984). Each of the Federal agencies developed initiatives for such research. Depending on the agency, smoking was the sole behavior targeted or, in other cases, one of a set of behaviors the agency sought to prevent. For instance, the National In- stitute on Drug Abuse (NIDA) was concerned with substance use more broadly, NHLBI with cardiovascular risk factors. The agencies within the Department of Health and Human Services (successor to the Department of Health, Education, and Welfare (DHEW)) with initiatives most directly bearing on the prevention of tobacco use among children and adolescents included NCI, the National Institute for Child Health and Human Development (NICHD), NIDA, NHLBI, and CDC. In addition, OSH (Bell and Levy 1984) (OSH is now part of CDC) developed such initiatives. Federal health agen- cy and OSH prevention initiatives included both research support leading to the development of prevention programs and the production of prevention resources and programs for direct use by schools and other organizations. In addition, guides of ex- isting resources are periodically produced by Federal agencies, including Smoking Programs for Youth (US DHHS 1980a) and Smokescreen: Guidelines for Helping Teenagers Become Nonsmokers (American Institutes for Research 1980), contracted by CDC. 396 Office on Smoking and Health The U.S. Public Health Service first officially became engaged in an appraisal of the available data on smoking and health in June 1956 when, under the direction of Sur- geon General Leroy Bumey, a scientific study group was established (Burney 1959). In 1957, the Public Health Service adopted the position that “excessive smoking is one of the causative factors in lung cancer” (Burney 1959). In 1964, DHEW became active- ly involved in efforts to discourage smoking. The seminal smoking-and-health event in this evolution of Federal involvement was the 1964 release of the Surgeon General's Report on Smoking and Health. At that time, Surgeon General Luther Terry established an office within the Public Health Service Chronic Disease Control Program (US DHHS 1986a) to help collect, organize, and analyze information on smoking and health. This office later became the National Clearinghouse for Smoking and Health and stil] later (March 1978), OSH. (See Chap- ter 7.) In the early years of the Clearinghouse, a number of innovative smoking control in- itiatives were supported, some of which are continued today by CDC, Center for Chronic Disease Prevention and Health Promotion (which now includes OSH), and by the Department of Education (US DHHS 1986a). Initially, the Clearinghouse developed curricula and teaching materials to educate young people about the hazards of tobacco use (US DHHS 1986a). Many of these materials are now being used in schools across the country. The Clearinghouse pioneered an effort to place PSAs in high school newspapers. It was also involved with mass distribution of pamphlets, program materials, and television PSAs. Between 1966 and 1971, the Clearinghouse conducted the first study of a communitywide smoking control intervention in San Diego Coun- ty, CA (US DHEW 1976). This project involved interventions aimed at schoolchildren, health professionals, and adult smokers. The San Diego project developed curriculum guides for students in grades | through 12, as well as newsletters to support the efforts of teachers and other health profes- sionals involved in the project. A “Youth-to-Youth” program, precursor to peer-led programs, was also included. Although evaluation of the project was limited, the data collected suggested that the intervention had been successful. Survey results show sig- nificant reductions between 1966 and 1975 in the percentage of teenage and adult smokers in San Diego compared with national samples (US DHEW 1976). The programs of the San Diego Community Laboratory led to the development of other comprehensive health curriculum projects such as the School Health Curriculum Project. Today, OSH continues its efforts for smoking prevention through the development and distribution of educational materials. It currently has a program of disseminating print PSAs through high school and college newspapers, as well as televised PSAs aimed at teenagers (US DHHS 1986a). OSH has been the only Federal office devoted solely to the smoking issue. Now part of CDC, the Office continues to perform the same functions that were established for the Clearinghouse in the 1960s (US DHHS !986a). OSH continues to serve as a repository for information on smoking and health and responds to thousands of public 397 inquiries for information each year. As part of its technical information service, it publishes a bimonthly bulletin of abstracts of published literature on smoking and heaith and periodically compiles a directory of ongoing research in smoking and health. OSH also periodically conducts surveys to estimate the prevalence of tobacco use among adults and adolescents and to determine the Nation’s attitudes, knowledge, and beliefs concerning smoking, tobacco use, and their health effects. OSH continues to plan, coor- dinate, and produce public and professional information and education programs on smoking and health that are distributed either directly or through other institutions such as voluntary health organizations and State and local health departments. It is the responsibility of OSH to prepare and disseminate the annual Surgeon General’s Report to Congress on the Health Consequences of Smoking, as required by Federal law (Public Law 91-222). Finally, OSH has new responsibilities under the Comprehensive Smok- ing Education Act of 1984 (Public Law 98-474) to collect information from the cigarette industry on cigarette additives, to transmit to Congress a biennial status report on smok- ing and health (US DHHS 1986a), and to provide staff support to the newly created Federal Interagency Committee on Smoking and Health (see Chapter 7). National Cancer Institute In the 1950s, scientists working at the NCI were among those who helped identify cigarettes as a cause of illness and premature death (Burney 1959). In 1955, NCI, in cooperation with the U.S. Bureau of the Census, sponsored the first large-scale nation- al survey of smoking patterns in the United States (Burney 1959). It was not until 1968, however, with the appointment of the Lung Cancer Task Force, that NCI established a formal research program to address the smoking issue. The Lung Cancer Task Force and a subcommittee of the Task Force, the Tobacco Working Group, established three objectives for the program: (1) production of a less hazardous cigarette, (2) identifica- tion of persons at increased risk of tobacco-related disease, and (3) development of pharmaceutical interventions to control smoking behavior. Development of a less haz- ardous cigarette was given a high priority until 1978, when this aspect of the program was abandoned. Prior to 1977, NCI funded little research on behavioral interventions for smoking. A major shift occurred in 1980, when prevention was identified as an NCI priority (NCI 1984). In 1982, NCI reorganized its smoking research program, establishing the Smok- ing, Tobacco, and Cancer Program (STCP) within the Division of Cancer Control (Cul- len 1986; Cullen, McKenna, Massey 1986; Glynn, in press). Included in STCP fund- ing was research to prevent adolescent tobacco use. In fiscal year 1985, STCP funded 14 grants on adolescent tobacco use and its prevention, with budgets totaling over 5.5 million dollars for the year. The studies were designed to include approximately 170,000 students in grades 6 through 12 (NCI 1984, 1986a). Twenty-three adolescent smoking intervention trials, involving approximately 1 million youth, were under way by early 1988 (Glynn, in press). In response to increased use of smokeless tobacco among young males in the 1970s and 1980s (US DHHS 1986c), NCI also took the lead in funding smokeless tobacco prevention programs. Seven of the 23 NCI-funded trials focus on the prevention of adolescent use of smokeless tobacco. 398 The prevention and control of smoking and other forms of tobacco use have become top priorities for cancer prevention within NCI (Fanning 1988). In 1987, 80 percent of the 37 million dollars spent on smoking research was allocated to studies of smoking behavior. Smoking research accounted for approximately 2.7 percent of NCI’s total budget in 1987. After funding intensive research for several years in the development and evaluation of smoking prevention programs, NCI has begun to emphasize the need for widespread dissemination of these and other smoking intervention programs (NCI 1986b) and has so far funded two new studies of the integration of tobacco education in the schools. National Heart, Lung, and Blood Institute NHLBI began funding smoking prevention efforts in 1974 through the Vermont Lung Center; NHLBI had received an expanded mandate (for research on the prevention of behavioral risk factors) legislated by the National Heart, Blood Vessel, Lung and Blood Act of 1972. Continuing through 1983, the Vermont Lung Center’s activities included a smoking prevention program aimed at youth aged 10 to 15 years (Stone 1985). During the mid-1970s, NHLBI supported the paradigm-setting work of Evans and his colleagues in the development of socially and psychologically based prevention programs (Evans 1976; Evans et al. 1981), and the development of the peer-taught smoking and substance abuse prevention program of McAlister and colleagues (Mc- Alister et al. 1980; Stone 1985). The majority of the smoking prevention programs sponsored by NHLBI in the years to follow were part of more comprehensive, and often communitywide, approaches to cardiovascular risk reduction. In the early 1980s NHLBI was sponsoring 15 school-based cardiovascular risk studies, 10 with explicit smoking prevention components—in all but 2 of the 10 studies, other risk factors such as nutrition and physical activity were also targeted (Stone 1985). National Institute on Drug Abuse In the mid-1970s, NIDA addressed the behavioral factors of cigarette smoking and the addictive properties of nicotine by supporting research and issuing a series of monographs on cigarette smoking by Jarvik and colleagues (1977) and Krasnegor (1979a,b). In addition to sponsoring research on nicotine dependence and treatment in their own right, NIDA has approached cigarette smoking as another form of substance abuse and as a possible “gateway drug” that could lead to the use of other substances (US DHHS 1986a). The new smoking prevention programs were used as a prototype for the prevention of other forms of substance abuse (Bell and Battjes 1985). National Institute for Child Health and Human Development NICHD began funding of research on smoking and health in the early seventies. During the mid-1970s, this effort was intensified as part of a program initiated by Secretary of Health, Education, and Welfare Joseph A. Califano. At that time the In- stitute identified two primary research areas: (1) factors related to risk-taking behavior 399 by children and the initiation of smoking, and (2) the effect of maternal smoking on the developing fetus. Emphasis on these two areas continues to the present. NICHD is working with the American College of Obstetricians and Gynecologists to develop a smoking cessation program for pregnant women,to be used in private obstetricians’ practices. Office of Disease Prevention and Health Promotion The Office of Disease Prevention and Health Promotion (ODPHP) coordinates all prevention activities in the Public Health Service. ODPHP has sponsored evaluation of school health curricula’s effects on smoking behavior (US DHHS 1986a) and sup- ported a national survey of 8th and 10th graders’ health knowledge, attitudes, and prac- tices, including their smoking behaviors (US DHHS, in press; see Chapter 5). Surgeon General’s Reports The Surgeon General’s Reports and the media coverage surrounding them are among the primary ways that the Federal Government informs the public about the health con- sequences of tobacco use. The themes, emphases, and detailed reviews of these reports reflect the knowledge and interests of a large group of scientists in the United States and abroad. (Chapter 1 provides a list of the major topics covered in each of the Sur- geon General’s Reports since 1964.) While not including a description of or specific recommendations for prevention programs, a section entitled “Taking Up Smoking” was included in the 1964 Report’s Chapter entitled “Psychosocial Aspects of Smoking.” The changing relationship of the child’s smoking to parental and peer smoking as the child grows older was noted in the 1964 Surgeon General’s Report: “As children grow older, they themselves, as well as their relationship to the home, change. With approaching adulthood and its associated new social patterns, other influences supplant those of the parents” (US PHS 1964, p. 369). Asa further indication of prevention programs’ roots ina stage approach to smok- ing acquisition, the 1964 Report continued, “It is quite possible that parents’ influence affects the age at which children start smoking much more than it affects the ultimate taking or not taking up of the habit” (p. 370). (See Chapter 5 regarding determinants of smoking behavior.) Consideration of young people and smoking in the Surgeon General’s Reports after 1964 was initially restricted to documenting the extent of health effects among young smokers. Then in the 1977—78 Report, under the heading “Implications for Action,” it was concluded that “dissuading young nonsmokers from starting to smoke” would result in the “greatest long-term benefits” compared with modifying the content of cigarettes or getting adult smokers to quit (US DHEW 1978, pp. 48-49). As for specific prevention approaches, the Report concluded that “health education of the young” was one of several antismoking efforts affected by “lack of knowledge on smoking behavior ...Although much is known about some of the principles contributing to effective health education of the young, these have not yet been incorporated into programmes, which 400 could provide convincing evidence of their ability to reduce smoking” (US DHEW 1978, p. 54). The 1979 Surgeon General’s Report was a watershed for smoking prevention, as well as other smoking issues. Two chapters were devoted exclusively to smoking among young people and its prevention, Chapter 17 (“Smoking in Children and Adolescents: Psychosocial Determinants and Prevention Strategies”) and Chapter 20 (“Youth Educa- tion”) (US DHEW 1979b). In merging considerations of psychosocial smoking deter- minants among youth with considerations of more traditionally phrased “educational” programs, the 1979 Report reflected a critical transition in the development of preven- tion approaches and in their treatment in the Surgeon General’s Reports. The introduc- tion to Chapter 17 began with “It is possible that prevention programs directed at children and adolescents have generally placed too much confidence in merely com- municating knowledge about the dangers of smoking” (p. 17-5). The Chapter then reviewed the range of psychosocial influences on youths’ decisions to smoke, and called for including developmental and social psychological theory in the conceptual basis of prevention programs. Demographic and psychosocial correlates of smoking among adolescents and smok- ing prevention approaches, with special reference to young girls and gender differen- ces, were reviewed in the 1980 Surgeon General’s Report on the health consequences of smoking for women (US DHHS 1980b). The 1981 Report on the changing cigarette (US DHHS 1981) did not consider smoking prevention per se, but briefly reviewed data on preferences among young smokers for cigarettes with various tar and nicotine levels. The natural history and prevention of smoking among adolescents were considered again in the 1982 Report on cancer (US DHHS 1982). Consensus was reached in this Report: the newly developed prevention programs based on social psychological theory were capable of a 50-percent reduction in smoking onset. The 1982 Report also included data on smoking cessation among adolescents. Prevention programs were not considered in the 1983 Report on cardiovascular disease (US DHHS 1983a), the 1985 Report on cancer and chronic lung disease in the workplace (US DHHS 1985a), or, with the exception of its review of nonsmoking policies in the schools, in the 1986 Report on involuntary smoking (US DHHS 1986b). While several smoking prevention programs were reviewed in the 1984 Report’s review of community studies of smoking control, it was noted that, for the most part, community studies focused on smoking cessation among adults, rather than on prevention (US DHHS 1984). Most recently, the 1988 Surgeon General’s Report on nicotine addiction concluded that smoking prevention should be integrated into substance abuse prevention programs for youth (US DHHS 1988), though the specific program options available were not reviewed. State Health Departments State health department initiatives to curb tobacco use have increased in the past decade (US DHHS 1986d). Many State health departments have established smoking education programs (US DHHS 1986a). State departments of education and depart- ments of health often serve as clearinghouses, compiling guides to existing prevention resources (e.g., University of the State of New York 1979). Several State health depart- 401 ments have organized special committees to develop comprehensive smoking control plans (Coye 1988; Minnesota Department of Health 1987; US DHHS 1986a), with most focusing on prevention rather than cessation. Several of these plans are cited in Chap- ter 7 (Table 20). Most notable among the plans is Minnesota’s, which, in addition to a broad range of other prevention program and policy components, earmarks a portion of the State cigarette excise tax to support smoking control initiatives (Minnesota Department of Health 1987). The 1986 inventory of State and local programs (US DHHS 1986d) described preven- tion programs operating through 20 State departments of health, State interagency coali- tions on smoking and health, and State departments of education. These prevention in- itiatives include a variety of approaches: implementation of existing health curricula, the development of specific new resources and guidelines, teacher training programs, promotion of resource centers, and community and parent programs. In an additional nine States, county organizations, including departments of health and interagency coalitions, were listed as undertaking specific smoking prevention projects that were most often curriculum based. Other Organizations and Agencies Although tobacco control is not their central mission, other institutions, agencies, and medical societies integrate smoking prevention programs into materials for distribution through schools and other settings. The program materials include the March of Dimes’ for (often) young, expectant mothers; National Institute on Alcohol Abuse and Al- coholism materials on substance abuse (US DHHS 1986a); and the American Dental Association materials on tobacco use, especially the use of smokeless tobacco and oral disease. Through their professional organizations and as individuals, physicians and other health researchers have designed materials and presentations, primarily for school as- semblies. The American Medical Association (AMA) (1987), the American Medical Women’s Association, and Doctors Ought to Care (DOC) are among those organiza- tions that have designed smoking prevention materials and currently promote their delivery through school assemblies. Volunteers for Health Awareness, a society of health researchers and health care providers in the Boston area, have delivered anti- smoking assemblies to junior high school students each year since 1969 (Reif 1976; US DHEW 1979b). In collaboration with ALA and researchers at Lawrence Hall of Science at the Univer- sity of California, Berkeley, the American Nonsmokers’ Rights Foundation (formerly California Nonsmokers’ Rights Foundation) has also developed smoking prevention curricula centered around a television documentary, “Death in the West” (Bailey 1985) and a film entitled “Second Hand Smoke” (American Nonsmokers’ Rights Foundation 1986). Addiction and tobacco industry tactics are highlighted in the curricula (Califor- nia Nonsmokers’ Rights Foundation 1983). The foundation has also developed an ad- junct peer-led program called “Teens as Teachers” to complement use of the films. By 1979, it was estimated that there were thousands of smoking prevention activities independently undertaken by schools and community groups, programs largely neither 402 formally described nor evaluated (Evans et al. 1979: US DHEW 1979b). While there is increasing documentation of programs on the national and State level (US DHHS 1986a, 1986b), program development and implementation by schools and communities, as special events or as part of existing health education curricula, are far less likely to be systematically recorded and evaluated. Problems in Dissemination of Smoking Prevention Programs Evaluation of the development and progress of prevention programs must include both controlled, scientific examination of program efficacy and study of the factors characterizing actual and potential widespread use of programs and their public health impact. This represents a merger of perspectives only recently formally considered in the field of smoking prevention programs (NCI 1986b; Best et al. 1988; Cleary et al. 1988; Flay 1985b). The current state of smoking prevention programs and resources reveals a gap be- tween these two approaches. The research-driven smoking prevention curricula have most often been developed without a mechanism for widespread application and use. In turn, many of the materials likely to be used in the field by public health profes- sionals, educators, and other policymakers responsible for young people’s health have had limited evaluation, except for the comprehensive health education curricula, and the extent and process of their dissemination have generally not been systematically documented. Once research-based programs are developed and initially found to have potential impact, there have not typically been mechanisms to encourage their active distribu- tion to school systems and other organizations. Most at best can only respond to specific requests for information about their program or dissemination of their materials. Recognizing this research gap, NCI (1986b) has initiated research to determine the most effective method to integrate tobacco education programs that have been proven to be efficacious into school programs. It is encouraging research that is focused more on application and dissemination than on the development of new curricula and interven- tions. Some of the issues bearing on program dissemination are reviewed in the smoking prevention literature (Best et al. 1988; Cleary et al. 1988); others are considered in broader literature on health education, program adoption, and the diffusion of innova- tion (Basch, Eveland, Portnoy 1986; Basch and Sliepcevich 1983; Murray 1986). Bar- riers specific to widespread institutionalization of smoking-specific programs within schools include demands on teacher time, cost of materials for specific programs and teacher training, and the variety of competing educational and health priorities found within a school system. (See also Kolbe and Gilbert (1984) for a discussion of obstacles to school implementation and maintenance of new health education programs.) Ideal- ly, the likelihood of distribution and use of prevention programs in the field should be considered throughout the course of program design and evaluation and not restricted to end-stage discussions of the feasibility of disseminating already developed and evaluated programs. 403 The availability of funding to bolster dissemination of existing programs has varied over time. Federal funding for implementation and demonstration of health education programs was provided by the 1979 Health Education Risk Reduction Grant Program (Kolbe and Iverson 1984). Additional funds were appropriated in 1980 for grants to deter smoking and use of alcohol by adolescents. The reorganization of such categori- cal grant programs into a block grant structure in 1981 resulted in a shift of Federal funds to the State level. However, the reduction of total available funds and the restructur- ing of the funding mechanism created competition within States for these funds and eliminated smoking-specific demonstration grants. It also made for less secure support of health education in general (Kolbe and Iverson 1984). Although a variety of or- ganizational, social, and political factors can affect the likelihood of adoption and use of a particular prevention program, the effect of availability of funds for teacher train- ing, purchase of materials, and even the simplest of evaluations must be considered in any analysis of the history and prospects of prevention efforts. Dissemination mechanisms also include providing information about programs. Federally funded databases and programs with potential for aiding the dissemination of smoking prevention programs are available. The Combined Health Information Database includes information on State and local programs listed in the National Status Report on Smoking and Health (US DHHS 1986a), as well as information on programs funded under the 1979-81 smoking and alcohol grant program (US DHHS 1986a). The NDN of the National Institute on Education includes data on extent of diffusion of evaluated and validated curricula. While health education is not its primary focus, NDN does include five comprehensive health education and substance abuse preven- tion programs into which smoking prevention has been integrated, including “‘Grow- ing Healthy” (NDN 1988b). Other promising programs, such as “Know Your Body,” are currently under review. By providing information on the programs, awarding grants to further the dissemination of selected curricula, and maintaining annual records on program dissemination among participants (NDN 1988a), NDN functions both in the active dissemination of programs and in monitoring the extent of use of various cur- ricula nationwide. Complementing the need to get research-derived programs into the hands of schools and other organizations, continued program evaluation is needed once they are out in the field. These data are needed to address questions concerning the applicability of programs, the extent and quality of implementation, and their effectiveness once out- side of controlled research settings. Additionally, through inquiry into factors affect- ing actual distribution and use of programs, these evaluations could also contribute to the development of guidelines supporting effective dissemination of smoking preven- tion programs. In these evaluations of the dissemination process, statistics need to go beyond data such as number of sets of program materials distributed, to include surveys of actual use and degree of implementation as well as program impact. The evaluation of two ACS elementary school health education programs, for example, included data on teacher use of materials (Pigg et al. 1985). There was considerable variation in the per- centage of teachers reported to have used materials in those schools that had kits avail- able. The ACS “Usage Report Card,” a record-keeping system for use by teachers to 404 document numbers of children exposed to the materials, was not always completed and mailed as requested, according to 75 percent of schools surveyed. Variability in extent of use and in documenting such use contributes to the difficulty of interpreting levels of implementation even when, in the case of this study, approximately 80,000 copies of the programs had been distributed to schools. Best and colleagues (1988) have outlined research needs on the diffusion of smoking prevention programs—tresearch the authors consider at least as vital as that evaluating effectiveness of program content. Diffusion studies, they conclude. should entail con- sideration of five sets of factors: planned diffusion strategies, program packaging, provider training, implementation monitoring, and costing (both cost of materials and cost-effectiveness of the program). Problems in Evaluation of Smoking Prevention Programs Prevention efforts within the psychosocial, more general health education, and media approaches have operated with very different goals, intended mechanisms for effect, and standards for evaluation. As reviewed above, the psychosocial influence smoking prevention curricula have been subjected to years of research development and evalua- tion (e.g., Best et al. 1988; Biglan and Ary 1985; Flay 1985b,; McCaul and Glasgow 1985; Snow, Gilchrist, Schinke 1985). The literature contains much detail about their effects in university-administered research projects. However, far fewer data are avail- able on the extent of their adoption and use by others in the field and on their impact when implemented in less-controlled settings (Best et al. 1988; Cleary et al. 1988). In most cases, active mechanisms for dissemination of the research products are lacking. These programs are most often not part of a system to ensure their dissemination once the typical 3- to 5-year development and evaluation phase of the research is complete. (See Prevention Section, Problems in Dissemination of Prevention Programs.) Prevention programs based on PSAs, posters, brochures, and other curriculum resour- ces sponsored by Federal agencies and professional and voluntary organizations have been widely distributed through the tremendous efforts of these agencies and organiza- tions. However, their effectiveness has generally been less thoroughly evaluated than that of the psychosocial smoking prevention curricula. Reflecting the priority of using their limited resources for dissemination, the programs and their outcomes rarely receive a level of evaluation comparable to that found in the peer-reviewed research literature on smoking prevention. Continuing methodological problems in prevention research include variations in criteria for measuring smoking outcomes in different studies, problems of attrition (Biglan et al. 1987; McAlister and Gordon 1986), limitation to white middle-class sub- jects (Gilchrist and Schinke 1985; Glynn in press), differences in level of analysis of effects and level of assignment to treatment or control group (Flay 1985a), and limited long-term followup. 405 Need for Long-Term Followup The need for long-term perspectives and followup of the effects of smoking preven- tion programs has been noted in the 1979 Surgeon General’s Report (US DHEW 1979b) and by Chassin and colleagues (1985), Evans (1984), and others. Prevention effects need to be maintained and monitored throughout the high school years to ensure that youth pass through this risk period without becoming smokers. Although long-term evaluation of prevention programs is frequently included in review article recommen- dations for future research (Biglan and Ary 1985; McAlister, Perry, Maccoby 1979), reports of 2-year or, less frequently, 3-year impact (for study subjects most often originally in junior high) constitute the most common long-term followups (Telch et al. 1982; Johnson et al. 1986; Chassin et al. 1985). A recent report by Flay, Thompson, and colleagues (1987) included results for a 6-year followup of students in the Water- loo Smoking Prevention trial. While prevention of onset of experimental smoking per- sisted through the end of grade 8, at the next assessment, during grade 12, no significant effect remained. Another NCI-funded smoking prevention project is currently tracing subjects through the important transition beyond high school (Murray, described in Glynn, in press). There are data suggesting that de/ay in initiation can constitute a desirable preven- tion outcome: delayed onset has been found to be associated with decreased mortality (US DHHS 1986a) and increased likelihood of quit attempts and cessation during the school years (Ershler et al., in press). However, variations in age of onset considered in these studies were naturally occurring and not the result of a specific prevention program. Thus, it remains to be confirmed that program-induced delays in onset among contemporary youth have the same relationship to later smoking behavior and health outcomes as do the naturally occurring variations. Construct Validity Another major methodological challenge posed in the evaluation of prevention programs is the problem of construct validity (Flay 1985a; McCaul and Glasgow 1985). With even the most highly developed programs, given their use of a multiple component format, it has been diffi