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ESTIMATION OF ENVIRONMENTAL TOBACCO SMOKE EXPOSURE ă 3.1. INTRODUCTION Environmental tobacco smoke (ETS) is composed of exhaled mainstream smoke (MS) from the smoker, sidestream smoke (SS) emitted from the smoldering tobacco between puffs, contaminants emitted into the air during the puff, and contaminants that diffuse through the cigarette paper and mouth end between puffs (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992). These emissions contain both vapor phase and particulate contaminants. SS is the major component of ETS, contributing nearly all of the vapor phase constituents and over half of the particulate matter. Overall, ETS is a complex mix of over 4,000 compounds. This mix contains many known or suspected human carcinogens and toxic agents. The information necessary to evaluate human exposures to each of the compounds of human health interest in ETS does not exist. Recognizing that it is impractical to characterize the many individual compounds that make up ETS and to then assess exposures to those compounds, this chapter focuses on the characterization of the complex ETS contaminant mix and exposure to it by nonsmokers. Available data on the physical and chemical properties of sidestream and mainstream smoke are compared to assess the potential for the release of known or suspected human carcinogens and toxic agents into indoor environments where human exposures occur. The available published data are reviewed to determine whether ETS constituents exist in elevated levels in various indoor environments where smoking occurs and whether human exposures ensue. Particular attention is focused upon environmental and biological marker compounds that serve as proxies for the complex ETS mix and the compounds of human health interest. The available biomarker data for ETS clearly show that levels of ETS contaminants encountered indoors by nonsmokers are of sufficient magnitude to be absorbed and to result in measurable doses. Chapters 6 and 8 and Appendix B use such biomarker data for estimating relative residential and nonresidential ETS exposures in calculating the associated risks for lung cancer and various noncancer respiratory effects. Epidemiologic studies relating exposure to ETS with lung cancer (Chapter 5) and respiratory disorders other than cancer (Chapter 7) frequently rely on questionnaires to assess level of exposure. This chapter reviews the limited number of studies that have attempted to validate questionnaires with objective measures of exposure. All of these are population surveys and not epidemiologic disease studies. The few studies that compare body cotinine levels with childhood respiratory disease occurrences are discussed in Chapters 7 and 8. This chapter concludes that (1) MS, SS, and ETS are chemically similar and contain a number of known or suspected human carcinogens and toxic compounds; (2) marker compounds for ETS are measurable in a variety of indoor environments; (3) exposure to ETS is extensive; and (4) there is a measurable uptake of ETS by nonsmokers. 3.2. PHYSICAL AND CHEMICAL PROPERTIES ČOver the past several years, there have been a number of reviews of the physical and chemical properties of mainstream and sidestream cigarette smoke (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992). A particularly detailed review is contained in the recent book by Guerin et al. (1992). This section summarizes the findings of these reviews to identify the similarities and differences in mainstream and sidestream emissions and to establish that known and suspected human carcinogens and toxic agents are released into occupied spaces from tobacco combustion. Data contained in these reviews, as well as recently published material, are also presented to document that sidestream emissions of notable air contaminants result in measurable increases of these contaminants in indoor locations where individuals spend time. The physical and chemical characterization of MS air contaminant emissions from cigarettes, cigars, or pipes is derived from laboratorybased studies that have typically utilized standardized testing protocols (FTC, 1990; Guerin et al., 1992). The data available are primarily for tobacco combustion in cigarettes and provide a substantial database on the nature of MS. These protocols employ smoking machines, set puff volumes and frequencies, and standardized air contaminant collection protocols (small chambers, Cambridge filters, chamber air flow rates, etc.). Existing standardized protocols reflect conditions representative of human smoking practices of over 30 years ago for nonfiltered cigarettes and may not reflect current human smoking parameters for today's filtered lowtar cigarettes (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992). It has been suggested that current standardized protocols, particularly for filter cigarettes, may underestimate MS deliveries (Guerin et al., 1992). MS air contaminant emission rates determined in these studies using standardized protocols can be affected by a number of factors, such as puff volume, air dilution rate, paper porosity, filter ventilation air flow around the cigarette, and moisture content of the tobacco. Actual smoking habits of individuals can also dramatically alter the MS deliveries. Variability in any of the factors can affect the nature and quantity of the MS emissions. Standardized testing protocols for assessing the physical and chemical nature of SS emissions from cigarette smoke do not exist, and data on SS are not as extensive as those for MS emissions. Protocols used for the generation and collection of SS emissions typically use standardized MS protocols (smoking machines, puff volumes, etc.) with modifications in the test devices (use of small chambers) that allow for the simultaneous collection of SS emissions for analysis (Dube and Green, 1982; McRae, 1990; Rickert et al., 1984). The protocols for the collection of SS emissions are such that results can be directly compared to MS emissions and thus provide valuable insights into the physical and chemical nature of ETS. It should be noted, however, that the SS emissions collected under these protocols may be somewhat different from ETS emissions. ETS also contains exhaled MS, which has not yet been characterized. Exhaled MS can contribute from 15% to 43% of the particulate matter in ETS, though little of the gas phase contaminants (Baker and Proctor, 1990). In addition, SS samples are not collected under conditions where the emissions are diluted and "aged," as is ETS. The aging and dilution of the SS emissions can produce changes in phase distribution of the contaminants. Results of laboratory evaluations have indicated substantial similarities and some differences between MS and SS emissions from cigarettes (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992). Differences in SS and MS emissions are due to differences in the temperature of combustion of the tobacco, Ph, and degree of dilution with air, which is accompanied by a corresponding rapid decrease in temperature. SS is generated at a lower temperature (approximately 600$C between puffs vs. 800900$C for MS during puffs) and at a higher Ph (6.77.5 vs. 6.06.7) than MS. Being slightly more alkaline, SS contains more ammonia, is depleted of acids, contains greater quantities of organic bases, and contains less hydrogen cyanide than MS. Differences in MS and SS are also ascribable to differences in the oxygen concentration (16% in MS vs. 2% in SS). SS contaminants are generated in a more reducing environment than those in MS, which will affect the distribution of some compoundsnitrosamines, for example, are present in greater concentrations in SS than in MS. SS is rapidly diluted in air, which results in a SS particle size distribution smaller than that for MS and in the potential for changes in phase distribution for several constituents. Nicotine, for example, while predominantly in the particle phase in MS, is found predominantly in the gas phase in ETS (Eudy et al., 1985). The shift to gas phase is due to the rapid dilution in SS. SS particle size is typically in the range of 0.011.0 %m, while MS particle size is 0.11.0 %m. The SS size distribution shifts to small sizes with increasing dilution (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992; Ingebrethsen and Sears, 1985). The differences in size distribution for MS and SS particles, as well as the different breathing patterns of smokers and nonsmokers, have implications for deposition of the produced particle contaminants in various regions of the respiratory tract. Estimates of from 47% to more than 90% deposition for MS and of 10% deposition for SS have been reported (U.S. DHHS, 1986). Despite quantitative differences and potential differences in phase distributions, the air contaminants emitted in MS and SS are qualitatively very similar in their chemical composition because they are produced by the same process. Over 4,000 compounds have been identified in laboratorybased studies of MS (Dube and Green, 1982; Roberts, 1988). In a 1986 IARC monograph evaluating the carcinogenic risk of tobacco smoke to humans (IARC, 1986), 42 individual MS components were identified as carcinogenic in bioassays with laboratory animals, with many of these either known or suspected human carcinogens. Many additional compounds in MS have been identified as toxic compounds. Although SS emissions have not been chemically characterized as completely as MS emissions, many of the compounds found in MS emissions, including a host of carcinogenic agents, are found in SS emissions (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992; Dube and Green, 1982; Roberts, 1988) and at emission rates considerably higher than for MS. Part of the data available from studies of MS and SS emissions is shown in Table 31 (extracted from NRC, 1986). These data are for nonfilter cigarettes and represent a summary of data from several sources. It is immediately obvious from Table 31 that SS and MS contain many of the same notable air contaminants, including several known or suspected human toxic and carcinogenic agents, and that SS emissions are often considerably higher than MS emissions. For the compounds shown in Table 31, all of the five known human carcinogens, nine probable human carcinogens, and three animal carcinogens are emitted at higher levels in SS than in MS, several by an order of magnitude or more. For example, Nĩnitrosodimethylamine, a potent animal carcinogen, is emitted in quantities 20 to 100 times higher in SS than in MS. Table 31 similarly shows that several toxic compounds found in MS are also found in SS (carbon monoxide, ammonia, nitrogen oxides, nicotine, acrolein, acetone, etc.). Again, for many of these compounds, SS emissions are higher than MS emissionsin some cases by an order of magnitude or higher. The SS/MS emission ratios shown in Table 31 can be highly variable and potentially misleading because, as noted earlier, a number of factors can have a substantial impact on MS emissions. A filtered cigarette, for example, can substantially reduce MS of total mass well below that shown in Table 31, thus resulting in a much higher SS/MS ratio. A number of recent studies (Adams et al., 1987; Guerin, 1987; Higgins et al., 1987; Chortyk and Schlotzhauer, 1989; Browne et al., 1980; Guerin et al., 1992) indicate that, quantitatively, SS emissions show little variability as a function of a number of variables (puff volume, filter vs. nonfilter cigarette, and filter ventilation). The lack of substantial variability in SS emissions is related to the fact that sidestream emissions are primarily related to the weight of tobacco and paper consumed during  Table 31. Distribution of constituents in fresh, undiluted mainstream smoke and diluted sidestream smoke from nonfilter cigarettes1 T ddxE !   ddxE !  T EEUEEUConstituentAmount in MSRange in SS/MSFFVapor phase:2@@ Carbon monoxide1023 mg2.54.700 Carbon dioxide2040 mg81100 Carbonyl sulfide1242 g0.030.1300 Benzene31248 g51000 Toluene100200 g5.68.300 Formaldehyde470100 g0.1 5000 Acrolein60100 g81500 Acetone100250 g2500 Pyridine1640 g6.52000 3Methylpyridine1236 g31300 3Vinylpyridine1130 g204000 Hydrogen cyanide400500 g0.10.2500 Hydrazine432 ng300 Ammonia50130 g3.75.100 Methylamine11.528.7 g4.26.400 Dimethylamine7.810 g3.75.100 Nitrogen oxides100600 g41022 NĩNitrosodimethylamine41040 ng2010022 NĩNitrosodiethylamine4ND25 ng<4022 NĩNitrosopyrrolidine4630 ng63000 Formic acid210490 g1.41.600 Acetic acid330810 g1.93.600 MethCyl chloride150600 g1.73.3 1,3Butadiene4,6 69.2 g36  ``(#8(continued on the following page)     Table 31. (continued)  T ddx R# P  ddx R# P T EEUEEUConstituent Amount in MSRange in SS/MSPPParticulate phase:200 Particulate matter7 1540 mg]i]]]1.31.900 Nicotine 12.5 mg]]]2.63.300 Anatabine 220 g]]]<0.10.500 Phenol 60140 g]]]1.63.000 Catechol 100360 g]]]0.60.900 Hydroquinone 110300 g]]]0.70.900 Aniline4 360 ng]]]3000 2Toluidine 160 ng]]]1900 2Naphthylamine3 1.7 ng]]]3000 4Aminobiphenyl3 4.6 ng]]]3100 Benz[a]anthracene5 2070 ng]]]2400 Benzo[a]pyrene4 2040 ng]]]2.53.500 Cholesterol 22 g]]]0.900 Butyrolactone5 1022 g]]]3.65.000 Quinoline 0.52 g]]]31100 Harman8 1.73.1 g]]]0.71.722 NĩNitrosonornicotine5 2003,000 ng]]]0.5300 NNK9 1001,000 ng]]]1422 NĩNitrosodiethanolamine4 2070 ng]]]1.200 Cadmium4 110 ng]]]7.200 Nickel3 2080 ng]]]133000 Zinc 60 ng]]]6.700 Polonium2103 0.040.1 pCi]]]1.04.000 Benzoic acid 1428 g]]]0.670.9500 Lactic acid 63174 g]]]0.50.700 Glycolic acid 37126 g]]]0.60.9500 Succinic acid 110140 g]]]0.430.62 PCDDs and PCDFs10 1 pg]]]2  ``(#8(continued on the following page)     Table 31. (continued) 1Data in this table come from the NRC report (1986), except where noted, which compiled data from Elliot and Rowe, 1975; Schmeltz et al., 1979; Hoffman et al., 1983; Klus and Kuhn, 1982; Sakuma et al., 1983, 1984a, 1984b; and Hiller et al., 1982. Full references are given in NRC, 1986. Diluted SS is collected with airflow of 25 mL/s, which is passed over the burning cone; as presented in the NRC report on passive smoking (1986). 2Separation into vapor and particulate phases reflects conditions prevailing in MS and does not necessarily imply same separation in SS. 3Known human carcinogen, according to U.S. EPA or IARC. 4Probable human carcinogen, according to U.S. EPA or IARC. 5Animal carcinogen (Vainio et al., 1985). 6Data from Brunnemann et al., 1990. PCDDs = polychlorinated dibenzopdioxins; PCDFs = polychlorinated dibenzofurans. 7Contains di and polycyclic aromatic hydrocarbons, some of which are known animal carcinogens. 81methyl9Hĩpyrido[3,4b]indole. 9NNK = 4(NĩmethylNĩnitrosamino)1(3pyridyl)1butanone. 10Data from L?froth and ZebGhr, 1992. Amount is given as International Toxic Equivalent Factor (ITEF). X` hp x (#%'0*,.8135@8: 18 years old) in 1988 (who reported that their workplace was not in their home) worked in locations where smoking was allowed in designated or other areas. Of the nonsmokers (79.2 million), 36.5% (28.5 million) worked at places that permitted smoking in designated (if any) and other areas. Of these nonsmokers, 59.2% (16.9 million) reported that exposure to ETS in their workplace caused them discomfort. The survey highlighted the importance of the workplace as a major source of ETS exposure in addition to the home. The available data on ETS exposure to children in the home are limited. However, based on the 1988 National Health Interview Survey on Child Health, 42% of children 5 years of age and under are estimated to live in households with current smokers (Overpeck and Moss, 1991). The home environment is clearly an important source of ETS exposure for children. Nationally based survey data needed to make direct estimates of the frequency, magnitude, and duration of ETS exposure for nonsmoking adults and children and the different indoor environments in which those exposures occur are not available. The survey data available, however, do indicate that due to the ubiquitous nature of ETS in indoor environments, some unintentional inhalation of ETS by nonsmokers is unavoidable. The combustion of tobacco results in the emission of a particularly complex array of air contaminants into indoor microenvironments. Data on the chemical composition of mainstream and sidestream cigarette emissions as well as measurements in indoor spaces where smoking occurs indicate that exposure to ETS will result in exposure to toxic and carcinogenic agents (Section 3.2). The nature of the ETS contaminant mix and eventual human exposure is the product of the interaction of several interrelated factors associated with the source, transport, chemical transformation, dispersal, removal, and remission from surfaces, as well as human activities. Efforts to determine adverse health effects of ETS must address the issue of exposure to a complex mixture, which can occur in a number of environments. Assessing exposure to ETS, as with any complex air contaminant mix, is inherently complicated in epidemiologic studies (Leaderer et al., 1992). Because of the many potentially toxic agents in ETS and the various possible toxicological endpoints of interest, it is neither feasible nor desirable to focus on any one contaminant. Rather, the focus is on gathering information on marker or proxy compounds or other indicators of ETS exposure. In assessing these exposures, both direct and indirect methods can be employed. Direct methods include personal monitoring and measurement of biological markers. Indirect methods employ models to estimate exposures. The modeling approach generally makes use of stationary monitoring and questionnaire data.Stationary monitoring is used to measure concentrations of air contaminants in different environments. These measured concentrations are then combined with timeactivity patterns (time budgets) to determine the average exposure of an individual as the sum of the concentrations in each environment weighed by the time spent in that environment. Monitoring of contaminants might also be supplemented with the monitoring of factors in the environment that affect the contaminant levels measured (meteorological variables, primary compounds, ventilation, etc.). Measurement of these factors, in a carefully chosen set of conditions, can lead to models that predict concentrations in the absence of measured concentrations and provide a means of assessing the impact of efforts to reduce or eliminate exposures. Questionnaires are used to determine timeactivity patterns of individuals, to provide a simple categorization of potential exposure, and to obtain information on the properties of the environment affecting the measured levels (number of smokers, amounts smoked, etc.). ETS exposure measurements, whether conducted to support epidemiological studies or to determine the extent of exposure in nonsmoking individuals, have typically employed air monitoring of indoor spaces, personal monitoring, and questionnaires. Modeling of ETS exposures, while useful in estimating, from measured data, the level of exposure in a variety of indoor spaces under varying conditions, is beyond the scope of this report. 3.3.1. Environmental Concentrations of ETS The SS emission data discussed in Section 3.2 and shown in Tables 31 and 32 clearly indicate that tobacco combustion will result in the release of thousands of air contaminants into the environments in which smoking occurs. The concentrations of the known and unidentified contaminants in the ETS complex mix in an enclosed space can exhibit a pronounced spatial and temporal distribution. The concentration is the result of a complex interaction of several important variables, including (1) the generation rate of the contaminant(s) from the tobacco (including both SS and exhaled MS emissions), (2) location in the space that smoking occurs, (3) the rate of tobacco consumption, (4) the ventilation or infiltration rate, (5) the concentration of the contaminant(s) in the ventilation or infiltration air, (6) air mixing in the space, (7) removal of contaminants by surfaces or chemical reactions, (8) reemission of contaminants by surfaces, and (9) the effectiveness of any air cleaners that may be present. Additional considerations relate to the location at which contaminant measurements are made, the time of sample collection, the duration of sampling, and method of sampling. Variations in any one of the above factors related to introduction, dispersal, and removal of ETS contaminants can have a marked impact on the resultant indoor ETS constituent concentrations. Any one of these parameters can vary by an order of magnitude or more. For example, infiltration rates in residences can range from 0.1 to over 2.0 air changes per hour, and house volumes can range from 100 to over 700 m3 (Grimsrud et al., 1982; Grot and Clark, 1979; Billick et al., 1988; Koutrakis et al., 1992). Smoking rates and mixing within and between rooms can also show considerable variability. The potential impact on indoor ETSrelated respirable suspended particle (RSP) mass concentrations due to variations in these parameters is demonstrated in Figures 31 and 32 (these figures were taken directly from Figures 54 and 55 in NRC, 1986). Figures 31 and 32 are based on the mass balance model for ETS (NRC, 1986) for a typical range of input parameters encountered in indoor spaces. These figures demonstrate that ETSgenerated RSP concentrations in indoor environments can range from less than 20 %g/m3 to over 1 mg/m3 depending upon the location and conditions of smoking. Numerous field studies in "natural" environments have been conducted to assess the contribution of smoking occupancy to indoor air quality. These studies, summarized in a number of reviews (e.g., NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992), have measured several ETSrelated contaminants of human health concern (e.g., particle mass, carbon monoxide, benzene, nicotine, polycyclic aromatic hydrocarbons, Nĩnitrosamines), in a number of enclosed environments (e.g., residential, office, transportation) and under a variety of smoking and ventilation rates. These studies demonstrate that (1) many of the contaminants of health interest found in SS are also found in ETS; (2) ETS contaminants are found above background level in a wide range of indoor environments in which smoking occurs; and (3) the concentrations of ETS contaminants indoors can be highly variable. These findings can be demonstrated for selected ETSrelated compounds presented in Figure 33 and in Table 33. Figure 33 principally utilizes data summaries presented in reviews of indoor measurements of ETSrelated compounds in a variety of indoor spaces (NRC, 1986; U.S. DHHS, 1986; and particularly Guerin et al., 1992). Only the range of average concentrations measured in  Figure 31. Diagram for calculating the respirable suspended particle mass (RSP) from ETS emitted into any occupied space as a function of the smoking rate and removal rate (N). The removal rate is equal to the sum of the ventilation or infiltration rate (nv) and the removal rate by surfaces (ns) times the mixing factor. The calculated ETSrelated RSP mass determined from this figure serves as an input to Figure 32 to determine the ETSrelated RSP mass concentration in any space in %g/m3. Smoking rates (diagonal lines) are given as cigarettes smoked per hour. Mixing is determined as a fraction, and nv and ns are in air changes per hour (ach). All three parameters have to be estimated or measured. Calculations were made using the equilibrium form of the massbalance equation and assume a fixed emission rate of 26 mg/m3 of RSP. Shaded area shows the range of RSP emissions that could be expected for a residence with one smoker smoking at a rate of either 1 or 2 cigarettes per hour for the range of mixing, ventilation, and removal rates occurring in residences under steadystate conditions. Source: NRC, 1986.   Figure 32. Diagram to calculate the ETSassociated respirable suspended particle mass (RSP) concentration in %g/m3 in a space as a function of total mass of ETSgenerated RSP emitted in mg (determined from Figure 31) and the volume of a space (diagonal lines). The concentrations shown assume a background level of zero in the space. The particle concentrations shown are estimates during smoking occupancy. The dashed horizontal lines (A, B, C, and D) refer to National Ambient Air Quality Standards (healthrelated) for total suspended particulates established by the U.S. Environmental Protection Agency. A is the annual geometric mean. B is the 24hour value not to be exceeded more than once a year. C is the 24hour air pollution emergency level. D is the 24hour significant harm level. Shaded area shows the range of concentrations expected (from Figure 31) for a range of typical volumes of U.S. residences and rooms in these residences. Source: NRC, 1986.  Figure 33. Range of average indoor concentrations for notable ETS contaminants associated with smoking occupancy for different indoor environments. Ranges of averages are principally from tables presented in Guerin et al. (1992), although other sources were used (NRC, 1986; U.S. DHHS, 1986; Turk et al., 1987). Background levels are subtracted. Maximum recorded values are typically orders of magnitude higher than averages shown. Table 33. Tobaccospecific Nĩnitrosamines in indoor air (ng/m3)1 X! | ddx\Z: D$b ddx\Z: D$b| *E E E E EEUE E E E EEU* 'SiteApprox. # of cigarettes smoked  Collection time (hours)Flow rate (liters/ min.) Tobaccospecific  Nĩnitrosamines  NNN2 NAT2 NNK2*P P *Bar I253533.222.89.223.8*P P *Bar II101533.28.36.29.6*P P *Bar III101533.24.33.711.3*P P *Restaurant3253062.151.81.51.4*P P *Restaurant3405082.1NDND3.3*P P *Car4133.32.155.79.529.3*P P *Train I50605.53.3NDND4.9*P P *Train II506063.3NDND5.2*P P *Office256.53.3NDND26.1*            *Smoker's Home303.53.3NDND1.9 XT!1Data corrected for recovery. 2NNN = NNNNĩnitrosonornicotine; NAT = NATNĩnitrosoanataline; NNK = NNK4methylInitrosoamino1(3 pyridinyl)1butanone. 3Smoking section. 4Windows partially open. ND = not detected (in some cases due to chromatographic interference). Source: Brunnemann et al., 1992. X` hp x (#%'0*,.8135@8:x3)  Figure 34. Mean, standard deviation, and maximum and minimum nicotine values measured in different indoor environments with smoking occupancy. References from which observations are reported and the number of environments monitored are also given.  3' REFERENCES FOR FIGURES 34 AND 35 ă XTJ00(#҇BTT JJ Figure 34 BTT JJ BT 1.JJ Leaderer and Hammond, 1991 BT 2.JJ Mumford et al., 1989 BT 3.JJ Marbury et al., 1990 BT 4.JJ Muramatsu et al., 1984 BT 5.JJ Coultas et al., 1990b BT 6.JJ Weber and Fischer, 1980 BT 7.JJ Vaughan and Hammond, 1990 BT 8.JJ Leaderer, 1989 BT 9.JJ Miesner et al., 1989 BT 10.JJ Hinds and First, 1975 BT 11.JJ Oldaker et al., 1990 BT 12.JJ Coghlin et al., 1989 BT 13.JJ Badre et al., 1978 BT 14.JJ Higgins, 1987 BT 15.JJ Nagda et al., 1990 BT 16.JJ Eatough et al., 1990 BT 17.JJ Mattson et al., 1989 BT 18.JJ Harmsden and Effenberger, 1957 BT 19.JJ Cano et al., 1970 B.0 Figure 35 BV-1.0Brunekreef and Boleij, 1982 BV-2.0Hawthorne et al., 1984 BV-3.0Moschandreas, 1981 BV-4.0Nitschke et al., 1985 BV-5.0Parker et al., 1984 BV-6.0Spengler et al., 1981 BV-7.0Spengler et al., 1985 BV-8.0Leaderer et al., 1990 BV-9.0Lebret et al., 1990 B,10.0Coultas et al., 1990b B,11.0Turk et al., 1987 B,12.0Weber and Fischer, 1980 B,13.0Sterling and Sterling, 1983 B,14.0Nelson et al., 1982 B,15. 0Quant et al., 1982 B,16.0Repace and Lowery, 1980 B,17.0Repace and Lowery, 1982 B,18.0Leaderer, 1989 B,19.0First, 1984 B,20.0Oldaker et al., 1990 B,21.0Ishizu, 1980 B,22.HusgafvelPursiainen et al., 1986 B,23.0Eatough et al., 1990 B,24.0Neal et al., 1978 B,25.0Nagda et al., 1990 B,26.U.S. Department of Transportation, 1971 B,27.0Elliot and Rowe, 1975X` hp x (#%'0*,.8135@8:x3)  Figure 35. Mean, standard deviations, and maximum and minimum concentrations of respirable suspended particle mass (RSP) measured in different indoor environments for smoking and nonsmoking occupancy. Also shown are outdoor concentrations. References from which observations are reported and the number of environments monitored are also given.  3'  Figure 36. Weeklong respirable suspended particle mass (RSP) and nicotine measurements in 96 residences with a mixture of sources. Numbers 19 refer to the number of observations at the same concentration. Source: Leaderer and Hammond, 1991.   Figure 37. Range of average nicotine concentrations and range of maximum and minimum values measured by different indoor environments for smoking occupancy from studies shown in Figure 34. Only those studies with sampling times of 4 hours or greater are included in the residential and office indoor environment summaries.  Figure 38. Range of average respirable suspended particle mass (RSP) concentrations and range of maximum and minimum values measured by different indoor environments for smoking occupancy from studies shown in Figure 35. RSP values represent the contribution to background levels without smoking. Background levels were determined by subtracting reported indoor concentrations without smoking. Only those studies with sampling times of 4 hours or greater are included in the residential and office indoor environment summaries. levels associated with smoking occupancy (Figure 38) were calculated by subtracting particle levels for nonsmoking occupancy (presented in the studies) from the smoking occupancy levels. Thus, the increase in particle mass concentrations associated with ETS is presented in Figure 38. Indoor RSP levels in residences without smokers are typically in the range of 1025 %g/m3, while background office levels are somewhat lower (Figure 35). The summary nicotine data (Figure 37) suggest that average nicotine values in residences with smoking occupancy will range from 2 to approximately 10 %g/m3, with high values up to 14 %g/m3 and low values down to 0.1 %g/m3. Offices with smoking occupancy show a range of average nicotine concentrations similar to that of residences, but with considerably higher maximum values. The data from other indoor spaces suggest considerable variability, particularly in the range of maximum values. The cumulative distribution of weekly nicotine measured in one study (Leaderer and Hammond, 1991) for a sample of 96 homes, with the levels for smoking occupancy emphasized, is shown in Figure 39. Particle mass concentrations in smokeroccupied residences show average increases of from 18 to 95 %g/m3, while the individual increases can be as high as 560 %g/m3 or as low as 5%g/m3 (Figure 38). Figure 310 (Leaderer and Hammond, 1991) highlights the distribution of weekly RSP concentrations for residences with smoking occupancy. In that study, smoking residences had RSP concentrations approximately 29 %g/m3 higher than nonsmoking homes. Concentrations in offices with smoking occupancy will be on average about the same as those in residences. Interestingly, in a large and possibly the most comprehensive study of particle mass concentrations associated with smoking and nonsmoking sites in office buildings (Turk et al., 1987), the geometric mean concentration for RSP in 32 smoking sites was 44 %g/m3 while the geometric mean for 35 nonsmoking sites was 15 %g/m3. The difference of 29 %g/m3 is the same as that found for smoking and nonsmoking residences (Figure 310). Restaurants, transportation, and other indoor spaces with smoking occupancy will result in a considerably wider range of average, minimum, and maximum increases in particle concentrations than the residential or office environments. As noted earlier, indoor air contaminant concentrations are the result of the interaction of a number of factors related to the generation, dispersal, and elimination of the contaminants. Source use is no doubt the most important factor. Few studies have measured contaminant concentrations as a function of the smoking rate in residences or offices, but some data are available. One study estimated an average weekly contribution to residential RSP of 25 %g/m3 per cigarette (Leaderer et al., 1990), while another study estimated that a packaday smoker would add 20 %g/m3 to residential levels (Spengler et al., 1981). Coultas et al. (1990b) estimated  Figure 39. Cumulative frequency distribution and arithmetic means of vaporphase nicotine levels measured over a 1week period in the main living area in residences in Onondaga and Suffolk Counties in New York State between January and April 1986. Source: Leaderer and Hammond, 1991. Figure 310. Cumulative frequency distribution and arithmetic means of respirable suspended particle mass levels by vaporphase nicotine levels measured over a 1week period in the main living area in residences in Onondaga and Suffolk Counties in New York State between January and April 1986. Source: Leaderer and Hammond, 1991. that one or more smokers in a home added approximately 17 %g/m3 to the residential RSP level. Variations in residential RSP levels as a function of the number of smokers and over a period of several months are demonstrated in Figure 311 (Spengler et al., 1981). An association between the reported number of cigarettes and weekly residential nicotine and RSP levels for a sample of 96 homes (Leaderer and Hammond, 1991) is shown in Figure 312a and 312b. Smoking clearly increases indoor concentrations of both nicotine and particle mass, and residential levels of both nicotine and particle mass increase with increasing levels of smoking. Since nicotine and particle mass are proxies for the complex ETS contaminant mix, other ETS air contaminants, including the toxic and carcinogenic contaminants, should, similarly, be elevated with smoking occupancy. This elevation for selected contaminants is shown in Figure 33 and Table 33, and for a wider range of contaminants in other publications (NRC, 1986; U.S. DHHS, 1986; Guerin et al., 1992; Turk et al., 1987; Brunnemann et al., 1992). Children have been identified as a particularly sensitive group at health risk from exposure to ETS in the residential indoor environment (NRC, 1986; U.S. DHHS, 1986). One study has measured smoking status of the parents and weekly nicotine concentrations in the activity rooms and bedrooms of 48 children under the age of 2 years (Marbury et al., 1990). The results, shown  Figure 311. Monthly mean respirable suspended particle mass (RSP) concentrations in six U.S. cities. Source: Spengler et al., 1981.   Figure 312a. Weeklong nicotine concentrations measured in the main living area of 96 residences versus the number of questionnairereported cigarettes smoked during the airsampling period. Numbers 19 refer to the number of observations at the same concentrations. Closed circles indicate that cigar or pipe smoking was reported in the houses, with each cigar or pipe smoked set equal to a cigarette. Data from residences in Onondaga and Suffolk Counties in New York State between January and April 1986. For panel (a), the standard errors for the intercept and slope are 0.014 and 0.002, respectively. For panel (b), the standard errors for the intercept and slope are 2.1 and 0.03, respectively. Source: Leaderer and Hammond, 1991.  Figure 312b. Weeklong respirable suspended particle mass (RSP) concentrations measured in the main living area of 96 residences versus the number of questionnairereported cigarettes smoked during the airsampling period. Numbers 19 refer to the number of observations at the same concentrations. Closed circles indicate that cigar or pipe smoking was reported in the houses, with each cigar or pipe smoked set equal to a cigarette. Data from residences in Onondaga and Suffolk Counties in New York State between January and April 1986. For panel (a), the standard errors for the intercept and slope are 0.014 and 0.002, respectively. For panel (b), the standard errors for the intercept and slope are 2.1 and 0.03, respectively. Source: Leaderer and Hammond, 1991. in Table 34, indicate that activity and bedroom concentrations of nicotine in the children's homes increase with the number of cigarettes reported smoked in the home by parents. Concentrations also increased with the number of reported smokers in the household. Correlation coefficients over 0.7 were calculated between nicotine concentrations and number of cigarettes smoked. Exposure of children to ETS is covered in greater detail in Chapter 8. It is important to note that while measurements of nicotine and ETSassociated RSP are good indicators of the contribution of ETS to air contaminant levels in indoor environments, their measurement does not directly constitute a measure of total exposure. The concentrations measured in all indoor environments have to be combined with timeactivity patterns in order to determine average exposure of an individual as the sum of the concentrations in each environment weighted by the time spent in that environment. Both the home and the work environment (those without policies restricting smoking) have highly variable ETS concentrations, with the ranges largely overlapping. Which environment is most important in determining total exposure will vary with individual circumstances (e.g., a person who lives in a nonsmoking home but works in an office with smokers will receive most ETS exposure at work, but for those exposed both at home and at work, the home may be more important because, over the course of a week, more time is generally spent at home). An additional issue to be considered is how well the general indoor concentrations represent exposures of individuals who may be directly exposed to the SS plume of ETS. Small children, particularly infants, held by smoking parents may receive exposures considerably higher than those predicted from concentrations reported for indoor spaces. Special consideration must be given to these significant subpopulations. 3.3.1.2.2. Personal monitors.  Personal monitoring allows for a direct integrated measure of an individual's exposure. Personal air monitoring employs samplers (worn by individuals) that record the integrated concentration of a contaminant to which individuals are exposed in the course of their normal activity for time periods of several hours to several days. The monitors can be active (employing pumps to collect and concentrate the air contaminant) or passive (working on the principal of diffusion). As with biomarkers, personal monitoring provides an integrated measure of exposure to air contaminants across a number of environments where an individual spends time but does not provide direct information on concentrations of the air contaminant of interest in individual environments or on the level of exposure in each environment unless samples are taken in only one environment or are changed with each change of environment. Supplemental  Table 34. Weekly average concentrations of each measure of exposure by parental smoking status in the crosssectional study, Minnesota, 1989 r ddx  3"40  ddx  3"40 r &p@@@@@Pp@@@@@P&Smoking status&@@@@@P@@@@@P&NonsmokersLight smokersFather onlyMother onlyBoth parents&SS&Number of subjects234867&&Total cigarettes (no./week)0.928.868.658.8227.6&&Activity room nicotine (%g/m3)0.150.322.455.5012.11&88&Bedroom nicotine (%g/m3)ܩ0.301.212.665.32 information (air monitoring of spaces, timeactivity patterns, etc.) is needed to determine the contribution of each microenvironment to total exposure. Relatively few studies have measured personal exposures to ETSassociated nicotine and RSP for nonsmoking individuals. The few reported studies of personal exposure to nicotine are summarized in Table 35. Personal exposures associated with specific indoor environments are presented. Indoor environments include the nonindustrial workplace, homes, restaurants, public buildings, and transportationrelated indoor spaces. Table 35 highlights the wide range of indoor environments in which ETS exposures take place and the wide range of personal exposures encountered in those environments. It is important to note, however, that relatively few observations are available and that observations for nonworkplace nicotine exposures are dominated by the Japanese data (Muramatsu), which may not be representative of personal exposures in the United States. Because the data are limited, specific conclusions about the contribution of different indoor environments to personal nicotine exposures associated with passive smoking cannot be drawn. The data do indicate, however, that a wide range of exposures to ETS takes place in a variety of indoor environments where smoking is permitted. The data also indicate that occupational and residential environments are important sources of exposure to ETS because of the levels encountered, which are comparable, and the amount of time individuals spend in them. Studies of personal exposure to RSP of nonsmoking individuals that have attempted to stratify the collected data by ETS exposure are shown in Table 36. Three of the five studies represent exposures integrated over several different microenvironments (residential, public Table 35. Studies measuring personal exposure to airborne nicotine associated with ETS for nonsmokers | ddx;  ddx; | *p@@@@@@Pp@@@@@@P*Nicotine, g/m3*P@@@@@@PP@@@@@@P*StudySettingSubjectNX(SD)RangeComments**Mattson et al., 1989AirplaneAttendants164.7 (4.0)0.110.54 attendants on 4 flights**Schenker et al., 1990RailroadClerks 40 6.9 Samples collected over work shifts**Coultas et al., 1990aWorkplaceNonindustrial1520.4 (20.6)**Muramatsu et al., 1984Office Laboratory Conference room Home Hospital lobby Hotel lobby Restaurant TransportationVolunteers10 8 5 3 1 4 15 2221.1 5.8 38.7 11.2 3.0 11.2 26.0 21.7Calculated from data presented*XX*Muramatsu et al., 1984Office Home Restaurant Car Public transportationVolunteers3 7 15 7 1 6.9 7.0 28.2 40.0 11.4Calculated from data presented  '3  t,  1  1 #`\  PQP#X` hp x (#%'0*,.8135@8:x3 ,  Table 36. Studies measuring personal exposure to particulate matter associated with ETS for nonsmokers  ddx`N``"  ddx`N``" .@@@@@ @@P@@@@@ @@P.Number of subjectsParticle mass, g/m3 Particle mass due to ETS.P@@@@@ @@PP@@@@@ @@P.StudySettingTotalNo ETS exp.ETS exp.X (SD)Rangeg/m3.SS.Spengler et al., 198124hr. day45NRNR20a..Spengler et al., 198524hr. day101 28 73NR NR NRNR NR NR 28a..Sexton et al., 198424hr. day48 NR NRNR 31.7 50.1NR NR NR 18.41..Coultas et al., 1990aWorkplace15 1 1463.941.5 4.0 68.239.54.0145.8 14.7145.8 642.88.Schenker et al., 1990Workplace86 3 XT1Calculated by authors from the regression line. 2Calculated from data presented, after the method of Leaderer and Hammond (1991). 3Calculated from nicotine exposure, after the method of Leaderer and Hammond (1991). NR = not reported. X` hp x (#%'0*,.8135@8:x3 ,  Table 37. Approximate relations of nicotine as the parameter between nonsmokers, passive smokers, and active smokers r ddxHHI T  ddxHHI T r &8@@@ @@ P8@@@ @@ P&Nonsmokers without ETS exposure (N = 46)Nonsmokers with ETS exposure (N = 54)Active smokers (N = 94)&cEEE EE UcEEE EE U&Nicotine/cotinineMean value% of active smokers' valueMean value% of active smokers' valueMean value&&Nicotine (ng/mL): in plasma in saliva in urine 1.0 3.8 3.9 7.0 0.6 0.2܃ 0.8 5.5 12.11 5.5 0.8 0.7܃ 14.8 673 1,750&&Cotinine (ng/mL): in plasma in saliva in urine 0.8 0.7 1.6 0.3 0.2 0.1܃ 2.01 2.52 7.72 0.7 0.8 0.6܃ 275 310 1,390 1Differences between nonsmokers exposed to ETS compared with nonsmokers without exposure: p < 0.01. 2Differences between nonsmokers exposed to ETS compared with nonsmokers without exposure: p < 0.001. Source: Jarvis, 1987.X` hp x (#%'0*,.8135@8: