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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