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OCR for page 24
2
Radon
INTRODUCTION
Of the several isotopes of radon, radon-222 has the most im-
portant impact on human health (see the box entitled "Isotopes of
Radons. An inert gas at temperatures above -61.8°C, radon-222 is
a naturally occurring decay product of radium-226, the fifth daugh-
ter of uranium-238. Both uranium-238 and radium-226 are present
in most soils and rocks in widely varied concentrations.2t As radon
forms from the decay of radium-226, it can leave the soil or rock
and enter the surrounding air or water. Radon gas thus becomes
ubiquitous, and its concentration is increased by the presence of a
rich source and by low ventilation in the vicinity of a source. As
illustrated in Figure 2.1, radon decays with a half-life of 3.82 days
into a series of solid, short-lived radioisotopes collectively referred to
as radon daughters or progeny (Figure 2-1) (see Annex 2B). Two of
these daughters, polonium-218 and polonium-214, emit alpha parti-
cles, which, when emission occurs in the lung, can damage the cells
lining the airways. The resulting biological changes can ultimately
lead to lung cancer.
Underground mining was the first occupation associated with
an increased risk of lung cancer. Uranium ores contain particularly
high concentrations of radium, and radon-daughter exposure has
been associated with Jung cancer in uranium miners. Miners of other
types of ore can also be placed at risk by the combination of a
sufficiently strong source of radon and inadequate ventilation.
24
OCR for page 25
RADON
25
ISOTOPES OF RADON
The committee's discussion of radon is limited to radon-
222, the most common isotope. Other radioisotopes of radon-
radon-219 (actinon) and radon-220 (thoron) occur naturally
and have alpha-emitting decay products. Actinon has an ex-
tremely short half-life (3.9 s). Accordingly, concentrations of
actinon and its daughters are extremely low, and decay of acti-
non contributes little to human exposure. Because of its short
hal£life (56 s), the concentration of thoron is also usually low.
Dosimetric considerations suggest that the dose to the tracheo-
bronchial epithelium from thoron progeny is, for an equal con-
centration of inhaled alpha energy, less by a factor of 3 than
that due to the progeny of radon-222.26 The potential for Jung
cancer due to inhalation of thoron cannot be addressed directly,
because the available epidem~ological data are based almost
exclusively on exposures to radon-222 and its daughters.
Radon progeny are also present in the air of dwellings. Their
source Is the underlying soil, but building materials, water used
routinely in the building, and utility natural gas also contribute. The
concentration of radon progeny in dwellings is highly variable and
depends mainly on the pressure in the house and on the ventilation.
Because of their wide distribution, radon daughters are a major
source of exposure to radioactivity for the general public, as well as
for special occupational groups. The estimated dose to the~bronchial
epithelium from radon daughters far exceeds that to any other organ
from natural background radiation.20 The recent recognition that
some homes have high concentrations of radon has focused concern on
the potential lung-cancer risk associated with environmental radon.
Measured concentrations of radon in homes in the United States
appear to follow a log-normal distribution.24
In addressing the risks associated with radon exposure, the com-
mittee responsible for this report considered the extensive infor-
mation accumulated during nearly a century of research on radon.
Epidemiological studies have described the risks associated with
radon-daughter exposure of underground miners; animal studies have
provided complementary data; and experimental and theoretical re-
search has provided insights into radon-daughter carcinogenesis. The
OCR for page 26
26
MASS
NUMBER
I t620y
, 1
RADON
~ 3.82d
218
214
210
206
HEALTH RISKS OF RAD ON AND O THER ALPHA-EMT TTERS
. _
.
... '...,
3.05m · ·.~ ASTATINE ~ RADON
(RAD!UM A) 0.019% .
. .,, ..
c~4 ~ ~
LEAD ~ ~ 1 ~ BISM ;T;I ·
' 26.8m · ~ ' 19.7m . . .
(RADIUM B) ~ _ (RADIUM C)
/3 ,POLOI IIUM.'
. ~ 0.0001648
_ (RADIUM C'
_ - · ~
THALLIUM | ~ _
3.1m
THE SHORT-LIVED
RADON DAUGHTERS
LEAD ,l3 _ r
22y ~
..
cx 0.000002% a 0.00013% crow
~1: I POLONIUM |
Sd r 138d
z~ ~
FIGURE 2.1 The radon decay chain. An arrow pointing downward indicates
a decay by alpha-particle emission; an arrow pointing to the right indicates a
decay by beta-particle emission. The historical symbols for the nuclides are in
parentheses below the modern symbols. Most of the decays take place along
the unbranched chain marked by the double arrows. The negligible percentage
of the decays going along the single arrows is shown at critical points. The end
of the chain, lead-206, is stable, not radioactive. Half-lives are shown for each
isotope with ~ = seconds, m = minutes, d = days, and y = years.
research, described in detail in the appendixes of this report, is briefly
summarized below.
DOSIMETRY
By convention, the concentration of radon daughters is mea-
sured In working levels (WL), and cumulative exposures over time
are measured in working-level months (WI.M) (see box entitled ~Spe-
cial Quantities and Units for Radon Exposures"~. As described in
Annex 2B, the relationship between exposure, measured as WI,M,
OCR for page 27
RADON
27
SPECIAL QUANTITIES AND UNITS
FOR RADON EXPOSURES
The working level (WL) is defined as any combination of
the short-lived radon daughters in 1 liter of air that results
in the ultimate release of 1.3 x 105 MeV of potential alpha
energy. As detailed in Annex 2B, this is approx~rnately the
amount of alpha energy emitted by the short-hal£life daughters
in equilibrium with 100 psi of radon. Exposure of a ratter to
this concentration for a working month of 170 h (or twice this
concentration for half as long, etc.) is defined as a working-level
month (W~M). Note that the cumulative exposure in W[M ~
the sum of the products of radon-progeny concentrations and
the tunes of exposure. For historical reasons, time is quantified
into blocks of 170 h when the concentration is expressed in WL.
This can lead to confusion in domestic environments, because a
3(}day month is 720 h. Exposure to ~ WL for 720 h results in
a cumulative exposure of 4.235 W[M. Home occupancy for 12
in/day at 1 WL would result in a cumulative exposure of about
2.12 W[M per month of occupancy.
and dose to target cells and tissues in the respiratory tract is ex-
tremely complex and depends on both biological and nonbiological
factors.20 Because of differences in the circumstances of exposure, it
cannot be assumed a priori that exposure to 1 W[M in a home and
to ~ W[M in a mine will result in the same dose of alpha radiation
to cells in the target tissues of the respiratory tract. Thus, an under-
standing of the dosimetry of radon daughters in the respiratory tract
is essential for extrapolating risk estimates derived from epidem~o-
logical studies of miners to the general population in indoor domestic
environments. Factors influencing the dosimetry of radon daughters
include physical characteristics of the inhaled air, breathing patterns,
and the biological characteristics of~the Jung (Table 2.1~.
Radon daughters are initially formed as condensation nuclei.
Although most of these attach to aerosols immediately after forma-
tion, a variable proportion remain unattached and are referred to as
the unattached fraction. This fraction is an important determinant
of the dose received by target cells; as the unattached fraction in-
creases, the dose also increases because of the efficient deposition of
OCR for page 28
28
HEALTH RISKS OF RADON AND OTHER ALPNA-E3MITTERS
TABLE 2-1 Factors Influencing the Dose to Target
Cells in the Respiratory Tract from Radon Exposure
Characteristics of Inhaled Air
Fraction of daughters unattached to particles
Aerosol characteristics
Equilibrium of radon with its daughters
Breathing Pattern
Tidal volume
Respiratory frequency
Nose or mouth breathing
Characteristics of Lung
Bronchial morphometry
Mucociliary clearance rate
Mucus thickness
Location of target cells
the unattached daughters in the airways. The particle size distribu-
tion in the inhaled air also influences the dose to the airways, because
particles of different sizes deposit preferentially in different genera-
tions of the Jung airways. The specific mixture of radon daughters
also affects the dose to target cells, but to a smaller extent.
The amount of radon daughters inhaled varies directly with the
minute ventilation, i.e., the total volume of air inhaled In each minute.
The deposition of radon daughters within the lungs, however, does
not depend in a simple fashion on the minute ventilation, but varies
with the flow rates in each airway generation. The flow rates vary
with both tidal volume and breathing frequency. The proportions of
oral and nasal breathing also influence the relationship between ex-
posure and dose. A substantial proportion of the unattached radon
daughters deposits in the nose with nasal breathing, whereas it is
likely that a smaller fraction deposits in the mouth with oral breath-
~ng.
Characteristics of the lung also influence the relationship be-
tween exposure and dose (Table ~-1~. The sizes and branching pat-
terns of the airways affect depositions and can differ between children
and adults and between males and females. The rate of mucociliary
clearance and the thickness of the mucus layer in the airways also
enter into dose calculations, as does the location of the target cells
in the bronchial epithelium. As outlined in Part 3 of Appendix VIT,
smoking and presumably other pollutants modulate these factors.
The effect of the physical and biological factors outlined in Table 2-1
on the dosimetry of radon daughters can be estimated by computer
modeling (see Annex 2B). The committee used the results of such
OCR for page 29
RADON
29
models to provide guidance on estimating the risk of lung cancer due
to radon in indoor environments.
HUMAN AND ANIMAL STUDIES
The association of radon-daughter exposure with human lung
cancer has been the subject of extensive epidemiological studies of
underground miners. The {ung-cancer hazard faced by underground
miners was first recognized by Harting and Hesse in 18797 on the
basis of their autopsy observations of European miners. Excess Jung-
cancer occurrence has been found in uranium miners in the United
States, Czechoslovakia, France, and Canada and in other under-
ground miners exposed to radon daughters, including Newfoundland
fluorspar miners, Swedish metal miners, British iron and tin miners,
Trench iron miners, Chinese tin miners, and American metal miners
(see Appendix IV). Epidemiological studies of these mining groups
have shown increasing lung-cancer risk as cumulative exposure to
radon daughters increases and have provided some insights into the
combined effects of cigarette smoking and radon-daughter exposure
(see Appendix VIl).
Exposures of animals to radon and its daughters have con-
firmed that exposure to radon daughters causes lung cancer (see Ap-
pendix HI). Animal experiments have also provided data on exposure-
response relationships and on the modifying effects of exposure rate
and the physical characteristics of the inhaled radon (see Appendix
NIT). Animal models have proved less useful for studying the inter-
action of radon daughters with cigarette smoking because of the
difficulties of replicating smoking patterns in humans with animals.
The committee also considered relevant information from the
extensive literature on the biology and epidemiology of lung cancer.
This malignancy, although relatively uncommon at the start of the
twentieth century, has become the leading cause of cancer death in
the United States.35 Most lung cancers are caused by cigarette smok-
ing; only 5-10%0 of the total cases occur in lifelong nonsmokers.35 38
In cigarette smokers, the risk of developing lung cancer increases
with the number of cigarettes smoked daily and with the number of
years of smoking.3 35 The risk of Jung cancer for a smoker is some 10
times higher than that for a nonsmoker, and up to 20 times higher
for heavy smokers. Because cigarette smoking predominates as the
cause of Jung cancer, the committee needed to address separately the
risks of radon-daughter exposure for smokers and for nonsmokers.
OCR for page 30
30
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
The committee's analyses of the interaction between radiation and
smoking are cliscussed in Part 2 of Appendix VIl.
The committee was faced with the challenge of using the epidemi-
ological and experunental evidence in combination with its under-
standing of the dosimetry of radon daughters to address the topical
issue of exposure In domestic environments. This followed from the
charge to the committee to develop risk coefficients applicable to
exposure to radon in homes. The rationale for this charge emerges
from recognition of the potential for radon in domestic environments
as a public-health hazard. The urgency of completing this task has
increased as more data have become available on indoor radon in
the United States. Radon concentrations in American homes have
not been systematically surveyed, but available data indicate that
some homes have levels approaching or greater than the control lev-
els in underground mines.25 Radon daughters are also a hazard for
underground miners. Thus, the committee was also charged with ad-
dressing the risks for occupational exposure to underground miners.
Other expert groups and individual investigators have derived
risk estimates for radon-daughter exposure (see Appendix VIl). The
approaches have been diverse and based variously on the epidemi-
ological data, on extensive dosimetric modeling, and on informal
expert judgment. The resulting risk estimates have a wide range.
The committee did not select any of the published lung-cancer risk
estimates associated with exposure to radon and its progeny as ap-
propriate for meeting its charge.
THE COMMITTEE'S APPROACH TO ESTIMATION OF LUNG-
CANCER RISK
Evaluation of the lung-cancer risk associated with radon daugh-
ters was the most challenging task faced by the committee. Nu-
merous studies of underground miners exposed to radon daughters
have shown an increased risk of lung cancer, in comparison with un-
exposed populations. Animal studies have confirmed this risk, and
the development of multicomponent dosimetric mo~lels has provided
an understanding of factors influencing the carcinogenic potential of
exposure. However, the human data are for occupational exposure
in an underground environment and do not address directly the risks
at the generally lower levels of exposure that are typically of concern
in the home.
OCR for page 31
RADON
31
Two approaches that have been used previously to characterize
the risks associated with radon-daughter exposure were considered
by the committee: dosimetric models of the respiratory tract and
statistical models applied to one or more of the epidemiological data
sets. The dosunetric approach provides an estimate of risk that is
based on modeling the dose to target cells in the respiratory tract. Di-
verse dosimetric models have been developed; all require assumptions
(some not subject to direct verification) concerning the deposition of
radon daughters in the Jung and the nature and location of the tar-
get cells for cancer induction. Additional assumptions concerning the
carcinogenic potential of alpha radiation in the respiratory tract are
also required. The comrn~ttee preferred an epidem~ological approach
that provides risk coefficients based directly on the substantial body
of available human data. While the committee did not use dosimet-
ric models for calculating the lung-cancer risk coefficients, it found
such models useful in applying its risk model, derived from studies
of underground miners, to the general population.
Rather than basing its risk estimates solely on review of pub
fished reports, the committee obtained and analyzed the original
exposure and follow-up data from four of the most important epi-
demiological studies of underground miners (see the next section).
Each of the studies has limitations, but a combined analysis of these
major data sets permitted a comprehensive assessment of the risk
associated with radon-daughter exposure and other factors influenc-
ing this risk. In analyzing the epidem~ological data, the committee
used a descriptive approach, rather than methods based on models
of carcinogenesis. The comm~ttee's analytical approach was appro-
priate for meeting its charge with a minimum of assumptions as to
the underlying mechanisms of cancer initiation and promotion. Al-
though a few epidemiological studies of Jung-cancer risk associated
with indoor domestic exposure to radon have been reported, these
studies have been preliminary and are inadequate for the purpose of
risk estimation. In the future, however, epidemiological studies of
indoor exposure may serve as a basis for lung-cancer risk estimates.
THE COMMITTEE'S ANALYSIS OF THE RISK OF LUNG
CANCER ASSOCIATED WITH EXPOSURE TO
RADON PROGENY
The committee's risk estimates for radon-daughter exposures are
based largely on its own reanalysis of the four principal data sets on
OCR for page 32
32
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
the epidemiological follow-up of underground miners. The commit-
tee obtained data based on two Canadian uranium-miner cohorts,
Eldorado Beaveriodget° and Ontario;~7~~9 on Swedish iron miners,
MaImberget;29 and on Colorado Plateau uranium miners. 9 i2 t3 37
(see box entitled "Characteristics of the Four Underground-Miner
Groups Analyzed by the Committees. The committee attempted
to obtain comparable data from the studies of Czechoslovakian ura-
nium miners, but was unsuccessful. For the first three of the cohorts,
we obtained data on individual miners; for the Colorado cohort, we
were able to obtain only detailed summaries of the type described
below. Some of the miners in the Colorado cohort were occupa-
tionally exposed to radon progeny prior to their employment in
uranium mines. Although exposures have been estimated for this
earlier period,~3 their accuracy is uncertain and they were not con-
sidered in the committee's analysis. Cigarette-smoking information
on all exposed subjects was available only for the Colorado cohort, so
the comm~ttee's primary dose-response analysis does not include this
factor. However, the committee's analyses of the combined effects
of smoking and radon exposure on the Colorado cohort, described
in Appendix VII, support the results presented here (and in Annex
2A).
Recent developments in statistical methods have provided better
approaches for analyzing data from occupational-cohort studies than
were available when these data were first analyzed. With these mul-
tivariate methods for analysm of the data, it is possible to examine
systematically many aspects of risk estimation that have been the
most uncertain in the past, particularly the temporal patterns of
excess risk. By analyzing the combined data from the four cohort
populations, it was the comm~ttee's intent to gain a clearer under-
standing of appropriate models for describing the risk associated with
exposure and to obtain a more meaningful comparison of the risks in
these primary cohorts.
The committee first carried out separate but parallel analyses
of the four cohorts to gain a clearer understanding of the determi-
nants of risk within each. The committee then carried out a formal
analysis of the combined cohort data to obtain better estimates of
the effects that seemed important and consistent in the separate
analyses. This approach led to the development of a relative-risk
time-since-exposure model, based on the combined data, which is
more complex than ordinarily used for estimating radiation risks.
However, it Is the simplest mathematical expression that adequately
OCR for page 33
33
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OCR for page 34
34
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
describes the level and temporal pattern of risk in the four cohorts.
This section provides a summary of the committee's approach and
results. Detailed discussion of our statistical models and methods
and of their application to these cohort data is given in Annex 2A.
Undoubtedly, many factors influence the occurrence of lung can-
cer in miners exposed to radon daughters. In carrying out its own
original analyses of the data on the cohorts, the committee focused
on the following potential risk factors: cumulative exposure, dura-
tion of exposure, age at which risk is being evaluated, age at first
exposure, time since cessation of exposure, and time since each part
of the exposure. In the one cohort for which it was possible to do
so (the Colorado Plateau uranium miners), the ejects of smoking
were also evaluated. The original investigators of these data relied
primarily on calculation of standardized mortality ratios (SMRs) by
exposure category, a method that provides a useful but limited anal-
ysis of the data. In addition to a thorough investigation of effects
of the above risk factors, a substantial part of the analysis was in
terms of comparisons purely within the cohort data, as opposed to
comparison with data on external populations, as in analyses based
on SMRs.
STATISTICAL MODELS AND METHODS
The committee's general approach was to examine how the age-
specific relative risk depends on the variables of interest. This was
done by making a cross-classification of numbers of Jung-cancer
cleaths and person-years at risk, by categories of these variables,
and then fitting models to the rates given by the ratio of deaths to
person-years in such a tabular cross-classification. The committee
fitted regression models with a Poisson probability mode] for the
number of deaths in each cell of the table, where the expected value
was taken as the product of the person-years at risk for the cell and
a cancer rate given by a parametric model. For the case of purely
internal cohort comparisons, not relying on external rates, this is a
grouped-data analog of the widely used Cox relative-risk regression
method.2 For the case of comparison with external rates, it is a gen-
eralization of standard SMR methods that provides more detailed
examination of the relative risk. (A very useful reference for these
methods is the survey paper by Bresiow.~)
The parametric models for this analysis were expressed in terms
of the excess relative risk, that is, the ratio of the excess risk to the
OCR for page 148
148 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
1.2
e
1.0
15~ 0.8
Oh
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Cal
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Or
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T
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10 15 20
BREATHING RATE l/min
FIGURE 2B-4 Mean bronchial dose as a function of minute volume.26
30
generations by as much as 50%, so that the total deposition in-
creases less rapidly than the increased alpha energy inhaled. Re-
cently, James27 has reported that the total deposition is proportional
to the square root of the minute volume over the range of particle
sizes in which deposition is due to particle diffusion.
The variation in the mean bronchial dose as a function of minute
volume for the three models is shown in Figure 2~4 for particles with
an AMAD of 0.15 ,um. Note that the curves are concave downward
because of the square root variation of dose with minute volume.
In summary, the results of efforts to mode! the dose to the Jung
show significant differences in the estimates of the dose per unit of
exposure in the tracheobronchial region of the lung: factors of 2 to
3 are typical. Unfortunately, there are few experimental data with
which these estimates can be compared, so it Is not possible to make
a fully informed choice among the models on the basis of measure-
ments. Recently, Cohen4 has reported on measurements leading to
correction factors of about 2 in an updated H-P five-Iobe mode.
OCR for page 149
RADON DOSIMETRY
149
Furthermore, some recent experiments indicate that the dose at bi-
furcations is not uniform and may be considerably larger than those
calculated with current models.3i These observations have not, how-
ever, been confirmed by Cohen's studies.4 Although the deposition
pattern predicted by any particular mode! cannot be validated in
viva, the average deposition patterns (and hence, the average dose)
for all the models are sufficiently s~rnilar so that any of them can be
used with about equal confidence.
Even though these three lung models give different values for
any particular case, the dose estimates are converging as more infor-
mation becomes available. A survey of dose calculations for miners
made in the period 1951-1981 by the National Council on Radiation
Protection and Measurements (NCRP)34 included 28 calculations
of the dose per W[M to the bronchial tissue. The results ranged
from 0.7 to 140 mGy/W[M (0.07 to 14 rad/W[M). In addition to
differences in the loci of the bronchi for which the dose was calcu-
lated, differences in input values of the parameters describing the
radon daughters in the air and of the parameters characterizing the
dosimetry models were responsible for much of the spread. Jacobi22
estimated that input of the same aerosol characteristics into these
models would reduce the spread to about 3 to 10 mGy/W[M (0.3
to 1 rad/W[M). Agreement is even better when the average dose
to the trachealobronchial tree is calculated. For the most advanced
calculations models, the variation in mean doses can be as little as
20~o.35 However, the degree of agreement is better for some aerosol
distributions then others, being best for air in mines and poorer
for the cleaner air in homes where the unattached fraction may be
higher.
EXTRAPOLATION OF DOSES FROM MINES TO HOMES
The committee's estimates of lung-cancer risks due to the inhala-
tion of radon and its progeny are based on data derived from coning
populations. These estimates can be used to calculate the risk per
W[M in nonoccupational situations, but the attendant assumptions
and uncertainties associated with this change in exposure conditions
must be considered. There are potentially important differences be-
tween the environmental conditions in which exposure is sustained
in a mine and a home and between the physical characteristics of
miners and members of the general population. Just as there is no
single lung mode} that has been shown to be best in all cases of radon
OCR for page 150
150 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
exposure, the committee finds that there is no single characterization
of the environment in mines or homes that can be called typical. For
the same working-level exposure, there can be a wide variation of
particle size, equilibrium factors, and percent unattached fraction.
In addition, a miner working underground! and a person living in a
home have different levels of activity and, thus, different breathing
patterns.
Rather than postulating some average or typical values for the
various factors that affect the dosimetry of radon progeny in mines
and homes and calculating appropriate dose per WI,M conversion
factors, the committee proposes a methodology that can be applied
when any radon environment is sufficiently characterized. By using
the ratio of the dose per W[M in nones to that in homes obtained by
means of the lung models described above, it is possible to extrapolate
the risk values obtained for underground miners to people living in
homes, at a reasonable level of approximation.
Let K be a dimensionless factor that, when multiplied by the
risk to miners per W[M, will give the risk to an individual in a home
per W[M.
(Ri~k~m (Rinks
K =
(WLM)m (WLM)h
(2B-2)
While miners exposed to 1 WL receive 1 W[M during a 17~h
working month, a person living in a home at 1 WL would normally
be exposed to more than 1 W[M in a month. If an occupancy factor
(O.F.) is defined as the fraction of a 72~h month that is spent in a
house, then 1 WI' will result in 720/170 O.F. W[M per month of
occupancy. Since risk is proportional to dose, K varies as the ratio
of the dose per W[M in houses and mines.
a, Riskh/WLMh
Riskm/WLMm ~ ~ Dosem/wLMm
Doseh/WLMh (2~3)
As described above, the dose to the lung depends upon both aerosol
and physiological factors. Therefore, to a first approximation, the
dimensionless proportionality constant K can be expressed in terms
of the partial dose conversion factors obtained from a specified lung
model.
K Oc Ph fh Fh (MV)h . . ./WLMh
Pm fm Em (MV)m · · ./WLMm
(2~4)
OCR for page 151
RADON DOSIMETRY
151
where P is dose conversion factor for particle size, f is dose conver-
sion factor for the unattached fraction, F is dose conversion factor for
the equilibrium factor, MV is dose conversion factor for the minute
volume; all these parameters have units of red per W[M. Physiolog-
ical factors such as mucus thickness, mucus transport rate, bronchial
morphometry, depth of the target cells, and the particle deposition
fraction can be assumed to be approximately equal in miners and
persons living in homes. These factors undoubtedly vary from per-
son to person; but except for the possibility of Correlated damage to
the lung, they should be about equal in miners and others, and there-
fore would largely cancel out in Equation 2~4. Differences between
smokers and nonsmokers, however, may be important (see Part 3 of
Appendix VIl).
The committee considered the possibility of systematic di~er-
ences between miners and others, for example, prevalence of ~nhala-
tion via the mouth, but found that data were not available for evalu-
ation. However, sex and age are factors to be considered. Although
most calculations of aerosol deposition are based on the anatomy of
the male, the female airway geometry is similar, and scaling factors
can be used for estimating the dimensions of individual airways.34 In
the case of the growing child, the alveolar area is not fully developed
at birth. However, the ciliated airways are complete. Calculated
deposition patternsi536 indicate higher relative deposition in the
first few generations in the lungs of children for aerosols of 0.2-,um
diameter or less.
For adults of working age and the same smoking status, it is
likely that mucociliary clearance rates are similar in miners and in the
general population. However, there is little information concerning
clearance in other groups in the population and none for children. It
is known that clearance in the elderly is delayed.~° Most lung models
show an increase of bronchial dose per unit exposure until about age
6, after which it falls off and becomes nearly constant after age 10.
The NEA Organisation for Economic Co-operation and Development
has recommended that age dependency of dose equivalent per unit
exposure be neglected.35
It is instructive to examine the variations of the proportionality
factor K, given by Equation 2B-4, under the various dosimetry mod-
els, as illustrated by the results shown in Figures 2B-2, 2B-3, and
2~4. In doing so, it will be shown that for a range of conditions
typical in mines and homes, under a given model, K is reasonably
OCR for page 152
152 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
stable, even though the variation between models in the calculated
dose per W[M varies by a factor of 2 or more.
The first three terms in Equation 2B-4, the conversion factors
for particle size, unattached fraction, and equilibrium factor, are rep-
resentative of the physical environment in the mine or home and are,
to some extent, interconnected. For example, with increasing aerosol
concentration the dose per W[M conversion factor for equilibrium
(F) generally increases somewhat, while that for the unattached frac-
tion (0 decreases. However, these factors are independent to a first
order and K can be approximated by the product of the ratios given
in Equation 2B-4.
George and colleagues.8 9 made particle size measurements in
homes in New York and New Jersey and in mines in Canada and
Colorado. They found that particle size was log normally distributed
with an activity mean diameter of 0.12 Am in homes and 0.17 Am in
the mines. From Figure 2B-3 it is seen that all three lung models give
about 1 rad/W~M for 0.12-pm particles compared to approximately
0.7 rad/W[M for 0.17-,um particles. For these particle distributions
Ph/Pm is about 1.4.
The amount of activity that is unattached depends on the am-
bient environment. Because of low ventilation, the mass concen-
tration of airborne dust was probably high in early mines and the
unattached fraction low. More recently, the ventilation in mines has
been greatly increased. However, the number concentration of air-
borne dust particles may have become higher due to the widespread
use of underground diesel equipment. In a careful study of several
uranium mines, George et al.9 found that the unattached fraction
ranged from 0.004 to 0.16, with a mean value of 0.04.
Recent investigations have provided some preliminary data on
the fractions of unattached RaA and the size distribution of the car-
rier aerosol for the attached fraction in the home environment.8 The
number and size of particles in the air of a home vary considerably
throughout the day, depending, among other factors, on the pres-
ence of cigarette smoke and the cooking of food. This, in turn, has
a large effect on how many ions become attached to particulates.
Particulate concentrations are generally lower at night but rarely fall
below 104 particles/mI. In the absence of specific aerosol sources in
the home, Reineking et al.38 calculated, on the basis of measured
concentrations of particulates, that the unattached fraction ranged
between 0.06 and 0.15 (mean value, 0.1~. With additional aerosol
sources, the unattached fraction fell below 0.05. This value for the
OCR for page 153
RADON DOSIMETRY
153
unattached fraction (0.1) ~ somewhat higher than those previously
assumed,~9 23 and is higher than the mean value (0.04) measured in
uranium mines.7 9 Although the unattached fraction of RaA may be
perhaps twice as high in homes compared to mines, extensive data
on homes and mines have yet to be published.
Assuming that the mines used to obtain the risk numbers for
radon had an unattached fraction (f m) of about 4%, the three models
shown in Figure 2B-4 give a conversion factor to the bronchial region
of about 0.5 0.6 rad/W~M. For a diffusion coefficient of 0.005 cm2/s
and an unattached fraction of To in homes, the same curves give
conversion factors between 0.5 and 0.7 rad/W[M. The ratio fh/lm
would then be about 1.2 (1.~1.4), depending on which lung model
is chosen.
- The equilibrium factor F is dependent on the ventilation rate.
High ventilation rates result In low values of F. Jacobi and Eisfeld24
have shown that variation of the equilibrium factor has very little
effect on the dose per unit exposure to the bronchial cells. Therefore,
even though Fh and Em may be different, the ratio of the conversion
factors is about I.
Physiological factors must be considered also. Underground min-
ers, usually adult males, spend about 40 h weekly engaged in mod-
erate to heavy activity ~ the course of their work. Nonoccupational
exposures of adults, both male and female, and children generally
occur in the home during light activity or while asleep. So, in addi-
tion to differing aerosols in homes and mines, the different breathing
patterns of miners and the population in homes must be considered.
The increased minute volume required for the metabolic cost
of exercise is achieved by an increase in both the tidal volume and
the frequency of breathing. The increased frequency of breathing
decreases the mean residence time of aerosols in the lung and, by so
doing, reduces the time available for diffusion to deposit particles on
the bronchial airways.
Exercise also has a role in how people inhale. With increasing
ventilation there is a shift from nasal to oral breathing. For example,
with exercise requiring ventilation of 35 liters/min, there is a shift
from a pattern of 80~o nasal breathing in the resting subjects to
about 50~o nasal breathing.37 Moreover, many normal people breath
oronasally,39 and those with any form of nasal obstruction have a
mainly oral form of breathing. The proportion of oral and nasal
breathing influences the bronchial dose since, as noted above, about
half of the unattached fraction is assumed to be deposited in the
OCR for page 154
154 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
nose. increased oral breathing, therefore, increases bronchial doses,
whereas increased nasal breathing reduces this dose. It can be argued
that the larger fraction of unattached RaA in the home compared
to that in a mine increases the dose to the bronchus for a given
concentration of radon progeny in air. However, the increased minute
ventilation of the miner is associated with more mouth breathing,
which would tend to increase his dose. The committee could not
find data on the pattern of nose or mouth breathing in miners and
therefore could not examine this factor analytically. It is an obvious
problem for further field investigation.
ICRP,~9 NEA,35 and NCRP33 assign a breathing rate of 20
liters/m~n to underground miners and base their dose estimates
on this minute volume. Ventilation rates in working coal miners
have been measure; values obtained ranged from about 30 to 40
liter/min when averaged throughout the working shift. This Is about
1.5 to 2 times the 2~liter/min value assigned to miners and 3 to 4
times the 12.5 liter/m~n value assignee] to the general population in
the NEA35 model. Moreover, individuals undertaking the same task
have differing minute ventilation. Heavier miners breathe more, as
do older miners. The very high ventilation rates found in coal miners
might not be representative of values for uranium miners.
In the case of the home environment, there are considerable
uncertainties in attempting to estimate overall deposition patterns
throughout the 24-h cycle. Not only is the distribution of oral/nasal
breathing a relevant factor, but the tidal volume and frequency of
breathing change continuously. The minute volume of a sleeping
person is low, and the convective diffusion component of bronchial
deposition may be insignificant.30
For a miner who averages a minute volume of 30 liters/m~n,
the conversion factors from the three models shown in Figure 2~4
would be on the order of 0.8 rad/WLM. The average person in a home
breathing, 12.5 liters/min would receive a dose of 0.45 rad/WLM.
Thus, the conversion factor ratio due to these different minute vol-
umes (MVh/MVm) would be 0.56. If the miners do a significantly
larger amount of mouth breathing than occurs in homes, this ratio
would be smaller.
For the mean bronchial dose, differences between the models
are small. The ratio of the conversion factors due to the different
minute volumes would remain nearly the same for any of the three
models because the shapes of the curves in Figure 2~4 are very
similar. However, for basal cells at 22-,um depths as the target
OCR for page 155
RADON DOSIMETRY
155
cells, the H-P mode] gives somewhat higher doses per unit exposure
than do the other two models, and the variation in the ratio of the
factor, MVh/MVm, in Equation 2B~2 due to the choice of the mode}
becomes larger.
As outlined in Equation 2~4, the four conversion factors making
up K have ratios in homes to mines of 1.4, 1.2, 1.0, and 0.56.
Therefore, for this specific case, the product of these factors is 0.94
and the mean dose received by a person exposed in a home to 1 WL
of radon for 170 h is very nearly the same as the dose to a miner
exposed to 1 WHIM. On the other hand, if the minute volume for
miners is taken as 20 liters/min, the ratio K is increased to about
1.3. In homes where the unattached fraction is low (Rio), this ratio
is less, about 0.8.
Other investigators have reached similar conclusions. After
reviewing the parameters relevant to a comparison of the WHIM
in a mine and in the home, the NCRP concluded that the alpha
dose to the surface of the bronchial tree (red per W[M) may be
somewhat higher for environmental exposure than for underground
exposure, largely due to a higher fraction of unattached RaA in
the home.34 In contrast, the NEA has estimated smaller doses per
WI,M for adult members of the general population than for miners.35
The NEA assumed a smaller unattached fraction (3%) than that
assumed by the NCRP (7%o) and a slightly lower breathing rate than
that assumed by the NCRP. Both the NCRP and the NEA analyses
assume that miners inhale 20 liters/min, that is, light activity. Upon
their review of the possible range of the input parameters for the
dosimetric models, the NCRP concluded that the dose per WHIM in
homes, as compared to that in mines, differs by less than a factor of
2.
~ summary, the committee believes that with the present state
of scientific knowledge, it can neither choose between the three major
radon lung models nor specify the best values of the factors which
characterize the dose in a home or in a mine. However, all of the
models are in agreement within about a factor of 3 or so. While the
method of ratios used here does not directly calculate a dose to the
lung tissues, it does allow the extrapolation of known risks in a mine
to a home where dosimetry factors have been established.
Future work on this methodology should be concentrated in
areas that will improve the quantification of the constant K. This
will include improving our knowledge of the environment in the
mines from which the risk estimates were obtained, characterizing
OCR for page 156
156 HEALTH RISKS OF RADON AND OTHER AlPHA-EMITTERS
the indoor environment of homes more completely, and determining
breathing characteristics of uranium miners by on-site measurements.
Finally, high priority should be given to creating and validating a
Jung mode} which retains the best features of the modem now in use.
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Representative terms from entire chapter:
radon daughters
