Reducing the Health Consequences of Smoking 25 YEARS OF PROGRESS a report of the Surgeon General 1989 Executive Summary U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service Centers for Disease Control Center for Chronic Disease Prevention and Health Promotion Office on Smoking and Health Rockville, Maryland 20857 Suggested Citation U.S. Department of Health and Human Services. Reducing the Health Cunsequen- ces of Smoking: 25 Years of Progress. A Report of the Surgeon General. U.S. 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. DEc291988 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 Suokfng 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 s-king 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. spoking 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 me". Smoking prevalence among me" 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 s-king 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 Aaerlcane 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 slake-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 Zlst century. Sincerely, Otis R. Bowen, M.D. Secretary Enclosure 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 Conseauences of Smokinsx 25 Years of Proaress, 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 s 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, 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. 2. 3. 4. 5. 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. 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. 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. 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. 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 0. 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 reaction on Wall 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-coveredReport were hand delivered to the West Wing of the White House at 7:30 on that Saturday morning. 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 111 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 small 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 50 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,ooO 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 will 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 198 1 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 3 1 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 general 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 learned 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 . . VI11 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., MS., 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 X 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. Sarnet, 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, Southwestern 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. Thomberry, 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. Bums, 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. Emster, 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. Garner, J.D., Professor of Law, Southern 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 Xl11 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. Lute, 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 0. 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 Mutt, 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., MSc., 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. Thomberry, 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 Attis, 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. Bonnet& Senior Editor, The Circle, Inc., McLean, Virginia Catherine E. Burckhardt, Editorial Assistant, Offtce 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 Health, 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 XVIII 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..i Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..iii Acknowledgments .................................................. ..i x 1. Historical Perspective, Overview, and Conclusions ...................... 1 2. Advances in Knowledge of the Health Consequences of Smoking .......... 33 3. Changes in Smoking-Attributable Mortality .......................... 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 ......................................... 465 8. Changes in the Smoking-and-Health Environment: Behavioral and Healthconsequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645 Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...685 Index.............................................................689 xxi CHAPTER 1 HISTORICAL PERSPECTIVE, OVERVIEW, AND CONCLUSIONS CONTENTS Historical Perspective ................................................. 5 Highlights of Conclusions and Findings .................................. 11 Major Conclusions . . . . . . . . . . . . . . . . 11 ,. 11 . . 13 . 16 Key New Findings . . . . . . . . . . . . _ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Overview . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Coverage of the Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1990 Health Objectives for the Nation . . . . . . . . . . . . . . . . . . . . . LimitationsofCoverage . . . . . . . . . . . . . . . . . . . .._...................... 19 Development of the Report . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 ChapterConclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...20 Chapter 2: Advances in Knowledge of the Health Consequences of Smoking . 20 Part I. HealthConsequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Part II. The Physicochemical Nature of Tobacco . . . . . . . . . . . . . . . . . 2 1 Chapter 3: Changes in Smoking-Attributable Mortality . . . . . . . . . . . . . . . . . . 21 Chapter 4: Trends in Public Beliefs, Attitudes, and Opinions About Smoking . 22 Chapter 5: Changes in Smoking Behavior and Knowledge About . . . . . . . . . . . . . . . . . . Determinants -. . . . . . . . . . . . . . . . . . . . . . . . Part I. Changes in Smoking Behavior . . . Part II. Changes in Knowledge About the Determinants of Smoking Behavior . . . . . . . . . . . . . . . . . . . . . . . . . . . . _ . . . . . Chapter 6: Smoking Prevention, Cessation, and Advocacy Activities . Part I. Smoking Prevention Activities . . . . . . . . . . . . . . . . . . . . . Part II. Smoking Education and Cessation Activities . . . . . . . . . Part III. Antismoking Advocacy and Lobbying . . . . . . . . . . . . . . Chapter 7: Smoking Control Policies . . . . . . . . . . . . . . . . . . . . . . . . . Part I. Policies Pertaining to Information and Education . . . . . . . 23 . 23 . 24 . . 25 . . 25 . . 25 . . 26 . . 26 . . 26 Part II. Economic Incentives .............................. 27 Part III. Direct Restrictions on Smoking ..................... 28 Chapter 8: Changes in the Smoking-and-Health Environment: Behavioral and HealthConsequences ........................................... ..2 8 References ......................................................... 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 195Os, 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 lung cancer was causal (Study Group on Smoking and Health 1957). On July 12 of that year, U.S. Surgeon General Leroy Bumey 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 Bumey said that "The weight of evidence at present implicates smoking as the principal factor in the increased incidence of lung cancer" (Bumey 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 5 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 I, 1961, the presidents ofthe 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 -esearch 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). 6 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 9 l-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 197 1-75 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 1 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- 7 TABLE l.-!Wgeon General's Reports on smoking and health, 1944-88 Year Subject/Highlights 1964 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 lung cancer in men and a suspected cause of lung cancer in women. Identified many other causal relationships and smoking+ilsease asxxiations (US PHS 1964). 1967 1968 1969 1971 1972 1973 Confirmed and strengthened conclusions of I964 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 informatlon 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 l/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 nonsyphiiitic 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 lmmunologxal 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 &ease: tobacco smoke contains hundreds of compounds, several of which have been shown to act as carcinogens, tumor initiators, and tumor promoters. ldentifled 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 healthy young men. Presented additional evidence on smoking as risk factor m peripheral vascular disease and problems of pregnancy (US DHEW 1973). 8 TABLE l.-Continued Year Subject/Highlights 1974 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). 1975 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). 1 976a Compiled selected chapters from 197 l-75 Reports (US DHEW 1976). 1977-78 Combined 2-year Report focused on smoking-related health problems unique lo women. Cited studies showing that use of oral contraceptives potentiates harmful effects of smoking on the cardiovascular system (US DHEW 1978). 1979 1980 1981 1982 I983 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 10 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 small 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). 9 TABLE l.-Continued Year Subject/Highhghts 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 1986 1986b 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 theu workplace environment. Risk of lung cancer from asbestos exposure characterized as multiphcative 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). 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). 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 l986b). 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 senes volumes m text because no new evidence war rewewed. hExcluded from count of senes volumer in text beau% it aas a Special Report. not m the ener of repon\ on vnokmg 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 Sectionof 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 . . . . . 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. 12 . 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 50million 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. o 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. 13 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 1. 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 Chapter 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 scientific-medical 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 I 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 III). 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, bum 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 1986~). 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 16 TABLE 2.-1990 health objectives for the nation pertaining to smoking Reduced risk factors I. By 1990, the proportion of adults who smoke should lx reduced to below 25 percent. 2. By 1990, the proportion of women 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. during pregnancy should be no greater than one-half the proportion of women overall who smoke. 4. By 1990, the sales-weighted average tar yield of cigarettes should be reduced to below IO 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 I2-year-olds should be able to identify smoking cigarettes with increased risk of serious disease of the heart and lungs. TABLE 2.-Continued Improved services/protection IO. By 1990, at least 35 percent of all workers should 13. By 1990, laws should exist in all 50 States and all be offered employer/employee-sponsored or -supported jurisdictions prohibiting smoking in enclosed public smoking cessation programs either at the worksite or in places, and establishing separate smoking areas at work the community. and in dining establishments. I I. By 1985, tar, nicotine, and carbon monoxide yields should be prominently displayed on each cigarette package and promotional material. 14. By 1990, major health and life insurers should be offering differential insurance premiums to smokers and nonsmokers. 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. Improved surveillance/evaluation 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. 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. 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. SOURCE: US DHHS (19Kob). tobacco use is one of 2 1 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 relative 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. 8. Studies dating from the 1950s have consistently documented the benefits of smok- ing cessation for smokers in all age groups. 9. 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 II. 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. 2. Forty-three carcinogens have been identified in tobacco smoke. 3. 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, 1959965, and CPS-II, 1982-86). Lung cancer death rates for younger male smokers fell about 30 to 40 percent during this period. 2. 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. 3. 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. 4. 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. 5. 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. 6. 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. 7. 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. 9. 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 1. 2. 3. 4. 5. 6. 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 7 1 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 having-a 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. 22 7. 8. 9. 10. 11. 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 5 I 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 3 1.7 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. 2. Annual per capita (I 8 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 198 1 and then fell to 574 billion in 1987. 3. 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. 11. 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 2 1. 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 2 1 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 so&demographic 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 198 1, after which this proportion fell slightly and then stabilized at 5 1 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 II. Changes in Knowledge About the Determinants of Smoking Behavior 1. 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. 24 2. 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. 3. 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 on a 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. 2. 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. 3. 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. 4. 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. 5. 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 2. 3. 4. 5. 6. 7. 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 1. 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. 2. 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. 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 wam- ing labels is now required for all cigarette and smokeless tobacco packaging and advertisements. 2. 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 26 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. 3. There is insufficient evidence to determine the independent effect of cigarette warning labels, particularly the rotating warning labels required since 1985, on public knowledge about the health effects of smoking or on smoking behavior. 4. 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. 5. Declines in adult per capitacigarette 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 a&smoking public service announcements were widely broad- cast on radio and television, as mandated by the Federal Communications Commission's Fairness Doctrine. 6. 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). 7. An estimated 1 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. 2. 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. 3. 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. 2. 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. 3. 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. 4. 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. 5. 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. 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. 2. 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. 3. 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). 4. 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. 5. 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 28 low-nicotine cigarettes in the 1970s. The net health impact of these product chan- ges is unknown. 6. 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 2 1 years. 7. 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., HLSAMICHI. S., TOMINAGA. S. (eds.) SmorC-ing 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, NC1 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. Squamous-cell epithelioma of the lip. A study of five hundred and thirty- seven cases. Journal of the Americ,an Medical Assncia~ion 74( 10):656&?4, March 6, 1920. BURNEY. L.E. Smoking and lung cancer. A statement of the Public Health Service. 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Journal of the American Medical Association 143:329-396, May 27. 1950. 32 CHAPTER 2 ADVANCES IN KNOWLEDGE OF THE HEALTH CONSEQUENCES OF SMOKING CONTENTS Introduction ........................................................ 37 -~~~ Partl: HealthConsequences ........................................ ..3 8 Smoking and Overall Mortality ...................................... 38 LungCancer ................................................... ..4 3 Introduction .............................................. ..4 3 Dose-Response Relationships .................................. 43 WomenandLungCancer .................................... ..4 6 Type of Lung Cancer and Smoking .............................. 50 PipeandCigar Smoking ....................................... 50 Determinants of Susceptibility .................................. 50 Familial Factors .......................................... 52 Other Host Factors ....................................... 52 Occupational Exposures ................................... 52 Ambient Air Pollution ..................................... 53 Indoor Air Pollution ...................................... 53 Diet ................................................. ..5 4 Smoking Cessation ........................................... 55 Laryngeal, Oral, and Esophageal Cancer ............................... 56 BladderandKidneyCancer ....................................... ..5 6 PancreaticCancer ............................................... ..5 6 Stomach Cancer ................................................... 57 CervicalCancer ................................................. ..5 7 Endometrialcancer ............................................. ..5 8 Coronary Heart Disease ............................................ 58 Epidemiology ............................................. ..5 8 Coronary Heart Disease Risk Factors ............................ 59 Pathophysiological Mechanisms ................................ 60 Clinical Correlations .......................................... 61 Smoking Cessation ........................................... 61 Cerebrovascular Disease (Stroke) ..................................... 61 Atherosclerotic Peripheral Vascular Disease ............................ 63 Atherosclerotic Aortic Aneurysm ..................................... 65 Chronic Obstructive Pulmonary Disease ............................... 66 Pathogenesis ................................................ 67 Pathophysiology ............................................. 67 Natural History of COPD and the Role of Cigarette Smoking ......... 68 PregnancyandInfantHealth ....................................... ..7 1 InfantBirthweight ......................................... ..7 2 Fetal and Perinatal Mortality ................................... 73 Congenital Malformations ..................................... 73 Fertility .................................................. ..7 5 Long-Term Effects on the Child ................................ 75 PepticUlcer .................................................... ..7 6 35 ............................................ 76 ............................................ 77 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...* 78 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Osteoporosis . . . . . . Involuntary Smoking . . Smokeless Tobacco . . . Addiction to Smoking . Part II: The Physicochemical Nature of Tobacco . . . . . . . . . . . . . . . . . , . . . . . . . . 79 The Changing Cigarette . . . . . . . . . . . . . . . . . . . . . . . . . . , . . . . , . . . . . . . . 85 Environmental Tobacco Smoke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 SmokelessTobacco . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90 Toxicity and Carcinogenicity of Tobacco Smoke . . . . . . . . . . . . . . . . . . . . . . . . 92 Nicotine . . . . . . . . . . Biological Markers . . Summary ............. Conclusions ........... . . . , . . . . . . . . ....................................... 93 ....................................... 94 ....................................... 97 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...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: I. 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 in men. 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 I964 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 I) (US DHEW 1979). Male cigarette smokers had approximately 70 percent higher overall death rates than nonsmokers: the excess mortality of female 3x TABLE L-Mortality ratios of current cigarette-only smokers, by cause of death in eight prospective epidemiologic studies Cause of death British Males in 25 States* U.S. Japanese Canadian Males in 9 Swedish' California doctors' 45-64 65-79 veterans' study4 veteran? States6 Males Females occupationss All cancersa ( 140-205) Cancer of lung and bronchus (162-163) 14.0 Cancerof larynx (161) Cancer of buccal cavity (140-141) 13.0b Cancer of pharynx (145-148) Cancer of esophagus ( 150) 4.1 Cancer of bladder and other ( I8 I ) 2. I Cancer of pancreas ( 157) 1.6 Cancer of kidney (180) Cancer,of stomach (I 5 I) Cancer of intestines (152-153) Cancer of rectum (I 54) 2.7 All cardiovascular disease (330-334, 40@468) CHD (420) 1.6 Cerebrovascular lesions (330-334) 1.3 Aortic aneurysm (nonsyphilitic) (451) 6.6 Hypertension (440-447) General arteriosclerosis (450) I .4 2.14 I .76 2.21 7.84 I I .59 12.14 6.09 8.99 9.96 4.09 9.90' 2.93' 12.54 4.17 I .J4 6.17 2.20 2.96 2.15 2.69 2.17 1.84 I .42 I .57 I .45 I .42 I .26 I.60 1.27 I.Old 1.17d 0.98 I.90 1.31 I .75 2.08 1.36 1.74 I .38 I .06 1.52 2.62 4.92 5.24 1.40 I .42 I .67 1.86 I .62 3.64 13.59 7.04 2.8 I 2.51 0.98 1.83 I.11 I .5 I I .27 0.91 1.96 1.14 2.5 I 14.2 3.9h 3.3 I.3 2. I I .4 I .9 I .4 0.6 I .6 0.9 1.8 I.6 3.3 I .97 10.73 13.10 2.80 6.60 2.40 I .50 2.30 0.50 0.80 I .57 1.70 1.30 1.20 2.00 7.0 1.8 3.1 0.9 1.7 1.0 1.6 1.3 2.0 4.5 15.9 1 .o I .6 0.7 2.5 6.0 2.3 0.8 0.9 1.3 2.0 I.1 I.8 1.4 I.0 2.0 TABLE I.--Continued Cause of death British Males in 25 States' U.S. Japanese Canadian Males in 9 Swedish' California doctors' 45-64 65-79 veterans 1 study4 veterans5 States6 Males Females occupation\x All respiratory disease (nonneoplatic) Emphysema and/or bronchitis Emphysema without bronchius (527. I ) Bronchitis (SOGSO2) Respiratory tuberculosis (001-008) Asthma (241) Influenza and pneumonia (4X&498) Certain other conditions Stomach ulcer (540) Duodenal ulcer (541) Cirrhosis (58 I ) t'arkinsonism (3SO) All causes 24.1 6.55 II.41 S.0 I .J I .86 I .72 2.5 4.06 4.13 4.13 2.86 I so 2.98 3.0 2.06 I.97 3.38 0.4 0.26 I .64 I .X8 I .43 I.84 IO.08 14.17 4.49 2.12 3.41 I .87 I .27 2.85 2.30 I .6 2.2' 4.3 1.7 Il.3 I .4 2.60 2.4 2.06' 6.9 2.16 0.5 1.35 2.3 I .93 2.4 0.X 4.0 I .22 I .52 1.70 I .4 I.2 I .78 "Number\ in parenthexes r~prcsent Intemar~onal C'lass~iication of Dlaeax\ (ICD) codes. "Includes cancers of larynx, buccal cavity. and pharynx. `Includes cancers of buccal cawry and pharynx. "Includes cancers of mrestine\ and rectum. elncludes stomach ulcer and duodenal ulcer. `Includes emphywzma. bmnchlw, and asthma. SOURCE: Studia cited arc as (bllows. `Doll and HIII (1956): `Hammond (1966): `Kahn (1966): "Hirayama (1967): `Best. Josie, Walker (1961); ' Hammond and Horn (1958); 7ceder]ofr,.a) (1975); `Dunn. Linden, Brealow (IY60). US DHEW (197')). 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 ofthe 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 I 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 I .43 at age 70 or more. Smoking remained the strongest 41 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, 19661979, by type of smoking Type of smoking' Cause of death Cancer of oral cavity and larynx (140-146.148. 161)b Cancer of esophagus ( 150) Cancer of liver and biliary passages (155-l 56) Cancer of pancreas ( 157) Cancer of trachea, bronchus, and lung ( 162) Cancer of bladder ( 188) Ischemic hean disease (4lWl4) Aortic aneurysm (nonsyphilitic) (41) Bronchitis and emphysema (490-492) Cigarettes Pipe only only 2.9 (8) 1.4 (3) 3.7 (9) 3.6 (6) 3.0(13) 1.7 (5) 3.3 (28) 2.8 (19) 7.4 (77) 7.2 (59) 4.2 (17) 4.0(16) 1.48 (399) 1.39 (366) 2.1 (II) 2.1 (11) 3.3 (18) 3.6 (16) Cigars only 0.6(l) 6.5 (2) 7.2 (4) 1.0(l) 7.6(11) 1.9(l) 1.16(42) 5.1 (4) 1.3(l) Peptic ulcer (53 l-534) Cirrhosis of liver (571) Suicide, accidents, and violence (E800-E999) All causes 2.0(11) 2.8 (13) 4.0 (3) 1.8 (21) 0.7 (4) 2.7 (3) 1.7 (90) 0.9 (35) 2.5 (10) 1.45 (I ,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 m 1%3, standardized for age and residence, was estimared to be 10.7 in cigarette smokers. 8.4 in pipe smokers, and 13.5 in cigar smokers. bNumhers in parentheses are KID-8 codes. SOURCE: Carstensen. Pershagen. Eklund (1987). 42 Lung Cancer Introduction One of the most prominent conclusions of rhe 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 a new epidemic. Clinical observations and early epidemiologic findings suggested that tobac- co smoking was associated with lung cancer. but hypotheses related to air pollurion. 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 1963 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 of regular smohing. For the purpose of illustration. selected examples ofdose-response relationships from two of the early. large prospective epidemiologic studies are reviewed here. Figure I 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 ofciparette smoke. These dataconfirm that even those who reported "just puffing"on cigarettes still had a significantly increased risk of lung cancer. Those wlho 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 I7 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 ofcarcinogenesis. 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 (197X) 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 1 to 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 (Pet0 1986). Cotnmercial cigarettes have continuously evolv,ed through the addition of filters and other modifications designed to reduce tar and nicotine yields (US DHHS I98 I ). Since extensive modification of the cigarette began in the I YSOs. it has only recently become possible to investigate smokers with predominant use of the newer products. Evidence from prospective and casr are performed on diabetics. Ap- proximately 3 1,000 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 of60 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 I6 percent of the non- smokers. Diabetics who stopped smoking for at least 3 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,OOO for men and 17.6/l ,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 I964 Report of the Surgeon General commented on the increased mortality rates fOJ 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 forabdominal aortic aneurysm was 2 to 8 times greater in cigarette smokers than in nonsmokers. A\ already noted, pathology studie\ have shown a rig- 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). However, 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 I97 I 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 focusedon 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 fOJ 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 numerou\ cross-sectional and longitudinal studies of mor- bidity and mortality. The longitudinal studies described the evolution of the cigarette- related decline in lung 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 pathogenesic, 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 defense\ 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 homorygous deficiency of alphat-antitrypsin. the major protease inhibitor. is associated with familial panlobular emphysema (Laurel1 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. Pathoph&ology 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 I Y6-l Report noted that smohcr\` I ung\ displayed air\bay> change\ and emphysema: however. the pathoph> Gological correlates of the\e changes Mere not explored. Suhquent in\c`stifution\. correl;tinf structural changes with function, have described the relationship between mohing-caused changes in lung structure and airtloti obstruction. Emphy~ttma and small-airway injury contribute to the phyciologi- cal impairment found in COPD: in individual\ with symptomatic airflow obstruction. either type of in,iuq ma> be predominant. but both are probably important (US DHHS IYXS). While the I%4 Report de\crihed effect\ of cigarette smoking on the airways. the importance of the small airMay\ as a \ite of airflow obstruction was not recognized until the late IYhOs (Hofg. Machlem. Thurlbech IY6Xj. More recent investigations have confirmed that measures of mall-airway injury are correlated with the degree of airflow obstruction (US DHHS I YX4: Hale et al. I YX-I: Nagai. West. Thurlbeck I YXS). Autopsy studies have shown that chan:;es in the small airways develop in the lungs of young smohers and antedate the development of symptomatic airflow obstruction (Niewoehner. Kleinerman. Rice lY71) The importance of emphysema in pro'.iucing chronic aifflow obstruction has also been amply documented %ince the IYh3 Report. Emphysema reduces the driving pressure for evpiratory tltru and contribute3 to i,lcrea\ed airways resistance by reducing tether- ing of small airMay\. In patient\ 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 IYX5). Thux. the \mohlng-cau\etl lung changes in the air\vay\ and parenchyma have both been unquivocalt~ linhed to airt`l~)w oh all the epidemiologic e\,idenr,e reviewed in the lY64 Report M;I~ cross-sec- tional in nature. These data estahli\hed that cigarette smohing increased respirator) symptom\ and reduced the level of ventilator\ function. but they did not provide in- Gght into the temporal evolution of COPD. Sub\equent cro\s-sectional studies have provided more complete quantitative description\ of the effects of cigarette smoking on lung function. and ncn longitudinal studies have partially dehcribcd the evolution of lung function change\ in mohcrs and the factory determining the rate ofchange over time. The numcrou\ cro\\-\ection;ll \tudie+, published \incz the IY6-l Surgeon General's Report have shop n that cigarette mokin, (7 is a strong determinant of the level of ven- tilator! function. LI hich is most often asressed b! the measurement of the I -set forced expiratory volume (FEV, ). The level of FEVt declines ;I> the amount of smoking in- crea\e\ CL'S DHHS IYXJ). Multiple re:;re\sion techniques have been applied to data from se\,erat different population\ to de\cribe the quantitati\,e relationship between the amount smohed and lot\ of ventilator\ function. These anal>\es indicate that ven- tilator! function decline\ in ;I lineart;t\hion u ith cumulative consumption ofcigarettes. usualI> e\;pre\\ed ;I\ pa&>ears (Burrows et al. lY77: Docker) et al. IYXX). For ex- ample. bused on anal) s~s of data from X. I Y I men and women from six U.S. cities. Dock- er\ and other\ ( 1 YXX) reported that male kImohers of a\ erage height lose 7.J mL of FEV I 6X on average for each pack-year and that women lo\e 3.4 mL per pack-year. Although the decline in mean level of FEV I appears hmall. the distributions of lung function level in smokers and in nonsmokers are different: the distribution for smokers is skewed toward lower levels co that a much greater proportion of smokers than nonsmokers have levels below the usual limit of normal (Figure I 1) (US DHHS 19X4: Burrows et al. 1977: Dockery et al. 19X8). 30 - 0 Pn-TRS x 2o * N=3303 IO- lOA=. 0+ I -3.0 -2.0 -1.0 0.0 1.0 2.0 3.0 .y ;ij~~:zs?"`" -3.0 -2.0 -1.0 3'. . 0.0 1.0 2.0 ~1409PK-TRS Ik638 -3.0 -2.0 -1.0 0.0 1.0 2.0 3.0 SE] ,& ~~~fP,~~"' -3.0 -2.0 -1.0 0.0 1.0 2.0 70 30 7 fy3," PK-YRF 20 . S 10. I;lA..8*1 04 -3.0 -2.0 -1.0 0.0 1.0 2.0 3.0 30 - s 2O . r E+,`,K-`"5 10. lOR1.966 07 -3.0 -2.0 -1.0 0.0 1.0 2.0 3.0 HElGhT ROJUSTEO FEYI RESIDUF4L iLITERS FIGURE Il.-Percent distribution of predicted values of forced expiratory volume in I-set (FEV I) in subjects with varying pack- years of smok- ing. NOTE Trmgle Indlcotz\ 111e3311. IQR I\ mtrrquart~le rany SOLRCE: Dochery et ~1. I IWX, The longitudinal studies published Gnce the 1964 Report have partially described the natural history of lung function changes in COPD (Fletcher et al. 1976: US DHHS 1984). Ventilatory function. ;1s measured by FEVt. 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. I I I I I t 25 35 45 55 65 75 FIGURE 12.-Decline of FEVI at normal rate (solid line) and at an accelerated rate (dashed line) 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 IO 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 I greater than 60 mL per year. Clinically, these subjects were not unique and none had alphat-antttrypsin 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 illness 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 19X5. the Center for Health Promotion and Education of the Centers for Disease Control. Atlanta. GA. defined the fetal tobacco syndrome as follows. (I) 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 nevvborn has symmetrical growth retardation at term, 37 weeks, defined as birthweight less than 3.500 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 Rirthweight 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 S4- and l30-percent increase. respectively, in the prevalence of new- borns weighing less than 2,500 g. A review of five studies including I I3.000 births in the United States. Canada, and Wales found that from 2 I to 39 percent of the incidence of low birthweight w*as 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 fetal 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 w'omen. 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 wjhites. Finally. a number of careful studie\ have found that the effect of cigarette smoking on birthueight is not mediated through decreased maternal appetite or weight gain (US DHHS 19X0). 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 (CO) in the blood. reduction of blood flow. or inhibition of respiratory enzymes. There is strong experimental evidence that maternal smoking causes fetal hyposia. 72 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 198X). In a 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 w/as 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 babie\ with higher birthweight than women who continued to smoke throughout pregnancy. Fetal and Perinatal Mortality Kleinman and colleagues (19X8) from the National Center for Health Statistics used Missouri birth records from 1979-83 (Table 3) tn study the relationship betvveen cigarette smoking in mothers and infant mortality. Among the 133.429 primiparas, the infant mortality rates (adjusted for age. parity. education. and marital status) were (per I.000 subjects) IS.1 for white nonsmokers. 1X.X for whites who smoked less than I pack of cigarettes per day. and 23.3 for whites who smoked more than I 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 I pack per day. 32.4: and for blacks who smoked greater than I 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 vvould be reduced by approximately IO 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 2X 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 IO cigarettes smoked per day and by 6 I 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 birth5 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 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 I .ooo) (per I .ooo) Whites Blacks Whites Blacks Adjusted odds ratios Whites Blacks Marital status Married Unmarried Education (years) I2 Age (years) I pack/day 14.5 25.4 15.9 29.5 I .OO I .oo 24.0 2X.6 2 I .o 27.2 1.33(1.1X-1.50) 0.92 (0.73-I. 16) 22.9 13.2 !9.X 33. I 1.36(1.16-1.59) IS.2 25.9 16.7 28.8 l.l4(1.02-1.28) 12.8 21.5 14.6 25.3 1.00 24.0 33.7 18.X 32.2 I .24 ( I .06-l .45) IX.2 26.0 16.3 27.9 1.08 (0.95-I .22) 14.2 23.4 15.2 26.0 1.00 13.2 27. I 16.1 27.6 I.06 (0.94-I .20) 16.1 19.9 I X.6 31.9 1.23(1.01-1.50) 25.4 69.3 31.1 52.9 2.09 (I .49-2.93) 13.9 25.3 15.1 26.0 19.1 33.7 18.8 32.4 24.3 41.5 23.3 39.9 1.00 1.25(1.13-1.39) I .56 ( I .37-I .77) SOURCE: Kleinman et al. (1988) offspring of women smoking more than 1 pack of cigarettes per day compared with women reporting no smoking during pregnancy. Similarly, Himmelberger, Brown, and Cohen (1978) reported a 2.3-fold higher risk of congenital abnormalities for smoking mothers than for nonsmokers. One study has also reported an increased frequency of congenital malformations based on the smoking habits of the father (Schardein 1985). The trends with paternal smoking were independent of maternal smoking level, maternal and paternal age. and social class. The relatively low incidence of congenital malformations, the different types of mal- formations, and the various possible biological mechanisms have made the study of the relationship between environmental factors and congenital malformations extremely difficult. New techniques to monitor pregnancy outcomes may enhance our under- standing of the interrelationship between cigarette smoking, other environmental fac- tors, and congenital malformations. Fertility A recent study has substantiated previous reports that suggested that women who smoke may have reduced fertility (Baird and Wilcox 1985). Data on smoking history and number of noncontraceptive cycles until conception were collected from 678 preg- nant women. Of nonsmokers, 38 percent conceived in their first cycle compared with 28 percent of smokers. Smokers were 3.4 times more likely than nonsmokers to have taken greater than 1 year to conceive. After adjustment for other risk factors, it was es- timated that the fertility of smokers was 72 percent of that of nonsmokers. Heavy smokers experienced lower fertility than light smokers. Fertility was not affected by the husbands' smoking. The effects of cigarette smoking on sperm quality in men (Ablin 1986) were also evaluated in relation to density, motility, and morphological abnormalities in 238 age- related smokers and 135 nonsmokers. Spermatozoa from smokers possessed sig- nificantly decreased density and motility compared with those from nonsmokers. Mor- phological abnormalities of the sperm were also noted more frequently among smokers than among nonsmokers (Ablin 1986). Long-Term Effects on the Child Relatively few studies have evaluated the long-term consequences of smoking during pregnancy on the child. One of the larger recent studies looked at neurological hand- icaps among children up to 14 years of age whose mothers had smoked during preg- nancy and among control children born in northern Finland in 1966 (Rantakallio and Koiranen 1987). Seventy-eight children of smokers and 62 controls had mental retar- dation (IQs less than 85), cerebral palsy, or epilepsy. The incidence of mental retarda- tion alone was 15.9/1.000 among the children of the mothers who smoked and 13.9 among the controls. For any combination of mental Letardation, cerebral palsy, and epilepsy, the rates were 42.8/l ,000 for children of smoking mothers and 34/l ,000 for the controls, a relative risk of 1.27 with confidence limits of 0.90 to 1.79. Naeye and Peters ( 19x4) investigated the mental development of smokers' children by comparing siblings whose mothers smoked in one but not in subsequent pregnan- cies and found that hyperactivity. short attention span, and lower scores on spelling and reading tests were more frequent for the children whose mother had smoked during pregnancy. but the differences were relatively small, the test scores being only 2 to 4 percent lower. Dunn also studied neurological and electroencephalographic abnor- malities among 6-year-old children of smokers and found these conditions to be slight- ly more common in the children of mothers who had smoked during pregnancy, but again the differences were not statistically significant. Small sample sizes in many of these studies and the relative infrequency of the events of interest limit interpretation of the studies (Dunn et al. 1977). Peptic Ulcer The 1964 Surgeon General`s Report noted an association between peptic ulcer and cigarette smoking. The 1979 Report stated that the relationship between cigarette smoking and peptic ulcer is significant enough to suggest a causal relationship. Peptic ulcer disease is more likely to occur, leis likely to heal. and more likely to cause death in smokers than in nonsmokers. Cigarette smoking retards the healins of peptic ulcer (Sontag et al. 1984: Lane and Lee 198X; Korman et al. 1983). A large trial of cimetidine, a drug used in the treatment of peptic ulcer. was reported in I984 by Sontag and associates. Ulcer recurrence was much more frequent among smokers compared with nonsmokers for both the placebo- and the cimetidine-treated groups. Nicotine decreases pyloric sphincter pressure and therefore permits increased retlux of duodenal contents into the stomach. Nicotine also decreases pancreatic bicarbonate secretion. This may impair neutralization of gastric acid in the duodenum, contributing to the formation and persistence of duodenal ulcers. Smoking cessation probably reduces the incidence of peptic ulcer and is an important component of peptic ulcer treatment ev/en with the available effective drug therapy. Osteoporosis The lY64 Report did not discuss osteoporosis. The interest in osteoporosis is fairly recent because of the increasing number of older individuals. especially women. at risk of fracture: the better methods of measuring bone mineral mass: and the understanding of osteoporosis pathophysiology and risk factors. Osteoporosis leading to fractures. especially of the hip. wrist. and spine, is an impor- tant cause of disability and death. predominantly among postmenopausal women. About IS to 20 million persons in the United States have osteoporosis. Each year about I .3 million fractures are attributed to this disease (Journal of the American Medical As- sociation 1983). Smoking may be a risk factor for osteoporosis (Willett et al. 1983). Women smokers have an earlier age of menopause, an important risk factor for osteoporosis (Willett et al. 1983 ). Smokers may have a lower intake of calcium during adolescence and young 76 adult life when maximum bone mineral mass is reached (Sandier et al. 1985). Smokers also weigh less than nonsmokers (US DHHS 1988). Obesity substantially reduces the risk of hip fracture (Kiel et al. 1987). Overweight women have higher endogenous estrogen levels and greater bone mass (Cauley et al. 1986). Exogenous estrogen intake among postmenopausal women results in a decreased risk of fracture (Emster et al. 1988). Women who smoke and are on estrogen therapy may have reduced levels of estrogens in their blood compared with levels for nonsmoking women. Among women who smoked and were given high doses of estradiol, blood levels of estrone and estradiol were only one-half of those among nonsmokers (Jensen. Christiansen, Rodbro 1985). Increased hepatic metabolism of exogenous oral estrogen may result in lower estrogen levels among postmenopausal cigarette smokers. Several case+control studies have evaluated the relationship between osteoporosis and cigarette smoking. Most find an increased risk of fractures among smokers. However, problems with study design. especially the potential effects of confounders such as obesity and age, have limited the interpretation of these studies. as have con- tradictory findings. For example, a large study of hip fractures among postmenopausal women in four Connecticut hospitals did not find any differences in risk between smokers and nonsmokers (Kreiger et al. 1982). A study in Iowa by Sowers (Sowers, Wallace. Lemke 1985) of 86 women aged 20 to 35 years did not find any relationship between forearm bone mineral mass and smoking during maximal bone mineralization. A study in Denmark (Jensen 1986) compared bone mineral content among 77 long- term smokers and 103 nonsmokers. Bone mineral content correlated with fat mass. For the same degrees of obesity, smokers did not have any lower level of bone mineral con- tent than nonsmokers. The results of these studies suggest that the effect of smoking as a risk factor for osteoporosis and fracture among postmenopausal women may be primarily determined by the inverse relationship between smoking and obesity. It is possible that the early age of menopause among smokers may also contribute to the risk of osteoporosis. Involuntary Smoking The issue of involuntary smoking was not raised in the 1964 Surgeon General's Report. The first report of the Surgeon General to address the possible health effects of involuntary smoking was published in 1972 (US DHEW 1972). Over the ensuing 15 years, evidence on the adverse consequences of involuntary smoking began to amass, with several hundred papers being published. In 19X6, the Surgeon General's Report (US DHHS 1986a) focused exclusively on this subject. Nonsmoking adults exposed to ETS have a higher frequency of symptomology, such as eye irritation and upper respiratory symptoms (US DHHS 1986a). The relationship between lung cancer among nonsmokers and ETS has been documented in both case- control and longitudinal studies. Most of these studies have measured the increased risk of lung cancer among nonsmoking women, usually wives exposed to their husbands' tobacco smoke. A I .3-fold increased risk of lung cancer has been estimated from these studies and is consistent with the amount of exposure to carcinogens from 77 ETS (US DHHS 1986a), the duration of exposure, and the differences in the distribu- tion of potential carcinogens between sidestream and mainstream smoke. The 1986 Surgeon General's Report on involuntary smoking concluded (US DHHS 1986a): 1. Involuntary smoking is a cause of disease, including lung cancer, in healthy non- smokers. 2. The children of parents who smoke compared with the children of nonsmoking parents have an increased frequency of respiratory infections, increased respiratory symptoms, and slightly smaller rates of increase in lung function as the lung matures. 3. The simple separation of smokers and nonsmokers within the same airspace may reduce, but does not eliminate, the exposure of nonsmokers to ETS. Another major review on involuntary smoking was released in 1986 by the Nation- al Research Council (NRC). This report concluded that the risk of lung cancer is ap- proximately 30 percent higher for nonsmoking spouses of smokers than it is for non- smoking spouses of nonsmokers (NRC 1986). Since release of the 1986 Surgeon General's Report, five additional studies examin- ing ETS exposure and lung cancer in nonsmokers have been published (Brownson et al. 1987; Dalager et al. 1986; Humble, Samet, Pathak 1987; Gao et al. 1987; Pershagen, Hrubec, Svensson 1987). All five noted a correlation between ETS exposure and lung cancer among nonsmokers. Thus, of the 16 epidemiologic studies in the scientific literature, 14 have noted a positive association. Smokeless Tobacco In 1979 the Surgeon General's Report included, for the first time, a review of the health consequences of using smokeless tobacco (snuff and chewing tobacco) (US DHEW 1979). In 1986, a special Surgeon General's Report, The Health Consequen- ces of Using Smokeless Tobacco (US DHHS 1986b), reviewed smokeless tobacco in depth and concluded that it can cause cancer in humans. The relationship between smokeless tobacco use and cancer is strongest for the use of snuff and for cancer of the oral cavity. Smokeless tobacco can also cause oral leukoplakia, which may progress to neoplastic transformation with continued use of smokeless tobacco. Addiction to Smoking The 1964 Surgeon General's Report referred to tobacco use as habituating. Fifteen years later, the 1979 Report concluded that smoking was "the prototypical substance abuse dependency" (US DHEW 1979). The entire 1988 Report (US DHHS 1988) was dedicated to an exhaustive review of tobacco use as an addiction. The 1988 Report concluded: 1. Cigarettes and other forms of tobacco are addicting. 2. Nicotine is the drug in tobacco that causes addiction. 3. The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin or cocaine. 78 These findings are discussed in greater detail in Part II of Chapter 5 on determinants of smoking behavior. PART II. THE PHYSICOCHEMICAL NATURE OF TOBACCO The 1964 Surgeon General's Report on Smoking and Health (US PHS 1964) gave impetus to intensified investigations on the physicochemical nature and composition of tobacco smoke and the identification of biologically active agents in tobacco and tobacco smoke and their modes of action. In 1936 Bruckner listed 120 known components in tobacco smoke. This number grew to about 450 in I959 (Johnstone and Plimmer 1959). to about 950 in 1968 (Sted- man 1968), to 3,875 in 1982 (Dube and Green 1982). and to 3,996 in 1988 (Roberts 1988). Today, the e$mated number of known compounds in tobacco smoke exceeds 4,000, including some that are pharmacologically active, toxic, mutagenic, or carcinogenic (US DHEW 1979; US DHHS 1983). Such diverse biological effects of cigarette smoke constituents provide a framework for understanding the multiple adverse consequences of smoking. Since about 1960. both the composition of cigarette tobacco and the componenta and shape of the cigarette itself have undergone significant changes that effected reductions in standardized measurements of tar, nicotine. and other toxic agents in the smoke (Nor- man 1982). Perhaps the greatest advances have been made in understanding the pharmacology and toxicology of nicotine (Benowitz 19X6: US DHHS 1988) and in de- lineating the nature and mode of action of the major carcinogens in tobacco smoke (US DHHS 1982; Hoffmann and Hecht. 1989). Processed, unadulterated tobacco contains at least 2,550 known compounds (Dube and Green 1982). The bulk of the dried tobacco consists of carbohydrates and proteins. Other important constituents are alkaloids (0.5 to 5 percent). with nicotine as the predominant compound (90 to 95 percent of total alkaloids). and terpenes (0. I to 3 per- cent), polyphenols (0.5 to 4.5 percent), phytosterols (0.1 to 2.5 percent), carboxylic acids (0. I to 0.7 percent), alkanes (0. I to 0.4 percent). and alkali nitrates (0.01 to 5 per- cent). In addition. tobacco contains traces of aromatic hydrocarbons. aldehydes. ketones, amines, nitriles. N- and 0-heterocyclic compounds, pesticides. and more than 30 metallic compounds (Wynder and Hoffmann 1967; US DHEW 1979). The composition of the processed tobacco in cigarettes influences the chemistry and toxicity of the smoke. Cigarettes manufactured in the United States are made with blends of bright. burley, and oriental tobaccos that generate weakly acidic mainstream smoke (pH 5.5 to 6.2) in which nicotine occurs in protonated form in the particulate matter. The sidestream smoke (SS) of these cigarettes is neutral to alkaline (pH 6.5 to 8.0), and part of the nicotine in SS is present in unprotonated form in the vapor phase (Brunnemann and Hoffmann 1974). These observations are important because un- protonated nicotine is readily absorbed through the buccal mucosa (US DHHS 1988). The 400 to 500 mg of mainstream smoke (MS) freshly emerging from the mouth- piece of a cigarette is an aerosol containing about IO" particles per mL: these range in diameter from 0. I to 1 .O pm (mean diameter 0.2 pm) and are dispersed in a vapor phase (Ingebrethsen 1986). About 95 percent of the MS effluents of a nonfilter cigarette are composed of 400 to 500 individual gaseous compounds with nitrogen. oxygen. and 79 22.5 mg. TPM (Wet) mmp. 67.5 mg. WHOLE VAPOR SMOKE PHASE 6.75 mg. 1 ESTERS 4.5 ACIDS UNIDENTIFIED COYP'DS SMOKE PIGMENT MISC. COMWS ALKANES TERPENOIO HVOROCARSON PHENOLS ESTERS OTHER AU(ALOID DER. NICOTINE ALCOnOLs ALDEHVOES L KETONES CARBOXVLIC ACIDS WATER ~2 METHANOL .2 HETEROCVCLIC COMPPS `NITRILES MISC. COMWS KLTONES ALDEHVOES lWDROCAR0ONS Total Cigarette Smoke Percentage of Smoke Weight FIGURE 13.--Composition of cigarette mainstream smoke SOI'RCE. Duhe .md Gwn t II)X21 carbon dioxide as major constituents; the particulate matter of MS contains at least 3.500 individual compounds (Figure 13 Dube and Green 1982). Like all organic combustion products tobacco smoke contains free radicals, highly reactive oxygen- and carbon-centered types in the vapor phase. and relatively stable radicals in the particulate phase. The principal of the latter appears to be a quinone/hydroquinone complex capable of reducing molecular oxygen to superoxide. and. ev/entually. to hydrogen peroxide and hydroxyl radicals (Nakayama. Kodama, Napata 1984: Church and Pryor 1985 ). For chemical analysis. the smoke is arbitrarily separated into vapor and particulate phases. Those smoke components of which more than SO percent appear in the vapor phase of fresh MS are considered volatile smoke constituents: all others are particulate phase components (Figure 13). Tables 5 .md 6 list the major types of components iden- tified and their estimated concentration in the smoke of one cigarette (US DHHS 1982; Hoffmann and Hecht 1989). The quantitative data presented here were obtained by machine making of cigarette5 under s:andardized laboratory conditions using the method of the Federal Tmde Commission (Pillsbury et al. 1969); therefore, the data do not fully reflect the human setting. This applies especially to smokers of low-yield cigarette\ who tend to compensate for the `ow nicotine delivery by drawing smoke more intensely and inhaling more deeply (US DHHS 198X). Table 6 doe\ not contain information about the nature and concentration of at least 30 metals in the smoke. These compounds are not listed because less than I percent of the metals in tobacco are transferred into the smoke and constitute together only 30 pg/g(Jenhin~. Goldey. Williamson 19X5). Tables 5 and 6 also lack descriptions of the x0 TABLE S.-Major constituents of the vapor phase of the mainstream smoke of nonfilter cigarettes Compound" Concrntrntton/cifarrtte Nitrogen Oxygen Cabon dioxide Carbon monoxide Water ArgWl Hydrogen Ammonia Nttrogen oxtde\ (NO,I Hydrogen cyanide Hydrogen wlfide Methane Other volatile alhanes (201 Volatile alkene\ (161 Iwprene Butadiene Acetylene Benrene Toluene Styrene Other volatile aromatic hydrwarhon\ t29) Formic acid Acetic actd Propiomc acid Methyl forma Other volattle acids (6) Formaldehyde Acetaldehyde Act&in TABLE S-Continued Compound" Concentration/cigarette Other volatile aldehydes (6) xo-14o~g Acetone 100-650 pg Other volatile ketones (3) 50-100&J Methanol X0-180 pg Other volatile alcohol\ (7) 1 O-30 pg' Acetonitrile IOO-15Opg Other volatile nitriles (IO) so-8a pg' hrdn m-40 PI Other volattle furans 14) 45- 12.5 jl&y Pyridine 20-200 pg Picolines (3) I S-80 pg SVinylpyridine I O-30 pg Other volatile pyridines (25) 20-so pgc Pyrrole O.l-IO& Pyrrolidine IO-18pg N-Methylpyrrolidine 2.0-3.0 p&7 Volatile pyrarines ( IX) 3.040 pg Methylamine 4-10 flp Other aliphatic amme\ (32) 3-10 pg "Numkr\ m parcnthere\ reprewn~ u~dwduul compounds Identilicd in a gwen group. "Percent of tot31 eflluent. `E\tmiw. SOURCE: Hoffmann and Hecht (1989). chemical nature and concentrations in cigarette smoke of agricultural chemicals and pesticides, which originate from the residues of such compounds in tobacco. There are many variations in the qualitative and quantitative aspects relative to such agents in tobacco from region to region and from year to year. Overall, the use of agricultural chemicals has also been greatly reduced (Wittekindt 1985). Nevertheless, it is fairly certain that commercial tobaccos contain up to a few parts per million of DDT, DDD, 82 TABLE &-Major constituents of the particulate matter of the mainstream smoke of nonfilter cigarettes Compound" pg/cigarette Nicottne Nomicotine Anatabine Anabasine Other tobacco alkaloids (17) Bipyrldyls (4) n-Hentriacontane (n-CItHM) Total nonvolatile hydrocarbons (45)b Naphthalene Other naphthalenes (23) Phenanthrenes (7) Anthracenes (5) Fluorenes (7) Pyrenes (6) Fluoranthenes (5) Carcinogenic polynuclear aromatic hydrocarbons ( I I )' Phenol Other phenols (45)b Catechol Other catechols (4) I ,00@3,000 S@lSO S-IS 5-12 NA l&30 IO0 3oo-400h 24 3Mb 0.2-0.4b 0.05-0.1h 0.6-I .ob 0.3-0.sb 0.3-o.45b 0.1-0.2s 8cL160 6C-1 80b 20@-400 loo-2ooh Other dihydroxybenzenes (IO) 2GO-400b Scopoletin 15-30 Other polyphenols (@ NA Cyclotenes ( 10)b 4&70b Quinones (7) 0.5 Solanesol 600-1.000 83 TABLE &-Continued Compound" Neophytadienes (4) Limonene Other terpenea (2W-2S0)h @cigarette 2W350 3cMo NA Palmitic acid 10@150 Stearic acid 5&75 Oleic acid 4&l 10 Linoletc acid 60-150 Linolenic acid 150-250 Lactic acid 6&80 Indole IO-15 Skatole 12-16 Other indoles ( 13) NA Quinolines (7) 24 Other N-heterocyclic hydrocarbons (55) NA Benrofurans (4 ) 200-300 Other 0-heterocyclic hydrocarbons (42) Stigmasterol NA 40-70 Sltosterol Camperterol Cholesterol Aniline Toluidiner Other aromatic amine, ( 12) Tobacco-spectfic N-nitrosamines (4)` 3wo 20-30 IO-20 0.36 0.23 0.25 0.3b2.7 Glycerol I20 NOTE: NA. not avddable. ZNumben m parenthew represent indwldual compounds identified m a given group. E,tlmate. `See Table 7 for detak SOURCE: Hoffmann and Hecht I 19X9). x3 and maleic hydrazide; fewer than 20 percent of these contaminants are transferred into the smoke stream. The 1964 Surgeon General's Report listed five polynuclear aromatic hydrocarbons (PAHs) and three N-heterocyclic hydrocarbons as known carcinogenic smoke con- stituents (US PHS 1964). By the criteria for carcinogenicity of chemicals as set by the International Agency for Research on Cancer (1986). the carcinogens identified to date in tobacco smoke include 11 PAHs, 4 N-heterocyclic hydrocarbons. 9 N-nitrosamines, 3 aromatic amines, 3 aldehydes, 6 volatile carcinogens, 6 inorganic compounds, and the radioelement polonium-210 (Table 7; Hoffmann and Hecht 1989). The Changing Cigarette As discussed in Part I. epidemiologic studies have documented a dose-response relationship between the number of cigarettes smoked and the development of cancer of the lung, larynx, oral cavity, esophagus. pancreas, bladder, and kidney (US DHHS 1982; IARC 1986). Bioassays for tumorigenicity with whole smoke and with tar have also demonstrated a dose-response relationship (US DHHS 1982). As tar and nicotine yields in cigarette smoke gradually declined, other toxic and tumorigenic agents, such as CO, volatile N-nitrosamines, and carcinogenic PAHs. were also successfully reduced (Hoffmann, Tso. Gori 1980; Hoffmann et al. 1984; US DHHS 1981). However, it was soon realized that the smoker of low-yield cigarettes tended to compensate for reduced nicotine delivery by intensified smoking (US DHHS 1988), and therefore exposure may not actually have been lowered. Based on values generated by smoking machines under standardized conditions, Figure 14 shows the reduction in sales-weighted tar and nicotine delivery of the average U.S. cigarette. Arrows in the graph point to the introduction of technical changes in the manufacture of cigarettes at various times. These changes have influenced the machine-measured sales-weighted average nicotine and tar deliveries (Norman 1982). Technical issues in the machine measurements of delivered tar and nicotine yields also arose during 1982; modifications of the testing procedure were suggested (Federal Trade Commission 1984). The data shown in Figure 14 are based on the consistent testing procedures. Since 1981, the tar delivery of U.S. cigarettes has averaged between 13.0 and 12.7 mg, while nicotine delivery has remained stable at 0.9 mg per cigarette. (See Chapter 5, Table 26.) In the smoke of popular U.S. low-yield cigarettes, the reduction of nicotine, the primary pharmacologic factor in tobacco addiction (US DHHS 198X), has not occurred to the same extent as has the reduction of tar. The same development has been observed with cigarettes in the United Kingdom (Jarvis and Russell 1985). Some modifications in the makeup of commercial cigarettes have led to a selective reduction of toxic and tumotigenic agents. Filter tips of cellulose acetate, the most com- mon cigarette filter material, can selectively remove phenols and volatile N- nitrosamines from the smoke stream. Perforated filter tips selectively reduce CO and hydrogen cyanide (HCN) levels, and charcoal filters may selectively reduce volatile al- dehydes and HCN. The incorporation into the tobacco blend of reconstituted tobacco sheets, expanded tobacco, and tobacco ribs has also contributed to a selective reduc- tion of PAHs in cigarette smoke. The incorporation of ribs and stems and the utiliza- 85 TABLE 7.-Tumorigenic agents in tobacco and tobacco smoke Compounds Processed tobacco (per gram) Mainstream smoke (per cigarette) Evidence for IARC evaluation of carcinogenicity In lab animals In humans PAH Benz(a)anthracene Benzo(b)fluoranthene Benzo(j)fluoranthene Benzo(k)fluoranthene Benzo(a)pyrene Chrysene Dibenz(a,h)anthracene Dibenzo(a,i)pyrene Dibenzo(a,l)pyrene Indeno( I ,2.3-c,d)pyrene S-Methylchrysene Aza-arenes Quinoline Dibenz(a,h)acridine Dibenz(a,j)acridine 7H-Dibenzo(c,g)carbazole N-Nitrosamines N-Nitrosodimethylamine N-Nitrosoethyl methylamine N-Nitrosodiethylamine N-Nitrosopytrolidine N-Nitrosodiethanolamine N'-Nitrosonomicotine 4-(Methylnitrosamino)- l- (3-pyridyl)- I -butanone N'-Nitrosoanabasine N-Nitrosomorpholine 0.1~90ng 20-70 ng &22 ng 621 ng 6-l2ng 20-40 ng @-@w 4 w I .7-3.2 ng Present 4-20 ng 0.6 ng Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient I-2 IQ 0.1 ng 3-10 ng 0.7 ng NA Sufficient Sufficient Sufficient ND-215 ng O.l-ISOng 3-13 ng Sufficient Sufficient N&360 ng NM,900 ng 0.3-89 pg 0.2-7 pg ND-25 ng 15IlOng ND-36 ng 0.12-3.7 Fg 0.08-0.77 pg Sufficient Sufficient Sufficient Sufficient Sufficient O.Ol-1.9ug 0.144.6 pg Limited ND-690 ng Sufficient NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA NA 86 TABLE 7.-Continued Compounds Processed tobacco (per gram) Mainstream smoke (per cigarette) Evidence for IARC evaluation of carcinogenicity In lab ammals In humans Aromatic amines 2-Toluidine 2-Naphthylamine 4-Aminobiphenyl Aldehydes Formaldehydea Acetaldehydea Crotonaldehyde Miscellaneous organic compounds Benzene Acrylonitrile I, 1 -Dimethylhydrazine 2.Nitropropane Ethylcarbamate Vinyl chloride Inorganic compounds Hydrazine Arsenic Nickel Chromium Cadmium Lead Polonium-210 I .&7.4 pg 1.4-7.4 mg 0.2-2.4 &y 60-147 pg 310-375 ng 14-51 ng 5OCk900 ng 2,ooo-6.~ ng I .00&2.000 ng I ,300-l ,600 ng &lo Pi% 0.2-I .2 pCi 3G-200 ng Sufficient l-22 ng Sufficient 2-5 ng Sufflclent 7&100 pgd I X- 1,400 mg' I@20 pg Sufficient Sufficient NA 12-48 pg 3.2-15 pg 0.73-1.21 pg 20-38 ng I-16 ng Sufficient Sufficient Sufficient Sufficient Sufficient Sufficient 24-43 ng 40-120ng 0-600ng 4-70 ng 41-62 ng 0.03-l .O pCi Sufficient Inadequate Sufficient Sufficient Sufficient Sufficient NA Inadequate Sufftcient Sufficient NA NA NA Sufficient Limited NA NA NA Sufficient Inadequate Limited Sufficient Limited Inadequate NA NOTE: ND, no data; NA, evaluation has not been done by IARC. `The Fourth Report of the Independent Scientific Committee on "Smoking and Health" (198X) published values for the 14 leading U.K. cigarettes in 1986 (51.4 percent of the market) of 2iSlO5 @cigarette (mean. 59 ~8) for formaldehyde and 550-1.150 pg/cigarette (mean. 910 pg) for acetaldehyde. SOURCE: Hoffmann and Hecht (1989). x7 Saks-weiightodbr(mg) Saks-weigMsd nkoUtm(mg) 40 30 20 10 0 1 F 1957-reconstituted tobacco Nkatim 1 1 I I , 1 5 1960 1965 1970 1975 1980 1985 4.0 3.0 2.0 1.0 0.0 FIGURE 14.-" Tar" and nicotine content of U.S. cigarettes, sales-weighted average basis, 1957-87 NOTE: Nicotme values for 195747 are estmates. SOL'RCE. lY57Lh7. U.Ach.m , I97hl. tourlh-qwter e\,,,nale\ tin each !cilr. I'JhX-X I. FTC ( IYX41: I'#-X7. dmved tion of more burley varieties in the tobacco blend have led to an increase in the nitrate content of the U.S. blended cigarette from 0.5 percent to between 1.2 to 13 percent. This development brought about a reduction of the smoke yields of tar, phenols, and PAHs. but has caused an increase of the nitrogen oxides in the smoke and thus has in- creased the potential for N-nitrosamine formation (US DHHS 1981. 1982; Hoffmann et al. 1983). The development of the low-yield cigarette has also necessitated an en- richment of the flavor "bouquet" in the smoke either by tobacco selection or by addi- tion of natural or synthetic flavor compounds. These facts and the practice of smoking low-yield cigarettes more intensely make it difficult toevaluate whetherthese new types of cigarettes are in fact less hazardous to the smoker (see Chapter 8). Changes in the market share of filtered cigarettes. lower yield cigarettes. mentholated cigarettes, and longer cigarettes are presented in Chapter 5. Environmental Tobacco Smoke SS is the smoke generated during smoldering of tobacco products between puffs. When it is obtained under standard laboratory conditions. undiluted SS contains far higher amounts of toxic and tumorigenic agents than MS, which is drawn puff by puff through the unlit end of the cigarette. Table 8 presents data for those toxic agents in SS that are known carcinogens, tumor promoters, and cocarcinogens. The release of volatile N-nitrosamines and aromatic amines into the SS is remarkably higher than that into MS (US DHHS 1988: Guerin 1987). Whereas filter tips, especially perforated TABLE &Come toxic and tumorigenic agents in undiluted cigarette sidestream smoke Compound Type of toxi,,ty Amount in sidestream smoke (per cigarette) Amount in sidestream smoke/ amount in mainstream smoke Vapor phase Carbon monoxide Carbonyl sulfide Benzene Formaldehyde 3-Vinylpyridine Hydrogen cyanide Hydrazine Nitrogen oxides (NO,) N-Nitrosodimethylamine N-Nitrosopyrrolidine Particulate phase Tar Nicotine Phenol Catechol o-Toluidine 2-Naphtylamine 4-Aminobiphenyl Benz(a)anthracene Benzo(a)pyrene Quinoline NNN NNK N-Nitrosodiethanolamine Cadmium Nickel Polonium-210 C C SC T C C C C 14-30 mg 1.1-15.7 T 2.1-46mg I .3-2 I TP 7S250 )~g I .3-3.0 cot 58-290 )~g 0.67-12.8 C 3M 18.7 C 70 ng 39 C l40ng 31 C 40-200 ng 24 C 4&70 ng 2.5-20 C 15-20 pg 8-1 I C 0.15-I .7 pg 0.5-5.0 C 0.2-I .4 ).lg 1 O-22 C 43 ng 1.2 C 0.72 pg 7.2 C 0.2-2s ).lg 13-30 C 0.5-I .6 pC1 1 M-3.7 26.841 mg 2-3 pg 400-400 KS I.500 pg 3OG450 pg l4-IlOpg 90 ng 5G+2,coo pg 20&l ,040 ng 3lS390 ng 2.5-14.9 0.034. I3 E-IO 50 24-34 o.w.4 3.7-12.8 20-130 6120 NOTE: C. carcinogenic; CoC, ccarcinogenic; SC, suspected carcinogen: T, toxic: TP, tumor promorer: NNN. N'-Nltrosonomicotine: NNK.4-(methylnitrosamino).(3.pyndyl)- I-butanone. SOURCE: Hoffmann and Hecht (I Y89). 89 ones, can signjficantly reduce the concentration of toxic and tumorigenic agents in MS, they have no reducing effect on the agents emitted into the SS (Adams, O'Mara-Adams, Hoffmann 1987). SS is the major source of ETS. The smoke diffusing through the cigarette paper, the smoke emerging from the burning cone during active smoking, and that portion of MS that is exhaled also contribute to ETS. Table 9 presents some data for toxic agents resulting from tobacco combustion in indoor environments (US DHHS 1988; Hoffmann _ ~~. and Hecht 1989). The concentrations of toxic agents in ETS appear low in comparison with their levels in undiluted cigarette MS. With regard to exposure factors, one needs to take into account the fact that the active inhalation of MS is limited to the time it takes to smoke each cigarette, whereas the inhalation of ETS is constant over several hours spent in the polluted environment. This is reflected in the results of measurements of the uptake of nicotine by active and passive smokers (US DHHS 1988). Smokeless Tobacco As noted above, the special Report of the Surgeon General, The Health Consequen- ces of Using Smokeless Tobacco, has shown that tobacco chewers and snuff dippers face an increased risk for cancer-of the oral cavity (US DHHS 1986b). In the United States the four primary smokeless tobacco types are plug tobacco, loose leaf tobacco, twist tobacco. and snuff. The composition of processed, unadulterated tobacco has been discussed. Chewing tobacco and snuff are made with various flavor additives (LaVoie et al. 1989). It is of special significance that the preparation of smokeless tobacco products, which en- tails curing. fermentation, and aging, occurs under conditions favoring the formation of tobacco-specific N-nitrosamines (TSNAs) from nicotine and other tobacco alkaloids such as nornicotine. anatabine. and anabasine (Figure 15). Of the six identified TSNAs in smokeless tobacco, N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-l-(3- pyridyl)- I -butanone (NNK) are strong carcinogens in mice, rats, and hamsters, induc- ing benign and malignant tumors of the oral cavity, nasal cavity, esophagus, lung, liver, and pancreas (Hecht and Hoffmann 1988; Rivenson et al. 1988). Table IO presents chemical-analytical data for TSNAs in U.S. smokeless tobacco products (Hoffmann and Hecht 1988). The concentrations of carcinogenic nitrosamines in smokeless tobac- co exceed those in otherconsumerproducts by at least 2 orders of magnitude (US DHHS 1986b). During tobacco chewing and snuff dipping, additional amounts of car- cinogenic TSNAs are most likely also formed endogenously in the oral cavity (Hoff- mann and Hecht 19X8). Carcinogenic TSNAs have been regarded as a major factor for the association of snuff-dipping with oral cancer in humans (Craddock 1983). Other carcinogens identified in smokeless tobacco are volatile nitrosamines (N- nitrosodimethylamine. <215 ppb), N-nitrosomorpholine (540 ppb), N-nitrosodiethyl- amine (<6.800 ppb), formaldehyde (17,OOCl ppb), crotonaldehyde (12,400 ppb), and benzo(u)pyrene (190 ppb). as well as traces of the radioelement polonium-210 (10.6 pCi/g) (US DHHS 1986; Hoffmann et al. 1987; Chamberlain, Schlotzhauer, Chortyk 1988). 90 TABLE 9.Come toxic and tumorigenic agents in indoor environments polluted by tobacco smoke Pollutant Nitric oxide Location Concentration/m' Workrooms 50-440 Ptz Restaurants 17-270 pg Bars 80-520 pg Cafeterias 2.5-48 pg Nitrogen dioxide Workrooms Restaurants Bars Cafeterias 688410 pg 4%190 pig 2-116pg 67-200 vg Hydrogen cyanide Benzene Formaldehyde Acrolein Acetone Phenols (volatile) N-Nitrosodimethylamine N-Nitrosodiethylamine Nicotine Benzo(a)pyrene Living rooms Public places Living rooms Public places Public places Coffee houses Restaurants, public places Restaurants, public places Public places Restaurants Workrooms Restaurants, public places 8-l 22 pg 2C-317 pg 23-50 pg 30-120 pg 36&5.800 pg 7.4-l I.5 ng O-240 ng O-200 ng 1-6PF3 3-10 M t-13.8 pg 3.3-23.4 ng SOURCE: Hoffmann and Hechr (1989). 91 FIGURE 15.-Formation of tobacco-specific N-nitrosamines TABLE IO.-Tobacco-specific N-nitrosamines in U.S. smokeless tobacco (ppb) Product NNN NNK NAT NAB Loose leaf tobacco 67Ck8.200 16') 380 ( 1) 2.300 ( 1) 140(l) Plug tobacco 3,4oc4,300(3J Snuff-moist 3.12(~-13.5.000(`6) 1CGl3.600(25) 1.340-339.000 (20) 1@-6,700(16) Snuff&dry `).(xx~.5?.wo(3) I.kWl3.000(3) 18,00&38,OCO(3) 6@-60,000 (3) VOTE: VW. n'-Nttro\onomicotlne: YNK.4-~methyl~itro\amtno~-l-(3-pyndyl)-l-but~none: NAT. U'-nltro\oan,ltahlnr. NAB. U'-n!tro\oanaha\me `Number m parenthew I\ the numkr oT~mpler analyzed. SOLRCE HoWmann end Hrcht , I%#). Toxicity and Carcinogenicity of Tobacco Smoke Undiluted tobacco smoke is too toxic to be tolerated by laboratory animals primari- ly becauw of the acute toxic effects of CO. CO in cigarette smoke increases with as- cending puff number from 2 to 5 volume percent (the average CO content of cigarette smoke ih 3.5 to 4.5 volume percent). The acute toxicity of tobacco smoke is also due to HCN. nicotine. and volatile aldehydes. In vitro short-term exposure to cigarette smoke cause\ ciliastasis. an effect primarily attributable to HCN (300 to 500 pg/cigarette) and volatile aldehydes (500 to 7.000 pg/cigarette). The long-term expo- wre of laboratory animals to diluted cigarette smoke causes impairment ofmucociliary clearance, mucus hypersecretion. and epithelial lesions. Cigarette smoke constituents responsible for this effect are both the gas phase. primarily HCN and volatile uldehydes. and the particulate phase (US DHEW 1979: US DHHS 19X-l). Long-term inhalation of diluted cigarette smoke by mice has resulted in adenomas and adenocarcinomas of the lung. whereas such inhalation in rats has only, led to a few isolated tumors of the lung. In Syrian golden hamsters, long-term smohe inhalation studies have regularly induced benign and malignant tumors of the larynx and only a few lung tumors. These obser\,ations strongly suggest. and studies of particulate deposition and determination ofcarboxyhemo~lobin (COHb) and nicotinexotinine in the blood of the smoke-exposed animals have confirmed. that laboratory animals do not inhale the smoke deeply. lntratracheal instillation of cigarette tar and one of its fractions has resulted in lung tumors. including bronchofenic carcinomas (Mohr and Reznik 197X: Dalbey et al. 1980: US DHHS 1982). The particulate matter (more often called "tar") suspended in organic solv,ents has in- duced carcinoma in the rat after subcutaneous injection and benign and malignant tumors in the skin of mice and rabbits after topical application. The major tumor in- itiators reside in the PAH-enriched neutral subfractions. whereas the tumor promoters and cocarcinogens are found in the weakly acidic fraction as vvell as in the polaric neutral subfraction (Wynder and Hoffmann 1967: Mohr and Reznik 197X: US DHHS 1982: Hoffmann and Hecht 198X). As discussed earlier. combined chemical-analytical studies have led to the identifics- tion of sev,eral organ-specific carcinogens in cigarette smoke. The diversity of these carcinogens and those identified as contact carcinogens may cause ambiguity as to which among them are most important. Table I I. which is based on extensive laboratory studies. lists the likely causative agents associated with the increased risk of cigarette smokers for cancer of the various organs (Hoffmann and Hecht 19X8). Nicotine It is generally held that nicotine is the active pharmacologic agent in tobacco that determines the addictive behavior of the tobacco smoker (US DHHS 1988). Nicotine, together with CO, is also regarded as a major contributor to cigarette smokers' increased risk of cardiovascular disease (US DHHS 1983. 198X). In addition to nicotine. tobac- co contains various other alkaloids. most of which are 3pyridyl derivatives. In the blended U.S. cigarette. nicotine constitutes 85 to 95 percent of the total alkaloids. During the smoking of a nonfilter cigarette. about IS percent of the nicotine appears in the MS, 35 to 30 percent appears in the SS. I5 to 20 percent is deposited in the butt. and the remainder is broken down into pyrolysis products. The major pyrolysis products of nicotine are CO, carbon dioxide, 3-vinylpyridine, 3-methylpyridine, pyridine, myosmine, and 2,3'-dipyridyl (US DHHS 1982). As discussed earlier. the absorption of nicotine from tobacco smoke is pH depend- ent. When tobacco smoke reaches the small airways and alv,eoli of the lung. nicotine ix rapidly absorbed. In chewing tobacco and snuff with their alkaline pH. nicotine is primarily absorbed through the mucous membranes of the oral cavity. Nicotine enters the blood and is rapidly transported to the brain, which has specific receptor sites for 93 TABLE Il.-Likely causative agents for tobacco-related cancers organ Initiator or carcinogen Enhancing agents Lung, larynx PAH Catechol (cocarcinogen) Weakly acidic tumor promoters NNK Polonium-210 (minor factor), acetaldehyde. formaldehyde Acrolein, crotonaldehyde (?) Esophagus Pancreas Bladder NNN NNK(?) 4-Aminobiphenyl 2-Naphthylamine Oral cavity (smoking) PAH NNK. NNN Ethanol Oral cavity (snuff dipping) NNK, NNN Irritation (?) Herpes simplex (?) Polonium-210 NOTE: PAH. polynucleararomatic hydrocarbons; NNK.4-(methylnitrosoamino)-l-(3-pyridyl)-l-but~one~ NNN. N'-Nttrosonomicotme. SOURCE: Hoffman and Hecht (1989). the drug. The effects of nicotine on the central nervous system are associated with the development of tobacco dependence (US DHHS 1988). Nicotine is metabolized primarily in the liver and. to a smaller extent. in the-lung. About IO to 15 percent of the absorbed nicotine is excreted unchanged in the urine. The primary metabolites of nicotine are cotinine and nicotine-N'-oxide. Cotinine is further metabolized extensively, with only 17 percent of it appearing unchanged in the urine (Benowitz 1986; Neurath et al. 1987; US DHHS 1988). Cotinine measurements in saliva, serum, or urine serve as an indicator for nicotine uptake by tobacco chewers, active smokers. and involuntary smokers. It takes I8 to 20 hr to eliminate one-half of the cotinine present in an active smoker through renal excretion; an involuntary smoker shows a considerably slower rate of elimination (Sepkovic. Haley, Hoffmann 1986; US DHHS 1988). Biological Markers Techniques for the determination of current and lifetime exposures to tobacco products include the examination of medical records and data from prospective and 94 case-control studies as well as the utilization of biological markers. The development of highly sensitive and reproducible methods has led to increased use of biological markers for uptake of tobacco smoke constituents. Table I2 lists those biochemical markers that are currently used to determine ex- posure to tobacco smoke components after active inhalation of MS and also after in- voluntary uptake of ETS. Some of these markers are also the basis for measuring the transfer of smoke constituents from the maternal bloodstream to a developing fetus. The tobacco-specific alkaloid nicotine and its major metabolite, cotinine, are most frequently used as serum and urine indicators of the uptake of tobacco smoke by active smokers and also to indicate ETS exposure in nonsmokers. Unlike CO, nicotine is not TABLE 12.-Biochemical markers for the uptake of tobacco smoke Smoke constituent Biochemical marker Substrate Method Sensitivity Critical valuea Nicotine Carbon monoxide (CO) Hydrogen cyanide WW Nitrogen oxides (NOA Ethylene (CHz=CHz ) 4-Aminobiphenyl Globin-adduct Tobacco-specific nitrosamines Globin-adduct Nicotine Cotinine COHb co Thiocyanate (SCK) Nitrosoproline Globin-adduct Serum Urine Serum Urine Saliva Serum Urine Saliva Serum Urine Blood Exhaled air Saliva Serum Urine Urine Blood Blood Blood GC RIA GC RIA Oximeter GC Autoanalyzer (color reaction) GC/l-EA Gc CC GC 1 ng/mL 0.2 ng/mL 5 ng/mL 1 ng/mL M.l% *I ppm f5 @mot/L tipmol/gHb 0 0 0 0 0.9 M.7% 5.6 i2.7 ppm 100 RmoUL 2.0 53 s kg/24 hours 58 f2.5 pmoUgHb ~70 pg/gHb Not established aCtitical values, values measured in nonsmokers. SOURCE: International Agency for Research on Cancer (1987). 95 only taken up by inhalation but also is absorbed through the mucous membranes in the oral cavity. Therefore, it is possible to determine user uptake of hydrophilic agents from chewing tobacco and snuff by means of nicotine-cotinine measurements. The analytical assessment of nicotine and cotinine in physiological fluids is done primarily by gas chromatography and radioimmunoassay (IARC 1986). Both methods are high- ly sensitive (between 0.2 and 5 ng/mL). and there is little or no interference by other smoke components. After environmental exposure, the average nicotine and cotinine levels in saliva, plasma, and urine of nonsmokers vary from 0.5 to 4.0 pg/mL, whereas the average amount of nicotine in the serum of cigarette smokers ranges from I5 to 40 ug/mL and lies between 500 and 2,000 pg/mL in saliva and urine. Cotinine concentra- tion varies from 1.50 to 350 ug/mL in plasma, from 150 to 400 pg/mL in saliva, and can go up to 2.000 ug/mL in urine (Jarvis et al. 1984: US DHHS 1988). In snuff dip- pers and tobacco chewers, plasma nicotine levels were found between 3 to 22 pg/mL and plasma cotinine was 200 to 400 l,tg/mL (US DHHS 1986). One of the oldest methods for estimating the inhalation of tobacco smoke is the deter- mination of COHb in blood. Since some CO is endogenously formed, the background values for COHb in the blood of nonsmokers without occupational exposure to CO range from 0.5 to 1.5 percent (National Research Council 1977). Smoking only a few cigarettes per day elevates COHb levels to 2.0 percent. In a study of men aged 34 to 64 years. cigarette smokers had average COHb concentrations of 4.7 percent; cigar smokers, 2.9 percent; and pipe smokers, 2.2 percent (Wald et al. 198 I: Wald and Ritchie 1984). The COHb values of nonsmokers after ETS exposure do not markedly exceed 1.5 percent: thus. COHb cannot serve as an indicator of exposure to ETS (NRC 1986). Since CO is only slowly released from the blood in the process of exhaling, the smok- ing intensity of a cigarette smoker can also be assessed by the analysis of CO in the ex- haled breath. The critical value for CO, the value above that of a nonsmoker, is 5.6f2.7 ppm in exhaled breath; again this method is not applicable to the dosimetry of non- smoker ETS exposures. HCN. a major tobacco smoke constituent (>I00 pg/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 umol 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 lrrnol/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 wsidely 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 TA 1538. 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 t-hat enable investigators to assay the uptake of tobacco smoke by individuals or by groups of individuals. Whereas analyses of exhaled CO, of COHb, and oSSCN- and nicotine-cotinine in saliva, serum, and urine are well suited for determining the smoking intensity of an active smoker, 96 only nicotine andcotinine determinations in serum and urine can also serve as indicators for the exposure of nonsmokers to ETS. Summary The 1964 Surgeon General`\ Report was a landmurh study that reviewed and arsesaed 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 making was found to increase overall mortality and tocause lung and laryngeal cancer. Several other important conclusions were also drawn (Table 13). Since 1964. 20 reports of the Surgeon General (includtng this Report) have been released on tobacco and health that substantiate and strengthen the original conclusions of the 1964 Report. These reports hav!e also established associations hetueen smoking :md disease in areas for vvhich 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 I3 allows the reader to sure ey quickly the state of hnow ledge on Ligarette smoking and health in I989 and to compare it with what was known in 1964. Of the 27 principal effects presented in Table 13. Ii were first noted in 1964; among those I3 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 nonsmohers and that smokeles\ 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 of43 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 I 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 is 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 TABLE 13.4ummary of the principal effects of cigarette smoking Effect first discussed in Surgeon General's Reports Year first discussed in a Surgeon General's Report Current knowledge in 1989 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 1964 Overall mortality increased in men and women 1967 Overall morbidity increased 1964 A major cause of coronary heart disease in men and women 1964 A cause of cerebrovascular disease (stroke) 1967 Increased mortality from atherosclerotic aortic aneurysm 1971 A cause and most important risk factor for atherosclerotic peripheral vascular disease 1964 The major cause of lung cancer in men and women 1964 The major cause of laryngeal cancer in men and women 1964 A major cause of cancer of the oral cavity (lip, tongue, mouth, pharynx) 1964 A major cause of esophageal cancer 1964 A contributory factor for bladder cancer 1967 A contributory factor for pancreatic cancer 1968 A contributory factor for renal cancer 1982 An association with gastric cancer 1982 An association with cervical cancer TABLE 13.-Continued Effect first discussed in Surgeon General's Reports Pulmonary Chronic bronchitis, the major cause Emphysema, increased mortality Women Low-birthyeight babies, associated with Unsuccessful pregnancy, associated with Year first discussed in a Surgeon General's Report 1964 1964 1964 1980 Current knowledge in I989 The major cause of chronic bronchitis The major cause of emphysema A cause of intrauterine growth retardation A probable cause of unsuccessful pregnancies Other effects Tobacco habit, related to psychological and social drives 1964 Involuntary smoking, irritant effect 1972 Peptic ulcer disease, associated with 1964 Occupational interactions, adverse 1971 Alcohol interactions, adverse 1971 Drug interactions, adverse 1979 Nonmalignant oral disease, associated with 1969 Smokeless tobacco. associated with oral cancer 1979 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 X2 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 19X9 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 uas briefly mentioned in the I964 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 for smokers of all ages. Part 1. Health Consequences I. The I964 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. Reportsofthe Surgeon General since 1963 have concluded that smoking increases mortality and morbidity in both men and women. Disease associations identified as causal since I963 include coronary heart disease. atherosclerotic peripheral vascular disease, lung and laryngeal cancer in women, oral cancer, esophageal cancer, chronic obstructiv/e 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 I979 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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The effects of maternal smoking on fetal and infant mortality. American Journal of Epidemiol- ogy 127(2):274-282, 1988. KORMAN, M.G., HANSKY, J., EAVES, E.R., SCHMIDT, G.T. Influence of cigarette smok- ing on healing and relapse in duodenal ulcer disease. Gastroenterology 85871-874, 1983. KREIGER, N., KELSEY, J.. HOLFORD, T.R., O'CONNOR, T. An epidemiologic study of hip fracture in postmenopausal women. American Journal ofEpidemiology 116( 1): 141-148, 1982. KULLER, L.. MEILAHN, E., TOWNSEND, M., WEINBERG, G. Control of cigarette smok- ing from a medical perspective. Annual Review of Public Health 3:153-178, 1982. LANE, M.R., LEE, S.P. Recurrence of duodenal ulcer after medical treatment. Lancer 1: 1147- 1149, May 21, 1988. LAURELL, C-B., ERIKSSON, S. The electrophoretic a-globulin pattern of serum in at-anti- trypsin deficiency. Scandinavian Journal of C/inica/ Investigations 15:132-140, 1963. LAVECCHIA, C., FRANCESCHI, S., DECARLI, A., FASOLI, M., GENTILE, A.,TOGNONI, G. Cigarette smoking and the risk of cervical neoplasia. American Journal of Epidemiology 123( 1):22-29, January 1986. LAVOIE, E.J., TUCCIARONE, P., KAGAN, M., ADAMS, J.D., HOFFMANN, D. Analyses of steam distillates and aqueous extracts of smokeless tobacco. Journal of Agricultural and Food Chemistry 37( 1): 154-157, January-February 1989. LAYDE, P.M., BERAL, V., KAY, C.R. Further analyses of mortality in oral contraceptive users. Royal College of General Practitioners' Oral Contraceptives Study. Lancer l(8219): 541-546, March 7. 1981. 108 LIEBERMAN, E., RYAN. K.J., MONSON. R.R., SCHOENBAUM, SC. Risk factors account- ing for racial differences in the rate of premature birth. New England Journal of Medicine 317( 12):743-748. 1987. LITHNER, F. Is tobacco of importance for the development and progression of diabetic vas- cular complications? Acta Medica Scandinavica 687(Supplement):33-36, 1983. LUBIN, J.H., BLOT, W.J.. BERRINO, F., FLAMANT, R., GILLIS. C.R., KUNZE, M., SCHMAHL, D.. VISCO. G. Patterns of lung cancer risk according to type of cigarette smoked. international Journal of Cancer 33(5):569-576. 1984a. LUBIN, J.H., BLOT, W.J.. BERRINO, F.. FLAMANT, R.. GILLJS, C.R., KUNZE, M.. SCHMAHL. D.. VISCO. G. Modifying risk of developing lung cancer by changing habits of cigarette smoking. British Medical JournaI 288(6435): 1953-1956. June 30. 1984b. LYNCH, H.T., FAIR, P.R., ALBANO, W.A., RUMA. T.A., BLACK, L., LYNCH, J., SHONKA, M. Genetic/epidemiological findings in a study of smoking-associated tumors. Cawer Genetic,s and Cyrogenetics 6(2): 163-I 69, June 1982. MACK, T.M., YU, MC., HANISCH. R., HENDERSON, B.E. Pancreas cancer and smoking, beverage consumption, and past medical history. Journal of the National Cancer institute 76( 1):4940, 1986. MARTIN, J.L.. WILSON, J.R., FERRARO, N., LASKEY, W.K., KLEAVELAND, J.P., HIRSHFELD, J.W. JR. Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease. Americ,an Journal ofCardiology 54( 1):56-60, July 1, 1984. MCLAUGHLIN, J.K., MANDEL, J.S., BLOT, W.J.. SCHUMAN, L.M., MEHL., E.S., FRAUMENI. J.F. JR. A population-based case, while the relative risk among former smokers was 1.20 (95percent 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 17 1) was 1.10 (95percent 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 95percent 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 K-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 (198246) Underlying cause of deatha Males Females CPS-I CPS-II CPS-I CPS-II CHD, age 235 1.83 1.94 1.40 l.78b CHD. age 35-64 2.25 2.81b 1.81 3.00b Cerebrovascular Lesions. age 235 1.37 2.24b 1.19 1 .84b Cerebrovascular Lesions, age 3564 COPD 1.79 3.67b I .92 4.80b 8.8 I 9.65 5.89 10.47 Cancer, Lip, Oral Cavity, and Pharynx 6.33 27.48 I.96 5.59 Cancer, Esophagus 3.62 7.60 1.94 10.25b Cancer, Pancreas 2.34 2.14 1.39 2.33 Cancer, Larynx 10.00 IO.48 3.81 17.78 Cancer, Lung 11.35 22.36b `See Tables 4-7 for International Classification of Disease codes. %S-percent confidence mtewals do not overlap between CPS-I and CPS-Il. SOURCE: Tables 4-7. 2.69 11 .94b 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 Cause of death ?ea 0 Fey$s b CHD. age 35-64 CHD, age a5 COPD 42 w-w &30) II 3.3 (9-14) (2.1-5.1) ;;9+ 67 (57-76) Cancer of lip, oral cavity, and pharynx :549-85) 27 (12-51) Cancer of larynx Cancer of esophagus 57 (36-76) &9) Cancer of lung 86 40 (82-88) (31-50) Cancer of pancreas 41 14 (30-53) (6-30) Cancer of bladder &6) &56) Cancer of kidney :P,-56) E42) Cerebrovascular disease, age 35.64 $36) :282-33) Cerebrovascular disease, age 265 2.0 1.3 (0.6-6.6) (0.24.5) `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-I. bFor females, attributable risks computed fmm prevalence rates in Table 2 and relative risks for all female smokers, past and present, in Table 5. `Numbers in parentheses are 9%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 lO.-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 CHD, age M5 COPD Cancer of lip, oral cavity, and pharynx Cancer of larynx Cancer of esophagus Cancer of lung Cancer of pancreas Cancer of bladder Cancer of kidney 51 9.5 (4&54)= (8.2-10.8) 25 6.0 (20-30) (3.9-9.4) 16 2.3 (15-17) (2.G2.7) 3.6 0.4 (2.9-4.2) (0.2-0.8) 1.9 0.i (1.42.2) (0.02-0.3) 2.4 0.1 ( I .5-3.2) (0.2-0.8) 35 3.1 (34-36) (2.638) 3.8 0.9 (2.8-4.9) (0.4-2.0) 3.0 1 .o (2.2-3.7) (0.5-1.5) 1.2 0.3 (0.7-I .9) (0.1-1.8) Cerebrovascular disease, age ~65 5.5 (4.2-7.2) .$78-L,) Cerebrovascular disease, age 265 I.5 1.0 (0.4-4.8) (0.2-5.9) Ten causes 150b (143-157) :;fxq NOTE: Computed from Table 9 and tabulations of deaths at ages 20 years or more by cause for 1965 (NCHS 1%7). Sums may not equal totals because of rounding. `Numbers in parentheses are 95percent confidence intervals. when the attributable risk estimates given in Note a of Table 9 were used. the total attributable deaths for males welt 158,ooO (95percent confidence interval, 15 1,WO to 166,ooO). Approximately two-thirds of the 8,000 additional deaths were from CHD. years or more. For the IO 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 Il.-Estimated attributable risks for 10 selected causes of death from cigarette smoking, males and females, United States, 1985 Cause of death Y% Females (%) CHD, age ~65 CHD, age 265 COPD Cancer of lip, oral cavity, and pharynx Cancer of larynx Cancer of esophagus Cancer of lung Cancer of pancreas Cancer of bladder Cancer of kidney Cerebrovascular disease, age ~65 Cerebrovascular disease, age 265 45 41 (40-50)" (3448) 21 12 ( 17-26) (9-15) 84 79 (78-88) (73-83) 92 61 (79-97) (45-76) 81 87 (57-93) (5697) 78 75 (62-89) (57-87) 90 79 (88-92) (75-82) 29 34 ( 18-43) (25-44) 47 37 (3 I-63) (1841) 48 G-64) l!Lw 51 55 (3ti5) (45-65) :P,35, 6 (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 pe rcent. For men 65 or older, the prevalences of current and former cigarette smoking were, respectively. 19.4 and 5 I. I 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 I 1 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). 8 I .8 percent of all COPD deaths (95percent con- fidence interval 78.3 to 85.3) and 21.5 percent of all CHD deaths (95percent 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 23 1,000 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 1 O-cause total; the relative importance of smoking-induced cancer fatalities has also increased. The total IO-cause smoking-attributable mortality for 1985 was 337,OOOdeaths. 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 I 1 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- tity 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 1 I and D* is a 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 - 11 (9-12) CHD, age 2665 44 26 (3654) m-34) COPD 37 20 (35-39) (18-21) Cancer of lip, oral cavity, and pharynx 5.1 1.6 (4.4-5.4) ( 1.2-2.0) Cancer of larynx 2.3 0.6 (1.62.7) (0.40.7) Cancer of esophagus 5.0 1.6 (4.0-5.7) (1.3-1.9) Cancer of lung 76 (74-77) &32) Cancer of pancreas 3.3 3.4 (2.1-5.0) (2.8-5.1) Cancer of bladder 3.1 (2.1-4.2) $!&I .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 4.8 R-17) (1.9-11.4) Ten causes 231 106 (22&242) (98-l 15) NOTE: Computed from Table I I and unpublished tahulatmns of deaths at agee, 20 years DT more by cause from NCHS. 1985. Sum of mdiwdual causes may not equal total\ because of rounding. `Numbers in parentheses are 95-percent confidence mrervals. 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 m- 60- 50- 40- 3D- 20- 10 - O- MRES FIGURE lO.-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. 2 36 832 - 30 FEWLES 2% 26 24 22 20 I8 16 14 12 10 6 6 4 2 0 CHI (85 FIGURE IL-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 incrwaduring 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 Activity or cause Annual fatalities per 1 million exposed persons Active smoking 7,oocf Alcohol 541 Accident 275 Disease 266 Motor vehicles 187 Alcohol-involved 95 Non-alcohol-involved 92 Work 113 Swimming 22 Passive smokingb 19 All other air pollutantsb 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. bCancer deaths only. SOURCE: Active smoking, CPS-II; NHlSs 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). 1. 2. 3. 4. 5. 6. 7. 8. 9. 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, 2 1 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 1 million per- sons at risk. 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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 ..................................................... ..17 5 DataSources .................................................... 175 Issues in Comparing Surveys ....................................... 177 Trends in Public Beliefs About the Health Effects of Smoking ............... 179 Overview ..................................................... ..17 9 Is Cigarette Smoking Harmful to Smokers in General? ................... 179 Heavy Versus Light Smoking .................................. 18 1 TarYield ................................................ ..18 3 Duration of Smoking ........................................ 185 Does Cigarette Smoking Cause: .. _ ............................. 185 LungCancer? .......................................... 185 HeartDisease? .......................................... 188 Chronic Obstructive Pulmonary Disease? ..................... 188 OtherCancers? ......................................... 195 What Are the Special Health Risks for Women? ................... 195 Effects of Smoking on Pregnancy Outcome ................... 197 Risk of Cardiovascular Disease Among Smokers Who Use Oral Contraceptives ........................... 197 Other Health Risks Related to Tobacco Use ...................... 200 Involuntary (Passive) Smoking ............................. 200 Is Smoking an Addiction? ................................. 200 Interaction Between Smoking and Other Exposures ............. 202 SmokelessTobacco .................................... ..20 2 Personal Health Risks for Smokers ................................... 202 How Harmful Is Smoking? ......................................... 204 AbsoluteRisk ............................................ ..20 6 RelativeRisk ............................................... 206 Attributable Risk and Smoking-Attributable Mortality .............. 206 ComparativeRisk ........................................... 207 Knowledge Among Adolescents About the Health Risks of Smoking ....... 212 General Health Effects ....................................... 2 12 PersonalizedRisk ......................................... ..215 Comparative Risk ........................................... 2 15 Addiction ............................................... ..216 SmokelessTobaccoUse .................................... ..217 Constituents of Tobacco Smoke ..................................... 217 Health Benefits of Smoking Cessation ................................ 219 Discussion .................................................... ..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 ....................... 223 173 Trends in Public Attitudes About Smoking and Smokers ................... 224 Involuntary Smoking as an Annoyance ............................... 224 Nonsmokers'Rights ............................................ ..22 4 Actions When Smokers Light Up .................................... 227 OpinionsofTeenagers .......................................... ..22 7 Trends in Public Opinion About Smoking Policies ........................ 230 Overview ....................................................... 230 Background .............................................. ..23 0 Limitations of the Surveys in Assessing Public Opinion About Smoking Policies .................................... 230 Restrictions on Smoking ........................................... 230 General ................................................. ..23 0 PublicPlaces ............................................. ..23 2 Workplace ................................................. 232 Airplanes ................................................ ..23 2 Restaurants ................................................ 235 OtherPlaces ............................................. ..23 5 Restrictions on the Sale and Distribution of Cigarettes ................... 235 Complete Ban on Sales ....................................... 235 Limiting Sales to Minors ..................................... 235 Banning Free Samples ....................................... 239 Policies Pertaining to Information and Education ........................ 239 Restricting or Prohibiting Tobacco Advertising ................... 239 Warning Labels for Cigarettes ................................. 24 1 EconomicPolicies .............................................. ..24 1 Taxation ................................................ ..24 1 Hiring .................................................. ..24 1 Conclusions ....................................................... 244 Appendix ....................................................... ..24 6 References ........................................................ 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 l.-Methodology of surveys Survey Survey firm Sample Age Response size (years) rate (%) Mode8 AUTS 1964 AUTS 1966 AUTS 1970 AUTS 1975 National Analysts National Analysts Opinion Research Chilton Chilron 5,794 5,768 5,200 12,ooo >21 221 76 P 72 P Tb P(9%c) T(91%) T(96%) P(4%c) Roper 1978 Roper 2,511 NHIS 1985 Census Bureau 33.630 AUTS 1986 Westat 13.03 I 118 217 P 90 P 74 T AMA 1986 Kane, Parsons 1.500 T AMA 1987 Kane. Parsons 1,500 T MTFd 1975-87 University Michigan of 18 Q ?`, personal interview; T. telephone interview; Q, self-administered questionnaire bNonrespondents to personal interviews. `Nontelephone households. dMonitoring the Future F'rojea, survey of high school senior. 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 (e.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 (e.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. In a 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 such a 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 3 1). 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 1 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 25year 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 so&demographic 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 SklhlS, so&demographic correlation data are not presented below. Because smoking rates 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 8 1 percent), as well as among never smokers (89 to 95 percent). 179 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 adults 1. AUTS' 1964 US DHEW 1969 70 91 89 89 81 2. AUTS' 1966 US DHEW 1969 78 89 89 89 85 3. ALJTS* 1970 US DHJZW 1973 79 92 92 4. AUTS' 1975 US DHEW 1976a 81 95 95 `Rrcentages include those who "strongly agree" or "mildly agree." NOTE: ACNE questions: I. 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 disagra). 92 87 95 90 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 othersa Kind I smoke probably more hazardous than othersa Kind I smoke probably less hazardous than othersa Kind I smoke probably about the same as others= Don't know Subtotal All cigarettes are probably about equally hazardousa Cigarettes are probably not hazardous to health at all Don't know or not stated if some are hazardous Total (6) (10) (8) (25) (25) (21) (14) (14) (13) (2) (2) (2) 47 51 45 43 41 50 4 5 2 6 4 3 100 100 100 `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 1973.1976~1; 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 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) Survey Ytar Reference hY amount Not hazardous I. Roper 1970 Roper 1978 47 45 5 2. Roper 1972 Roper I978 48 42 6 3. Roper 1974 Roper 1978 54 39 4 4. Roper 1976 Roper 1978 54 38 4 5. Roper 1978 Roper 1978 61 31 5 6. AUTS 1986 US DHHS, in press 72 20 81 13 85 II ~Respondents were ailowed to choose only one answer. The `*no1 hazardous" response was not availaMe for the AUTS. bPcrcentagcs of respses in Roper surveys refer to all respondents; in AUTS 1986, percentages represent cumnt, former, and never smokers. respectively. NOTE: Actual questions: l-5. How hazardous is smoking ,?,(any amoun1, only heavy smoking. not hazardous, don't knowy 6. Do you think that1 only heavy smoking is hazardous or that any smoking is hazardous'? (only heavy smoking, any smoking. don't know] 3 4 3 4 4 5 (current smokers) 4 (former smokers) 4 (never smokers) 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, 8 1, 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 a health 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: "It 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 TABLE S.-jPublic 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) I 2-4 5-9 IO-14 15-24 25-39 aul Don't know Current smokers 14 4 8 12 17 3 17 25 Former smokers 17 6 10 13 19 2 9 22 Never smokers 21 9 10 I1 19 1 9 20 %e queslion was open ended. Responses were grouped in the calegories l-9. l&24. and 225 cigarettes per day 10 conform to the common definitions of light, moderate, and heavy smoking. SOURCE: AUTS 19R6 (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. 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 all 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 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 "bore likely to get lung cancer? (percentage indicating the following number of years ) 59 lcLl9 2&29 Em Don't know/ no answer Smokers not more likely to get lung cancer Current smokers 10 12 12 II 10 43 Former smokers 17 17 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. bRegardless of number of cigarettes per day. SOURCE: AUTS 1964 (US DHEW 1969). 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) I5 Never Don't know Current smokers 23 15 10 8 3 10 0.6 30 Former smokers 24 13 I3 IO 3 9 0.4 29 Never smokers 36 I6 IO 6 2 5 0. I 25 %IC 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 6.5 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 TABLE S.-Trends in public knowledge about smoking and lung cancer Cigarette smoking causes lung cancer (percentage who agree by smoking status) Survey Year Reference Current Former Never All All smokers smokers smokers nonsmokers adults I. Gallup I954 Gallup I98 I 41 2. Gallup 3. Gallup 4. AUTS 5. AUTS 6. Gallup 7. Gallup 8. Gallup Y. Gallup I957 Gallup 1981 50 1958 Gallup I98 I 44 1964 US DHEW 1969 1966 US DHEW 1969 1969 Gallup 1981 53 75 7s 75 66 57 79 70 72 66 71 1971 Gallup I98 I 71 1977 Gallup 1981 81 1978 Gallup 1978 72 87 81 IO. Gallup 1981 Gallup I98 I 69 91 X3 TABLE K-Continued Survey Year Reference Current smokers Cigarette smoking causes lung cancer (percentage who agree by smoking status) Former Never All smokers smokers nonsmokers All adults II. 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. NHISb 19x7 83 92 92 89 "And unpublished data. hPreliminary first-quarter data (unpublished). Year-end percentage for all adults is 89 percent. NOTE: Actual questions: , l-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?' IS- IO. 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) I I. Tell me if you think cigarette smoking detinitely 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 smokmg 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 1ikely"to get lung cancer. TABLE 9.-Trends in public knowledge about smoking and heart disease Smoking cigarettes causes heart disease (percentage who agree by smoking status) Survey Year Reference Current Former Never All All smokers smokers smokers nonsmokers adults I. AUTS 2. AUTS 3. AUTS 4. Gallup 5. Gallup 6. Gallup 7. Gallup 8. NHIS 9. AUTS 1964 US DHEW 1969 1966 US DHEW 1969 1966 US DHEW 1969 1969 Gallup I98 1 1917 Gallup 198 I I978 Gallup 1978 1981 Gallup 1981 1985 NCHS 1988 1986 US DHHS, in press 32 51 44 46 40 33 53 43 41 42 `46 65 58 60 54 60 68 63 72 68 59 82 74 88 93 92 92 90 71 84 80 81 78 TABLE 9.-Continued Smoking cigarettes causes heart disease (percentage who agree by smoking status) Survey Year Reference Current smokers Former smokers Never smokers All nonsmokers All adults IO. NHISa 1987 73 82 77 77 %eliminary first-quarter data (unpublished). Year-end percentage for all adults is 76 percent. NOTE: Actual questions: l-2. Do you thmk 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 ugarertes or people who do smoke cigarettes'! 3. Cigarette smokers are more likely to die from heart dibeaae than people who don't smoke cigarettes. (strongly agree. mildly agree. no opinion. mildly disagree. strongly disagree)' 4-7. Do you think that cigarette smokmg is or is not one of rhe causes of hean disease'? R. Do you think cigarette smokmg definitely increases, probably increases. probably dwa not. or definitely does not increase a person's chances of getting hean disease?' 9. Do you think a person who smokes is any more likely lo get heat-i 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? `Percentages include those who "strongly agree"or"mildly agree." `Percentages include those who believe that smoking "definitely" or"probably" increase\ the risk. ' "Percentages include those who believe smokers are "much more likely"or"somewhat more likely" to get heart disease. TABLE lO.-Trends in public knowledge about smoking and emphysema or chronic bronchitis Percentaae who agree bv smoking status Survey Year Reference Current Former Never All smokers smokers smokers nonsmokers All adults 1. AUTS 2. AUTS 3. NHIS 4. AUTS 5. Gallup 6. NHIS' 7. AUTS 8. NHIS 1964 Smoking is a cause of emphysema/chronic bronchitis US DHEW 1969 42 60 1966 1985 US DHEW I%9 NCHS 1986b 46 60 Smoking is a cause of emphysema 89 94 1986 US DHHS, in press 85 92 1987 ALA 1987 75 91 55 56 52 54 91 92 90 91 90 1987 1966 US DHEW 1969 19 87 Smoking is a cause of chronic bronchitis 50 56 84 65 56 1985 NCHS 1986b 82 89 88 88 50 51 91 89 85 84 59 86 TABLE lO.-Continued Percentage who agree by smoking status Survey Year Reference Current smokers Former smokers Never smokers All nonsmokers All adults 9. AUTS 1986 US DHHS, in press 73 84 83 84 81 10. NHISa 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: l-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 emphysema.' think cigarette smoking definitely increases, probably increases, probably does not. or definitely does not increase a person's chances of getting the following problems 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 crgarette smoking is related to emphysema? 7. Cigarette smoking causes chronic bronchitis. (strongly agree, mildly agree, no opmion. 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 followmg 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 whobelieve 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 (9 1 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 acausal 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 3 1 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 TABLE Il.-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 1917 Gallup 1981 79 2. Gallup 1978 Gallup 1978 13 82 79 3. Gallup 1981 Gallup 1981 69 87 81 4. NHIS 1985 NCHS 1986h 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 13 85 83 80 %`reliminary first-quarter data (unpublished). Year-end percentage for all adults is 80 percent. hAnd unpublished data. NOTE: Actual questions: l-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 , cancerofthe larynx or voice box (question 4). cancer of the esophagus (question 5): 6. Do you think a person who smokes is any mwe 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 consequexes 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 IX to 44 veurs 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 aho smokes. 197 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 Survey Year smokers smokers smokers nonsmokers Smoking during pregnancy increases the chances of premature birth 1. AUTS 1966 25 43 34 2. NHIS 1985 (all) 64 71 75 2. NHIS 1985 (men) 2. NHIS 1985 (women) All adults 70 64 76 Smoking during pregnancy increases the chances of stillbirth 3. NHIS 1985 (all) 57 3. NHIS 1985 (men) 3. NHIS 1985 (women) Smoking during pregnancy increases the chances of miscarriage 4. NHIS 1985 (all) 66 4. NHIS 1985 (men) 4. NHIS 1985 (women) Smoking during pregnancy increases the chances of having a low-birth,weight baby 5. NHIS 1985 (all) 14 5. NHIS 1985 (men) 5. NHIS I985 (women) A woman taking birth control pigs is more likely to have a stroke if she smokes 6. NHIS 1985 (all) 59 6. NHIS 1985 (men) 48 6. NHIS I985 (women) 70 67 75 82 67 57 80 72 79 83 64 65 62 54 55 52 72 74 72 66 63 68 74 72 75 80 74 85 TABLE 12.-Continued Survey Year Current smokers Percentage who agree by smoking status Former Never All All 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 b{ 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. (J987) and NCHS (1986) and mclude only those people I8 to 44 year?, of age. Roper data for 1980 are from thefTC(l981). bPreliminary first-quarter data (unpublished). Year-end percentage for all adults is 89 percent. NOTE: Actual questions: I. -Women who smoke during pregnancy are mme likely to have premature babies than women who do not smoke (strongly agree. mildly agree. no opmion. mildly disagree. strongly dtsagree).' 2. Does cigarette smoking during pregnancy definitely increase, probably increase, probably not or definitely not increase the chance\ of premature bmh?' 3. of stillbirth?' 4. of 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 wcnnan 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 I~`L true. thmk 11`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 whobelieve that smoking "detinitely"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), 8 1 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 (8 1 percent) (Table 13). In the 1986 AUT'S, 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 TABLE 13.-Trends in public knowledge about the health risks of passive smoking Smoking is haLardous lo nonsmokers' health (percentage who agree bv smoking status) Survey YetiI Reference Current smokers Former smokers Never smokers All nonsmokers All adults I. Roper 1974 Roper 1978 30 57 46 2. Roper 1976 Roper 1978 38 61 52 3. Roper 1978 Roper 1978 40 69 58 4. AUTSa 1986 US DHHS, in press 69 82 87 85 81 5. NHISb 1987 68 85 88 81 6. Gallup 1987 ACS 1988b 64 86 89 81 `Percentages presented here are slightly lower than those previously published (CDC 1988) because the lauer did not include "don't know" respomeh in the denommator. %eliminary first-quarter data (unpublished). Year-end percentage for all adults is 81 percent. NOTE: Actual questions: l-3. Is smoking hazardous tononsmokers' 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 nor harmful to people who are near them? (yes, harmful; no, not harmful; can't ray/no op~mon) `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 concerning 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 1986~). 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 (7 1 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 regarding 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 198 1 and 1985. The proportion of current smokers answering in the affirmative increased from 80 percent in 198 1 to 90 percent in 1985. These data, at first glance, suggest that a high percentage of smokers 202 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) Survey YGU Reference Current smokers Former smokers Never smokers All nonsmokers All adults I. 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: l-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 concerned 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 TABLE 15.-Trends in smokers' concern about the effects of smoking on their own health Concern about the possible effects of cigarette smoking on your health (percentage who responded by level of concern) Survey Year Very concerned Fairly concerned Only slightly concerned Not Any concerned concerna I. AUTS 1964 13 18 19 50 50 2. AUTS 1966 12 17 18 53 47 3. AUTS 1970 29 22 19 31 69 4. AUTS 1975 25 23 19 32 68 5. AUTS 1986 `Very. fairly, or only slightly concerned. NOTE: Actual questions: 18 22 34 24 75 l-5. Are you in any way concerned about the possible effects of cigarette smoking on your health? SOURCE: US DHEW ( 1969. 1973, 1976a): 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 198 1). 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 198 1). 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 3 1 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: lO,OOOdeaths, 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 lb 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 P reCention magazine (Harris 1983). Respondents were asked to rank 24 health and safety factors on a l-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 lb 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 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 31 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). U.: In helping people m general to IIVB a long ano nealrny me, now woulu you rate the importance of . . . M Utmost 01 Low ,. Impodancs 9 8 7 6 5 4 1 I I I I I I w Never dnvmg after drmking 9.25 (.05) HI Keeping air quality acceptable 9 11 (.05) W Keeping water quality acceptable 8.95 (.OS) ct( Havmg smoke detectors in home 8.89 ( 06) i-w Keeping close to recommended weight 8.54 ( 05) l-w Havmg blood pressure readmg annually 8 51 ( 06) ccl Takmg steps to control stress 8.38 (.06) l-o-i Gettmg enough wtamms, minerals 8.37 (.06) Y Exerclsmg regularly 8.32 (.06) I+-f Not smoking 8.25 ( 08) H( Having fnends. relabves. neighbors 8 18 ( 06) +o-f lnherthng genes from parents for long life 8 16 ( 06) m Recetvlng advice from doctor on health habits 8 13 ( 06) l-o-4 Not eatmg too much sodium 8.10 (.06) l-u Gettmg 7-8 hours sleep 8.04 (.06) I+A Eahng enough fiber 7 98 (.06) I-VI Wearmg seatbelts all the bme in front seat 7 89 ( 07) c-c( Not eating too much fat 7.88 (.07) w Gettmg enough calcium 7.84 (.06) &o-f Not eating too much sugar 7 81 ( 07) w Ealmg breakfast daily 7.61 ( 08) M Not getting loo much cholesterol 7 42 ( 07) m Dnnking alcohol moderately 6 53 ( 09) w Dnnkmg no alcohol 6 42 ( 09) FIGURE l.-Adult public's rating of 24 health and safety factors NOTE: Shown &we is the mean importance raring f~,r each factor given by l-2.54 adulta using a I to IO scale. Given III parentheses is the standard emor of the mean. The 95.percent confidence inlerval around each mean is graphically displayed as a band or range consisting of k two standard errc~r values. SOURCE: Harris (1983). 0.: Thinking about the uverall health of the general populatfon, how important is it for adults to . . . M Utmost OfLOW l-v Not smoke 9.78 ( .09) Wear seatbelts all the bme m front seat 9.16 (.12) t - i Never drive after drinking 9.03 (.18) I z I Have smoke detectors in home 8.53 ( .17) 1 = 4 Live where drmking water IS of acceptable quality 8.41 (. 17) t = 1 Have friends, relabves. neIghbars 8.31 (.16) t = I Exercise regularly 8.20 (.16) I = i Drink alcohol moderately 6.15 (.19) t - I Not eat tw much fat 7.82 (.15) .' Keep close to recommended weight 7.71 (.15) Receive advlce from doctor on health habits 1 71.67 (.22) r = I Have blood pressure reading annually 71.62 (.21) I I Inherit genes from parents for long life 7.62 (.28) t c 4 Take steps to control stress 7.58 (. 18) I = I Eat enough fiber 7.41 (.17) t c 4 Get enough Cal&urn (for women) 7.28 (.19) 1 ; 4 Not get too much cholesterol 7.15 (.19) I = I Live where air is acceptable 7.12 (.22) 1 - I Get enough vitamins and minerals 7.12 (.22) I I Not eat too much sodium 7.04 (. 19) i : I Noteat toomuchsugar 6X1(.19) 1-t Get 7-8 hours sleep 6.71 (.20) l-1 Eat breakfast daily 6.16 (.25) Drink no alcohol 3.15 (.23) t-1 FIGURE 2.-Experts' rating of 24 health and safety factors NOTE: Shown above is the mean importance ratmg for each factor given by 103 experts using a I m IO scale. Given in parentheses is the standarderror of the mean. An indicator of the variability of individual ratings around each mean is grapbi- tally displayed as a band or range consisting off two standard error values. SOURCE: Harris (1983). TABLE 17.-Public knowledge about the harmfulness of cigarette smoking compared with other risks, 1986 Percentage who agree Percentage who disagree Current smokers Former smokers Never smokers Current smokers Former smokera Never 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. 4x 30 28 41 54 57 Smoking cigarettes is less dangerous than driving without a 36 25 26 52 58 68 seat belt. Smoking is less harmful than being 20 pounds overweight. 31 19 IX 59 69 71 NOTE: Percentages of those who agree include those who "strongly agree" or "somewhat agree." Percentages of those who diwgree include those who Wrongly disagree" or "somewhat disagree." SOURCE: AUTS I986 (US DHHS. in press). riculum Program during the 1980-S 1 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; cigarettesmoking, 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: (I) 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 TABLE l&-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 a 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 I I 6 28 63 98 1982 2 2 7 30 61 97 1983 1 2 7 29 61 97 1984 I 2 6 27 64 97 1985 2 2 6 24 67 97 1986 I 1 5 26 66 97 "Slight. moderate. or great risk of harm combined. SOURCE: Bachman, Johnston, O'Malley ( I9XOa.b. 1981. 19X4. 198% 1987): Johnston and Bachman (19X0): Johnston. Bachman, O'Malley ( I9XOa.b. 19x2. 19X4. 19%) 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 gnat risk, moderate risk, sltght risk. no risk, don't know. SOURCE: Bachman. Johnston, O'Malley (1987). tional Institute on Drug Abuse) forevery 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; 5 1 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 In a survey 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 likely, 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 risk. 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 11 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). In a 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-l 8) either did not know (21 per- cent) or said "no" (29 percent); 45 percent of adults (aged 29-3 1) 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) TN = 109) ST use con 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 II 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 detined as follows: has never dipped or chewed. or has only tried tt a few times or twxe 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 2 1). 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 numberof 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 h) t-2 0 TABLE tl.-Public knowledge about the health benefits of smoking cessation in relation to years of abstinence, 1986 I2 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. I 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 Fast 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 24.1 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. I 19.0 Maryland 29.7 31.5 28.1 36.3 20.1 282 TABLE &-Continued Education Overall Males Females 512 years >12 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. I Florida 31.7 35.5 28.4 36.8 25.4 Fast 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 Id&O 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. Percentageof 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). 2. 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 a1.1987a). 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. 3. The smoking continuum. This is a lo-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 R2 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 3 1.5 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 I965 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=O.Ol). The difference in the rate of change between black and white females is in the opposite direction but is not statistically significant (p=O.31) 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 be en 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 TABLE 9.-Trends in smoking quit ratio (o/o), 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 graduate graduate college 1 965a 29.6 31.4 24.6 30.5 22.8 1966 29.5 3 1.4 24.2 30.4 22.6 33.3 28.0 28.7 1970 35.3 37.9 29.2 36.7 23.2 38. I 33.6 34.9 1974 36.3 39.3 30.8 38.0 21.8 38.0 35.2 36.6 1976 37.1 39.9 32. I 38.4 26.3 39.5 35.0 37.2 1977 36.8 40.3 31.3 38.2 24.8 38.3 34.0 36.8 1978 38.5 41.3 33.8 39.9 27.5 38.7 36.3 41.0 1979 39.0 41.5 34.0 40.3 28.0 40.8 36.7 37.5 I980 39.0 41.5 34.0 40.4 27.7 39.4 36.5 40.6 1983 41.8 44.1 37.6 43.3 29.3 42. I 38.7 41.2 1985 45.0 49.0 40.0 46.7 31.8 41.3 40.5 46.0 1987b 44.8 48.7 40. I 46.4 31.5 39.7 40.9 46.9 Trend information (1965-85) Changec/ year +0.68 io.73 +0.73 i-O.72 +0.43 +0.4 I co.57 +0.73 Standard error (k) 0.05 0.06 0.05 0.06 0.07 0.06 0.07 0.10 R2 0.95 0.94 0.96 0.94 0.82 0.85 0.89 03X College graduate 39.7 48.2 47.9 46. I 48.6 49.7 50.6 48.7 54.9 61.1 61.4 +0.x5 0.16 0.78 NOTE: Quit ratio = (Former Smokers/Current + Former Smokers) `For 1965, data stratified by education were not avadable. %ovisional 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 lO.-Smoking continuum, adults aged 17 years and older, United States, 1986 Percentage of Percentage of population ever smokers Category 1 Category 2 Category 3 Category 4 Category 5 Category 6 Category 7 Category 8 Category 9 Category 10 Never smokers Former smokers who had quit 5 or more years ago Former smokers who had been abstinent for 1 to 5 years Former smokers who had been abstinent for 3 to 12 months Former smokers who had quit within the last 3 months Current smokers who had quit for 7 or more days m the past year Current smokers who had quit for Id days in the past year Current smokers who had quit previously but not in the last year Current smokers who had never tried to quit but who had thought about it or would quit if there was an easy way to do so Current smokers who had never tried to quit. had not thought about it, and would not try to quit even if there was an easy way to do so 47.3 14.7 27.9 5.7 10.8 2.0 3.8 3.2 6.1 3.9 7.4 2.0 3.8 11.6 5.4 22.0 10.2 4.5 8.5 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 1 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, 2 1.1 percent of ever smokers stopped smoking for at least I 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; 4.5 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 .-- w ._ _ __._ _. __-- ~- ___ __ _-_.- ___.e_.-- -----. ----. --__- - -__--x TABLE ll.Smoking continuum by sex and education, percentage of ever smokers, United States, 1986 Males (%) Sex Females 51 I years (%) (%) Education 12 years 13-15 years 516 years (%) (%) (%) Smoking continuum Smokers who never tried to 8.3 (8.3)b quit (IO)" Smokers who never tried to 9.1 (17.4) quit (9) Smokers not quitting in the last 2 I .5 (38.9) year (8) Smokers quitting 16 days in 3.4 (42.3) the last year (7) Smokers quitting 7 or more 6.5 (48.8) days in the last year (6) Ex-smokers tL3 months (5) 6.8 (55.6) Ex-smokers 3-12 months (4) 3.6 (59.2) Ex-smokers I-5 (3) years 10.9 (70. I) Ex-smokers 25 (2) years 30.1 (loo) `Category on the smoking continuum (see Table IO for definitions). bNumbers in parentheses are cumulative percentages. t SOURCE: AUTS 1986 (US DHHS, in press, a). 9.1 (9.1) 9.8 (9.8) 9.5 (9.5) 7.7 (7.7) 5.7 (5.7) 9.6 ( 18.7) 9.8 (19.6) 9.5 (19.0) 10.9 (18.6) 5.7 (I 1.4) 23.9 (41.7) 23.9 (43.5) 22.5 (41.5) 22.5 (41.1) 17.7 (29. I) 4.6 (46.3) 4.4 (47.9) 4.9 (46.4) 2.6 (43.7) 1.5 (30.6) 8.6 (54.9) 7.4 (55.3) 7.9 (54.3) 8.6 (52.3) 5.0 (35.6) 5.2 (60.1) 6.6 (61.9) 5.4 (59.7) 6.0 (58.3) 7.0 (42.6) 4.3 (64.4) 3.4 (65.3) 4.1 (63.8) 4.7 (63.0) 3.7 (46.3) 10.7 (75. I) 7.8 (73. I) 10.7 (74.5) 12.8 (75.8) 14.0 (60.3) 25.1 (100) 27.2 (100) 25.3 (100) 24.4 (100) 39.2 (100) TABLE 12.-Smoking continuum by race and age, percentage of ever smokers, United States, 1986 Whites (%) Race Age Blacks IS-24 years 25-44 years 4564 years 265 years (%) (%) (90) (%) (So) Smoking continuum Smokers who never tried 8.7 (8.7)b to quit ( 10)a Smokers who never tried 8.9 (17.6) to quit (9) Smokers not quitting in the last 22.2 (39.8) year (8) Smokers quitting l-6 days in 3.6 (43.4) the last year (7) Smokers quitting 7 or more 7.0 (50.4) days in the last year (6) Ex-smokers O-3 months (5) 5.9 (56.3) Ex-smokers 3-12 months (4) 4.0 (60.3) Ex-smokers l-5 (3) years 10.8 (71.1) Ex-smokers t5 (2) years 28.8 (100) "Category on the smoking continuum (see Table IO for definitions). bNumbers in parentheses are cumulative percentages. SOURCE: AUTS 1986 (US DHHS, in press. a). 8.6 (8.6) 9.1 (9.1) 6.9 (6.9) 8.3 (8.3) 7.4 (7.4) 12.3 (20.9) 18.4 (27.5) 10.6 (17.5) 7.5 (15.8) 3.6 (1 1.0) 22.2 (43.1) 16.3 (43.8) 26.4 (43.9) 21.6 (37.4) 14.5 (25.5) 6.9 (50.0) 7.2 (51.0) 4.4 (48.3) 3.2 (40.6) 2.1 (27.6) 10.7 (60.7) 19.3 (70.3) 8.6 (56.9) 4.7 (45.3) 2.0 (29.6) 7.5 (68.2) 7.2 (77.5) 5.8 (62.7) 6.2 (5 I .5) 8.2 (37.X) 3.3 (71.5) 9.0 (86.5) 4.3 (67.0) 3.2 (54.7) 2.5 (40.3) 9.4 (80.9) 10.3 (96.8) 1 I .4 (78.9) 9.9 (64.6) IO. I (50.4) 19.0 (loo) 3.0 (loo) 20.6 (100) 35.6 (100) 49.7 (loo) 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-l 12). 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=O.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 1988~). 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.-Seif-reported cigarettes smoked per day (percentage of current smokers), United States, aged 20 years and older, 1974-S Number of cigarettes smoked per day Year 1-14 IS-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. I 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 197445; 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 (e.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 30 25 P) 020 z : 15 t n 10 1974 1975 1976 1977 1978 1979 1960 1961 1962 1963 1964 1965 YEAR FIGURE I.-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. i-k74 t 1975 , 1976 1977 1 1976 I 1979 1 1960 1961 I 1962 I 1963 / 1984 I 1985 I YEARS - White Males - Black Males -+ White Females - 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: NH& 197&E% unpublished data, Office on Smoking and Health. 294 295 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 lS.-Crade by which ever smokers smoked their fmst cigarette (o/o), reported by high school seniors, United States, 1986 Grade Total Males Females Whites Blacks Higher education plans 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 72.5 72.7 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 II 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 lOth-grade students, United States, 1987 Males Females 36 Cumulative % % Cumulative % By grade 4 11.0 II.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 4.6 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 2 1 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 2 1. 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 2 1 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 2 1. 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 3 1.1 percent in 1987 at a rate of change (1965-85) of -1.19 percent- age points per year. In contrast, smoking prevalence among young females has fallen 298 TABLE 17.-Proportion of ever smokers (9%) who started smoking before various ages, by gender, birth cohorts from NHISs Age at smoking initiation 1910-14 1915-19 1920-24 Year of birth 1925-29 1930-34 1935-39 1940-44 1945-49 1950-54 I&15 >I5 Total Menthol cigarette smokers Total Sex Males Females Age 17-19 2624 25-44 454 265 Race White Black Other Education I\. lY72-Xl 0 13.8 Redboo~ 1970-x I 0 16.1 X0-l E: `rl.~+,/~ne, h.~cd ,~~ludcj d rn,n,mum ot 60 health-related an&x I" r& year\ rurxyed SW KC L- I).ilC , 14x2 / of media coverage of smoking and health has been developed recently; some of it, however. date5 back half a century (Seldes 1941). Formal analytical studies of the phenomenon that control for potential confounding influences are limited in number; 508 existing analyses are based primarily on correlations between magazines' cigarette ad- vertising revenues and their coverage of smoking and health (Whelan et al. I98 I; Dale 1982; Jacobson and Amos 1985; White and Whelan 1986: Warner and Goldenhar, in press). One of these studies found that between 1967 and 1979. there were a total of 8 fea- ture articles that seriously discussed quitting or the dangers of smoking in IO prominent women's magazines that carry cigarette advertisements. Of the 10 magazines, 4 car- ried no antismoking articles in the entire 12-year period. By contrast. 2 prominent magazines that do not accept cigarette advertising. Good Ho~rsekeepin~~ and Se\,entern, ran 11 and 5 such articles, respectively. On average, the magazines that accepted cigarette advertisements published from 12 to 63 times as many articles on individual topics such as nutrition, contraception. stress, and mental health as they did on the an- tismoking theme. The ratio was much smaller for Good Hnusekeeping and Selvnteen (Whelan et al. 1981). In another empirical study by the same organization, researchers examined coverage of smoking and health in prominent magazines recognized for their general interest in health matters. Publications selected for study published at least 60 articles on health topics between 196.5 and 1981. The proportion of health articles devoted to smoking was compared with the proportion of advertising revenues derived from cigarette advertisements. Only four of the magazines had as many as IO percent of their health-related articles devoted to smoking. Of these four, the top three did not accept cigarette advertising. The fourth had the lowest proportionate share of adver- tising income derived from cigarette ads of the remaining magazines. There was no substantial correlation between the volume of advertisements and smoking coverage within the remaining magazines (Dale 1982; Table `7). A more recent study compared changes over time in coverage of smoking and health by 39 national magazines that published cigarette ads and I I magazines that did not. The study also compared these changes with those found in coverage by The New York Times and The Chrisban Science Monitor, as well as with the collective cigarette ad- vertising revenue of the first group of magazines. The two newspapers were selected as measures of the "inherent newsworthiness" of the subject. Comparing two 1 l-year periods, one preceding the broadcast media ban on cigarette advertising ( 1959-69) and the other following it (1973-83). the authors found that ( 1) the magazines that included cigarette ads experienced an increase in real cigarette ad revenues, controlling for in- flation, of 727 percent (cigarette ads rose from 1.9 percent of total magazine ad revenues in the first period to 11 .O percent in the second); (2) these magazines decreased their coverage of smoking and health by 65 percent, while the magazines that did not carry cigarette ads decreased their coverage by 29 percent, a statistically significant dif- ference; (3) the two newspapers' coverage fell by 21 percent (the Times, which accepts cigarette advertising) and 3 percent (the Monitor; which accepts no cigarette advertis- ing). Both decreases were significantly smaller than that of the magazines that included cigarette ads, but not significantly different from that of the magazines not including cigarette ads (Warner and Goldenhar, in press). In addition to these correlational studies, there is extensive anecdotal evidence about the influence of advertising revenues on magazine coverage of smoking and health. Writers, editors, and publishers have described numerous instances of purported cen- 509 sorship attributed directly to publications' fears of alienating cigarette advertisers (Smith 1978; Whelan et al. 1981; Bagdikian 1983; Warner 1985; Okie 1985; Magnus 1986). Although the anecdotal evidence pertains mainly to magazines, it includes other media. including newspapers (ABC News 1983; Gitlitz 1983) and the broadcast media prior to the removal of cigarette ads (Bagdikian 1983). Furthermore, there are allega- tions of advertising-induced censorship related to other tobacco products, such as smokeless tobacco (Connolly 1986). Federal Advertising Restrictions The Federal agency responsible for regulating the advertising of tobacco and other consumer products is the FTC. The Federal Trade Commission Act of 1914, amended in 1938, empowers the FTC "to prevent persons, partnerships, or corporations . . . from using unfair or deceptive acts or practices in commerce" (Wagner 1971 b). The FTC's efforts to regulate unsubstantiated claims in tobacco advertisements began well before 1964. From the 1930s through the 1950s. many cigarette advertisements made claims that smoking the advertised brand improved health or at least offered health benefits compared with smoking other brands (Neuberger 1963; Tye 1986). Be- tween 1938 and 1968, the Commission invoked its adjudicatory (quasi-judicial) authority 25 times with respect to cigarette advertising (Fritschler 1969). Between 1945 and 1960, the Commission completed seven formal cease-and-desist order proceedings against cigarette manufacturers involving medical or health claims made in advertising (FIX 1964b). For example, according to Wagner ( 197 I b): A 1945 complaint lodged against R.L. Swain Tobacco prohibited representations that respondent's cigarettes were endorsed or approved by the medical profession; that they would soothe the nose, throat, or mouth; that they contained no irritating properties; and that they produced little or no stain on fingers and teeth. In 1950, the FTC moved successfully to curb R.J. Reynolds Tobacco Company from claiming that Camels aided digestion; did not impair the wind or physical condition of athletes: would never harm or irritate the throat or leave an aftertaste; were soothing, restful, and comforting to the nerves; and contained less nicotine than any of the four other largest selling brands. A 1942 complaint against Brown and Williamson Tobacco Company prohibited claims that Kools would keep the head clear in winter and give extra protection against or cure colds. Because the adjudicatory judgments obtained by the FTC applied only to the parties to the case, other cigarette companies engaging in the same or similar deceptive acts were not immediately affected. Fritschler (1969) concluded that "in the case of cigarette advertising, the Commission found itself putting out brush fires of deception while the inferno raged on." The FTC first promulgated industrywide cigarette adver- tising guidelines in September 1955. These guidelines were "for the use of its staff in the evaluation of cigarette advertising" (FTC 1964b), as opposed to formal trade regula- tion rules, which would have the force of law. The guidelines, among other things, sought to prohibit: (1) representations in cigarette advertising of medical approval of cigarette smoking in general or of smoking a particular brand; (2) advertising claims that referred either to the presence or absence of any physical effects relating to cigarette 510 smoking in general or smoking a particular brand, or relating to filters or filtration; and (3) unsubstantiated advertising claims relating to tar and nicotine levels. In June 1962, the FTC announced the adoption of general rule-making procedures, which it used on three occasions the following year to regulate various nontobacco products (Fritschler 1969). As noted in the section on warning labels, 1 1 days after the release of the 1964 Report of the Surgeon General's Advisory Committee on Smoking and Health, the FTC announced three proposed trade regulations on cigarette labeling and advertising (FTC 1964a). Rule 2 would have strictly regulated the imagery and copy of cigarette ads in order to prohibit explicit or implicit health claims. However, the proposed rule was vacated (FTC 1965) after the Federal Cigarette Labeling and Ad- vertising Act of 1965 (Public Law 89-92) was signed into law. In the meantime, in April 1964, the major U.S. cigarette manufacturers had adopted their own Cigarette Advertising Code, intended to apply to broadcast advertising. It prohibited making health claims in advertisements and directing advertising to young people. Cigarette manufacturers agreed to avoid ads that represented `*cigarette smoking as essential to social prominence, distinction, success, or sexual attraction" and to avoid showing smokers engaged in activities "requiring stamina or athletic conditioning beyond that of normal recreation" (Emster 1988; Friedman 1975). In its 1968 report to Congress, the FTC recommended a ban on cigarette advertising on television and radio (FTC 1968). In February 1969, the FCC announced a proposed trade regulation rule that would have banned cigarette commercials from television and radio (FCC 1969). On July 8, 1969, the National Association of Broadcasters an- nounced a plan to phase out all cigarette advertising on the air over a j-year period beginning January 1, 1970 (Whiteside 1971). At a Senate subcommittee hearing 2 weeks later, the cigarette industry offered voluntarily to end all cigarette advertising on television and radio by September 1970, provided that Congress would grant the com- panies immunity from antitrust laws to allow them to act in concert (Whiteside 1971). Ultimately, Congress approved the Public Health Cigarette Smoking Act of 1969, which was signed into law on April I, 1970. The Act prohibited cigarette adver- tising in the broadcast media effective January 2, 197 1. Subsequent Federal legislation extended the ban on advertisements in the broadcast media to little cigars and to smokeless tobacco products. In September 1973, the Lit- tle Cigar Act of 1973 (Public Law 93-109) banned broadcast advertising of "little cigars," defined as "any roll of tobacco wrapped in leaf tobacco or any substance con- taining tobacco . . as to which one thousand units weigh not more than three pounds." Over a decade later, smokeless tobacco advertising in the broadcast media was banned by the Comprehensive Smokeless Tobacco Health Education Act of 1986 (Public Law 99-252). The ban took effect on August 27, 1986. In recent years, the FTC has again had its attention drawn to the content of print ad- vertising. As discussed in a prior section, the FIG successfully obtained an injunction against one manufacturer for incorrectly stating the tar yield of one cigarette brand, Barclay, in packaging and advertising (FTC v. Brown and Williamson 1983). In addi- tion, the Tobacco Institute (Tobacco Institute 1983) and R.J. Reynolds (RJR) have advertised in national print media with statements that challenged the link between smoking (active and involuntary) and disease. During 198.5, RJR published an advertisement (R.J. Reynolds 1985a) entitled "Of Cigarettes and Science," which discussed, among other things, the procedures that scientists use to test scientific hypotheses, and presented information about the Multi- ple Risk Factor Intervention Trial (MRFIT) (MRFIT Research Group 1982). In April 1985, the American Heart Association, the American Cancer Society, and the American Lung Association, acting through the Coalition on Smoking OR Health, petitioned the FTC with regard to this ad. On June 16, 1986, the FTC issued a complaint alleging that the advertisement falsely and misleadingly represented that the purpose of the MRFIT study was to determine whether heart disease is caused by smoking, that the MRFIT study provides credible scientific evidence that smoking is not as hazardous as the public has been led to believe, and that the MRFIT study tends to refute the theory that smoking causes coronary heart disease. The complaint also charged that in light of the representations made in the ad, the advertisement failed to disclose certain material facts about the study, specifically, that the men in the study who quit smoking had a significantly lower rate of coronary heart disease than men who continued to smoke and that the study results are consistent with previous studies showing that those who quit smoking experience a substantial decrease in coronary heart disease mortality. On June 26, 1986, RJR moved to dismiss the complaint on the grounds that the ad- vertisement was noncommercial speech that was fully protected by the first amend- ment, even if it was false and deceptive. An Administrative Law Judge agreed and dis- missed the complaint on August 4, 1986. In an order and decision dated March 4, 1988, the FTC reversed the judge's order, holding that "the content of the Reynolds adver- tisement includes words and messages that are characteristic of commercial speech." RJR unsuccessfully appealed this decision to the U.S. Court of Appeals of the District of Columbia; trial before an FTC Administrative Law Judge on this matter is set for January 30. 1989. (Also see White 1987.) (As of October 1988. all documents related to this administrative matter were maintained in FTC Docket No. 9206.) State and Local Advertising Restrictions The preemption clause of the Public Health Cigarette Smoking Act of 1969 (Public Law 9 l-222) prevents States from regulating or prohibiting cigarette advertising or promotion for health-related reasons. The Act defines "State" to include "any politi- cal division of any State." This preemption was left intact by subsequent congressional legislation, including the I984 Comprehensive Smoking Education Act (Public Law 98-474). which amended other sections of the original law, such as the requirement for warning labels. The stated purpose of the preemption was "to avoid the chaos created by a multiplicity of conflicting regulations" (U.S. Senate 1970). There is no preemp- tion of State and local advertising restrictions for smokeless tobacco in the Comprehen- sive Smokeless Tobacco Health Education Act of 1986 (Public Law 99-252), although the Act does prevent States from requiring additional warning labels on smokeless tobacco products or advertisements. States and localities may have some jurisdiction in regulating the location of adver- tising when the medium is not national in scope. For example, cities may be able to prohibit tobacco advertising on their transit systems. The extent of such jurisdiction is 512 not clear from the preemption clause itself, and there is no body of case law. Several States and local jurisdictions have adopted statutes or regulations banning certain types of purely local cigarette advertising or promotion. The most common restrictions, described below, are bans on transit advertising and on the distribution of free cigarette samples. In some cases, these regulations apply to all tobacco products. None of these policies has been challenged in court. The strongest State law has been adopted in Utah, where tobacco advertisements are banned on "any billboard, streetcar sign, streetcar, bus, placard, or on any other object or place of display" (Utah 1978). Bans on tobacco advertising in public transit systems have been adopted in several cities. In August 1984, the Board of Directors of the Regional Transportation District in the Denver, CO, area voted to prohibit transit ad- vertising for tobacco products and alcoholic beverages on its buses and in its two downtown transit centers (Schmitz 1984). Similarly, the Massachusetts Bay Transpor- tation Authority (MBTA) in the Boston metropolitan area adopted an administrative policy prohibiting tobacco advertisements on buses and trollies and in stations, effec- tive October 1986 (Boston Herald 1986). The town of Amherst, MA, enacted a bylaw prohibiting tobacco advertising "on or in any bus, taxicab, or any other vehicle used for public transportation" within the town in 1987 (Amherst 1987). The Bay Area Rapid Transit (BART) District in the San Francisco Bay Area of California has eliminated the advertising of tobacco products and alcoholic beverages from its trains and stations. BART covers San Francisco, Alameda, and Contra Costa counties. Based on a vote of the BART Board of Directors, the policy was phased in between May 1987 and May 1988 to allow existing advertising contracts to expire (Collier 1987). In Minnesota, the Metropolitan Sports Commission voted in January 1988 to end tobacco advertising in Minneapolis' professional sports stadium, the Hubert H. Humphrey Metrodome. The new policy will take effect after expiration of the existing IO-year cigarette advertising contract in 1992. Cigarette advertising revenue under this contract has been approximately 300,000 dollars per year (Marty 1987). Cities and States have also acted to restrict or ban the distribution of free tobacco product samples, a major form of tobacco promotion. At least 14 cities have banned all distribution of free samples: these include Minneapolis, St. Paul, and Albert Lea, MN; Boston, Newton, Cambridge, Amherst, Somerville, and Worcester, MA; Honolulu, HI; Bowie, MD; Atlanta, GA (Davis and Jason 1988); Austin, TX (Austin 1988); and Cincinnati, OH (Smith 1988). The earliest of these ordinances were adopted by Minneapolis and St. Paul in 1979. Two States (Utah and Minnesota) have prohibited the distribution of free smokeless tobacco samples (Davis and Jason 1988). A larger number of States and cities have banned the distribution of free samples to minors, al- though the success in enforcing these selective sampling restrictions is uncertain. (See Part III, section on minors' access to tobacco.) Effects of Government Actions to Restrict Tobacco Advertising In general, there has been little formal evaluation of the impact of government ac- tions concerning tobacco advertising and promotion. 513 The relationship between government policy and tobacco consumption has been studied only in the case of the Fairness Doctrine and the subsequent ban on cigarette advertising in the broadcast media. Evaluation of the effectiveness of the broadcast ad ban is complicated by three factors. First, the ban removed the obligation of stations to air the Fairness Doctrine PSAs. To the extent that the PSAs were effective in dis- couraging smoking, their disappearance serves to undermine any positive effect from the broadcast advertising ban. Second, the savings from reduced advertising in the short term may have allowed the cigarette companies to hold down the. price of cigarettes temporarily, which in turn would have served to increase sales (Schneider, Klein, Murphy 1981). Third, after several years of reduced advertising expenditures following the broadcast advertising ban, the cigarette industry dramatically increased expenditures for print media advertising (especially billboards) and for promotional activities (Warner 1986b; Popper 1986a; Davis 1987). To the extent that cigarette advertising in these media and other promotional activities may increase total sales, this also may have served to decrease the net effectiveness of the broadcast ban. As mentioned in the previous section on the broadcast media, per capita cigarette sales decreased by 6.9 percent during the 3-year period (1968-70) when PSAs were mandated by the Fairness Doctrine, but increased by 4.1 percent during the 3-year period (1971-73) following the end of Fairness Doctrine PSAs and the beginning of the broadcast advertising ban. This suggests that any beneficial effects of the broad- cast ad ban may have been outweighed by disappearance of the PSAs, at least in the short run. In a regression analysis of the effects of both cigarette ads and the Fairness Doctrine PSAs, Hamilton ( 1972) found that the antismoking PSAs retarded per capita cigarette consumption far more than the cigarette ads boosted it. In an analysis taking into account cigarette price, advertising, and counteradvertising, Schneider, Klein, and Murphy (198 1) concluded that the net effect of the broadcast advertising ban was to in- crease cigarette consumption. However, Hamilton ( 1972) and Warner ( 1979) both sug- gested that the net effect of the two policies may have been to increase cigarette con- sumption in the short term, although they cautioned that the net effect in the long term is difficult to gauge. It is difficult to evaluate the effect on smoking behavior of FTC actions to regulate the content of advertising. FTC rulings did block misleading advertising, but as the MRFIT case demonstrates, the regulatory process is slow. Delays inherent in the regulatory process limit the impact of the ultimate decisions. The effect on smoking behavior of State and local restrictions on cigarette advertis- ing and promotion is not known because no evaluations have been conducted. No data are available regarding the effectiveness of sampling bans in reducing the availability of cigarettes. Even if such policies have no direct influence on smoking, however, these restrictions (and the publicity surrounding their enactment) may promote increased public awareness of the issue of smoking and health and may serve as important sym- bols of social disapproval of tobacco use. More is known about the financial impact of local advertising bans on transit authorities, for whom the bans result in lost advertising revenue. Information from two of the four jurisdictions that have enacted transit tobacco advertising bans indicates that transit authorities have been able to recoup lost advertising revenue in a relatively short 514 time. Cigarette advertisements accounted for approximately 800,000 dollars, or 36 per- cent,of MBTAs 2.2 million dollars in advertising revenue in 1985 (Boston Herald 1986; AdEast 1986). According to MBTA, it regained its previous (1985) level of advertis- ing revenue in 1987 (Grealy 1988). Similarly, in San Francisco, BART officials reported only a minimal. temporary advertising revenue loss during the year of im- plementation (Healy 1988). The effect, if any, of transit and sampling bans on nation- al advertising and promotional expenditures by tobacco companies is unknown. Policies Under Consideration Currently, as reviewed above, the Federal Government bans tobacco advertising in the broadcast media and regulates the content of tobacco advertising by FTC actions and by the requirement that warning labels appear on cigarette and smokeless tobac- co advertisements. A number of proposals that would further restrict tobacco advertis- ing and promotion are now under consideration by the public health community, State legislatures, and Congress. Some of the proposals are mutually exclusive and should be considered as alternatives, whereas others could coexist. Nationally prominent proposals are mentioned here. Their major strengths and weaknesses are considered in detail elsewhere (Warner et al. 1986a). One group of proposals would have theGovernment morestringently regulate the im- agery and content of advertising, either by developing and enforcing an advertising and promotion code or by severely restricting the permissible format of advertisements; the latter is so-called "tombstone advertising." With the former approach, a code defining permissible imagery in advertisements and a mechanism to ensure monitoring of and compliance with the code would have to be developed and implemented. For such a code to be effective, it would have to encompass both advertising and nonadvertising forms of promotion, the latter of which now represents over half of total cigarette ad- vertising and promotional expenditures (FTC 1988b). The advantages and disad- vantages of such a code have been discussed (Taylor 1984; FK 1981b; Warner et al. 1986a). An alternative proposal would limit the imagery and graphics of tobacco ad- vertisements to so-called "tombstone advertising," with no models, slogans, scenes, or colors permitted. The tombstone proposal does not address other forms of promotion. The merits of this proposal are considered elsewhere (e.g., FTC 198lb; Warner et al. 1986a). A second set of proposals would restrict the availability of tobacco advertising and promotion. These range from a total ban on all advertising and promotion to more limited policies that would prohibit advertising in certain media; prohibit certain promo- tional techniques, such as the distribution of free tobacco product samples (Davis and Jason 1988); or ban advertising and promotion accessible to children. Currently, the most widely discussed proposal is to ban all forms of advertising and promotion for all tobacco products. The proposal's prominence reflects its advocacy by organizations such as the American Medical Association, American Cancer Society, American Heart Association, American Lung Association, and American Public Health Association, and the fact that it has been the basis of several bills before Congress (e.g., H.R. 1272, 100th Congress, 1st Session) and the subject of congressional hearings (Subcommittee 515 on Health and the Environment 1986). A total ban on tobacco advertising and promo- tion was enacted in Canada in June 1988, scheduled to go into effect in stages begin- ning January 1, 1989 (Bums 1988; House of Commons of Canada 1988). The ad ban proposal raises a wide range of complex issues whose full discussion is beyond the scope of this Report and has been covered elsewhere (Warner et al. 1986a). The most visible and fundamental is the question of commercial free speech: What is the right of the producers of a legal product to advertise and what is the right of con- sumers to have access through advertisements to information on legal products (White 1984; Miller 1985; Weil 1986; Neubome 1986; Reimer 1986; Covington and Burling 1986; Blasi and Monaghan 1986,1987)? Among the more pragmatic issues is concern that withdrawal of cigarette advertising and tobacco company sponsorship might jeop- ardize the existence of some publications, advertising agencies, and sports and arts in- stitutions (Warner 1986b). From a public health perspective, the central issue is one of effectiveness: Would an advertising ban in fact achieve its desired end-reductions in smoking prevalence? If so, would a less restrictive policy achieve the same effect without raising first amendment concerns? A third set of proposals seeks to neutralize the influence of advertising by mandat- ing the publication or broadcast of antitobacco messages by the media. An example of this so-called "counteradvertising" was the FCC requirement for antismoking PSAs in the broadcast media under the Fairness Doctrine from 1967 through 1970; these were discussed in a previous section. The apparent effectiveness of these PSAs led to proposals for the Government to establish a source of substantial and continuous fund- ing for an antitobacco advertising campaign (Warner 1986b,c). Several mechanisms have been proposed to raise the resources for a paid campaign. One would require tobacco advertisers to pay for an amount of counteradvertising space that is equivalent to or some fraction of what they devote to protobacco advertising. Another proposal would earmark a proportion of the Federal cigarette excise tax to fund a paid counterad- vertising campaign (Warner 1986~). A fourth approach seeks to create an economic disincentive for tobacco manufac- turers to advertise by eliminating their ability to deduct tobacco advertising and promo- tional expenditures as business expenses for income tax purposes. This proposal has also been put into the form of congressional legislation (S. 446, 100th Congress, 1st Session, and H.R. 1563, 100th Congress, 1 st Session) and its merits have been debated in congressional hearings (Weil 1986; Stark 1986; Bradley 1986). The majority of proposals to restrict tobacco advertising and promotion are designed for action at the Federal level, because current Federal legislation preempts States from regulating cigarette advertising. Repeal of the Federal preemption clause has been proposed as a means of encouraging State and local regulatory actions (Bailey 1986; Warner et al. 1986a). Summary There is no scientifically rigorous study available to the public that provides a defini- tive answer to the basic question of whether advertising and promotion increase the level of tobacco consumption. Given the complexity of the issue, none is likely to be 516 forthcoming in the foreseeable future. The most comprehensive review of both the direct and indirect mechanisms concluded that the collective empirical, experiential, and logical evidence makes it more likely than not that advertising and promotional ac- tivities do stimulate cigarette consumption. However, that analysis also concluded that the extent of influence of advertising and promotion on the level of consumption is un- known and possibly unknowable (Warner 1986b). This influence relative to other in- fluences on tobacco use, such as peer pressure and role models, is uncertain. Although its effects are not wholly predictable. regulation of advertising and promotion is likely to be a prominent arena for tobacco policy debate in the 1990s. In part this reflects the high visibility of advertising and promotion; in part it reflects the perception that these activities constitute an influence on tobacco consumption that is amenable to govem- ment action. Reporting Requirements Current Federal legislation mandates that DHHS and the FTC issue reports to Con- gress on tobacco-related subjects at regular intervals. By virtue of the extensive media coverage and wide dissemination of many of these reports, they often provide informa- tion not only to Congress but also to the general public, journalists, other policymakers, health professionals, and researchers. Surgeon General's Reports As discussed in Chapter 1, the Federal Cigarette Labeling Act of 1965 and the Public Health Cigarette Smoking Act of 1969 require that the Secretary of Health, Education, and Welfare (now the Secretary of Health and Human Services) transmit an annual report to Congress on current information about the health consequences of smoking and such recommendations for legislation as he or she may deem appropriate. This Report is the 20th in the series of reports on the health consequences of smoking, generally referred to as Surgeon Generals' Reports, which began with the 1964 Report of the Surgeon General`s Advisory Committee on Smoking and Health. The 1986 Report of the Advisory Committee to the Surgeon General, The Health Consequences of Usirrg Smokeless Tobacco (US DHHS 1986c), was not produced in response to a specific legislative mandate. Biennial Status Reports The Comprehensive Smoking Education Act of 1984 requires the Secretary of Health and Human Services to transmit a report to Congress biennially containing the follow- ing information about smoking control efforts: (1) an assessment of Federal activities to inform the public; (2) a description of the extent of public knowledge about the health consequences of smoking: (3) a report of the activities of the Federal Interagency Com- mittee on Smoking and Health, the research and educational activities of DHHS relat- ing to smoking. and State and local laws relating to the use and consumption of ciga- rettes; (4) information on private actions taken to reduce the effects of smoking on health; and (5) recommendations for legislation and administrative action that the Secretary deems appropriate. The first such report, entitled Smoking and Health: A NationalStatus Report, was released in November 1986 (US DHHS 1986e). A similar reporting requirement exists for smokeless tobacco. The Comprehensive Smokeless Tobacco Health Education Act of 1986 requires that the Secretary of Health and Human Services transmit a report to Congress biennially on (I) the effects of health education efforts on the use of smokeless tobacco products, (2) the public's use of smokeless tobacco products, (3) the health effects of smokeless tobacco products and areas appropriate for further research, and (4) appropriate legislation and administra- tive action. The first report pursuant to this requirement was released in May 1987 (US DHHS 1987a). Federal Trade Commission Reports The Federal Cigarette Labeling and Advertising Act of 1965 and the Public Health Cigarette Smoking Act of 1969 require the FTC to transmit an annual report to Con- gress concerning (1) the effectiveness of cigarette labeling, (2) current practices and methods of cigarette advertising and promotion, and (3) such recommendations for legislation as it may deem appropriate. The first provision was eliminated by the Com- prehensive Smoking Education Act of 1984. FTC Reports have been submitted an- nually to Congress since 1967. These reports generally include data on aggregate and per capita cigarette sales, domestic market share of filter and nonfilter cigarettes and menthol and nonmenthol cigarettes, domestic market share by cigarette length and tar and nicotine yields, and cigarette advertising and promotional expenditures broken down by type of advertising or promotion and type of cigarette (FTC 1988b). The tar, nicotine, and carbon monoxide yields of all cigarettes are to be provided in future reports. The Comprehensive Smokeless Tobacco Health Education Act of 1986 requires that FTC report to Congress every other year on current sales, advertising and marketing practices, and recommendations for legislative or administrative action. Effectiveness One method for assessing the effectiveness of reporting requirements as a means of disseminating information is to evaluate the quantity and quality of information made available and the extent to which policymakers and the public are aware of the reports or their contents. The information in these reports may influence policy development, tobacco use, and public awareness of the health effects of smoking, but these relation- ships are difficult to measure. In fact, there has been little formal evaluation of report- ing requirements or the reports themselves on any of these outcomes. There is some empirical evidence that the Surgeon General's Reports, or at least the first Report in 1964, may have had a direct or indirect effect on cigarette consumption. Adult per capita consumption of manufactured cigarettes in the United States (total cigarettes consumed annually divided by the population 18 years of age and older) reached an all-time high of 4,345 in 1963. After the release of the 1964 Report of the Surgeon General's Advisory Committee on Smoking and Health (US PHS 1964) and the attendant publicity, per capita consumption fell to 4,195 in 1964 before increasing to 4,259 in 1965 (Chapters 5 and 8). In an analysis comparing actual cigarette con- sumption to projections based on previous trends, Warner (1977, 1981, 1989) es- timated that the Advisory Committee's Report and associated publicity induced a 5- percent decrease in cigarette consumption in 1964. Schneider, Klein, and Murphy (198 1) estimated that the 1964 Report decreased per capita consumption of tobacco by 39 percent during the 1964-78 period. Similarly, British researchers (Russell 1973; Peto 1974) have credited the Royal College of Physicians' 1962 Report on Smoking and Health with decreasing cigarette consumption 4.6 to 9 percent that year. No published studies have evaluated the effects of other Surgeon General's Reports upon tobacco use. The impact of the 1964 Surgeon General's Advisory Committee Report may be unsurpassed, compared with that of subsequent reports, because of the widespread publicity surrounding the first Report and the "newness" of its findings. Public knowledge of the health hazards of tobacco use has increased substantially since 1964 (Chapter 4). Because of the many factors that may have affected public knowledge and attitudes about smoking, it is difficult to estimate the degree to which the Surgeon General's Reports have by themselves influenced beliefs, attitudes, and opinions. Despite the lack of empirical data, it is widely acknowledged that the Sur- geon General's Reports have become recognized as authoritative documents and sum- maries of the literature on the health consequences of smoking (Walsh and Gordon 1986). The quality of the reports can be attributed, at least in part, to the large number of expert contributors and an extensive peer review process (summarized in the ac- knowledgments of this and previous reports). Because of the large and expanding literature on tobacco and health, there is no doubt that the Surgeon General's Reports have served a useful purpose by providing detailed and current reviews of information on tobacco and health. One of the principal intended audiences of the 1988 Surgeon General's Report on Nicotine Addiction (US DHHS 1988) was physicians. Two weeks after the release of the Report, Lakeside Pharmaceuticals sponsored a telephone survey of 159 randomly selected physicians from three primary care specialities. Ninety-one percent of physicians interviewed knew about the Report, and 70 percent thought that the conclusions of the Report would alter the way physicians treat patients for smoking (Ad Factors/Millward Brown 1988). These data suggest that the Report was effective in conveying information on smoking to health care providers. 519 The findings of the Surgeon General's Reports have often been cited as the scientific basis for public and private policies designed to reduce tobacco use. Similarly, the find- ings and legislative recommendations of FTC reports have been cited in support of strengthening existing cigarette warning labels. For example, in the legislative history of the Public Health Cigarette Smoking Act of 1969, the Senate Report (U.S. Senate 1970) recommended a stronger cigarette warning label by citing the findings of pre- vious Surgeon General's Reports, the conclusion of the 1967 FTC Report that the original warning label was ineffective, and the legislative recommendation of the 1969 FTC Report for a stronger warning label. Thus, although empirical data are lacking, anecdotal reports suggest that the mandated Federal Government documents have played an important role in providing a knowledge base to support the development of smoking control policies. Government Expenditures and State Smoking Control Plans Government activities on smoking and health have, for the most part, been informa- tional and educational. The extent of these activities is determined in part by the availability of funds to support them. Funding, in turn, reflects broad government priorities. Consequently, government decisions about expenditures on smoking and health can be considered as "policies" and will be reviewed in this Section. Federal Expenditures There are two sources of information about Federal expenditures on smoking and health. The Office on Smoking and Health (OSH), the successor of the National Clearinghouse for Smoking and Health (NCSH), is the only Federal office wholly devoted to smoking control. Its activities (Chapter 6) include providing information and education to health professionals, policymakers, and the general public and spon- soring national surveys of smoking behavior. Its budget is an index of categorical ap- propriations for activities related to smoking and health. In addition, since 1979, agen- cies within DHHS have reported their expenditures in 15 prevention priority areas, including smoking and health, to the Office of Disease Prevention and Health Promo- tion. This information has been published for fiscal years 1979 through 198 1 and 1983 through 1986 (US DHHS 1981b, 1982b, 1985b, 1987b) and includes a list of projects funded by each reporting agency. 520 The budgets of OSH and NCSH are shown in Table 8 for fiscal years 1966 through 1988. Congressional appropriations designated for "smoking and health" have in- creased from 2.0 million dollars in 1966 to 3.5 million dollars in 1988. Expressed in constant 1966 dollars. the 1988 appropriation is 0.95 million dollars, 48.5 percent of the 1966 appropriation. For the past 5 years, the annual budget of OSH in current dol- lars has been approximately 3.5 million dollars. Expenditures on smoking and health reported by agencies within DHHS for fiscal years 1979 through 1981 and 1983 through 1986 (US DHHS 1981b, 1982b, 1985b, 1987b) are shown in Table 9. Reported expenditures increased from approximately 2 1 million dollars in fiscal year 1979 to approximately 40 million dollars in fiscal year 1986. Increased expenditures by several agencies contributed to this change, but it is primarily attributable to sharply increased allocations by the National Cancer Institute (Chapter 6). Expenditures on smoking and health have accounted for a growing share of all DHHS prevention efforts, but remain a small proportion of the total prevention budget. In fiscal year 1986, smoking and health activities accounted for 1 .O percent of the DHHS prevention budget (4.1 billion dollars) and 1.2 percent of the Public Health Service's prevention budget (3.3 billion dollars) (US DHHS 1987b). The data on expenditures reported by DHHS agencies should be interpreted with cau- tion. These figures may vary slightly from figures contained in other documents be- cause each agency applied its own criteria, within general guidelines, for identifying these expenditures. In addition, some prevention expenditures within certain block grants or certain programs (e.g., medicaid) are not accessible by current reporting sys- tems and thus may not be included in these figures. It should also be noted that these data do not include possible expenditures on smok- ing and health by other Federal departments or agencies. For example, the Department of Defense (DOD) has recently funded approximately 97,000 dollars in publications and 324,000 dollars in radio and television messages relating to smoking and health. Many of the radio and television spots are being used in the Armed Forces Radio and Television Network overseas (US DOD 1987). DOD has received assistance from voluntary health agencies in disseminating information and materials to military ser- vice members (US DOD 1987) (Chapter 6). These data also do not include Federal agency expenditures on tobacco where the goal is not smoking control. Examples of this are the Department of Agriculture's tobacco agriculture program (Warner 1988) and efforts by the Office of the U.S. Trade Representative to secure freer access to foreign markets for American cigarette manufacturers (Connolly 1987). 521 TABLE S.-Appropriated funds and positions for the Office on Smoking and Health (OSH) (197847) and its predecessor, the National Clearinghouse for Smoking and Health (NCSH) (196677) Fiscal year Appropriated fundsa (millions of dollars)b PositionsC 1966 (NCSH) 1.955 30 1967 2.144 37 1968 2.075 37 1969 2.100 35 1970 2.250 35 1971 2.156 29 1972 2.380 43 1973 I .600 (+ 0.306jd 43 1974 0.986(+ 1.862)d 36 1975 1.028(+0.813)d 35 1976 0.825(+0.295)d 12 1977 1.200 12 1978 1.200 I2 1979 (OSH) 2.500 12 1980 2.519e 25 1981 2.062e 25 1982 1.944 23 1983 2.098 21 1984 3.521 21 1985 3.538 17 1986 3.375' 17 1987 3.471 18 1988 3.466 18 `The difference between these figures and those III Table 9 reflect the fact that the figures in Table 9 may exclude salaries and other"overhead" expendmres (travel, postage. photocopying, etc.). bFigures not adjusted for inflation. `Beginnmg in 1980. the number of allocated "posirmns" was redefined as the number of allocated "full-time equivalents (FTEs)." FTEs allow the hinng of mwe than one person for a given FTE (e.g.. two half-time employees for one FTE). which was not passable under the previous system. dAddttional funds transferred from other agencies. `An additmnal IO million dollars was appropnated to support a smoking and alcohol demonstration grant program For chddren and adolescents. This money was later transfened from the Office on Smoking and Health (which at that ttme was within the Office of the AssIstant Secretary for Health) to the Centers for Disease Control. `A total oF3.526 million dollars was origmally appropriated. but 174,GllO dollars were withheld ("sequestered") pursuant to Section 5 IS of F'ubltc Law 99- 190. SOURCE: Office on Smoking and Health (unpubhshed data). 522 TABLE 9.-Expenditures on smoking and health by DHHS, fiscal years 1979-81 and 1983-86 Fiscal year expendituresa (in thousands of dollars) Agency 1979 1980 1981 1983 I984 1985 1986 ADAMHA CDCb HRSAC NIHe NC1 NHLBI OASH OSHb d TOTALe (smoking and health) 153 1,184 1,579 2,024 2,353 2,796 213 4,400 445 50 380 755 377 457 386 l&5.50 16,150 12.93 1 13,810 21.520 26,850 33,112 12,845 13,235 10,182 9.476 16,721 21,131 27,099 2,550 2,900 2,637 2,210 2,700 3.315 3,360 I.853 2,074 1,555 2,024 3,273 2.503 2,862 1,706 1,961 1,555 1,895 3.148 2,495 2,857 21,146 23,081 16,50 1 17,413 26,867 32,086 39,525 TOTAL of all pre- vention activities 2.971.171 3,530,405 3,571,060 3.577.069 3,823.993 3,908,524 4,088,465 Smoking and health, as % of all prevention activities 0.7 0.7 0.5 0.5 0.7 0.8 1.0 NOTE: ADAMHA. Alcohol. Drug Abuse. and Mental Health Admmistration (includes National Institute on Drug Abuse); CDC, Centers for Disease Control; HRSA, Health Resources and Services Administration; NIH, National Institutes of Health; NCI. National Cancer Institute (part of NIH): NHLBI, National Heart. Lung, and Blood Instttute (part of NIH); OASH, Office of the Assistant Secretary for Health; OSH, Office on Smoking and Health. aFigures not adjusted for inflation. bOSH was transferred administratively from OASH to CDC in September 1986. `For fiscal years 1979-81. expenditures were reported separately for the Health Resources Administration and the Health Services Administration. but are combined in this table under HRSA. which now subsumes these two agencies. %he difference between these expenditure figures for OSH and those in Table 8 reflect the fact that the figures m this table may exclude salaries and other "overhead" expenditures (e.g., travel. postage. photocopying). `Figures differ slightly from pubhshed data because of revised NC1 figures. SOURCE: US DHHS (198lb, 1982b, 1985b, 1987b). The figures in this inventory may vary shghtly from figures contained in other documents because each agency applied its own criteria, within general guidelines, for identifying these expenditures. Some prevention expenditures within certain block grants or certain programs (e.g., medicaid) are not available with current reporting systems and thus may not be included in the figures in this table. Figures for NC1 budget year were provided by the Deputy Director, Divismn of Cancer Prevention and Control. 523 State Smoking and Health Plans Data on expenditures relating to smoking and health by State and territorial health departments were not available for this Report. However, the existence of a State Smoking and Health Plan is an indicator of a well-developed State smoking control program. State smoking control plans may be produced by a State health department acting alone or in conjunction with other public and private organizations in the State that are interested in smoking and health. They may also be produced by an advisory commit- tee or "citizens' panel" on smoking and health appointed by the Governor or State health officer. Table 10 provides a list of selected State Reports on smoking and health. The most comprehensive reports provide State-specific information on tobacco use, smok- ing-attributable mortality and economic costs, current tobacco control activities, and recommendations for tobacco control programs and policies and for information col- lection. A similar report has also been produced by the City of New York (New York City Department of Health 1986). The Minnesota Plan for Nonsmoking and Health (Minnesota Department of Health 1984,1987'b) isoften cited as a particularly well-developed program. In 1983, the Min- nesota Commissioner of Health established the Minnesota Center for Nonsmoking and Health. The three-member staff of the Center organized the Minnesota Technical Ad- visory Committee on Nonsmoking and Health, with representation from a variety of sectors: wholesale-retail sales; labor; medicine; nursing; hotels. resorts, and res- taurants: law; large and small business; education: insurance; economics; advertising; State legislature; local government; and community action. In September 1984, the committee issued a 198-page document, The Minnesorcr Plan for. Non.sn~oking and Health (Minnesota Department of Health 1984). with 39 recommendations. During the same year, nearly 30 public and private organizations joined to form the Minnesota Coalition for a Smoke-Free Society by the Year 2000. In June 1985. the Minnesota legislature ratified smoking control legislation. several provisions of which were based on recommendations of The Minnesota Piun. One of these provisions was a 5-cent increase in the State cigarette excise tax. One cent of the tax increase was earmarked for a public health fund, one-quarter of which was set aside for tobacco use prevention. The revenues have been used to fund special project grants for local smoking control projects, surveillance of adult and teenage use of tobacco in the State. a mass media educational campaign, and evaluation of the impact of these interventions. Eight Western States (Arizona, Colorado, Montana. New Mexico, North Dakota. South Dakota, Utah, and Wyoming) are cooperating on the first regional tobacco-and- health "plan." the Rocky Mountain Tobacco-Free Challenge. The eight State health departments are coordinating a competition among these States to achieve specific goals by the year 2000. These goals include a 50-percent reduction in the prevalence of tobac- co use by adults and youth, a SO-percent reduction in consumption of all tobacco products, and a 25-percent reduction in deaths related to tobacco use. The Governors of these eight States signed a declaration in early 1988 endorsing the competition and the year 2000 goals (Vilnius 1988). 524 TABLE lo.-Selected State and local reports on smoking and health Information in reporl State Year Origin of report" Prevalence of smoking mortality Recom- mendations Colorado Maine Massachusetts Michigan Minnesota New Jersey New York City North Dakota Pennsylvania 1986 AC 1983 SHD 1988 SHD 1980 AC 1984 SHD 1984 SHD 1987 SHD 1988 AC 1986 AC 1986 SHD 1986 cc X X X X X X X X Xh X X X X XC X X dAC. Advisury Committee or Cmzens' Panel: SHD. State Health Department; CC, Consensus Conference. hBy State Senate district. `State- and county-spafic data. SOURCE: Colorado Department of Health (1986); Mame Department of Human Services (1983): Massachusetts Department of Public Health (1988): Michigan Department of Public Health (19X0. 1984); Mmnesota Department of Health (1984, 1987b); New lersey Commission on Smoking or Health (1988); New York City Department of Health t 1986): North Dakota State Department of Health (1986); Pennsylvania Plan for Tobacco or Health (1986). 525 PART II. ECONOMIC INCENTIVES Economic as well as educational factors can influence tobacco consumption by in- creasing the costs of manufacturing, distributing, selling, or consuming cigarettes. Direct increases in consumer costs affect consumption patterns directly, but cost in- creases to suppliers ultimately affect consumers too, to the extent that supplier costs are passed on to consumers. This Section considers two economic instruments, taxation and insurance, and discusses how public and private policies have created economic disincentives for tobacco use. The simplest economic disincentive to consumption is to raise the price of a product. Governments have done so by imposing a tax on tobacco, usually an excise tax, which offers the benefit of generating public revenue. Insurers' policies work more indirect- ly to discourage smoking. Premium differentials make insurance more expensive for smokers to purchase; this effectively increases the cost of being a smoker, although its impact is not felt directly at the point of cigarette purchase. Health insurers' decisions about the reimbursability of smoking cessation treatment costs also create economic incentives. For the smoker, reimbursement removes a financial impediment to cessa- tion; for the provider, reimbursement presumably would stimulate the availability of cessation services. Unlike taxation, insurance mechanisms are largely private policies; however, they can be encouraged and supported by government actions. In addition, government acts as a health insurer through publicly funded programs, such as medicare, and theoretically could use insurance mechanisms to promote nonsmoking. It is important to note that taxation and insurance incentives may influence smoking behavior through more than purely economic mechanisms; they also remind smokers that smoking is a harmful and socially discouraged behavior. Other policies that act via economic mechanisms are not discussed. Chief among these is the Federal policy of tobacco price supports and the allotment system. As an agricultural policy not oriented toward tobacco consumption (although it may have an indirect impact) (Warner 1988; Johnson 1984), it is not within the scope of this Chap- ter. Also not discussed in this Chapter is a current high-visibility antitobacco activity with potentially important economic effects relevant to consumption: the ongoing ef- forts to establish the legal liability of tobacco manufacturers for the diseases caused by their products (Daynard 1988). Although product liability suits themselves are not policies, policymaking pertaining to them could influence the number and ultimate im- pact of these suits. For example, recent legislative action in California attempts to limit the legal liability of tobacco manufacturers and vendors for claims brought in that State. California's Civil Liability Reform Act of 1987 (California Chapter 1498) includes a section specifically exempting manufacturers or sellers of tobacco products from product liability actions. Economic incentives are not limited to public and private policies. Smoking cessa- tion programs have used economic incentives to encourage participation or success. and employers have offered employees economic incentives not to smoke. These non- policy uses of incentives are identified in Chapter 6 and are discussed elsewhere (Warner and Mutt 1984). 526 Tobacco Excise Taxation Excise taxes are sales taxes on specific commodities such as tobacco products. AI- though accounting for only a small percentage of aggregate tax receipts in the United States today. excise taxes provide revenue for Federal, State, and local governments. The primary fiscal attraction of excise taxes is their low administrative cost relative to the revenue they can generate. In theory, to generate substantial revenue, excise taxes should be placed on commodities with a broad base of consumption that is not substan- tially reduced by the imposition of the tax. Hence, during the Middle Ages, the salt tax was an important source ofrevenue. In the United States, tobacco, alcohol, and gasoline have emerged as commodities subject to special excise taxes. In addition to being an attractive source of revenue, excise taxes on tobacco have a history as measures designed to reflect public morality by taxing "sinful" behaviors. More recently, as attention has focused on the deleterious health effects of cigarette smoking, it has been recognized that excise taxes have the potential to enhance public health by reducing the consumption of tobacco. The capacity to simultaneously raise revenue and enhance public health has made the tobacco excise tax a particularly at- tractive public policy tool (Lewit 1985; Warner et al. 1986b). This Section reviews the history and current status of cigarette excise taxation at the Federal, State, and local levels. focusing on the period since 1964. It examines the relationship between changes in taxes on cigarettes and changes in cigarette consump- tion, with particular attention to the consequences of the doubling of the Federal excise tax in 1983, and it identifies tax-related policies under serious consideration. History and Current Status Federal Excise Taxes Tobacco was one of the first goods to be taxed in North America, first by the British and then by the newly independent Republic in the early 1790s (Tobacco Institute 1988). The early tax on snuff was eliminated in 1804 and revived briefly as a wartime measure in 1814. A number of Federal tobacco taxes, including a tax on cigarettes, were imposed in 1864 as part of a package of taxes to finance the Civil War. Federal excise taxes on tobacco in one form or another have remained a part of the Federal tax system since that time. The tax on tobacco was a particularly important source of revenue to the Federal Government prior to the enactment of the income tax in 19 13. Generally, the Federal tax on cigarettes over the 120-year period from 1864-1983 tended to fluctuate with the revenue requirements of the Government, corresponding to alternating periods of war and peace. The Federal tax on cigarettes, introduced during the Civil War, was raised briefly during the Spanish American War, and again during World Wars I and II. In November 195 I, during the Korean War, the Federal excise tax was increased from 7 to 8 cents per pack. It remained at this level for over three decades, until March 1, 1983, when it was temporarily doubled to I6 cents per pack as part of the Tax Equity and Fiscal Responsibility Act of 1982. After several temporary 527 extensions, Congress made the 16-cent rate permanent in 1986. A Federal excise tax on smokeless tobacco was levied by the Omnibus Budget Reconciliation Act of 1985, which imposed taxes of 24 cents per lb on snuff and 8 cents per lb on chewing tobac- co. This is equivalent to a 1 .I)-cent tax on a 1.2-0~ can of snuff and a 1 .O-cent tax on a 2-02 pouch of chewing tobacco. In the year ending June 30, 1987, Federal tobacco taxes grossed 4.8 billion dollars. Over 98 percent of Federal tobacco tax revenues were provided by the tax on cigarettes (Tobacco Institute 1988). Cigarette excise taxes have provided a declining share of total Federal revenue during the post-World War I1 period. Accounting for over 3 per- cent of Federal revenues in 1950, the share of total Federal revenues attributable to cigarette excise taxes fell from 1.76 percent in 1964 to 0.52 percent in 1987 (see Figure 3). This occurred despite a doubling of the tax in nominal terms in 1983 and an in- crease in total tax receipts of over 2.8 billion dollars between fiscal 1964 and fiscal 1987. $ billion % 6 l- 6 /`. - `../' ' -.- "\./.,, -5 -4 -3 2 T----"~ - `. --____. \ -2 :x. \ -. `. 1 .-_x---- ______ 1. --._ \ -1 ._---_ .w. ------___,- _-*----____ 0' I I I 1 1 , I-0 1963 1967 1971 1975 1979 1983 1987 Year - Fed TX Rev S Bil _ _ _ _ ;e;;,`,"" Sl TX Rev 5 Bill % Tot St `-' Revenue 528 The Federal excise tax has declined in real terms since 1964, despite the rising con- cern about the adverse effects of smoking on health that followed the release of the 1964 Surgeon General's Report and the adoption of specific Federal tobacco control policies. One reason for the decline was the lack of legislated increases in the tax rate. Only the prospect of huge Federal budget deficits that accompanied the 1981 tax cuts prompted renewed interest in the cigarette excise tax as a source of funds to help reduce the projected deficits (Toder 1985). Inflation also eroded the real excise tax rate be- cause the excise taxes on cigarettes are unit rather than ad valorem taxes. A unit tax is a constant nominal rate per unit of a well-defined product, whereas the ad valorem tax is a constant fraction of either wholesale or retail price. Current Federal taxes on cigarettes, cigarette papers and tubes, smokeless and smoking tobacco, and small cigars, as well as most State and local taxes on cigarettes, are unit taxes. Federal taxes on large cigars and most State taxes on noncigarette tobacco products are ad valorem taxes. Cigarette taxes fall relative to the price of cigarettes when cigarette taxes are not changed by at least as much as the rate of general inflation or the rate of increase in cigarette prices. The Federal tax has increased only once since 195 I. Accordingly, the real tax (in 1987 value) fell from 30.4 to 9.8 cents per pack of 20 cigarettes between 1964 and 1982. The doubling of the nominal tax from 8 to 16 cents per pack in 1983 caused the tax to nearly double in real terms, to 19 cents (1987 value), between 1982 and 1983. However, inflation since 1983 has gradually eroded the tax to less than 16 cents (1987 value) today. During this same period, the Federal tax as a percentage of average retail price (including taxes) declined from 30.3 to 10.7 percent between 1964 and 1982, increased to 17.8 percent in 1983, and declined again to 13.7 percent in 1987 (Figure 4). State and Local Excise Taxes All States, the District of Columbia, and nearly 400 localities currently impose ex- cise taxes on cigarettes in addition to the Federal tax. In 192 1, Iowa became the first State to tax cigarettes. By 1964,49 States had enacted cigarette taxes. The last State to enact an excise tax on cigarettes, North Carolina, did so in 1969. Since then, a num- ber of States have modified their cigarette taxes, as described below. As of June 30, 1988, State excise tax rates ranged from a low of 2 cents per pack in North Carolina to a high of 38 cents in Minnesota. The average State tax was 18.2 cents per pack. In the year ending June 30, 1987, State tobacco taxes generated revenues of 4.8 billion dol- lars; almost 98 percent was provided by State cigarette taxes. In addition, 40 States and the District of Columbia imposed general sales taxes on cigarettes in 1987. In 35 States, the sales tax value base included the State excise tax. As a result, sales taxes added up to 10 cents per pack to the price of cigarettes in the highest tax States (Connecticut and Washington) in 1987. States have also increased their taxation of smokeless tobacco. In 1964, only 14 States taxed smokeless tobacco. By 1987, this number had nearly doubled to 27 (Tobacco Institute 1988). During the local fiscal crises that resulted from the Depression of the 1930s. municipal governments also began to enact tobacco taxes. The spread of cigarette taxes has not been as rapid or extensive among municipal governments as it was among State 529 o----o 1963 1967 1971 1975 1979 1983 1987 Year - Tot TX Rt _ _ _ _ kriig Fed TX Rt . -. ,-, St TX Rt Current S % of Price % of Price FI( ;I RE -I.--Federal and Statecigarettee\cise ta\ rates and relail cigarette prices. I WLJ-x7 governments. As of 1987. 369 cities and 20 counties in 6 States imposed local taxes on tobacco products. Taxes are levied by communities in Alabama, Illinois, Missouri, New York. Tennessee, and Virginia. In the year ending June 30, 1987, these taxes ranged from 1 to 15 cents per pack and yielded revenues of 197 million dollars. Over 70 percent of local cigarette tax revenues are collected in New York City and Chicage Cook County, IL, where the local tax rates are 8 and 23 cents per pack, respectively. During the period following the 1964 Surgeon General's Report, State cigarette ex- cise tax receipts grew much more rapidly than Federal receipts (Figure 3), but their share of total State tax revenue declined. State tax receipts averaged a fairly constant 5 percent of total State revenues during the initial part of the period, but the proportion has declined steadily since 1972. Gross receipts from local taxes on cigarettes have grown from 58 million dollars in 1964 to 197 million dollars in 1987, less than the growth rate of State tax receipts but more rapid than Federal tax receipt change in the same period. The number of local jurisdictions taxing cigarettes has not increased ap- preciably (Tobacco Institute 1988). 530 FIGURE L-State cigarette excise tax rates (as of June 30, 1988) SOURCE. Tobacco Instm~e t IYKXai Between 1963 and 1987, the average State tax on cigarettes in current dollars in- creased almost annually, but because the rate of increase slowed relative to the rate of inflation after 1972, the real tax rate and the tax rate as a percentage of retail price have each declined by over 40 percent in the past 15 years. The rate of increase in State taxes accelerated after 1980, so that on average, it has kept pace with the general rate of in- flation since that time (Figure 4). Considerable differences in cigarette tax rates among States have persisted over the last 25 years (Figure 5). Not until 1969 did all States tax cigarettes. At that time, the maximum State tax rate was 16 cents, and the difference between the tax rate in the highest and lowest tax States was 14 cents (Table 1 I). The range of State cigarette taxes in constant dollars was greatest in 197 1 and fell steadily through 198 1. This decline occurred because the lowest tax State maintained a constant nominal tax rate and taxes in the high-tax States failed to keep pace with inflation. Since 1982, tax increases in high-tax States have tended to keep pace with the rate of inflation. The major tobac- co-producing States of North Carolina, Kentucky, and Virginia have maintained low cigarette tax rates since 1964. The largest tax increases have occurred in Oregon, which did not even tax cigarettes in 1964, in Minnesota, and in California in November 1988. Differences in cigarette tax rates among States and local jurisdictions can create problems with the enforcement of State and local tax laws andcan result in lost revenues to some jurisdictions. In particular. large differences in cigarette tax rates among and within States provide an incentive for bootlegging: that is, purchasing of cigarettes in low-tax jurisdictions for consumption or resale in high-tax jurisdictions. A variety of tax evasion activities have been identified: casual smuggling (individuals buying 531 TABLE 1 I.-Dispersion in cigarette excise tax rates among States, 1963-87 Year Number of taxing Statesa Minimum Maximum Minimum Maximum tax, current tax, current tax, 1987 tax, 1987 dollars Range, 1987 dollars dollars dollars dollars (cents/pack) (cents/pack) (cents/pack) (cents/pack) (cents/pack) I963 48 I964 49 1965 49 1966 SO I967 so 1968 51 1969 51 1970 51 1971 51 1972 51 1973 51 1974 51 197s Sl I976 51 I977 51 1978 51 1979 51 I980 51 1981 51 1982 Sl 1983 51 19x4 51 I985 51 I986 51 1987 SJ 0.0 8.0 0.0 29.6 29.6 0.0 8.0 0.0 29.3 29.3 0.0 11.0 0.0 39.6 39.6 0.0 1 I.0 0.0 38.5 38.5 0.0 13.0 0.0 44.2 44.2 0.0 IS.0 0.0 49.0 49.0 2.0 16.0 6.2 49.5 43.3 2.0 18.0 5.8 52.6 46.8 2.0 21.0 5.6 S8.9 53.3 2.0 21.0 S.5 56.9 51.5 2.0 21.0 5.1 53.7 48.5 2.0 21.0 4.6 48.3 43.7 2.0 21.0 4.3 44.3 40.0 2.0 21.0 3.9 41.9 31.9 2.0 21.0 3.7 39.3 35.6 2.0 21.0 3.5 36.5 33.0 2.0 2 I .o 3.2 32.9 29.7 2.0 2 1 .o 2.1 28.9 26.2 2.0 21.0 2.5 26.2 23.1 2.0 25.0 2.4 29.4 27.0 2.0 26.0 2.3 29.6 21.3 2.0 26.0 2.2 28.4 26.2 2.0 26.0 2.1 27.5 25.3 2.0 3 I .o 2.1 32. I 30.0 2.0 38.0 2.0 38.0 36.0 cigarettes in neighboring lower tax jurisdictions for their own consumption), illegal or- ganized or commercial smuggling for resale, tax-free mail order purchase of cigarettes (technically illegal since 1949), purchase of cigarettes through tax-free outlets (inter- national ports of entry. military stores, and Indian reservations), and illegal diversion of cigarettes within the traditional distribution system (forged tax stamps and under- reporting) (Advisory Commission on Intergovernmental Relations (ACIR) 1977, 1985L 532 As the differential in State tax rates increased during the late 1960s and early 1970s. the level of cigarette tax evasion increased substantially. Although casual smuggling between neighboring States (e.g., Massachusetts and New1 Hampshire. Washington and Oregon) had long been a problem, government officials reported a substantial increase in organized smuggling over long distances and in the illegal diversion of cigarettes from the legal distribution system (ACIR 1977). The problem was also reported in the media. In response, the Federal Cigarette Contraband Act was enacted. It prohibited the transportation, receipt, shipment, possession, distribution. or purchase of more than 60.000 cigarettes not bearing the indicia of the State in wnhich the cigarettes vvere found. Enforcement of this Act was made the responsibility of the Bureau of Alcohol, Tobac- co. and Firearms of the U.S. Treasury Department. A second study by the Advisory Commission on Intergovernmental Relations ( 1985) suggested that this act had been effective in reducing the level of organized smuggling. ACIR ( 1985) has suggested earmarking a portion of the revenue generated by increases in State cigarette excise taxes for antismoking law enforcement activities. The law enforcement problems stemming from organized interstate cigarette boot- legging were also a factor in the deceleration of State tax increases in high-tax States (ACIR 1985). In real terms, the difference between the rate in the highest and lowest rate States (53 cents, 1987 value) peaked in 197 1. The decline in the range of real prices means that interstate bootlegging has become less profitable since that time. This decline in profitability, combined with the increased Federal enforcement effort, probably accounted for the decline in bootlegging (Warner 1982). More recent in- creases in State taxes and the resultant widening of real differentials between high- and low-tax States have again increased the incentives for smuggling. In addition, many States and the FederalGovernment have reduced the level of resources allocated to en- forcing State tax laws as the problem of bootlegging abated. Cigarettes sold on military bases and Indian reservations are exempt from State and local tobacco excise taxes. Tax-exempt sales at these locations represent a revenue loss to the States, which would collect a tax on these sales if the tax-exempt options did not exist. These cigarette sales represent "the major sources of current revenue losses for most states" (ACIR 1985). In 1986, DOD discussed but did not adopt a proposal to remove the State and local tax exemption for cigarettes sold in the military. as part of an overall strategy to discourage smoking in the military (US DOD 1986~). Effects of Excise Taxes on Smoking and Health Price Elasticity of Demand for Cigarettes One of the few nearly universal relationships in economics is the law of dowmvard sloping demand; that is, demand for a commodity declines as its price increases. Numerous econometric studies have confirmed that this relationship holds for ciga- rettes. Because excise taxes increase the price of cigarettes, fluctuations in excise tax rates should influence the demand for cigarettes, and excise tax increases should reduce tobacco consumption. The basis for estimating the consumption effects of a change in excise tax rates is an analysis of the price elasticity of demand for cigarettes. Elasticity, a measure of the de- gree of responsiveness of demand to changes in price, is defined as the percentage change in the quantity of cigarettes demanded divided by the percentage change in price. An elasticity of -0.5, for example, means that a lo-percent increase (decrease) in price would reduce (increase) by 5 percent the quantity of cigarettes demanded. Be- cause cigarette taxes account for only a fraction of the total retail price of cigarettes, the price elasticity of demand would have to be multiplied by the percentage change in price that resulted from a tax change to determine the elasticity of demand with respect to the tax. Accordingly, the elasticity of demand with respect to a tax change will be less than the price elasticity of demand. Numerous attempts have been made to measure the price elasticity of demand for cigarettes, with estimates ranging from -0.2 to -1.3. Miller (1982) suggested that -0.7 was the midpoint of recent studies and noted that the Tobacco Institute used that figure for its analyses of cigarette tax effects. Table 12 reports the results of studies published since 1980 on the price elasticity of demand for the United States. The substantial chan- ges in the market for cigarettes and in the demographics of the smoking population that have occurred since 1964 suggest that earlier estimates may be inappropriate today. The estimates reported in Table 12 derive from econometric studies that attempt to explain differences in cigarette consumption as functions of the price of cigarettes, in- come, and demographic variables. Some of the variability in results is a consequence of methodological differences among studies. The studies derive estimates of demand from different sources, including time series of per capita cigarette consumption (for the United States as a whole and for cross-sections of States) and cross-sectional sur- vey data on the smoking behavior of individuals at a point in time and over time. Each of these methods has inherent limitations that can cloud the interpretation of results. In time series studies, the estimates of price and income elasticities are sensitive to the method of accounting for the effects of concurrent social influences on smoking, such as the growing public knowledge about its harmful effects and changing cigarette ad- vertising policies. In addition, time series estimates are not stable because the inde- pendent variables tend to be highly correlated with each other. Moreover, price elas- ticities estimated with time series data may represent short-term responses to price fluctuations rather than the long-term responses that are typically of greater interest to policymakers. On the other hand, estimates of cigarette price elasticities based on cross-sections of State tax-paid sales may be biased upward because some cigarettes sold in low-tax States are ultimately consumed by smokers in higher tax States. As a result, tax-paid sales may overstate actual consumption in low-tax States and understate consumption in high-tax States, and the estimated price elasticity of sales will exceed the price elas- ticity of actual consumption. Some studies have attempted to control for short-distance, casual smuggling (ACIR 1977,1985; Becker, Grossman, Murphy 1987; Chaloupka and Saffer 1988) and long-distance, organized smuggling (Becker, Grossman, Murphy 1987; Chaloupka and Saffer 1988) by using a set of carefully constructed variables. While these are imperfect measures of the smuggling phenomena, the careful attempt to control for the problem should reduce the bias associated with the use of this type of data. 534 TABLE 12.-Recent estimates of the price elasticity of demand for cigarettes Study Estimated aggregate price elasticity Method of estimation Comments Fujii (1980) a.45 Ridge regresston Schneider, Klein. Murphy (1981) Lewit, Coate, Grossman (1981) Teenage smoking Lewit and Coate (1982) Adult smoking Young (I 983) Price increase Price decline Bishop and Yoo (1985) ACIR (1985) Mullahy (1985) Baltagi and Levin (1986) Porter ( 1986) Chaloupka (1988) Long run Becker, Grossman, Murphy (1987) Long run Chaloupka and Saffer (1988) -1.23 -1.44 a.42 a.33 a.6 I -0.45 -0.45 -0.47 a.14 -0.21 -0.26 -0.40 -0.75 -0.28 Instrumental Time-series aggregate data, variables 1930-78 Ordinary least- U.S. Health Examination Survey, squares I2- 17.yearolds. 196670 Ordinary least. squares Ridge regression Three-stage least- Time-serves aggregate data. squares U.S., 1954-80 Ordinary least- Pooled-time series of State squares cross-sections, 198183 Probit, instrumental variables 1979 Health Interview Survey, by sex Instrumental Pooled-time series cross-section variables of 46 States. 1963-80 Two-stage least- Time-series aggregate data, squares 1947-82 Instrumental variables instrumental variables HANES2 full sample; also by age, sex. race, or education Pooled-time series of State cross- sections, 195685 Two-step endogenous law model Time-series aggregate data, 1929-73 1976 Health Interview Survey. elasticities by age and sex. 2&74-yearolds Fujii', model with asymmetrical responses Pooled-time series of State cross- sections, 1975-85 535 An additional limitation of most econometric studies is that they use aggregate or per capita cigarette consumption as their dependent variable. As a result, they provide es- timates of the price elasticity of aggregate or per capita cigarette consumption but can provide no information on the effects of price changes on smoking rates, smoking ces- sation and initiation, or quantity and type of cigarette smoked by smokers. Also, they cannot identify differences by separate demographic groups in response to price chan- ges. Accordingly, aggregate studies are useful for economic and fiscal planning but are of limited usefulness when considering the behavioral or health effects of changes in cigarette tax policy. In contrast to studies focused on aggregate consumption effects, Lewit and colleagues ( 198 1, 1982) used data on individuals from two national surveys to investigate the ef- fects of price (tax) differences on smoking behavior. With data on a sample of 19,288 individuals aged 20 through 70 years from the 1976 NHIS, Lewit and Coate (1982) es- timated an overall price elasticity of -0.42 for cigarettes. They corrected for bias in two ways: first, by using consumption reported by individuals rather than tax-paid sales as the unit of observation, and second, by removing from the sample those households within 30 miles of States with lower prices. The former eliminates some of the error in the measurement of consumption, and the latter partially corrects for errors in the price measure that result when households purchase cigarettes outside their own localities. Lewit and Coate's study also gave a more detailed breakdown of the smoking response than in previous studies. They found that cigarette prices affected smoking primarily by reducing smoking prevalence (the "participation rate," or number of smokers). The estimated effects on the number of cigarettes per smoker were not statis- tically significant. There were also differences in the estimated price elasticities among groups: reported price elasticities were much higher for adult males than for adult females and much higher for people aged 20 to 25 years than for other age groups. Their estimates are summarized in Table 13. In a methodologically similar study, Lewit, Coate, and Grossman (198 1) analyzed teenage smoking by using data from Cycle III of the U.S. Health Examination Survey (HES), a national sample of 6,768 youths between the ages of 12 and 17 years who were surveyed between March 1966 and March 1970. They reported that price elas- ticities of demand for cigarettes among teenagers are larger in absolute value than price elasticities for adults. As in the adult study, smoking participation (or prevalence) is more responsive to price than is the quantity of cigarettes smoked. Their estimated smoking participation elasticity for teenagers was -1.20, and the quantity-smoked elas- ticity (conditional on smoking) was -0.25 (Table 13). The estimated elasticities based on HES data for teenagers were generally confirmed in a related study by Grossman, Coate, and Lewit (1983) and summarized by Grossman (1983). The study used a similar methodology to estimate price elasticities for teenagers on the basis of the four U.S. National Surveys on Drug Abuse (NSDA) con- ducted in 1974, 1976, 1977. and 1979. Estimates based on these surveys must be in- terpreted with caution because they are based on much smaller samples than those from the previous studies. Adjusting for this fact, Grossman's summary estimate of NSDA 536 TABLE 13.-Estimates of the price elasticity of demand for cigarettes Elasticities Age group (year\) Total Participation Quantity per smoker 12-17 -1.40 -1.20 4.15 2&Z 4.89 4.74 4.20 2635 -0.47 a.44 4.03 3674 A).45 4.15 4. I.5 All adults (X-74, 4.42 426 4. IO All (12-74) age\ -0.47 -0.31 4.1 I participation elasticity was -0.76, which is smaller in absolute value than the HES es- timate but almost 3 times larger than the NHIS elasticity for adults. Most economic studies of the demand for cigarettes, including those cited above, have not explicitly allowed for the addictive nature of cigarettes (US DHHS 1988). Part of the reason for this omission was that the consumption of addictive goods in general was not thought to conform to the rational. utility-maximizing model that is the paradigm of standard economic analysis. Recently, however, Becker and colleagues (Becker, Grossman, Murphy 1987: Becker and Murphy 1988). among others, have developed models of "rational addiction" that are conducive to economic analysis. In general, this work recognizes that the demand for cigarettes depends on the levels of both past and future consumption, permitting incorporation of the notions of tolerance, reinforcement, and withdrawal, which are generally used to distinguish addictive from nonaddictive substances. The findings of preliminary empirical research are consistent with the characteriza- tion of smoking as an addiction and suggest that failure to consider addiction explicit- ly may lead to underestimation of the long-term response to changes in cigarette price (Becker, Grossman, Murphy 1987; Chaloupka 1988). The application of the rational addiction model to cigarette consumption is a recent development that will require fur- ther empirical investigation and theoretical refinement before its contribution to the un- derstanding of smoking behavior can be fully evaluated. The range of estimates of the long-term price elasticity of demand for cigarettes derived under the assumptions of the model is not inconsistent with previously published estimates. however, which suggests that insights gained from analyses of recent tax increases are not likely to be invalidated by further refinement of the addiction model. The principal message of this body of research on price elasticity of demand is that an increase in the price of cigarettes appears to curtail smoking, particularly the initia- tion of smoking by teenagers. Because adolescents are more responsive to changes in cigarette prices than are adults and because price changes appear to have stronger ef- fects on smoking prevalence than on daily consumption by smokers, the studies sug- 537 gest that excise tax increases may be useful tools to prevent or delay the onset of smok- ing by adolescents. Because aggregate cigarette consumption and smoking prevalence are dominated by the behavior of adults, the short-term effects of an increase in cigarette excise taxes would likely be modest. The long-term impact of such an increase could, however, be considerably more substantial. If the current situation, in which very few individuals start smoking after age 20 (see Chapter 5) continued, it is possible that the cohort of young persons who do not begin to smoke as a result of a tax increase would never be- come smokers. If the tax increase were maintained in real terms, it could continue to discourage successive generations of youths from starting to smoke. Gradually, the smoking prevalence of adults might be reduced as these cohorts moved through the age spectrum. Over a period of several decades, aggregate smoking and its associated health effects might decline more substantially than would be evident in the years im- mediately following a tax increase. In addition to its relevance for cigarette taxation, research demonstrating the inverse relationship between tobacco price and demand has implications for the armed forces. As described in Chapter 5, the prevalence of smoking among military personnel ex- ceeds that of the general population. One factor probably contributing to the differen- tial in smoking rates is the lower price paid by military personnel for tobacco products. The current pricing structure of the military resale system results in approximate 35percent and 1 g-percent reductions in cigarette price in military commissaries and exchanges, respectively, when compared with commercial retail outlets (US DOD 1986~). Cigarettes sold in these military stores are exempt from State and local excise taxes and, if outside the United States, are also exempt from the Federal excise tax. Cigarette sales in the military resale system totaled 1,046 million packs in fiscal year 1985, though sales have been decreasing in the 1980s (US DOD 1986c. 1987). Price elasticity of demand data suggest that increasing the price of cigarettes could contribute to reducing tobacco use by military personnel. In 1986, DOD considered banning the sale of tobacco in commissaries or raising the price of tobacco products on military installations as part of a broad program to discourage tobacco use. Neither of these policies was adopted (US DOD 1987) although, as discussed in Part III and Chapter 6, DOD has instituted new smoking restrictions and has launched antismoking activities on a large scale. Effects of an Excise Tax Increase Research addressing the temporary doubling of the Federal excise tax in 1983 and its six temporary extensions prior to permanent adoption in 1986 generated several es- timates of the effect of the tax increase on cigarette consumption and smoking prevalence. For example, Harris (1982) used the Lewit-Coate estimate of the adult- smoking participation price elasticity of -0.26 and the Lewit-Coate-Grossman estimate of the teenage-smoking participation price elasticity of -1.20 to forecast the impact of the doubling of the Federal excise tax rate in 1983. He predicted that the number of adult smokers would decline by 1.5 million and the number of teenage smokers by 0.7 million. 538 In an analysis performed in 198.5, during the period of uncertainty as to whether the Federal tax increase would be extended permanently or allowed to lapse, Warner (1986a) used the Lewit-Coate and Lewit-Coate-Grossman age-specific elasticity es- timates to project the changes in cigarette consumption that would have accompanied an g-cent tax decrease or 8- and 16-cent tax increases (Table 14). Altogether he es- timated that an g-cent decrease in the tax would induce almost 2 million persons to smoke who would not do so if the tax were to remain unchanged at 16 cents per pack. In contrast, a doubling of the tax to 32 cents per pack would have encouraged almost 3.5 million Americans to forego smoking, a figure that included more than 800,000 teenagers and almost 2 million young adults aged 20 to 35 years. TABLE lrl.-Expected percentage changes in cigarette consumption resulting from changes in the Federal cigarette excise tax I-cent decrease ¢ increase l¢ increase Age .ww Total Smoking Total Smoking Total Smoking consumption prevalence consumption prevalence consumption prevalence 12-17 11.9 10.2 -11.1 -9.5 -21.1 -18.1 20-25 1.6 6.3 -7.0 -5.9 -13.4 -11.2 2635 4.0 3.1 -3.7 -3.5 -7.1 -6.6 36-74 3.8 1.3 -3.6 -1.2 -6.8 -2.3 All adults (20-74) 3.6 2.2 -3.3 -2.1 A.3 -3.9 SOURCE: Warner (1986a). Lewit (1985) examined the actual decline in aggregate cigarette consumption follow- ing the 1983 tax increase. He noted that in anticipation of the January 1, 1983, tax in- crease, the tobacco companies increased the wholesale price of cigarettes four times between August 1982 and January 1983. Cigarette prices were increased twice again in 1983, and 16 States increased their cigarette excise taxes during 1982 and 1983. As a consequence, the average retail price of cigarettes increased by about 40 percent be- tween November 1, 198 1, and November 1, 1984, from approximately 70 cents per pack in 1981 to almost 98 cents in 1984 (Tobacco Institute 1988). During this same period, the price of cigarettes adjusted for inflation rose by 26 percent. Based on an overall price elasticity of -0.47 for adults and teenagers, per capita consumption should have declined by about 12 percent over this period. Department of Agriculture data in- dicate a decline of 11 to 12 percent. Although per capita cigarette consumption had been slowly declining at the rate of about 1 percent per annum since the mid-1970s. the very rapid acceleration in the rate of decline following the excise tax increase and as- 539 sociated price increases is consistent with the cross-sectional studies and serves as fur- ther evidence that excise taxes may be a potent tool to discourage smoking. Harris (1987) conducted an extensive review of the 1983 Federal tax increase. On the whole, his findings for the period 1981-86 are consistent with those reported by Lewit (1985). Harris' discussion of the cigarette manufacturers' response to the tax in- crease is. however, of particular interest. It has been generally assumed that changes in tax rates would be fully passed on to consumers. Accordingly, Warner's analysis (1986a) and Harris' earlier analysis (1982) assumed that an g-cent tax increase would raise the retail price of cigarettes by 8 cents. Harris (1987) reports evidence to suggest, however. that the preannounced 1983 Federal tax increase appeared to have served as a focal point for coordinating an oligopolistic price increase by tobacco producers that exceeded the amount of the tax. He concludes that "Quite contrary to the convention- al view of the incidence of excise taxes, the federal excise tax may have actually had a multiplier effect upon price." He estimates that the g-cent-per-pack tax increase in- duced a 16-cent-per-pack increase in the market price of cigarettes. Health Consequences of Tax Changes Given the deleterious health effects of cigarette smoking and the important changes in both cigarette consumption and smoking prevalence that would accompany a sub- stantial tax change, it appears that a policy of aggressive increases in the tax on ciga- rettes would lead to large reductions in smoking-induced illness. To assess fully the effect of a cigarette tax change on the health of the population, information is needed on who actually cuts down on cigarettes, who quits, and who does not start smoking. Only a portion of such information is available. However. both Warner (I 986a) and Harris (1987) provide crude estimates of some of the health effects that may result from the 1983 Federal tax increase. Basing his es- timates on the conservative assumption that one lifelong smoker out of every four dies of smoking-related illness (Mattson et al. 1987), Warner obtained upper bound es- timates of the mortality impact of increases or decreases in the Federal excise tax. He estimated that an g-cent tax increase, maintained in real value over time, would avert 450.000 premature deaths in the cohort of Americans 12 years of age and older in 1984 and that this number would rise to 860,000 following a 16-cent increase. An g-cent tax decrease, however, would result in an increase of more than 480,000 premature smok- ing-induced deaths. Focusing specifically on the post- 1983 tax-induced price changes and their impact on consumption. Harris estimated that 100,000 additional persons will live to age 65 as a result of the tax increase. Of these 100,000, he estimated that 54,000 will result from having discouraged 600,000 teenagers from starting to smoke. Thus, the major effect of the tax increase on mortality will not be realized for decades. On the other hand, al- though no estimates of the impact of the tax increase on other health measures have been published. reductions in smoking-induced morbidity and disability should raise aggregate health levels long before the projected mortality reductions are fully realized. Policies Under Consideration Among the public policy tools with a potential to reduce tobacco use, the cigarette excise tax has received particular attention because its public health benefits are well documented, and it has the additional advantage of generating public revenues (Warner et al. 1986b). Currently discussed proposals to modify Federal, State, or local cigarette excise taxes fall into two categories: (1) proposals to increase the amount of the tax or the method of calculating the tax rate, and (2) proposals to channel the revenues generated from excise taxes for specific purposes. The first category includes proposals to increase the Federal excise tax rate, raise State and local excise tax rates (especially in States in which rates are currently below the national or regional average), and switch from a specific unit tax to an ad valorem tax, thereby tying the tax rate to a measure that changes with inflation. This last proposal often accompanies the others because it permits the real tax rate to keep pace with inflation. Proposals in the second category would dedicate (or earmark) some portion of tax receipts for purposes such as funding tobacco control programs or paying for the excess health care costs of smokers. Tobacco Excise Tax Increases Increasing the Federal excise tax beyond the 16-cent-per-pack level first set by Con- gress in 1983 and made permanent in 1986 is the most widely discussed and most broad- ly supported tax proposal. It has been endorsed by a wide range of voluntary health or- ganizations and organized medical societies, including the American Medical Association, American Public Health Association, American Cancer Society, American Heart Association, and American Lung Association. Proponents of a Federal excise tax increase note that the real value of the tax has fallen since 1964 and that in- flation since the last increase in 1983 has continued to erode the real value of the tax. Opponents of Federal excise tax increases have raised several issues, primarily based on tax equity considerations. Chief among them is that cigarette excise taxation is regressive, requiring the poor to pay a greater proportion of their income on the tax than the rich. More pragmatic concerns have been raised about the effect on State tax revenues. Because the consumption of cigarettes tends to decline as price rises, State cigarette tax receipts may fall after a Federal tax increase if State tax rates remain con- stant. In the aggregate, this did not happen after the 1983 Federal excise tax increase because State tax rates also increased. Increases in State excise taxes have received less attention, although the effect of such a policy change on consumption and revenue would be expected to resemble that of a Federal tax change. The variability in State taxes adds an additional concern about interstate bootlegging of cigarettes, which could be avoided if excise tax rates were preferentially raised in States with relatively low tax rates. Beyond excise tax changes, cigarette taxes could also be increased in those States that now exempt cigarettes from the regular sales tax by removing that exemption. Massachusetts did so in June 1988, resulting in a 5-cent increase in the tax on cigarettes (Mohl 1988). 541 Switch to an Ad Valorem Tax With the exception of the State excise tax in Hawaii, all Federal, State, and local cigarette taxes are specific unit taxes; that is, the tax rate is a constant nominal amount per unit. While a specific unit excise tax has the advantage of administrative simplicity, it has the disadvantage that the real revenue yield tends to decline with inflation. Unit excise taxes must be raised periodically if real revenues-and consequent impact on tobacco consumption-are to be maintained. Replacing unit taxes on cigarettes and other tobacco products with equivalent-yield ad valorem taxes would allow revenues to keep pace with inflation-induced increases in cigarette prices, and real cigarette prices would be more likely to be maintained over time. As mentioned above, Federal taxes on large cigars and most State taxes on noncigarette tobacco products are ad valorem taxes. An alternative to switching to an ad valorem tax on cigarettes is to index the unit tax to changes in either the general price level or to a price index for cigarettes (Toder 1985). This would maintain the administrative simplicity of per-unit taxes and eliminate the need to periodically reevaluate the unit tax rate to maintain real revenues. Earmarking of Revenues Tobacco taxes may also be earmarked (dedicated) for specific tobacco- or health-re- lated purposes. Proposals have included using tax revenues to support the cost of health care for tobacco-related illnesses or to fund tobacco prevention and cessation programs delivered in schools or via the media (Warner 1986~). Earmarking a portion of the Federal cigarette excise tax to fund the medicare program has been proposed to Con- gress (Committee on Ways and Means 1986), and survey data show that a majority of the public would support an increase in the cigarette excise tax to fund medicare (Chap- ter 4). Several States have used cigarette tax revenues to finance tobacco-related health programs. In Nebraska, revenue from a I-cent-per-pack cigarette tax is used to fund the State's Cancer and Smoking Disease Research Program (CDC 1987). In Minnesota, the Omnibus Nonsmoking and Disease Prevention Act of 1985 increased the cigarette excise tax by 5 cents per pack and earmarked 1 cent of the additional revenues for a public health fund. As noted previously, one-quarter of this fund is dedicated to assist local school boards to implement tobacco use prevention programs. Funds are also provided for an active public tobacco control and prevention program overseen by the Commissioner of Health (Minnesota Department of Health 1987a,bj. In Utah, a portion of revenues generated from an I l-cent increase in the State cigarette excise tax is dedi- cated for tobacco control programs (Utah 1987). A newer proposal would earmark a portion of the estimated excise tax revenue generated from sales of tobacco products to minors to support tobacco prevention and cessation programs for youth (Slade 1988a). In Indiana, a portion of the State tobacco excise tax is earmarked to support subsidized child care programs (Lewin 1988). The most substantial earmarking of tobacco excise tax revenues is in California, the result of passage of a ballot initiative in November 1988 raising the State's cigarette excise tax by 25 cents per pack. With the exception of funds to cover the administra- 542 tive and collection costs associated with the tax, three-quarters of all revenues are dedi- cated to health education, research, medical treatment, and environmental conservation programs. In its first full year of operation, the tax is expected to generate 650 million dollars for these purposes (Tobacco Tax and Health Protection Act of 1988; Wilson 1988b). Insurance and the Treatment of Smokers At the time of the 1964 Surgeon General's Report. whether a person smoked was not a consideration in the premiums paid for insurance. No major life, health, disability, homeowner, or auto insurer offered discounts to nonsmokers, and no major health in- surer covered the expenses of smoking cessation programs. In fact, the consensus of a panel of the Society of Actuaries convened in 1963 was that consideration of smoking in calculating life insurance premiums seemed to be impractical (Novemberet al. 1964). Over the subsequent 25 years, this situation has changed considerably, but changes have come at different rates in the three major segments of the insurance industry- life, health and disability, and property and casualty. Currently, almost all life insurers, including two that are subsidiaries of major tobacco firms, offer premium discounts to individuals who do not smoke cigarettes (Trenk 1986). In contrast, only about 15 per- cent of companies writing health and disability insurance policies offer discounts to nonsmokers, and even fewer reimburse health care providers for smoking cessation treatment (National Association of Insurance Commissioners (NAIC) 1987~). Only 1 of the 10 leading writers of homeowner and personal passenger auto policies offers dis- counts to nonsmokers on both (Wasilewski 1987a,b). Although the underwriting prac- tices and administrative exigencies vary considerably among these three types of in- surance, sentiment has been building for insurers, primarily those in life and health, to offer premium differentials and cover the costs of smoking cessation treatment (Brailey 1980; Stokes 1983; Davis 1986; Engstrom 1986; Walsh and Gordon 1986; US DHHS 1988). Premium differentials based on smoking behavior are generally referred to as non- smoker discounts rather than as smoker surcharges. The terminology, which implies that smoking is the majority condition, is no longer correct, but it persists for historical and marketing reasons; the premium differentials were developed when smoking was a more common behavior, and a discount sounds like a positive incentive, while a sur- charge has the negative connotation of a penalty. Smoker-nonsmoker premium dif- ferentials are the result of insurer business decisions, based primarily on differences be- tween insured smokers and nonsmokers in mortality rates, health care costs, and auto and homeowner claims. For the policyholder, a premium differential may serve as an economic disincentive for smoking. This Section will examine separately each of the three major industry segments to address the extent to which insurers in each category consider policyholder smoking status when calculating premiums or coverage, reasons the three segments handle the issue differently, and the potential effects of the insurance industry's premium struc- ture and reimbursement policies on smoking behavior. 543 Life Insurance Life insurance policies are sold on an individual, family, or group basis. Policies pur- chased on an individual or family basis are referred to as ordinary life insurance and are the most common type of life insurance. Sixty-two percent of households in the United States had ordinary life insurance policies in 1987 (American Council of Life Insurance (ACLI) 1987). Life insurers price their products according to the mortality experience of the insured population. Higher premiums are set for classes of individuals with greater mortality rates. Smoker-nonsmoker premium differentials were adopted by the industry when actuarial studies confirmed that the excess mortality of smokers, previously observed in epidemiologic studies, was also present in the insured population (Cowell 1985). Some insurers offer an alternative to smoker-nonsmoker premium differentials. These policies are based on overall health behavior or health status and are typically available only to applicants who meet health standards with regard to weight, blood pressure, and exercise and who do not smoke. History of Premium Differentials Three months after the 1964 Surgeon General's Report was released, State Mutual Life Assurance Company became the first company to offer life insurance to non- smokers at discounted rates. The company believed that its statistical evidence of "much higher death rates among persons who smoke was so overwhelming. that the company could no longer ignore it in pricing insurance" (Cowell 1985; Cowell and Hirst 1980). This action was consistent with aposition that nonsmokers should not sub- sidize the higher insurance costs resulting from smokers' excess death claims. Between 1965 and 1975, more than 30 other companies introduced premium dis- counts for nonsmokers, based on their estimates of the effects of smoking on mortality in the insured population. Their estimates resulted at least partly from examination of mortality studies discussed in the early Surgeon General's Reports (Crowne and Shapiro 1980). However, most of the industry did not develop nonsmoker premium discounts at that time. Their reluctance derived primarily from a paucity of actuarial data. Furthermore. only half of the primary market of policyholders-adult males- stood to benefit from these discounts, because in 1965,50 percent of adult males smoked (Chapter 5). Companies also had to address the uncertainties of marketing and ad- ministering a new product. These factors were sufficient to slow the adoption of smoker-nonsmoker premium differentials (Cowell 1985; Cowell and Hirst 1980). In 1979. State Mutual analyzed the mortality differences between its insured smokers and nonsmokers. The analysis showed that the overall mortality of smoking policyholders was 2 to 2 l/2 times that of nonsmoking policyholders. The higher death rates of smokers were not confined to older ages but were apparent even at early ages. These findings were statistically significant and large enough to be used for insurance underwriting and pricing purposes (Cowell and Hirst 1980). This landmark report was a stimulus to rapid change in the industry. After State Mutual made public its ex- perience, so did other life insurers, including those that had previously not issued their 544 findings in the mistaken belief that the differences were too large to be true. Within 3 years, 400 companies offered discounted premiums to nonsmokers (Shaman 1982). In 1983, at the request of NAIC. a Society of Actuaries' task force examined the smoking-related mortality data of insurance companies. The Task Force on Smoker/Nonsmoker Mortality determined the mortality differences between smoking and nonsmoking insured persons of ages 15 to 99 years and divided the mortality tables used to value the reserves on life insurance into those appropriate for pricing separate smoker and nonsmoker products. The group did not specifically address the nature of the association between smoking and increased mortality that it so clearly observed. For their purposes, it was sufficient only that premium rates reflected the actual mor- tality experience of groups of insured smokers and insured nonsmokers (Society of Ac- tuaries 1983). By addressing these issues, the task force facilitated greater acceptance of smoker- nonsmoker premium differentials by insurance companies and the State government officials who regulate them. NAIC used the Society of Actuaries' work to develop the "Model Rule (Regulation) Permitting Smoker/Nonsmoker Mortality Tables For Use In Determining Minimum Reserve Liabilities and Nonforfeiture Benefits"(NAIC 1985b). The rule permitted insurers to use standard underwriting and actuarial practices to set different premium rates for smokers and nonsmokers, as insurers would for any other accepted risk classification in their normal conduct of business. Proposed in January 1984 to Commissioners of Insurance in all States, the model rule or a similar variation had become law in 33 States as of July 1987 (NAIC 1987f). Once the empirical basis for smoker-nonsmoker premium differentials was estab- lished, life insurers had to consider how to market and administer the new products. A central concern was the possibility that individuals would misrepresent their smoking status (Lipson 1988). Misrepresentation is not a new problem; insurance companies have had to deal with it since their beginning. One solution was to require biochemi- cal validation of nonsmoking status. A growing number of insurers now require this validation before selling a policy (Lyons 1986). One reason nonsmoking discounts are less often offered on group policies is that persons within groups are rarely examined or have their smoking status verified (Brailey 1980). A second approach has been to investigate claims made by nonsmokers. When con- fronted with a claim from an individual who has misrepresented his or her smoking status, insurance companies have usually done one of the following: (1) reduced the benefit to the amount that the premium actually paid would have purchased for a smoker, (2) paid the claim in full, (3) returned the premiums paid with interest, (4) deducted the premium differential from the benefits, or (5) rescinded the policy and refused to pay. How often insurers use each of these options is not known, but the last option, by far the most severe deterrent to misrepresentation, has recently garnered much industry support (Lyons 1986). It has also been upheld in the courts. In a January 4, 1988, decision in Mutual BenefitLife Insurance Company v. JMR Electronics Corp., the U.S. District Court of the Southern District of New York absolved the insurer of liability for a policy where the insured had misrepresented his smoking status: To allow recovery would condone such fraudulent Statements, for applicants would have everything to gain and nothing to lose by gambling on getting full coverage and at worst 545 getting the coverage they are actually entitled to (Tobacco Products Litigation Reporter 1988). In May 1988, the U.S. Court of Appeals upheld that opinion (Hagedom 1988). Current Status of Premium Differentials In 1987,89 percent of 215 companies responding to an industry survey reported that they offered health-behavior-related discounts on individual life insurance policies; 14 percent also offered them on group life insurance policies. Almost all of these health- behavior-related discounts included discounts to nonsmokers (Center for Corporate Public Involvement 1987). Thirty percent of all individual life insurance policies purchased in the United States and 39 percent of the amount of coverage are so-called universal life policies, which offer the policyholder the option of varying the amount of coverage or the timing of premium payments (ACLI 1986). All of the top five life insurers, which as a group are responsible for 23.4 percent of life insurance premiums generated in the United States, offer nonsmoking discounts on universal policies, varying by the age of the insured by as much as 30 percent (A.M. Best 1987a). Nineteen of the top 25 companies, respon- sible for 46 percent of the total amount of life insurance premiums, offered universal policies in 1987 (A.M. Best 1987a). Of those 19 companies, 16 gave discounts to non- smokers, some as high as 40 percent for both males and females. Discounts varied by the age and sex of the insured (Table 15). The discounts were smallest for younger per- sons, increased steadily to a peak at age 45 years, and dropped slightly for older in- dividuals. At all ages, discounts were larger for men than for women, The average dis- counts for newly insured males and females in 1987 ranged from 12.5 to 22.5 percent. TABLE K-Average premium discount (%) offered to nonsmokers purchasing universal life insurance policies, 1986-87 Average age (years) 2s 35 45 55 Male 14.5 IS. I 22.5 Female 12.5 14.3 17.0 NOTE. D~\counts bawd on the m,n,mum ilm~unt of ~nwrance that can be purchased SOURCE: A.M. Beat (1987~3,. 20.4 16.5 The average dollar amount of discounts varied not only by sex and age but also by policy amount (Table 16). Savings for nonsmokers increased with the amount of the policy and the age of the insured, and they were larger for men than for women. The average size of an ordinary life insurance policy in force in 1986 was 25,538 dollars (ACLI 1987). On a 25,000 dollar policy written for males, the annual savings in premium cost ranged from 15 dollars at age 25 to 114 dollars at age 55. Savings on the same size policy written for females varied between 10 dollars at age 25 and 61 dollars 546 TABLE 16.-Average difference ($) between annual premiums paid by smokers and nonsmokers purchasing universal life insurance policies, 1986-87 Age (years) Policy amoum 2s 35 45 s5 $25.000 policy" Male Female $50,000 policyh Male Female I5 30 72 114 IO IX 39 61 4x 79 170 299 34 55 IO9 192 NOTE. Figures are baxd on polx~r\ offered by the 25 largest life muren `Average value of an ordmary (indiwdual) hfe insurance p+hcy in force m 1986 ud\ 3.538 dollar\ (ACLI 1987). Not all companies offer th!\ amount of co~rape hAverage value of an ordinary lmdrvldual) life ~nrurance policy purchawd in 19X6 wa\ 55.535 dollars (ACLI 1987). SOLRCE: A.M. Best (19x76). at age 55 (A.M. Best 1987a). The average size of ordinary life insurance policies pur- chased in 1986 was 55,535 dollars (ACLI 1987). Annual savings on a 50,000 dollar policy averaged from 48 dollars at age 25 years to 299 dollars at age 55 in men, and from 34 dollars at age 25 years to 192 dollars at age 55 in women (A.M. Best 1987a). Health Insurance Approximately 85 percent of Americans are covered by health insurance, which is most frequently offered by commercial carriers, Blue Cross-Blue Shield (BC/BS) plans. and health maintenance organizations (HMOs). Unlike life insurance, which is largely sold to individuals and families, 80 percent of health insurance is purchased on a group basis, usually as an employment benefit (Health Insurance Association of America (HIAA) 1987). As a result, these policies are seldom tailored to individual health profiles or health risks to the degree common in individual life insurance underwriting, where a physical examination is typically required before a policy is written. In keeping with this situation, smoker-nonsmoker premium differentials are much less commonly offered by health than by life insurers, as described below. Current Status of Premium Differentials Individual health insurance policies are far less common than group plans. They ac- count for only 20 percent of the health insurance market (HIAA 1987). The most com- plete study of premium differentials for individual health and disability policies was conducted in 1987 by NAIC (NAIC 1987a,b,c,d), which sent a survey to all 603 car- riers offering individual health and disability insurance in Illinois and all BC/BS plans in the United States. Seventy-six percent of commercial carriers and 77 percent of 547 BUBS plans responded. Fourteen percent of the commercial carrier respondents either offered discounts to nonsmokers or imposed surcharges on smokers for health (hospi- tal-medical) or disability (loss of income) policies. Sixteen percent of BC/BS plans offered discounts to nonsmokers on hospital-medical policies. Average nonsmoker discounts on health insurance offered by commercial carriers ranged from 9 to 15 per- cent, with an industry average of 10 percent. Average discounts offered by the BC/BS plans ranged from 8 to 10 percent, with an industry average of 9 percent. For disability policies, the average nonsmoker discount ranged from 3 to 14 percent, with an industry average of 8 percent, whereas the average smoker surcharges ranged from 10 to 14 per- cent, with an industry average of 13 percent. Health insurers are much less likely to offer nonsmoker discounts with their group health products, despite an NAIC resolution supporting premium differentials in group as well as in individual health policies (NAIC 1985a). In 1980, Provident Indemnity Life Insurance Company became the first to use smoking as a risk factor in establishing health insurance premiums for small groups (less than 25 employees) (Hellauer 1988). Few insurers have followed suit. The use of smoking status in the calculation of premiums for HMOs has been slowed by Federal regulations. Federally qualified HMOs were required by the original HMO Act of 1973 (Public Law 93-222) to calculate their group premiums by community rating, reflecting the health cost experience of the overall community, not of special groups such as young, healthy employees. In the HMO Amendments of 1981 (Public Law 97-35) Congress modified that requirement and allowed HMOs to become more competitive by setting their community rates by class. Classes subsequently permitted by the Secretary of Health and Human Services include age, sex, family size, and in- dustry of the insured. Because smoking status is not one of these, each HMO must in- dividually petition the Federal Government to use smoking as one of its classification factors. As of March 1988, only one had applied for permission and received it. The Contra Costa Health Plan in 1987 became the first federally qualified HMO to use smoking as a factor in calculating its group health premiums. To do so, it received ap- proval by the Office of Prepaid Health Care, Department of Health and Human Ser- vices. Contra Costa based its request, and the Federal office its approval, on a study (Brink 1987) that reported that nonsmokers incurred 18.5 percent lower health care costs than smokers (Contra Costa Health Plan 1987). In summary, as of 1987, approximately one in seven commercial health carriers and BC/BS plans offered nonsmoking discounts on individual policies; these discounts ranged from 3 to 15 percent. A few carriers have introduced discounts of 2 to 3 per- cent on group policies where certain percentages of the groups are nonsmokers. Only one federally qualified HMO offers a nonsmoker discount; it is approximately 5 per- cent of premium cost. Factors Influencing Decisions About Premium Differentials Several factors have contributed to the slower development of smoker-nonsmoker premium differentials by health and disability insurers compared with life insurers. First, there are fewer actuarial data to document that nonsmokers incur fewer health 548 care costs. Second, most health insurance is purchased on a group basis, which makes calculating discounts more difficult and makes validation of smoking status nearly impossible because no individual examination is undertaken. Third, as discussed above. current Federal regulations for HMOs preclude the use of smoking status in calculating premiums. Health insurers have offered nonsmoker discounts with little supportive actuarial ex- perience that nonsmokers incur fewer claims. Many insurers have not developed such data because they have not had the ability to separate the claims experience of smokers from nonsmokers. In addition, smaller companies may not have the statistical resour- ces to collect or analyze such data. In one recent survey, only 32 percent of commer- cial carriers with premium differentials and 70 percent of BC/BS plans had the ability to develop the appropriate actuarial data (NAIC 1987~). The first major compilation of claims data was made in 1987 by NAIC (1987~). It supported smoker-nonsmoker premium differentials in most cases. Analysis of the claims experience of eight commercial carriers justified a nonsmoking discount of 28 percent on hospital-medical policies, whereas a similar analysis of five BC/BS plans justified a l9-percent discount (Table 17). Claims data from all five BC/BS plans jus- tified nonsmoking discounts that were more than or equal to that offered. The ex- perience was not so clearcut for commercial carriers. The data from one company, with more than half of the total claims experience, supported a larger discount. However, claims experience justified nonsmoker discounts for only three of the seven smaller companies. This inconsistency may be explained by the misclassification of smokers in the "nonsmoker" policyholder category. This is suggested by the fact that only 20 percent of all adjusted earned premiums were held by policyholders classified as smokers, a much lower percentage than the prevalence of smoking in the general population. This discrepancy may result from smokers misrepresenting their status, TABLE 17.4ummary of smoker-nonsmoker health and disability claims experience Adjusted earned premiums ($) Loss ratio= Nonsmoker Smoker Nonsmoker Smoker Hospital/medical insurance Commercial carrier Blue Cross-Blue Shield Disability insurance Commercial carrier h'onsmoker discount Smoker surcharge Blue Cross-Blue Shteld 120.694.007 29.857.057 49.1 68.7 55.79 I .022 32.449.964 71.6 88.2 I l/W,976 3,931,357 30.4 25.1 50.404.495 $,182,015 31.3 61.1 26.226.456 10322.819 76.9 104.8 aRatio of claims incurred to earned premiums. multtplied by 100. A loss ratm of 100 indicates that chms mcurred equal earned premiums. SOURCE: NAIC (1987~) 549 from excessively lenient eligibility standards for nonsmoker status, or from certain plans having an excess number of older former smokers who had quit smoking because of smoking-related illness. For disability insurance policies, a nonsmoking discount of 25 percent was justified by the analysis of seven commercial carriers and one BC/BS plan (Table 17). However, as with hospital-medical policies, the claims experience of a single large insurer over- whelmed those of the others. Only one of the other carriers had experience that jus- tified a discount. On the other hand, analysis of claims data from the five commercial carriers that charged smokers a premium surcharge rather than offering nonsmokers a discount supports these increased rates for smokers. Another reason health insurers have been reluctant to offer nonsmoking discounts is that most insurance is purchased by groups. Premiums paid by groups are commonly "experience rated"; premiums paid in a given year are based largely on the overall costs of claims incurred by the group in the previous year or years. In theory, the experience rating mechanism should eventually result in lower premiums to groups with relative- ly more nonsmokers, if their health care costs are in fact lower than those of smokers. A group with fewer smokers should incur fewer health care costs, which should be reflected in their subsequent premiums. Adding a premium discount based on the proportion of nonsmokers in the group simply adds administrative problems with deter- mining and validating the proportion of nonsmokers in the group. Finally, because the difference in health care costs between smokers and nonsmokers differs across various age groups, computation of discounts is complicated and must involve adjustment by the age mix of the employee group (Hellauer 1988). Property and Casualty Insurance There is a clear rationale for offering nonsmoker discounts on homeowner policies. Between 198 1 and 1985, smoking materials caused 7.1 percent of all home fires, 8.0 percent of all home fire property damage, and 3 1.3 percent of all home fire civilian deaths (National Fire Protection Association 1987). In 1985 alone, smoking materials in the United States caused almost a quarter million home fires. Associated with those fires were 1,703 deaths, 3,997 injuries, and 422 million dollars in direct property damage (Hall 1987). Smoker-nonsmoker premium differentials on auto insurance are based on studies demonstrating that nonsmokers have fewer motor vehicle accidents. Farmers' In- surance Group, the first property and casualty insurer to offer these discounts, instituted its nonsmoker discounts because of an early study reporting an association between smoking and vehicular accidents (Adams and Williams 1965, 1966). Farmers' own in- ternal study of several thousand of its policyholders revealed that its nonsmokers had a lower accident rate and fewer claims than smokers. Subsequent claims experience has confirmed the original findings, as has nonindustry research (McGuire 1972; Grout et al. 1983; DiFranza et al. 1986). The specific reason for the better safety record of nonsmokers is not clearly under- stood, and the relationship may not be causal. Several potential explanations for smokers' higher accident rate have been suggested: (1) smoking while driving may 550 result in less attentive driving; (2) smokers may engage in more risk-taking behavior in operating their vehicles; (3) smokers use alcohol and illegal drugs more frequently than nonsmokers; and (4) nicotine or some other constituent of cigarette smoke may impair complex behaviors such as driving (DiFranza et al. 1986). In the industry's view, whether there is a causal link between smoking and motor vehicle accidents is irrelevant; the better safety record of nonsmokers has been shown repeatedly and is the basis for the discounts. Periodic reviews by Farmers' have been kept proprietary but support continuing discounts for nonsmokers (Clemans 1988). Similarly, Hanover In- surance Group's experience-that smokers have a 24percent higher rate of claims than do nonsmokers-demonstrates that actuarial differences support premium differentials (DiFranza et al. 1986). The first property and casualty insurer to offer premium discounts to nonsmokers, the Farmers' Insurance Group of Companies, includes the third largest private pas- senger auto insurer and the third largest homeowner insurer in the United States. Non- smoking discounts were offered on auto policies beginning in 197 1 and on homeowner policies in 1974 (Clemans 1988). This company remains the only 1 of the 10 leading writers of homeowner and private passenger auto insurance to offer discounts to non- smokers on both types of policies (Wasilewski 1987a,b). Currently Farmers' offers nonsmokers and former smokers who have not smoked for at least 24 months discounts of 3 to 7 percent on homeowner policy base rates and discounts of 10 to 25 percent on auto policies, depending on State of residence. Other insurers that offer nonsmoker discounts on auto policies include Preferred Risk Group and Hanover Insurance Company (NAIC 1987e). On the basis of its own claims experience, Hanover increased discounts from the original 5 percent, instituted between 1974 and 1978, to the current 10 percent. The company provides the discounts on both auto and homeowner policies nationwide, except in States where regulatory bodies prohibit them. Fifty-two percent of its policyholders have nonsmoker discounts (Wein- man 1988). Factors that have prevented the more widespread industry adoption of nonsmoker discounts on auto and homeowner policies include difficulties in the verification of smoking status and regulations in some States that prohibit nonsmoking discounts or prohibit rescission of benefits in cases of misrepresentation. Effects of Insurance Premium Differentials on Smoking Behavior Insurers' use of smoking behavior as a factor in setting premiums may have both economic and educational effects that discourage smoking. Premium differentials may serve as economic disincentives for smoking because they effectively, if indirectly, in- crease the cost of smoking cigarettes. This may reduce tobacco consumption and en- courage cessation. In addition, payment of a higher premium may reinforce smokers' knowledge of the harm caused by smoking and serve as another social message to smokers about the disadvantages of smoking and desirability of cessation. It is less likely that insurance premium differentials will have a strong role in discouraging smok- ing initiation, because most individuals make decisions about smoking during adoles- cence, before many purchase insurance. 551 Empirical studies, reviewed in the previous section, have demonstrated that changes in cigarette prices affect tobacco consumption. Elasticities have been calculated for the effect on demand of changes in the price of cigarettes at the point of purchase, but not for economic policies that indirectly alter a smoker's costs. No empirical studies have examined the effect on smoking prevalence or cigarette consumption of higher in- surance premiums for smokers or of reimbursement for the cost of smoking cessation programs. The potential educational effects of premium differentials on public knowledge or attitudes have not been studied; effects will be difficult to distinguish from other social influences discouraging smoking. The expected effects of excise taxes and premium differentials are not identical, be- cause of inherent differences between buying cigarettes and purchasing insurance. A smoker can respond to higher excise taxes by reducing consumption without giving up smoking, but a smoker can reduce insurance premiums only by stopping smoking al- together. Insurance premium differentials may be less powerful economic incentives than are changes in actual cigarette prices, because higher insurance premiums do not translate directly into an increase in the price of cigarettes at the point of sale. Further- more, a smoker buys cigarettes far more often then he or she pays insurance premiums. On the other hand, the magnitude of an insurance premium differential is greater than a tax-induced change in the price of a pack of cigarettes. Other factors may blunt the impact of insurance premium differentials based on smok- ing behavior. First, smokers may forget or not even know that they are being penal- ized if there is no reminder of that fact on their insurance bill or payroll receipt. Some life and health insurers may not inform smoking policyholders that they use control- lable risk factors when setting premiums. The educational value of the premium dif- ferential is largely lost after the policy is issued if periodic reminders of the basis of premium are not sent with the insurance bill. Furthermore, part of the economic incen- tive is lost if no mechanism exists for smokers who quit smoking after the policy is is- sued to become eligible for a lower premium. Second, the individual may not pay the full cost of insurance premiums. Health and life insurance is often included in employee benefit packages, with the employee paying only a portion of the total premium. The employee's contributions to the insurance premiums may be small or nonexistent. Third, most health insurance policies are group policies that do not include smoker- nonsmoker differentials. Those that do set premiums based on the smoking prevalence of the group, so that a smoker's higher premium cost is partly borne by nonsmoking members of the group. Finally. because not all insurers offer nonsmoking discounts, even smokers purchasing individual insurance have the option of purchasing insurance from companies that do not tie premiums to smoking behavior. Health Insurance Coverage for Smoking Cessation Treatment Insurers who reimburse for the costs of attending a smoking cessation program or of purchasing a cessation aid effectively reduce the cost of quitting smoking, thereby removing a financial disincentive to quit. This reimbursement may also serve as an economic incentive to the provider of the treatment to offer more services, thereby in- creasing availability of cessation treatment. 552 Currently, few health insurance carriers cover the costs of smoking cessation programs. Only I I percent of 263 health insurance carriers surveyed in 1985 included smoking cessation treatment as a covered benefit. Insurers that reimbursed for smok- ing cessation programs did so only to treat established smoking-related diseases, not to prevent these diseases (Gelb 1985). Among BC/BS plans, smoking cessation is usual- ly not an approved benefit for groups unless it is included as part of a wellness pack- age purchased by the employer (Moore 1988). A similar situation holds for the reim- bursement of pharmacologic treatment to promote smoking cessation. Health insurers usually limit reimbursement of drug treatment to drugs that are approved by the Food and Drug Administration (FDA) and are prescribed for treatment of a diagnosed medi- cal illness in a patient who has prescription drug coverage. Currently, nicotine polacrilex gum is the only drug approved by the FDA to aid in smoking cessation. Nevertheless, its prescription is usually not reimbursable for smokers who do not al- ready carry a diagnosis of a smoking-related disease (Moore 1988). Several barriers impede greater coverage of smoking cessation treatment by health insurers. Traditionally, health insurance has covered the cost of treating, not prevent- ing, illness. A major reason for this was that insurers' were not convinced of the finan- cial feasibility of covering preventive services. however socially desirable such a policy might be. Similarly, insurers have only gradually come to cover the costs of drug and alcohol treatment (American Hospital Association 1987). Smoking cessation programs might be classified as either preventive care or as treatment of substance abuse. Regard- less of how it is classified, it appears that insurers are not convinced of the financial feasibility of covering smoking cessation treatment. In part, this stems from a lack of data with which to make appropriate calculations. To be in the health insurers' economic interests, the cost of a treated smoker (the cost of cessation treatment in addition to other health claims) must be less than the claims paid to a smoker who does not attend a cessation program. This calculation requires the estimation of several factors that have not been well studied, including the difference in annual health care costs of current and former smokers, the costs and success rates of different smoking treatments, the likelihood that a smoker will quit without a program, the length of time that the smoker remains insured by the same insurer, and the discount rate at which future costs are evaluated. Furthermore, because health in- surance is usually provided by employers, and employees change jobs, it is possible that the health insurer who pays for a policyholder's smoking cessation may not reap the benefits of any reduced health care costs that individual experiences. Even if reimbursement for smoking cessation treatment were shown to be financial- ly advantageous for insurers, practical problems would remain to slow the implemen- tation of reimbursement. For example, insurers would have to define which programs, drugs, or other aids would be covered and which providers would be reimbursed. Summary The Public Health Service's 1990 Health Objectives for the Nation include twogoals for smoking and insurance: 553 1. By 1985. the collection and publication by insurers of actuarial experience on differential life experience and hospital utilization by specific cause among smokers and nonsmokers, by sex; 2. By 1990, differential insurance premiums for smokers and nonsmokers by major life and health insurers (US DHHS 1981 b. 1986d). Progress has been made toward meeting both of these goals. The actuarial basis for life insurance premium differentials has been established, and data are beginning to be collected on hospitalization rates (US DHHS 1986d). However, more information on the total health care costs of smokers and nonsmokers, including ambulatory care, would help to establish a firmer rationale for offering premium discounts for health and disability insurance and for covering the costs of smoking cessation treatment. The second objective has been partially met. Although nearly all life insurers offer non- smoker discounts, only a minority of health insurers do. This is partly because, unlike life insurance, most health insurance is sold to groups, which, as discussed above, presents greater operational obstacles to the development and implementation of non- smoker discounts. Much of the accomplishment to date is a result of the insurance industry's voluntary initiatives, which seem likely to continue (Walsh and Gordon 1986). Collection and publication of claims experience by industry groups such as the Society of Actuaries are steps that could be taken to increase the use of smoker-nonsmoker premium dif- ferentials in health and disability insurance. State and Federal governments have the opportunity to act as facilitators and educators to encourage insurers-aspecially health insurers-to offer premium discounts to nonsmokers and to reimburse for smoking ces- sation treatment. Government officials at both levels could act to remove those legal barriers that prevent insurers from adopting nonsmoker discounts and to disseminate research findings that support these discounts and coverage for smoking cessation. HMOs may be more likely to use smoking status as a factor in setting premiums if cur- rent Federal restrictions preventing it, except on a case-by-case basis, are removed. Although the insurance industry is State regulated, regulation has generally been limited to ensuring the financial integrity of insurers. Some have suggested that aState- regulated industry could be subject to other controls in the public interest (Hiam 1987/88). Since the 1960s. all States have mandated certain types of coverage that in- surers must provide as a condition of doing business in the State (Glantz 1985). State health insurance commissioners or legislatures could require smoker-nonsmoker premium differentials as a condition for writing policies within their States. In several States, bills have been filed that would mandate insurance premium differentials, al- though none have been enacted (CDC 1980, 1981). The few remaining life insurers without premium differentials might be encouraged to adopt them if the NAIC model rule regarding smoker-nonsmoker mortality tables were adopted by legislatures and insurance commissioners in the States that have not yet done so (NAIC 1985b). Publicly funded health insurance such as medicare and medicaid is more directly amenable to government action. Measures have been introduced into Congress that would restructure medicare premiums to offer discounts to nonsmokers and to cover preventive care, including smoking cessation treatments (past bills include S. 357 and S. 358 in 1985). In the preface to the 1988 Surgeon General's Report (US DHHS 1988). 554 the Surgeon General stated, "Treatment of tobacco addiction should be more widely available and should be considered at least as favorably by third-party payors as treat- ment of alcoholism and illicit drug addiction." Research to establish the cost-effective- ness of preventive care coverage by insurers, especially for smoking cessation, would be useful in reaching that goal. PART III. DIRECT RESTRICTIONS ON SMOKING The policies discussed so far discourage tobacco use indirectly, either by educating the public about the health hazards or by creating economic disincentives to smoke. A third category of public policies acts more directly; their aim is to reduce smoking by limiting either public access to tobacco products or the opportunity to use them. The most extreme potential policy in this category would be a total ban on the sale, posses- sion, or use of tobacco products, analogous to current statutes on such other addictive drugs as heroin or cocaine. Short of that are policies that restrict or ban smoking in specific places, such as indoor public places and workplaces, prohibit the sale of tobac- co products in particular places, or prohibit the use of tobacco by a particular group of individuals, namely minors. Tobacco occupies a position unlike that of any other consumer product (or phar- maceutical agent) in the United States; it was widely used, socially accepted, and economically vital to strong agricultural and manufacturing interests long before its ad- verse health effects and addictive potential were appreciated. These facts have made the most stringent regulatory option-total ban on sale or use-impractical and un- desirable, Such a policy did exist in some States in the early part of this century, when a moral crusade against cigarettes like that against alcohol led to the passage of laws in a dozen States banning the sale of tobacco products (Walsh and Gordon 1986). These laws proved difficult to enforce and were all repealed by 1927. Although a total prohibition on tobacco is unlikely, there is a long tradition of restrict- ing children's and adolescents' access to tobacco. According to established social con- vention, the rational use of certain products, like tobacco, alcohol, or the material sold in adult bookstores, requires an informed decision that minors are deemed to be too young to make. The growing awareness of the addictive nature of nicotine (US DHHS 1988) strengthens that convention in the case of tobacco products. Policies limiting smoking in public places or workplaces have a different rationale; they restrict the smoker's behavior for the sake of the nonsmoker. Although the primary aim of these policies is to protect the nonsmoker from the health consequences of involuntary tobac- co smoke exposure, they may have the side effect of discouraging tobacco use by reduc- ing opportunities to smoke and changing public attitudes about the social acceptability of smoking. The direct restrictions discussed so far address the consumer (smoker or potential smoker). Policies directed at tobacco manufacturers include regulations on the con- tents of tobacco products to reduce their harmfulness. Such policies have the inherent difficulty of defining an acceptable level of tobacco or smoke exposure because, as documented in Chapter 2, there is no known safe level of tobacco use. 555 This Section considers three types of policies that put direct restrictions on smoking or tobacco products. First, it examines policies that restrict smoking in public places and workplaces, including both government actions and policies initiated in the private sector. Second, policies that would restrict minors' access to tobacco products are dis- cussed. Finally, the Section considers the treatment of tobacco products by Federal regulatory agencies. Government Actions to Restrict Smoking in Public Places and Workplaces In 1986. the Surgeon General's Report documented "a wave of social action regulat- ing tobacco smoking in public places" (US DHHS 1986b) that was then occurring. It reviewed public and private policies designed to protect individuals from environmen- tal tobacco smoke (ETS) exposure by regulating the circumstances in which smoking is permitted. Since the 1986 Report, the pace of action appears to have increased in both the public and private sectors. Restrictions on smoking in public places are the result of government actions at the Federal, State, and local levels, particularly State and local legislation. The Federal Government has largely acted via regulatory mechanisms and has addressed smoking in Federal facilities and in public transporta- tion. The major exception is recent congressional legislation restricting smoking on commercial airliners. Accompanying government actions are a wide range of private initiatives; these have become widespread in this decade. Smoking restrictions in the workplace are the most common private sector action, but hospitals, schools, hotels and motels, and other institutions are also adopting no-smoking policies. This trend reflects two forces: a growing scientific consensus about the health risks of involuntary smok- ing (US DHHS 1986b; NAS 1986b) and changing public attitudes about the social ac- ceptability of smoking. As documented in Chapter 4, a growing majority of Americans now supports the right of nonsmokers to breathe smoke-free air and favors restricting smoking in public places and the workplace. This Section addresses the scope and impact of government actions to restrict smok- ing in public places and workplaces. Private initiatives to regulate smoking are dis- cussed in the subsequent section. Both sections summarize and update the findings of Chapter 6 of the 1986 Surgeon General's Report. Smoking Restrictions in Public Places A public place has usually been defined as any enclosed area to which the public is invited or in which the public is permitted (Americans for Nonsmokers' Rights (ANR) 1987a. b). This broad definition encompasses a diverse range of facilities that share the characteristic of being indoor enclosed spaces that permit the general public rela- tively free access. Beyond this general agreement, laws and regulations differ in their operational definition of public place. They even differ in the degree to which the con- cept is specified. Public place is commonly interpreted to include government build- ings, banks, schools, health care facilities, public transportation vehicles and terminals, retail stores and service establishments, theaters, auditoriums, sports arenas, reception areas, and waiting rooms. Although they fit the definition, restaurants are usually 556 treated separately in these laws. Private businesses are also separately addressed, and private homes specifically excluded. As noted in the 1986 Surgeon General's Report, the degree to which smoking is restricted in public places also depends on history or tradition, the level of involuntary smoke exposure that is likely (determined by size, ventilation, and amount of smok- ing), the ease with which smokers and nonsmokers can be separated, and the degree of inconvenience that smoking restrictions pose to smokers. Public places may be owned by government or private interests. As a consequence of these factors and others, there is considerable variability in the methods by which new regulations have been proposed and the ease with which they have been adopted. Smoking restrictions have been most easily adopted in public facilities, especially facilities where smoking has traditionally been prohibited for safety reasons, where smoking is not associated with the activity taking place, and where the public spends limited time. Such considerations explain the relatively slower acceptance of smoking restrictions in restaurants. bars, and private businesses (US DHHS 1986b). Federal Actions Until recently, actions at the State and local Government level- primarily legisla- tion-accounted for the bulk of smoking regulations in public places. Since 1986, the Federal Government has taken new steps, including the first congressional actions (covered below), to restrict smoking in two categories of public places: transportation facilities and Government worksites. The Federal Government has enacted no restric- tions on smoking that apply to a broad range of nongovernmental public places. State Legislation Although the health hazards of smoking were not widely appreciated until the 1960s the fire hazard was recognized much earlier, giving rise to the first State laws regulat- ing smoking. For nearly a century cigarette smoking has been regulated by State law to prevent fires and prevent the contamination of food being prepared or packaged for public consumption. This was the extent of State law in 1964, when the first Surgeon General's Report was issued. At that time, 19 States prohibited smoking near ex- plosives or fireworks, in or near mines, or near hazardous fire areas. Five States banned smoking in food processing factories or restaurant preparation areas (US DHHS 1986e; BNA 1987). These laws affected only a small proportion of the population and did not alter smoking in public places. In addition, by 1964, 13 States had adopted some restrictions on smoking in specific public places. This legislation, also enacted to prevent fires, had some potential to reduce smoking in public places, even though that was not its primary intent. Six States permitted employers to ban smoking in mills and factories as long as signs were posted, and six States restricted smoking in public transportation vehicles or terminals or in auditoriums and theaters. The remaining laws sought to discourage smoking by children: three States prohibited smoking (at least by minors) on school grounds, build- ings, or buses (US DHHS 1986b: BNA 1987). This remained the basic extent of smok- ing restrictions through the 1960s as the health hazards of smoking became widely known. In the 197Os, a new form of smoking legislation emerged, differing in both intent and content. The specific rationale behind this legislation was the safety and comfort of nonsmokers, reflecting growing interest and, later, scientific evidence of the health hazards of passive smoke exposure (US DHHS 1986b; BNA 1987). These Clean In- door Air Acts regulated smoking in a larger number of places and for the first time man- dated smoking restrictions in private facilities. Over time, the language of the laws be- came more restrictive, first permitting, then requiring nonsmoking sections, then making nonsmoking the principal condition, with an option for smoking areas. The legislation was developed and promoted by the growing nonsmokers' rights movement, for the most part a grassroots movement consisting of Californians for Nonsmokers' Rights (later changed to Americans for Nonsmokers' Rights) and a number of other State and local groups, many using the name Group Against Smoking Pollution (GASP). These organizations focused their attention on achieving legislative goals at the State and local levels (see Chapter 6). In doing so, they sometimes worked in con- junction with the voluntary health organizations. The prevalence and content of State legislation on smoking changed dramatically over the ensuing two decades (Figure 6). Current smoking restrictions in public places are largely the product of legislation enacted at the State level beginning in the early 1970s (Tables 18 and 19). Between 1970 and 1979, smoking restrictions were enacted by legislatures in 24 additional States; in 7 others, existing restrictions were extended. In 1975 alone, 13 States enacted laws, more than double the number that had done so in the previous decade (1964-74). Not only the quantity but also the content of these laws was different. In 1973. Arizona became the first State to restrict smoking in a number of public places, and the first to do so explicitly because smoking was a public health hazard. Although not com- prehensive by current standards, the law was regarded as comprehensive when passed. The first State law to include smoking restrictions in restaurants was passed in Connect- icut in 1974. Coverage of worksite smoking also began at this time with the landmark Minnesota Clean Indoor Air Act. Passed in 1975, it extended smoking restrictions to many public places, restaurants, and both public and private worksites. It became the model for other comprehensive State legislation that began to be passed in the mid- 1970s. After a relative lull in the early 198Os, there was another notable increase in passage of State laws in the middle of the decade, probably reflecting greater scientific consen- sus about the health consequences of involuntary smoking. By the end of 1985,41 States and the District of Columbia had passed laws regulating smoking in at least one public place (US DHHS 1986b). In 1987, the year after two national groups separate- ly reviewed the evidence on passive smoking and reached similar conclusions about its health effects (US DHHS 1986b: NRC 1986b), 20 States passed legislation regulating smoking, more than ever before in a single year. Moreover. the legislation being passed grew more comprehensive in its coverage. From the start of 1985 to the end of the 1987 legislative sessions, there was a doubling in the number of States restricting smoking 558 Numkrot States with bwsinsfk~ct j- I- i- I- i- 41 4( 3: 3( 2: 2( 1: I( 5 0 l- j- 1960 1964 1970 1975 1980 1985 1987 Year 45 40 35 30 25 20 15 10 / 5 0 FIGURE &-Prevalence and restrictiveness of State laws regulating smoking in public places, 1960-1987 NOTE: Index of restricrweness: 0 = none. no \tatewde re~tnctions: 0 25 = nommal. State regulates smoking m one to three pubhc places, excluding restaurants and private workutes: 0.50 = barlc. State regulates vnoking m four or more pubhc places. excluding restaurants and private worksttes: 0.75 = moderate. State regulates vnoking m restaurants but not pnvate worksltes: I SKI = extensive. State regulate\ smoking m private work~e\. SOURCE: US DHHS (1986b); unpublished data. OSH. 559 TABLE M.-State laws restricting smoking, 1964-87 Year Number of States Number of States Number of States Number Cumulative restricting restricting restricting of States number of smoking in smoking in smoking in enacting States with restaurants private worksites public worksites laws laws Enacting/cumulative Enacting/cumulative Enacting/cumulative 1964 196.5-56 1967-68 1969-70 1971 1972 1973 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 1985 1986 1987 0 0 2 0 2 1 3 3 13 5 6 2 6 I 7 1 4 3 9 6 20 13 13 14 14 16 17 20 22 1 1 29 2 3 1 32 3 6 I 35 2 7 0 36 1 8 0 38 2 10 2 38 0 10 0 39 I II 0 39 0 11 0 40 1 12 1 41 1 12 0 42 4 16 4 42 1 16 3 43 (84%") 10 23 (45%) 4 4 4 I 5 3 8 1 9 2 11 0 II 3 13 0 13 2 15 2 15 5 20 4 22 15 31 (61%) NOTE: Includes the Dwnct of Columbia. aPercentage of total States. SOURCE. BNA (19X71: US DHHS l1986b): indwdual State law. in private workplaces (from 4 to 13), public workplaces (15 to 3 l), and restaurants (10 to 23) (Table 18). Recently adopted laws are more likely to include three provisions that strengthen the position of nonsmokers: ( 1) protection against discrimination for supporters of worksite smoking policies, (2) priority to the wishes of nonsmokers in any disagreement about the designation of an area as smoking or nonsmoking, and (3) permission for cities and counties to enact more stringent ordinances. In 1985, Maine was the first of five States to adopt a nondiscrimination provision, which makes it illegal for employers to dis- cipline, discharge, or otherwise discriminate against employees who assist in the im- plementation of nonsmoking policies (BNA 1987). The second provision first appeared 560 TABLE 19.Ctate laws regulating smoking in public places and worksites, through October 1,1988 AL AK AZ AR CA CO CT YEAR(S) 1975 1973.81 1977 1971.76 1977 1973.74 LEGISLATION I984 1986.87 1985. x7 19x0. Xl 1985" 1983.87 ENACTED 19x2. x7" PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationh Elevators Indoor cultural or recreational facrlitieh Retail storesd Restaurantse Schools Hospitals Nursing homes Government buildings Public meeting rooms Libraries Other' X X' x X X X X X X X X X X X X X X X X X X XL X X X X X X X X x x X X X x X' x X X X x X X X X X x X WORKSITE SMOKING RESTRICTIONSg ' Public worksites D B.D ED l3 C,D" C Private worksites A C IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers X X ENFORCEMENT (PENALTIES) Against smokers' For failure to post signs' X X X X X X X LOCAL ORDINANCES Specifically allowed Specifically preempted X X OVERALL RESTRICTIVENESS OF STATE LAWk 0 3 2 2 3 2 4 561 TABLE 19.-Continued DE DC FL GA HI ID IL YEAR(S) 1960 1975.79 1974,83 1975 1976,87 1975,85 LEGISLATION 1988 198.5 ENACTED PL'BLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationb X Elevators lndoor cultural or recreational facilities Retail storesd Restaurantse Schools Hospitals Nursing homes Government buildings Public meeting rooms Libraries Other' X X 2: XC XC X X X X X X X X X X X X X X X WORKSITE SMOKING RESTRICTION@ h Public worksites B.D B.D D Private worksites B.D IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers ENFORCEMENT (PENALTIES) Against smokers' X X X X X X For failure to post stgns' X X X LOCAL ORDINANCES Spectfically allowed Specifically preempted X X OVERALL RESTRICTIVENESS OF STATE LAW' I 3 4 I 3 3 0 562 TABLE 19.-Continued IN IA KS KY LA ME MD YEAR(S) 1987 1978.87 1975.87 1972 1954.81 1957,75 LEGISLATION 1988 1983.85 1987a ENACTED 1987.88 1988 PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationb Elevators Indoor cultural or recreational facilities Retail storesd Restaurantse Schools Hospitals Nursing homes Government buildings Public meeting rooms Libraries Other' X X X X X X X X X X X X X X X X X X' XC X X X X X X X X X X X X X X X X X X X X X X Xa X X WORKSITE SMOKING RESTRICTIONSg h Public worksites C.D D CD B.D B" Private worksites D BD IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers X X ENFORCEMENT (PENALTIES) Against smokers' X X X X X X For failure to post signs' X X X LOCAL ORDINANCES Specifically allowed X X Specifically preempted OVERALL RESTRICTIVENESS OF STATE LAWk 2 4 3 I 0 4 2 563 TABLE 19.-Continued MA MI MN MS MO MT NE YEAR(S) 1947,75 1967.68 1971.75 1942 1979 1979 LEGISLATION 1987,88 197% XI 1987 1986 ENACTED I986,87 1988 PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationh xc x X X X X Elevators XC X X XC X Indoor cultural or recreational facilities X X X X X Retail storesd X X X X X Restaurantse X X X X X Schools X X X X Hospitals X X X X X Nursing homes X X X X X Government buildings X X X X X Public meeting rooms X X X X X Libraries X X Other' X X X X WORKSITE SMOKING RESTRICTIONS' h Public worksites C.Da D CD D D Private worksites C.D D D IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimmation agamst nonsmokers X X ENFORCEMENT (PENALTIES) Against smokers' X X X X X For failure to post signs' X X LOCAL ORDINANCES Specifically allowed Spectfically preempted OVERALL RESTRICTIVENESS OF STATE LAW' 3 3 4 I 0 4 4 564 TABLE 19.-Continued NV NH NJ NM NY NC ND YEAR(S) 1911.75 1981 1953 1985 1921.53 1977 LEGISLATION 1979 1986 1979 1975 1987 ENACTED 1987 1987 1985 1976 PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationh X X X Elevators X X X X Indoor cultural or recreational facilities X X X Retail storesd X X X Restaurantse X X X Schools X X X Hospitals X X X Nursing homes X X X Government buildings X X X X Public meeting rooms X X X X Libraries X X X Other' X X X X X X X X X X X X X X X X X WORKSITE SMOKING RESTRICTIONS" h Public worksites D B,C CD CD Private worksites A B B.C A IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers X ENFORCEMENT (PENALTIES) Against smokers' X X X X X X For failure to post signs' X X X LOCAL ORDINANCES Specifically allowed Specifically preempted X OVERALL RESTRICTIVENESS OF STATE LAWk 3 4 4 2 2 0 3 565 TABLE 19.-Continued OH OK OR PA RI SC SD YEAR(S) 1953,81 1975 1973,75 1927 1976 1937 1974 LEGISLATION l981,84 1987 1977 1947 1977 1987 ENACTED 1988 1981 1977 1986 PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationb X X X= Elevators X X X Indoor cultural or recreational facilities X X X X Retail storesd X X Restaurantse X X Schools X X X Hospitals X X X X Nursing homes X X X X Government buildings X X X Public meeting rooms X X X Libraries X Other' X X X X X X X X X X X X X X X X X X X X X X WORKSITE SMOKING RESTRICTIONSB h Public worksites D C.D D B Private worksites B IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers X X X ENFORCEMENT (PENALTIES) Against smokers' X X X X X X For failure to post signs' X X LOCAL ORDINANCES Specifically allowed Specifically preempted X OVERALL RESTRICTIVENESS OF STATE LAWk 2 3 3 2 4 1 2 566 TABLE 19.-Continued TN TX UT VT VA WA WV YEAR(S) 1975 1976 I892 1984 1913 LEGISLATION 1987 1979 1987 1985 1919 ENACTED 1986 1985 PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationb Elevators Indoor cultural or recreational facilities Retail storesd Restaurar& Schools Hospitals Nursing homes Government buildings Public meeting rooms Libraries Othef X X X X X X X X X X X X X X X X X X XC X XC X' XC XC X XC X X X X X X' XC X X X WORKSITE SMOKING RESTRICTIONSg h Public worksites D B.D D Private worksites D BD D A IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers X X X ENFORCEMENT (PENALTIES) Against smokers' For failure to post signs' X X X X X X X LOCAL ORDINANCES Specifically allowed Specifically preempted X OVERALL RESTRICTIVENESS OF STATE LAWk 0 2 4 4 0 4 1 TABLE 19.-Continued TOTAL STATES WI WY N % YEAR(S) 1983 LEGISLATION ENACTED PUBLIC PLACES WHERE SMOKING IS RESTRICTED Public transportationb X Elevators X Indoorcultural or recreational facilities X Retail storesd X RestaurantC' X Schools X Hospitals X Nursing homes X Government buildings X Public meeting rooms Libraries Other' 36 32 30 25 24 32 34 32 31 27 21 70.6 62.7 58.8 49.0 47.1 62.7 66.7 62.7 60.8 52.9 41.1 WORKSITE SMOKING RESTRICTIONS" h Public worksites D 31 60.8 Private worksites 13 25.5 IMPLEMENTATION PROVISIONS Nonsmokers prevail in disputes No discrimination against nonsmokers 8 15.7 5 9.8 ENFORCEMENT (PENALTIES) Against smokers' X 40 78.4 For failure to post signs' 17 33.3 TOTAL 41 80.4 LOCAL ORDINANCES Specifically allowed X 7 13.7 Specifically preempted 3 5.9 OVERALL RESTRICTIVENESS OF STATE LAW' 3 0 568 TABLE 19.-Continued NOTE: Laws clted do not include restrtctions on unokmg near explos~vea. firework?. or hazardow areas: in or near mmes; or m food preparation or handling areas of restaurants or food procewng factones. aExecutwe order. % school buses only m AR, FL, and SC. Smokmg IS prohtbtted on all forms of mtrastate transponat~on m CA. `Smoking iy never permitted m this area. %opnetorr of retad stores m CO are encouraged to establich no-smoking areas Smoking I\ prohIbIted only m grocery stores in AK, CA. CT, MA, NV, and RI. ?`ropnetors of restaurants m NJ and CO are encouraged 10 establnh no-smokmg areas. In AK, FL, HI. MI. NH. OK. RI. and WI. restaurants seating 50 or more persons must have a no-smokmg section In CA, restaurant\ in a publicly owned buildmg seating 50 or more must have a no-smokmg cectmn. In CT and MA, restaurants seatmg 75 or more must have a no-smokmg salon. `Smokmg I\ restricted mJur) rooms m AK, FL. ME, MA. MI. MN. OR. and SD: m day-care centers m .AK. AZ. AR. MA, and MN: in mdls, factones. barns. or stables m ME. MA, NV. RI. VT, and WV: m pollmg placer m NH and NY: in pnsons. at the prison offiaals dncretron. m FL and PA: and m the asbestos hazard abatement proJect m OH. `A. employer must post a stgn where smokmg is prohibtted: B. employer must have a written smoking pohcy; C. employer must have a pohcy that provtdes for a nonsmoking area: D, no cmokmg except m derignated area. Only B. C. and D count as having a worksite policy m calculation of totals. %nployers must pat sagm designatmg smoking and no-smokmg area\ m AK. MI. MN. NE. NJ. and UT public worksites. and in MN, NE, NJ, and UT pnvate worksites: in smokmg areas only in FL, ND. and WI pubhc worksltes: and in nosmokmg areas in NH and NM publtc worksites. Depending upon then pohcy. employers mu\1 post either smoking or no-smoking signs m MT public and private worksltes. Smoking 1s not re,tncted m factones, warehouse\. and similar worksites not usually frequented by the public in MN and NE. Smokmg i\ prohIbIted m any mdl or factory m which a no-smoking sign is posted in NV. NY, VT, and WV. `Persons who smoke m a prohibited area are subject to the followmg maxlmbm finer: $5, AK, KY, VT: $10, IA, OR. PA: $2@-25,CT. DE, HI, KS. NM, WI; $50. ID. ME. NH; $100. AR, CA. DC,GA. NE. NV. NY. ND. OK, RI. WV: $100 per day, WA: $200. NJ: $300, MD: $500. FL, MI; $50 or up to IO days ~a11 OT bath. MA. minor rmsdemeanor. OH; petty misdemeanor, MN; misdemeanor, MS, TX: petty offense, AZ, SD: mfractton, IN, UT. `Persons who are required IO and fall to post smoking and/or no-tmokmg signs are subject to the following maxmwn fines: $10, IA; $2&25. MT; $50, KS. NH; $100. ME, ND. OR. VT: $200. NJ; 5300. AK. DC: $500. FL. MI: $500 per day, HI, RI; ciwl actIon, WA; infraction. CT `Restnctiveness key: 0. none (no statewide restnctions); I, nommal (State regulates smokmg m l-3 pubhc places, ex- cluding restaurants and pnvate worksites): 2. basic (State regulates smokmg m 4 or more public places. excluding res- taurants and private worksites); 3. moderate (State regulates smokmg in restaurants but not pnvate worksites): 4. exten- sive (State regulates smoking in private worksites). SOURCE: BNA (1987): Tobacco-Free America Project 1987. 1988a. b: US DHHS (1986b): individual State laws. in the Minnesota Clean Indoor Act (1975) and is incorporated into statutory language in six other States. Seven States include the third provision, which specifically permits local governments to enact ordinances more stringent than the State law (BNA 1987). Conversely, following intense legislative debate that included heavy lobbying by the tobacco industry, Florida (1985) enacted a State law that preempted more stringent local laws, as have Oklahoma (1987) and New Jersey (BNA 1987). Similar legislation has been proposed in other States. By the end of 1987, smoking was restricted in at least 1 public place in 42 States and the District of Columbia. Table 19 summarizes the provisions of these laws, which most often restrict smoking in public transportation facilities (36 States), hospitals (34 States), schools (32 States), elevators (32 States), government buildings (3 1 States), and recreational facilities (30 States). As of January 1988, over 82 percent of the United States population resided in States that restricted smoking in at least one public place; this compares with a previous estimate of 8 percent in 197 I (US DHHS 1986b). Over 569 17 percent of Americans lived in States with laws requiring smoking restrictions at the worksite for nongovernment workers, whereas over half lived in States with such restrictions for State government employees. More than 40 percent of Americans live in States requiring no-smoking areas in restaurants, and two-thirds live in States that limit smoking in health care facilities. The 1986 Surgeon General's Report documented geographical variation in State smoking laws. Southern States had fewer and less comprehensive laws. This remains true (Table 20). Excluding the major tobacco-producing States (North Carolina, Ken- tucky, South Carolina, Virginia, Tennessee, and Georgia), over 80 percent of States in each region, including the South, have enacted smoking restrictions. Of the major tobacco-growing States, only Georgia, which ranked sixth in production, had enacted restrictions on smoking in any public places other than school facilities or vehicles. State laws also vary in their implementation and enforcement provisions. Health departments are responsible for policy implementation in most States (US DHHS 1986b). Nearly all States with laws (40 of 43) provide penalties for smokers who vio- late restrictions (Table 19). Seventeen States also have penalties for employers and proprietors who do not establish nonsmoking policies or post signs as required (BNA 1987). It is not known how often these penalties are actually imposed. Local Legislation As noted in the 1986 Report, efforts to pass Clean Indoor Air Laws spread from the State to the local level in the 1980s spearheaded by actions in California (US DHHS 1986b). Local ordinances generally extend the scope of smoking restrictions beyond that provided for in corresponding State laws. Usually they include provisions to restrict or ban smoking in restaurants and public and private worksites, in addition to a broad range of public places. An accurate record of local ordinances nationwide is dif- ficult to obtain because there is no single reference library for local legislation. Recent- ly, two organizations have monitored local no-smoking ordinances on a nationwide basis. Their data indicate that local ordinances are being enacted at a rapid pace. As of August 1988, ANR (1988b) identified 321 local ordinances with provisions for sig- nificant nonsmoker protection. The Tobacco-Free America Project (1988~) reported in October 1988 that 380 local communities had passed laws restricting smoking in public places. These numbers represent a nearly fourfold increase in the estimate of 89 communities with smoking ordinances in 1986 (US DHHS 1986b). The most complete information on the prevalence and content of local ordinances is available for California, where ANR has kept an ongoing compilation of laws (ANR 1988a). According to their records, the first local ordinances were passed in 1979. In 1982, San Diego became the first large California city to enact a workplace ordinance. Although not the first local action to include the private workplace, the passage of San Francisco's worksite smoking ordinance in 1983, in the face of heavily subsidized tobacco industry opposition, attracted widespread publicity and stimulated further ac- tion (US DHHS 1986b). The following year, Los Angeles passed a law requiring smok- ing policies in workplaces with five or more employees (ANR 1988a). 570 TABLE 20.-Regional variation in restrictiveness of State laws limiting smoking Mean States Mean rcstrictivenessb States with different degrees Total restrictivenessb with lawsC of laws in effect of restrictivenessb Regiona States in October 1988 N (la) October 1988 1.00 0.75 0.50 0.25 0.00 Northeast 9 .861 9 (1W .861 6 I 2 0 0 Midwest 12 .625 10 (83 ,750 3 4 3 0 2 West 13 .692 12 (92) .750 3 6 3 0 I South 17 ,324 12 (71) ,458 I 2 3 6 5 Major tobacco producer 6 ,125 3 (50) ,250 0003 3 Other I1 ,432 9 (82) .528 1 2 3 3 2 Total 51 ,583 43 (84) ,692 13 13 11 6 8 `Regions are defined by the Bureau of the Census Northeast: Cf, MA, ME, NH. NJ, NY, PA, RI. VT Midwest: IA, IL. IN, KS, MI, MN, MO. ND. NE.OH, SD, WI West: AK, AZ. CA, CO. HI, ID, MT. NM. NV, OR, UT. WA, WY South: AL, AR, DC, DE, FL, GA. KY, LA, MD, MS. NC, OK. SC, TN, TX, VA, WV Major tobacco producers: GA, KY. NC, SC. TN, VA ?ndex of restrictiveness (from US DHHS 1986b): 0.00 = None; no statewide restrictions. 0.25 = Nominal; State regulates smoking in one to three public places, excluding restaurants and private worksites 0.50 = Basic; State regulates smoking in four or more public places, excluding restaurants and private worksites. 0.75 = Moderate; State regulates smoking in restaurants, but not private worksites. I .@I = Extensive; State regulates smoking in private worksites. CDifference in prevalence of laws, South versus all other: chi square (using Yates correction)=1 3.40, p to fall. Advertising expenditures did decrease in 197 1, immediately following the broadcast ad ban. but they increased in succeeding years such that real expenditures (i.e.. controlling for in- flation) exceeded pre-ban levels by the mid- 19704 (Federal Trade Commih\lon 1988). Real cigarette price actually increased in the first 2 year\ of the ban period. although real manufacturers' wholesale prices declined during those >`ear\ (escihe taxeb account- ing for the increase). Several analysts have concluded that broadcast bans have decreased consumption. albeit typically quite modestly (Bishop and Yoo 1985: Peto 197-l). A common assess- ment, particularly in studies of the British broadcast ad ban. ha5 been that the consump- tion impact of the ban trailed off. with consumption returning to baseline wfithin 2 to 5 years (McLeod 1986: Witt and Pass 1983: Atkinson and Skegg 1973). As noted in Chapter 7, however, none of these analyses was designed to asses\ the long-run social influence of entire generations not being exposed to broadcast advertising of cigarettes (Warner 1979). Many observers believe that the seminal smoking-and-health event in the United States in the past 15 years has been the growth of the nonsmokers' rights movement, reflected in passage of State and local laws and private business policies restricting smoking in public places and workplaces. Laws and policies and their effects were reviewed in the preceding chapter and. in greater depth. in the 1986 Surgeon General's Report (US DHHS 1986) and other recent publications (Bureau of National Affairs 1986, 1987). As noted in the last chapter, to date few statistical studies using objective consump- tion data have examined the relationship between smoking restriction policies and per capita consumption. Three econometric analyses found a significant inverse relation- ship between restrictions and consumption, but none concluded that the relationship was causal. In one study, an index of the growth of State-level smoking restriction laws correlated strongly with the decline in adult per capita consumption after 1973 (Figure 3), but the author concluded that "This correlation seems unlikely to reflect causation. Rather, bothdecliningconsumption and growth in legislation probably reflect a prevail- ing nonsmoking ethos and the conversion of modified knowledge and attitudes into be- havioral change" (Warner 198 1 a). In the second econometric study. the author found a Ggnificant reduction in smok- ing associated with laws categorized as restrictive. but no Ggnificant reduction as- sociated with less restrictive laws. The study could not determine, however, whether passage of restrictive laws preceded or followed decreases in consumption (Lewit 1988). In the third study, the authors concluded that the significant correlation between passage of laws and reduced cigarette demand likely reflected reverse causality; that is, that cigarette demand has a significant negative effect on the probability of passing a clean indoor air law (Chaloupka and Saffer 1988). Aggregate Effects While numerous econometric studies have contributed to understanding the impact of major individual smoking-and-health events, regression analysis has also been used by Warner ( 1977, 1981a, 1989) to estimate changes in per capita consumption associated with changes in the smoking-and-health environment over the entire period since 1964. In the two more recent studies, to estimate what consumption would have been in any given year without the antismoking campaign, Warner added the values of the relevant antismoking variables in the regression, multiplied by their corresponding coefficients, to the year's actual per capita consumption. (With the previous year's con- sumption included among the independent variables as a measure of the addiction effect, an antismoking effect was also carried forward into future years and was in- cluded in the analysis.) The resulting estimates of per capita consumption in the ab- sence of the campaign were then compared with the realized levels of consumption to measure the aggregate impact of the campaign in the year in question. Figure 4 presents the results of the most recent analysis (Warner 1989). The solid line in the Figure tracks actual adult per capita cigarette consumption from 1932 through 1987. (The regression covered the post-World War II period, 1947 through 1987.) The dashed and dotted lines are two estimated patterns that consumption would have fol- lowed from 1964 through 1987 had the demand for cigarettes never been influenced by the development and dissemination of scientific knowledge on the hazards of smoking and the associated social and policy developments. The distinction between the two estimated lines lies in how price changes are treated. The dotted line results from the assumption that the pattern of price changes was itself a function of legislators' reactions to the emerging evidence on smoking and health (Warner 198 1 a,b). In particular, the real price of cigarettes rose every year from 1964 through 1972 and again from 198 1 through 1987. The intervening period of real price decreases has been attributed to reduction in new State excise tax increases due to con- cern about interstate cigarette smuggling, the result of tax-based price differentials be- tween low- and high-tax States (Advisory Council on Intergovernmental Relations 198.5; Warner 1982). The resumption of real tax increases in 198 1 may reflect reduced concern about smuggling, as a consequence of the diminishing real value of interstate tax differences during the preceding decade. (See Chapter 7.) To reflect the assump- tion that this pattern of price changes was a function of the antismoking campaign, the dotted line in Figure 4 treats price as if it had been constant (in real terms) in the years after 1963. This permits an assessment of the effects on consumption of price fluctua- tions possibly resulting from the campaign. 662 6000 1930 1940 1950 1960 1970 1980 1990 Year FIGURE 4.-Comparison of actual per capita cigarette consumption (solid line) with estimated consumption in the absence of the antismoking cam- paign (dashed line = actual cigarette prices; dotted line = real price held constant) SOURCE: Warner (1989) The dashed line treats the pattern of realized prices as independent of the antismok- ing campaign; actual experienced prices are reflected in the dashed line. Warner inter- preted the gap between the solid line (actual consumption) and dashed line (estimated consumption, actual prices) as a measure of the " `pure' publicity effect" of the cam- paign, whereas the gap between the dashed line and dotted line (estimated consump- tion, constant prices) measured the impact on consumption of changing prices. TO the extent that the latter was attributable to smoking-and-health concerns of legislators, Warner considered it a measure of price-related campaign-induced changes in con- sumption. While the precise pattern of estimated per capita consumption without the antismok- ing campaign depends on the treatment of price change, each of the estimated lines in- dicates a generally increasing pattern of consumption over time, in contrast to the pat- tern actually experienced. According to the analysis, in 1987, without the antismoking campaign, and treating price changes as independent of the campaign (i.e., the dashed 663 line in Figure 4), per capita consumption would have been 79 percent greater than the level actually experienced. When the pattern of price changes is removed (the dotted line in Figure 4), the estimate rises to 89 percent, indicating that price fluctuations con- tributed to decreased consumption, but to a much smaller degree than did the publicity effect. An alternative way to interpret the 1987 figures is to observe that actual con- sumption was from 53 to 56 percent of the expected level in the absence of the anti- smoking campaign. Two observations support the magnitude of the campaign impact estimated in this per capita consumption analysis. First, the finding of a substantial impact of the anti- smoking campaign is consistent with the cohort analysis of prevalence reviewed above. Second, continued diffusion of smoking among women to levels comparable to those attained by men prior to the mid- 1960s. combined with the maintenance of men's smok- ing rates, would have produced rates of per capita consumption higher than those es- timated here (Warner 1977). Filter-Tipped and Low-Tar and -Nicotine Cigarettes Whereas quitting smoking or avoiding initiation constitutes the most obvious reac- tion to campaign-related health or social concerns, switching to cigarettes perceived as less hazardous better reflects some smokers' responses, in part because actions short of quitting allow smokers to respond to their concerns without having to take the more drastic step of ceasing an addictive behavior. In this regard, two of the best markers of smokers' reactions to antismoking publicity have been the rapid spread of filtered cigarettes in the 1950s and low-tar and -nicotine cigarettes in the 1970s (Schneider, Klein, Murphy 198 1). While evidence linking cigarette smoking with cancer dates back at least to the 1930s the period of sustained, intensive scientific investigation began in the late 1940s and early 1950s. (See Chapters 1 and 2.) A few popular publications transmitted the new scientific findings to the lay public soon thereafter, including Reader's Digest (Riis 1950; Norr 1952; Lieb 1953; Miller and Monahan 1954) and ConsumerReports (1953, 1954, 1955). At the same time, cigarette manufacturers were developing and market- ing new filtered cigarettes. Cigarette filters were advertised as a technology to remove the harmful elements of smoke (Calfee 1986; Davis 1987; Tye 1986; Warner 1985b; Whelan 1984). As the data in Chapter 5 indicate, the shift to filtered cigarettes at this time was swift. While filtered cigarettes had been available since the 193Os, they composed only 1 per- cent of the market in 1952. By 1954 the proportion of filtered cigarettes had increased to 9 percent. The filter-tip market share rose by at least 9 percentage points each of the next 3 years, reaching 38 percent in 1957. Three years later, the filtered cigarette be- came the dominant product on the market. This first widespread public concern about smoking and health was also associated with a 2-year decline in adult per capita cigarette consumption in 1953 and 1954 (Figure 3). Two decades later, in the mid-1970s. the rapid shift toward low-tar and -nicotine cigarettes represented a second major change in consumers' choice of cigarette product. In the late 1960s. low-tar and -nicotine cigarettes (defined as cigarettes yield- 664 ing 15 mg tar or less, as measured by the Federal Trade Commission) constituted from 2 to 3 percent of the cigarette market. In the early 1970s. cigarette manufacturers in- itiated an advertising campaign for low-tar and -nicotine cigarettes, which resulted in 50 percent of advertising dollars being dedicated to these products by 1977 (Schneider, Klein, Murphy 198 1: Federal Trade Commission 1988). Many of the ads made health claims for the products, most implicitly (Altman et al.. in press; Davis 1987; Tye 1986; Warner 1985b). From 1970 through 1974, the market share of low-yield cigarettes increased from 4 to 9 percent. Three years later, with 50 percent of all cigarette ads devoted to the low- yield products, market share had increased to 23 percent. By the end of the decade, the market share exceeded 40 percent, and it hit 56 percent in 198 1. Thereafter, the per- centage backed off a few points, but the low-tar and -nicotine cigarette remained the principal product on the market (Federal Trade Commission 1988). Surveys in the 1970s found that large proportions of the smoking public believed that some cigarettes posed little or no health risk (Federal Trade Commission 1981). (See Chapter 4.) As such, many smokers may have perceived low-tar and -nicotine ciga- rettes as an alternative to quitting smoking that would not compromise health. Some analysts have concluded that the shift to low-tar and -nicotine cigarettes, and before it to filter-tipped cigarettes, was the smoking public's principal behavioral response to concerns about the health hazards of smoking (Schneider, Klein, Murphy 198 1). Health Consequences of the Campaign Given the health consequences of smoking, described in Chapters 2 and 3, the be- havioral impact of the antismoking campaign implies that the campaign has had sig- nificant effects on the health of the American public. These health effects may be quite varied, reflecting the number and variety of behavioral changes, ranging from outright smoking cessation to shifts to low-tar and -nicotine cigarettes. In addition to reductions in the amount of smoking-related mortality, the mix of smoking-related deaths may have been altered by campaign responses, as a result of changes in the nature of the product and its disease-producing properties. (See Chapters 2 and 3 and US DHHS 1981.) Similarly, patterns of morbidity and disability may have been affected. While smoking-related deaths have been averted as a result of people's responses to the antismoking campaign (as discussed below), it is also possible that some addition- al deaths have occurred because of campaign response. The latter could result, for ex- ample, if industry advertising, responding to smokers' health concerns. prompted smokers who otherwise would have quit smoking to switch to low-yield cigarettes. There is a clear consensus that among the principal factors motivating the growth of filtered cigarettes and the shift toward brands lower in tar and nicotine yield were con- cerns about the health effects of smoking--on the part of consumers, the Federal Trade Commission (which decided in 1967 to publish standardized tar and nicotine measure- ments), and the cigarette manufacturers in response (US DHHS 198 1, 1988; Gerstein and Levison 1982; Schneider, Klein, Murphy 1981; Miles 1982). As noted above, analysts have concluded that, at the time of the shifts to filtered and low-yield ciga- rettes, cigarette advertising stressed the new products' health "advantages," with the 665 apparent intent of allaying consumer fears and thereby discouraging quitting of smok- ing (Calfee 1986; Davis 1987; Tye 1986; Warner 1985b; Whelan 1984; Altman et al., in press). A number of factors complicate assessment of the net health consequences of reduced-yield cigarettes. These include the unknown health effects of additives in low- yield cigarettes and the tendency toward nicotine regulation, both discussed in detail in previous reports of the Surgeon General (US DHHS 198 1, 1988); the possibility that many low-yield-cigarette smokers would have quit smoking in the absence of the availability of lower yield products; and the possibility that the availability of low-tar and -nicotine brands may account in part for the increase in smoking by teenage girls and young women in the 1970s (Harris 1980). To date, the net health effects of the in- troduction and consumer acceptance of filtered and low-yield cigarettes have not been determined. Furthermore, no formal analysis has attempted to assess how much of the switch to lower yield products constitutes response to the antismoking campaign. Only one measure of health impact of the campaign has been evaluated quantitative- ly: aggregate mortality associated with changes in smoking prevalence. The conclud- ing section of this Chapter reviews the relevant findings. Mortality Postponed by Campaign-Related Decreases in Smoking Prevalence While the net health effects of filter and low-tar and -nicotine cigarettes have not been determined, Warner (1989) has estimated the mortality postponed as a result of campaign-induced decisions of smokers to quit and of nonsmokers not to start smok- ing. Updating an earlier analysis (Warner and Murt 1983), Warner applied epidemiologic data on age-sex-specific mortality rates of smokers, former smokers, and never smokers to the cohort-specific changes in smoking prevalence summarized above in Tables 1 and 2. The reduced mortality rates of former smokers (compared with continuing smokers) were multiplied by the estimated number of campaign-in- duced quitters and noninitiators (i.e., people influenced by the campaign not to start smoking) in each cohort and in each year from 1964 through 1985. This procedure generated estimates of the number of additional smoking-related deaths that would have occurred had the antismoking campaign not encouraged quitting and noninitiation. (See Chapter 3 for discussion of smoking-related deaths.) The analysis also produced estimates of life-years saved. These represent the life expectancy gained by campaign- induced quitters and noninitiators who avoided or postponed premature smoking-re- lated deaths. Given the need to make several assumptions to perform the study, Warner subjected his findings to four sensitivity analyses. He altered each of four variables' assumed values in a conservative direction to determine whether the specific values selected for the base case fundamentally affected the qualitative findings of the study. While the sensitivity analyses reduced the estimates of deaths postponed by the campaign, the author concluded that none reduced them sufficiently to alter the essential qualitative finding: from 1964 through 1985, hundreds of thousands of smoking-related prema- ture deaths were delayed or avoided as a result of campaign-induced decisions to quit smoking or not to start. Table 4 presents estimates of deaths postponed for each of the 12 age-sex cohorts identified in Tables I and 2, from 1964 through 1985. For Americans born after 1900, the total number of deaths postponed as a result of campaign response was estimated as 789,200. The distribution between men and women and across birth cohorts is seen in the individual cells of Table 4. TABLE 4.-Deaths postponed by campaign-related smoking cessation and noninitiation, 1964-85 (in thousands) Birth year Males Females Total 1901-10 103.6 16.7 120.3 1911-20 182.0 46.0 228.0 1921-30 182.7 59.6 242.3 193 I-40 83.2 22.7 105.9 1941-50 44.0 15.5 59.5 1951-60 29.0 4.2 33.2 Total 624.5 164.7 789.2 SOURCE: Warner (1989). According to the estimates in Table 4, nearly four times as many men as women real- ized additional years. In part this reflects the greater consumption impact of the cam- paign on men, as well as their higher mortality rates. However, Warner's analysis util- ized male smoker mortality ratios from an insurance study (Cowell and Hirst 1980) and adopted as a conservative assumption an estimate that women's excess smoker mor- tality ratios were half those of men. New data from the American Cancer Society's sur- vey, analyzed in Chapter 3, demonstrate that women's excess smoker mortality ratios are closer to two-thirds those of men. Consequently, the data in Table 4 likely under- estimate the number of women's deaths postponed relative to those of men. Warner also estimated the number of life-years saved as a result of campaign-related smoking cessation and noninitiation. In total, the 12 cohorts gained 16.3 million addi- tional life-years. The average number of life-years saved per death postponed was 20.6. Figure 5 plots the cumulative number of smoking-related deaths estimated to have occurred within the 12 cohorts between 1964 and 1985 and the study's estimate of the number that would have occurred without the antismoking campaign. By 1985, when the cumulative number of postponed deaths was approaching 800,000, the number of smoking-related deaths during the period had totaled 5.7 million. Thus, life-savings at- tributable to the campaign equaled 12 percent of actual plus avoided smoking-related mortality. In Warner and Murt's earlier study, campaign-related life-savings through 1978 equaled 5 percent of actual plus avoided smoking-related mortality (Warner and Murt 1983). The increase reflects greater numbers of quitters and the health benefits of the passage of time, as former smokers' excess (smoking-related) mortality risks fall as years of smoking increase. Comparing the two analyses, one sees that almost three- 667 1960 1965 1970 1975 1980 1985 YEAR FIGURE K-Comparison of estimated cumulative smoking-related deaths (solid line) with estimate of the number that would have occurred without the antismoking campaign (dashed line), 1964-S quarters of the postponement of deaths occurred in the most recent 7 years of the 22 years studied. In particular, 1 12,400 deaths-14 percent of the total-were postponed in I985 alone (Warner 1989). For the youngest cohorts in the study, low overall death rates translated into relative- ly few deaths postponed through 1985. Given the substantial impact of the campaign on the smoking patterns of these cohorts, however, major life-saving accomplishments of antismoking efforts mounted to date will be realized two to three decades hence, when these cohorts reach the age at which smoking-related illnesses begin to take their greatezt toll. Similarly. recent campaign-related quitting in the middle-aged cohorts will translate into large numbers of smoking-related deaths postponed or avoided in fu- ture years. a\ these recent quitters experience reduced smoking-related mortality rates. Thus. the health benefits of the antismoking campaign will continue to expand, both in abholute term5 and as a percentage of the total potential burden of smoking-related mor- tality. This is illustrated by Warner's (1989) estimate that campaign-induced quitting and noninitiation through 19X.5 will result in the postponement or avoidance of an additional 2. I million smokmg-related deaths between 1986 and the year 2000. The finding that men have realized a much greater collective health benefit from their responses to the antismoking campaign than have women reflects the fact that more men than women quit or did not initiate smoking as a result of the campaign, as well as the ahsurned lower smoker mortality ratios and death rates of women. As women's 66X smoking patterns have approached those of men in recent years (see Chapter 5), the dis- parity between male and female smoker mortality ratios has diminished. (See Chapter 3.) Particularly in the younger cohorts, if women respond to the relatively new em- phasis on the health consequences of their smoking (US DHHS 1980). the male-female differential for postponed deaths would be expected to decrease in the future (Warner and Murt 1983; Warner 1989). The authors of these studies acknowledged that their estimate of deaths postponed as a result of the antismoking campaign was an incomplete measure of the health conse- quences of the campaign (Warner and Murt 1983: Warner 1989). As noted above, the net health effects of the switch to filtered and low-yield cigarettes have not been established, and no formal analysis has assessed the impact of campaign-related reductions in smoking prevalence on smoking-related morbidity and disability. Nevertheless. Warner and Murt concluded that the estimated life-savings associated with responses to the campaign constitute a major public health accomplishment. They cautioned, however, that the magnitude of the remaining burden of smoking "places the impressive successes of the antismoking campaign in context" (Warner 1989). 1. 2. 3. 4. 5. 6. 7. Conclusions 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, 669 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. I million smoking-related deaths between 1986 and the year 2000. 670 Appendix Selected Developments Related to Smoking and Health, 1964-88 1964 . Smoking and Health: Report of the Advisory Committee to the Surgenn General. the first major U.S. report on smoking and health, is published. Concludes that cigarette smoking is a cause of lung cancer in men and a suspected cause in women. Identifies many other causal relationships and smoking-disease as- sociations. Calls for "appropriate remedial action." . National Interagency Council on Smoking and Health, the first national anti- smoking coalition, is formed. . National Association of Broadcasters (NAB) amends its television advertising code to discourage portrayal of cigarette smoking as a behavior worthy of im- itation by youngsters. . Cigarette manufacturers establish voluntary Cigarette Advertising Code for television and radio. . Federal Trade Commission (FTC) announces proposed Trade Regulation Rule on Cigarette Labeling and Advertising. . National Center for Health Statistics begins collecting information on smoking as part of the National Health Interview Survey. Collected periodically there- after. . American Medical Association (AMA) officially calls smoking "a serious health hazard." . Public Health Service (PHS) and Indian Hospitals discontinue distributing free cigarettes. The Department of Defense and the Veterans Administration soon do the same in their medical installations. . State Mutual Life Assurance Company becomes the first company to offer life insurance to nonsmokers at discounted rates. 1965 . Congress passes the Federal Cigarette Labeling and Advertising Act, requiring health warning on all cigarette packages: `Caution: Cigarette Smoking May be Hazardous to Your Health." . PHS establishes the National Clearinghouse for Smoking and Health. 671 1966 . Health warning label appears on all cigarette packages. . Congress enacts the Fair Packaging and Labeling Act to require fair, nondecep- tive packaging and labeling. Tobacco and tobacco products are excluded. 1967 . Report of the Surgeon General concludes smoking is the principal cause of lung cancer. . Federal Communications Commission (FCC) rules that the Fairness Doctrine applies to cigarette advertising. Stations broadcasting cigarette commercials must donate air time to antismoking messages. . PHS, American Cancer Society (ACS). American Lung Association (ALA) (then known as the National Tuberculosis Association), and American Heart As- sociation (AHA) launch public service advertisjng campaigns against smoking. . FTC releases the first report on tar and nicotine yield in cigarette brands. . National Institutes of Health initiates research planning for developing "less haz- ardous" cigarettes. . First World Conference on Smoking and Health is held in New York City. 1968 . Action on Smoking and Health is formed to serve as a legal action arm for the antismoking community. . National Clearinghouse for Smoking and Health produces the first Government antismoking poster. . CBS airs "National Smoking Test" during prime time. 1969 . NAB endorses phasing out of cigarette ads on television and radio. . ACS sponsor5 a quit-smoking series on PBS. . ALA introduces its first smoking cessation materials. 612 1970 . Congress enacts the Public Health Cigarette Smoking Act of 1969 (passed in 1970), banning cigarette advertising on television and radio and requiring a stronger health warning on cigarette packages: "Warning: The Surgeon General Has Determined that Cigarette Smoking is Dangerous to Your Health." . Due to the new statutory prohibition on broadcast advertising, the voluntary Cigarette Advertising Code is disbanded. . Due to the broadcast ban, the FCC rules that the Fairness Doctrine no longer will apply to cigarette advertising (effective 197 1). . First National Conference on Smoking and Health is held in San Diego. . World Health Organization takes a public position against cigarette smoking. . Congress enacts the Controlled Substances Act. Tobacco is excluded from jurisdiction. 1971 Surgeon General proposes a Government ban on smoking in public places. Cigarette advertising ends on radio and television. Fairness Doctrine antismok- ing messages also end. Cigarette manufacturers' voluntary agreement to list tar and nicotine yield in all advertising becomes effective. Six major cigarette companies agree voluntarily to include health warnings in all printed advertising. The FTC announces intent to proceed against cigarette companies for false and deceptive advertising. Second World Conference on Smoking and Health is held in London. Interstate Commerce Commission implements rules to restrict smoking to rear seats (not to exceed 20 percent of capacity) on interstate buses. 1972 . First Report of the Surgeon General to identify involuntary smoking as a health risk. . Under a consent order with the FTC, six major cigarette companies agree to in- clude a "clear and conspicuous" health warning in all cigarette advertisements. 673 . Congress enacts the Consumer Product Safety Act. Tobacco and tobacco products are excluded from jurisdiction. . Supreme Court upholds congressional action banning cigarette commercials from television and radio. . Department of Health, Education, and Welfare issues policy directive to estab- lish no-smoking rules in departmental conference rooms, cafeterias, and certain work areas. . ALA sponsors first State-level "no-smoking day" in Oklahoma. 1973 . Congress enacts Little Cigar Act of 1973, banning little cigar ads from television and radio. . Civil Aeronautics Board requires no-smoking sections on all commercial airline flights. . General Services Administration issues guidelines on smoking in Federal build- ings. . Arizona becomes the first State to restrict smoking in a number of public places and the first to do so explicitly because environmental tobacco smoke exposure is a public health hazard. 1974 . Connecticut passes the first State law to apply smoking restrictions to restaurants. . ACS, ALA, and AHA cosponsor no-smoking day in Minnesota. 1975 . Cigarettes are discontinued in K-rations and C-rations provided to soldiers and sailors. . Third World Conference on Smoking and Health is held in New York City. Con- ferees call for a unified worldwide campaign against smoking. . Minnesota passes landmark comprehensive statewide clean indoor air law. 1976 . Interstate Commerce Commission modifies interstate bus rules to permit smok- ing in 30 percent of seats. 674 . Interstate Commerce Commission prohibits smoking in railroad dining cars and requires separate smoking and nonsmoking passenger cars. . Congress amends the Federal Hazardous Substances Act to exclude tobacco and tobacco products from jurisdiction. . Congress enacts the Toxic Substances Control Act. Tobacco and tobacco products are excluded from jurisdiction. . ACS appoints National Commission on Smoking and Public Policy to hold hear- ings on major policy. Report issued in 1978. 1977 . Secretary of Health, Education, and Welfare establishes Task Force on Smok- ing and Health. . ACS sponsors the first national "Great American Smokeout." . Doctors Ought to Care is formed to provide a focal point for physicians' antismoking advocacy, especially through counteradvertising. 1978 . Secretary of Health, Education, and Welfare announces major Government in- itiative against smoking. Calls smoking "Public Health Enemy Number One." . National Clearinghouse for Smoking and Health is renamed Office on Smoking and Health and transferred from Atlanta to Washington, DC. Given expanded function to coordinate Federal smoking and health activities. . AMA releases "Tobacco and Health," summarizing findings of a tobacco re- search program that included 15 million dollars in financial support from the tobacco industry. Concluded that smoking is harmful to health. . Utah enacts the first State law banning tobacco advertisements on any billboard, streetcar sign, streetcar, or bus. 1979 . Fifteenth Anniversary Report of the Surgeon General is issued. Most com- prehensive review of smoking and health ever published. . National Institute of Education survey shows that girls are smoking more than boys. . Fourth World Conference on Smoking and Health is held in Stockholm. . Minneapolis and St. Paul become the first cities to ban the distribution of free cigarette samples. 1980 . Report of the Surgeon General highlights health consequences of smoking to women. . PHS announces Health Objectives for the Nation, which include a goal to reduce smoking to below 25 percent among adults by 1990. . The FTC begins testing cigarettes for carbon monoxide yields. 1981 . Report of the Surgeon General focuses on "The Changing Cigarette." Concludes no cigarette or level of consumption is safe. . The FTC concludes existing cigarette warning label is no longer effective. Recommends rotational warning label system. . National Conference on Smoking or Health is held in New York City, sponsored by ACS. Leads to formation of Coalition on Smoking OR Health. (See 1982.) 1982 . Report of the Surgeon General focuses exclusively on smoking and cancer. . Congress temporarily doubles the Federal excise tax on cigarettes to 16 cents per pack, to be in effect January 1, 1983, to October 1, 1985. First increase since 1951. . Congress enacts No Net Cost Tobacco Program Act of 1982 to reduce taxpayers' costs for the tobacco price support program. . ACS, ALA, and AHA form a tripartite Coalition on Smoking OR Health, primarily to coordinate Federal legislative activities related to smoking control. . National Cancer Institute reorganizes its smoking research program, as the Smoking, Tobacco and Cancer Program, to focus on smoking behavior research and interventions. 1983 . Report of the Surgeon General focuses exclusively on smoking and cardiovas- cular disease. 676 . Fifth World Conference on Smoking and Health is held in Winnipeg. . National Institute on Drug Abuse declares smoking to be the Nation's "most widespread form of drug dependency." . New York State Journal of Medicine publishes the first U.S. medical journal all- tobacco edition focusing on health and social issues. . San Francisco passes law to include smoking restrictions in private workplaces. 1984 . Report of the Surgeon General focuses exclusively on smoking and chronic obstructive lung disease. . Congress enacts the Comprehensive Smoking Education Act, requiring rotation- al health warnings on cigarette packages and advertisements: "SURGEON GENERAL'S WARNING: Smoking Causes Lung Cancer, Heart Disease, Emphysema, and May Complicate Pregnancy." `SURGEON GENERAL'S WARNING: Quitting Smoking Now Greatly Reduces Serious Risks to Your Health." "SURGEON GENERAL'S WARNING: Smoking by Pregnant Women May Result in Fetal Injury, Premature Birth, and Low Birth Weight." "SURGEON GENERAL'S WARNING: Cigarette Smoke Contains Carbon Monoxide." . Federal Interagency Committee on Smoking and Health, an advisory committee chaired by the Surgeon General, is established. . Food and Drug Administration approves nicotine polacrilex gum as a "new drug." . Congress enacts the Cigarette Safety Act of 1984, requiring research and a report on "fire-safe" cigarettes. . Tobacco Products Liability Project is formed to support efforts to bring product liability suits against cigarette manufacturers as a public health strategy. . Surgeon General announces his goal of a smoke-free society by the Year 200O. 1985 . Report of the Surgeon General covers smoking and occupational exposures. 677 . AMA calls for a ban on all tobacco advertising and promotion, consistent with similar calls by ALA, ACS, AHA, and numerous other health and medical or- ganizations. . Office on Smoking and Health initiates a national educational campaign regard- ing smoking during pregnancy. . National Heart, Lung, and Blood Institute establishes a Smoking Education Program. . ALA produces a television series, "Freedom from Smoking@ in 20 Days." . Minnesota enacts the first State legislation to earmark a portion of the State cigarette excise tax to support antismoking programs. . STAT (Stop Teenage Addiction to Tobacco) is formed to focus on teenage tobac- co use. . Maine becomes the first State to adopt a law protecting supporters of worksite smoking policies against discrimination. 1986 . Report of the Surgeon General focuses exclusively on the health consequences of involuntary smoking. . Special Report of the Surgeon General documents the health consequences of using smokeless tobacco. . Congress enacts the Comprehensive Smokeless Tobacco Health Education Act of 1986. Requires rotation of three health warnings on smokeless tobacco pack- ages and advertisements and bans smokeless tobacco advertising on broadcast media. . Congress extends permanently the 16 cents per pack Federal excise tax on cigarettes. . Congress enacts the Tobacco Program Improvement Act of 1986, further revis- ing the price support program. . Department of Health and Human Services releases the first biennial National Status Report to Congress on Smoking and Health. . Department of Defense launches extensive antismoking education campaign for the military and other Department of Defense employees. . Americans for Nonsmokers' Rights becomes National. Originally formed as California GASP (Group Against Smoking Pollution) in 1976. 678 . Minnesota enacts the first State law to ban free distribution of smokeless tobac- co samples. . Congress imposes a Federal excise tax on smokeless tobacco products. 1987 . General Services Administration implements regulations to prohibit smoking in Federal buildings, except in designated areas. . Department of Health and Human Services (DHHS) establishes a smoke-free environment in its facilities, affecting 120,000 DHHS employees nationwide. . Food and Drug Administration determines "Masterpiece Tobac" (chewing gum containing tobacco) to be an "adulterated food" subject to its jurisdiction, and "Favor" (a "smokeless cigarette" not containing tobacco leaf) to be a "drug" subject to its jurisdiction. Both products withdrawn from the market. . Sixth World Conference on Smoking and Health is held in Tokyo. . ACS, ALA, and AHA launch a joint project, "Tobacco-Free America." . Minnesota Sports Commission votes to ban tobacco advertising in the Metrodome Sports Stadium effective 1992, the first such action in the United States. . Minnesota passes a law requiring all hospitals in the State to ban smoking by 1990. 1988 . Report of the Surgeon General concentrates exclusively on nicotine addiction. . Congressionally mandated smoking ban takes effect on domestic airline flights scheduled for 2 hours or less. Northwest Airlines voluntarily bans smoking on all fights in North America. . ALA sponsors the first annual "Non-Dependence Day." . In Cipollone v. Liggert Group, Inc., plaintiff wins the first jury verdict against a tobacco company in a smoking and disease case. . New York City clean indoor air ordinance takes effect, banning or severely limit- ing smoking in a wide variety of public places. Applies to over 7 million people, almost 3 percent of the U.S. population. . New York Metropolitan Transit Authority (NYMTA) bans smoking on Long Is- land Railroad and Metro North Commuter Rail and trains, affecting 452,000 679 daily riders. Action prompted by a law Congress passed in 1987 to withhold Federal transportation funds to NYMTA unless it banned smoking. . California implements statewide law banning smoking on all intrastate airplane, train, and bus trips. . California suit against manufacturers and retailers of cigars, pipe tobacco, and roll-your-own cigarette tobacco seeks compliance with State law requiring label- ing of consumer products containing carcinogens or reproductive toxins. Cigar Association of America indicates that most cigars sold in the United States will carry a warning label. . R.J. 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Inter- national Journal of Social Economics lO(3): 18-33, 1983. 684 GLOSSARY AAFP AAP AARC AC ACCP ACHE ACS ADAMHA AHA ALA AMA ANR AR ASH ASHA AUTS BATF BART BC/BS BIOSEP BRFS CAB cc CDC CHD CIS CNR CNS co COHb COLD COPD CPS CPS-I CPS-II CPSA American Academy of Family Physicians American Academy of Pediatrics American Association for Respiratory Care advisory committee American College of Chest Physicians American College of Healthcare Executives American Cancer Society Alcohol, Drug Abuse, and Mental Health Administration American Heart Association American Lung Association American Medical Association Americans for Nonsmokers' Rights attributable risk Action on Smoking and Health American School Health Association Adult Use of Tobacco Survey Bureau of Alcohol, Tobacco, and Firearms Bay Area Rapid Transit Blue Cross-Blue Shield Biofeedback Smoking Education Project Behavioral Risk Factor Surveillance System Civil Aeronautics Board Consensus Conference Centers for Disease Control coronary heart disease Cancer Information Service Californians for Nonsmokers' Rights central nervous system carbon monoxide carboxyhemoglobin chronic obstructive lung disease chronic obstructive pulmonary disease Current Population Survey Cancer Prevention Study I Cancer Prevention Study II Consumer Product Safety Act 685 CPSC CVD DBP DHHS DOC DOD EPA ETS FAA FCC FDA FEVt FFDCA FHSA F-l-C FI-E GAS0 GASP GSA HCN . HDL HES HHANES HIAA HMO HRSA IAC ICC ICD-9 ICD-7 IPPB IQ JCAHO LFL LIRR MBTA MRFIT MS NAB NAIC NASHS NAT NCHS NC1 NCSH Consumer Product Safety Commission cardiovascular disease diastolic blood pressure Department of Health and Human Services Doctors Ought to Care Department of Defense Environmental Protection Agency environmental tobacco smoke Federal Aviation Administration Federal Communications Commission Food and Drug Administration 1 -set forced expiratory volume Federal Food, Drug, and Cosmetic Act Federal Hazardous Substance Labeling Act Federal Trade Commission full-time equivalents Great American Smokeout Group Against Smoking Pollution General Services Administration hydrogen cyanide high density lipoprotein Health Examination Survey Hispanic Health and Nutrition Examination Survey Health Insurance Association of America health maintenance organization Health Resources and Services Administration Interagency Committee Interstate Commerce Commission International Classification of Diseases, Ninth Revision International Classification of Diseases, Seventh Revision Intermittent Positive Pressure Breathing Trial I Quit Joint Commission on Accreditation of Healthcare Organizations "Live for Life" Long Island Railroad Massachusetts Bay Transportation Authority Multiple Risk Factor Intervention Trial mainstream smoke N'-nitrosoanabasine National Association of Insurance Commissioners National Adolescent Student Health Survey N'-nitrosoanatabine National Center for Health Statistics National Cancer Institute National Clearinghouse for Smoking and Health 686 NDN NHANES NHES NHIS NHLBI NICHD NIDA NIH NNK NNN NNS NRC NSBA NSDA NSFG OASH occ OSH OSHA OTA PAH PHS r-M PSAs RJR SCN SEP SES SHCP SHD ss ST STAT STCP TEFRA TPLP TSG TSNA USDA USP VA WHO National Diffusion Network National Health and Nutrition Examination Survey National Health Examination Survey National Health Interview Survey National Heart, Lung, and Blood Institute National Institute of Child Health and Human Development National Institute on Drug Abuse National Institutes of Health 4-(methylnitrosoamino)- 1-(3-pyridyl)- 1 -butanone N'-nitrosonomicotine National Natality Survey National Research Council National School Boards Association National Survey on Drug Abuse National Survey of Family Growth Office of the Assistant Secretary for Health Office of Cancer Communications Office on Smoking and Health Occupational Safety and Health Administration Office of Technology Assessment polynuclear aromatic hydrocarbon Public Health Service parts per billion public service announcements R.J. Reynolds Tobacco Company thiocyanate Smoking Education Program socioeconomic status School Health Curriculum Project State Health Department sidestream smoke smokeless tobacco Stop Teenage Addiction to Tobacco Smoking, Tobacco, and Cancer Program Tax Equity and Fiscal Responsibility Act Tobacco Products Liability Project Technical Study Group tobacco-specific N-nitrosamine U.S. Department of Agriculture U.S. Pharmacopeia Veterans Administration World Health Organization 687 INDEX ADDICTION central nervous system, 340 conditioning of smoking habit, 78-79, 340,342 development of smoking habit, 333-334 health warnings, recommendations. 486 historical perspective, 329-330. 340-342 National Institute on Drug Abuse, re- search programs, 399 nicotine, psychosocial and pharmacologic forces, 331, 334, 340. 342 public beliefs about tobacco use, 200, 2 16 relationship to price elasticity, 537 withdrawal symptoms, 343-344 ADOLESCENTS access to tobacco, 235, 238, 596604,606 advertising effects, 339,503-504,660 behavioral risk factors compared with smoking, beliefs, 2 15 beliefs about smoking, 212-215,216. 222-223 cessation attempts, British and American teenagers, 596 cigarette consumption, 660 developmental stage models, peer pres- sure and coping patterns, 386 drug and alcohol use vs. smoking, beliefs. 214,215 free tobacco product samples, 597 High School Seniors Surveys, 302-303, 306 initiation of smoking, 215. 296-297, 333- 335,537-539 knowledge about smoking and smokeless tobacco use, 2 17,22 1,222-223 parental and peer influences, 336-338, 389,390 perceptions about smokers their own age, 227-229 prevention of smoking, programs. 394- 396,398,407-408 Price elasticity of demand for cigarettes, 536539 psychosocial curricula. 385,389.390 smokeless tobacco and oral neoplasm risk, 217. 218 smoking cessation programs, 392-393 social trends and smoking prevalence, 409 Surgeon General's Reports. smoking prevention, 4OWOl ADULT USE OF TOBACCO SURVEYS (AUTSs) airplane smoking restrictions, 573 employee smoke exposure after restric- tion implementation, 594 cigar and pipe smoking, 322. 326328 methodology and scope, 246-247 public service announcements, 497 smokeless tobacco use. 3 19-32 1 smoking continuum of quitting process, 286.288-289.292 smoking prevalence, 266.27 l-272 tar yields of cigarettes, 3 15 tobacco use. 359 workplace smoking policies, prevalence, 582 ADVERTISING (SW also PROMOTION) broadcast bans. 5 1 I, 5 14,66M61 Cigarette Advertising Code, 5 11 consumption effects. 501-503,514,660- 661 decreased motivation to stop smoking, 502 disincentives, 5 16 expenditures, 499%500,503,507,5 14, 661 Fairness Doctrine, application to ciga- rettes, 414-415 Federal Trade Commission action against R.J. Reynolds. 512 Federal Trade Commission guidelines for evaluation, 5 I O-5 I I guidelines, cigarette smoke constituents, 488-490 health warnings, 476,479,483-484 imagery and content regulation, proposals, 5 15 689 initiation of smoking, 501 legibility of advertisements. 483484 low-tar and -nicotine cigarettes, 665 market maturity and segmentation, strategy, 506 preemption of State and local restrictions, 512 public health impact, 50 I public transit bans, 513, 514-515 recall by children, effect on smoking be- havior, 505-506 recidivism, 502 regulation of health claims by cigarette manufacturers, 5 10 restrictions or prohibition, 178, 239-240, 515-516 revenues, media coverage, 508-5 10 stadium ban, Minneapolis, 5 13 teenager targets, 338-339,503-504 tobacco industry questions about harmful- ness of smoking, 5 I l-5 I2 ADVOCACY American Lung Association, 4 17,442 attempts to shift public perceptions. 436- 437 Coalition on Smoking OR Health, 439, 440,443 Comprehensive Smoking Education Act of 1984,437 educational and behavioral programs, policy initiatives, 383 Fairness Doctrine, antismoking lobbying. 441-442 National Commission on Smoking and Public Policy, 443 National Interagency Council on Smok- ing and Health, 437-438 nonsmokers' rights movement. 415,442- 443,558 objectives, 437439 organizational characteristics of smoking control groups, 432-440 State and local antismoking lobbying, 444 Tobacco-Free America Project, 383 AGE FACTORS adult smokers and ex-smokers at risk, 134-137 Alameda County Study, mortality, 4 I antismoking campaign effects among birth cohorts, 65 1457 cigar and pipe smoking, 327-328 coronary mortality, sex ratio, 144-145 initiation of smoking, 296-300,537-539 lung cancer mortality, sex ratio, 143-144 mortality postponed or avoided, 667,668, 669 smokeless tobacco use, males, 322-324 smoking continuum, 289,291,292 statistical analysis and relative risk, women, 127 tar yields or menthol cigarettes, 3 I6 ANTISMOKING CAMPAIGNS American Cancer Society, 4 14 American College of Chest Physicians, 4 19-420 American Heart Association, 4 14 American Medical Association, 4 18-420 Coalition on Smoking OR Health, 418 Department of Defense, 425-427,575 Doctors Ought to Care, 419 Fairness Doctrine, application to cigarette advertising, 414-415 Federal Government efforts, 396-401, 649-651 funding sources, 5 16 Great American Smokeout day, 416-417, 426 Health Objectives for the Nation, 16-19. 433 health professional associations, 4 18420 mass-media-based programs, 384-385 mortality postponed or avoided, 666-669 National Cancer Institute, 398-399,421- 423 National Heart, Lung, and Blood In- stitute, 399,423-425 National Institute for Child Health and Human Development, 399-400 National Interagency Council on Smok- ing and Health, 395-396.437438 national voluntary health organizations, 394-395,417418 nationwide, net health consequences, 665-669 nonsmokers' rights movement, 4424l3 Office of Disease Prevention and Health Promotion, 425 Office on Smoking and Health, 397-398, 421 organizational characteristics of advocacy groups, 43940 State health departments, 427 Surgeon General's Reports, 40@401 ANTISMOKING MATERIALS American Academy of Family Physicians, 420 American Cancer Society, 395 American Heart Association, 394-395 690 American Lung Association, 394.414 American Society of internal Medicine. 420 National Cancer Institute programs. 421- 423 ARTERIOSCLEROSIS aortic and coronary atherosclerosis, 6C-61 claudication and aortic aneurysm mor- tality, 65-66 peripheral vascular disease claudication, 63. 65 Asian Americans/Pacific Islanders See ETHNIC GROUPS ATTITUDES (See also ADULT USE OF TOBACCO SURVEYS; CANCER PREVEN- TION STUDIES; NATIONAL HEALTH INTERVIEW SUR- VEYS; SMOKING SURVEYS) addictive nature of tobacco use, 200,202 adolescents, 212-215.216,217-218, 227-229.409 air pollution, health risks, 207, 209-210, 211 alcohol consumption, health risks, 207- 212 asbestos exposure and smoking, lung neoplasm risk, 202 ban on free samples, 239 blacks, risk factors for cardiovascular dis- eases, 2 12 bladder neoplasms, smoking relationship, 195 broadcast antismoking messages, impact on public opinion, 4 I5 carbon monoxide in tobacco smoke, 2 17 cessation of smoking, health effects, 219. 220 children, harmfulness of smoking, Weekly Reader survey, 2 15-2 16 chronic obstructive pulmonary disease, smoking relationship, 188, 193-194, 195 consumption of cigarettes, health risks, 184 coronary heart disease, smoking relation- ship, 188, 191-192 duration of smoking, health risks, 185, 186-187 smoking-and-health reports, effects on public knowledge, 5 19 esophageal neoplasms, smoking relation- ship, 195, 196 health effects of smoking, 179-181, 219, 221-222 heavy vs. light smoking, 181-184. 221 hiring of smokers, 241 inflight smoking bans, 573,574 involuntary smoking, 200.20 1,224, 225 laryngeal neoplasms, smoking relation- ship, 195, 196 life expectancy, risks of smoking, 206 low-yield cigarettes, health risks, 183. 185,221 lung neoplasms, smoking relationship. 185, 186, 188, 189-190 neoplasms. smoking as risk factor, 212 nonsmokers rights, 224,226 obesity, health risks, 207-212 oral contraceptives, interactions and risks, 197-199 peer influence on smoking, 336338 pregnancy, dangers of smoking, 197 restrictions on smoking in public, 23& 239,578 risk models, 262 I2 smokeless tobacco use, mouth and throat neoplasms, 202 smokers, personal risk, 202-204.205 smoking-and-health advocacy groups, at- tempts to change public perceptions, 436-431 survey methodology. 176-l 78 tobacco access laws, law enforcement of- ficials, 605-606 types of cigarettes, harmfulness, 18 1 women, dangers of smoking, 195,197- 199 workplace restrictions, 578,589,600-601 BEHAVIOR, HUMAN actions of smokers among nonsmokers, 227 child risk taking, 399400 estimated risks of various activities, 160 health risk knowledge vs. smoking habit, 344-345 self-efficacy and smoking cessation, 351 self-reported smoking status, 265-266 switching cigarette types, antismoking campaign, 664-665 BIOASSAY biochemical markers, mainstream and sidestream smoke, 94-97 smoking status validation, vs. self reports, 265 thiocyanates and diet, 96 691 BIRTH DEFECTS parental smoking. 73. 75 cessation of smoking, 73 fetal hypoxia and carbon monoxide, 72 maternal smoking, dose-response effect, 72 BLACK AMERICANS adolescents, smoking prevalence, 303- 306 cardiovascular disease risk, beliefs, 2 12 initiation of smoking, 301-302 maternal smoking, 72,73-74, 275 prevalence of smoking, 269-27 1 quit ratios, gender, 286 self-reported daily cigarette consumption, heavy smokers, 295 statistical bias, lung cancer risk among women, 129 tar and nicotine content, beliefs about health risks, 183. 185 CALIFORNIA nonsmokers' rights group, proposition on `smoking restrictions, 442 public transit bans. 5 13, 574 restaurant smoking restrictions, Beverly Hills, 57 I Safe Drinking Water and Toxic Substan- ces Enforcement Act. 6 12 San Diego study, National Clearinghouse for Smoking and Health, 397 warning labels, tobacco products. 612 workplace smoking restrictions, 57fL57 1. 577 CANADA ban on tobacco advertising and promo- tion, 5 16 public beliefs about addictive nature of tobacco use. 200,202 Tobacco Products Control Act. 487 transportation smoking restrictions. 574, 58X-589 CANCER PREVENTION STCDIES (AMERICAN CANCER SOCIETY) chronic obstructtvJe pulmonary disease and smoker mortality. 146 comparability with other studies. 14&141 coronary heart disease and smoker mor- tality. 143-145 estimated relative risks, cancer. coronary and pulmonary diseases, 146-152 lung cancer and smoker mortality. 143- I44 mortality, 122, 142 relative risk changes, 131-132 sampling bias and validity. 128-J 29 CARBON MONOXIDE advertising guidelines, 4881189 carboxyhemoglobin. biochemical markers, 96 public beliefs about tobacco smoke con- stituents. 217 CARCINOGENESIS adenomas, adenocarcinomas. and car- cinomas, long-term smoke exposure, 93 polynuclear aromatic hydrocarbons and N-heterocyclic hydrocarbons, 8.5 tumorigenic agents in tobacco, 8687 reduction by tobacco additives, 614 CEREBROVASCULAR DISORDERi drug therapy efficacy, 63 estimated relative risks, 1960s and 1980s. 147-152 Japanese-American men, Hawaii, 62 mortality and morbidity, 6142 public beliefs about smoking and oral contraceptive use, 197, 198 risk factors, 61-62, 63 women and smoking habit, 6263 CESSATION OF SMOKING adolescent attempts, Britain and United States, 596 advertising and promotion of tobacco, ef- fects. 502 brand-switching as alternative, health con- sequences, 665-666 cardiovascular disease risk reduction, 423424 cerebrovascular disease risk reduction, 147,152 ethnic and demographic differences, 286 287 expectancy-value and health-belief decisionmaking models, ?5&351 gender differences. 354 historical perspectives, 330.433336 hospital restrictions, impact. 589. 592 immediate vs. long-te,m effects of tobac- co, 393 indicators of quitting activity, 285 insurance, 55 l-552,552-553 lung cancer risk reduction. 55, 127 nicotine dependence, 339 outcome expectations, 352 692 pharmacologic processes and condition- ing. 349 physician impact, 418-420 precontemplation, contemplation. and ac- tion stages, 348 pregnant women, 353.400 public beliefs about health effects. 219, 220 reimbursement of drug treatment, 553 restrictions as incentive. 578-579 role of disease incidence. 352-3S3 self-efficacy model, 35 l-352 smoking continuum of quitting process. 288-289.292 stage model. opportunities for older adolescents, 386 stages, 413 trends. 287 workplace policies. 354-355.589. 563 workplace restrictions. impact. 592 young smokers. quit attempts, 392 CESSATION OF SMOKING, hlETHODS acupuncture, 43 I American Lung Association materials. 414 clonidine, 428 commercial programs, 427.431-432 computer-assisted program, 43 I filter systems, 430 Great American Smokeout day, 4 16-4 17 history of aids and treatments, 409-413 How to Quit Smoking workplace program, 432 how-to-quit materials, 430 hypnosis. 431 interpersonal support, 354-355 Live for Life workplace program, 432- 433 lobeline sulfate capsules, 428 nicotine polacrilex gum. 428429, 553, 616 nonpharmacologic aids. 430-43 1 pharmacist's antismoking materials, 425 pharmacologic cessation aids, 428-429 physician advice and materials, 418-4 i9, 422-423 quit rates for different treatments, 4lO- 413 Schick Stop Smoking program, 432 silver acetate, 428 Smoke Stoppers program. 433 smokeless cigarettes, 430 Smokeless program, 433 SmokEnders program, 43 1 CHILDREN access to tobacco. 59GS97. 599-603, 603-604 beliefs about harmfulness of smoking, Week/~ Reader survey, 2 I S-2 I6 intervention approaches for young smokers. 386 maternal smoking, long-term effects. neurological handicaps, 75-76 parental smoking effects. 336338 penalties for tobacco possession, 603 psychosocial approaches to antismoking education. 385 recall of cigarette advertisements. effect on smoking behavior. 505-506 revenue from tobacco sales to minors, 605 States prohibiting free tobacco samples for minors. 599-602 Surgeon General's Reports, smoking prevention. 40@4Ol CHRONIC OBSTRUCTIVE PULMONARY DISEASE age-specific death rates. 146 attributable risks, sex ratio, 153-161 morbidity and mortality, 6667. 71. l4l- 142 pathogenesis, enzyme activity, 67 pathophysiology. emphysema and small- airway injury, 67-68 public beliefs about smoking relationship, 188,193-194,195 respiratory function tests, 68-70 ventilatory function, 68-7 I CIGAR SMOKING age-adjusted relative risks, 153 gender, age, race, socioeconomic and demographic factors. 322, 326-328 lung cancer mortality, 50 mortality, vs. pipes vs. cigarettes. 4142 prevalence rates, men, I34 CIGARETTES, LOW-NICOTINE alternative to cessation. antismoking cam- paign, 664665 lung cancer mortality, 44.46 public beliefs about health risks, 183, 1 X5 yield, sales, consumption, 313-3 14 CIGARETTES, LOW-TAR alternative to cessation, antismoking cam- paign, 6-65 changes in tobacco products, risk assess- ment, I39 lung cancer mortality, 44.46 693 public beliefs about health risks, 183, 185,221 safety and public perceptions, 416 yield, sales, consumption, 3 13-3 15 CIGARETTES, LOW-YIELD alternative to cessation, antismoking cam- paign, 664-665 consumption, 658 health effects, 315-316,666 market share, 665 public health concerns, 183, 185,490 safety and public perceptions, 416 tar and nicotine reductions in filtered products, 85.88 COGNITION developmental model of smoking acquisi- tion and prevention, 391-392 health effects of smoking, knowledge, 335-336,344-345 Health Objectives for the Nation, 1990, public knowledge, 223-224 health warnings, effectiveness of wording and format, 484 risk assessment, understanding by public, 222 smoking cessation, 348-349,350-35 1, 351-352.353 COLORADO Aspen, smoking ordinances, effects on business, 572 CONDITIONING biological effects of nicotine, 343 environmental smoking cues, 349-350 pharmacologic effects of nicotine in smoking cessation, 349 withdrawal symptom relief, 343-344 CORONARY HEART DISEASE age-specific death rates, 144-145 attributable risks, 153-161 avoidable risk from smoking, I3 I Cancer Prevention Studies, risk factors and potential bias, 128 changes in risk behavior, with smoking, 139-140 diabetes as risk factor, 59 estimated relative risks, 147-15 1 myocardial infarct risk, mortality and treatment, 58-59,61 nonsmoker mortality, 141-142 pathophysiologic mechanisms, 60-61 public beliefs about smoking relationship, 188. 191-192 risk factors and smoking, 59-60 smoking cessation effects, 61 survey of patients' siblings on risk fac- tors, smoking, 2 12 DEMOGRAPHIC FACTORS bias in risk assessments, 128 cigar and pipe smoking, 327-328 education, 269,27 1,286,287,289-290, 292,301-302,303-306,316 gender, 276,322-326 gender, socioeconomic, and personality variables, smoking habit, 329 personal characteristics and smoking, 347 region, gender, education, and smoking prevalence, 279,282-283 smoking cessation and relapse, 353 variation among antismoking strategies, 408-409 DIET cholesterol, 207,209-210,212 hypercholesterolemia, 139-140 lung cancer and protective effects of vitamins, 54 DRUG ABUSE adolescent beliefs, smoking vs. other sub- stance use, 214,215 cigarettes as a "gateway drug," 399 integration of smoking prevention programs into substance abuse programs, 401 marijuana smoking, public beliefs, 207, 211 school health education programs, 388- 389 ECONOMICS ban on cigarette sales, public opinion, 235,237 cigarette prices in military commissaries, 426 consumer demand and production factors, 6-61 institutional dependence on tobacco in- dustry, effect on consumption, 502 price elasticity, 533-538,662-664 public service announcements, effects on cigarette consumption, 498 public transit advertising ban, impact, 514-515 restaurant smoking ban, effect on busi- ness, Aspen, 572 trends in per capita cigarette consump- tion, 267-268 694 Education See DEMOGRAPHIC FACTORS; HEALTH EDUCATION EMPHYSEMA airflow obstruction, 67-68 morbidity and mortality, chronic obstruc- tive lung disease, 66-68 protease-antiprotease activities in pathogenesis, 67 public beliefs about smoking relationship, 188, 193-194, 195 Environmental tobacco smoke See INVOLUNTARY SMOKING ETHNIC GROUPS (See also BLACK AMERICANS) Asian Americans, Hawaii, smoking prevalence, 275 cigar and pipe smoking, 327-328 Hispanics, smoking prevalence, 274 Native Americans and Alaskan Natives, smoking prevalence, 274 race and smoking continuum, 289,291, 292 racial differences in smoking onset and prevalence, 338 smokeless tobacco use, 322-324 tar yields and menthol cigarettes, 316 EX-SMOKERS age factors, 136 attributable risk, lung cancer, and women, 127 health benefits of smoking cessation, 666, 667 lung cancer risk reduction, 55 measurement of quitting activity, 285 mortality, sex ratio, 147-152 prevalence, 132-134,288-289 public beliefs about risk reduction after smoking cessation, 2 19,220 self-attained cessation of smoking, 413 FILTERS lung cancer mortality, 44,46 reduction of toxic and tumorigenic agents in cigarettes, 85 sales, Consumption, 3 13-3 14 shift from unfiltered, antismoking cam- paign, 664665 use, lower yield cigarettes, 138-l 39 FIRES fire-safe cigarettes, development and feasibility, 614 Insurance. smonmg-reuueu UG~LILI P~IU damage, 550 smoking-related deaths, 614 Former smokers See EX-SMOKERS HEALTH EDUCATION advocacy group activities, 438 budgets of Federal agencies, 52&523 Comprehensive Smokeless Tobacco Health Education Act, 478,481,490, 511.512.518 Comprehensive Smoking Education Act, 478,479,481,490.512,517-518 Department of Defense, 426,521 integration of programs with policy initia- tives, 383 national goals, l6- I9 National Heart, Lung, and Blood In- stitute, Smoking Education Program, 424-425 national voluntary health organizations, 394-395,413418 prevention of smoking programs, 335- 336,385,397-398,401-402,403405, 406.407-408 school-based programs, 388-389.390, 391,491494 Surgeon General's Reports, smoking prevention, 401 teacher training, State requirements, 494, 495 youth programs, cessation of smoking, 392-393 Hispanic Americans See ETHNIC GROUPS INDIANA designated smoking areas in hospitals, 586 Inhalation patterns See SMOKING CHARACTERISTICS INITIATION OF SMOKING advertising and promotion of tobacco, 501 age, adults vs. adolescents, 296 campaign-related decreases, 666667 delay, smoking prevention programs, 406 developmental stages models, 385-386 knowledge of health effects, 335-336 lung cancer mortality, men, 45 National lnstitute for Child Health and Human Development, 399-400 peer pressure, 389-390 695 pharmacologic processes and condition- ing, 333-335 prevalence of smoking, 135-l 36, I37 price effects, 537-538 risk personalization, 2 15 social influence and life skills training ap- proaches, 390-391 trends, gender, race, and education, 301 INSURANCE auto, 550-55 1 biochemical validation of smoking status, life insurance, 545 coverage of smoking cessation treatment, 552-553,557 nonsmoker premium discounts, 543,544, 546-55 I premium calculations, smoking status, health maintenance organizations, 548 premium differentials, incentives to stop smoking, 551-552 INVOLUNTARY SMOKING biochemical markers, 95-97 exposure risks, lung cancer, nonsmoking women, 77-78 Federal workplace policy to limit expo- sure, 575 indoor air pollution, lung cancer risk, 53- 54 nonsmokers' rights movement, 442-443 public annoyance, survey results, 224,225 public beliefs about risk, 200,201 regulation of environmental tobacco smoke, 6 I 3 sidestream effects, toxic and tumorigenic agents, 88-91 workplace exposure, restriction ration- ales, 58G58 I, 594 LABELING LEGISLATION (See also TAXATION) Cigarette Labeling and Advertising Act, 441 Cigarette Safety Act, 614 Clean Indoor Air Acts, 558,572,613 Comprehensive Smokeless Tobacco Health Education Act, 443,478,48 I, 490.51 I, 512,518,612 Comprehensive Smoking Education Act, 398, 437,443,478, 479,48 I, 490.5 12, 517-518 Consolidated Omnibus Budget Recon- ciliation Act, 443 Consumer Product Safety Act, 61 I Controlled Substances Act, 610-611 Federal Cigarette Contraband Act, 534 Federal Cigarette Labeling and Advertis- ing Act of 1965,7, 19, 137,475-476, 482,517,518 Federal Food, Drug, and Cosmetic Act, 609 Federal Hazardous Substance Labeling Act, 610,611 Food and Drugs Act of 1906,608609 Little Cigar Act, 477.486.5 I I Minnesota Clean Indoor Air Act, 558 Occupational Safety and Health Act, 612- 613 Omnibus Budget Reconciliation Act, 528 Public Health Cigarette Smoking Act, 441.476,477,496,511,512,517,518, 520 Public Health Service Act, 613 Safe Drinking Water and Toxic Substan- ces Enforcement Act, 6 12 tobacco access laws, 597-598,606,607- 608 Tobacco Products Control Act, Canada, 487 Federal Cigarette Labeling and Advertis- Toxic Substances Control Act, 61 I ing Act of 1965,7.475>76,477,482, 518,519 Federal Trade Commission requirements, 475-476 ..- -.- health warnings, 479-482,484-487,6 I2 nicotine polacrilex gum package inserts, 482 oral contraceptives, 481-482 oral snuff warning labels, Massachusetts, 617 LITIGATION Action on Smoking and Health v. Harris, 611 American Public Health Association v. Consumer Product Safety Commission, 611 Austin v. Tennessee, 598 Cippollone v. Liggett, 611612 Federal Trade Commission v. Brown and --- Palmer v. Liggett. 6 I2 public opinion, 24 I, 242 Williamson, 489,5 I I Federal Trade Commission v. Liggett and Myers, 608-609 6% Federal Trade Commission v. RJ. Reynolds. 5 I2 Illinois Cigarette Service Co. v. City of Chicago, 598 Mutual Benefit Life Insurance Company v. JMR Electronics Corp., 545-546 Palmer v. Liggett. 6 12 Parker v. City School Superintendent, 606 U.S.A. v. Liggett, 476 U.S.A. v. R.J. Reynolds. 476 Lobbying See ADVOCACY LUNG NEOPLASMS age-specific mortality rates, 143-144 asbestos exposure. smoking and risk, 202 dose-response relationships, 4346 familial determinants, 52 female mortality, 4649, 125-l 26 histologic type, 5&51 inhaled tobacco carcinogens. 93 International Classification of Diseases, 130 male mortality, 44-45 nonsmoker mortality, 141-142 public beliefs, smoking and risk, 185, 186, 188, l89-190,202 radon and risk, 53-54 vitamins, protective effects, 54 MASS MEDIA advertising restrictions, 239-240 advertising revenues, 502.508-510 American Cancer Society, television ad- vertisements, smoking cessation, 414 American Lung Association, series for news broadcasts, 417-4 I8 broadcast ban of tobacco advertisements, 496,511 Cigarette Advertising Code, 5 11 coverage of smoking and health related to cigarette advertisers, 509 national voluntary health organizations, television campaigns, 41%416 news media coverage of health risks, 222 public service announcements, 497-500 video news releases, 388 MASSACHUSETTS availability of tobacco to adolescents, 604405 Cambridge, smoking restrictions, 577 local smoking ordinances, prevalence, 572 oral snuff, warning labels, 6 I2 public opinion about smoking restric- tions, 578 public transit advertising ban, 5 13 MATERNAL SMOKING birth defects, dose-response, 72 blacks, 72,73-74,275 demographic factors, 275-276 fetal and perinatal mortality, 73 hypoxia. fetal and neonatal effects, 72 infant birthweight, 72-73 infant mortality, 73-74 long-term effects, 75-76 National Institute for Child Health and Development, 400 neurological handicaps, 75-76 public beliefs about smoking effects, 195, 197,221 socioeconomic status, 276 spontaneous abortion and chromosomal abnormalities, 73 MATHEMATICAL MODELS attributable risks from cigarette smoking, 153-161 attributable, relative, and absolute risks, hazardous exposure variables, 123-125 avoidable deaths from cancer and coronary heart disease, 13 1 consumption patterns, changes in smok- ing-and-health environment, 662&G% dose-response relationships, 44 lung cancer rates among females, 125- 126 mortality postponed or avoided, 666-669 smoking prevalence, 270,651-657 synergy of radon exposure and cigarette smoking, 125 MINNESOTA Clean Indoor Air Act, 558 excise funding of smoking prevention program, 402 hospital smoking ban, 586 smoking control program, 524,542 stadium advertising ban, 573 MORTALITY (See also MATHEMATICAL MODELS) age factors, 41-42.45 all and specific causes, smokers and ex- smokers, 146-l 52 attributable risks from smoking, 13s 132, 154-156.206-207 cancer, 47,48 697 cardiovascular and respiratory disease, cancer, 3940 diabetes and coronary heart disease, 59 esophageal neoplasms. 56 laryngeal neopiasms. 56 misclassification of cause, International Classification of Diseases, 130 oral neoplasms, 56 overall rates, 38-41 pancreatic neoplasms, 5657 postponed deaths, campaign-induced, 666-669 public beliefs about risks, 206 relative risk, lung cancer, women, 126 smoker vs. nonsmoker, 544-545 smoking-attributable total, I60 statistical bias, lung cancer risk among women, 129 stomach neoplasms, 57 stroke, 6162.64 tax-related changes, 540 MULTIPLE RISK FACTOR INTER- VENTION TRIAL (MRFIT) advertising by R.J. Reynolds, mis- representation of study, 5 I2 mortality and morbidity, smoking habit. 41 program history, National Heart, Lung, and Blood Institute, 423-424 NATIONAL HEALTH INTERVIEW SURVEYS (NHISs) daily cigarette consumption, 292-293, 295 gender, race, education, 267,269-270 initiation of smoking, 297, 301 methodology and scope, 25&25 I population-weighted mortality data. 122 prevalence data, self-respondents and proxies, 132-133 quit ratios, 286, 287 sampling errors, I29 smokeless tobacco use, 319-320 smoking prevalence, 272-274,298,299 Native Americans or Alaska Natives See ETHNIC GROUPS NEOPLASMS attributable risks, sex ratio, 1965 and 1985, 153-161 avoidable risk from smoking, 131-132 bladder and kidney, smoking dose- response, 56 public beliefs about smoking risk, 212 NEW YORK Clean Indoor Air Act, 572 commuter rail smoking ban, 573 compliance with restaurant smoking restrictions, 577 public opinion about smoking restric- tions, 577-578 workplace smoking policies, 582 NICOTINE advertising guidelines, 488-489 alkaloids in tobacco, 79 biochemical marker, 95-97 conditioning and smoking, neurohumoral effects, 343 deposition, absorption, and metabolism, 93-94 historic perspective, smoking behavior, 329-330 metabolism, 94-96 peptic ulcer, 76 proposed Federal regulation of cigarette content, 6 10 regulation of blood level, 342 trend for cigarette content, 88 NICOTINE DELIVERY alternative products, 615-616 nicotine aerosols, 616 nicotine polacrilex gum, 616 reduced-smoke cigarettes, 617 smokeless cigarettes, 3 18-3 19 tobacco chewing gum, 616 tobacco toothpaste, 6 16 Nicotine polacrilex gum See NICOTINE DELIVERY; CESSA- TION OF SMOKING, METHODS NONSMOKERS beliefs about personal risks of smoking, 203,204 health claims, 549 insurance premium discounts, 546-548 lung disease, involuntary smoking, 77-78 mortality rates, 141-145 prevalence, 288-289 workplace smoking restriction, 575,584, 590,59 1 Nonsmokers' rights See ADVOCACY OCCUPATIONAL DISEASES asbestos exposure, public beliefs about smoking risks, 202 698 workplace exposures, lung cancer risk, 52-53, 128 OCCUPATIONS blue-collar workers. 272-274 industry type, 585 managers, 585 military personnel, 277-278,347,425- 427 white-collar workers, 272 Passive smoking See INVOLUNTARY SMOKING PEER GROUPS initiation and maintenance of smoking, 336-338 smokers vs. abstainers, 355 social support, smoking, and cessation, 354-355 PERCEPTION health risks of smoking, health warnings, 485 positively perceived effects of smoking, 342 social acceptability of smoking, 347 PERSONALITY extraversion, 336,345 internal vs. external locus-of-control dimension, 346 marketing campaigns and personality characteristics, 339 negative affect smoking, 346 neuroticism, delinquency, and smoking status, 336 psychosocial factors, smoking habit, 329 relapse rates after smoking cessation, 353 PIPE SMOKING age-adjusted relative risks, 153 lung cancer mortality, 50 mortality, vs. cigars and cigarettes, 41-42 prevalence among men, 134 socioeconomic and demographic factors, 322,326-328 PREVENTION OF SMOKING, PROGRAMS American College of Chest Physicians, 419-420 American Nonsmokers' Rights Founda- tion, 402 American Pharmaceutical Association, 423 construct validity, 406-407 demographic and historic factors, 408- 409 Department of Defense, 425-427 design and target audiences, trends, 384 dissemination, 403-405 evaluation, 405 Federal Government support, agencies and reports, 396-401 Federal guides of existing resources, 396 general school health education levels, 389 Great American Smokeout day, 416-417 health professional organizations, 402- 403 historic perspective, 330 long-term followup, 406 mass media, 387-388 National Cancer Institute, 398-399,421- 423 National Heart, Lung, and Blood In- stitute, 399.423-425 National Institute on Drug Abuse, 399 National Interagency Council on Smok- ing and Health, 395-396 Office of Disease Prevention and Health Promotion, 400,425 Office on Smoking and Health, 397-398, 421 psychosocial curricula, 389-392 school health education, 388-389 State, 401-402.427 voluntary health organizations, 394-395, 407-418 workplace, 425,432434 youth, 392-393 POLICIES advertising imagery and content, proposals, 5 15 categorization of tobacco control efforts, 472.473 educational and behavioral interventions and initiatives, 383 Fairness Doctrine, 441-442,496,660- 661 Health Objectives for the Nation, 16-19, 223-224 history of smoking-and-health research and regulation, 5-6 national goals for insurance, nonsmoker premiums and actuarial data, 553-555 restriction of advertising and promotion, 515-516 restriction of smoking, impact on per capita consumption, 661-662 taxonomy of workplace smoking policies, 581 trends. 409413 warning labels, Federal Trade Commis- sion requirements, 475-476 PROMOTION (See also ADVERTISING) decreased motivation to stop smoking, 502 encouragement of smoking initiation. 501 encouragement of recidivism, 502 expenditures, 499-500 free distribution of tobacco products, 239. 513,514,597,603-604 nicotine polacrilex gum, 429 proposed restrictions, 5 15 States prohibiting tobacco sales to minors, 599-602 tobacco consumption. 501-502 Public service announcements See ADVERTISING; ADVOCACY; HEALTH EDUCATION; SMOK- ING CONTROL PROGRAMS RECIDIVISM advertising and promotion of tobacco, 502 body weight and smoking cessation, 354 coping responses, 350 gender differences, 354 prevention strategies, 4 IO, 4 13 socioeconomic and demographic factors, 353 stress, negative affect, 349 triggers to relapse. 349-350 RESTRICTION OF SMOKING airplanes, 232.573-574.588-589 airports, 574 Clean Indoor Air Act, New York, 572 consumption impact. 591-592.661662 Department of Defense, 575 economic impact. 594595 educational institutions. 561-568, 587- 588 Federal Government workplaces, 574575 fire hazards, 557 health care facilities, 561-568. 585-586, 561-562 industry type and prevalence of smoking policy, 585 local ordinances, 57g572.577 penalties for noncompliance, 561-568 pharmacies. 587 physician offices and medical organiza- tions, 586 provisions of laws, 560,568 public places, 232-233,556557,558 public transportation, 561-568.573.574 regional variation, 570.57 I restaurants and hotels, 235, 236, 569, 570,577 State laws, 558-560,56l-569,569-570, 599-602 target occupational groups, 595 tobacco access laws, 603,604-606,607- 608 trends in public beliefs, 23G23 I vending machines, access, 603604 workplace policies, 232, 56l-568,6OCL 601,577,581-585,590,591,593,594- 595 SEX RATIO age-specific death rates, 144-145, 146 antismoking campaign effects, 650-657 attributable risks for cancers, coronary and pulmonary diseases, 154-l 56 initiation of smoking, 296300 lung cancer mortality, 46 mortality postponed or avoided, 667,668- 669 nonsmoker mortality, 141-142 self-reported daily cigarette consumption, 295 smokeless tobacco use, 32CL322 smoking cessation and relapse, 354 smoking continuum, 289-290 smoking prevalence, 132-133. 134-135, 136-l 37, 138,269-270,272,279.282- 283,298,301,302,303-305,307-312, 316 SMOKE STREAMS mainstream chemical analysis, vapor and particulate phases, 79-85 sidestream effects, toxic and tumorigenic agents, cigarettes, 88-91 SMOKELESS TOBACCO advertising strategy, graduated use, 507 antismoking pamphlet, American Dental Association, 420 Comprehensive Smokeless Tobacco Health Education Act, 478,48 I, 490, 511.512,518 disclosure of nicotine content. require- ments, 500 Federal excise tax. 528 700 health warning requirements. 478. 479. 4x0.4x I nitrosamine formation and oral cancer. 90. 92 snuff-dipping and oral cancer. leukoplakia. 78 State excise taxes. S3Y SMOKELESS TOBACCO USE adolescent\. 217.393 National Cancer Institute prevention programs. 398 prcv~alence among male\. 3 19-322. 325 316.657 puhl~c beliefi. mouth and throat neopla\ms. 202 S.MOKING BEHAVIOR adults. 133-13s. 140. 298. 302 advertismg effects. 501-502. 506507 appetitive model, smoking cues. 344 Asian Americans, 275 chronic obstructive pulmonary disease. 6849 cigarette consumption. 267-268.293- 294.5 18-5 19.592.657-662 determinants of smoking, stages, 334 development. maintenance, cessation. 33 l-332.334 estimated prevalence in absence of anti- smoking campaign, 65 l-657 gender. race, education. 269-270,302- 306 heavy vs. light smoking, 18 1-I 84,22 I Hispanics. 274 intensity. biochemical markers, 95-97 maintenance, pharmacologic processes and conditioning, 340,342 men, 269-270 military personnel, 276278, 575 Native Americans, 274 nicotine dependence, 33 I, 349 opponent-process theory, aversive wtithdrawal symptoms, 343-344 oral contraceptive use, 140 personal characteristics, 336.345-347 pregnant women, 275-276 price elasticity and smoking prevalence, 536539 public beliefs about duration and health risks. 185, 186-187 public service announcements. 497-500, 514 self-reported status vs. biochemical validation. 265 socioeconomic and demographic factors, 329 State legislative impact. 578-579 State-specific prevalence. 2X@-28 I Third World countries. I9 workplace policies. 584. 589,591-592 SMOKING CHARACTERISTICS compensation, 3 l6,3 I7 inhalation patterns and lung cancer mor- tality. 45 length of cigarette, market share. 3 17-3 18 menthol cigarettes. inhalation, 317 sex ratio. 132-l 33 SMOKING CONTROL PROGRAMS hospital prohibition of cigarette sales, 586 knowledge among smokers about health effects, 221 Minnesota. 525.542 Office on Smoking and Health, 397 Rocky Mountain Tobacco-Free Chal- lenge. 524 tobacco taxes as funding source, 542-543 Utah, excise revenues. 542 SMOKING SL'RVEYS (See also ADULT USE OF TOBACCO SURVEYS; CANCER PREVEN- TION STUDIES; NATIONAL HEALTH INTERVIEW SURVEYS) American Medical Association, 247 Behavioral Risk Factor Surveillance Sys- tem, 247-248,278-279,280-281 Chilton Survey, 1979,248 Collaborative Perinatal Study, 276 Current Population Survey. 248,279, 282-283.322 Department of Defense, 276278,427 Gallup Surveys, 248-249 High School Seniors Surveys, 296,302- 303.306 Hispanic Health and Nutrition Examina- tion Survey, 251 I 274 Lieberman Research, Inc., 249 methodology, public attitudes on health effects of smoking, 175-l 77 National Adolescent Student Health Sur- veys, 250,296297.3-307 National Health and Nutrition Examina- tion Surveys, 251 National Household Surveys on Drug Abuse, 3 I2 National Institute on Drug Abuse High School Seniors Surveys on Drug Use, 251-252 701 National Maternal and Infant Health Sur- vey. 215 National Natality Surveys, 275 National Survey of Family Growth, 276 Native Americans and Alaskan natives, 274 Roper surveys, 252-253 teenagers, 307-309.3 1 O-3 12 U.S. Department of Health, Education, and Welfare Teenage Smoking Sur- veys, 253 SNUFF ban on sales, 6174 I 8 marketing and labeling, 615 warning labels, Massachusetts, 612 SNUFF-DIPPING adolescents, beliefs about harmfulness, 217,218 adults. 1964 to 1986, 319-322 males, 3 19-322 prevalence and proposed ban, 615 SOCIOECONOMIC STATUS birthweight and maternal smoking, 73 blacks vs. whites, smoking prevalence, 269-270 cessation and relapse, 353 cigar and pipe smoking, 328 educational level and occupation, 139 personal characteristics and smoking, 347 pregnant women, 276 smokeless tobacco use among males, 322-323 students with blue-collar backgrounds, 408 SOUTH CAROLINA local smoking restrictions, 572 STATISTICAL ANALYSIS (See also MATHEMATICAL MODELS; SMOKING SURVEYS) adolescent smoking, weekly vs. daily rates, 307, 3 12 advertising expenditures and tobacco con- sumption, 504-505 age adjustment and relaiive risk, 127 aggregation vs. precision, lung cancer risk among women, I27 attributable risk, causation, and mortality, 122-123 bias in risk assessments, 128 Cancer Prevention Studies, age adjust- ment of relative risks. 141 data errors, exposures and causes of death, 129-l 30 data sources, 264 methodology of public opinion surveys, 175-178 per capita consumption studies, 657-658 risk factor interaction with smoking, 50- 51 synergy and statistical bias, 128 STRESS consumption and initiation, smoking habit, 329 public beliefs about risks of smoking, 207-210.212 reduction, biological effects of nicotine, 346347 smoking cessation and relapse, 353 STUDENTS adolescents, personalization of smoking risks, 215 beliefs on health effects of smokeless tobacco, 217,218 litigation. school smoking lounges, 606 parental awareness of school-based programs, 387 program failure to reach dropouts, 407- 408 school health education curricula, 38% 389 school smoking restrictions, 587-588 TAR CONTENT advertising guidelines, 488489 chemical analysis of particulate matter in mainstream smoke, 83-84 proposed Federal regulation of cigarettes, 610 reductions, 85,88,6 I7 smokers' gender, age, race, education, 3 16 TAXATION ad valorem tax on cigarettes, revenues, 542 cigarette price changes, 662 evasion of cigarette taxes, cigarette boot- legging, 531-533, 541 excise taxes, 264 Federal and State tobacco tax increase, ef- fects, 541 Federal excise tax, 527-528,529,530, 540 Indiana, cigarette excise tax. 542 licensing requirement for tobacco sales, 604 702 Minnesota. cigarette excise tax, 402,525 Nebraska, cigarette excise tax, 542 price elasticity of demand. 533-538 sales tax exemption. 54 I smoking-related deaths, effects of tax rates, 540 State and local excise rates and prevalence, 528-532 tax-exempt cigarette sales, impact on States, 533 tobacco tax revenues for State smoking control programs, 542-543 unit tax on cigarettes, 542 Utah, cigarette excise tax, 542 TEXAS smoke-free hospital rooms, 586 workplace smoking restrictions, 583 TOBACCO ADDITIVES changes in cigarettes, I39 disclosure requirements, 490 menthol cigarettes, health effects, 3 I7 pesticide traces, 82,85 reduction of carcinogens, 6 14 risks and disclosure, 613 TOBACCO INDUSTRY advertising refuting claims about harmful- ness of smoking, 51 I-512 censorship of smoking and health items, 509-510 Cigarette Advertising Code, 5 I I code regarding free samples, 597 compliance with health warning legisla- tion, 476,483 disincentives to advertise, 5 I6 lobbying efforts, 440-441 marketing of low-yield cigarettes, 665 restrictive policies, 595 vending machine sales, 604 TOBACCO SMOKE physical chemistry, carcinogenic and mutagenic effects, 79-85 tar and neoplasms. 93 toxicity and carcinogenicity, 92-93 UTAH public transit advertising ban, 5 13 smoking control program. 542 UTERINE NEOPLASMS cervical cancer, smoking and other risk factors, 57-58 endometrial and cervical cancers, risk vs. protective factors. I52 endometrial cancer and estrogen levels, 58 VIRGINIA local smoking restrictions. 572 WOMEN all-cause and specific mortality. 146147, 149, 151-152 attributable risk, cancers, cardiovascular and pulmonary diseases, 157-l 58 attributable risk, lung cancer, 126 cancer mortality risk, 47 cervical and endometrial cancer, 57-58 fertility and smoking, 75 initiation of smoking, 299, 300, 301,302 lung cancer mortality risk, 46-49, 144 mortality postponed or avoided, smoking cessation or noninitiation, 667,668-669 National Institute for Child Health and Human Development, cessation of smoking program, 400 oral contraceptive use, 140, 197-199, 481-482 osteoporosis, calcium intake, estrogen, and obesity, 7677 pregnancy, dangers of smoking, public beliefs, 195, l97-199,221 pregnancy, demographic factors, smoking prevalence, 275-276 pregnancy, smoking cessation programs, 418.427 public beliefs about dangers of smoking, 195. 197-199 response to antismoking campaigns, 650- 651,653-657 smoking prevalence, 1965 to 1987,269- 270 stress, smoking cessation and relapse, 353-354 stroke and smoking habit, 6243 eU.S.G.p.0. 1989 623-880/10288 703