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, 6 and cotinine in the plasma or urine of nonsmokers exposed to ETS - are about 1 percent of the mean values observed in active smokers. ' Several studies have indicated that urinary cotinine concentrations ' in infants and children increase as the numbers of reported smok- ers ers increase in the home. At present, there may be difficulty in - interpreting the relative cotinine levels in.nonsmokers compared with smokers because of the reported slower clearance of eotinine in nonsmokers. Absorption, metabolism, and excretion of ETS constituents, including nicotine, need to be carefully studied in or- der to evaluate whether there are differences between smokers and nonsmokers in these Jaetors. Ptirther epidemiologic studies using biological markers are needed to quantify exposure-dose relation- ships in nonsmokers. Thiocyanate, as measured in saliva, serum, or urine, does not appear to be sufficiently sensitive as an Indicator of ETS exposure. Similarly, exhaled carbon monoxide and carboxyhemoglobin are not sufficiently sensitive to moderate or low levels of ETS exposure - and thus are not particularly useful biological markers for expo- sure to ETS, except in experimental, acute exposure situations. There are several other sources of carbon monoxide in the environ- ment that equal or exceed the concentrations of carbon monoxide attributable to ETS. Other suggested biological markers of exposure are N-nitroso- proline, nitrosothioproline, and some of the aromatic amines that are present in high concentrations in SS. However, data on sensi- tivity and reliability of laboratory procedures for these markers are not eufl'icient to recommend their use at this time in epidemiologic studies of ETS. Laboratory assays have shown mutagenic activity in the urine of smokers and ETS-exposed nonsmokers. The mutagenicity of urine is a function of many factors--such as dietary constituents, occupational exposures, and other environmental factors-which render any findings of mutagenicity nonspecific. Research is needed to clarify the appropriate methods for estimating mutagenicity and to isolate and identify the active agents in body fluids o f ETS- exposed nonsmokers. DNA adducts derived from tobacco-related chemicals can be measured in the blood. However, -these chemicals, such as b®nzo[a]pyrene, are not unique to ETS. Studies are needed that can measure adducts of tobacco-specific chemicals. 90G99448 IN VIVO AND IN VITRO STUDIES Laboratory studies can contribute to a better understanding of the factors and mechanisms involved in the induction of disease by environmental agents. There have been numerous bioassays conducted on MS. In examining the effects of MS, many research workers have used condensates of the smoke painted on the shaved skin of mice. This contrasts with the human exposure that is mainly in the respiratory tract. Nonetheless, these skin-painting studies have been useful in examining the carcinogenicity of dif_ ferent tobacco constituents and thus advancing knowledge of the actions of MS on a gross exposure level. Similar work with skin painting has not been done with ETS and would be of value for assessing the differential toxicity ojETS and MS. In constrast to MS exposure, ETS exposure involves propor- tionately more exposure to gas phase than to particulate phase ecinstituents. There have not, however, been studies of the effects of exposure to aged ETS. The relative in vivo toxicity of MS, SS, and ETS needs to be assessed. Some studies have attempted to evaluate the gas phase of MS. SS, and ETS in short-term, in vitro assays. A solution of the gas phase of MS has been shown to induce dose-dependent increases -- in sister-chromatid exchanges in cultured human lymphocytes. Mutagenic activity has been found in the particulate matter of SS --- -- - - - an.d in condensates of ETS. However, the work done to date is too sparse to permit any estimates of the mutagenicity of ETS per ae, - - even though most of ETS consists of SS. Further in vitro assays of ETS are needed. HEALTH EFFECTS This report reviews both chronic and acute health effects as- sociated with ETS exposure in nonsmokers. Most epidemiologic studies of chronic health effects have been conducted on persons who have had long-term exposures to ETS from household mem- bers. The studies do not directly address chronic,health effects in individuals who are exposed at work or have occasional exposures in the home or elsewhere. Hecause the physicochemical nature of ETS, MS, and SS dif- fer, the extrapolation of health effects from studies of MS or of

i a active smokers to nonsmokers exposed to ETS may not be appro- priate. However, chemicals known to be toxic and carcinogenic in MS are also present in ETS. Laboratory studies in conjunction with epidemiologic investigations are needed to help clarify possible - - health effects of exposure to ETS in nonsmokers. Acute, Noxious Effects The most common acute effects associated with exposure to ETS are eye, nose, and throat irritation, and objectionable smell of tobacco smoke. Tobacco smoke has a distinct and persistent - odor, making control through ventilation particularly difficult. In closed rooms where smoking is allowed, a ventilation rate of greater than 50 cubic feet per minute per occupant is necessary to achieve air quality that is acceptable to more than 80% of adults entering the room as contrasted with rates of less than 10 cubic - feet per minute per occupant when there is no smoking or other pollution. Annoyance with noxious tobacco odor largely governs the reactions of visitors, while occupants of smoky rooms are more likely to complain about Irritating effects to the eye, nose, or throat. Particle filtration appears to lead to little or no decline in odor and irritation, suggesting that the effects are produced by gas-phase constituents. During exposure to ETS, eye blink rate is correlated with sensory irritation, such as burning eyes and nasal irritation. For some persons, eye tearing can be eo intense as to be incapacitating. There is some evidence that nonsmokers are more sensitive to the noxious qualities of cigarette smoke than are smokers. Objective physiological or biochemical indices should be sought to validate reports ojnosious reactions and chronic irritation associated with ETS. Smoke contains immunogens, that is, substances that can ac- tivate the immune system. Approximately half of atopic (allergy prone) individuals react to various extracts of tobacco leaf or amoke presented in skin tests.. However, the components of the extract that are responsible for this reaction have not been iso- lated. There is little correlation between positive reactions to skin tests and self reported complaints of tobacco smoke sensitivity. Research is needed to evaluate the medical importance in stopic persons of these positive reactions to skin tests using ETS extracts and to relate immune response on skin tests to subjective complaints about the noxious, irritating properties of tobacco smoke. 9 Respiratory Symptoms and Lung Function Respiratory symptoms, such as wheezing, coughing, and spu- tum production, are increased in children of smoking parents. These symptoms are more common in children of smokers than children of nonsmokers. The largest studies place the increased risk of 20 to 80%, depending on the symptom being assessed and number of smokers in the household. Also, respiratory infections manifested as pneumonia and bronchitis are significantly increased in infants of smoking parents.. Some studies have reported that in- fants fants of smoking parents are hospitalized for respiratory infections more frequently than children of nonsmokers. Among children aged under 1 year, studies are remarkably consistent in showing an increased risk of respiratory infections among children living in homes where parents smoke. There is a dose-response relationship that relates more to maternal smoking than paternal smoking. The association persists after allowing for possible confounding factors such as occupational data, respiratory illness in the parents, and birthweight. The mechanisms of the increased risk may either be - - a direct effect of ETS or due to a higher risk of cross-infection in such homes. Regardless of the mechanism, the exposure of small children to smoking in the home appears_ to put them at risk of - --- - respiratory illness. Since children exposed to ETS from parental smoking have an increased frequency of pulmonary symptoms and respiratory infections, it is prudent to eliminate ETS exposure from the envi- ronments of small children. There is some evidence that parental smoking may affect the - rate of lung growth in children. In children with one or more par- ents who smoke, lung function increase, which is a normal growth phenomenon, shows a small decrease in the rate of growth. An important issue currently unresolved is whether a child who is affected by exposure to ETS from parental smoking may be at an increased risk for the development of chronic airflow obstruction in adult life. In all studies of children, it is difficult to distin- guish - guish between the role of ETS exposure in utero and postnatally. Research is needed to address the issues of ETS exposure during childhood and fetal life and its possible relationship with airway hyperresponsiveness and pulmonary diseases in adult life. 4OG9gLtae

10 Three studies have shown a small reduction in pulmonary - function in normal adults exposed to ETS. Interpretation of these findings is difficult because pulmonary effects in normal adults are likely to reflect the cumulative burden of many environmental and occupational exposures and other insults to the lung. Thus, the effects of ETS on the lungs of adults are likely to be confounded by many other factors, making it difficult to attribute any portion of the effect solely to ETS. In some studies of asthmatics, in whom pulmonary reactions to ETS should be more readily produced, no effects on lung function were reported. In other studies, asthmatics reported complaints upon exposure to ETS and showed significant pulmonary func- tion changes after experimental smoke exposure. .Future studies of asthmatics exposed to ET3 should be designed so as to limit the distortion produced by heterogeneous patient groups, varying medication schedules, and psychogenic effects of ETS. Lung Cancer Considering the evidence as a whole, exposure to ETS in- creases the incidence of lung cancer in nonsmokers. Estimates of the magnitude of the increased risk vary. Among studies of var- ious populations in Europe, Asia, and North America, the risk of lung cancer is roughly 30% higher for nonsmoking spouses of smokers than it is for nonsmoking spouses of nonsmokers. There is consistency among the studies in that all of the studies indi- vidually include the 30% increased risk within the 95% confidence intervals. Patterns and extent of exposure may vary in different communities and countries. Based on presently available epidemi- ologic ologic data, the estimate of the increased risk from the American studies is lower than the average for all the studies, though not sig- _- nificantly so. These estimates are almost exclusively derived from the comparison of persons identified as exposed, or unexposed, on the basis of their spouse's smoking habits. Certain errors in the reporting of smoking habits have proba- bly contributed to the risks observed in the epidemiologic studies. Misclassification of current or examokers as nonsmokers would tend to produce an observed relative risk that is larger than the true risk. This effect was studied in detail using estimates of the ex- tent of the errors involved and judged to contribute only a portion tent - - of the excess risk. Underestimation of the increased risk might also 80698448 11 be introduced because ause the supposedly unexposed population had some exposure to ETS, although they were classified as unexposed in the studies. Taking both types of errors into account produces an estimate of the excess lung cancer risk for nonsmokers married to smokers compared with completely unexposed individuals that is similar to the relative risk observed in the epidemiologic studies considered. Since carcinogenic agents contained in ETS are inhaled by nonsmokers, in the absence of a threshold for carcinogenic effects, gn increased risk of lung cancer due to ETS exposure is biologi- cally plausible. Laboratory studies would be important in determin- ing the concentrations of carcinogenic constituents of ETS present in typical daily environments. The use of biological markers in epidemiologic studies is recommended to more precisely. quantify dose-response relationships between ETS exposure and lung cancer occurrence. Other Cancers There have been few studies of risk for cancers other than lung in nonsmokers exposed to ETS. Some of the sites considered have been brain, hematopoetic, and all sites combined. The results of these studies have been inconsistent. Whether or not there is an association between ETS exposure and cancers of any site other than lung is an important topic for future epidemiologic inquiries. Cardiovascular Disease Since active smoking has an adverse effect on cardiovascular disease morbidity and mortality, ETS exposure has also become - suspect. Reports have noted an excess risk of cardiovascular r dis- ease in ETS-exposed nonsmokers; however, methodologic prob- lems in the designs and analyses of these studies preclude any firm conclusions about the results. Studies reporting that ETS can precipitate the onset of angina pectoris among people who already have this condition are subject to the same-precautionary note. - Exposure to ETS produced no statistically significant effects on heart rate or blood pressure in school-aged children or healthy adult subjects, either during exercise or at rest. Data are not available as to possible adverse cardiovascular effects in suscepti- ble ble populations, such as infants, elderly, or diseased individuals.

12 Further esperimental and observational studies ahould be conducted to assess the effect of long-term and acute ETS exposure on cardiac function, blood pressure, and angina in nonsmokera. Other Health Considerations in Children Several other health outcomes have been studied that relate to the growth and health of children. For all postnatal outcomes, it is often not possible to differentiate the effect of in utero exposure to ETS from subsequent childhood exposures to ETS. Nonsmoking pregnant women exposed to smoking spouses have been reported to produce babies of lower birthweight than nonsmoking women with nonsmoking spouses. Some studies have noted a dose-response relationship between the number of ciga- rettes smoked by fathers and birthweight of the offspring. Ad- ditional studies of intrauterine fetal growth retardation associated with ETS exposure of nonsmoking mothers need to be conducted with better assessments of the magnitude of ETS exposure. Several studies have examined possible relationships between chronic exposure to ETS by children and parameters of growth and development. Growth is an.especially difficult phenomenon to study since many factors-such as genetics, nutrition, social class, and ethnicity-play important roles. It is difficult to assign proportional causality to each factor. Moreover, height and weight ratios and other growth measures are not reliably obtained in standard pediatric surveys. A few studies have shown that children of smokers have reduced growth and development, and one study reported a dose-response relationship between reduced height and increasing numbers of cigarettes smoked in the home by either the mother or the father. Further work is needed to determine the nature of this association. Otitis media is a common occurrence in young children. In several studies, parental smoking, along with several other risk factors, has been linked to increased risk of chronic ear infections in children. Further work is needed to determine whether the asso• ciation is causal. 1 Introduction Environmental tobacco smoke (ETS) occurs in homes, at - workplaces, and in public places. The acute irritating and nox- ious effects of involuntary exposure to ETS, or °paasive smoking," are well established. Based in part on these irritating proper- ties of ETS, a recent report of the NRC recommended a ban on - - smoking in the small enclosed spaces of airliner cabins (National Research Council, 1986). More than 20 states and numerous lo- cal governments have enacted legislation and policies restricting smoking (1985 information obtained from the Office on Smoking and Health, personal communications). Such public information campaigns and other actions have convinced a large portion of the population that active cigarette smoking is dangerous to health. To many, this also implies that exposure to ETS can affect health. This report, in part, evaluates whether the latter beliefs are war- ranted. It also makes recommendations for future exposure moni- toring and epidemiologic research. The issues are complex. In some cases the conclusions are - uncertain, because much of the scientific data necessary to shed light on these concerns does not exist. Thi4 report addresses the following major issues pertaining to ETS: • The nature of the smoke. What constitutes ETS? What are the chemicals in ETS and what are the dilutions therein? There are two physical phases of smoke: particulate phase and vapor phase. What chemicals are in each phase? Are any of these chemicals carcinogenic or toxic, as determined in bioassays? E'iQ698L49 ~ 13

14 • Factors affecting exposure and the assessment of exposure. To what extent is the nonsmoker exposed to harmful chemicals that can be measured in ETbZ How can we measure exposure to _- ETS? Can ambient monitoring be used in epidemiological studies7 How reliable is questionnaire information? What constitutes the dose a person may receive? Are there objective measures of dose received, such as tobacco-smoke-specific biological markers? What choices and reasons for choice are there among the markers? • Effects of exposure. What are the health effects, if any, - consequent to exposure to ETS? Are these health effects related to discomfort or irritant effects only, or more serious disease? Are the potential health effects reversible when exposure ceases? What are the data from human studies? Do interactions with other environmental agents at workplaces or in homes need to be considered? Are there biologically plausible explanations for the various effects ascribed to ETS exposure? The report considers sensitive populations such as children, pregnant women, older persons, and those with persisting respira- tory illnesses. It does not consider the established effects on the fetus carried by a pregnant, smoking woman because this is not an instance in which a nonsmoking individual breathes ETS gen- erated by other people. However, a pregnant, nonsmoking woman might be affected by exposure to ETS, as may her fetus. The health effects considered include respiratory symptoms and- lung function, and other respiratory ailments (especially in children), such as asthma and allergic responses, cancer at various sites, and cardiovascular disease, among others. Some attention is paid to irritation, annoyance, and associated responses. DEFINITIONS Environmental tobacco smoke (ETS) originates from the smol- dering end of the tobacco product in between puffs, known as sidestream smoke' (SS), and from the smoker's exhaled smoke. [T-he smoke that the smoker inhales is known as mainstream smoke (MS).] Other contributors to ETS include minor amounts of smoke that escape during the puff-drawing from the burning cone and some vapor-phase components that diffuse through the cigarette paper into the environment. These various components are re- leased into the environment and are diluted by ambient air. They 15 may also aggregate with pollutants already in the environment and thereby change character. The composition of this complex mix- ture, known as ETS, has different physicochemical characteristics than the MS. There.are various terms in the literature that refer to the inhalation of ETS by nonamokers, e.g., "passive smoking," "in- voluntary smoking," and "breathing other people's smoke." We will refer to the inhalation of ETS by using the terms "passive smoking" and "exposure to ETS by nonsmokers" interchangeably. TRENDS IN CIGARETTE USAGE Exposure of nonsmokers to ETS is a function of several vari- ables, one of which is the number of active smokers with whom the nonsmoker comes into contact throu hout some g period of time. The percent of the population who smoke steadily increased over the first two-thirds of this century but has declined more recently. - - In 1980, 32% of the adult population considered themselves to be - - - cigarette smokers (U.S. Department of Commerce, 1984). This percentage, now roughly equal for men and for women, reflects ts a reduction of almost one-third in men since the publication of the first Surgeon General's Report on Smoking and Health in 1964 (U.S. Public Health Service, 1964). Figure 1-1 shows the trends in cigarette usage between 1955 and 1985 for males and females. Table 1-1 gives cigarette consumption since 190U. Table 1-2 il- lustrates an overall increase in cigar and pipe smoking, followed by a decline during the past decade. The actual probability of exposure to ETS is complex, affected by ventilation rates, size of houses, restrictions on where tobacco products may be smoked, and changes in the cigarette itself. The consequence of Figure 1-1 is that the general probability of being exposed to some_ ETS for the nonsmoker has increased until quite recently. The magnitude of exposure to ETS will depend upon the number of cigarettes and/or cigars and pipes smoked in a given environment, as well as other factors such as ventilation. Light smokers are more likely to stop smoking than heavy smokers, which might explain why over the past 30 years the number of - cigarettes per smoker and the total consumption (Figure 1-2) have not declined as rapidly as the percentage of people who smoke (see also cigar and loose tobacco consumption in Table 1-2). From a peak consumption in the early 1960s, there has been a decline of 0169g449

18 . 50 Mele. 40 30 rT 20 10 0 f I 1 1 I I 1 I1 1955 1960 1'88S 1970 1975 1980 1985 YEAR FIGURE 1-1 Percentage of current smokers In the United States. Adult population, by .ex, 1966-1983. From Shopland and Brown (1986). 20°rli in the per capita (U.S.) consumption of cigarettes (Shopland and Brown, 1985). These data, however, are averaged over the total U.S. population, including smokers and nonsmokers. Among persons who consider themselves smokers, the cigarette consump- tion per adult smoker actually has increased from 27.3 to 30.0 cigarettes per day. Table 1-a demonstrates that, for both sexes, the percent of smokers who are heavy smokers hes steadily in- creased over the past 30 years. Therefore, the consumption per active smoker indicates that the nonsmoker who has close contact with a smoker may be exposed to greater amounts of smoke in 1985 than in 1955, although the total number of hours a nonsmoker is exposed to ETS would have declined. Counteracting this trend of increased exposure has been the trend of reduction in amount of tobacco used to fill each cigarette. Physical changes of the leaf due to modern ntethods of processing, the use of filter tips (United States, >90% of all cigarettes since 17 TASI,E 1-1 U.S. Cigarette Consumption, 1900 to 1983a ear otal Billions Number Per Capita, 18 Years and Older ear otal BHlions Number_ Capita, 18 Years and Older ear otal Billions Number - Per Per Capita,. 18 Years and Older 1900 2 5 - - . 54 1930 119.3 1,485 1960 484.4 4 171 1901 2.5 S3 1931 114.0 1,399 1961 502.5 , 4 266 ' 1902 2.8 60 ' 1932 102.8 1,245 1962 508.4 , 4 265 1903 3.1 64 1933 111.6 1,334 1963 523.9 , 4.345 1904 3.3 66 1934 125.7 1,483 1964 511.3 4,195 1905 3.6 70 193S 134.4 1,564 1965 528.8 4,259 1906 4.5 86 1936 152.7 1.754 1966 541.] 4,287 1907 5.3 99 1937 162.8 1,847 1967 549.3 4,280 1908 5.7 105 1938 163.4 1,830 1968 545.6 4 186 1909 7.0 125 1939 172.1 1,900 1969 528.9 , J,993 1910 8.6 151 1940 181.9 1,976 1970 536.5 3,985 1911 10.1 173 1941 208.9 2,236 1971 555.1 4 037 1912 13.2 223 1942 245.0 2,585 1972 566.8 , 4,043 1913 15.8 260 1943 284.3 2,956 1973 589.7 4,148 1914 16.5 267 1944 296.3 3,039 1974 599.0 4,141 1915 17.9 285 1945 340.6 3,449 197S 607.2 4,123 1916 25.2 39S 1946 344.3 3,446 1976 613.5 4,092 1917 35.7 SS1 1947 345.4 3.416 1977 617.0 4,051 1918 45.6 697 1948 358.9 3.S0S 1978 616.0 3,967 1919 48.0 727 1949 360.9 3,480 1979 621,5 3,861 1920 44.6 66S 1950 369.8 3,522 1980 631.5 3,851 1921 50.7 742 19S1 397.1 3.744 1981 640 0 3 840 1922 53.4 770 1952 416.0 3.886 1982 . 634.0 , 3 753 1923 64.4 911 1953 408.2 3,778 1983 600.0 , 3 502 1924 71.0 9s2 1954 387.0 3,546 1984 600.41 , 3,461k 1925 79.8 1,085 1955 396.4 3.597 1985 595.09 3,384` 1926 89.1 1,191 1956 406.5 3,650 1927 97.5 1,279 1957 422.5 3,755 1928 106.0 1.366 1958 448.9 3,953 1929 118.6 1,504 - 1959 467.5 4,073 "lncludes o.ereees forcer, 1917-1919 and 1940 to date. Commodity Economics Division, Economic Research Service, USDA. 6SubJect to revision. `Estimated. SOURCE: U.S. Department of Agriculture, 1985, TI6954L8

i8 650 600 400 350 1955 1960 196$ 1970 1975 1980 1985 YEAR FIQURE 1-2 Total cigare«9 consnmptioa (domestic salee), 1955- 1985, 1978; Griese, 1984), and variationa in the compOsition oI tobacco blends for cigarettes (Norman, 1982) have made this reduction possible. In 1956, the U.S. average ~~ce then, tar n and ln'a ot e yie de rng and 2.69 mg, respectl/ y_ nicotine in have steadily decreased to 13.2 mg tar and 0.95 mg 1980 (The Tobacco inetitute', 1981). liowever, tar and nicotine yields in the SS of cigarettes have not eignificantly changed except 19 TABLE 1-2 U.S. Consumption of Cigars and Tobacco for Pipes and Hand-rolled Cigarettes Year Cigars, Tobacco, millions Mn.lb• Year Cigars, millions Tobacco, Mn.lb' Year Cigars, millions 1920 8,609 1950 . 5.608 104.3 1980 5,386 1921 7.435 1951 5,778 97.4 1981 5,231 1922 7,527 1952 6,037 92.9 1982 4,901 1923 7,505 1953 6.107 84.3 1983 4,884 1924 7,189 1954 6,024 81.2 1925 66.949 1955 6,078 77.8 1926 7,008 1956 6,039 70.0 1927 7,008 1957 6.194 68.9 1928 6,874 1958 6,586 74.4 1929 6,972 1959 7,377 71,9 1930 6,272 1960 7.434 72.2 1931 5,656 196t 7,083 72.7 1932 4,724 t962 7,103 69.8 1933 4.553 1963 7,434 69.7 1934 4.818 1964 9,899 81.7 1935 4,943 1965 8,949 69.8 1936 5,362 1966 8,610 68.6 1937 5,516 1967 8.403 66.4 1938 55.294 1968 8.331 69.6 1939 5,469 1969 8.579 68.3 1940 5,491 1970 8,881 74.0 1941 5,933 1971 8,830 69.5 194; 6.339 1972 11,125 66.8 1943 5,350 1973 11,126 59.5 1944 4,878 1974 9,339 1945 5,027 1975 8,663 1946 S,924 1976 7.492 1947 5,706 1977 6,792 1948 5,860 1978 6,231 1949 5,625 1979 5,706 'Tobaccn for pipes and hand-rolled dgarettes not available prior to 1950. SOURCES: Lee, 1975; Tobacco Reporur, 1984. i

20 TABLB 1-3 Number of Cigarettes Smoked per Day, as a Percentage of Current Smokers, by Sex Less Than 15 IS-24 25 or More M.les 1965 30.1 45.7 24.1 1976 24.9 44.4 30.7 1980 24.2 41.7 34.2 1983 23.5 42.9 33.6 Females 1965 46.2 40.8 13.0 1976 37.6 43.4 19.0 1980 34.7 42.0 23.0 1983 33.8 45.6 20.6 SOURCE: Shopland and Brown, 1985. in the case of cigarettes designed for ultralow yields of tar and nicotine. Certain other components, in particular volatile, toxic components, are released into SS in significantly greater amounts than into rlS. Furthermore, ETS contains significantly smaller _ particles than MS, and nicotine, and perhaps other smoke con- stituents, is volatilized to a greater extent in SS than in MS. This means that the gas-phase composition of SS differs substantially frum that of NiS. The health implications to nonsmokers of exposure to ETS_ may not be a simple extrapolation from the studies of active smokers. The complexities of such extrapolations will be discussed. Children represent a large population of nonsmokers who may be exposed to environmental smoke. Several cohort studies of chil- dren are reviewed in Chapter 11. Although there is some variation among these studies, they indicate, mainly through questionnaires, that between 50 and 6-5 percent of the children have been exposed to tobacco smoke in the home during the past 20 years. Health implications of this exposure for the developing child will be dis- cussed. cussed. ORGANIZATION This report begins with a discussion of the components of ETS (Chapter 2) and what in vivo and in vitro studies have determined about ETS (Chapter 3). Various methods of exposure assessment 21 are considered in Chapters 4 through 8, including physical effects, questionnaires, and biological markers. Chapters 9 through 15 review epidemiologic studies of possible health effects of these ex- posures. The health consequences examined range from irritation - and allergic reactions to cancer and cardiovascular disease. Only - studies that assess exposures under experimental conditions or in - the home are included. ETS potentially interacts with constituents of the ambient air. This makes the evaluation of possible health effects due to workplace exposure complex and specific to each situation because of the varying nature of contaminants. Each chapter concludes with a summary of what is currently known, the strength of that knowledge, and what additional information would further clarify the relationship of ETS and possible health effects. Some recommendations for additional research are also given. REFERENCES ,tiriese, V.N. Market growth of reduced tar cigarettes. Recent Adv. Tob. Sci. 10:4-14, 1984. Lee, P.N., Fd. Tobacco Consumption In Various Countries, pp. 82-84. Lon- don, England: Tobacco Research Council, 1975. National Research Council, Committee on Airliner Cabin Air Quality. Air- liner Cabin Environment: Air Quality and Safety. Washington, D.C.: National Academy Press, 1986. 303 pp. Norman, V. Changes In smoke chemistry of modern day cigarettes. Recent Adv. Tob. Sci. 8:141-177, 1982. Shopiand, D R., and C. Brown. Changes in cigarette smoking prevalence in - - the U.S.: 1966-1983. Ann. Behav. Med. 7;6-8, 1986, The Tobacco Institute. U.S. tar/nicotine levels dropping. The Tob. Observ. 6:1, 1981. Tobacco Reporter. Cigars In the U.B.: Is the upturn real? Tob. Rep. 111:45-48,1984. U.S. Department of Agriculture. Tobacco: Outlook and Situation Report. DOA Publ. No. TS-129. Washington, D.O : U.S. Government Printing OtRce,1986. U.S. Department of Commerce. Statistical Abstract of the United States: 1986. Washington, D.C.: U.S. Department of Commerce, Bureau of the Census, 1984. 119 pp. CTf 9g44A

I PHYSICOCHEMICAL AND TOXICOLOGICAL STUDIES OF ENVIRONMENTAL TOBACCO SMOKE PU9R449

2 The Physicochemical Nature of Sidestream Smoke and Environmental Tobacco Smoke INTRODUCTION Mainstream smoke (MS) is the aerosol drawn into the mouth of a smoker from a cigarette, cigar, or pipe. Sidestream smoke (SS) , is the aerosol emitted in the surrounding air from a smoldering tobacco product between puff-drawing. SS is a major source of environmental tobacco smoke (ETS), i.e., air pollution caused by the burning of tobacco products. Other contributors to ETS are the exhaled portion of MS and the smoke that escapes from the burning part of a tobacco product during puff-drawing. In -- - addition, some volatile components (e.g., carbon monoxide) diffuse through cigarette paper and contribute to ETS. _ Tobacco smoke aerosols are diluted with air by the time they are inhaled as ETS air pollutants. Furthermore, the physical char- acteristics and chemical composition of ETS change as the pollu- tants "age" : nicotine is volatilized; particle sizes decrease; nitrogen - -- oxide gradually oxidizes to nitrogen dioxide; various components of the ambient air (e.g., radon daughters) can be adsorbed on the - - - - particles; and other physicochemical changes can occur. In the scientific literature, the terms "passive smoke," "passive smoking," and "involuntary sm4king" are used often. These terms do not adequately describe ETS and its inhalation, but they are used interchangeably with "ETS" in this report. Most of the reported data on MS, SS, and ETS pertain to cigarette smoking. Few comparative data on smoke pollutants from other tobacco products are available. ST69gZ48 25