Chapter 29 A Reconsideration of Cells at Risk and Other Key Factors in Radon Daughter Dosimetry A. C. James National Radiological Protection Board, Chilton, Didcot, Oxfordshire 0X11 0RQ, United Kingdom In assessing dose to lung from radon daughter exposure, it is appropriate to consider secretory cells as well as basal cells as sensitive targets; hence, it is more defensible to average dose over the whole thickness of bronchial epithelium. The mean bronchial absorbed dose calculated in this way is higher by about 60% for the unattached fraction of potential alpha-energy and about 30% for the attached aerosol than the dose to basal cells alone. The data on bronchial dimensions, airway deposition and clearance of radon daughters are reviewed and a model consistent with these data is formulated. This gives dose conversion factors of 130 mGy per WLM exposure for unattached radon daughters and approximately 8 mGy per WLM for the aerosol fraction. The latter value is sensitive to the particle size distribution, varying inversely with aerosol AMD. Breathing rate and age are shown to be minor factors in determining lung dose. Assuming that radon daughter aerosols do not grow in size at physiological humidity, one finds that typical exposure conditions in the home may be assessed by an effective dose equivalent of 15 mSv per WLM. Consideration of the inverse variation of equilibrium factor and unattached fraction in room air leads to a relatively constant dose per unit concentration of radon gas, which facilitates the interpretation of monitoring data. The risk of lung cancer from exposure to radon daughters in homes is derived by assessing lung dose, either absolutely by evaluating an effective dose equivalent (UNSCEAR, 1982; ΝΕΑ, 1983) or by scaling the 0097-6156/87/0331-0400$06.00/0 Published 1987 American Chemical Society
29. JAMES
401
Cells at Risk and Other Key Factors
excess rate of lung cancer incidence in uranium miners in proportion to dose rates i n mines and homes (NCRP, 1984; Jacobi and Paretzke, 1985; E l l e t t and Nelson, 1985). Lung dose must be calculated by modelling the sequence of events involved in inhalation, deposition, clearance and decay of radon daughters within the bronchial airways. Various models have shown that dose for a given exposure depends on environmental and personal factors, p r i n c i p a l l y the aerosol size d i s t r i b u t i o n , breathing rate and lung s i z e . An improved understanding of the physical behaviour and size d i s t r i b u t i o n of radon daughter aerosols i n room a i r i s emerging (Porstendôrfer, 1984), supported by an increasing body of data. It i s therefore worthwhile reconsidering the influence of environmental conditions on lung dose and taking this opportunity to incorporate improved knowledge of the parameters and processes involved in modelling that results from recent research. R e a l i s t i c models of lung dose proceed by defining the tissue at r i s k and the location of sensitive c e l l s . The 'basal c e l l s ' l i n i n g the basement membrane of bronchial epithelium are generally assumed to be targets for cancer induction, but a different consensus is now emerging. There are also differences of opinion on the extent of sensitive bronchial tissue. The concept of an effective dose equivalent c a l l s for dose to be averaged over the whole tissue (ΝΕΑ, 1983), whereas some researchers prefer to focus attention on dose to a few larger airways where the majority of cancers are thought to occur (NCRP, 1984; E l l e t t and Nelson, 1985). These fundamental issues are being considered by a Task Group set up by the ICRP to review the current lung model (Bair, 1985). In this paper I s h a l l attempt to formulate a model for radon daughter dosimetry consistent with the Task Group's present views and to examine the p r a c t i c a l import. Cells at r i s k The h i s t o l o g i c a l types of lung cancer seen to excess i n uranium miners r e f l e c t those in the population at large (Masse, 1984). These occur almost entirely i n bronchial airways. Approximately 207 are adenocarcinomas which occur in peripheral bronchioles (Spencer, 1977) where there are no basal c e l l s . Squamous c e l l cancers predominate in miners exposed early in l i f e to r e l a t i v e l y low concentrations of radon daughters (Saccomanno et^ a_l. , 1982). These are considered l i k e l y to arise from the secretory small mucous granular c e l l s which undergo c e l l d i v i s i o n and extend to the e p i t h e l i a l surface (Masse, personal communication). Division of these c e l l s i s accelerated after i r r i t a t i o n by toxicants such as cigarette smoke or infectious diseases (Trump et a l . , 1978). It i s reasonable to conclude that dose to c e l l s throughout the bronchial tree may contribute to the r i s k of lung cancer and not just the dose received by certain c e l l s i n the large central airways. It i s probably also appropriate to evaluate the dose absorbed by c e l l s throughout the depth of bronchial epithelium, i . e . the mean dose, o
402
RADON AND
ITS DECAY PRODUCTS
rather than focus on basal c e l l s alone (Masse, 1984). conclusions underlie the revised dosimetry developed below.
These
Dose per disintegration The dose received by c e l l s in the bronchial epithelium from decay of the alpha-emitting radon daughters at the airway surface decreases rapidly with depth in tissue. The data available show that the thickness of bronchial epithelium i s highly variable (Gastineau et al., 1972) but the d i s t r i b u t i o n of values can be formalised (Wise, 1982) by the summary shown i n Table I.
Table I. Normal Distribution of E p i t h e l i a l Thickness
Airways Main bronchi Lobar bronchi Segmental bronchi Transitional bronchi Bronchioles
Mean 80 50 50 20 15
(urn)
Standard Deviation 6 12 18 5 5
Figure 1 shows the range of doses to basal c e l l s calculated for one alpha-decay of RaA or RaC' per cm^ of airway surface in each bronchial generation. The hatched areas show the effect of considering radon daughter a c t i v i t y in the mucosa, i . e . the airway wall, rather than e n t i r e l y in mucus (minimum values) (James et a l . , 1980; ΝΕΑ, 1983). The location of radon daughter decays r e l a t i v e to basal c e l l s is c l e a r l y important i n the upper airways, including the segmental bronchi (generations 3-5) which are commonly regarded as a major s i t e of lung cancer (NCRP, 1984; E l l e t t and Nelson, 1985). The Figure also shows the values adopted by the NCRP (Harley and Pasternack, 1982) which assume a target c e l l depth of 22 pm in the upper airways and 10 urn in the bronchioles and the range of values used in other dosimetric models (Jacobi and E i s f e l d , 1980; Hofmann, 1982). These different dosimetric factors, a r i s i n g from different assumptions about target c e l l depth, should be taken into account when comparing the results of various models. The conversion factor varies much less when the mean dose to a l l e p i t h e l i a l c e l l s i s evaluated (Figure 2). This i s especially marked for RaC decays which contribute most of the dose. In this case, very similar doses are calculated i f the complex depth distributions of Table I are represented by a single e p i t h e l i a l thickness of 50 urn in the bronchi, i . e . generations 1-10, and 15 urn in bronchioles. Lung models Most dosimetry models have incorporated the so-called Weibel Ά' airway dimensions (Weibel, 1963) in order to calculate aerosol deposition, clearance and the density of alpha-decays per unit surface
403
Cells at Risk and Other Key Factors
JAMES
7;
-Activity
in
mucosa Po-2%
Po-218 250 r
Y777? 200
oOS.
NCRP 78, 198i
C
Ο
Jacobi-Eisfeld, 1980 • Hofmann, 1982 o
72
3-5
9,10
Bronchial
1 2
11-15
9,10
3-5
11-15
generation
Figure 1. Doses to basal c e l l s i n each bronchial generation from 1 disintegration of RaA or RaC per cm 2 airway surface. -Activity
in
mucosa
"
mucus Po-2%
Po-218 250
p™ K'UZZL
15
è
200
I
150 0) /
*
/
> >
50 pm 0)
-8
50
1 2 Bronchial
3-8
9,10
11-15
1 2
3-8
9,10
11-15
generation
Figure 2. Doses averaged over a l l e p i t h e l i a l c e l l s i n each bronchial generation from 1 disintegration of RaA or RaC per cm 2 airway surface.
404
RADON AND ITS DECAY PRODUCTS
area. The Yeh-Schum airway model (Yeh and Schum, 1980) has also been used (James et a l . , 1980; Harley and Pasternack, 1982) and dosimetric results from both models have been compared (ΝΕΑ, 1983; NCRP, 1984). A further model of the bronchial tree, referred to here as UCI', has been reported more recently (Phalen et a l . , i n press). This includes novel data for children's lungs at various ages. Both the Weibel 'A' and Yeh-Schum models need to be reduced in scale to represent adult human lung at a normal level of i n f l a t i o n corresponding to 3000 ml functional residual capacity (FRC) (Yu and Diu, 1982). P a r t i a l scaling has been included in some dosimetric models (ΝΕΑ, 1983; James, 1984) but not i n others. In a l l cases the airway sizes used to represent adult lung correspond to a higher level of i n f l a t i o n than the standard FRC, leading to general but relatively small underestimates of bronchial dose. The volumes and surface areas of airways in each generation that result from scaling the Weibel Ά', Yeh-Schum and UCI lung models to the standard FRC (Yu and Diu, 1982), are shown i n Figure 3. The residual differences in airway size are appreciable, but there is no overriding reason to prefer a p a r t i c u l a r model. Dosimetric results are therefore evaluated below for a l l three. !
Deposition Diffusion i s the dominant mechanism of lung deposition for radon daughter aerosols. It i s generally assumed that airflow i s laminar i n the smaller airways and that deposition i n each airway generation can be calculated adequately (Chamberlain and Dyson, 1956; Ingham, 1975). However, there i s no such consensus on the treatment of deposition i n the upper bronchi. Some authors (Jacobi and E i s f e l d , 1980; NCRP, 1984) have considered deposition to be enhanced by secondary flow, on the basis of experimental results (Martin and Jacobi, 1972). It has been shown that t h i s assumption reduces the calculated dose from unattached radon daughters by a factor of two (James, 1985). The deposition of sub-micron aerosols i n a hollow cast of human bronchi has recently been measured under r e a l i s t i c conditions (Cohen et a l . , in press). Typical data are shown in Figure 4. These are inconsistent with convective enhancement of deposition but support the c l a s s i c a l treatment of deposition by d i f f u s i o n (Chamberlain and Dyson, 1956). The deposition model used here includes expressions for d i f f u s i o n (Ingham, 1975) sedimentation (Pich, 1972) and impaction (Egan and Nixon, 1985) and a r e a l i s t i c treatment of lung v e n t i l a t i o n . It can be shown that this predicts the aerosol deposition measured in the lungs of human subjects (summarised by Rudolf (1986)) over the range of aerosol size from 5 nm to 5 urn diameter, and for a l l breathing conditions tested, to within 20% of measured values. Loss by f i l t r a t i o n in the nose or mouth of radon daughter a c t i v i t y attached to aerosols can be neglected. The few data available for unattached daughters (George and Breslin, 1969) indicate that about 50% of a c t i v i t y inhaled through the nose i s lost but only a negligible amount during mouth breathing. These values are consistent with human data obtained recently for a range of p a r t i c l e sizes down to 5 nm diameter ( S c h i l l e r , 1986) which suggest that nasal deposition e f f i c i e n c y increases with the square root of the p a r t i c l e d i f f u s i o n
405
Cells at Risk and Other Key Factors
29. JAMES
Weibel Ά'
ο Yeh-Schum
° UCI
1000
100 r~ ZV,
ΣΑ,
cm-
z
cm
90
» 3100
β
• 122
> 3200
ο •
'
ι 2500
85
,
100 10 •8 • •
10
0
5
Bronchial
15
10
15
10 generation
Figure 3 . Volumes and surface areas of airways i n each bronchial generation of the Weibel Ά ' , Yeh-Schum and UCI lung models, with t o t a l volumes 2 V and areas Σ Α .
02pm, •
3
1
3
OMpm.
~0-5£>m h'
Bifurcations
ο Airway -
1
~048m h-
lengths
Martin & Jacobi, 1972
2
Bronchial
3
U
5
6
1
2
3
4
5
generation
Figure 4. Deposition of submicrometer aerosols measured f o r c y c l i c flow through a hollow cast of the human bronchial tree, compared with calculated values.
6
406
RADON AND ITS DECAY PRODUCTS
c o e f f i c i e n t , under constant breathing conditions. However, the estimation of nasal f i l t r a t i o n of unattached radon daughters f o r different breathing rates and ages remains uncertain. Knowledge of the mechanism involved i s needed. Clearance Radon daughters are deposited on the surface of mucus l i n i n g the bronchi. I t i s generally assumed that the daughter nuclides, i.e. polonium-218 (RaA), lead-214 (RaB) and bismuth-214 (RaC), remain i n the mucus and are transported towards the head. However, one dosimetric model assumes that unattached radon daughters are rapidly absorbed into the blood (Jacobi and E i s f e l d , 1980). This has the effect of reducing dose by about a factor of two. Experiments in which lead-212 was i n s t i l l e d as free ions onto nasal epithelium i n rats have shown that only a minor f r a c t i o n i s absorbed rapidly into the blood (Greenhalgh et al., 1982). Most of the lead remained in the mucus but about 307o was not cleared in mucus and probably transferred to the epithelium. The absorption c h a r a c t e r i s t i c s of radon daughters remain somewhat uncertain, as do the rates of mucous clearance at various levels i n the bronchial tree. Accordingly, the effect on calculated doses of a range of assumed clearance behaviour i s examined below. It i s considered that the following postulates determine the possible range of doses: (i) insoluble daughters t o t a l l y transported i n mucus ( i i ) insoluble daughters with no clearance ( i i i ) p a r t i a l l y soluble daughters with 307» transferred to mucosal tissue.
Dose per unit exposure Figure 5 shows, on logarithmic scales, absorbed doses averaged over a l l e p i t h e l i a l c e l l s i n the bronchial and alveolar regions of the lung, f o r the wide range of aerosol size associated with radon daughters in room a i r . The size range can be divided into two bands, corresponding to unattached and attached daughters. The aerosol parameter determining dose i s the AMD ( a c t i v i t y median diameter). It i s assumed that free atoms and small ion clusters are 1 nm and 3 nm i n diameter, respectively. Larger attached species are assumed to be distributed i n p a r t i c l e s i z e , with geometric standard deviations of 1.5 at an AMD of 0.01 /jm and 2.0 f o r AMDs larger than 0.05 urn. A breathing rate of 0.75 m^ per h i s assumed to characterise domestic exposure of adult males (UNSCEAR, 1982; ΝΕΑ, 1983). Doses calculated using the Weibel Ά ' or UCI lung dimensions are uniformly about 307 higher than values obtained with the Yeh-Schum model (Figure 5). The bands of dose plotted here show variation due to the three different assumptions of clearance behaviour. The effect of clearance i s e n t i r e l y negligible for radon daughters attached to aerosols, but for unattached daughters, v a r i a b i l i t y in bronchial dose due to clearance amounts to about + 307 . Larger uncertainty could possibly be introduced by habitual mouth breathing. Conversely, o
o
29. JAMES
Cells at Risk and Other Key Factors
Unattached
|
|
407
Attached
AMD, ρ m
Figure 5. Doses averaged over a l l e p i t h e l i a l c e l l s i n the bronchial and alveolar regions of the lung per unit exposure to potential alpha-energy as a function of aerosol s i z e , compared with doses to basal c e l l s ; for several models of airway size and clearance behaviour.
408
RADON A N D ITS DECAY PRODUCTS
bronchial dose from unattached daughters i s r e l a t i v e l y independent of p a r t i c l e size, but the dose decreases markedly as the aerosol AMD becomes larger. Dose to a l v e o l i i s always less than 10% of that to the bronchi and can be safely neglected. The range of doses calculated when only basal c e l l s are assumed at r i s k i s also shown in Figure 5. For unattached daughters, doses are approximately one half and for attached daughters three quarters of values derived by averaging over a l l c e l l s . These doses are to be compared with the range derived by the ΝΕΑ (ΝΕΑ, 1983). The reference values recommended by the ΝΕΑ and adopted by UNSCEAR (UNSCEAR, 1982) l i e at the bottom of the range of doses to basal c e l l s derived here. Table II l i s t s values of mean bronchial dose obtained by weighting equally the results from a l l three lung models and clearance assumptions. I propose these as reference values.
Table I I . Reference Values of Mean Bronchial Dose from Exposure to 1 WLM Potential Alpha-energy in Homes Aerosol size (AMD, um) Unattached 0.05 0.1 0.15 0.2 0.3 0.4 - 0.5
Absorbed dose (mGy per WLM) 130 20 10 7 5 4 3
It can be concluded that mean bronchial dose i s inversely proportional to the AMD of the inspired aerosol over the size range 0.05 - 0.2 um. This corresponds to the range reported for room a i r under normal conditions (Reineking et ajL. , 1985). However, i t i s not certain that the size of radon daughter aerosols i s stable once inspired. It i s quite possible that they could grow rapidly to roughly double their ambient size by absorbing water (Martonen and Patel, 1981). In absolute terms, therefore, bronchial dose from the attached fraction of radon daughter a c t i v i t y could be as low as half that indicated by environmental measurements. It would be useful to resolve this uncertainty experimentally. Figure 6 shows doses averaged over e p i t h e l i a l c e l l s i n the segmental bronchi, i . e . generations 3 - 5. In t h i s case the Yeh-Schum and UCI lung dimensions give similar results, whereas the Weibel 'A' model alone gives results about 30% higher. The dose to shallow basal c e l l s assumed by the NCRP (NCRP, 1984) to represent exposure to the domestic radon daughter aerosol (0.125 ^jm diameter) l i e s within the range of values calculated here. Doses averaged over a l l e p i t h e l i a l c e l l s in segmental bronchi are seen i n Figure 6 to be uniformly double those to basal c e l l s only. In the case of unattached daughters, the l a t t e r are similar to the value of about 140 mGy per WLM assumed by the NCRP.
29.
JAMES
409
Cells at Risk and Other Key Factors
It can be seen by comparing Figures 5 and 6 that doses averaged over a l l c e l l s or to basal c e l l s alone are within a factor two of each other. Thus, irrespective of aerosol size, doses to segmental bronchi are s i m i l a r to the average value for the whole bronchial region. Within c e r t a i n bounds, the effect of increasing the size of c a r r i e r aerosol p a r t i c l e s , i . e . the attached f r a c t i o n of radon daughter a c t i v i t y , i s to reduce lung dose proportionally. The position i s more complex for unattached daughters. Increasing aerosol size in this range serves to reduce proportionally dose to the upper airways, i . e . segmental bronchi. However, this has the e f f e c t of increasing deposition and dose in smaller airways, maintaining the mean bronchial dose more or less constant. Influence of breathing rate. Figure 7 relates average doses to e p i t h e l i a l c e l l s at various breathing rates. Doses are normalised to values calculated at each aerosol size for an adult male breathing at the reference rate of 1.2 m^ per h ( c f . a miner) (ICRP, 1981). Apart from the values at unusually large aerosol sizes, results for both the bronchial region as a whole and for segmental bronchi are remarkably constant at each breathing rate. The l a t t e r are represented well by the fine broken lines which show values proportional to the square root of breathing rate. This relationship results from the combination of intake rate (simply proportional to breathing rate) and deposition probability, which has been shown in human subjects to be proportional to the square root of residence time i n the lung when deposition occurs predominantly by d i f f u s i o n (Gebhart and Heider, 1985). It can be concluded that uncertainties i n breathing rate are r e l a t i v e l y unimportant in determining lung dose and that dose varies with p a r t i c l e size in much the same manner over the whole physiological range of breathing rates. Age dependence The main parameters influencing lung dose as a function of age are the breathing rate and lung dimensions. Breathing rates have been assessed from data on dietary intake as a function of age (Adams, 1981). It i s assumed that oxygen consumption i s proportional to energy expenditure and thus dietary intake. The following expression has been developed (Adams, 1981) to relate the energy expenditure rate R i n a c h i l d of age t (years) and mass M(t) (kg) to that of an adult: R = (M(t)/70).exp[0.047(21 - t ) ] .
t < 21
Using this expression, with data on body weight as a function of age (Altman and Dittmer, 1972), one gets the breathing rates r e l a t i v e to adult values shown in Figure 8. These correspond to rates of 0.095, 0.34, 0.48 and 0.61 m 3 per h at b i r t h , 2, 6 and 10 years, respectively, r e l a t i v e to an adult rate of 0.75 m 3 per h. The ΝΕΑ and NCRP have assumed generally lower rates of intake by children (ΝΕΑ, 1983; NCRP, 1984). The UCI lung model (Phalen et a l . , i n press) includes for the f i r s t time measurements of airway diameter and length throughout the bronchial tree i n 20 lungs taken from children or young adults at various ages, including neo-natal specimens. Linear regressions of
RADON AND ITS DECAY PRODUCTS
7000 p-
Unattached κ \
Attached H
h
Mouth \
breathing
\
100 Weibel Ά' Yeh-Schum I UCI
è £
10
•δ c ο
Basal
I
φ
Q) I/)
0-1
_L
cells
NCRP 78
' I I I I I
1
001
0001 AMD,
01
0-5
pm
Figure 6. Doses averaged over e p i t h e l i a l c e l l s i n segmental bronchi per unit exposure to potential alpha-energy.
0-001 AMD,
001
0-1
0-5
pm
Figure 7. Doses to the bronchial region and segmental bronchi as a function of breathing rate, r e l a t i v e to values for miners breathing at 1.2 m^h" . 1
29.
JAMES
Cells at Risk and Other Key Factors
411
both diameter and length were reported for the trachea and 15 bronchial generations with respect to height. These functions can be used to scale for age the airway dimensions in each of the three models of adult lung discussed e a r l i e r . The resulting scaling factors for diameter and area are shown in Figure 9. It i s seen that the diameters of bronchioles (averaged over generations 11 - 15) vary l i t t l e with age. The increase in bronchial size i s greater, but s t i l l less than might be expected i f airways are simply scaled for overall body dimensions ( i l l u s t r a t e d by the dashed curves i n Figure 9, which are functions of body weight W). Since bronchiolar diameter does not change much with age i t i s l i k e l y that the thickness of bronchiolar epithelium i s also r e l a t i v e l y constant. However, in the case of the bronchi, i t i s reasonable to assume that e p i t h e l i a l thickness i s proportional to bronchial diameter. Thus, i t is necessary to use age dependent conversion factors between the surface density of alpha-decays and dose to c e l l s . The effect of these considerations on mean dose to e p i t h e l i a l c e l l s at various ages r e l a t i v e to adult values i s shown in Figure 10. It is seen that the mean bronchial dose i s only marginally increased in young children. This effect i s smaller than the age dependence considered e a r l i e r (ΝΕΑ, 1983; NCRP, 1984) and can surely be regarded as i n s i g n i f i c a n t . A greater age dependence of dose to segmental bronchi i s shown i n Figure 10, but this i s s t i l l not large except for neonates. Dose conversion factors It has been shown elsewhere that the individual radon daughters, ie RaA, RaB and RaC, contribute to lung dose s t r i c t l y in proportion to the amount of potential alpha-energy associated with each radionuclide and not in proportion to their individual a c t i v i t i e s (Jacobi and E i s f e l d , 1980; James, 1984). This leads to the theoretical expectation that r i s k i s proportional to the special quantity 'exposure to potential alpha-energy', under otherwise similar environmental conditions (ΝΕΑ, 1983; ICRP, 1981). In p r a c t i c e , i t i s often neither possible nor convenient to monitor 'exposure to potential alpha-energy', whereas monitoring of exposure to radon gas by means of the time-integral of the radon concentration in a i r i s r e l a t i v e l y straightforward (ΝΕΑ, 1985). Hence, the additional parameter F, known as the equilibrium factor, has been devised for p r a c t i c a l application (UNSCEAR, 1982). F expresses the airborne concentration of potential alpha-energy as a fraction of the highest possible value achieved when a l l the daughters have the same a c t i v i t y as the measured radon gas. Thus, the potential alpha-energy concentration i s 1 WL when the radon concentration i s 3700 Bq per m3 and F = 1, i . e . radon and daughters are i n radioactive equilibrium. The annual exposure to potential alpha-energy, Ε , i s then related to the average radon concentration, C_ by: ^ Rn
E
p
[WLM]
= F χ C
Rn
[Bq m"3]
χ η χ 8760 / 170 / 3700
where 8760 = number of hours per year 170 = number of hours per working month η = fraction of time spent indoors (occupancy)
RADON AND ITS DECAY PRODUCTS
1-2
r
Age,
Figure 8.
y
Breathing rate and body weight as a function of age.
Diameter
S
q
ιι
ι
ι
0 2 Age,
6
ι 10
Area
ι 21
Iι ι 0 2
1 6
1
1
10
21
y
Figure 9. Diameters and surface areas of bronchial airways as a function of age, according to the UCI lung model.
29. JAMES
Cells at Risk and Other Key Factors
413
Taking η as 0.8 (UNSCEAR, 1982; ΝΕΑ, 1983), the annual exposure to potential alpha-energy i s given by F χ 0.011 (WLM per y per Bq m-3). This conversion procedure can be used with dosimetric factors chosen from here or elsewhere to estimate dose rates as a function of the average radon gas concentration for different environmental conditions. A conversion factor of 130 mGy per WLM i s recommended here (Table II) for that part of the exposure associated with unattached daughters, i . e . the unattached f r a c t i o n . However, for the attached fraction, i t i s necessary to specify the aerosol AMD, bearing in mind that dose i s inversely proportional to AMD. A value of 0.12 pm may well be t y p i c a l of domestic rooms. In this case, a dose conversion of about 8 mGy per WLM i s recommended (Table I I ) . It should be noted here that the numerical factor could be as high as 20 under unusual conditions (Reineking et a l . , 1985), or as low as 4 i f aerosol growth in the humid airways of the lung i s i n fact s i g n i f i c a n t . Figure 11 shows the annual absorbed doses, D^ , calculated by applying these recommended dose conversions to the range of unattached fractions and equilibrium factors that might normally be encountered in rooms (Porstendôrfer, 1984). The equilibrium factor, F, generally increases with aerosol concentration. This w i l l lead to a proportionally higher t o t a l exposure to potential alpha-energy for a given concentration of radon gas in room a i r . However, the fraction of the exposure associated with unattached daughters, fp , decreases dramatically for high F. The net effect of these changes i s that the dose rate for a given radon concentration i s r e l a t i v e l y independent of room conditions. On this basis, a single conversion factor could be recommended, with a value somewhere between 50 and 100 uGy per y per Bq m-3 radon gas concentration. It i s to be noted that the conversion factor of 20 mSv effective dose equivalent per 200 Bq m""3 equilibrium equivalent radon concentration, considered by the ICRP (ICRP, 1984) i n recommending an 'Action Level' for remedying high indoor radon concentrations, corresponds to a dose rate of about 40 uGy per y per Bq m~3 radon gas concentration. Effective dose equivalent. If i t i s assumed that the weighting factor for bronchial dose equivalent i s 0.06, the unattached fraction of potential alpha-energy i n room a i r i s t y p i c a l l y about 5%, and that the aerosol AMD i s t y p i c a l l y 0.12 ρ (Reineking et aJL. , 1985), the dosimetry developed here gives a conversion factor to effective dose equivalent of approximately 15 mSv per WLM exposure i n homes. This i s three times higher than the value commonly used (UNSCEAR, 1982). Conclusions (i) In order to assess r i s k , i t now seems more defensible to consider the average dose to a l l e p i t h e l i a l c e l l s than just the dose to deeplying basal c e l l s . A dosimetric model formulated i n this way gives mean bronchial doses higher than heretofore by about 60% for the unattached f r a c t i o n of potential alpha-energy and about 30% for radon daughters attached to room aerosols.
RADON AND ITS DECAY PRODUCTS
414
AMD,
pm
Figure 10. Doses to the bronchial region (solid curves) and to segmental bronchi i n newborn infants and children of various ages, r e l a t i v e to values for adults.
0-25 r
020
QQ
015
Q)
.S •g ο
0-10 Q)
005
I 0 1
ο 5
^
Aerosol
concentration,
Z,
^ Ci
cm~^
Figure 11. Variation of unattached f r a c t i o n of potential alphaenergy and equilibrium factor according to a model of room aerosol behaviour and the effect on bronchial dose rate per unit radon gas concentration.
29. JAMES
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(ii) Refinement of the assumptions made in modelling lung deposition and clearance, based on recent experimental data, leads to an estimate of absorbed dose per unit exposure to unattached daughters three times higher than that adopted by UNSCEAR (UNSCEAR, 1982). The new value of 130 mGy per WLM is similar to that recommended by NCRP (NCRP, 1984). (iii) This pointer to higher dose conversion factors is reinforced by an emerging congruence of experimental results, indicating that exposure to unattached daughters is higher in homes than previously assumed and that the attached aerosol is typically smaller. The combined effect of these factors suggests an increase in the estimate of conversion factor to effective dose equivalent in homes by a factor of three, to about 15 mSv per WLM. (iv) It has been shown that both breathing rate and age are minor factors in determining dose per unit exposure. (v) According to the dose conversion factors developed here and current understanding of the inverse relationship between equilibrium factor and unattached fraction, lung dose rate is simply proportional to the radon gas concentration over a wide range of conditions. This has beneficial implications for domestic and occupational monitoring schemes. (vi) In order to reinforce or refute these conclusions priority should be given to experimental studies and predictive modelling of aerosol size and unattached fraction in room air. It is important also to know if radon daughter aerosols grow significantly in size at physiological humidity and to refine our understanding of nasal deposition of unattached daughters. Acknowledgment This work was partly funded by the Commission of the European Communities, under contract BI6-116-UK. References Adams, Ν., Dependence on Age at Intake of Committed Dose Equivalents from Radionuclides, Phys. Med. Biol. 26:1019-1034 (1981). Altman, P.L. and D.S. Dittmer, Biology Data Book, Vol 1, pp. 195-201, Federation of American Societies for Experimental Biology, Bethesda, MD (1972). Bair, W.J., ICRP Work in Progress: Task Group to Review Models of the Respiratory Tract, Radiol. Prot. Bull. 63:5-6 (1985). Chamberlain, A.C. and E.D. Dyson, The Dose to the Trachea and Bronchi from the Decay Products of Radon and Thoron, Br. J. Radiol. 29:317-325 (1956). Cohen, B.S., N.H. Harley, R.B. Schlesinger and M. Lippmann, Nonuniform Particle Deposition on Tracheobronchial Airways: Implications for Lung Dosimetry, Ann, occup. Hyg. in press. Egan, M.J. and W. Nixon, A Model of Aerosol Deposition in the Lung for Use in Inhalation Dose Assessments, Radiat. Prot. Dosim. 11:5-17 (1985).
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RADON AND ITS DECAY PRODUCTS
Ellett, W.H. and N.S. Nelson, Epidemiology and Risk Assessment, in Indoor Air and Human Health (R.B. Gammage and S.V. Kaye, eds) pp. 79-107, Lewis, Chelsea, MI (1985). Gastineau, R.M., P.J. Walsh and N. Underwood, Thickness of Bronchial Epithelium with Relation to Exposure to Radon, Health Phys. 23:857-860 (1972). Gebhart, J. and J. Heyder, Removal of Aerosol Particles from Stationary Air within Porous Media, J. Aerosol Sci. 16:175-187 (1985). George, A.C. and A.J. Breslin, Deposition of Radon Daughters in Humans Exposed to Uranium Mine Atmospheres, Health Phys. 17:115-124 (1969). Greenhalgh, J.R., A. Birchall, A.C. James, H. Smith and A. Hodgson, Differential Retention of Pb-212 Ions and Insoluble Particles in Nasal Mucosa of the Rat, Phys. Med. Biol. 27:837-851 (1982). Harley, N.H. and B.S. Pasternack, Environmental Radon Daughter Alpha Dose Factors in a Five-lobed Human Lung, Health Phys. 42:789-799 (1982). Hofmann, W., Dose Calculations for the Respiratory Tract from Inhaled Natural Radionuclides as a Function of Age - II. Basal Cell Dose Distributions and Associated Lung Cancer Risk, Health Phys. 43:31-44 (1982). ICRP; International Commission on Radiological Protection, Limits for Inhalation of Radon Daughters by Workers, Publication 32, Ann, of ICRP 6:1-24 (1981). ICRP; International Commission on Radiological Protection, Principles for Limiting Exposure of the Public to Natural Sources of Radiation, Publication 39, Ann. of ICRP 14:1-8 (1984). Ingham, D.B., Diffusion of Aerosols from a Stream Flowing through a Cylindrical Tube, Aerosol Sci. 6:125-132 (1975). Jacobi, W. and K. Eisfeld, Dose to Tissues and Effective Dose Equivalent by Inhalation of Radon-222, Radon-220 and their Short-lived Daughters, GSF Report S-626, Gesellschaft fur Strahlen-und Umweltforschung, Munich-Neuherberg (1980). Jacobi, W. and H.G. Paretzke, Risk Assessment for Indoor Exposure to Radon Daughters, Sci. Total Environ. 45:551-562 (1985). James, A.C., J.R. Greenhalgh and A. Birchall, A Dosimetric Model for Tissues of the Human Respiratory Tract at Risk from Inhaled Radon and Thoron Daughters, in Radiation Protection. A Systematic Approach to Safety, Vol 2, pp. 1045-1048, Pergamon, Oxford (1980). James,A.C.,Dosimetric Approaches to Risk Assessment for Indoor Exposure to Radon Daughters,Radiat.Prot. Dosim. 7:353-366 (1984).
29. JAMES
417
Cells at Risk and Other Key Factors
James, A.C., Dosimetric Assessment of Risk from Exposure to Radioactivity in Mine Air, in Occupational Radiation Safety in Mining (H. Stocker, ed) Vol 2, pp. 415-425, Canadian Nuclear Association, Toronto (1985). Martin, D. and W. Jacobi, Diffusion Deposition of Small-sized Particles in the Bronchial Tree, Health Phys. 23:23-29 (1972). Martonen, T.B. and M. Patel, Modelling the Dose Distribution of HSO Aerosols in the Human Tracheobronchial Tree, Am. Ind. Hyg. Assoc. J. 42:453-460 (1981). 2
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Masse, R., Cells at Risk, in Lung Modelling for Inhalation of Radioactive Materials (H. Smith and G. Gerber, eds) pp. 227-246, EUR 9384 EN, CEC, Brussels (1984). NCRP; National Council on Radiological Protection, Evaluation of Occupational and Environmental Exposures to Radon and Radon Daughters in the United States, NCRP Report No. 78, Bethesda, MD (1984). ΝΕΑ; Nuclear Energy Agency Group of Experts, Dosimetry Aspects of Exposure to Radon and Thoron Daughter Products, OECD Nuclear Energy Agency, Paris (1983). ΝΕΑ; Nuclear Energy Agency Group of Experts, Metrology and Monitoring of Radon, Thoron and their Daughter Products, OECD Nuclear Energy Agency, Paris (1985). Phalen, R.F., M.J. Oldham, C.B. Beaucage, T.T. Crocker and J.D. Mortensen, Postnatal Enlargement of Human Tracheobronchial Airways and Implications for Particle Deposition, Anat. Rec. in press. Pich, J., Theory of Gravitational Deposition of Particles from Laminar Flow in Channels, Aerosol Sci. 3:351-361 (1972). Porstendörfer, J., Behaviour of Radon Daughter Products in Indoor Air, Radiat. Prot. Dosim. 7:107-113 (1984). Reineking, Α., Κ.Η. Becker and J. Porstendôrfer, Measurements of the Unattached Fractions of Radon Daughters in Houses, Sci. Total Environ. 45:261-270 (1985). Rudolf, G., J. Gebhart, J. Heyder, C. Schiller and W. Stahlhofen, An Empirical Formula Describing Aerosol Deposition in Man for Any Particle Size, J. Aerosol Sci. 17:350-355 (1986). Saccomanno, G., V.E. Archer, O. Auerbach, M. Kuschner, M. Egger, S. Wood and R. Mick, Age Factor in Histological Type of Lung Cancer in Uranium Miners, a Preliminary Report, in Radiation Hazards in Mining (M. Gomez, ed) pp. 675-679, Society of Mining Engineers, New York (1982).
418
RADON AND ITS DECAY PRODUCTS
Schiller, Ch.F., Diffusionsabscheidung von Aerosolteilchen im Atemtrakt des Menshen. PhD Thesis, J.W. Goethe-Universitat, Frankfurt/Main (1986). Spencer, Η., Carcinoma of the Lung, in Pathology of the Lung, Vol 2, pp. 773-859, Pergamon, Oxford (1977). Trump, B.E., E.M. McDowell, F. Glavin, L.A. Barrett, P. Becci, W. Schurch, H.C. Kaiser and C.C. Harris, The Respiratory Epithelium IV. Histogenesis of Epidermoid Metaplasia and Carcinoma in Situ in the Human, J. Natl. Cancer Inst. 61:563-575 (1978). UNSCEAR; United Nations Scientific Committee on the Effects of Atomic Radiation, Ionizing Radiations: Sources and Biological Effects, Report to the General Assembly, Annex D, United Nations, New York (1982). Weibel, E.R., Morphometry of the Human Lung, Academic Press, New York (1963). Wise, K.N., Dose Conversion Factors for Radon Daughters in Underground and Open-cut Mine Atmospheres, Health Phys. 43:53-64 (1982). Yeh, H.C. and G.M. Schum, Models of Human Lung Airways and Their Application to Inhaled Particle Deposition, Bull. Math. Biol. 42:461-480 (1980). Yu, C.P. and C.K. Diu, A Comparative Study of Aerosol Deposition in Different Lung Models, Am. Ind. Hyg. Assoc. J. 43:54-65 (1982). RECEIVED November 13, 1986