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