Tobacco Documents Online

Introduction Development and Organization of the 1986 Iteport The 1986 Report was developed by the Office on Smoking and llealth of the U.S. DeparUnent of /lealth and Human Services as part of the Uepartment's reshonsibility, under Public Law 91-222, to report new and current information on smoking and health to Lite United States Congress. The scientific content of this Report reflects the contributions of more than 60 scientists representing a variety of disciplines. individual manuscripts were written by experts known for their understanding of and work in specific content areas. These maiiu- scripts were refined through a series of meetings attended by the authors, OfGce on SAioking llealth staff and consultants, and the Surgeon General. Upon receipt of Lite final manuscripts frorm Lite authors, the Office and its consultants edited and consolidated the individual manu- scripts into appropriate chapters. These draft chapters were subjec- ted to an extensive outside peer review (see Acknowledgments for individuals and their afliliations) whereby each was reviewed by up to seven experts. Their comments were integrated and Lite entire volume was assembled. This revised edition of Lite Report was resubjected to review by l7 distinguished scientists outside the Federal Government, both in this country and abroad. Parallel to this review, the entire Report was also submitted to various institutes and agencies within the U.S. Public Health Service for review and comment. The 1986 Report cotrt:aiiis a Foreword by the Assistant Secretary for Health, a Preface by the Surgeon General of the U.S. Public IlealtlrService, and the followiiig chapters: Chapter 1. Introduclion, Overview, and Summary and Conclu- sions Chapter 2. l lealth Effects of Environmental Tobacco Smoke Exposure Chapter 3. Environinental Tobacco Smoke Chemistry and Expo- suresof Nonsmokers Chapter 4. Deposition and Absorption of Tobacco Smoke Constit- - uents Chapter 5. Toxicity, Acute Irrit:ant Effects, and Carcinogenicity of Environmental Tobacco Smoke Chapter 6. Policies Restricting Smoking in Public Places and the Workplace Overview Inhalation of tobacco smoke during active cigarette smoking remains the largest single preventable cause of death and disability

I I ; t I f r I /or the U.S. }rulrulutiun. Tlre health currsertuences of cigarette smoking and of the use of other tobacco products have been extensively documented in the 17 previous Reports in the health consequences of smoking series issued by the 'J.S. Public ilealtli Service. Cigarette smoking is a major cause or cancer; it is most strongly associated with cancers of the lung and respiratory tract, but also causes cancers at other sites, including the pancreas and urinary bladder. It is the single greatest cause of chronic obstructive lung diseases. It causes cardiovascular diseases, including coronary heart disease, aortic aneurysm, and alherosclerotic peripheral vascular disease. Maternal cigarette smoking endangers felal and neon-Mal health; it contributes lo perinatal mortality, low birth weight, and complications during pregnancy. More than 300,UUU prenrature dealhs occur in the United States each year that are directly attribut:able to tobacco use, particularly cigarette smoking. This Report examines in detail the scienlif ic evidence on involun- tary smoking as a potential cause of disease in nonsmokers. Nonsnrokers' exposure to environmental tobacco smoke is termed involuntary snroking in this Report because the exposure generally occurs as an unavoidable consequence of being in proximity to smokers, particularly in enclosed indoor envirorrments. The term "passive smokitig"'is also used throughout the scientific literature to describe this exposure. The magnitude of the disease risks for active smokers secondary to their "high dose" exposure to tobacco smoke suggests that the "Io.ver dose" exposure to tobacco smoke received by involuntary smokers may also have risks. Allhoul;h the risks of involuntary smoking are smaller than lhe risks of active smokiirg, the number of indi'viduals injured by involuntary smoking is larf;c both in absolute lerms ancl in comparison with the number injured by some other agents in the general environment thut are regulated to curtail their potential to cause human illness. This Report reviews the evidence on the characteristics of main- stream tobacco smoke and of environmmrtal tobacco smoke, on the levels of exposure to environmental tobacco smoke that occur, and on the health effects of involuntary exposure to tobacco smoke. The composition of lhe tobacco smoke inhaled by active smokers and by involuntary smokers is examined fur similarities and differences, and the concentrations of tobacco smoke components that can be measured in a variety of settings are explored, us is smoke deposition and absorption in the respiratory tract. The studies that describe the risks of environmental tobacco smoke exposure for humans are carefully reviewed for their findings and their validity. The evidence on the health effects of involuntary smoking is reviewed for biologic plausibility, and compared with extrapolations of the risks of active

snrukint; to the luwer duse of exlxrsure to tub:rctv smoke IuunJ in nonsmokers. This review leads to three major conclusions: 1. Involuntary smoking is a cause of disease, including lung cancer, In hcalthy nonsmokers. 2. The children of parents who smoke compared with the children of nonsmoking parents have an increased frequency of respiratory infections, increased respira- tory symptoms, and slightly smaller rates of increase in lung function as the lung matures. 3. The simple separntion of smokers and nonsmukers " within the same air space may reduce, but clves not elimir-ate, the exposure of nonsmokers to envirowimen- tal tobacco smoke. The subsequent chapters of this volume describe in detail the evidence Lhat supports these conclusions; the evidence is briefly summarized here. Environmental Tobacco Smoke Constituents lmportant considerations in exarnining the risks of involunt.ar,y smoking are the corrrtwsitivn of environmental tobacco smoke (L I'S) and its toxicity and curcincrgenicity relative to the tobacco smoke inhaled by active smokers. Mainstream cigarette smoke is the smoke drawn through the tobacco into the smoker's mouth. Sidestream smoke is the smoke emitted by the burning tobacco between pulfs. Environmental tob.lcco smoke results from the combination of sidestream smoke and the Iraction of exlialed mainstream smnke not retained by the srnuker. In contrast with mainstream smoke, ETS is diluted into a lar6er volume of air, and it ages prior to inhalation. The cornparison of the chemical composition of the smoke inhaled by active smokers with that inlraled by involuntary smokers suggests that the toxic and carcinogenic effects are qualitatively similar, a similarity that is not too suri-risinK because both mainstream smoke and environmental tobacco smoke result from the combustion of tobacco. Individual mainstream smoke constituents, with appropri- ate testing, have usually been tound in sidestream smoke as well. Ilowever; differences between sidestream smoke and mainstrenm smoke have been well documented. The ternperature.of combustion during sidestream smoke formatibn is lower than during main- stream smoke formation. As a result, Rreateramounts of many of the organic constituents of smoke, including some carcinogens, are generated when tobacco burns and forms sidestrearn smoke than when mainstream smoke is produced. For example, in contrast with mainstream smoke, sidestream smoke contains greater amounts of arnmonia, benzene, carbon monoxide, nicotine, and the carcinogens

2-napthylamine, 4-aminobiphenyl, N-nitrosamine, benzja} anthracene, and benzo-pyrene per milligram of tobacco burned. Although only limited bioassay data comparing mainstream smoke and sidestream smoke are available, one study has suggested that sidestream smoke may be more carcinogenic. Extent of Exposure Although sidestream smoke and mainstream smoke differ some- what qualitatively, the differing quantitative doses of smoke compo- nents inhaled by the active smoker and by the involuntary smoker are of greater importance in considering the risks of the two exposures. A number of different markers for tobacco smoke exposure and absorption have been identified for both active and involuntary smoking. No single marker quantifies, with precision, the exposure to each of the smoke constituents over the wide range of environmental settings in which involuntary smoking occurs. However, in environments without other significant sources of dust, respirable suspended particulate levels (RSP) can be used as a marker of smoke exposure. Levels of nicotine and its metabolite cotinine in body fluids provide a sensitive and specific indication of recent whole smoke exposure under most conditions. Widely varying levels of environmental tobacco smoke can be measured in the home and other environments using markers. The time•activity patterns of nonsmokers, which indicate the time spent in environments containing ETS, also vary widely. Thus, the extent of exposure to ETS is probably highly variable among individuals at a given point in time, and little is known about the variation in exposure of the same individual at different points in time. Lung Cancer - The American Cancer Society estimates that there will': be more than 135,000 deaths from lung cancer in the United States in 1986, and 85 percent of these lung cancer deaths are directly attributable to active cigarette smoking. Therefore, even if the number of lung cancer deaths caused by involuntary smoking were much smaller than the number of lung cancer deaths caused by active smoking„the number of lung cancer deaths attributable to involuntary exposure would still represent a problem of sufficient magnitude to warrant substantial public health concern. Exposure to environmental tobacco smoke has been examined in numerous recent epidemiological studies as a risk factor for lung cancer in nonsmokers. These studies have compared the risks for subjects exposed to ETS at home or at work with the risks for people not reported to be exposed in these environments. Because exposure to ETS is an almost universal experience in the more developed countries, these studies involve compnricon of more exposed nnci less

exposed people, rather than comparison of exposed and unexposed people. Thus, the studies are inherently conservative in assessing the consequences of exposure to E75. Interpretation of these studies must consider the extent to which populations with different ETS exposures have been identified, the gradient in ETS exposure from the lower exposure to the higher exposure groups, and the magni- tude of the increased lung cancer risk that results from the gradient in ETS exposure. To date, questionnaires have been used to classify ETS exposure. Quantification of exposure by questionnaire, particularly lifetime exposure, is difficult and has not been•validated. However, spousal and parental smoking status identify individuals with different levels of exposure to ETS. Therefore, investigation has focused on the children and nonsmoking spouses of smokers, groups for whom greater ETS exposure would be expected and for whom increased nicotine absorption has been documented relative to the children and nonsmoking spouses of nonsmokers. Of the epidemiologic studies reviewed in this Report that have examined the question of involuntary smoking's association with lung cancer, most (11 of 13) have shown a positive association with exposure, and in 6 the association reached statistical significance. Given the difficulty in identifying groups with differing ETS exposure, the low-dose range of exposure examined, and the small' numbers of subjects in some series, it is not surprising that some studies have found no association and that in others the association did not reach a conventional level of statistical significance. The question is not whether cigarette smoke can cause lung cancer; that question has been answered unequivocally by examining the evi- dence for active smoking. The question is, rather, can tobacco smoke at a lower dose and through a different mode of exposure cause lung cancer in nonsmokers? The answer must be sought in the coherence and trends of the epidemiologic evidence available on this low-dose exposure to a known human carcinogen. in general, those studies with larger population sizes, more carefully validated diagnosis of lung cancer, and more careful assessment of ETS exposure status have shown statistically significant associations. A number of these studies have demonstrated a dose-response relationship between the level of ET5 exposure and lung cancer risk. By using data on nicotine absorption by the nonsmoker, the nonsmoker's risk of developing lung cancer observed in human epidemiologic studies can be compared with the level of risk expected from an extrapolation of the dose-response data for the active smoker. This extrapolation yields estimates of an expected lung cancer risk that approximate the observed lung cancer risk in epidemiologic studies of involuntary smoking.

Cigarette smoke is well established as a human carcinogen. The chemical composition of EI'S is qualitatively similar to mainstream smoke and aidestream smoke and also acts as a carcinogen in bioassay systems. For many nonsmokers, the quantitative exposure to ETS is large enough to expect an increased risk of lung cancer to occur, and epidemiologic studies have demonstrated an increased lung cancer risk with involuntary smoking. In examining a low-dose exposure to a known carcinogen, it is rare to have such an abundance of evidence on which to make a judgment, and given this abundance of evidence, a clear judgment can now be made: exposure to ETS is a cause of lung cancer. The data presented in this Report establish that a substantial number of the lung cancer deaths that occur among nonsmokers can be attributed to involuntary smoking. However, better data on the extent and variability of ETS exposure are needed to estimate the number of deaths with confidence. Respiratory Disease Acute and chronic respiratory diseases have also been linked to involuntary exposure to tobacco smoke; the,evidence is strongest in infants. During the first 2 years of life, infants of parents who smoke are more likely than infants of nonsmoking parents to be hospital- ized for bronchitis and pneumonia. Children whose parents smoke also develop respiratory symptoms more frequently, and they show small, but measurable, differences on tests of lung function when compared with children of nonsmoking parents. Respiratory infections in young children represent a direct health burden for the children and their parents; moreover„ these infec- tions, and the reductions in pulmonary function found in the school- age children of smokers, may increase susceptibility to develop lung diseased as an adult. Several studies have reported small decrements in the average level of lung function in nonsmoking adults exposed to ETS. These differences may represent a response of the lung to chronic exposure to the irritants in ETS, but it seems unlikely that ETS exposure, by itself, is responsible for a substantial number of cases of clinically significant chronic obstructive lung disease. The small magnitude of the changes associated with ETS exposure suggests that only individuals with unusual susceptibility would be at risk of develop- ing clinically evident disease from ETS exposure alone. However, ETS exlrnure may be a factor that contributes to the development of clinical disease in individuals with other causes of lung injury. Cardiovascular Disease A few studies have examined the relationship between involun- tary smoking and cardiovascular disease, but no firm conclusion on

the relationship can be made owing to the limited number of deaths in the studies. Irritation Perhaps the most common effect of tobacco smoke exposure is tissue irritation. The eyes appear to be especially sensitive to irritation by ETS, but the nose, throat, and airway may also be affected by smoke exposure. Irritation has been demonstrated to occur at levels that are similar to those found in real-life situations. The level of irritation increases with an increasing concentration of smoke and duration of exposure. In addition, participants in surveys report irritation and annoyance due•to smoke in the environment under real-life situations. Determinants of Exposure Exposure to ETS has been documented to be common in the United States, but additional data on the extent and determinants of exposure are needed to identify individuals within the population who have the highest exposure and are at greatest risk. Studies with biological markers and measurements of ETS components in indoor air confirm that measurable exposure to ETS is widespread. How- ever, within exposed populations, levels of cotinine excretion and presumably ETS exposure vary greatly. In a room or other indoor area, the size of the space, the number of smokers, the amount of ventilation, and other factors determine the concentration of tobacco smoke in the air. The technology for the cost-effective filtration of tobacco smoke from the air is not currently available, and because of their small size, the smoke particles remain suspended in tl.ie air for long periods of time; thus, the onlyy way to remove smoke from indoor air is to increase the exchange of indoor air with clean outdoor air. The number of air changes per hour required to maintain acceptable indoor air quality is much higher when smoking is allowed than when smoking is prohibited. Environmental tobacco smoke originates at the lighted tip of the cigarette, and exposure to ETS is greatest in close proximity to the smoker. However, the smoke rapidly disseminates throughout any airspace contiguous with the space in which the smoking is taking place. Dissemination of smoke is not uniform, and substantial gradients in ETS levels have been demonstrated in different parts of the same airspace. The time course of tobacco smoke dissemination is rapid enough to ensure the spread of smoke throughout an airspace within an 8-hour workday. In the home, the presence of even one smoker can significantly increase levels of respirable suspended particulates. These data lead to the conclusion that the simple separation of smokers and nonsmokers within the same airspace will reduce, but

not eliminate, exposure to !;l'S, particularly in those settinge where exposure is prolonged, such as the working environment. The exposure of an individual nonsmoker to ETS is also deter- mined by that person's time-activity pattern; that is, the amount of time spent in various locations. For adults, the duration of time spent in smoke-contaminated environments at work or at home is the principal determinant of ETS exposure, along with the levels of smoke in those environments. For infants and very young children, the smoking habit of the primary caretaker, as well as that person's time-activity pattern, is likely to play a major role in determining ETS exposure. Policies Restricting Smoking Policies regulating cigarette smoking with the objective of reduc- ing explosion or Gre risk, or of safeguarding the quality of manufac- tured products, have been in force in a number of States since the late 1800s. More recently, and with steadily increasing frequency, policies regulating smoking on the basis of the health risk or the irritation of involuntary smoking have been promulgated. State and local governments have enacted laws and regulations restricting smoking in public places. These policies have been implemented with few problems and at little cost to the respective governments. The public awareness of these policies that results from the media coverage surrounding their implementation proba- bly facilitates their self-enforcement. Public awareness may best be fostered by encouraging the establishment of these changes at the local level. Policies limiting smoking in the worksite have also become increasingly widespread and more restrictive. However, changes in worksiUe policies have evolved largely through voluntary rather than governmental action. In a steadily increasing number of worksites, smoking has been prohibited completely or litnited too relatively few areas within the worksite. The creation of a smoke- free workplace has proceeded successfully when the policy has been jointly developed by employees, employee organizations, and man- agement; instituted in phases; and accompanied by support and assistance for the smokers to quit smoking. This trend to protect nonsmokers from ETS exposure may have an added public health benefit-helping those smokers who are at- tempting to quit to be more successful and not encouraging smoking by people entering the workforce. Summary and Conclusions of the 1986 Report The three major conclusions of this report are the following:

1. Involuntary smuking is a cause of disease, including lung cancer, in healthy nonsmokers. 2. The children of parents who smoke compared with the ' children of nonsmoking parents have an increased frequency of respiratory infections, increased respira- tory symptoms, and slightly smaller rates of increase in lung function aa the lung matures. 3. The simple separation of smokers and nonsmokers within the same air space may reduce, but does not eliminate, the exposure of nonsmokers to environmen• tal tobacco smoke. Individual chapter summaries and conclusions follow. Health Effects of Environmental Tobacco Smoke Exposure 1. Involuntary smoking can cause lung cancer in nonsmokers. 2. Although a substantial number of the lung cancers that occur in nonsmokers can be attributed to involuntary smoking, more data on the dose and distribution of ETS exposure in the population are needed in order to accurately estimate the magnitude of risk in the U.S. population. 3. The children of parents who smoke have an increased frequen- cy of hospitalization for bronchitis and pneumonia during the first year of life when compared with the children of nonsmok- ers. 4. The children of parents who smoke have an increased frequen- cy of a variety of acute respiratory illnesses and infections, including chest illnesses before 2 years of age and physician- diagnosed bronchitis, tracheitis, and laryngitis, when com- pared with the children of nonsmokers. 5. Chronic cough and phlegm are more frequent in children whose parents smoke compared with children of nonsmokers. The implications of chronic respiratory symptoms for respira- tory health as an adult are unknown and deserve further study. 6. The children of parents who smoke have small differences in tests of pulmonary function when compared with the children of nonsmokers. Although this decrement is insufficient to cause symptoms, the possibility that it may increase suscepti- bility to chronic obstructive pulmonary disease with exposure to other agents in adult life, e.g., active smoking or occupation- al exposures, needs investigation. 7. }{ealthy adults exposed to environmental tobacco smoke may have small changes on pulmonary function testing, but are unlikely to experience clinically significant deficits in pulmo-

nary function as a result of exposure to environmental tobacco smoke alone. 8. A number of studies report that chronic middle ear effusions are more common in young children whose parents smoke than in children of nonsmoking parents. 9. Validated questionnaires are needed for the assessment of recent and remote exposure to environmental tobacco smoke in the home, workplace, and other environments. 10. The associations between cancers, other than cancer of the lung, and involuntary smoking require further investigation before a determination can be made about the relationship of involuntary smoking to these cancers. 11. Further studies on the relationship between involuntary smoking and cardiovascular disease are needed in order to determine whether involuntary smoking increases the risk of cardiovascular disease. Environmental Tobacco Smoke Chemistry and Exposures of Nonsmokers - 1. Undiluted sidestream smoke is characterized by significantly higher concentrations of many of the toxic and carcinogenic compounds found in mainstream smoke, including ammonia, volatile amines, volatile nitrosamines, certain nicotine decom- position products,,and aromatic amines. 2. Environmental tobacco smoke can be a substantial contributor to the level of indoor air pollution concentrations of respirable particles, benzene, acrolein, N-nitrosamine, pyrene, and carbon monoxide. ETS is the only source of nicotine and some N- nitrosamine compounds in the general environment. 3. Measured exposures to respirable suspended particulates are higher for nonsmokers who report exposure to environmental tobacco smoke. Exposures to E'I'S occur widely in the non- smoking population. 4. The small particle size of environmental tobacco smoke places it in the diffusion-controlled regime of movement in air for deposition and removal mechanisms. Because these submicron particles will follow air streams, convective currents will dominate and the distribution of ETS will occur rapidly through the volume of a room. As a result, the simple separation of smokers and nonsmokers within the same airspace may reduce, but will not eliminate, exposure to ETS. 5. It has been demonstrated that ETS has resulted in elevated respirable suspended particulate levels in enclosed places.