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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