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7
Exposure-Dose Relationships for Environmental Tobacco Smoke

ESTIMATING DOSE

When considering the risks of exposure to environmental tobacco smoke (ETS) by nonsmokers, it is not enough to evaluate exposure and response. The actual dose received should be considered. Typically, for smokers, the exposure is given in terms of number of cigarettes smoked per day or cumulative pack-years. For nonsmokers, the exposure is usually characterized in terms of particle or gas concentration in micrograms per cubic meter. But what is known about the total integrated dose to the respiratory tract resulting from exposure to ETS by nonsmokers? What fraction of inspired particles and gases is deposited and fails to exit with the expired air? Moreover, what is the fate of the deposited smoke?

Although highly variable in concentration, ETS includes many of the same constituents as the smoke entering the active smoker’s lungs. Both particulate and gaseous phases are present, as described in Chapter 2. In principle, the retained dose for either inhaled particles or gases can be approximated in a straightforward manner:

(7–1)

The deposited dose, in micrograms per hour, equals the ventilation rate in cubic meters per hour times the concentration of particle or gas in the inspired air in milligrams per cubic meter ([C]), times the collection efficiency (CE). CE has no dimensions; it is the fraction of the inhaled particle or gas that deposits and thus



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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects 7 Exposure-Dose Relationships for Environmental Tobacco Smoke ESTIMATING DOSE When considering the risks of exposure to environmental tobacco smoke (ETS) by nonsmokers, it is not enough to evaluate exposure and response. The actual dose received should be considered. Typically, for smokers, the exposure is given in terms of number of cigarettes smoked per day or cumulative pack-years. For nonsmokers, the exposure is usually characterized in terms of particle or gas concentration in micrograms per cubic meter. But what is known about the total integrated dose to the respiratory tract resulting from exposure to ETS by nonsmokers? What fraction of inspired particles and gases is deposited and fails to exit with the expired air? Moreover, what is the fate of the deposited smoke? Although highly variable in concentration, ETS includes many of the same constituents as the smoke entering the active smoker’s lungs. Both particulate and gaseous phases are present, as described in Chapter 2. In principle, the retained dose for either inhaled particles or gases can be approximated in a straightforward manner: (7–1) The deposited dose, in micrograms per hour, equals the ventilation rate in cubic meters per hour times the concentration of particle or gas in the inspired air in milligrams per cubic meter ([C]), times the collection efficiency (CE). CE has no dimensions; it is the fraction of the inhaled particle or gas that deposits and thus

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects fails to exit with the expired air. Thus, the dose is directly proportional to three variables: ventilation, pollutant concentration, and the fraction deposited. First, consider ventilation . The standard 70-kg adult at rest breathes about 7.5 L/min (International Commission on Radiological Protection, 1975). However, a value of 20 L/min would be more appropriate for adults in indoor environments who periodically stand, walk, type, or perform other modest tasks. During heavy exercise, ventilation can increase by a factor of as much as 10, to exceed 100 L/min (International Commission on Radiological Protection, 1975). The concentration of various constituents in ETS ([C]) that might be encountered in various situations has been discussed in Chapters 2 and 5. PARTICLE SIZE For particles, collection efficiency (CE) is determined primarily by two factors: particle size and breathing pattern. If the geometric size, shape, and density of the individual particles or droplets are known, then the distribution of particle diameters can be described. Because it is a better predictor of the behavior of the particle in the respiratory tract, aerodynamic diameter rather than optical measurement is used to express the range of particle sizes. Aerodynamic diameter is defined as the diameter of a sphere of unit density that has the same settling velocity as the particle being measured. It may be expressed as the count median aerodynamic diameter (CMAD) or mass median aerodynamic diameter (MMAD). These are, respectively, the diameters for which half of the number (or mass) of the particles are less than that diameter and for which half exceed it. The particles in mainstream cigarette smoke have been measured by several investigators using a variety of analytical devices. Because of the different apparatus and methods of smoke generation and dilution, results vary. However, to an order of magnitude, the findings are reasonably consistent. McCusker et al. (1983) used a device called the single particle aerodynamic relaxation time (SPART) analyzer to size mainstream particles from several brands of cigarettes, with and without filters. The MMAD for all brands averaged approximately 0.46 mm and was not markedly

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects different when the filters were removed. Particulate concentrations per milliliter ranged from 0.3×109 to 3.3×109, depending on whether the cigarettes were rated ultralow, low, or medium in tax content. Hinds (1978) compared the particulate size distribution in cigarette smoke using an aerosol centrifuge and a cascade impactor. Although these devices are based on different physical principles, the MMAD values were comparable to those measured by McCusker et al. (1983), ranging from 0.37 to 0.52 µm. Variations depend primarily on the dilution of the smoke. Keith and Derrick (1960) used a specially modified centrifuge, termed a conifuge, to analyze cigarette smoke and reported MMAD and concentration values similar to Hinds (1978) and McCusker et al. (1983). Particulate analysis by a light-scattering photometer yielded a MMAD of 0.29 µm and particulate concentrations of 3×1010/ml. Time and concentration can modify tobacco smoke. Cigarette smoke aerosols contain volatile components, and evaporation gradually reduces particle diameters. It is also true that when the particle concentrations are extremely high, like those encountered in mainstream smoke, the aerosol can agglomerate rapidly because nearby particles collide with each other and coalesce. If smoke is cooled (reducing the vapor pressure of volatile components) and diluted in room air (reducing the probability of particle collisions), the size of the particles will become more stable. Particle size may also change within the human respiratory tract. After air containing smoke is drawn into the mouth and upper respiratory tract, it becomes humidified. Smoke particles can grow in size because of their affinity for water, termed hygroscopicity (Hiller, 1982a). BREATHING PATTERN Particle size is a critical factor in determining the collection efficiency, but breathing pattern is also important For example, large slow tidal volumes will favor alveolar deposition, while high inspiratory flows will promote deposition at bifurcations in the airways. Breath-holding is also important. The greater the elapsed time before the next expiration, the higher the fraction of inspired particles deposited, since there is more time for particles to sediment or diffuse. Individual anatomic differences may influence the amount and distribution of deposited particles. The cross section of airways will influence the linear velocity of the inspired air.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Increasing alveolar size decreases alveolar deposition. Preexisting disease can also modify the deposition of smoke. For environmental tobacco smoke (diameters of particles ranging from 0.1 µm to 1 µm) the sedimentation and diffusion mechanisms will be the primary mechanisms of deposition. Changes in the rate and pattern of breathing associated with exercise can also affect the total dose of cigarette participates deposited in the lungs. Bennett et al. (1985) reported that exercise increased the percent deposition of experimentally generated aerosols (MMAD of 2.6 µm) in human subjects. The reason for this observation was that during exercise, breathing patterns change so that flow rates are increased. Increasing the flow rates also increases the inertial impaction. Also, exercise is frequently associated with a shift from nose to mouth breathing. Consequently, the filtration of large particles that takes place in the upper respiratory tract no longer occurs. Increased deposition was also measured in exercising hamsters that inhaled a radiolabelled aerosol (activity median diameter of 3 µm) (Harbison and Brain, 1983). These results are relevant to those who breathe air containing ETS when their minute ventilation is increased while working or during periods of exercise. DEPOSITION OF CIGARETTE SMOKE PARTICLES The factors discussed in the previous sections indicate that experimental measurements of the concentration of smoke aerosols in indoor environments, i.e., exposure concentrations, are insufficient for predictions of smoke deposition. ETS smoke is constantly changing, thereby complicating the collection of accurate and reproducible data regarding its particulate size. In addition, alterations in respiratory structure and respiratory rate can affect deposition of particulates. These complexities stress the importance of actual measurement of regional deposition of cigarette smoke particles in human lungs. However, little is published on this important area, despite the prevalence of passive smoking and concerns about its impact on human health. The majority of the available information on deposition of particles present in cigarette smoke is based on theoretical or physical models of the lungs and measurements of differences between the concentrations of tobacco smoke aerosol or model aerosols in inhaled and exhaled air.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects A model to predict the percent of deposition of particles based on MMAD was developed by the Task Group on Lung Dynamics (1966) of the International Commission on Radiological Protection. The respiratory tract was divided into three main regions: nasopharynx, trachea and bronchi, and the alveolar. In conjunction with estimates of particle clearance, deposition calculations were made for these regions at three different inhalation volumes. This model suggests that about 30% of the particles within the size range present in cigarette smoke will deposit in the alveolar region and 5–10% in the tracheobronchial region. This model also emphasizes the impact of particle solubility on the total integrated dose with time. Brain and Valberg (1974) developed convenient nomograms and a computer program to calculate how particle solubility and particle size significantly affect the net amount of particulates retained in the lungs. Although the basic outline of the model is generally correct, more recent measurements suggest that values for alveolar deposition of particles 0.1–1.0 µm are too high by a factor of at least 2 (Heyder, 1982). The extent to which ETS particles are hygroscopic and increase in size within the respiratory tract is an important and unresolved issue that adds further uncertainty. Aerosol deposition has also been studied in airway casts. Physical models of the upper airways of human lungs have been made by a double-casting technique to study particulate deposition at several airway generations (Schlesinger and Lippman 1972). Different flow rates and particle sizes were used to study deposition patterns. Schlesinger and Lippman (1978) reported a correlation between the deposition sites of test aerosols in their lung casts and the most common sites of origin of bronchogenic carcinoma in smoking humans. Both occurred preferentially at bifurcations. Martonen et al. (1983) added an oropharyngeal compartment and a replica cast of the larynx to the tracheobronchial casts in order to better simulate airflow patterns in the upper respiratory tract. They used these models to evaluate the amount of cigarette smoke condensate deposited in the airways at different flow rates. More condensate was present in areas where airways branched and especially at the bifurcation points, indicating increased levels of impaction. Aerosol was also deposited preferentially along posterior airway walls of the branching regions. Hiller et al. (1982a) measured the collection efficiency in adults of an aerosol containing three different sizes of polystyrene latex

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects spheres in nonsmoking humans. They measured a 10% deposition for 0.6-µm (MMAD) spheres, which is similar to the results of Davies et al. (1972) and Muir and Davies (1967) using 0.5-µm aerosols and Heyder (1982) using aerosols that were 0.2 to 1.0 µm in size. The size ranges of these aerosols are comparable to those experimentally measured in cigarette smoke, as previously discussed. In contrast to passive smoking, the estimates of the collection efficiency of smoke particles during active smoking are substantially higher (about 70%) for at least two reasons (Hiller et al., 1982b). First, the much higher particulate concentrations in mainstream smoke may give rise to more agglomeration and greater hydroscopic growth in the respiratory tract. Both processes produce larger particles with higher collection efficiencies. Second, and more important, the breathing pattern used by the active smoker is markedly different than normal breathing. It is characterized by a slow deep inspiration followed by breath-holding. This increases the average residence time of the smoke particles and thus increases the fraction of inhaled particles that deposit in the lung. To compare the amount of smoke deposited in the lungs of an active smoker with an individual exposed to ETS, first consider a pack-a-day smoker (about 20 cigarettes during an 8-hour period). The average tar rating in mainstream smoke (MS) over the past couple of decades has been about 14 mg/cigarette. Therefore, the total amount of tax inspired is 280 mg/8 h. Assuming a collection efficiency of 70%, the amount of tar deposited is 196 mg/8 h. As pointed out in Chapter 5, smoke particles can range from 50 to 500 µg/m3 in public places where smoking occurs and from 20 to 150 µg/m3 in homes with smokers. Consider a nonsmoker who breathes at 10 L/min, or 4,800 L/8 h. With modest exercise, this could increase to 20 L/min, or 9,600 L/8 h. Based on estimates by Hiller et al. (1982a,b), the collection efficiency of particles in ETS is about 10%. Therefore, the total amount of smoke particles deposited in a nonsmoker in these environments for 8 h could range from approximately 0.0096 mg/8 h=20 µg/m3×4.8 m3/8 h×0.1 to an extreme of 0.5 mg/8 h=500 µg/m3×10 m3/8 h×0.1. This would be approximately 0.005% to 0.26% of that amount of tar deposited in the active smoker’s lungs after smoking 20 cigarettes. The active smoker, of course, also breathes the ETS, so that the total dose received by the active smoker is the mainstream smoke plus a passive smoking dose equivalent to that received by the

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects nonsmoker exposed to ETS. However, since the dose received due to breathing ETS-contaminated air is so small, this additional contribution to the total dose is negligible. Benzo[a]pyrene (BaP) is one of the primary constituents of particles in mainstream smoke. From Table 2–10 one can estimate that a nonsmoker exposed to ETS receives a higher relative dose of BaP than of RSP. However, the ambient measurements, which are used to estimate the dose for the nonsmoker, may be elevated in view of the high outdoor concentrations that are reported in these studies. More data on the fate of BaP in ETS and on ambient concentrations are needed before estimates of the relative doses can be made meaningfully. Although the amount of smoke deposited in the lungs of nonsmokers during exposure to ETS is small compared with that encountered by the active smoker regarding mainstream smoke, it may differ in composition and toxicity. For example, as discussed in Chapter 2, certain constituents are present in much higher concentrations in sidestream smoke as compared with mainstream smoke (Weiss et al., 1983). These possible differences in composition must be explored. PARTICLE RETENTION IN THE LUNGS The amount of particles present at different sites in the lungs is not only dependent on deposition. Retention of smoke depends on the balance between the amount of each constituent that deposits in the respiratory tract and the efficiency of the lung clearance mechanisms in the airways and alveoli. Clearance mechanisms are a dynamic component of normal lung function and operate to keep the lung clean and sterile. Particles depositing in the airways are entrained in the mucus layer that lines the airway. This layer is swept toward the mouth by the action of ciliated cells and eventually swallowed. Mucus transport is approximately 1–2 cm per minute in the trachea, but is slower in smaller airways. In addition, macrophages present in the airways may phagocytose deposited particulates and be carried towards the mouth by the mucociliary transport system. Particulates reaching the alveolar region—those that are usually less than several micrometers—are soon engulfed by alveolar macrophages. Some of these cells gradually migrate towards the airways and exit the lung via the

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects mucociliary escalator. Dissolution of particles is an additional important clearance mechanism. Lung disease and cigarette smoking itself can affect particle clearance and retention in smokers’ lungs. Previous studies have shown that smokers have different aerosol deposition patterns and slower clearance rates than nonsmokers (Albert et al., 1969; Sanchis et al., 1971; Cohen et al., 1979). These alterations in clearance are, in part, caused by components within cigarette smoke that affect the quantity and rheological properties of the mucous. Components of cigarette smoke, also, can impair phagocytosis by alveolar macrophages (Ferin et al., 1965). Clearance mechanisms in smokers may be further compromised by lung diseases, such an emphysema and fibrosis, and by exposure to other air pollutants. Measurements of the long-term retention of compounds associated with cigarette particulates in the lungs are difficult to estimate from data obtained with airway casts or from differences between inhaled and exhaled aerosol concentration, since these methods do not take into account clearance mechanisms. Unfortunately, few data are available regarding the actual retention and sites of deposition of cigarette smoke particles in either nonsmoking humans or animals exposed to ETS. The most accurate method that could be used is quantification of particulate deposits in individual pieces of tissue dissected from the lung. Impossible in living animals, this is a tedious procedure in animal lungs or human material obtained at surgery or autopsy and is especially difficult for large lungs. One can also attempt to quantify dose by examining saliva, serum, or urine. These possibilities are discussed in Chapter 8. GASES IN ENVIRONMENTAL TOBACCO SMOKE In addition to the particulate phase, we must also consider exposure-dose relationships for gases in ETS. As before, breathing pattern influences gas uptake. Of particular importance is the difference between oral and nasal breathing. Breathing by mouth increases the exposure of the airways, while breathing by nose (as would be true for nonsmokers exposed to ETS most of the time) offers some protection for the lower respiratory tract. The most important variable determining the amount and site of uptake is the water solubility of the gas in question. Gases that are highly soluble in water, such as formaldehyde or acrolein, will

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects be almost completely removed by the upper respiratory tract, especially during nasal breathing. The concentration of other gases, such as the oxides of nitrogen, which have an intermediate solubility, will decrease as the inspired bolus penetrates deeper and deeper into the lungs. There will be uptake of gas in the upper airways, but significant amounts will also penetrate to respiratory bronchioles and alveoli. Finally, there are gases of low solubility, such as carbon monoxide. No significant uptake of CO occurs in the upper airways, and it is only slowly absorbed across the air-blood barrier. In the absence of heavy exercise and very high ventilation rates, many hours are required to establish an equilibrium between inspired GO and carboxyhemoglobin in the blood. As was true for particles, we can estimate the gas uptake for active smokers and for passive smokers. As reviewed in Chapter 2, CO from ETS can range from less than 1 to 8 ppm. If the background air has little or no CO, even the upper estimates of 8 ppm will have a negligible effect on carboxyhemoglobin levels. Almost 2 hours would be required to reach 1% carboxyhemoglobin (Peterson and Stewart, 1975). This is approximately the same as background levels of carboxyhemoglobin, which are associated with endogenous production of carbon monoxide. Even after 15 hours, when the equilibrium value of 1.7% COHb is finally reached, the effect should be insignificant. However, if air pollution from mobile and stationary sources produces higher background levels of CO, then an incremental exposure of 1 to 8 ppm could produce some added burden of carboxyhemoglobin. Reactive or highly soluble gases such as formaldehyde, acrolein, or oxides of nitrogen present a different situation. Acrolein has a very high water solubility (40 g/100 ml). Because of this high solubility in the airway lining fluids, one would anticipate a collection efficiency approaching 100%. Moreover, this would occur rapidly, so that acrolein is classified as an upper respiratory tract irritant. According to Table 2–10, there are between 60 and 100 µg of acrolein generated per cigarette. Thus, from 20 cigarettes, 1.2 to 2.0 mg of acrolein would be deposited in the respiratory tract of the active smoker. Chapter 2 suggests that levels of acrolein in public places where smoking is permitted could range from 10 to 50 µg/m3. Using similar assumptions to that made for particles, we estimate that the nonsmoker would inhale 4.8 to 10 m3 of air per 8 hours. Assuming a collection efficiency of 100%, the total amount of

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects acrolein deposited in the passive smoker would be approximately 0.048 to 0.5 mg. We select 1.6 mg/8 hours as the mid-range dose for the active smokers, which assumes 20 cigarettes smoked per 8 hours with 80 µg acrolein per cigarette. Using this value, the nonsmoker exposed to ETS for 8 hours would then receive approximately 3 to 31% of that received by the active smoker. When the contribution of ETS is included for the active smoker, the nonsmoker exposed to ETS for 8 hours would receive between 5 and 24% of that of an active smoker. The relatively high dose of acrolein received by the nonsmoker reflects the high collection efficiency for this hydrophilic component and the persistence of vapor-phase components in the air even when filtration is used. Table 2–10 gives comparisons of the amount of other materials inspired for both active smokers and individuals exposed to ETS over shorter periods of time. SUMMARY AND RECOMMENDATIONS A number of studies have measured the levels of specific constituents of ETS under natural conditions (reviewed in Chapters 2 and 5). The extrapolation from relative exposures to relative doses received is difficult. Variation in the percent of time individuals spend in particular environments such as home, workplace, and so forth, and the variations in uptake and clearance, discussed in this chapter, will affect the actual dose received. Using a simple, first-approximation model for exposure and retention, the relative daily dose received for a nonsmoker exposed to ETS can be compared with the dose received by an active smoker. For RSP, the estimates were up to 0.26%. For acrolein, a hydrophillic, vapor-phase constituent, the relative dose is estimated to be much higher, 3 to 31%, whether or not the ETS exposure of the active smoker is considered. Nicotine, another constituent that appears primarily in the vapor phase of ETS, has an estimated relative dose of up to 1% (see Chapter 8). The extent to which these are indicative of the relative exposures to specific constituents that are important for particular health effects in active smokers or in nonsmokers exposed to ETS cannot be determined for any of the health effects reviewed later in this report. Nevertheless, the estimated relative exposures give

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects some idea of the potential range of relative exposures, for constitutents that are found both in the vapor phase and in the particulate phase. Because of the range of estimated relative doses, it would be ideal to make estimates of the relative dose based on the specific constituent(s) that are most relevant to the health effect being assessed. However, many of these specific constituents, for instance the carcinogenic constituents such as benzo[a]pyrene, N-nitrosodimethylamine, and N-nitrosodiethylamine, are difficult to measure; therefore, there are not enough data available to make meaningful estimates of the relative doses of these constituents. Also, biological markers might be potentially informative indicators of the relative doses. However, as reviewed in Chapter 8, to date only carbon monoxide, nicotine, and cotinine have been measured extensively in humans. What Is Known Particle size and breathing pattern are critical factors in the deposition of ETS in humans. Theoretical models predict that 30 to 40% of the particles with the size range present in cigarette smoke will deposit in the alveolar region and 5 to 10% in the tracheobronchial region. The collection efficiency of smoke particles during active smoking has been measured to be about 70%. On the other hand, the collection efficiency is estimated to be only 10% for nonsmokers exposed to ETS. What Scientific Information Is Missing Actual measurement of regional deposition of cigarette smoke particulates in human lungs is not available. There are little data regarding the actual retention and sites of deposition of ETS particulates in either humans or animals. The concentrations of various components in vapor and particulate phases of MS and ETS differ. Consequently, research is needed, particularly for vapor-phase components, to see how these differences affect dose.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects REFERENCES Albert, R.E., M.Lippmann, and W.Briscoe. The characteristics of bronchial clearance in humans and the effect of cigarette smoking. Arch. Environ. Health 18:738–755, 1969. Bennett, W.D., M.S.Messina, and G.C.Smaldone. Effect of exercise on deposition and subsequent retention of inhaled particles. J. Appl. Physiol. 59:1046–1054, 1985. Brain, J.D., and P.A.Valberg. Models of lung retention based on ICRP Task Group report. Arch. Environ. Health 28:1–11, 1974. Cohen, D., S.F.Arai, and J.D.Brain. Smoking impairs long-term dust clearance from the lung. Science 204:514–517, 1979. Davies, C.N., J.Heyder, and M.C.Subba Rama. The breathing of half-micron aerosols. I. Experimental. J. Appl. Physiol. 32:591–600, 1972. Ferin, J., G.Urbankova, and A.Vlokova. Influence of tobacco smoke on the elimination of particles from the lungs. Nature 206:515–516, 1965. Harbison, M.L., and J.D.Brain. Effects on exercise of particle deposition in Syrian golden hamsters. Am. Rev. Respir. Dis. 128:904–908, 1983. Heyder, J. Particle transport onto human airway surfaces. Eur. J. Respir. Dis. 63(Suppl. 119):29–50, 1982. Hiller, F.C., M.K.Mazumder, J.D.Wilson, P.C.McLeod, and R.C.Bone. Human respiratory tract deposition using multimodal aerosols. J. Aerosol. Sci. 13:337–343, 1982a. Hiller, F.C., K.T.McCusker, M.K.Mazumder, J.D.Wilson, and R.C.Bone. Deposition of sidestream cigarette smoke in the human respiratory tract. Am. Rev. Respir. Dis. 125:406–408, 1982b. Hinds, W.C. Size characteristics of cigarette smoke. Am. Ind. Hyg. Assoc. J. 39:48–54, 1978. International Commission on Radiological Protection (ICRP), Task Group of Committee 2 of the International Commission on Radiological Protection. Physiological data for reference man, pp. 346–347. In ICRP. Report of the Task Group on Reference Man (ICRP 23). New York: Pergamon, 1975. Keith, C.H., and J.C.Derrick. Measurement of the particle size distribution and concentration of cigarette smoke by the “conifuge.” J. Colloid Sci. 15:340–356, 1960. Martonen T.B., and J.E.owe. Cigarette smoke pattern in a human respiratory tract model. Proc. Ann. Conf. Eng. Med. Biol. 25:171, 1983 (abstract). McCusker K., F.C.Hiller, J.D.Wilson, M.K.Mazumder, and R.Bone. Aerodynamic sizing of tobacco smoke particulate from commercial cigarettes. Arch. Environ. Health 38:215–218, 1983. Muir D.C.F., and C.N.Davies. The deposition of 0.5 µm diameter aerosols in the lungs of man. Ann. Occup. Hyg. 10:161–174, 1967. Peterson, J.E., and R.D.Stewart. Predicting the carboxyhemoglobin levels resulting from carbon monoxide exposures. J. Appl. Physiol. 39:633–638, 1975. Sanchis J., M.Dolovich, R.Chalmers, and M.T.Newhouse. Regional distribution and lung clearance mechanisms in smokers and non-smokers, pp. 183–191. In E.H.Walton, Ed. Inhaled Particles, Part III. Surrey, England: Unwin Brothers Ltd., 1971.

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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects Schlesinger R.B., and M.Lippmann. Particle deposition in casts of the human upper tracheobronchial tree. Am. Ind. Hyg. Assoc. J. 33:237–251, 1972. Schlesinger R.B., and M.Lippmann. Selective particle deposition and bronchogenic carcinoma. Environ. Res. 15:424–431, 1978. Task Group on Lung Dynamics. Deposition and retention models for internal dosimetry of the human respiratory tract. Health Phys. 12:173–207, 1966. Weiss S.T., I.B.Tager, M.Schenker, and F.E.Speizer. The health effects of involuntary smoking. Am. Rev. Respir. Dis. 128:933–942, 1983.