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Comparative Dosimetry of Radon in Mines and Homes (1991)

Chapter: Breathing, Deposition, and Clearance

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Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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7
Breathing, Deposition, and Clearance

INTRODUCTION

Although epidemiological and animal studies provide information on the risks of lung cancer in relation to exposure, linkage of exposure to dose is essential for extrapolating the risk from the mining to the indoor environment. Since exposure does not equal absorbed dose, it is important to describe adequately the variables that determine exposure-dose relationships.

This chapter summarizes aerosol deposition and clearance mechanisms and discusses how both of these influence the amount of alpha energy from radon progeny delivered to target sites. The chapter also discusses approaches that can be used to describe the amount and distribution of doses and, finally, some factors that are known to influence the amount and distribution of retained aerosols.

A major goal of this chapter is to understand and predict differences in response to similar concentrations of inhaled radon progeny among different groups. However, exposure-dose relationships can vary in different individuals (e.g., children versus adults). Thus, even if the inspired concentration of radon progeny were similar, the dose deposited in the lungs may vary. Such factors as metabolic rate, breathing pattern, and lung structure determine the deposition of radon progeny and may differ among individuals. The impact of changes in breathing pattern and the effects of chronic lung disease on particle retention are also discussed in this chapter.

Many aspects of the deposition of aerosols in mammalian lungs have

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

captured the energy and imagination of many investigators, and only a brief summary is provided here. Published symposia serve as excellent sources of information in this area, for example, the First (Oxford), Second (Cambridge), Third (London), Fourth (Edinburgh), Fifth (Cardiff), and Sixth (Cambridge) International Symposia on Inhaled Particles (Davies, 1961, 1964; Walton, 1971, 1977, 1982; Dodgson and McCallum, 1988). In addition, many papers and books reviewing deposition and clearance processes are available (Altshuler et al., 1957; Hatch and Gross, 1964; Aharonson et al., 1976; Brain et al., 1977; Lippmann, 1977; Raabe et al., 1977; Brain and Valberg, 1979, 1985; Heyder et al., 1980; Lippmann et al., 1980; Clarke and Pavia, 1984; Stuart, 1984; Morén et al., 1985).

The distinction between retention (the amount of an aerosol present in the lungs at any time) and deposition (the initial attachment of suspended particles to a surface) should be kept in mind. Retention, but not deposition, is influenced by clearance and translocation. Even during a brief exposure to radon progeny (30 to 60 min), there may be loss and redistribution of deposited particles, especially in the large ciliated airways. To acknowledge the possibility of particle redistribution during a measured exposure period, the term retention is used to refer to the amount and distribution of particles in lungs at any time after an exposure to an aerosol.

Many parameters that influence aerosol deposition have been studied. Total deposition in the lungs depends on particle size (Morrow, 1966), tidal volume (Taulbee et al., 1978), breathing frequency (Altshuler, 1961; Muir and Davies, 1967; Valberg et al., 1982), and lung volume (Davies et al., 1972). To date, little is known about the actual anatomic distribution of deposited radon progeny within the lungs, especially at the level of small airways and parenchyma. Since the rates and pathways of clearance are determined by the sites of aerosol deposition, it is necessary to study factors such as exercise and disease that strongly influence the distribution of the retained aerosol in the lungs.

DEPOSITION OF RADON PROGENY: GENERAL PRINCIPLES

Deposition is the process that determines what fraction of the inspired particles is caught in the respiratory tract and, thus, fails to exit with expired air. It is likely that all particles that touch a wet surface are deposited; thus, the site of contact is the site of initial deposition. Distinct physical mechanisms operate on inspired particles to move them toward respiratory tract surfaces. Major mechanisms are inertial forces, gravitational sedimentation, Brownian diffusion, interception, and electrostatic forces. The extent to which each mechanism contributes to the deposition of a specific particle depends on the particle's physical characteristics, the subject's breathing pattern, and the geometry of the respiratory tract. Radon progeny are unusual in that they tend to be smaller than

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

most aerosols of concern to health (see Chapters 2 and 6), and thus, Brownian diffusion and sedimentation dominate, as discussed below.

Detailed treatments of particle deposition have been given by Brain and Valberg (1979), Lippmann et al. (1980), Heyder et al. (1980, 1986), Morgan et al. (1983), Raabe (1982), Stuart (1984), and Agnew (1984). Comprehensive treatises on aerosol behavior are also available (Fuchs, 1964; Davies, 1967; Mercer, 1981; Hinds, 1982; Reist, 1984).

The behavior of a particle in the respiratory system is largely determined by its size and density. Particles of varying shape and density may be compared by their aerodynamic equivalent diameter (Dae). Aerodynamic diameter is the diameter of the unit density (1 g/cm3) sphere that has the same gravitational settling velocity as that of the particle in question. Aerodynamic diameter is proportional to the product of the geometric diameter and the square root of density.

FACTORS ACTING TO DEPOSIT PARTICLES IN THE LUNGS

Diffusional

Radon progeny undergo Brownian diffusion—a random motion caused by their collisions with gas molecules; this motion can lead to contact and deposition on respiratory surfaces. Diffusion is significant for particles with diameters of less than 1 µm; only then does their size approach the mean free path of gas molecules. Thus, this is probably the dominant mechanism for radon progeny since most of the alpha activity resides on such small particles. Unlike inertial or gravitational displacement, diffusion is independent of particle density; however, it is affected by particle shape (Heyder and Scheuch, 1983). For these particles, size is best expressed in terms of a thermodynamic equivalent diameter, Dt, the diameter of a sphere that has the same diffusional displacement as that of the particle. The probability that a particle would be deposited by diffusion increases with an increase in the quotient (t/Dt)1/2, where t is the residence time. Deposition is also independent of respired flow rate. Diffusion, like sedimentation, is most important in the peripheral airways and alveoli, where dimensions are smaller. However, as particle size becomes very small, diffusion may become an important mechanism even in the upper airways.

Gravitational

Gravity accelerates falling bodies downward, and terminal settling velocity is reached when viscous resistive forces of the air are equal and opposite in direction to gravitational forces. Respirable particles reach this constant terminal sedimentation velocity in less than 0.1 ms. Then, particles can be removed if their settling causes them to strike airway walls or alveolar surfaces. The

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

probability that a particle will deposit by gravitational settling is proportional to the product of the square of the aerodynamic diameter (Dac2) and the residence time. Thus, breathholding enhances deposition by sedimentation. Sedimentation is most important for particles larger than about 0.2 µm and within the peripheral airways and alveoli, where airflow rates are slow and residence times are long (Heyder et al., 1986).

Inertia

Inertia is the tendency of a moving particle to resist changes in direction and speed. It is related to momentum: the product of the particle's mass and velocity. High linear velocities and abrupt changes in the direction of airflow occur in the nose and oropharynx and at central airway bifurcations. Inertia causes a particle entering bends at these sites to continue in its original direction instead of following the curvature of the airflow. If the particle has sufficient mass and velocity, it will cross airflow streamlines and impact on the airway wall. The probability that a particle will deposit by inertial impaction, therefore, increases with increasing product of Dae2 and respired flow rate. Generally, inertial impaction is an important deposition mechanism for particles with aerodynamic diameters larger than 2 µm. Thus, it is probably unimportant for radon progeny in indoor air. It can occur during both inspiration and expiration in the extrathoracic airways (oropharynx, nasopharynx, and larynx) and central airways.

As particle size decreases, inertia and sedimentation become less important, but diffusion becomes more important. For example, a 2-µm-unit-density spherical particle is displaced by diffusion (Brownian displacement) by only about 9 µm in 1 s. It is important to know that this displacement varies with the square root of time. It settles by gravity by about 125 µm in the same period. However, as the particle size drops to 0.2 µm, the diffusional displacement in 1 s increases to 37 µm whereas gravitational displacement drops to only 2.1 µm. At 0.02 µm, gravitational displacement is only 0.013 µm/s while diffusional displacement in 1 s has soared to 290 µm. A comparison of settling and diffusion displacements for a range of particle sizes is shown in Table 7-1.

Other Forces

Deposition can also occur in the lungs when particles have dimensions that are significant relative to those of the air spaces. As aerosols move into smaller and smaller air structures, some particles may reach a point where the distance from their center to a surface is less than their radius. The resulting contact is called interception. Interception is most important for the deposition of fibers, but it is probably insignificant for most radon progeny unless they are attached to larger particles.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

TABLE 7-1 Root Mean Square Brownian Displacement in 1 Second Compared with the Distance Fallen in Air in 1 Second for Unit-Density Particles of Different Diameters

 

Particle Diameter (µm)

Brownian Displacement (µm)

Distance Fallen (µm)

Settling greater in 1 s

50

1.7

70,000

 

20

2.7

11,500

 

10

3.8

2,900

 

5

5.5

740

 

2

8.8

125

 

1

13

33

Diffusion greater in 1 s

0.5

20

9.5

 

0.2

37

2.1

 

0.1

64

0.81

 

0.05

120

0.35

 

0.02

290

0.013

 

0.01

570

0.0063

NOTE: Temperature = 37°C; gas viscosity = 0.19 × 10-3 poise. Appropriate correction factors were applied for motion outside the range of validity of Stokes' law.

Electrical forces may cause charged particles to deposit in the respiratory tract by the creation of image charges on airway walls. Image charges form within the airways when charged particles attract ions that have the opposite charge and repel airway ions of the same charge. Generally, electrical forces are a minor mechanism of deposition, unless the inspired particles are highly charged. When they are, electrical forces may cause significant losses within the device used to generate the aerosol. Deposition of 1.0-µm charged particles is increased over that of uncharged particles once there are about 40 charges on the particle; for 0.6-µm particles, an increase is seen once there are 30 charges, and for 0.3-µm particles only 10 charges are needed (Melandri et al, 1983). Ambient aerosols that have been airborne for several hours tend to be uncharged. However, fresh aerosols 1 to 10 µm in diameter produced by a grinding or cutting process may have hundreds of electrostatic charges per particle, which are sufficient to enhance deposition. The extent to which charge influences deposition of radon progeny is largely unknown. Other forces acting to affect deposition such as acoustic forces, magnetic forces, or thermal forces, are normally not significant in the respiratory tract.

The effectiveness of these deposition mechanisms depends on (1) the effective aerodynamic diameters of the particles, (2) the pattern of breathing, and (3) the anatomy of the respiratory tract. These factors determine the fraction of the inhaled particles that is deposited as well as the site of deposition.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Aerosol Characteristics

A major factor governing the effectiveness of the deposition mechanisms is the size of the inspired particles. The effective aerodynamic diameter is a function of the size, shape, and density of the particles and affects the magnitude of forces acting on them. For example, while inertial and gravitational effects increase with increasing particle size, the displacements produced by diffusion decrease. The importance of particle size cannot be overemphasized. It is featured prominently in most discussions of aerosol deposition in the respiratory tract (Altshuler et al., 1957; Brain et al., 1977; Lippmann, 1977; Raabe et al., 1977; Brain and Valberg, 1979; Heyder et al., 1980, 1986; Lippman et al., 1980; Agnew, 1984; Stuart, 1984).

Radon decay products have a particular size as molecular species but then attach to particles with a wide range of sizes. Since size helps to determine the site of deposition within the lungs, it is important to quantify the mass of particles within the size range that can penetrate the oropharynx. Aerosol mass distributions are characterized by two values, the mass median aerodynamic diameter (MMAD) and the geometric standard deviation (GSD). The MMAD denotes the particle size at which half of the total aerosol mass is contained in larger particles and half is contained in smaller particles. Since the MMAD is expressed as an aerodynamic diameter, it describes how the aerosol behaves in the respired air and can be used to estimate where and by what processes the aerosol deposits in the respiratory tract. The GSD denotes the spread of particle sizes. Most aerosols have sizes that are distributed log-normally; that is, on a plot of the frequency distribution versus particle diameter, the distribution looks Gaussian. An aerosol that is composed of particles of the same size would have a GSD equal to 1.0 and would be termed monodisperse. An aerosol with a GSD of 1.22 or larger is called polydisperse (Fuchs, 1964). Almost all naturally occurring aerosols are polydisperse. An aerosol with a MMAD of 2.0 µm and a GSD of 2.0 would have 1 GSD or 68% of its mass contained in particles between 1.0 and 4.0 µm in aerodynamic diameter. An important implication of a log-normal distribution is that much of the aerosol mass can be contained in the large particles, since mass is proportional to the cube of the diameter. Where these large particles deposit in the respiratory tract governs, to a large extent, where much of the dose is deposited.

Mass can be measured gravimetrically by pulling air containing the aerosol through an absolute filter at a known volumetric flow rate. Particle size can be estimated by using light or electron microscopy to examine collected particles. Optical methods utilizing light scattering can give continuous estimates of particle size and/or concentration. These methods, however, describe only the cross-sectional or geometric diameter of the aerosol. Aerodynamic diameter is a more meaningful predictor of deposition site, since it accounts for particle size, shape, and density. Several devices can provide aerodynamic diameter directly,

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

including cascade impactors and aerosol centrifuges. Real-time aerodynamic size measurements are possible using laser Doppler velocimeters (Hiller et al., 1978; Bouchikhi et al., 1988) or laser diffraction particle sizers (Clay et al., 1983).

Accurate measurement of aerosol size distributions is complex because particle size is frequently dynamic. Evaporation, hygroscopicity, and agglomeration may cause rapid changes in particle size. Once hygroscopic particles are inhaled and mix with the warm humid air in the respiratory tract, they stop shrinking and start to adsorb water and grow in size. The relative humidity in the lungs beyond the major bronchi at resting inspiratory rates is about 99.5% (Ferron et al., 1988a); this is sufficient to cause dry salt particles to increase 3 to 4.5 times in diameter (Ferron and Gebhart, 1988). Thus, aerosol size measurements of hygroscopic particles made after drying or at a low relative humidity drastically underestimate their size in the lungs. In such cases it is possible to estimate the size attained in the lungs by taking into consideration the relative humidity, the molecular weight of the salt, and the number of ions into which it dissociates in water, among other factors. Such particle growth equations are presented by Ferron (1977, 1987) and Persons et al. (1987).

Particle size may not be constant as a generated pharmacological aerosol moves through a delivery system and the respiratory tract. Volatile aerosols composed of Freon propellant or water become smaller through evaporation (Mercer, 1973), whereas hygroscopic aerosols such as sodium chloride particles may grow dramatically, especially as the relative humidity nears 100% (Cinkotai, 1971; Ferron, 1977; Ferron and Gebhart, 1988).

The effect of hygroscopicity on deposition has been studied both experimentally (Blanchard and Willeke, 1983; Tu and Knutson, 1984) and theoretically (Ferron, 1977; Martonen et al., 1985; Xu and Yu, 1985; Persons et al., 1987; Ferron et al., 1988a,b), and has recently been reviewed (Morrow, 1986). The overall effect borne out in these studies is that, with increasing hygroscopicity and relative humidity, deposition fraction as a function of particle size is shifted to smaller particle sizes. That is, whereas the deposition minimum for nonhygroscopic particles is about 0.5 µm, the minimum for dry NaCl particles that grow in the 99.5% relative humidity of the lungs is about 0.1 µm (Xu and Yu, 1985). Consequently, the deposition of hygroscopic particles with diameters of greater than 0.1 µm when inhaled exceeds the deposition of nonhygroscopic particles of the same size. For example, a 1-µm NaCl particle has a deposition fraction or collection efficiency 3.8 times greater than that of a 1-µm nonhygroscopic particle (Xu and Yu, 1985). Many pharmacological aerosols are hygroscopic; the hygroscopic growth and deposition characteristics of histamine, for example, are similar to those of NaCl (Ferron, 1987).

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Breathing Pattern

Another important factor affecting deposition is the breathing pattern. Minute volume defines the average flow velocity of the aerosol-containing air in the lung and the total number of particulates to which the lung is exposed. Respiratory frequency affects the residence time of aerosols in the lungs and, hence, the probability of deposition by gravitational and diffusional forces. A change in the lung volume alters the dimensions of the airways and parenchyma.

Anatomy of the Respiratory System

The anatomy of the respiratory tract is important since it is necessary to know the diameters of the airways, the frequency and angles of branching, and the average distances to the alveolar walls. Furthermore, along with the inspiratory flow rate, airway anatomy specifies the local linear velocity of the airstream and the character of the flow. A significant change in the effective anatomy of the respiratory tract occurs when there is a switch between nose and mouth breathing. There are inter-and intraspecies differences in lung morphometry; even within the same individual, the dimensions of the respiratory tract vary with changing lung volume, with aging, and with pathological processes.

CLEARANCE OF RADON PROGENY: GENERAL PRINCIPLES

The response to the alpha energy produced by radon progeny depends not only on the amount of aerosol deposited but also on the amount retained in the lungs over time. Retention is the amount of material present in the lungs at any time and equals deposition minus clearance. An equilibrium concentration is reached during continuous exposure to radon progeny when the rate of deposition equals the rate of clearance. The amount of particles retained within a specific lung region over time is a key determinant of dose.

As discussed elsewhere in this chapter, such factors as particle size, hygroscopicity, and breathing pattern affect the site of deposition within the respiratory tract. In turn, where particles deposit in the lungs determines which mechanisms are used to clear them and how fast they are cleared. This influences the amount retained over time. Examples of the implications of particle characteristics on integrated retention were given by Brain and Valberg (1974) using a model developed by the Task Force on Lung Dynamics. They showed that the total amount as well as the distribution of retained dose among nose and pharynx, trachea and bronchi, and the pulmonary and lymphatic compartments were dramatically altered by particle size and solubility.

Particles that deposit on the ciliated airways are cleared primarily by the mucociliary escalator. Those particles that penetrate to and deposit in

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

the peripheral, nonciliated lung can be cleared by many mechanisms, including translocation by alveolar macrophages, particle dissolution, or movement of free particles or particle-containing cells into the interstitium and/or the lymphatics. These pathways are of great importance for materials that have a long biological half-life, such as silica, asbestos, or plutonium. However, one must realize that these fates are of relatively little importance for short-lived radon progeny. This is because the majority of the energy produced by alpha-particle emission is dissipated during the first hour. Thus, the movement of radon progeny very soon after deposition is relevant to dosimetry. What happens weeks or months later is irrelevant. Reviews of clearance processes have been prepared by Kilburn (1977), Pavia (1984), and Schlesinger (1985a).

Mucociliary Transport

Less soluble particles that deposit on the mucous blanket covering pulmonary airways and the nasal passages are moved toward the pharynx by cilia. Also present in this moving carpet of mucus are cells and particles that have been transported from the nonciliated alveoli to the ciliated airways. At the pharynx, mucus, cells, and debris coming from the nasal cavities and the lungs meet, mix with salivary secretions, and enter the gastrointestinal tract after being swallowed. In humans, the ciliated epithelium extends from the trachea down to the terminal bronchioles. The particles are removed with half-times of minutes to hours; the rate depends on the speed of the mucous blanket. The speed is faster in the trachea than it is in the small airways (Serafini et al., 1976). There is little time for solubilization of slowly dissolving materials. In contrast, particles deposited in the nonciliated compartments have much longer residence times; there, small differences in in vivo solubility can have great significance. The speed of mucous flow can be affected by factors influencing either the cilia or the amount and quality of the mucus.

Ciliary action may be affected by the number of strokes per minute, the amplitude of each stroke, the time course and form of each stroke, the length of the cilia, the ratio of ciliated to nonciliated area, and the susceptibility of the cilia to intrinsic and extrinsic agents that modify their rate and quality of motion. The characteristics of the mucus are critically important. The thickness of the mucous layer and its rheological properties may undergo wide variations. Wanner (1977) and Camner and Mossberg (1988) reviewed many of these factors that influence clearance, including clinical implications.

Mucociliary transport has been studied by a variety of techniques, such as monitoring the movement of inert or radiolabeled particles deposited on the tracheal mucus via a bronchoscope or as an inhaled bolus. Tracheal mucus velocity (TMV) can then be estimated from the distance the particles moved over time, as observed with either movies taken through a bronchoscope or by a gamma camera (Yeates et al., 1975; Chopra et al., 1979). Bronchoscopic

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

techniques yield higher numbers for TMV (15-21 mm/min) than the noninvasive bolus techniques do (4.4 mm/min). These values are only characteristic for the trachea and large central airways. Transport in the small peripheral airways is slower probably due to the discontinuous mucous layer (Van As, 1977).

Many investigators have estimated mucociliary transport from whole-lung clearance curves. These curves are generated by monitoring the amount of radioactivity in the lungs over time (hours to days) following the inhalation of a radiolabeled aerosol.

Albert and Arnett (1955) first used this method and noted that the clearance curve can be divided into two phases: a fast and a slow phase. The fast phase was complete within 24 to 48 h and has generally been attributed to tracheobronchial clearance; the slow phase has been attributed to alveolar clearance (Booker et al., 1967; Morrow et al., 1968; Lippmann and Albert, 1969). This interpretation has been widely accepted and has been used to study clearance in normal and abnormal individuals (Lourenco et al., 1971; Sanchis et al., 1972; Poe et al., 1977; Camner and Philipson, 1978; Stahlhofen et al., 1980). However, evidence indicates that clearance from the airways might not be complete in the first 24 h. This may be even more pronounced in patients with lung disease. Gore and Patrick (1982) noted that particles instilled into the trachea can be sequestered in epithelial cells. Stahlhofen et al. (1986) noted fast and slow phases of clearance even in humans given a bolus of particles delivered only 45 cm3 beyond the larynx. Another approach is to examine deposition and clearance of particles in central versus peripheral regions (Smaldone et al., 1988). The uses of this type of analysis in the interpretation of clearance curves have recently been noted in an editorial by Foster (1988).

More studies are needed to elucidate the best methodology to model mucociliary clearance and to understand its role and importance in patients with pulmonary disease. Clearly, it is also essential to understand the initial deposition pattern of an inhaled aerosol in order to assess the importance of mucociliary clearance on the disappearance of the aerosol from the lungs.

Nonciliated Regions

Particles deposited in the nonciliated portion of the lungs either are moved toward the ciliated region, primarily within alveolar macrophages, or they enter the lung connective tissue either as free particles or within macrophages. Macrophages are credited with keeping the alveolar surfaces clean and sterile. These cells rest on the continuous epithelial layer of the lung. It is their phagocytic and lytic potentials that provide most of the bactericidal properties of the lungs. Rapid endocytosis of insoluble particles by macrophages prevents particle penetration through the alveolar epithelia and facilitates alveolar-bronchiolar transport. Particles in connective tissue may slowly dissolve or may be transported to new sites through lymphatic pathways. Particles remaining on alveolar

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

surfaces are cleared with biological half-times estimated to be days to weeks in humans, whereas particles that have penetrated into fixed tissues are cleared with half-times ranging from a few days to thousands of days depending on their solubility. Brain (1985) has summarized the biology of lung macrophages and in a recent review (Brain, 1988) has emphasized that many kinds of lung macrophages exist. These include alveolar, airway, connective tissue, pleural, and intravascular macrophages.

Cough

The function of cough is the removal of material from the respiratory tract when mucociliary transport is overwhelmed. Thus, there would probably be little or no transport of radon progeny in the airways produced by cough in individuals with normal amounts of secretions. However, in chronic smokers and other subjects with chronic bronchitis, cough can produce significant and rapid mucus transport. Whether cough is initiated by cough receptors or voluntarily, the subject's first action is usually inspiration. Following the inspiratory phase, the glottis is closed. At about the same time, expiratory muscles in the abdomen and chest wall contract, producing pleural and alveolar pressures of 100 mm Hg or more. When the glottis is opened abruptly, the result is extremely high linear velocities which may be hundreds of miles per hour. The kinetic velocity of this airflow is coupled to mucus and causes it to be propelled along the airways. Several reviews of cough are available (Brain et al., 1985; Leith et al., 1986).

DIFFERENCES BETWEEN WORKERS AND THE PUBLIC

The mechanisms responsible for deposition and clearance have already been discussed. The effectiveness of these mechanisms depends on various factors. Some major influences on the fraction of the inspired aerosol that deposits within the respiratory tract and its distribution are discussed here.

Anatomic Variations

The configuration of the lungs and airways is important since the efficiency of deposition depends, in part, upon the diameters of the airways, their angles of branching, and the average distances to alveolar walls. Furthermore, along with the inspiratory volumetric flow rate, airway anatomy specifies the local linear velocity of the airstream and, thus, whether the flow is laminar or turbulent. There are inter-and intraspecies differences in lung morphometry (Soong et al., 1979; Schlesinger and McFadden, 1981; Phalen, 1984; Nikiforov and Schlesinger, 1985); even within the same individual the dimensions of the respiratory tract vary with changing lung volume, with aging, and with pathological processes. Among individuals who breathe in the same manner,

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

total deposition has been found to have a coefficient of variation of as large as 27%, much of which is believed to be due to intersubject differences in airway geometry (Heyder et al., 1982). This finding has been supported by other theoretical and experimental studies (Yeates et al., 1982; Yu and Diu, 1982). Within one person, a decrease in lung volume from 4,800 to 2,400 ml not only increases deposition but also causes the major site of particle deposition to shift from the lung periphery to the central airways (Agnew, 1984). At low lung volumes, central airways have smaller cross-sectional areas and, thus, higher linear velocities. For a given flow rate, this enhances deposition by impaction in more central intrapulmonary airways. As a person ages, anatomical changes of the respiratory tract also appear to affect deposition. It has been predicted theoretically that total deposition in children may be as much as 1.5 times higher than that in adults (Xu and Yu, 1986). Children have smaller tidal volumes and residence times, and these compensate in part for their smaller lung dimensions.

The dimensions of the airways and alveoli vary among individuals because of age, body size, genetics, and disease. However, the overall pattern of conducting airways changes little since it is established at birth. It is true that terminal bronchioles can develop into respiratory bronchioles and become more alveolated, but in general, the newborn's airways simply enlarge into the adult tracheobronchial tree (Hogg et al., 1970; Hislop et al., 1972; Burri, 1985). Between birth and adulthood, airways enlarge in length and diameter by a factor of around 3. Lung volume would thus be expected to grow 27-fold during this period of time (Dunill, 1962).

However, ventilation per gram of body weight is clearly higher in children than it is in adults. In addition, some of the more peripheral airways appear to grow less during childhood and adolescence than do more central airways. Phalen et al. (1985) have predicted that deposition is highest in newborns and decreases with increasing age to adulthood. Phalen and colleagues have also suggested that smaller individuals receive more particle deposition within the conductive zone than do larger individuals at the same level of ventilation.

There are substantial changes in the gas-exchange region during growth that reflect an enormous increase in the number and surface area of alveoli. However, these changes should not influence the deposition or clearance of radon progeny in airways, the primary region of concern.

In addition to age, gender and ethnicity may also influence airway size. Up to age 14 yr, boys were found to have lungs larger than those of girls (Thurlbeck, 1982). There are also dramatic differences in the sizes, dimensions, and structural proportions of the larynx between males and females.

Breathing Pattern

The way each underground miner or member of the general population breathes also affects deposition. Minute volume defines the average flow

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

velocity of air in the lungs and the total number of particles to which the lungs are exposed. Respiratory frequency, tidal volume, and lung volume will affect the residence time of aerosols in the lungs and, hence, the probability of deposition by gravitational and diffusional forces. Flow rate governs the degree and extent of turbulent flow in the upper airways that enhances particle deposition. A change in lung volume also alters the dimensions of the airways and parenchyma. High levels of ventilation and breath holding represent extremes of breathing patterns that give rise to markedly different deposition patterns. Valberg et al. (1978) exposed excised dog lungs to a submicrometric radioactive aerosol while the dogs were using different breathing patterns. Even though the same particle size was used throughout, when the pattern was rapid and shallow, airway deposition was predominant, but when the pattern was slow and deep, deposition on alveolar surfaces was greater.

Activity Level and Exercise

There are compelling reasons why exercise and the resulting changes in breathing pattern should influence particle deposition in the respiratory tract. First, the level of ventilation is a major determinant of the mechanism of deposition. Inertial impaction depends on the velocity of the airstream, whereas the importance of diffusion and settling depends on the residence time in the lungs and the distance the particles must travel to reach lung surfaces. Inertial impaction is more important in central airways, where linear velocities are high; diffusion and settling are more important in peripheral airways and alveoli, where residence times are longer and distances are smaller. Second, minute volume (respiratory frequency x tidal volume) determines the total particle mass that enters the respiratory tract. Hence, even if the deposition fraction or collection efficiency is constant, an increase in the minute volume increases particle deposition in the lungs. Dennis (1971) has reported that during exercise, the deposition fraction increases with minute volume in some human subjects, particularly for larger particles (1.0 to 3.0 µm); thus, the amount of aerosol deposited in the lung per unit time increases in two ways. Both the amount entering the respiratory tract as well as the percentage deposited were elevated.

Landahl and associates (1952) demonstrated that the percentage of airborne particles deposited in the respiratory tract increases with increasing minute volume. In exercising hamsters (Harbison and Brain, 1983), the deposition of a 0.4-µm 99mTc-labeled aerosol increased as their oxygen consumption increased. Exercising animals consumed twice as much oxygen as sedentary animals did but they retained 2.5 to 3 times as many particles in their lungs. Enhanced retention probably reflects both an increase in ventilation and an increase in collection efficiency. It is likely that different relationships may pertain with larger particles. Then, increased flow rates may be more effective at depositing particles in the nose, pharynx, larynx, and large airways, leading to diminished

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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particle deposition deep in the lungs. Recently, Zeltner et al. (1988) found the same absolute number of 1.0-µm particles deposited in the parenchyma of exercising hamsters compared with that in resting animals, whereas deposition in the upper airways increased in exercising hamsters. It is possible that for still larger particles, exercise could actually lower the particle dose to the parenchyma.

In humans who are exercising vigorously, minute volumes can exceed 120 liters/min, greatly increasing the amount of aerosol inspired. Even at rest, inspiratory flows are elevated during speech (Bouhuys et al., 1966; Bunn and Mead, 1971). The high velocities (2 m/s) achieved in the main bronchi enhance inertial impaction and turbulence. Experimenting with 0.5-µm monodisperse particles, Muir and Davies (1967) found that the percentage of particles deposited increased linearly with tidal volume and decreased with the square root of breathing frequency. Expiratory reserve volume also influenced this percentage (Davies et al., 1972).

Oral Versus Nasal Breathing

A highly significant change in the effective anatomy of the respiratory tract occurs when there is a switch between nose and mouth breathing or when the nose is bypassed by a tracheostomy or by an endotracheal tube. The nose has a central role as a collector of inhaled aerosol particles and as a conditioner that warms and humidifies inspired air. The combination of a small cross section for airflow, sharp curves, and interior nasal hairs helps to maximize particle impaction. Abundant evidence indicates that significant fractions of inhaled particles and gases can be deposited in the nose and pharynx. Excellent reviews of particle deposition in that region are available (Hounam and Morgan, 1977). Deposition and clearance of particles in the head during nose breathing have been studied extensively by Pattle (1961), Hounam et al. (1969), Lippmann (1970, 1977), Märtens and Jacobi (1974), Swift and Proctor (1982), and Heyder et al. (1986). Collectively, these reports indicate that although the nose is an inefficient filter for submicrometric particles, large quantities of large particles (>5.0 µm) are deposited in the nasopharyngeal region. The probability for particle deposition increases with increasing particle diameter, flow rate, and nasal flow resistance. Almost all particles larger than 10 µm are trapped in the nose. Large individual variations are apparent, possibly because of intersubject differences in the distensibility of the nasal passages that affect nasal resistance.

The loss of the filtering capacity of the nose may be important. With rising levels of exercise-enhanced metabolism and increasing ventilation, the high-resistance nasal pathway is progressively abandoned in favor of the low-resistance oral pathway. As the nose is bypassed, more and more particles penetrate to and deposit in the airways of the lungs. With exercise, the amount

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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of aerosol depositing in the lungs may increase in excess of that predicted by the increased ventilation.

The surface area of the human nose is small relative to the 140 m2 of the total respiratory tract, but it has a rich vasculature that is well designed for heating or cooling and for rapid exchange of dissolved substances between the mucus, tissues, and blood vessels. Most capillaries have fenestrated endothelial linings enclosed by porous basement membranes.

Proctor (1973) estimates that the nasal surface area between the bony opening into the nasal cavity and the posterior end of the turbinates is 160 cm2, or 0.016 m2. The volume of air within the human nasal passages is about 20 ml. At an inspiratory flow rate of 0.4 liters/s, the residence time of the inspired gas in the nose is only 0.05 s. Despite this brief contact time with the nasal mucosa, special anatomic features help to condition the inspired gas. At modest flow rates, inspired gas is warmed and humidified before it reaches the subglottal area. However, the upper airways are less effective at higher flow rates, especially when the inspired air is cold and dry. The nose also has a major role as a collector of inhaled aerosol particles. A small cross section for airflow and the resulting high linear velocities, sharp curves, and interior nasal hairs all help to promote particle impaction.

In both animals and humans, particle deposition and clearance rates are markedly affected by the choice of pathway to the trachea. Shifts from the nasal to the oral route are of major significance. An excellent review of particle deposition in the nose is that of Hounam and Morgan (1977). Deposition and clearance of particles in the head during nose breathing have been extensively studied by Pattle (1961), Hounam and coworkers (1969), Lippmann (1970), and Märtens and Jacobi (1974). Collectively, these reports indicate that substantial quantities of particles larger than 5.0 µm are deposited in the nasopharyngeal region. There are large individual variations, depending on the structure and aerodynamic properties of the nose. Hounam et al. (1969) showed an increase in the percentage of inspired particles deposited in the nose as the resistance to airflow increased. Forsyth and associates (1983) have demonstrated that nasal resistance decreases dramatically with exercise, probably because of mucosal shrinkage mediated by the effects of the sympathetic nervous system on the nasal microcirculation. Lower nasal resistance would decrease the particle collection efficiency in the nose and would increase particle penetration to the pulmonary airways and parenchyma. The nose would become a less efficient filter.

The nasal route is more efficient at removing large particles from inspired air than is the oral route. In bypassing the nose, mouth breathers deposit more particles in their lungs and may concomitantly increase the risk of pulmonary damage. Mouth breathing is common under conditions of heavy exercise, during speech or singing (Bouhuys et al., 1966; Bunn and Mead, 1971), and in those who have decreased nasal conductance caused by infection or allergy. This

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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may result in markedly increased exposure of the airways and alveoli to large particles.

Some inhaled toxins and the diseases they produce may induce changes that in turn affect where radon progeny deposit. For example, sulfur dioxide and sulfate particles alter the dimensions of the upper and lower airways in both humans and experimental animals. The principal effect in acute experiments is to increase pulmonary flow resistance; this reflects the bronchoconstrictive action of the pollutant. Chronic exposure may lead to chronic bronchitis, and again, airways may be narrowed. In either case, the reduction in airway cross section increases linear flow velocities and turbulence, with the result that more particles deposit by impaction. Thus, chronic exposure to air pollutants or tobacco smoke is likely to be associated with changes in the uptake of radon progeny.

OTHER MODIFYING FACTORS INFLUENCING DEPOSITION AND/OR CLEARANCE OF RADON PROGENY

Preexisting Disease

Respiratory diseases can influence the distribution of inspired radon progeny. Bronchoconstriction or obstruction of airways leads to diversion of flow to less obstructed airways. With advancing disease, the remaining healthy airways and alveoli may be increasingly exposed to inspired particles. Narrowing of airways by mucus, inflammation, or bronchial constriction can increase the linear velocities and turbulence of airflow, enhance inertial deposition, and cause more central deposition patterns (Albert et al., 1973; Goldberg and Lourenco, 1973; Taplin et al., 1977; Kim et al., 1983a). In very sick patients with chronic obstructive pulmonary disease (COPD), there may be increases in aerosol deposition that may be associated with flow limitation (Smaldone and Messina, 1985).

One factor that determines where radon progeny are deposited in the lungs is the distribution of ventilation. Particles are carried into the lungs with the inhaled air and therefore reach only areas that are ventilated. It is known that nonventilated regions of the lungs exist in patients with a variety of pathological conditions (Milic-Emili, 1974). Because diseased lungs are nonuniformly affected, they are more likely than normal lungs to have large alterations in the distribution of ventilation. Disease may impair ventilation in some regions because of airway closure, atelectasis, or obstructing mucous plugs (Macklem, 1971), and fewer particles reach these regions. Conversely, the remaining ventilated areas of the lungs may be exposed to increased toxic loads when a significant amount of the lung is not ventilated. Maintaining patent airways and open alveoli requires a balance between surface tension and tissue forces (Macklem, 1971; Weibel and Gil, 1977; Hoppin et al., 1986). Alterations

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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in these forces can cause alveoli to collapse, especially when breathing at low lung volumes (Bachofen et al., 1979; Gil et al., 1979). Thus, airway and alveolar patency during breathing depends upon surface and tissue forces, and any disruption in lung structure can lead to the creation of nonventilated areas of the lung.

Chronic pulmonary disease alters the architecture of the lungs. Emphysema involves alveolar wall destruction, which leads to enlarged air spaces. When radial traction forces of the alveolar septa are reduced and surface tension is diminished because of loss of alveolar surface area, intrapulmonary bronchi are poorly supported and tend to collapse during expiration (American Lung Association, 1981). Similarly, the increase of secretions in patients with chronic bronchitis favors airway obstruction by mucous plugs and the regional thickening of alveolar walls in interstitial fibrosis makes alveoli less compliant and thus favors local hypoventilation. In each of these cases, the changes in airway and alveolar properties cause changes in the distribution of ventilation. Although airway closure has been noted in patients with chronic lung disease (Macklem, 1971), little is known about the anatomic distribution of poorly ventilated regions of the lungs and how this distribution changes during the disease process.

Radioactive aerosols have been used in humans to detect airway obstruction in COPD (Lourenco et al., 1972; Goldberg and Lourenco, 1973; Ramanna et al., 1975; Dolovich et al., 1976; Pavia et al., 1977; Taplin et al., 1977; Itoh et al., 1981; Kim et al., 1983a,b). Scintigraphic analysis of particle deposition shows that deposition is greater in the central airways of patients with airway obstruction than in airways of normal patients (Lourenco et al., 1972; Ramanna et al., 1975; Taplin et al., 1977; Itoh et al., 1981). Investigators have quantified this phenomenon by calculating a penetration index to assess how deeply the aerosol enters the lungs (Thomson and Pavia, 1973; Dolovich et al., 1976; Agnew et al., 1981). Penetration of aerosol has been found to correlate inversely with airway obstruction. Other investigators have used aerosol rebreathing techniques to measure total deposition in normal individuals versus that in patients with obstructed airways (Kim et al., 1983a). Theoretical analyses of these data suggest that aerosol deposition may be a more sensitive indicator of airway abnormalities than is measurement of overall airway resistance (Kim et al., 1983b). Total deposition in the lungs of humans with airway obstruction is enhanced compared with that in the lungs of normal patients (Kim et al., 1983a).

Since human disease is progressive, experiments such as those described above are complicated and difficult to interpret. Nevertheless, some conclusions can be made from these studies. Two types of airway obstruction can occur in patients with COPD: physical obstruction of the airways with mucous plugs, as in those with chronic bronchitis, and obstruction caused by too-small bronchioles that collapse during expiration. Airway collapse or closure does not occur in

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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normal individuals who are breathing at rest, but can occur during normal breathing in humans with emphysema (Macklem, 1971).

Obstruction of small airways has three effects on aerosol deposition. First, particles deposit more centrally because they fail to reach the terminal air units. Second, deposition is enhanced at the site of obstruction in both obstructed airways and in those that collapse during expiration. Smaldone and associates (1979) examined the latter type of obstruction and showed that deposition is enhanced around the site of closure because of changes in airflow patterns. Turbulent eddies enhance deposition at the constriction site; collapse brings particles in close contact with airway walls.

Third, Macklem and associates (1973) have postulated that obstructed airways cause inspired gas to be diverted to the healthier regions of the lungs; thus, particles preferentially deposit in healthy regions. Because of the increased linear velocity of the gas in these healthy regions and enhanced penetration to alveoli, deposition would be enhanced (Macklem et al., 1973).

Animal models have been used to explore how aerosol deposition is influenced by lung pathology. In these studies, variable factors in humans like age, environmental exposure, and extent of disease can be controlled. In 1979, Hahn and Hobbs studied both papain-and elastase-induced emphysema in hamsters. Intratracheal instillation of elastase produced focal destruction and enlargement of alveoli accompanied by loss of lung elastic recoil (Hayes et al., 1975; Snider et al., 1977, 1986).

Hahn and Hobbs (1979) exposed hamsters to an aerosol of 137Cs-labeled aluminum silicate particles 21 days after elastase or papain administration. The emphysematous hamsters, examined 3 h after the aerosol exposure, retained 45 to 65% fewer particles in their lungs than did the control hamsters. This decrease in initial dose of aerosol in emphysematous lungs was also observed by Damon and associates (1983) in rats exposed to iron oxide particles and by Lundgren and associates (1981) in rats exposed to 169Yb-labeled plutonium oxide particles.

Sweeney et al. (1983a, 1985, 1987) have studied the progressive influence of emphysema, chronic bronchitis, and fibrosis on the distribution of deposited submicrometric particles throughout rodent lungs. One common result in all three diseases is that the presence of detectable pulmonary disease always results in less uniform patterns of particle retention throughout the lungs. This pattern could not be explained by differences in breathing pattern (Sweeney et al., 1983b, 1986). With a restrictive lung disease, such as fibrosis, deposition was more heterogeneous in the early stages when the fibrotic lesions were focal. As the fibrosis became more uniformly distributed throughout the lungs, particle retention also became more uniformly distributed. These changes were inversely correlated with the presence of pulmonary fibrosis; fibrotic lung regions retained fewer particles than the more normal regions of the lung did (Sweeney et al., 1983a).

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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For pulmonary emphysema, the heterogeneity of deposition increased with increasing severity of the disease, as measured by changes in the mean linear intercept of the parenchyma (Sweeney et al., 1987). Variations in local deposition could not be explained by the anatomic distribution of emphysema throughout the lungs. In animals with emphysema, although the parenchyma is the primary site of the lesion, airways are also influenced in the later stages of the disease. Loss of elastic recoil caused by tissue destruction would tend to reduce airway caliber. With the progressive loss of supportive parenchymal tissue as emphysema progresses, the decreasing airway caliber would favor enhanced airway deposition and increased overall heterogeneity of deposition. Airway changes caused by physical obstruction of the airways because of mucus plugging (as in animals with chronic bronchitis) also produce increased heterogeneity with enhanced deposition in the affected airways (Sweeney et al., 1985).

Nevertheless, extrapolation of these findings in animals to humans with chronic obstructive pulmonary disease or idiopathic pneumonitis with fibrosis must be done cautiously. These data in animals can be used to identify some factors influencing deposition, and thus risk, but they are limited in predicting causal relationships in human disease.

Smoking

There are many reasons to believe that smokers may have altered exposure-dose relationships as well as altered responses to radon progeny. First, and probably most important, there are mechanistic interactions among the carcinogens and irritants in tobacco smoke and radon progeny. However, in addition, smoking can alter the structure of the lung and thus alter both deposition and clearance kinetics. Cigarette smoking frequently leads to chronic bronchitis, a disease characterized by proliferation of mucus-secreting cells and glands. Thus, chronic bronchitis is often characterized by narrowing of airways, and this can enhance airway deposition. This should lead to increased deposition of radon progeny. Also enhancing the dose from radon progeny would be diminished clearance rates from airways. Counteracting this would be the protective effect of an increased mucous layer thickness.

OTHER CHARACTERISTICS OF WORKERS AND THE PUBLIC

Occupancy Data

If one wants to compare exposure-dose relationships between miners and the general population, one factor that must be considered is where people spend their time. For early miners, the number of hours spent underground on a weekly basis has not been well described in published literature. Contemporary underground miners spend about 35 or 40 h/week in mining environments where

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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radon progeny are encountered. The actual time spent there is probably less than that, since some time is spent preparing for work and descending into and ascending the mine. Clearly, the general population spends a much greater portion of its time in indoor environments. In 1955, Stewart et al. reported that the general population spent approximately 90% of its time indoors in the United Kingdom. In 1982, the United Nations Scientific Committee on the Effects of Atomic Radiation used a value of 80%. More recently, Francis (1987) produced a report describing indoor occupancy in the United Kingdom. On average, 92% of time was spent indoors. That was divided into 77% spent in their own residence and 15% spent in other indoor locations. Of the 77% spent indoors in their own residence, 42% was in the bedroom, 18% was in the living area, and the remaining 17% was in the kitchen, dining room, and bathroom. Similar data have been reported for adults in the United States; in a survey of 44 U.S. cities, participants spent less than 10% of their time outdoors (Szalai, 1972).

The data suggested that occupancy patterns are relatively independent of season, but differences among different days of the week were noted. For example, Sundays in the winter yielded the highest indoor occupancy in residences (about 90%). They also encountered some variation among various population subgroups. Housewives spent approximately 97% of their time indoors; 88% was spent in their own residence, while 9% was spent in other indoor locations. Furthermore, of the remaining 3% that was spent outdoors, about half of that was taken up with traveling.

Ethnic Differences

Another issue that has been raised in relation to comparisons between miners and the general population are ethnic differences. Is it possible that different ethnic groups have different lung geometries, lung volumes, or breathing patterns? Recently, Roy and Courtay (in press) reviewed the existing literature in relation to ventilation rates and lung volumes. They assessed more than a dozen papers providing information in relation to black, Chinese, Japanese, Indians, Caucasian Americans, and other ethnic groups in the United States. The general conclusion was that there are some differences in lung size among different ethnic groups. American Caucasians tended to have greater portal capacities than did American blacks or Americans of Asian descent. Nevertheless, variability in ventilation among these groups was relatively small, especially when compared with variations in activity and therefore ventilation within individuals. A compelling conclusion is that ethnicity is not a major factor influencing exposure-dose relationships for inhaled particles.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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Altitude

Frequently, underground miners, especially in the United States, work at elevated altitudes. Many of the uranium miners in the Colorado Plateau worked at altitudes of between 5,000 and 8,000 feet above sea level. The related effects caused by changes in oxygen concentration and gas density on breathing are slight in relation to work-ventilation relationships and other concerns addressed in this report. It is true that changes in gas density can affect deposition mechanisms such as sedimentation, but again, these effects are likely to be relatively small.

Species Differences

Animal models of radon deposition and retention have been used (Cross, 1988). However, even when the same aerosol size distribution is breathed by different species, very disparate lung doses may still result. There are both systematic and unusual variations in ventilation, collection efficiency, and lung anatomy among species that influence the amount and distribution of deposited aerosols. Thus, the problem of extrapolating findings from one species to another and from animals to humans is difficult. Several scientists (Palm et al., 1956; Friedlander, 1964; Kliment, 1973; Stauffer, 1975; McMahon et al., 1977; Raabe et al., 1977; Schlesinger, 1980; Phalen, 1984; Xu and Yu, 1986) have made either theoretical or experimental contributions, but the problem is far from solved. How well aerosol deposition in humans and animals compares has been reviewed recently by Schlesinger (1985b) and by Brain et al. (1988). It is essential to realize that different rates of clearance among species can also influence retention and thus the total dose retained by the lung.

CONCLUSIONS

Determination of the distribution of inhaled radon daughters within the respiratory tract is one dimension of the more general problem of determining exposure-dose and dose-response relations. It is likely that some of the variability in response among different individuals and various animal species may result from differences in the concentration of radon progeny at the site of action as well as variations in the inherent responsiveness of specific active tissues. Furthermore, the properties of the bronchial epithelium are important, since many radon daughters may breach epithelial barriers and come into contact with more reactive cells.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

REFERENCES

Agnew, J. E. 1984. Physical properties and mechanisms of deposition of aerosols. P. 49 in Aerosols and the Lung: Clinical and Experimental Aspects, S. W. Clarke and D. Pavia, eds. Boston: Butterworths.

Agnew, J. E., D. Pavia, and S. W. Clark. 1981. Airways penetration of inhaled radioaerosol: An index to small airways function? Eur. J. Respir. Dis. 62:239-255.

Aharonson, E. F., A. Ben-David, and M. A. Klingberg, eds. 1976. Air Pollution and the Lung. New York: Halsted Press-Wiley.

Albert, R. E., and L. C. Arnett. 1955. Clearance of radioactive dust from the lung. Arch. Environ. Health 12:99.

Albert, R. E., M. Lippmann, H. Peterson, J. Berger, K. Sanborn, and D. Bohning. 1973. Bronchial deposition and clearance of aerosols. Arch. Intern. Med. 131:115.

Altshuler, B. 1961. The role of the mixing of intrapulmonary gas flow in the deposition of aerosol. Pp. 47-54 in Inhaled Particles and Vapours, C. N. Davies, ed. Oxford: Pergamon Press.

Altshuler, B., L. Yarmus, E. D. Palmes, and N. Nelson. 1957. Aerosol deposition in the human respiratory tract. I. Experimental procedures and total deposition, A.M.A. Arch. Ind. Health 15:293.

American Lung Association. 1981. Chronic Obstructive Lung Disease, 5th ed. New York: American Lung Association.


Bachofen, H., P. Gehr, and E. R. Weiber. 1979. Alterations of mechanical properties and morphology in excised rabbit lungs rinsed with a detergent. J. Appl. Physiol. 47:1002-1010.

Blanchard, J. D., and K. Willeke. 1983. Total deposition of ultrafine sodium chloride particles in human lungs. J. Appl. Physiol. 57:1850.

Booker, D. V., A. C. Chamberlain, J. Rudo, D. C. Muir, and M. L. Thompson. 1967. Elimination of 5 micron particles from the human lung. Nature 215:30.

Bouchikhi, A., M. H. Becquemin, J. Bignon, M. Roy, and A. Teillac. 1988. Particle size study of nine metered dose inhalers, and their deposition probabilities in the airways. Eur. Respir. J. 1:547.

Bouhuys, A., D. F. Proctor, and J. Mead. 1966. Kinetic aspects of singing. J. Appl. Physiol. 21:2-10.

Brain, J. D. 1985. Macrophages in the respiratory tract. Pp. 447-471 in Handbook of Physiology, Vol. 1, Circulation and Nonrespiratory Functions, A. P. Fishman and A. B. Fisher, eds. Bethesda, Md.: American Physiological Society.

Brain, J. D. 1988. Lung macrophages—How many kinds are there? What do they do? Am. Rev. Respir. Dis. 137:507.

Brain, J. D., and P. A. Valberg. 1974. Models of lung retention based on the Report of the ICRP Task Group. Arch. Environ. Health 28:1-11.

Brain, J. D., and P. A. Valberg. 1979. Deposition of aerosols in the respiratory tract. Am. Rev. Respir. Dis. 120:1325-1373.

Brain, J. D., and P. A. Valberg. 1985. Aerosols: basics and clinical considerations. Pp. 594-603 in Bronchial Asthma: Mechanisms and Therapeutics, 2nd ed., E. B. Weiss, M. S. Segal, and M. Stein, eds. Boston: Little, Brown and Co.

Brain, J. D., D. F. Proctor, and L. M. Reid, eds. 1977. Respiratory defense mechanisms. In Lung Biology in Health and Disease, Vol. 5. New York: Marcel Dekker.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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Brain, J. D., P. A. Valberg, and S. Sneddon. 1985. Mechanisms of aerosol deposition and clearance. Pp. 123-147 in Aerosols in Medicine. Principles, Diagnosis and Therapy, F. Morén, M. T. Newhouse, and M. B. Dolovich, eds. Amsterdam: Elsevier Science Publishers.

Brain, J. D., P. A. Valberg, and G. A. Mensah. 1988. Species differences. Pp. 89-103 in Variations in Susceptibility to Inhaled Pollutants, J. D. Brain, B. D. Beck, A. J. Warren, and R. A. Shaikh, eds. Baltimore: Johns Hopkins Press.

Bunn, J. D., and J. Mead. 1971. Control of ventilation during speech. J. Appl. Physiol. 31:870-872.

Burri, P. H. 1985. Lung development and growth. Pp. 1-46 in Handbook of Physiology, S. R. Geiger, ed. Sect. 3: The Respiratory System, A. P. Fishman and A. B. Fisher, eds. Bethesda, Md.: American Physiological Society.

Camner, P., and B. Mossberg. 1988. Mucociliary disorders: A review. J. Aerosol Med. 1:21-28.

Camner, P., and M. S. Philipson. 1978. Human alveolar deposition of 4 micron teflon particles. Arch. Environ. Health 33:181.

Chopra, S. K., G. V. Taplin, D. Elam, S. W. Carson, and D. Golde. 1979. Measurement of tracheal mucociliary transport velocity in humans—smokers versus non-smokers (preliminary findings). Am. Rev. Respir. Dis. 119(Suppl.):205.

Cinkotai, F. F. 1971. The behavior of sodium chloride particles in moist air. J. Aerosol Sci. 2:325.

Clarke, S. W., and D. Pavia, eds. 1984. Aerosols and the Lung. Boston: Butterworths.

Clay, M. M., D. Pavia, S. P. Newman, and S. W. Clarke. 1983. Factors influencing the size distribution of aerosols from jet nebulizers. Thorax 38:755.

Cross, F. T. 1988. Radon inhalation studies in animals. Radiat. Prot. Dosim. 24:463-466.


Damon, E. G., B. V. Mokler, and R. K. Jones. 1983. Influence of elastase-induced emphysema and the inhalation of an irritant aerosol on deposition and retention of an inhaled insoluble aerosol in Fischer-344 rats. Toxicol. Appl. Pharmacol. 67:322-330.

Davies, C. N., ed. 1961. Inhaled Particles and Vapours. Elmsford, N.Y.: Pergamon Press.

Davies, C. N., ed. 1964. Inhaled Particles and Vapours II. Elmsford, N.Y.: Pergamon Press.

Davies, C. N., ed. 1967. Aerosol Science. New York: Academic Press.

Davies, C. N., J. Heyder, and M. C. S. Ramu. 1972. Breathing of half-micron aerosols. I. Experimental. J. Appl. Physiol. 32:591-600.

Dennis, W. L. 1971. The effect of breathing rate on the deposition of particles in the human respiratory system. Pp. 91-102 in Inhaled Particles III, W. H. Walton, ed., Surrey, England: Unwin Brothers.

Dodgson, J., and R. I. McCallum, eds. 1988. Inhaled Particles VI. New York: Pergamon Press.

Dolovich, M. B., J. Sanchis, C. Rossman, and M. T Newhouse. 1976. Aerosol penetrance: A sensitive index of peripheral airways obstruction. J. Appl. Physiol. 40:468-471.

Dunill, M. S. 1962. Postnatal growth of the lung. Thorax 17:329-333.


Ferron, G. A. 1977. The size of soluble aerosol particles as a function of the humidity of the air: Application to the human respiratory tract. J. Aerosol Sci. 8:251.

Ferron, G. A. 1987. A method for the calculation of aerosol particle growth and deposition in the human respiratory tract. Pp. 105-110 in Deposition and Clearance of Aerosols in the Human Respiratory Tract, W. Hoffman, ed. Vienna: Facultas.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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Ferron, G. A., and J. Gebhart. 1988. Estimation of the lung deposition of aerosol particles produced with medical nebulizers. J. Aerosol Sci. (in press).

Ferron, G. A., B. Haider, and W.G. Kreyling. 1988a. Inhalation of salt aerosol particles. I. Estimation of the temperature and relative humidity of the air in the human upper airways. J. Aerosol Sci. 19:343.

Ferron, G. A., W. G. Kreyling, and B. Haider. 1988b. Inhalation of salt aerosol particles. II. Growth and deposition in the human respiratory tract. J. Aerosol Sci. 19:611-631.

Forsyth, R. D., P. Cole, and R. J. Shephard. 1983. Exercise and nasal patency. J. Appl. Physiol. 55:860-865.

Foster, W. M. 1988. Editorial: Is 24 hour lung retention an index of alveolar deposition? J. Aerosol Med. 1:1.

Francis, E. A. 1987. Patterns of building occupancy for the general public. NRPB-M129. National Radiation Protection Board.

Friedlander, S. K. 1964. Particle deposition by diffusion in the lower lung: Application of dimensional analysis. Am. Ind. Hyg. Assoc. J. 25:37.

Fuchs, N. A. 1964. The Mechanics of Aerosols. Elmsford, N.Y.: Pergamon Press.

Gil, J., H. Bachofen, P. Gehr, and E. R. Weibel. 1979. Alveolar volume-surface area relation in air-and saline-filled lungs fixed by vascular perfusion. J. Appl. Physiol. 47:990-1001.

Goldberg, I. S., and R. V. Lourenco. 1973. Deposition of aerosols in pulmonary disease. Arch. Intern. Med. 131:88-91.

Gore, D. J., and G. Patrick. 1982. A quantitative study of the penetration of insoluble particles into the tissues of the conducting airways. Ann. Occup. Hyg. 26:149.


Hahn, F. F., and C. H. Hobbs. 1979. The effect of enzyme-induced pulmonary emphysema in Syrian hamsters on the deposition and long-term retention of inhaled particles. Arch. Environ. Health 34:203-211.

Harbison, M. L., and J. D. Brain. 1983. Effects of exercise on particle deposition in Syrian golden hamsters. Am. Rev. Respir. Dis. 128:904-908.

Hatch, T. F., and P. Gross. 1964. Pulmonary Deposition and Retention of Inhaled Aerosols. New York: Academic Press.

Hayes, J. A., A. Korthy, and G. L. Snider. 1975. The pathology of elastase-induced panacinar emphysema in hamsters. J. Pathol. 117:1-14.

Heyder, J., and G. Scheuch. 1983. Diffusional transport of nonspherical aerosol particles. Aerosol Sci. Technol. 2:41.

Heyder, J., J. Gebhart, W. Stalhofen, and B. Stuck. 1982. Biological variability of particle deposition in the human respiratory tract during controlled and spontaneous mouth-breathing. Ann. Occup. Hyg. 26:137.

Heyder, J., J. Gebhart, G. Rudolf, C. F. Schiller, and W. Stahlhofen. 1986. Deposition of particles in the human respiratory tract in the size range 0.005-15 µm. J. Aerosol Sci. 17:811.

Heyder, J., J. D. Blanchard, H. A. Feldman, and J. D. Brain. 1988. Convective mixing in human respiratory tract: Estimates with aerosol boli. J. Appl. Physiol. 64:1273.

Hiller, F. C., M. K. Mazumder, J. D. Wilson, and R. C. Bone. 1978. Aerodynamic size distribution of metered dose bronchodilator aerosols. Am. Rev. Respir. Dis. 118:311.

Hinds, W. C. 1982. Aerosol Technology—Properties, Behavior, and Measurement of Airborne Particles. New York: Wiley-Interscience.

Hislop, A., C. F. Muir, M. Jacobson, G. Simon, and L. Reid. 1972. Postnatal growth and function of the pre-acinar airways. Thorax 27:265-274.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Hogg, J. C., J. Williams, J. B. Richardson, P. T Macklem, and W. M. Thurlbeck . 1970. Age as a factor in the distribution of lower-airway conductance in the pathologic anatomy of obstructive lung disease. N. Engl. J. Med. 282:1283-1287.

Hoppin, F. G., J. C. Stothert, I. A. Greaves, Y.-L. Lai, and J. Hildebrandt. 1986. Lung recoil: Elastic and rheological properties. Pp. 195-215 in Handbook of Physiology, Section 3, The Respiratory System, Volume III, The Mechanics of Breathing, Part 1, P. T. Macklem and J. Mead, eds. Bethesda, Md.: American Physiological Society.

Hounam, R. F., and A. Morgan. 1977. Particle deposition. Pp. 125-156 in Respiratory Defense Mechanisms, J. D. Brain, D. F. Proctor, and L. M. Reid, eds. New York: Marcel Dekker.

Hounam, R. F., A. Black, and M. Walsh. 1969. Deposition of aerosol particles in the nasopharyngeal region of the human respiratory tract. Nature 221:1254-1255.

Itoh, H., Y. Ishii, H. Maeda, G. Todo, K. Torizuka, and G. C. Smaldone. 1981. Clinical observations of aerosol deposition in patients with airways obstruction. Chest 80(Suppl.):837-839.


Kilburn, K. H. 1977. Clearance mechanisms in the respiratory tract. In Handbook of Physiology, Section 9, Reactions to Environmental Agents, D. H. K. Lee, H. L. Falk, and S. D. Murphy, eds. Bethesda, Md.: American Physiological Society.

Kim, C. S, L. K. Brown, G. G. Lewars, and M. A. Sackner. 1983a. Aerosol rebreathing method for assessment of airway abnormalities: Theoretical analysis and validation. Am. Ind. Hyg. Assoc. J. 44:349-357.

Kim, C. S., L. K. Brown, G. G. Lewars, and M. A. Sackner. 1983b. Deposition of aerosol particles and flow resistance in mathematical and experimental airway models. J. Appl. Physiol. 55:154-163.

Kliment, V. 1973. Similarity and dimensional analysis, evaluation of aerosol deposition in the lungs of laboratory animals and man. Folia Morphol. 21:59.


Landahl, H. D., T. N. Tracewell, and W. H. Lassen. 1952. Retention of airborne particulates in the human lung. Arch. Ind. Hyg. Occup. Med. 6:508-511.

Leith, D. E., J. P. Butler, S. L. Sneddon, and J. D. Brain. 1986. Cough. Pp. 315-336 in Handbook of Physiology, The Respiratory System, Section 3, Volume III, Part 1, P. T. Macklem and J. Mead, eds. Bethesda, Md.: American Physiological Society.

Lippmann, M. 1970. Deposition and clearance of inhaled particles in the human nose. Ann. Otol. Rhinol. Laryngol. 79:519-528.

Lippmann, M. 1977. Regional deposition of particles in the human respiratory tract. Pp. 213-232 in Handbook of Physiology, Section 9, Reactions to Environmental Agents, D. H. K. Lee, H. L. Falk, and S. D. Murphy, eds. Bethesda, Md.: American Physiological Society.

Lippmann, M., and R. E. Albert. 1969. The effect of particle size on the regional deposition of inhaled aerosols in the human respiratory tract. Am. Ind. Hyg. Assoc. J. 30:257.

Lippmann, M., D. B. Yeates, and R. E. Albert. 1980. Deposition, retention, and clearance of inhaled particles. Br. J. Ind. Med. 37:337.

Lourenco, R. V., M. F. Klimek, and C. J. Borowski. 1971. Deposition and clearance of 2 micron particles in the tracheobronchial tree of normal subjects—smokers and nonsmokers. J. Clin. Invest. 50:1411.

Lourenco, R. V., R. Loddenkemper, and R. W. Canon. 1972. Patterns of distribution and clearance of aerosols in patients with bronchiectasis. Am. Rev. Respir. Dis. 106:857-866.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Lundgren, D. L., E. G. Damon, J. H. Diel, and F. F. Hahn. 1981. The deposition, distribution, and retention of inhaled 239PuO2 in the lungs of rats with pulmonary emphysema. Health Phys. 40:231-235.

Mackleto, P. T. 1971. Airway obstruction and collateral ventilation. Physiol. Rev. 51:368-436.

Macklem, P. T., W. E. Hogg, and J. Brunton. 1973. Peripheral airway obstruction and particulate deposition in the lung. Arch. Intern. Med. 131:93-97.

Märtens, A., and W. Jacobi. 1974. Die in vivo Bestimmung der Aerosolteilchendeposition im Atemtrakt bei Mund-bzw. Nasenatmung. Pp. 117-121 in Aerosole in Physik, Medizin und Technik , W. Stahlhofen, ed. Bad Soden, West Germany: Gesellschaft für Aerosolforschung.

Martoner, T. B., A. E. Barnett, and F. J. Miller. 1985. Ambient sulfate aerosol deposition in man: Modeling the influence of hygroscopicity. Environ. Health Perspect. 63:11.

McMahon, T. A., J. D. Brain, and S. R. LeMott. 1977. Species differences in aerosol deposition. In Inhaled Particles IV, W. H. Walton, ed. Elmsford, N.Y.: Pergamon Press.

Melandri, C. V., G. Tarroni, V. Prodi, T. DeZaiacomo, M. Formignani, and C. C. Lombardi. 1983. Deposition of charged particles in the human airways. J. Aerosol Sci. 14:657.

Mercer, T. T. 1973. Aerosol Technology in Hazard Evaluation. New York: Academic Press.

Mercer, T. T. 1981. Production of therapeutic aerosols; principles and techniques. Chest 80(Suppl.):813.

Milic-Emili, J. 1974. Small airway closure and its physiological significance. Scand. J. Respir. Dis. 85(Suppl.):181-189.

Morén, F., M. T. Newhouse, and M. B. Dolovich, eds. 1985. Aerosols in Medicine—Principles, Diagnosis, and Therapy. New York: Elsevier.

Morgan, W. K. C., H. W. Clague, and S. Vinitski. 1983. On paradigms, paradoxes, and particles. Lung 161:195.

Morrow, P. E. 1986. Factors determining hygroscopic aerosol deposition in airways. Physiol. Rev. 66:330.

Morrow, P. E., Chairman, Task Group on Lung Dynamics. 1966. Deposition and retention models for internal dosimetry of the human respiratory tract. Health Phys. 12:173-188.

Morrow, P. E., F. R. Gibb, and K. M. Gazioglu. 1968. A study of particulate clearance from the human lungs. Am. Rev. Respir. Dis. 96:1209.

Muir, D. C. F., and C. N. Davies. 1967. The deposition of 0.5 µm diameter aerosols in the lungs of man. Ann. Occup. Hyg. 10:161-174.


Nikiforov, A. T., and R. B. Schlesinger. 1985. Morphometric variability of the human upper bronchial tree. Respir. Physiol. 59:289.


Palm, P. E., J. M. McNerney, and T. Hatch. 1956. Respiratory dust retention in small animals: A comparison with man. A.M.A. Arch. Ind. Health 13:355.

Pattle, R. E. 1961. The retention of gases and particles in the human nose. Pp. 302-309 in Inhaled Particles and Vapours, Vol. I, C. N. Davies, ed., Oxford: Pergamon Press.

Pavia, D. 1984. Lung mucociliary clearance. In Aerosols and the Lung: Clinical and Experimental Aspects, S. W. Clarke and D. Pavia, eds. London: Butterworths.

Pavia, D., M. Thomson, and H. S. Shannon. 1977. Aerosol inhalation and depth of deposition in the human lung. Arch. Environ. Health 32:131-137.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Persons, D. D., G. D. Hess, W. J. Muller, and P. W. Scherer. 1987. Airway deposition of hygroscopic heterodispersed aerosols: Results of computer calculation. J. Appl. Physiol. 63:1195.

Phalen, R. F., ed. 1984. Inhalation Studies: Foundations and Techniques. Boca Raton, Fla.: CRC Press.

Phalen, R. F., M. J. Oldham, C. B. Beucage, T. D. Crocker, and J. D. Mortensen. 1985. Tracheobronchial airways and implications for particle deposition. Anat. Rec. 212:368-380.

Poe, N. D., M. B. Cohen, and R. L. Yanda. 1977. Application of delayed lung imaging following radioaerosol inhalation. Radiology 122:739.

Proctor, D. F. 1973. The upper respiratory tract and the ambient air. Clin. Notes Respir. Dis. 12:2-10.

Raabe, O. G. 1982. Deposition and clearance of inhaled aerosols. In Mechanisms in Respiratory Toxicology, Vol. I, H. Witschi and P. Nettesheim, eds. Boca Raton, Fla.: CRC Press.

Raabe, O. G., H.-C. Yeh, G. J. Newton, R. F. Phalen, and D. J. Velasquez. 1977. Deposition of inhaled monodisperse aerosols in small rodents. In Inhaled Particles IV, W. H. Walton, ed. Elmsford, N.Y.: Pergamon Press.

Ramanna, L., D. P. Tashkin, G. V. Taplan, D. Elam, R. Detels, A. Coulson, and S. N. Rokaw. 1975. Radioaerosol lung imaging in chronic obstructive pulmonary disease. Chest 68:634-640.

Reist, P. C. 1984. Introduction to Aerosol Science. New York: McMillan.

Roy, M., and C. Courtay. In press. Daily activities and breathing parameters for use in respiratory tract dosimetry. Radiat. Protect. Dosim.


Sanchis, J., M. Dolovich, R. Chalmers, and M. Newhouse. 1972. Quantitation of regional aerosol clearance in the normal human lung. J. Appl. Physiol. 33:757.

Schlesinger, R. B. 1980. Particle deposition in model systems of human and experimental animal airways. In Generation of Aerosols and Facilities for Exposure Experiments, K. Willeke, ed. Ann Arbor, Mich.: Ann Arbor Science Publishers.

Schlesinger, R. B. 1985a. Clearance from the respiratory tract. Fund. Appl. Toxicol. 5:435.

Schlesinger, R. B. 1985b. Comparative deposition of inhaled aerosols in experimental animals and humans: A review. J. Toxicol. Environ. Health. 15:197.

Schlesinger, R. B., and L. McFadden. 1981. Comparative morphometry of the upper bronchial tree in six mammalian species. Anat. Rec. 199:99.

Serafini, S. M., A. Wanner, and E. D. Michaelson. 1976. Mucociliary transport in central and intermediate size airways and effect of aminophyllin. Bull. Eur. Physiopathol. Respir. 12:415.

Smaldone, G. C., and M. S. Messina. 1985. Flow limitation, cough, and patterns of aerosol deposition in humans. J. Appl. Physiol. 59:515.

Smaldone, G. C., H. Itoh, D. L. Swift, and H. N. Wagner. 1979. Effect of flow-limiting segments and cough on particle deposition and mucociliary clearance in the lung. Am. Rev. Respir. Dis. 120:747-758.

Smaldone, G. C., R. J. Perry, W. D. Bennett, M. S. Messina, J. Zwang, and J. Ilowite. 1988. Interpretation of ''24 hour lung retention'' in studies of mucociliary clearance. J. Aerosol. Med. 1:11.

Snider, G. L., C. B. Sherter, K. W. Koo, J. B. Karlinsky, J. A. Hayes, and C. Franzblau. 1977. Respiratory mechanics in hamsters following treatment with endotracheal elastase or collagenase. J. Appl. Physiol. 42:206-215.

Snider, G. L., E. C. Lucey, and P. J. Stone. 1986. Animal models of emphysema. Am. Rev. Respir. Dis. 133:149-169.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
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Soong, T. T., P. Nicolaides, C. P. Yu, and S. C. Soong. 1979. A statistical description of the human tracheobronchial tree geometry. Respir. Physiol. 37:161.

Stahlhofen, W., J. Gebhart, and J. Heyder. 1980. Experimental determination of the regional deposition of aerosol particles in the human respiratory tract. Am. Ind. Hyg. Assoc. J. 41:385.

Stahlhofen, W., J. Gebhart, G. Rudolf, and G. Scheuch. 1986. Measurement of lung clearance with pulses of radioactively-labelled aerosols. J. Aerosol Sci. 17:333.

Stauffer, D. 1975. Scaling theory for aerosol deposition in the lungs of different mammals. J. Aerosol Sci. 6:223.

Stewart, N. G., R. N. Crooks, and E. Fisher. 1955. The radiological dose to persons in the UK due to debris from nuclear test expolsions. AERE HP/R1701. Harwell: Atomic Energy Research Establishment.

Stuart, B. O. 1984. Deposition and clearance of inhaled particles. Environ. Health Perspect. 55:369.

Sweeney, T. D., J. D. Brain, A. F. Tryka, and J. J. Godleski. 1983a. Retention of inhaled particles in hamsters with pulmonary fibrosis. Am. Rev. Respir. Dis. 128:138-143.

Sweeney, T. D., W. A. Skornik, J. J. Godleski, and J. D. Brain. 1983b. Collection efficiency is decreased in hamsters with pulmonary fibrosis. Fed. Proc. 42:1349.

Sweeney, T. D., J. D. Brain, W. A. Skornik, and J. J. Godleski. 1985. Chronic bronchitis produced by SO2 alters the deposition pattern of inhaled aerosol in rats. Am. Rev. Respir. Dis. 131:A195.

Sweeney, T. D., W. A. Skomik, J. J. Godleski, and J. D. Brain. 1986. Collection efficiency of inhaled particles is decreased in hamsters with pulmonary emphysema. Am. Rev. Respir. Dis. 133:147.

Sweeney, T. D., J. D. Brain, S. A. Leavitt, and J. J. Godleski. 1987. Emphysema alters the deposition pattern of inhaled particles in hamsters. Am. J. Pathol. 128:19-28.

Swift, D. L., and D. F. Proctor. 1982. Human respiratory deposition of particles during oro-nasal breathing. Atmos. Environ. 16:2279.

Szalai, A. 1972. The Use of Time: Daily Activities of Urban and Suburban Populations in 12 Countries. Paris: Mouton.

Taplin, G. V., D. P. Tashkin, S. K. Chopra, D. E. Anselmi, D. Elam, B. Calvarese, A. Coulson, R. Detels, and S. N. Rokaw. 1977. Early detection of chronic obstructive pulmonary disease using radionuclide lung-imaging procedure. Chest 71:567-575.

Taulbee, D. P., C. P. Yu, and J. Heyder. 1978. Aerosol transport in the human lung from analysis of single breaths. J. Appl. Physiol. 44:803-812.

Thomson, M. L., and D. Pavia. 1973. Particle penetration and clearance in the human lung. Arch. Environ. Health 29:214-219.

Thurlbeck, W. M. 1982. Postnatal human lung growth. Thorax 37:564-571.

Tu, K. W., and E. O. Knutson. 1984. Total deposition of ultrafine hydrophobic and hygroscopic aerosols in the human respiratory system. Aerosol Sci. Technol. 3:453.


United Nations Scientific Committee on the Effects of Atomic Radiation. 1982. Ionizing Radiation: Sources and Biological Effects. 1982 Report to the General Assembly. New York: United Nations.


Valberg, P. A., J. D. Brain, S. R. LeMott, S. L. Sneddon, and A. Vinegar. 1978. Dependence of aerosol deposition site on breathing pattern. Am. Rev. Respir. Dis. 117:262A.

Valberg, P. A., J. D. Brain, S. K. Sneddon, and S. R. LeMott. 1982. Breathing patterns influence aerosol deposition sites in excised dog lungs. J. Appl. Physiol. 53:824-837.

Suggested Citation:"Breathing, Deposition, and Clearance." National Research Council. 1991. Comparative Dosimetry of Radon in Mines and Homes. Washington, DC: The National Academies Press. doi: 10.17226/1799.
×

Van As, A. 1977. Pulmonary airway clearance mechanisms: a reappraisal. Am. Rev. Respir. Dis. 115:721.

Walton, W. H., ed. 1971. Inhaled Particles III. Surrey, England: Unwin Brothers.

Walton, W. H., ed. 1977. Inhaled Particles IV. Elmsford, N.Y.: Pergamon Press.

Walton, W. H., ed. 1982. Inhaled Particles V. Oxford: Pergamon Press.

Wanner, A. 1977. Clinical aspects of mucociliary transport. Am. Rev. Respir. Dis. 116:73-125.

Weibel, E. R., and J. Gil. 1977. Structure-function relationship at the alveolar level. Pp. 1-81 in Lung Biology in Health and Disease, Vol. 3, Bioengineering Aspects of the Lung, J. B. West, ed. New York: Marcel Dekker.


Xu, G. B., and C. P. Yu. 1985. Theoretical lung deposition of hygroscopic NaCl aerosols. Aerosol Sci. Technol. 4:455.

Xu, G. B., and C. P. Yu. 1986. Effects of age on deposition of inhaled aerosols in the human lung. Aerosol Sci. Technol. 5:349.


Yeates, D. B., N. Aspin, H. Levison, M. T. Jones, and A. C. Bryan. 1975. Mucociliary transport rates in man. J. Appl. Physiol. 39:487.

Yeates, D. B., T. R. Gerrity, and C. S. Garrard. 1982. Characteristics of tracheobronchial deposition and clearance in man. Ann. Occup. Hyg. 26:259.

Yu, C. P., and C. K. Diu. 1982. A probabilistic model for intersubject deposition variability of inhaled particles. Aerosol Sci. Technol. 1:355-362.

Yu, C. P., and G. B. Xu. 1986. Predictive models for deposition of diesel exhaust particulates in human and rat lungs. Aerosol Sci. Technol. 5:337-347.


Zeltner, T. B., T. D. Sweeney, W. A. Skornik, and J. D. Brain. 1988. Effects of exercise on the retention of inhaled 0.9 µm particles in hamsters. Am. Rev. Respir. Dis. (Abs.) 137:315.

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Studies of underground miners have provided a wealth of data about the risk of lung cancer from exposure to radon's progeny elements, but the application of the miner data to the home environment is not straightforward.

In Comparative Dosimetry of Radon in Mines and Homes, an expert committee uses a new dosimetric model to extrapolate to the home environment the risk relationships found in the miner studies. Important new scaling factors are developed for applying risk estimates based on miner data to men, women, and children in domestic environments. The book includes discussions of radon dosimetry and the uncertainties concerning other risk factors such as age and smoking habits.

The book also contains a thorough technical discussion of the characteristics of radioactive aerosols in domestic environments, the dose of inhaled radon progeny to different age groups, identification of respiratory tract cells at the greatest risk of carcinogenesis, and a complete description of the new lung dose model being developed by the International Commission on Radiological Protection as modified by this committee.

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