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CHAPTER 7 EXPOSURE ASSESSMENT IN PASSIVE SMOKING James L. Repace, MSc. Indoor Air Division Office of Air and Radiation U.S. Environmental Protection Agency introduction There are currently no direct measures of the dose of ETS absorbed in a population under study; however, exoosures to ETS can be assessed by personal air contaminant monitoring, modeling of concentrations (based on air sampling, time activity patterns, and questionnaires), or biological markers. (NRC, 1986) Exposure to ETS is determined by the following paradigm: exposure equals the product of respiration rate, concentration, and duration. concentration is directly proportional to the product of number of smokers, smoking rate, and emissions per tobacco product, and is inversely proportional to the product of space volume and removal rate. The nonsmokers' total exposure to ETS is determined by the product of the time-weighted sum of the concentrations encountered in various microenvironments, and the individual's respiration rate during exposure. (IARC, 1987) In the epidemiologic studies of passive smoking and lung cancer described under Hazard Assessment, exposures were estimated on the basis of a questionnaire which assesses smoking status, and typically asked simple questions of the sort: "if you are a nonsmoker, do you live with, or work with, or have regular contact with persons who are nonsmokers?" (NRC, 1986) Some studies assessed past exposure history and spouses' smoking rate as well. This kind of question, though useful, is not likely to be fully reliable or precise, particularly for non-domestic exposures. (NRC, 1986; IARC, 1987) On the other hand, it has been shown that those nonsmokers who report exposure to ETS at home tend to have higher non-domestic exposures as well.(NRC, 1986; Wald, 1986) Ideally, the health effects of ETS exposures might be assessed by quantifying the time-dependent exposures and doses for each of the several thousand compounds in tobacco smoke and defining dose-response relationships for these compounds in producing disease, both as isolated compounds and in various combinations. However, the enormity of this task has led to simpler approaches which attempt to use measures of exposure to individual smoke constituents as estimates of whole smoke exposure. For this reason, exposures to ETS are often assessed using markers of the 79

FIGURES AND TABLES FOR CHAPTER 7 91

International 11: 3-22. Repace, JL, and Lowrey, AH (1988). Sexton, K; Spengler, JD; Trietman, RD (1984). Personal exposure to respirable particulates: a case-study in Waterbury, Vermont. Atmos. Environ. 18: 1385-1398. Surgeon General (1986). The Health Consequences of involuntary smoking. U.S. Dept. of Health i Human Services, WAshington, DC. Spengler, JD; Treitman, RD; Tosteson TD; Mage DT; and Soczek ML (1985). Personal exposures to respirable particulates and implications for air pollution 'epidemiology. Environ. Sci. & Technol. 19:700-707. Tobacco Institute (1987). Tobacco industry profile, 1987. Washington, DC. Wald, NJ; Nanchanai, K; Thompson, SG; Cuckle, HS (1986). British Med J. 293:1217-1222. F 94

microenvironments each year from cigarette smoking alone. Assuming cigars produce 3 times as much RSP as cigarettes and that pipes produce as much RSP as a cigarette, (Repace and Lowrey, 1982) where pipes and hand-rolled cigarettes are assumed to contain 1 q of tobacco, then all cigars are estimated to contribute as much RSP indoors as 11 billion cigarettes, while all pipes and hand-rolled cigarettes are estimated to contribute as much as 15 billion regular cigarettes, increasing the estimated total RSP generated in US indoor microenvironments from all cigarettes, pipes, and cigars to nearly 13,000 metric tons per year. As exemplified by data from EPA's TEAM study, ETS predominates over other sources of RSP indoors (see Fig. 3.) Although the percentage of the population that smokes has declined from nearly 50% in the 1960's to about 30%-presently (0SH,1988), the percent of smokers who are heavy smokers has increased steadily over the past 30 years; thus although the percentage of smokers has gone down, the increase in smoking rate may tend to offset that trend towards lowering nonsmoker exposure to ETS.(NRC,1986). B. Indoor air transport of LTs Nonsmokers are exposed to ETS in indoor spaces. The determinants of these enclosed-space exposures include smoking occupancy, source air-contaminant emission characteristics, source use, building characteristics, space volume, infiltration or ventilation rates, efficiency of air mixing, surface sorption, chemical transformation, and the efficiency of air cleaning equipment. The interaction of these variables in determining the resultant concentrations of ETS has been evaluated in both controlled laboratory settings and in field studies within the theoretical framework of the mass-balance equation. The mass- balance equation may be applied to tobacco smoke either as an equilibrium model (time-independent) or as a dynamic model (time- dependent). Dynamic and equilibrium models are useful in laboratory studies; equilibrium models are best suited to evaluating and predicting ETS concentrations in field studies, particularly when average concentrations over a period of days or longer are of interest. (NRC,1986) Laboratory and field studies typically utilize some form of a single-compartment equilibrium model to evaluate the input parameters of the mass-balance equation, to evaluate field study data, and to project RSP concentrations from ETS indoors. These studies have reduced the general single-compartment mass-balance equation to the following simplified form: Cp - G(m(N. + N.)V] ~ (1), where Cp is the equilibrium concentration of ETS-generated RSP in a space, expressed in units of micrograms per cubic meter 81

smokers are present, and also are based on the room density of habitual smokers (number of habitual smokers per 100 cubic meters). Thus, the presence of a typical or "habitual" smoker (i.e., one who is assumed to smoke at an average rate of 2 cigarettes per hour at 10 minutes per cigarette, with an emission factor of about 22 mg of SS RSP per cigarette) is the modeling parameter rather than the room density of burning cigarettes.(IARC, 1987) These derivative equations are given as follows: Cp - 217 Dh./N„ (3) r where c,q is the equilibrium concentration in units of micrograms per cubic meter, Dh, is the number of habitual smokers per 100 cubic meters of space volume, and N, is the number of space air changes per hour. Eq. 3 assumes that the number of habitual smokers in the space is 3 or more, so that the generation of smoke is steady. If the number of habitual smokers being modeled is only 2, then eq. (4) applies, yielding: C,y = 145 Dh./Nv (4), for the 2-smoker equation, where the smaller coefficient approximates the effect of the non-steady generation of ETS. Similarly, if the number of habitual smokers to be modeled is one, then eq.(5) is used: C,y a 72 Di„/N„ (5), for the single-smoker equation. The use of such equations is illustrated as follows: As part of the the Harvard 6-City study of indoor and outdoor air quality, Spengler and colleagues (1981) collected RSP samples in 55 homes in 6 cities between May 1977 and April 1978. The number of smokers living in each home was recorded. The quantity of tobacco smoked was not reported, nor was the number of hours each smoker spent in the home, and the air exchange rates were not measured. The average "background," or mean indoor RSP level in the homes of nonsmokers was about 24 ug/m3; using regression analysis, the authors estimated that the average impact of a single smoker (a composite averaged over both sexes) on 24-hr average RSP levels in a residence was about 20 ug/m3. On average, two such habitual smokers would make about 40 ug/m3 (24-hrs)p allowing for 8 hours of sleep, the 16-hr average would be 60 ug/m3. Although the air exchange rates were unknown, Fig. 4 shows a histogram of the frequency of occurrence of various air exhange rates (called infiltration rates) during the heating season for typical middle income housing (R. Grot, personal communication) for 266 homes in 14 cities around the US in 1978 (SG,1986). Occupants were asked to keep windows and doors closed during the tests. Under these conditions, the mean air exchange rate found 83

FIGURE 3. EPA's TEAtt Study demonstrates that smoking provides the dominant source of RSP in many buildings (Sheldon, et al, 1986) Nine SrC.ws I a % / / % / Mean Cont:entration ~ 1";~, in nonsmoking area ~ 5:00 PM 5:30 6:00 6:30 rM 11eso1raY.e partccu:a:es :- lr•- `:cor :cun{e c! t.•.e eilarl~ home-: (3::=~61). ~ ~ ~ ~ ~ W ly

Nicotine is found in measurable concentrations in the saliva and urine of most urban nonsmokers, and is present in higher concentrations in those with soma recent exposure. Estimating the magnitude of the passive smoking dose is difficult, and it is of doubtful validity to extrapolate from the uptake of one marker to another. Over a period when one cigarette equivalent of carbon monoxide is absorbed, the dose of nicotine appears to be only between 1/10 and 1/3 of a cigarette equivalent. Similarly, under extreme conditions of indoor pollution, it has been calculated that a nonsmoker would inhale volatile nitrosamines equivalent to 10 nonfilter cigarettes or 35 filter cigarettes.(IARC, 1987) The average concentration of. cotinine in the blood of habitual smokers is about 300 ng/ml, and is calculated to represent the consumption of about 36 mg of nicotine per day. On this basis, and on the assumption that formation of cotinine from nicotine and clearance from the body does not differ substantially from smokers to nonsmokers, present data suggest that average urban nonsmokers (in the UK) take in 0.2 mg of nicotine per day.(IARC, 1987) [.2 mg represents .6% of the smokers' doseJ The highest plasma cotinine concentration observed in a nonsmoker corresponds to an approximate maximum dose of 2.5 mg of nicotine per day, 10 times higher, and 7% of the average smoker's dose. Recent studies of salivary cotinine in schoolchildren in the UK showed, in the case where both parents smoked, average concentrations just over 14 of the levels seen in heavy cigarette smokers.(IARC, 1987) There is little data on nicotine levels in nonsmoking US adults. However, one recent study of personal exposures to airborne nicotine in 4 US office workers showed about a .1 mg mean;exposure (mean personal nicotine conce3ntration of 15 ± 9 ug/m , daily workday average, times a 0.8 m/hr inhalation rate times an 8-hr workday). The nonsmokers were exposed to the smoke of a co-worker who smoked 9 cigarettes per workshift, about half the rate of the average US smoker. (Hammond et a1.,1987) This result, although limited, is consistent with the UK data. [N.B.: At an RSP/nicotine ratio of 13:1, (Hammond et al., 1987) the associated 8-hr av. RSF level from ETS in this office is calculated at 195 ug/m .) Although the ratio of nicotine to other tobacco smoke constituents differs in MS and SS smoke, nicotine uptake may still be a valid marker for total ETS exposure. Nicotine uptake in nonsmokers has been estimated in terms of cigarette equivalents from various studies to vary between 1/6 to 1/3 of a cigarette per day. The NRC reports various estimates of cigarette equivalents based upon cotinine in nonsmokers ranging from 0.1 to 1 cigarette per day, and utilizes a ratio of urinary cotinine in ETS-exposed nonsmokers (25.2 ng/ml) to that in active smokers (1826 ng/ml) yielding a 1.4% result.(NRC, 1986) (Assuming a usage of 32 89

vapor phase or particulate phase. Although biological markers show promise as measures of exposure, they also have limitations. Another consideration is averaging time. For chronic diseases such as cancer, average exposures occuring over a year or lifetime are of greater importance than short-term exposures.(SG, 1986) I The two most promising markers for ETS are respirable suspended particles in the size range <2.5 um (RSP) and nicotine and its metabolite cotinine.(NRC,1986; SG,1986; IARC,1987) A majority of field studies have used RSP as an indicator of exposure to ETS because of the substantial emission of RSP in indoor spaces from tobacco combustion. ETS is the dominant contributor to the indoor level-s of RSP. The total RSP, as measured by personal monitors, has been found to be substantially elevated for those who report exposure to ETS relative to those who report no exposure. Both air monitoring and modeling clearly indicate that RSP concentrations will be elevated over background levels in indoor spaces when even low smoking rates occur.(NRC, 1986) Although lacking specificity for tobacco smoke, the prevalence and number of smokers correlates well with RSP levels in homes and other enclosed areas.(SG,1986) RSP is the single largest component of ETS by weight, and RSP is currently the best and most-utilized general category of air contaminants to represent ETS.(NRC,1986) The biological markers that have been most useful for assessing recent exposures to ETS are nicotine and its metabolite cotinine, which derive exclusively from tobacco products, of which tobacco smoke is the most important source. Almost all nicotine shifts from the particulate phase in MS and fresh SS smoke to the vapor phase in ETS. Nicotine and cotinine can be quantified in saliva, blood, and urine. Generally, the mean concentrations of nicotine and cotinine in plasma or urine of nonsmokers exposed to ETS under natural conditions is about 1 percent of the mean values in smokers, (NRC,1986) reflecting the fact that smokers are present in nearly all environments, including most•workplaces,-restaurants, and transit vehicles, making it almost impossible for nonsmokers to avoid some exposure to ETS.(SG,1986) A. Sources of ET8 In 1986, an estimated 50,000,000 US smokers aged 117 yrs smoked about 584 billion cigarettes annually. (NRC, 1986; Tobacco Institute, 1987) They consumed an additional 3.2 billion cigars, as well as an estimated 24.4 million pounds of tobacco for pipes and hand-rolled ciqarettes.(NRC, 1986) The average US cigarette smoker smokes 32 cigarettes per day at a rate of 2 cigarettes per hour and emits about 22 mg of RSP per cigarette.(IARC, 1987) Since the average person spends about 90% of the time indoors, an estimated 12,000 metric tons of RSP are emitted into US indoor m 80 Go O OD W O 1~

nonsmoker appears to carry a daily body burden of about 0.2 milligrams (mg) of nicotine. The cotinine-based estimates have the advantage that they reflect actual dose of an ETS constituent. They have the disadvantage that they do not reflect a wide distribution of target populations, are based mostly on UK ETS exposures, and may substantially underestimate exposures to other constituents of ETS. The RSP-based estimates have the advantage that they are model-based, can be used to estimate exposures in a variety of microenvironments, represent the great bulk of ETS carcinogens, and can be compared with atmospheric measurements of RSP. They have the disadvantage that they do not represent whole smoke exposure, and do not reflect absorbed dose. The greatest source of uncertainty is that neither cotinine nor RSP measurements are based on a national probability sample, and on an absolute scale, represent a limited amount of data. Nevertheless, the NRC(1986), the SG(1986), and IARC(1987) have utilized this data base for exposure assessment purposes. Estimates of the adult nonsmoking population's exposure to RSP from ETS suggest that the range of exposure is from 0 to 14 mg per day, with the population average put at 1.5 mg per day, where the peak-to-mean ratio is about a factor of 10, consistent with the biomarker-based findings. 92

(ug/m}), G is the RSP generation rate from tobacco combustion in units of micrograms per hour (ug/hr), N„ is the ventilation or infiltration rate in units of airchanges per hour (ach), N, is the loss rate of RSP due to surface removal in a space in air changes per hour, V is the volume of the space in cubic meters (m3), and m is the mixing rats expressed as a fraction. The above model assumes no air-cleaning devices, either in the space or recirculated airt Leaderer (1984) has given a detailed review of this model. Under laboratory conditions, these input parameters can be controlled and evaluated. In conducting field studies or in estimating past RSP levels indoors, the values on the right side of eq.l have to be determined from available data. This equation assumes equilbrium conditions, and to the extent that any of the generation or removal terms are intermittent (e.g. smoking rate) or variable (e.g. ventilation rate), errors are introduced. (NRC,1986) The most extensive use of the mass-balance equation for assessing RSP levels due to ETS in occupied spaces has been due to Repace and Lowrey..(1980). (NRC,1986) Drawing upon the "best available data" from several sources, including both measured and estimated parameters, they proposed and applied in field observations a condensed version of the mass-balance equation for estimating RSP exposures due to ETS in a variety of indoor microenvironments.(NRC,1986) Their model is: Ceq - 650 D./N„ (2), where C., is the equilibrium concentration of RSP due to ETS in units of micrograms per cubic meter, D. is the density of ictive smokers (burning cigarettes) observed in a space per 100 m over the sampling time, and N„ is the ventilation or infiltration rate in ach.(NRC,1986) The constant term (650) is calculated from a standard set of assumed conditions for smoking rates, RSP emission rates, mixing factors, ventilation rates, and sink rates. These standard sets of conditions are derived largely from experimental data-and building standards.(NRC,1986) In applying equilbrium mass balance models such as eq.(2), gathering data on easily measured input parameters such as smoking rates or volume can substantially reduce the variablity of the estimated RSP levels. However, the NRC stated that additional field testing of eq.(2} as well as a better understanding of the variability of the input parameters was needed.(NRC,1986) More recently, the*International Agency for Research on Cancer (IARC) has published derivatives of eq.2 which incorporate advances in understanding.(IARC,1987) Eq.(2) assumes a steady generation of tobacco smoke, which is generally only valid when 3 or more smokers are present in a space. It is also limited for modeling purposes by being based on the room density of active smokers. The derivative equations incorporate adjustments which allow for intermittent generation of smoke when less than 3 82

levels; smoking data points 'A' thru 'T' encompassed a wide variety building microenvironments,including 10 restaurants, 3 cocktail lounges, 3 bingo games, 2 dinner-dance halls, 1 bowling alley, 1 sports arena, 1 hospital waiting room, and a residence during a dinner party. Studies of the dispersion of RSP from ETS in US homes showed at most a factor of 2 difference among various rooms in residences, averaged over 24 hrs. In a setting such as a work environment, where the average exposure is several hours, ETS would be expected to disseminate throughout the airspace where smoking is occuring.(SG, 1986) Although most people spend approximately 90 percent of their time in just two microenvironments (home and work), important exposures can also be encountered in other microenvironents, e.g., in transit, which accounts for 0:5 to 1.5 hrs per day for most people..(SG, 1986) Exposures on aircraft can also be considerable. (Repace and Lowrey, 1988) I D. Exposure of nonsmoking populations to ITS In the general population (both sexes) aged >_ 17 years in 1980 (160,798,000 persons),_a majority has smoked at some time: 32.6% were current smokers, and 21.3% were exsmokers, while 46.1% had never smoked (see Table 9). Among current 1980 smokers, 53% were male, and 47% were female, with some race- and gender-specific differences : white males, 35.9%, black males, 42.0%; white females, 29.3%, black females, 29.7%. (R. Wilson, NCHS, personal communication) In terms of the population at risk, both lifelong nonsmokers and former smokers, 66.7% of the adult population and the overwhelming majority of children are potentially at risk from involuntary exposure to ETS (in 1970, Bonham and Wilson (1970) found in a national probability sample of children, that 62t of US homes with children contained 1 or more smokers). Exposure to various subpopulations or individuals, however, may vary considerably. For example, the prevalence of smoking among subgroups of the population who proscribe smoking on religious grounds (such as Mormons and Seventh-Day Adventists) is much lower: for example, in 1980, only 1.7% of Seventh Day Adventist men and 0.5% of Seventh Day Adventist women reported current smoking, although 35% of the total were exsmokers. The incidence of lung cancer -- a disease for which the majority of cases occur in smokers -- among SDAs is 21% of that in the general population. Thus, SDA homes would be, in general, expected to be ETS-free. The microenvironments of importance for exposure to ETS will be those where the population spends the bulk of its time. As Table 10 (Ott, 1981)(based on 1972 data) shows, employed men spend an estimated 56% of their time at home, and 28% of their time at work, for a total of 84% of the time at home and at work; employed women spend 64% of their time at home, and 22% of the time at work, for total of 86% of the time at home and at work; while homemakers spend 85% of the time at home. When time spent 86

office buildings in 7 states with different climates is shown in Fig. 7, and these generally approximate the ASHRAE 62-81 ventilation standards for offices (20 cfm per occupant, equivalent to 0.84 ach, for smoking buildings), on average, although there are some buildings significantly lower. A recent EPA study of air exchange rates in 6 buildings (3 new, 3 old) did not show significant differences between the new (.5 ach) and old (.5 ach) buildings' airchange rates, although for a given building nighttime measurements tended to be lower. (Sheldon, et a1.,1987) In summary, limited field tests of the general equilibrium model, in which some of the input parameters are measured and others are estimated from either chamber studies or building codes, have predicted RSP levels reasonably well over a wide range of values of input parameters. It is clear that both models and observations based on personal monitoring or area monitors in various microenvironments yield consistent results: RSP levels when smoking is allowed will result in substantial increases over RSP levels in nonsmoking occupancy.(NRC,1986) C. Measured concentrations of RSP from ETS Both chamber and field studies (Table 8) have demonstrated that tobacco combustion has a major impact on the mass of suspended particulate matter in occupied spaces in the size range <2.5 um, defined here as RSP. RSP is a major component of ETS. Even under conditions of low smoking rates, easily measurable increases in RSP have been recorded above background levels (Table 8). The term RSP, however, encompasses a broad range of particulates of varying chemical composition and size emanating from a number of sources (outdoors, cooking indoors, kerosene heaters, etc.)(NRC, 1986) The apportionment of RSP indoors depends primarily on the presence of these other sources, however, there are few indoor sources generating concentations which approach in strength those due to ETS. As section II indicates, there appears to be little variability between brands of cigarettes or tobaccos for RSP emissions, although cigars will produce greater emissions than cigarettes. Thus, it may be inferred from Table 8 that from a comparison of smoking and nonsmoking buildings, the bulk of the RSP found in buildings where there is smoking is due to ETS. For example, by comparison of the data of First (1984), Leaderer, et al (1986) and Repace and Lowrey (1980,1982) for a total of 42 smoking buildings and 21 nonsmoking buildings, the wei?hted average RSP level in the smoking builjings is 262 ug/m, while in the nonsmoking buildings it is 36 ug/m , suggesting that about 85% of the indoor RSP levels in those buildings is due to ETS. Most of the buildings involved were public access buildings. Figure 8, (IARC, 1987) a plot of the data of Repace and Lowrey (1980, 1982) illustrates the large impact of smoking on RSP 85

I exposures. However, additional data on the distribution of smokers in the nonsmokers' environment as well as the distribution of ETS levels in that environment, are needed in order to characterize the actual ETS exposure of the population. In the absence of such data, population exposures can be estimated by models or by extrapolation from biological markers from existing studies. (SG, 1986; IARC, 1987) In summary, exposures to ETS can be assessed by personal air contaminant monitoring, modeling of concentrations based upon air sampling, time-activity patterns, and questionnaires, or upon biological markers. The two best methods at present are based upon the biological markers, nicotine and its metabolite, cotinine, which are present in the saliva, plasma, and urine of active and passive smokers, and upon RSP from the particulate phase of ETS, which has been used by a majority of field studies because of the substantial emission of RSP from tobacco combustion. In US, ETS is generated by 50 million smokers, who smoke the equivalent (including pipes and cigars) of 610 billion cigarettes annually,- Although the number of smokers has been declining, the percentage of heavy smokers has been increasing. There are models in use, based on the mass-balance equation, and validated both under laboratory and limited field conditions, which can predict the concentrations of RSP from ETS to a reasonable degree of accuracy. Application of such models, together with field studies of RSP concentrations and behavioral studies, has shown that exposure to ETS is very widespread in the population. Field studies of RSP in buildings where smoking occurs suggest that RSP from ETS contributes 80 to 90 percent of the particulate load during the period of smoking, and that it persists for long periods after smoking ends at typical building air exchange rates, thus prolonging nonsmokers' exposures. E. Zntegrated exposure analysis Exposure to ETS can be quantified either by atmospheric or biological markers:, Of the latter, expired carbon monoxide, carboxyhemoglobin, plasma thiocyanate, plasma, urinary or salivary nicotine, and plasma, urinary, or salivary cotinine have been used to evaluate exposure to ETS. However, successful attempts to quantify the degree of exposure have been limited largely to measurements of nicotine and cotinine. Urinary nicotine is a sensitive indicator of recent ETS exposure, while cotinine appears to be the short-term marker of choice for epidemiologic studies. Nicotine and cotinine are the best markers currently available. Levels in body fluids may be elevated 10 or more times in the most heavily exposed groups compared with the least exposed groups. Mean levels of urinary nicotine and cotinine in body fluids increase with an increasing self-reported ETS exposure and with an increasing number of cigarettes smoked per day by active smokers. (SG, 1986) 88

was 1.1 ± 0.9 ach (Grot & Clark, 1979); this value is likely to be lower than a full seasonal average with no restrictions on door and window openings. Based on time-budget studies, in a two- smoker home, on average, an estimated 21 cigarettes per day (cpd) would be smoked in the home by the homemaker, and 11 cpd by the wage-earner, for a total of 32 cpd, by a smoking couple (i.e., assuming 2 cigarettes per hour, this implies that smoking occurs in the home 16 hrs out of 24).(Repace and Lowrey, 1985) The utility of Eq. 4 depends on the assumption of an air exchange rate. Eq. 4 f r a two-smoker home (q„ w 0.58) predicts a value of Cp - 60 ug/m~ 16 hr average or 40 ug/m3 24-hr average, for a value of N, - 1.4 achI .ddinq the 24 ug/m3 background yields an estimated 64 ug/m for a 24-hr average. Extrapolating from this to a single smoker home would place the estimated 24-hr RSP ~oncentration at 44 ug/m3, and to a 3 smoker home yields 84 ug/m . This is consistent with observations as shown in fig.5. Thus, by assuming an air exchange rate only a third of a standard deviation from the 14 city mean, the 6-city RSP levels in smokers' homes.can..be..fit exactly. If the 14 city mean of 1.1 ach were used for N, instead, the predicted concentrations would still be within 27% of observations. This example illustrates the utility of models in estimating nonsmokers' exposures to ETS. As a second example, consider the measured aerosol mass concentration in a 700 m3 (25000 ft2 floor area) office with one smoker (smoking rate not reported), and a measured air exchange rate of 1 ach (see Fig. 6); the large impact on the office aerosol concentration caused by smoking is apparent by comparing the daytime and evening RSP concentrations.(IARC, 1987) The predictions of eq. 5 for Dh, - 1 smoker (smoking at a rate of 2 cph) per 7 hundred cupsic meters and N, - 1 ach yields C - 10 ug/m3; wit~ an 18 ug/m background added, the predicted RSP level is 28 ug/m . The predicted value (eq. 3) for chainsmoking (6 cph) is 48 ug/m3, which is consistent with the daytime data in Fig. 6. It is clear from fig. 6 and also from models, that ETS can be very persistent in indoor environments: at an air exchange rate of 1 ach, it takes 3 hrs for 954 of the smoke from 1 cigarette to be removed (IARC, 1987) Recent research has revealed several interesting factors in large office building air exhange. There are many pathways for floor-to-floor air communication, particularly return air shafts, where the existence of such pathways can cause a building's air exchange characteristics to closely approximate those of a single large open space; it does not require unusual numbers or sizes of openings to create these conditions.(A.Persily, personal communication7 Persily and Grot,1986) This implies that ETS may diffuse throughout a large office building, exposing nonsmokers even in private offices. Nicotine measurements in office buildings support this observation. (Williams, et al., 1985) A sampling of whole-building air-exchange rates in 8 large federal 84

of average exposure in passive smoking to that in active smoking, was about 0.3%. This translates into 3% of the smoker' exposure for the most-exposed passive smokers, reasonably consistent with estimates based on doses from nicotine and cotinine, above. Table 13 gives estimates of the probability-weighted exposures to ETS for US nonsmoking adults at home and at work, the two most-frequented microevironments.(Repace and Lowrey, 1985) Table 13 is derived from RSP concentration modeling based upon Eq.'s 2- 5, and from assessments of exposure probability based on a limited national survey of top management and health officials concerning prevalence of smoking in the workplace in 3000 US corporations, large, medium, and small (29% response), and a national probability sample of the prevalence of smoking in homes with children (used as a surrogate for all homes). Exposure probabilities were a weighted average taken over the number of workers in white-collar and blue-collar occupations, and including the different exposure probabilities for white and blue collar workers. Air exchange rates and building occupancies were taken from ASHRAE Standard ventilation rate tables for white- collar workplaces (which were used as surrogates for blue-collar workplaces). Table 13 estimates average the workplace ETS exposure probability at 63%, and the average estimated domestic ETS exposure probability at 62%, where the focus was on estimation of ETS exposures in the 1950's to mid-1970's, since these exposures were held to be of primary significance for the studies of passive smoking and lung cancer, given the long latency for lung cancer. comparison of these exposure probability estimates to adult life ETS exposure histories taken by Kabat and Wynder (1986) for 215 60-yr old female nonsmokers, 654 at home and 67% at work, shows good agreement. Table 13 estimates a 0.45 mg/day RSP exposure for nonsmokers at home, (weighted for male and female time-activity pattern dif~erences, and for respiration rate) corresponding to a 19 ug/~a 24-hr average, in good agreement with results (19 ug/m per smoker) published in the 6- City study.(Repace and Lowrey, 1985) Table 13 also estimates a 1.82 mg/day RSP exposure for workers, (again weighted for male- female time-activity patterns and for respiration rate) corresponding to about a 230 ug/m3 workplace concentration, using ASHRAE Standard 62-73 for workplace occupancy and performing a weighted average workday for the different hours worked by men and women (Repace and Lowrey, 1985). This is in good agreement with the weighted average concentrations (262 ug/m3) reported for ETS in public access buildings (See section III-C). In summary, using either the best biological marker (cotinine) or the best atmospheric marker (RSP) produces a consistent assessment of ETS exposure, i.e., of the order of 1% of that in smokers. The most-exposed individuals appear to have levels about ten times higher. Based upon limited data, the typical 91

References Bonham, G: Wilson, RW (1981). Children's health in families with cigarette smokers. Amer. J. Public Health 71: 290-293. First, MW (1984). Environmental tobacco smoke measurement: retrospect and prospect. Eur. J.Respir. Dis. 5(Suppl.):9-16. Garfinkel, L (1981). Time trends in lung cancer mortality and a note on passive smoking. J. Natl. Cancer Inst. 66:1061-1066 Greenburg, RA; Haley, NJ; Etzel, RA; Loda, FA. Measuring the exposure of infants to tobacco smoke: Nicotine and cotinine in urine and saliva. New England J. Med. 310: 1075-1078. Grot, RA, & Clark, RE (1986). 178-194. Measured air infiltration and ventilation rates in 8 large office buildings. ASTM Spec. Pub. 904, Ed. H. Trechsel & P. Lagus, ASTM, Philadelphia 151-183. Hammond, SKr Leaderer, BP; & Roche, A. (1987). Collection and analysis of nicotine as a marker for environmental tobacco smoke in personal samples. Atmos. Env. Jarvis, MJ; Russell, MAH: Feyerabend, C; Eiser, JR; Morgan, Mi et al (1985). Passive exposure to tobacco smoke: saliva cotinine concentrations in a representative population sample of nonsmoking school children. Br. Med. J. 291: 927-929. Leaderer, BP: Cain, WS; Isseroff, G; Berglund, LG. (1984). Ventilation requirements in buildings. II Particulate matter and carbon monoxide from cigarette smoking. Atmos. Environ. 18: 99- 106. National Research Council (1986). Environmental tobacco smoke -- measuring exposures and assessing health effects. National Academy Press, Washington, DC. Office on Smoking and Health (1988). Estimates of the mortality from smoking. Centers for Disease Control, Washington, DC. Ott, WR. Human activity patterns: A review of the literature for estimation of exposure to air pollution. U.S. Environmental Protection Agency, Washington, DC. Repace, JL, and Lowrey, AH (1980). Indoor air pollution, tobacco smoke, and public health. Science 208: 464-472. Repace, JL, and Lowrey, AH (1982). Tobacco smoke, ventilation, and indoor air quality. ASHRAE Trans. 88= 894-914. Repace, JL, and Lowrey, AH (1985). A quantitative estimate of nonsmokers' lung cancer risk from passive smoking. Environment 93

in other peoples' homes and in non-work places of business are added in, the population averages about 88% of its time in homes and workplaces. These sites, therefore, must, on average, predominate as potential sites for exposure to ETS for the general nonsmoking population. A UK study of exposure to ETS in 20 nonsmoking men whose wives smoked showed that 784 of the men's reported hours exposure came from outside the home; by contrast, 90% of the ETS exposure of 101 nonsmoking men whose wives did not smoke was reported to come from non-domestic microenvironments. (Table 11). Since the second largest source of time spent by men is in the workplace (Table 10), this suggests the workplace may be an important source of exposure for nonsmoking men. One recent questionnaire survey of exposure to ETS in a California population subscribing to a health-maintainance plan indicated that 634 of nonsmokers surveyed reported exposures to tobacco smoke (Friedman, 1983)p this occurred despite the fact that in the 1980's California has has been in the forefront of restrictions on smoking in public, with 44% of its population currently living in communities that have enacted workplace smoking restrictions.(SG, 1986) Garfinkel (1981), in a study of 176,000 nonsmoking US women (1960-1972), found 72% had smoking husbands. Kabat and Wynder (1986), in a recent study of 215 sixty-year-old US women nonsmokers, found that 65% were exposed at home.and 67% reported exposure at work, averaged over adulthood. Studies of the concentration of nicotine and cotinine in the body fluids of nonsmokers report similar results (Table 12); Fig. 10 (Jarvis & Russell, 1984) shows that in a study of about 100 UK nonsmokers, only 124 of the subjects had undetectable cotinine levels. Moreover, in the latter study, surprisingly, nearly 50% reported no exposure, suggesting that ETS permeates indoor atmospheres to such an extent that many nonsmokers are unwittingly exposed. This is borne out by a study of 46 US infants, 40% of whom were reported by their mothers to be unexposed to ETS, but only 20% had undetectable urinary cotinine levels (Fig. 11).(Greenberg, 1986) In a third UK study (Wald, 1986) of urinary cotinine in 221 nonsmokers, the 20% who reported no exposure had mean urinary cotinine levels which were 21% of the remainder of the group who reported exposure. The foregoing illustrates that exposure to ETS is very widespread in the population, even among those nonsmokers who believe themselves to be unexposed, however it tends to be greater in those who say they are exposed at home, possibly indicating a greater tolerance for ETS among men with nonsmoking spouses. Although there have been numerous measurements of ETS concentrations in various indoor settings, these data do not represent a comprehensive description of the actual distribution of ETS exposures in the US population. Spengler et al.(1985) and Sexton et al. (1984) demonstrated by personal monitoring of RSP and the use of time-activity questionnaires that exposures to ETS both at home and at work are significant contributors to personal 87

FIGURE 4. Air exchange rates in homes are one determinant of nonsmokers' exposures to ETS. Low air exchange rates mean higher exposures. Shown is a histogram of infiltration values in a sample of 266 older US middle class homes around the country. Average heating season values are shown. The median of the distribution is 0.9 ach and the mean is 1.1 ± 0.9 ach.(Grot and Clark, 1979)(NRC, 1986) ---°-°------------------------------°------------------------- ALL 14 CITIES H 40 No. OF NOUSES • 211 No. OF NEAOINCS • 1011 ~ 30 12 NR', p=1 0 . I r3 o< O•O.I/NR" 0 20 \ ~ s \ i 10 \ \\ \\\\ \ MMM 0 to 0.5 1.0 1.5 2.0 tS 10 3.5 4.0 4.5 AIR EXCHANGE RATE IHR") Figure 3. HSstoEram of ineasured natural air infiltration rates for 14 weatherization sites 92 b

1 cigarettes per day by habitual smokers based upon cigarette sales (Repace and Lowrey, 1980), this yields 57 ng/ml/cigarette, or 0.44 cigarette equivalents per day. Adjusting this by multiplying by the ratio of cotinine clearance in nonsmokers to that in smokers reported in one study (Fig.1), 49.7 hrs/18.5 hrs - 2.67, yields a higher value, 1.1 cigarette equivalents per day or 3.6% of the smokers' dose.] In summary, based upon the limited studies (none of which are a probability sample of US nonsmokers) of cotinine in body fluids of nonsmokers (see Table 11, SG, 1986), nonsmokers appear to have of the order of 1% of the nicotine uptake of smokers. However, these estimates must be interpreted with caution; relative absorption of nicotine in smokers and nonsmokers may substantially underestimate exposure to other components of ETS. (SG,1986) Alternatively, human exposure to ETS can be estimated using approaches similar to those used for other airborne pollutants. Measures of exposure to individual atmospherie smoke constituents can be used as estimates of whole smoke exposure. The accuracy of this approach is limited by changes in the composition of ETS with time and conditions of exposure. One widely reported marker of ETS is respirable suspended particulate matter (RSP). Although lacking specificity for tobacco smoke, the prevalence and number of smokers correlates well with RSP levels in homes and other enclosed areas. In the Harvard study of indoor air pollution in 6 cities, Spengler et al. and Sexton et al. demonstrated by the personal monitoring of RSP and the use of time-activity questionnaires that exposures to ETS at home and at work are significant contributors to personal exposures. In general, measurements in a large number of locations using measures of smoke generation such as the number of people smoking or the number of cigarettes being smoked have shown a definite relationship of smoke generation to particulate levels. In US homes, there are few other sources of RSP, and therefore, the relationships of RSP measurements to ETS are quite accurate.(SG, 1986) Repace and Lowrey (1980) measured RSP concentration using a piezobalance in several public and private locations, in both the presence and absence of smoking. They then developed an empirical model utilizing the mass balance equation (Eq.2). Using both measured and estimated parameters as input to the model, they validated the model for predicting an individual's exposure to ETS.(SG, 1986) Kuller et al (1986) in a review of estimates of the nonsmoking population's exposure to ETS, observed that cigarette smoking is probably the single most important source of indoor RSP; that a higher percentage of nonsmokers appear to be exposed out of the home, usually at work (Friedman, 1983); and that modeling of RSP has estimated that the average exposure of the nonsmoking adult population to tars from ETS was 1.43 mg/day, varying from 0 to 14 mg (Repace and Lowrey, 1985). Kuller et al. (1986) in reviewing the latter estimate, observed that the ratio 90

FIGURE 5.application of L\RC model (ZARC, 1987) vs. observations for monthly mean RSb concentrations in six US cities (Spengler, at al., 1981; NRC, 1986) The effect of smoking is to increase backgound residential RSP levels (24 uq/m3) an average of about 2o uq/m3. The theoretical values from eq.4 are shown (horizontal solid lines) for comparison, estimated for 1,2, and 3 smoker homes by assuming a mean air exchange rate of 1.4 ach. -------°----------------°----°--°----°-------------°-°- I I I 1 I I I I I I I V 1 I 1 I 1 S 1 %*w O.c Jan Peo tiyr oo• May jkn dw ap S.e Oc+ Nav Oa .un c.o Ma. av 1976 1977 _ 1978 92 c o +Ouhloor : . Indoor, no smokers ~ ~ . Indoor, I fR10kH ~\ LU 110 ~ . s[ndo0a, >i smoker J . V•• / 3 smckers 2 smokers 1 smoker C smokers

Table 11 COTININE IN NONSMOKERS /FROlt DOetESTIC AND NONDONESTIC EXPOSURES.(NRC, 1986) 91% of the~•ETS exposure of the nonsmoking husbands of smoking wives came from non-domestic sources compared to 71t of the exposure of the nonsmoking husbands of smoking wives. The most probable non-domestic source of exposure is the workplace. ----------°------°--------------------------°----------------- Tast.e 12•2 Urinary Cotinine Concentration and Number of Reported Hours of Exposure to Other People's Tobacco Smoke Within the Past 7 Days in Nonsmoking Married Men According to Smoking Habits of Their Wives Urinary Cotinine Concentration Exposure to Other People's Smoke in Preceding Week, h Smoking Cate o No. of , ng/ml Total Outside Home g ry of Wife Men Mean (SE) Median Mean (SE) Median Mean (SE) Median Nonsmoker Smoker 101 20 g.5(1.31" 25.2(14.g) 5.0 9.0 11.0(l.2)6 23.2(4.!) 6.5 21.1 10.0(1.2)` 16.4(3.31 6.0 10.7 NOTE: Differences (nonsmoking wife versus smoking wife): 'p < 0.05; bp < 0.001; `p < 0.06 (Wilcosin rank sum test). SOURCE: Wald and Ritchie (19&/). 92 k

TABLE 10.(Repace and Lowrey, 1985) Time spent in %anous microenvironments by persons in 44 U.S. cmes. expressed in average hours per day. tOtt, in press: NRC. 1981: Stalau. 1912). Microenvironment Employed Men, All Days Employed w'omen, All Days Married Housewives. All Days Inside one's home 13.4 15.4 20.5 Just outside one's home 0.2 0.0 0.1 At one's workplace 6.7 5.2 - In transit 1.6 1.3 1.0 In other people's homes 0.5 0.7 0.8 In places of business 0.7 0.9 1.2 In restaurants and bars 0.4 0.2 0.1 In all other locations 0.5 0.3 0.3 Total ' 24.0 24.0 24.0 92 j

R 111111111 111111111 1 1 I I I 1 I'I,1 1 ~ =tl 111111111 111111111 7 ' 62E608~,8 Mt'xFP.Cr °ccc:cGC= ~ aaa a ~ ~ 7 ~

FIGURE 6. The effect of smoking on workplace RSP levels in a Minneapolis office building. The contrast between daytime RSP levels, when smoking occured, and night-time RSP levels, when it did not, is marked. --__--------°--------°----------------------------------°--- Aer^sol m ass Concentrahon tn a?00-mi office with one smoker (NBISon ef a/. 1982! ie smoking instrument and smoking rate were not specified. However, the air exchange rate ror the space may be calculated by means of equation 2. For the decay of ETS on Thursday. July 9, a non-linear regression analysis of the ASP levels, with an 18 Ng/m3 background levef subtraction, yields C,=1.0 ach (rz=0.95). This value is close to the ASHRAE-recommended ventilation rate for office space. aav ' I I I ~ aw I j I I I ~ I r I I ' ' I I I I I 1 I I ~eo I '~ I ~ .e e I ~toe I too use ltee 1300 ~aee e ~ear wON r,ur TUE ea.. WED eaRr THU +e ,u.. trRl ~r xr SAT 92 d

FIGURE 7. Air exchange rates in cotamercial buildings are c determinant of nonsmokers' exposures to ETS in the vorkplac.. Shown are air exchange rates (infiltration plus ventilation) in eight large federal office buildings in 8 US cities in 7 states. Air exchange rates in the tighter buildings failed to meet ASHRAE standards for occupied office space, (20 cfm/occ or 0.84 ach). The mean annual air exchange rate for all eight office buildings is 0.71 ± 0.25 air changes per hour, about one third less than in the sample of homes in fig.(&^.(Grot and Persily, 1986). ----------------------------- }-____-_--------------'----------___ t Fayetteville Pittsfield FIG. 1-Location of the tight federal office baildints. HUILDING DIlD.+NSIONS (100 m2 x 1000 ft2) Occupiable Floor 7 Volume. &Lr archa.nae rate Loaation Area. m m' (ach) Anchorage 45 500 174 000 0.82 ± .35 Ann Arbor 4 900 31 700 1.04 ± .69 Columbia 24 700 159000 0.85 ± .23 Fayeneville 3 400 21 300 0.37 ± .09 Huron 6 420 27 500 0.32 ± .16 Norfolk 17 300 60300 0.79 ± .19 Pittsfield 1 730 8 520 0.70 ± .19 m Springfield 13 500 57 700 0.79 ± .18 ~ m 2 e O Cb W N O

F 12 Na YYt9Y go aa •a aaaaa aa ~ ~ ~~ 6C sirUMN, Ir ~ A ~ ~ szesas4s . ~ ~~ ~e si~es ~e ~FE cs5caaacg "aa33aaaa ~ ~ FE aa Rya b + ~. ~CC e a gCCC~ a r 4 c E c t I ~ S

FIGURE 8.(IARC, 1987) .--• ) _...t.or -0^ _IS eero30, :,e^erally .n000r yvws at PSO n OuomnQS rne•e ra.^.: S sr•O.ea i,lip ;raary e.caee trose •oune n omiamqs .Nere to0acco s -ot smO.ea -ps a= - o^e•e !oeaew ras sme.ee, iie .,SA vaoonai amo,em air Ouaj:tv %Aw5• •erti 'Cr rotai SVSCe9ceO OarOCj41es ?SP, were encee0e0 '2:C I , vu0t iaw ar fiONrfiCaNT w.eM UvfL !ON TS• I VaS 24 waV ue eOLLYTIGNMlOfNCLlVil r0T!e I . ......................................... ~ 3C0- 9 ,c  SMOef N OSNSiTr fSTiMaTfO • MfaSUefO DATA 0 C<LCULaTSOlOY4tSnYMLlVSL ' tx~ .CC: 00 e_ •G N~aOe 1~M e1~MaNT lfVll f0~ TS• -.-.-. «;.-.-:u . .- - .-.-1 200C • ,• Ki Naa03 1/ • SlCOMOaaT LLViL !ON TS• -•-•-•-'-'- - -----'-'-'-'---'-'- e . iv M y L. SO 'CC.~~P~iP•O _ 1 NaaOfaNNWt111rMaRTLlVtL/OeiN / ~ 11 OaTa IOiNTS I~ 5 •J 'S 2•7 2: 70 ]S ACIR'e S/O•t« anelfy (100 a aLML" C/"r•ffN PM N!j) 92 h

I TABLE 8. contd.(NRC, 1986) 5IYd\ 1\m 4 PrtY11tW l.dunh'. 0.'eupam'Y m, ~.nuLe.m r\f1\' RJIf V S U-partmcnl n nnmcv.S - M- .4 rran\ryv. mtan, lo•I p/anc\ IO mrlnarv T = ---IIn S - M- Welnrand planl:\ 4aoffkr. T = IAl-:IV S - N.M - F\cher. I WN '.SCtne \Ilw\ken per 10p In' 'Grama iK mhacar v.nrumed. ' Snme smMms .a: tcpp.ned dunng 4 M Ihe 280 .ampks ''Meawred durmt 3a-h permdc by Ihe perfluntnearlnn vanr lechnlque. 'Snme revdenat bd d.mhmalrona nl vwrrn tkernecne h<atcn. +md vo.n..ve.l and nn ctyarettn. ' Aclne \mnkcn densn, per 100 m'' t..m~pnlratnT\ M•~nnMm~ MUn Iranlta•i. r\p[ Tlme Vf m~ Cmm~Mnl\ G I-1 4. NM(hCnl-/ FSP 7 1 ' h * n-'h 4 10•1:111-1 TSP P 2 mtn 117 - 1.V1 RSPV mml/a f.Vl ea l I On: peak 1 EaekRmund k.N 4BBREVIATIONSS ach = Alt ManRes per hnur G >< Gnennetrr M ~ MeManral mnubinm 9 = Natural anulalan `I$ = Nn tmnkers Q ~ Optical mGnltor P = PieaOekQM Ealanee OCMI a: Quality Crystal MitteOaNnse Cenade Impaam RSP = Rekplralk sospended panrks S = SmuWen T = Taat ereupants TSP = Twal suspended particles reslr. = bulk4ing .nh unohmg RNnntan 92 g

TABLE 8. (NRC, 1986) PsrueulJic L.•ci• I.IeJwrelJ in Inda-r En•,rr.nmunlc. Ineludine SmokmQ and Vn„amnkm¢ Oeeup.lla. I.It .1 I..inm. 1. ~.~I.~~u.n Vl.,mmrme Ncan.rane.' ..! mG.mmrm. rt.-nr I.Pr rim< . .. ......, ------ - - i_'0-wn _ •--. -mn tln~..•..;I inJ 1«..dcn.r. •S 1. {L.Ir~I ~u•; - n ] nle r"dcncc. 5: 1 - V- G 7 mn 1!51M-!c01 1'SP a~n.nnn. IJ rr•.dcnrc• t . - V_ G'-mn " Iz] in0-IJUI ISP.rn•nnn. I.r..d.a<r <i 2mn 1151-1 TSPvn•.urn• owm.,.. - c ! ml. _ /l1.-11 tvArf.na.a 7u•crna S=i-Jn - V.MI-n.0 t:Vn JJn12!3•uM1.l fSP.enulaIn.n .•1 .11 . IV 1. Fll.a and Nu.e 19'j v5 ='-!M T = In-1M 1 arcnu. NS - - G 2a n 55142-u21 1 arrna• S - N- G OJ h 31011i8•6201 T r !.OM- IJ_'-- Flral. IVM I K'h.M.l VS Haahnrne . e, 11 . 1494 fl public S hulldlnea N_ P- 20f-1 V.M - P'- 2n0140-IM01 II resldenm NS I50-n-J M 018-0,9n QCMI:S-IS min Inver 6 hl 8 resldenns ^IS 150-n'4 M 0.2MI.98 OCMI•5-15 min Iner6hl 1 nadenan S 140-n'J M 0.2'-I.J7 QCMI,5-15min Ir..er 6 hl Leaderer 1 puMla V5 Ihl-1.Rn M'0.P-S.nJ G•a-21 h et al.. huddmp M:0 -'-s 53'r Cn 2-!a h pernnal • putrue 1.T-a.SY 1118-hOD cnmmuni- nuadinys T = 2•e e11Mn N..w /r.urdrv... .r.J I•1.1 rc.rrlrnar• VC I !~n ra.~A. n.c. 1 IIna4.... _ _ _ . :J h (7 ! 1 h V.I..h4c UuIM..r• - rI.J IVna IV ...nlcn.r. 4t II r.••rACnm t Paracr rl .li I r.•ulence VS VM r - 1 ! r..IMnce. S + 1-2 r + 1-J Rcpac<and Uuldnnn - Ln.re.. lurtl. lue2 ]' PuMS sl I3-3 4' nruldmyc Sr.rne rl ,~ fAnlh..r. - IVI.J IV 11../11e• 24 rca.knce• VS' arumllrr Ourd.nm - rl nl . tunl K n/nrncc. VS I b mlr4nce• 1' I 9 rc•rAenrc. S - . Vrrnch+ Uul.h.n• - IVM: -1 rr•nkerr• VS !4 I •rllrllrr• t Grrlme ann 1.dLae V rear b.rlmV. IVnI ~-nlLeh t V n a I I... h 11 ! 1 h Vlla"Il.,.h [I!Jh - _ f: I nn u=-I.na v _ U Ir.nn 92 f 111 • 04011-;41 !h n • -. in.nhl TSP f5P TSP TSP RSP..insa•summee- np swrces RSP. snser+wmmn- snurcei RSP. smerisummec- sourcef - nt. TSP. Iepeu nelausing, all ru. Meawred (160.0 peak) MSL reP a/... mea•urcd HSp.ISPaW. mrawrrcd HW I\r.lh.. mc+.nrnl Ntr. 1 tr Jla. muawrcd HSI' 11.r .rl'r+r n c.l.oe•. v,.rrcc m/: HSI• alt.n ma-+•nm. I SI'mr a m.• Itr NSP. a.mlle..f ! nun yrnple. RSPP a.erauc.d S.mnl vmpks H\P rrlw+s..nry.4c. t'•cd frnpIaaz. RSP. rclwa/ nwnvnn HSP rcpcas mr+.un:. NSP rclleal mav...re• RSP rrA'a1 mcawre. RSI' mreal mcJ.rse. RSPP repa•n In..l.orn IISP, rr(%al nh'J.V/r. rsp TSP ----------- -------

TABLE 9• Number of persons 17 years and over, by cigarette smoking status, race, sex, and age: United States, 1980. (Unpublished data, National Center for Wilson, personal communication) Health Statistics, R• °-----------------°---------- c J a l ~ ..,.~L.. 7....... ...•~... . r• .c - - ~ ili0_ ..,~, Z i I i ~ . rv..0 i1.eC ~+/7 I III 6q71/ I I .! 7G4i. I ~ (!~t . 7. ! I ji..l J/J i,. J.O 7 l.•'" y`"` ~•. I o . ~:. la r ~• r ~T. ., ~•rp i ~L~~. I J't•bM ya.... . yr •6 v Og•..r /il~ 7~. =530t' ~'1• / 1~r5{n /l;/7~ f j / /,~~ 7. I _ . . . .... e ..1 ?Yn~ ,ef7 y~ll ,Jer LkGSr ~ :G ~r• . ' ~h.i ~ ~ . I 7~7?7 ~9oY . a7 Itsl I ~y 7 I o~7 . S •L,ts17. I / 7 -t Y GGY , s4'l , 4fi j s0 73 P• it•ry y ~ts ~ t .I a ' ~ s ~ ' P Y i ~ I Jretpt• 1 1 6 lGSS :IJ.JIl ,,s~!. !so ~at i , Gt ~G/ ( ~ 14.3 y~• lr 3 7 .... . ... !,f ~. ;;~~tp. ~7/ t I ~ y ~ j yy*r ~..-ds n~......J... . y~rp1• 47542 aM.IfP qr+~a / rss l7-f~/~a.+i a.r.MY ~r .j/41'/h7. 'J~yY~• ;(..LY :37LA I. ~ J l . IM14/• O/l I lSel'. i.o.1, I ~~l~~'1~ a ! 171, !7 7• ~ tS-•Y I~a~Y S l,P:fJ. ~ ' 1"17 s~r.T. fG ,3Y!at. I! ~..A.,._ Yiylt =1 / I 1 `I,1I Ifl>• ~. i7at.,.a....(....+ _ n•rY ....• IJ1I0I + q?f! 1j#.0M~1. a/13~a tMt i ,MY.dI /e ~1 II I41.11,• L~73/. ~ i!7.T7 i~M is 449 . nraa r __ as•w I /Yy ~i " , oaJ r ' , : YssM ~.' 7rY7P ~Ya,i. _ l ilptf; t. •;y1 tL~a ~ ~ A.~• IG.Si11. • iqJK! Yt t . 1 rS ql 1417 zJt s 9 sp !e t !~ ' ql! 10 f 41 Y!•! t e, _L3l.dt -t ~ : . , . ~ i ~ Ap • ' n Yp`''' ps •yY ~r...' Y.o.11 ~,65f f• LYd/ ~3i sF I /AG a 4 js7 i/1=t I aGay ~ I 17 .. ~ !1H! .u ~ ;1 Tf.7y<.... I y.71• .'.'Y .7I• !i~ b ~ ~ li 3h 1 7r ~ .Lf,71/1 I lS csy.......1,,,. ; xPlt • 7JG ,. ,1'y6 :7Y ' 3fl• I. JG! /a I 7YLS• , ,~S I Z 3 1 YG , , 7e•!t• '/ist , !/l1i• at ?i,. alti . . 1~Oa . ::3do2 a 7L 27531 . 9s _ ~SJ• , SY .•••V yF ia.... ~ - y s•t * sLJ at•' lr/. ii• ! laI• ta• w ac. sa fL, /GL• ~j•.... , ,.,. 92 1 87808325