DRC-1993-001001 - 0901a068807b32d6

PREFACE
At its 1990 meeting, the Commission established a Task Group of Committee 4 to
prepare a report on protection against radon in buildings. In 1991, it set up a Working
Party to prepare a report on limits for the radiation exposure of workers in mines.
The members of the Commission Working Party were W. Jacobi (Chairman) and
H. J. Dunster. Members of the Committee 4 Task Group were R. V. Osborne
(Chairman), J. H. Harley*, A. C. James, M. C. O’Riordan, A. G. Scott,
G. A. Swedjemark and P. Zettwoog.
Both reports were submitted to the Commission for discussion at its meeting in
November 1992. It was then decided to combine the two studies into a single report on
protection against radon in dwellings and workplaces, including mines. This combined
report was prepared by a Commission Task Group with the following membership:
R. H. Clarke (Chairman)
H. J. Dunster
W. Jacobi
R. V. Osborne.
A draft of the report was issued by the Commission for consultation in April 1993. A
revised text was approved for publication in September 1993.
1. INTRODUCTION
(1) The naturally radioactive noble gas radon ( 222Ftn) is present in the air outdoors
and in all buildings, including workplaces. It is thus an inescapable source of radiation
exposure both at home and at work. High radon levels in air can occur in buildings,
including workplaces, in some geographical locations. This applies particularly in
workplaces such as underground mines, natural caves, tunnels, medical treatment areas
in spas, and water supply facilities where ground water with a high radon concentration is
treated or stored.
(2) This report summarises the extent of current knowledge about the health effects of
inhaled radon and its progeny and makes recommendations for the control of this
exposure in both dwellings and workplaces. It aims to give guidance to national advisory
and regulatory agencies and to practitioners of radiological protection concerned with
radon in dwellings and workplaces.
1.1. The Structure of the Report
(3) In its 1990 recommendations, ZCRP Publication 60 (ICRP, 1991), the Commission
deals separately with practices and intervention and with occupational and public
exposure. Exposures to radon have implications in all these situations. Radon is present
in all buildings. In existing dwellings, the exposures can be reduced only by some form of
intervention. In workplaces, it is necessary to consider both the need for intervention (as
in dwellings) and the continued control of radon exposures as part of the practice carried
out in the workplace. The future exposure in new buildings also has to be considered.
This report, which is intended to deal coherently with all these issues, has the following
structure.
(4) The rest of Section 1 provides introductory material about radon and the
quantities and units used in specifying radon concentrations and exposures, followed by a
summary of the main principles of protection applicable to radon. Throughout the
report, the term “radon” is used most often to include its short-lived progeny, not
necessarily in equilibrium. The term “radon concentration,” however, relates to the
concentration of the parent nuclide alone.
(5) Section 2 deals with the current information about the health effects of exposure
to radon. It provides estimates of both the fatality and detriment coefficients for lifetime
exposure to radon progeny of workers and the general public. These coefficients are then
used to give a direct conversion, based on equal detriment, between radon exposure and
effective dose.
(6) Section 3 deals briefly with radon in buildings, indicating the practical approaches
to reducing the concentrations of radon and its progeny. Section 4 deals with the policy
for limiting radon in dwellings, leading up to recommendations for action levels of radon
in dwellings, above which remedial measures (intervention) should be taken. The
requirements for new buildings are also discussed.
(7) Section 5 deals with radon in workplaces. Radon occurs in all workplaces and
action may be needed to reduce existing concentrations. Guidance is given on the
concentration of radon above which remedial measures (intervention) to reduce radon
2 REPORT OF A TASK GROUP OF COMMITTEE 4
concentrations should be taken. The Commission recommended in ZCRP Publication 60
that exposure to radon at work should be excluded from its system of protection for
practices unless the relevant regulatory agency has ruled otherwise. Section 5 gives
guidance on the level of exposure to radon that should be used in making that ruling.
(8) Once the decision to apply the Commission’s system of protection is made, it
becomes necessary to apply an exposure limit. This has been derived to correspond to
the same level of detriment as that resulting from an effective dose equal to the
Commission’s recommended dose limit. Some additional guidance is given on practical
control measures in workplaces.
1.2. The History of Radon
(9) The existence of a high mortality rate among miners in central Europe was
recognised before 1600, and the main cause of death was identified as lung cancer in the
late nineteenth century (Haerting and Hesse, 1879). It was suggested that the cancers
could be attributed to radon exposure in 1924 (Ludewig and Lorenser, 1924).
(10) Early environmental measurements were largely confined to outdoor air for the
study of diverse phenomena such as atmospheric electricity, atmospheric transport and
exhalation of gases from soil. The first indoor measurements were made in the 1950s
(Hultqvist, 1956), but attracted little attention. In recent years, there has been an upsurge
in the interest in radon in dwellings and workplaces.
(11) A more comprehensive review of the history of radon is given as a separate
publication in this issue of the Annals of the ZCRP.
1.3. Radon and its Progeny
(12) The two significant isotopes of radon are radon-222, the immediate decay
product of radium-226, deriving from the uranium series of natural radionuclides, and
radon-220, the immediate decay product of radium-224, deriving from the thorium
series. Because of their origins, the two isotopes are commonly known as radon and
thoron. The element is a noble gas and both isotopes decay to isotopes of solid elements,
the atoms of which attach themselves to the condensation nuclei and dust particles
present in air. The problems posed by radon-220 (thoron) are much less widespread,
and generally more tractable, than those posed by radon-222. For protection against
thoron, it is usually sufficient to control the intake of the decay product, lead-212, which
has a half-life of 10.6 hours. This report is concerned with protection against radon-222.
The main decay properties of the short lived progeny are shown in Table 1. Radon-222
decays by alpha emission to polonium-218 with a half-life of 3.82 days. Polonium-214
decays to lead-210 which has a half-life of 23.3 years and which eventually decays to
stable lead-206.
(13) The biological processes linking the inhalation of radon and its progeny to the
generation of an increased risk of lung cancer are complex. The special quantities that
have been developed for use with radon have proved useful in practice in the provision
of simple relationships between exposure and risk. However, their quantitative
significance for this purpose may be modified by physical factors not included in the
definition of the quantities themselves, such as the unattached fraction (see Annex C).
PROTECTION AGAINST RADON-222
Table 1. Decay properties of radon-222 and short lived progeny
3
Radionuclide Half-life
Main radiation energies and yields (y)
Alpha Beta Gamma
Energy Energy (max) Energy
(MeV) (& (MeV) (i, (MeV) (44
222Rn
2’8Po
3.824 days 5.49 100
3.05 min 6.00 100 -
2L4Pb 26.8 min - - 1.02 6 0.35 37
0.70 42 0.30 19
0.65 48 0.24 8
214Bi 19.9 min - - 3.27 18 0.61 46
1.54 18 1.77 16
1.51 18 1.12 15 ?14Po 164 ,us 7.69 100 - - - -
Sources: Browne and Firestone (1986) and ICRP (1983).
1.4. Special Quantities and Units
(14) This section sets out the special quantities and units that are used to
characterise the concentration of the short-lived progeny of radon in air, and the
resulting inhalation exposure.
Potential alpha energy
(15) The potential alpha energy, ep, of an atom in the decay chain of radon is the
total alpha energy emitted during the decay of this atom to stable 210Pb. The potential
alpha energy per unit of activity (Bq) of the considered radionuclide is tp/Ar= (&,t,/ln2)
where 1, is the decay constant and t, the radioactive half-life of this nuchde. Values of E,,
and EJA, are listed in Table 2.
Table 2. Potential alpha energy per atom and per unit activity
Potential alpha energy
Radionuclide Half-life
Per atom Per unit of activity
(MeV) (lo-l2 J) (MeV Bq-‘) (1O-‘o J Bq-‘)
Radon (222Rn) progeny:
2’SPo 3.05 min
2’4Pb 26.8 min
“4Bi 19.9 min
“4P. 164 .us
13.69 2.19 3615 5.79
7.69 1.23 17 840 28.6
7.69 1.23 13 250 21.2
7.69 1.23 2x 10-3 3x 10-b
Total (at equilibrium), Bq per of radon 34 710 55.6
Concentration in air
(16) The potential alpha energy concentration, cp, of any mixture of short-lived
radon progeny in air is the sum of the potential alpha energy of these atoms present per
4 REPORT OF A TASK GROUP OF COMMITTEE 4
unit volume of air. Thus, if ci is the activity concentration of a decay product nuclide i,
the potential alpha energy concentration of the progeny mixture is
cp = C Ci(Ep,illZr,i)
i
This quantity is expressed in the SI unit J me3 (1 J me3 = 6.242 x 1012 MeV mT3).
(17) The potential alpha energy concentration of any mixture of radon progeny in air
can be also expressed in terms of the so-called equilibrium equivalent concentration, ce,,
of their parent nuclide, radon. The equilibrium equivalent concentration, corresponding
to a non-equilibrium mixture of radon progeny in air, is the activity concentration of
radon in radioactive equilibrium with its short-lived progeny that has the same potential
alpha energy concentration, cr,, as the actual non-equilibrium mixture. The SI unit of the
equilibrium equivalent concentration is Bq rnm3.
(18) The equilibrium factor, F, is defined as the ratio of the equilibrium equivalent
concentration to the activity concentration of the parent nuclide, radon, in air. This
factor characterises the disequilibrium between the mixture of the short-lived progeny
and their parent nuclide in air in terms of potential alpha energy.
Inhalation exposure of individuals
(19) The quantity “exposure,” P, of an individual to radon progeny is defined as the
time integral of the potential alpha energy concentration in air, cr, or the corresponding
equilibrium equivalent concentration, ce,, of radon to which the individual is exposed
over a given period T, e.g. one year.
Potential a energy exposure P,(T) = 1 c,(t) dt
0
7
c
Equilibrium equivalent exposure p,,t T) = J c,,(t) dt
(20) The unit of the exposure quantity Pp is J h rne3; for the exposure quantity P_,
the unit is Bq h m- 3. The potential alpha energy exposure, P,,, of workers is often
expressed in the historical unit Working Level Month (WLM). 1 WL was originally
defined as the concentration of potential alpha energy associated with the radon
progeny in equilibrium with 100 pCi C - * (3700 Bq L - ‘). This concentration was about
1.3 X lo5 MeV C - r , but the precise value depended on the estimates of alpha energy per
disintegration. The Working Level is now defined as a concentration of potential alpha
energy of 1.300 x lo8 Me V m- 3. Since the quantity was introduced for specifying
occupational exposure, 1 month was taken to be 170 hours, Since 1 MeV= 1.602 X lo- l3 J,
the relationship between the historical and the SI units is as follows:
1 WLM=3.54mJhmb3
1 mJ h me3 = 0.282 WLM
(21) Here, and elsewhere in this report, values that will be used in later calculations
may be given to more significant figures than are usually needed and sometimes to more
than the precision of the data justifies. Whenever rounded values are given for
quantities that will be used in subsequent calculations, the unrounded values are
retained for use in these calculations. Most values are given in SI units. However, the
PROTECTION AGAINST RADON-222 5
historical units are still widely used and converted values are also given where it is likely
that this will be helpful.
(22) The conversion coefficients between the concentration quantities, potential
alpha energy, cF, and equilibrium equivalent concentration, Ces; and between the
exposure quantmes, potential alpha energy exposure, Pp, and equilibrium equivalent
exposure, Peg, are given in Table 3.
Table 3. Conversion coefficients for the different
concentration quantities and for the corresponding
exposure quantities for radon-222
Quotient Conversion coefficients
5.56 x lo+ (J m-‘) per (Bq m-‘)
1.80 x lo8 (Bq m-‘) per (J m-?
PJPC, 5.56 X 10d9 (J h rne3) per (Bq h mm3)
1.57 x 10d6 WLM per (Bq h md3)
pc,/p, 1.80 x lo8 (Bq h md3) per (J h mm3)
6.37 x IO5 (Bq h mm3) per WLM
Quantities: c,~ concentration of potential alpha
energy, c,,--equdibrium equivalent concentration of
radon, Pp - time-integrated exposure to potential
alpha energy concentration, Te9 - time-integrated
exposure to equilibrium concentration of radon.
(23) The relationship between the annual exposure and the radon concentration at
home or at work can be obtained from Table 3. For most purposes, it is adequate to use
an equilibrium factor of 0.4 and an occupancy of 2000 hours per year at work or
7000 hours indoors (UNSCEAR, 1988). On this basis, a continued exposure to a radon
concentration of 1 Bq mm3 results in an annual exposure at home of 1.56 X 10e2 mJ h mm3
(4.40x 10m3 WLM). The corresponding figure at work is 4.45 X lob3 mJ h mm3
(1.26 x 1O-3 WLM).
1.5. The Principles of Protection
(24) In ZCRP Publication 60, attention is drawn to the need for protection against
natural sources of radiation both in dwellings and workplaces. Key extracts from the
recommendations as they relate to radon are presented here.
(25) The Commission distinguishes between two circumstances of exposure to
radiation, one where human activities introduce new sources or modes of exposure and
thus increase the overall exposure and the other where they decrease the exposure to
existing sources. The first it calls practices and the second intervention. It also identifies
the circumstances under which exposure to radon at work may need to be subject to the
Commission’s system of protection for practices and where the need for action against
exposure to radon in homes should be considered. Radon occurs in all buildings and the
concentrations vary widely from building to building. In the workplace, there is
sometimes a difficulty in making a sharp distinction between radon concentrations that
should be treated as being due to a practice or as due to an existing situation for which
6 REPORT OF A TASK GROUP OF COMMITTEE 4
intervention may be needed. One of the aims of this report is to give guidance on that
distinction.
(26) The system of radiological protection recommended by the Commission for
proposed and continuing practices is based on the following general principles. Here,
and throughout the document, direct quotations and paragraph references from ICRP
Publication 60 are itaiicised. This extract is from Paragraph 11.2.
“(a) No practice involving exposures to radiation should be adopted unless it produces
sufficient benefit to the exposed individuals or to society to offset the radiation
detriment it causes. (The justification of a practice.)
“(b) In relation to any particular source within a practice the magnitude of individual
doses, the number of people exposed, and the likelihood of incurring exposures
where these are not certain to be received should all be kept as low as reasonably
achievable, economic and social factors being taken into account. This procedure
should be constrained by restrictions on the doses to individuals (dose constraints),
or the risks to individuals in the case of potential exposures (risk constraints), so
as to limit the inequity likely to result from the inherent economic and social
judgements. (The optimisation of protection.)
“(c) The exposure of individuals resulting from the combination of all the relevant
practices should be subject to dose limits, or to some control of risk in the case of
potential exposures. These are aimed at ensuring that no individual is exposed to
radiation risks that are judged to be unacceptable from these practices in any
normal circumstances. Not all sources are susceptible of control by action at the
source and it is necessary to specify the sources to be included as relevant before
selecting a dose limit. (Individual dose and risk limits.)”
(27) For intervention, the Commission recommends that two general principles be
followed. These general principles are set out in Paragraph 113 of which the relevant
part reads:
“(a) The proposed intervention should do more good than harm, i.e. the reduction in
detriment resulting from the reduction in dose should be sufficient to justify the
harm and the costs, including social costs, of the intervention.
“(b) The form, scale, and duration of the intervention should be chosen so that the net
benefit of the reduction of dose, i.e. the benefit of the reduction in radiation
detriment, less the detriment associated with the intervention, should be
maximised.”
(28) The Commission qualifies this advice in Paragraph 131, of which the relevant
part reads:
“The dose limits recommended by the Commission are intended for use in the control
of practices. The use of these dose limits, or of any other pre-determined dose limits, as
the basis for deciding on intervention might involve measures that would be out of all
proportion to the benefit obtained and would then conflict with the principle of
justification. The Commission therefore recommends against the application of dose
limits for deciding on the need for, or scope of, intervention. Nevertheless, at some level
of dose, approaching that which would cause serious deterministic effects, some kind of
intervention will become almost mandatory..”
More detailed accounts of the Commission’s policy are given in Sections 4 and 5.
PROTECTION AGAINST RADON-222 7
2. THE HEALTH EFFECTS OF INHALED RADON AND
ITS PROGENY
(29) Estimates of the consequences to health of exposures to ionising radiation are
best based on epidemiological studies of human populations. In the context of radiation,
epidemiology is concerned with the establishment of statistical associations between
exposures and health effects. These studies have established beyond any reasonable
doubt that radiation is a causative agent of cancer in many organs and tissues of the
body, including the lung. The establishment of quantitative association is more difficult.
(30) It is a vital tenet of statistics that events that are correlated in time or space are
not necessarily correlated in cause. Indeed, chance associations have a definite
likelihood of occurrence. To establish a quantitative causal relationship it is necessary to
supplement the epidemiological data by the use of models based on biological evidence.
When a range of such models is proposed, it is legitimate to use epidemiology to
indicate statistical preferences between them. Epidemiology may also suggest
improvements to the proposed models or further possible models. However, it is not
legitimate to create or modify models solely to improve the statistical fit of the data in a
single epidemiological study. There must also be confirmatory findings in other studies
and plausible biological support.
(31) Epidemiological studies have shown a correlation between exposure to radiation
and excess lung cancer. These include the Life Span Study of the survivors of the atomic
bombs at Hiroshima and Nagasaki, patients treated for ankylosing spondylitis, cancer of
the cervix, Hodgkins disease and breast cancer, and miners exposed to radon at work. The
two main sources of quantitative information about the risks resulting from the exposure of
the lungs to radiation are the Life Span Study and the studies of miners. The Life Span
Study provides estimates of the cancer fatality coefficient for exposure, principally to
gamma radiation, that is fairly uniform over the whole lung. The studies on miners provide
information on the relationship between the incidence of fatal lung cancer and the
concentration of radon progeny in the mining environment.
(32) In the last ten years or so, there have also been many studies aimed at detecting
a correlation between the incidence of lung cancer and exposure to radon in dwellings.
Some of these have shown positive correlations, but many have not. Reviews of these
studies has been made by Samet (1989) and Stidley and Samet (1993). Most of these
studies have been geographical correlation studies. These involve selecting two or more
areas, some of high and others of low, average concentration of radon in dwellings. The
current lung cancer incidences are examined and a statistical comparison made.
(33) Unfortunately, geographical correlation studies are difficult to interpret, even
qualitatively, because of the presence of several serious confounding factors. One
possible confounding factor is a correlation of radon concentrations with other
environmental features. Areas of high radon are often in rocky and hilly regions rather
than in the river valleys and alluvial plains where populations and industrial
developments are likely to be concentrated. There may thus be an inverse correlation of
radon concentration and industrialisation. If, as is likely, there is a direct correlation
between lung cancer and industrialisation, probably associated with smoking, this may
mask, or appear to reverse, any link between lung cancer and radon.
(34) Even if an allowance can be made for confounding factors, it remains difficult
to draw quantitative conclusions, because many of those who die in an area have not
consistently lived in that area. The concentrations observed are then not typical of the
8 REPORT OF A TASK GROUP OF COMMITTEE 4
exposures of individuals. These difficulties can largely be avoided by the use of cohort
and case-control studies. Several of these are currently (1993) in hand.
(35) When the problem of confounding factors is recognised, case-control studies of
radon (e.g. Schoenberg et aZ., 1990) in dwellings are not inconsistent with the mining
studies, but, as yet, most of them provide no quantitative data. However, some
quantitative data, albeit statistically weak, are provided by two case-control studies from
Sweden (Pershagen et aZ., 1992, 1993). For the present, the Commission continues to
rely mainly on the data from epidemiological studies on miners, because of the lack of
statistical power in the studies on dwellings.
(36) There are several sources of uncertainty in the radon epidemiology. These
include the statistical limitations imposed by the size of the exposed populations, the
need to select a projection model to estimate lifetime risks and the need to postulate an
exposure-response relationship to provide estimates of risk at levels of exposure below
those for which there are directly observable excess risks. In addition to the statistical
uncertainties, there are several sources of non-random uncertainty in these studies:
(a) the uncertainty of individual exposure estimates;
(b) the difficulty of selecting an appropriate control group;
(c) the different working atmospheres in the mines, including the influence of other
non-radioactive ore dusts;
(d) the different smoking habits; and
(e) the differences (by a factor of about two) in the mean follow-up periods.
Furthermore, the quantity inhaled potential alpha exposure may not be the most
appropriate quantity, because of variation in physical parameters such as the particle
size distribution of the inhaled aerosols. However, this is the quantity in which all the
epidemiological data for miners are expressed.
(37) The Commission has adopted an improved dosimetric model of the respiratory
tract for use in a very wide range of circumstances (ICRP, 1994). The practical
applications of this model are still being developed. The use of this model for assessing
the fatality and detriment coefficients for inhaled radioactive materials is complicated
by uncertainties in several important areas. The deposition and retention aspects of the
model lead on to dosimetric stages involving the geometrical relationship between the
deposited material and the cells at risk. It is then necessary to assess the relative
importance of the dose to cells in different parts of the tract. The present estimates of
the probability that these doses will result in cancer depend on the estimation of risk
coefficients for lung cancer caused by uniform, high dose-rate exposure to low LET
radiation obtained from the Life Span Study. Statistical limitations prevent the direct
observation of the excess relative risk at low doses. The use of these data for estimating
the risk from radon exposures in homes and workplaces therefore depends on the
choice of the dose and dose rate effectiveness factor for the induction of lung cancer by
low LET radiation and of the radiation weighting factor for alpha radiation.
(38) Although there are uncertainties in both above approaches, they do not lead to
widely different results. The Commission has concluded that the use of the
epidemiology of radon in mines is more direct, and therefore involves less uncertainty
and is more appropriate for the purposes of this report than the indirect use of the
epidemiology of low LET radiation from the Japanese data. The Commission therefore
recommends that the dosimetric model should not be used for the assessment and
control of radon exposures. The fatality coefficients in this report are therefore based
PROTECTION AGAINST RADON-222 9
on the epidemiological studies on miners exposed to radon. Since these results relate
essentially to adult males, it is necessary to make further judgements to predict the risks
to females and children from the observed risks to males. See Sections 2.2.1 and 2.2.3.
2.1. Lung Cancer in Radon-Exposed Miners
(39) There have been several epidemiology studies of lung cancer in miners exposed
to radon. These are continuing and the results are combined and reviewed from time to
time, both by individuals and groups (e.g. U.S. National Research Council, NRC).
Several studies and reviews are in preparation or in press at the date of preparation of
this report. As an indication of the methodology of such studies, and to give a general
indication of typical results, the Commission has conducted a limited review,
summarised in Annex A of this report. In this developing situation, the Commission has
not made its own definitive analysis.
2.1.1. Epidemiological studies
(40) The epidemiological evidence for the induction of lung cancer following
inhalation of radon comes from several cohort and case-control studies of underground
miners, particularly uranium miners. These findings have been summarised and
reviewed in other reports (UNSCEAR, 1986, 1988; NRC, 1988; IARC, 1988; ICRP,
1991). For the quantitative risk analysis, the following studies of uranium miners
cohorts are of special importance: Bohemia (Sevc et al., 1988, 1993), Colorado, USA
(Whittemore and McMillan, 1983; Hornung and Meinhardt, 1987), New Mexico, USA
(Samet et aZ., 1989, 1991), Ontario, Canada (Muller et al., 1985, 1989), Saskatchewan
(Beaverlodge), Canada (Howe et aZ., 1986; SENES, 1991; Chambers et al., 1992),
France (Tirmarche et al., 1992a) and Port Radium, Canada (Howe et al., 1987). An
excess rate of lung cancer has also been observed in iron miners in Malmberget, Sweden
(Radford and Renard, 1984), fluorspar miners in Newfoundland, Canada (Morrison et
al., 1988), workers in a tin mine in Yunnan, China (Lubin et al., 1990, Xiang-Zhen et al.,
1993) and gold miners in Ontario (Kusiak et al., 1991).
(41) Many of these studies are consistent with a proportional (linear, non-threshold)
relationship between excess risk and cumulative exposure. Some, however, show
evidence of a higher excess relative risk per unit exposure at low exposures compared
with the mean value for the whole exposed group (Darby and Doll, 1992). Studies on
rats, reviewed by the US Department of Energy (DOE, 1988), support a non-threshold,
linear, exposure-risk relationship at low levels of exposure. There are several possible
explanations of this discrepancy. The expression of the exposure in terms of potential
alpha energy concentration may conceal the effect of other factors, such as particle size
distribution, ventilation rate, and the unattached fraction. The exposure-risk
relationship might also be distorted by the presence of other carcinogens, such as
arsenic.
(42) When the results of several studies have been amalgamated, it has usually been
on the basis of the estimated excess relative risk per unit exposure. This implies the use
of a causative relative risk model in which the excess risk results from a multiplication
of the age-specific baseline risk (including any enhancement from smoking). However,
any enhancement of the baseline risk caused by earlier parts of the occupational
exposure is ignored. If it were included, the model would show the excess risk rising
10 REPORT OF A TASK GROUP OF COMMITTEE 4
more rapidly than linearly at higher levels of exposure. Such a rise has not apparently
been observed. If there is a true causative relative risk model, it seems to be more
complex than is usually assumed.
2.2. Lung Cancer Risk Estimates for Chronic Exposure
(43) The epidemiological findings have to be extended to provide information for
long periods of exposure, for lifetime risks, and for other populations than those
studied. For estimating lifetime risk from data covering shorter periods, the Commission
has used a multiplicative projection model rather than an additive one (ICRF’, 1991). It
warned, however, that there was no adequate basis for choosing between a relative and
an absolute risk model for transferring estimates from one population to another. In this
report, the estimates of absolute excess risks are assumed to apply to a wide range of
populations. There is, as yet, no a priori basis for selecting a model for transferring the
risk estimate for males to the risk estimate for females. The choice is complicated by the
interaction of the effects on the lung of radiation and of smoking. This issue is discussed
in Section 2.2.1.
(44) The general policy of the Commission towards protection makes use of the
attributable lifetime risk and detriment from stochastic radiation effects. It is therefore
necessary to estimate the lifetime absolute probability of attributable death starting from
the data over the more limited follow-up periods provided by the epidemiology studies.
2.2.1. Risk projection models for lung cancer
(45) Different types of risk projection models, some with modifications for factors
such as time since exposure, have been proposed to estimate the possible lifetime risk of
lung cancer from inhaled radon progeny from the results of the epidemiological studies
with limited follow-up periods (Harley et al., 1981; NCRP, 1984a,b; ICRP, 1987; NRC,
1988; Jacobi, 1992).
(46) At present, multiplicative projection models, which assume a correlation with
the age dependency of the normal baseline rate of lung cancer, are considered to be
more representative of the time distribution of the excess risk. Assuming a proportional
exposure-risk relationship, these relative risk models proceed from the age specific
mortality rate for lung cancer to the age specific excess rate resulting from chronic
exposure starting at 18 years of age. The integration considers a time lag (minimum
latency) between exposure and the expression of lung cancer from inhaled radon
progeny.
(47) In ZCRP Publication 60, the Commission used a projection model with a
constant multiplier (relative risk factor) for most cancers and low-LET radiation.
However, the epidemiological findings from radon-exposed miners now yield
convincing evidence that the excess relative risk factor for lung cancer varies strongly
with time since exposure and with attained age. This follows from the analysis of the
data from the uranium miners in the USA and Canada in the BEIR IV study (NRC,
1988) and from the data of the uranium miners in Bohemia (Sevc et al., 1988, 1993).
On the basis of these findings, modified multiplicative risk projection models have been
developed (NRC, 1988; Jacobi et al., 1992). They are compared in Annex A.
(48) With respect to smoking, some studies on lung cancer in radon-exposed miners
suggest qualitatively a synergistic or multiplicative effect, whereas some do not. Some
PROTECTION AGAINST RADON-222 11
quantitative information comes from a large case-control study among the Colorado
uranium miners. This study yields a somewhat less than multiplicative effect of smoking
and rejects an additive model (Whittemore and McMillan, 1983; Hornung and
Meinhardt, 1987). It should be noted, however, that these miners were exposed to very
high radon levels. Furthermore, it has been reported that, with increasing follow-up, this
relationship is moving towards an additive model (Jacobi, 1991). A similar result is
reported in the New Mexico studies (Samet et al., 1989). The latter tendency might be
related to the different latency distributions of small-cell and squamous cell carcinoma,
which are two most common types of carcinoma included in the generic term lung
cancer. In short, the epidemiological evidence from miners does not yet provide a firm
quantitative conclusion on the influence of smoking (IARC, 1988).
(49) In this context, it should be mentioned that the Life Span Study of the atomic
bomb survivors yields for females an excess relative risk of lung cancer per unit
equivalent dose to the lung that is 3 to 4 times higher than that for males (Shimizu et aI.,
1988). The absolute excess risk per unit dose was much the same in males and females.
It has been demonstrated that this sex difference in relative risk diminished after
adjustment had been made assuming additivity of the effect of smoking and external
radiation exposure (Kopecky et al., 1986).
(50) It is biologically plausible that the absolute risk coefficient should be about the
same for men and women of similar habits, including smoking. In the absence of a cleai
indication to the contrary, the Commission has now decided to use, for protection
purposes, the same absolute lifetime risk per unit exposure to radon progeny for both
males and females. In so doing it is recognised that the risk factor may be over-cautious
for females. The use of the same relative risk would have predicted a lower absolute
fatality coefficient for females, probably related to a lower level of smoking.
2.2.2. Lifetime risk from chronic occupational exposure
(51) As in ZCRP Publication 64 the Commission has adopted nominal probability
coefficients for chronic exposure of workers (ages 18 to 65 years). Since the
epidemiology is all related to the exposure to concentrations of potential alpha activity,
rather than to intake, the coefficients relate to exposure. They can be converted to
nominal coefficients for intake using a standard breathing rate of 1.2 m3 h-l. The
published estimates of risk are similar to those in the BEIR IV report (NRC, 1988).
This report gave a lifetime fatality coefficient of 3.5 X 10e4 per WLM for a U.S.
population, 9.99 x 10e5 per (mJ h m-3). The Commission’s reference population has
baseline values of survival probability, and of the age-specific lung cancer mortality rate,
corresponding to the reference data for the “average population” and defined as the
unweighted average of the values listed by Land and Sinclair (1991) for the populations
of Japan, the United States, Puerto Rico, the United Kingdom and China. This
population has a somewhat lower baseline cancer mortality. On this basis, the
Commission has adopted a nominal probability coefficient (fatality) for males and
females of 8.0 X low5 per (mJ h me3). The corresponding value in historical units is
2.83 X 10m4 per WLM, which has been rounded to 3 X 1OmJ per WLM.
2.2.3. Lifetime risk from chronic exposure of the public
(52) The fatality probability coefficient for the general public might be somewhat
larger than that for miners because of the inclusion of children. However, the effect of
any high relative risk in the period soon after exposure of children would be offset by
JAICRP 23:2-B
12 REPORT OFATASK GROUP OFCOMMITTEE 4
the decreasing excess relative risk with time. For the mortality coefficient for cancer in
general, the Commission has used fatality coefficients of 5 x lo-* per Sv for the public
and 4 x lo-* per Sv for workers-a factor of 1.25 (ICRP, 1991). However, for exposure
to radon, the Commission knows of no reason to adopt a lifetime risk coefficient for
children different from that for adults. Many other factors may influence the difference
in coefficient for occupational and public exposure to radon progeny. They include dust
loading, particle size, the degree of attachment of radon progeny to condensation nuclei
and dust particles, and the properties of the respiratory tract as a function of age. To
adjust the risk coefficient, it is necessary to consider all these factors.
(53) On balance, variations in the values of the physical and biological parameters
suggest a lower dose (and therefore risk) per unit exposure in buildings than in mines.
Several authorities have made adjustments for this difference, either implicitly or
explicitly. The results are expressed as the factor by which the risk coefficient for
exposure in mines should be changed to give the coefficient for exposure in buildings.
Calculations by NEA (1983) yield a factor of 0.65, by NCRP (1984b) a value of 1.4 in
the case of adult males, and by Harley (1984) a range from 0.8 to 1.2. ICRP (1987)
adopted a value of 0.8, NRC (1988) adopted a default value of unity, but later
calculated a range from 0.6 to 0.9 (NRC, 1991).
(54) Despite the importance of the unattached fraction, these adjustments are all
close to unity. Taking this into account, and accepting the implicit degree of
approximation, the Commission has concluded that, for protection purposes, there is
insufficient justification for adopting a nominal probability coefficient (fatality) for the
public different from that for workers, i.e. 8 x 10e5 per (mJ h mM3).
2.2.4. Detriment coeficients
(55) In order to establish a consistent policy for exposure to radon and to other
radiation sources, it is necessary to take account of the factors that convert mortality
into detriment. In ICRP Publication 60 (ICRP, 1991), the Commission took account of
non-fatal cancer, hereditary effects and the length of life lost or impaired. The principal
detriment due to the inhalation of radon and its progeny is that associated with the fatal
lung cancer. There is a slight addition due to curable lung cancer and a slight reduction
due to a smaller length of life lost than for the average of all cancers. From the values in
Table B-20 of ZCRP Publication 60, the detriment coefficient for lung cancer is 0.95
times the fatality coefficient. There will also be some detriment resulting from the
exposure of tissues outside the lung as the result of radon transferred to these tissues by
the blood, and of radon progeny inhaled. The information in Annex B shows that these
will result in an increase in detriment of about 2%. In view of these various factors, the
Commission has concluded that the selection of a detriment coefficient different from
the fatality coefficient for radon exposure is not justified.
2.2.5. The conversionfrom exposure to effective dose
(56) Because most workers exposed to radon will also be exposed to other sources
of radiation, it is helpful to provide a conversion from radon exposure to effective dose.
Since the Commission has not used a dosimetric approach for radon, this conversion
has been obtained by a direct comparison of the detriment associated with a unit
effective dose and a unit radon exposure. The detriment per unit effective dose is
5.6 X 10e5 per mSv for workers and 7.3 X low5 per mSv for the general public (ICRP,
1991). The detriment per unit exposure to radon progeny is 8.0 X 10T5 per (mJ h me3)
PROTECTION AGAINST RADON-222 13
for workers and the same for members of the public. In terms of detriment, an exposure
to radon progeny of 1 mJ h rnA3 is equivalent to an effective dose of 1.43 mSv for
workers or 1.10 mSv for members of the public. The corresponding figures for 1 WLM
are 5.06 mSv for workers and 3.88 mSv for members of the public. This difference is
entirely due to the different detriment coefficients for effective dose in ZCRP
Publication 60. The conversions obtained in this way are called conversion conventions.
They are based on an equality of detriment, not on dosimetry. Rounded values are given
in Table 7.
3. RADON IN BUILDINGS
(57) A building above ground, especially if it is made of traditional earthen materials
quarried locally and has a basement, may be considered as a transition between the
lithosphere and the atmosphere. If all the doors and windows are open, indoor air will
not be very different from the outdoor air: if the openings are all tightly closed, the
indoor radon concentration will be appreciably higher than that outdoors.
(58) Underground workings, such as those involved in tunnelling, are not strictly
buildings and the options for reducing the concentration of radon and its progeny are
somewhat different from those available in buildings. A description of the mining
environment is given in ZCRP Publication 47 (ICRP, 1986) and is relevant to other
underground workings.
3.1. Radon Concentrations in Buildings
(59) For both dwellings and workplaces, the distributions of radon concentrations
are approximately lognormal, with some tendency for high concentrations to lie above
those predicted by the lognormal distribution. The geometric mean (GM) and geometric
standard deviation (GSD) describe the distribution. The arithmetic mean (AM) is used
to estimate the average probability of detrimental health effects. Comprehensive data on
indoor radon concentrations are compiled by the United Nations Scientific Committee
on the Effects of Atomic Radiation. The Committee concluded (UNSCEAR, 1988) that
the worldwide, population-weighted, values of these parameters for dwellings are
AM=40 Bq rne3, GM=25 Bq rnM3 and GSD = 2.5. It also adopted a typical value of
0.4 for the equilibrium factor.
(60) Radon concentrations in dwellings differ between countries because of
differences in geology and climate, in construction materials and techniques, and in
domestic customs. National values mask marked regional variations in radon
concentrations. Elevated regional values ranging up to several times the central
UNSCEAR values occur fairly widely and values of several thousands of Bq mm3 have
been found in thousands of houses in Finland (Castren, 1987) and Sweden
(Socialstyrelsen, 1988). Systematic investigations of above-ground workplaces are still
rare, with the principal exception of public buildings such as schools and nurseries.
3.2. Building Occupancy
(61) To calculate the radon exposure from measured concentrations, a value of the
occupancy factor is needed. UNSCEAR (1988) uses 0.80 indoors and 0.20 outdoors
for worldwide calculations. In northern countries, the indoor occupancy factor seems
14 REPORT OF A TASK GROUP OF COMMITTEE 4
to be higher according to studies in the UK (Brown, 1983) and Sweden (Mjiines, 1986;
Westrell, 1984). On average, more than 90% of time in the UK is spent indoors, 75%
being spent in dwellings; differences between summer and winter are small. The
Swedish studies show that about 85% to 90% of time is spent indoors, 65% being spent
in dwellings: this changes to 60% when the holiday period is included. Some 5% to 10%
of time is spent outdoors, and the same percentage is used for travelling. The occupancy
factor for women who remain at home in France is said to be 90% (Roy and Courtay,
1991). A rounded occupancy factor of 0.8 is adopted here, corresponding to
7000 hours per year. For workplaces, it is customary to assume an occupancy of
2000 hours per year. These values are reasonable reference values but do not
necessarily reflect the conditions in any particular building. This uncertainty reinforces
the need to use rounded, but fairly representative, occupancy values.
3.3. The Value of Identifying Radon-Prone Areas
(62) In the Commission’s view, there is merit in defining radon-prone areas in which
the concentration of radon in buildings is likely to be higher than is typical of the
country as a whole. This allows attention to be focused on radon where it is most
exigent and action to be concentrated where it is most likely to be effective. Any
definition of radon-prone areas will have to be in fairly general terms, so it must be
remembered that some locations with high radon concentrations may occur outside
radon-prone areas. One way of selecting areas to be treated as “radon-prone” is to use
the results of surveys in dwellings and to define a radon-prone area in terms of a
selected proportion of dwellings with concentrations above some selected value. The
choice of these figures is discussed in Section 4.2.2.
(63) Whereas knowledge of the geology and the type of soil is important in
identifying likely radon-prone areas, especially in the first phase of a radon programme,
the most reliable way to delineate radon-prone areas is by measuring the radon
concentrations in a representative sample of existing dwellings. The radiological
information, which also reflects the nature and use of the dwellings, may then be used to
improve the use of the geological information in identifying other radon-prone areas.
Correlations with superficial and bed-rock geology, soil radon and permeability may be
used to adjust or explain the boundaries of the areas (Miles et al., 1992). In some
regions, the correlations may be strong enough for geological criteria to be applied
directly (Akerblom et al., 1990; Clavensjo and Akerblom, 1992), but what succeeds in
some cases may not succeed in all.
3.4. Remedial and Preventive Measures
(64) The principal methods for reducing high radon concentrations indoors are as
follows:
(a) To reduce the radon supply by reversing the pressure differential between the
building and the soil, often called soil depressurisation. This is most easily
achieved by using a small fan to withdraw the radon from the region under the
floor, either in a porous area under (or close to) the dwelling or in the space
under a suspended floor.
(b)
(cl
Cd)
(4
PROTECTION AGAINST RADON-222 15
To reduce the radon supply by raising the resistance of the foundations to soil gas
entry or by treating building materials to reduce radon escape. This process of
sealing is difficult to make effective in existing buildings because there are many
routes of entry for radon from the ground.
To remove the radon source, which is likely to be feasible only for the water
supply and in, extreme cases, solid materials such as the underlying soil.
To dilute the radon and its progeny by increasing the ventilation rate. The
effectiveness of this process is limited because the ventilation rate in most
buildings is already as high as the occupants want, and further ventilation will
increase heating or cooling costs. Some forms of ventilation will decrease the
pressure in the building, thus increasing the radon input.
To reduce the concentration of radon progeny, e.g. by filtration or by increased
movement of indoor air to enhance the deposition of radon progeny.
Some of these remedial measures, e.g. (a) and (d), depend on a continued expenditure if
they are to be effective. Local circumstances and the material giving rise to the radon
will influence the choice of methods.
(65) Table 4 shows a qualitative summary of the costs and effectiveness of the
various options for radon remedial work. The cost and effectiveness of the methods are
likely to vary locally and national authorities are best placed to adapt their policies to
their particular circumstances.
Table 4. Guide to the cost and effectiveness of various remedial
measures for buildings
Method cost Effectiveness”
Soil depressurisation
Floor sealing
Water treatment
Subsoil removal
Increased ventilation
Increased air movement
Moderate
Moderate
Moderate
High
Moderate
Low
High
Moderate
High
High
Low
Low
il The effectiveness is judged in terms of the effect on the part of
the concentration of radon progeny to which the remedial measure
applies.
4. THE APPROACH TO PROTECTION IN DWELLINGS
4.1. Policy Issues
(66) Radon in dwellings is singled out for special attention by the Commission in
IC’RP Publication 60 because of the magnitude of individual and collective doses
(Paragraphs 216-218). The Commission has dealt with radon in dwellings only in the
context of intervention. It has not treated the occupancy of dwellings as a practice. It
envisages that intervention would involve “modifications to the dwellings or to the
behaviour of the occupants”. Behaviour is taken here to mean the manner in which
occupants use a dwelling.
16 REPORT OF A TASK GROUP OF COMMITTEE 4
(67) The Commission goes on to recommend the use of action levels for initiating
intervention:
,, . . . to help in deciding when to require or advise remedial action in existing dwellings.
The choice of an action level is complex, depending not only on the level of exposure,
but also on the likely scale of action, which has economic implications for the
community and for individuals’: Whereas owner-occupiers may be left to decide
whether to take action, firm national action levels may be required.”
In a crucial passage, the Commission recommends that
“the best choice of an action level may well be that level which defines a significant, but
not unmanageable, number of houses in need of remedial work. It is then not to be
expected that the same action level will be appropriate in all countries.”
(68) By dealing with radon in dwellings in this way, the Commission has emphasised
intervention to protect the more highly exposed individual members of the population.
In this report, it has not dealt with the wider public health implications of the exposures
to the whole population. Any action affecting the whole housing stock of a country
would be extremely costly, although it might still be cost-effective in terms of the
reduction in the national collective dose. It is for national authorities to decide whether
the necessary funds would be available and best spent on general radon reduction or
other aspects of housing improvement.
(69) Following the policy set out in Section 1.5, consideration is given in this section
to the circumstances under which the principles of protection against natural sources of
radiation might be applied to radon in buildings and to the practical procedures for
doing so. The section deals primarily with dwellings, but many of the issues are equally
relevant to buildings used as workplaces. The special problems of workplaces are dealt
with in Section 5.
(70) It is clear that elevated levels of radon do occur in some dwellings, that it is
possible to identify the conditions under which they arise, that remedial and preventive
measures are usually simple and of moderate cost, and that there are appreciable risks
attendant on elevated exposures. Intervention is therefore feasible. The main matter is
the d e termination of the action level at which intervention should be undertaken.
4.2.1
(7 1
4.2. Practical Protection in Dwellings
Action level for intervention in dwellings
) It is now appropriate to examine the basis for adopting an action level for
intervention in dwellings. Here, and throughout the report, action levels relate to the
annual mean concentration of radon in a building. It is important that the action taken
should be intended to produce substantial reduction in radon exposures. It is not
sufficient to adopt marginal improvements aimed only at reducing the radon
concentrations to a value just below the action level. Once intervention is decided, the
degree of the intervention should be optimised.
(72) It seems clear that some remedial measures against radon in dwellings are
almost always justified above a continued annual effective dose of 10 mSv. For simple
remedial measures, a somewhat lower figure could be considered, but a reduction by a
factor of five or ten would reduce the action level to a value below the dose from
natural background sources. The choice of action level for annual effective dose is thus
PROTECTION AGAINST RADON-222 17
limited to the range of about 3-10 mSv. The Commission recommends that the action
level should be set within this range by the appropriate authorities.
(73) The corresponding rounded value of radon concentration is about
200-600 Bq me3, with an annual occupancy of 7000 hours and an equilibrium factor of
0.4. Continuous domestic exposures at average concentrations of 200 Bq rnd3 and
600 Bq rnT3 would imply annual exposures as in Table 5.
Table 5. Annual exposures for action levels of 200 (Bq me3) and 600 (Bq me3) in
dwellings
Action level (effective dose) 3 (mSv y-j) 10 (mSv y-l)
Action level (radon concentration) 200 (Bq mm3) 600 (Bq m-3)
Annual exposure to radon gas 1.4 (MBq h rne3) 4.2 (MBq h m-3)
Annual exposure to progeny 3.11 (mJ h me3) 9.33 (ml h me3)
0.88 WLM 2.63 WLM
4.2.2. Implementation of action levels
(74) It is for national authorities to decide whether to make action levels mandatory
or advisory. Much will depend on the view taken of the social and legal circumstances.
If there is a high proportion of rented dwellings together with a legal system based on
statutes, there may be a willingness to oblige landlords to comply with the action level.
In common-law jurisdictions with a preponderance of owner-occupiers, compulsion
may be deemed undesirable. In either case, it is of considerable importance to ensure
that occupiers, both tenants and owners, are fully aware of the risks of radon and the
remedial options. Because of the uncertainty inherent in any measurement of indoor
radon level, it is also important to allow some flexibility in cases marginally above or
below the action level. It must also be remembered that the risk estimates relate to a
mixed population of smokers and non-smokers. Unless the effect of smoking is purely
additive, the action level will be over-cautious in relation to the risks to non-smokers.
The conventional conversion from radon exposure to effective dose will also
over-estimate the risks to non-smokers. In a few situations, the readily available
counter-measures may not be sufficient to bring the radon concentrations in a dwelling
down to the action level. It must then be remembered that the action level recommended
by the Commission relates only to the simple measures discussed in this section. More
severe measures, such as relocation, would not be appropriate unless the irreducible
concentrations were an order of magnitude or more higher than the action levels adopted.
(75) Although exposure to radon is unlikely to be an acute threat to health, it will be
wise not to delay remedial action unduly once an elevated level has been found.
National authorities recognise the importance of this point and have developed various
protocols. In Sweden, for example, householders are advised to take simple precautions
temporarily, such as increasing the ventilation, until a permanent remedy can be
effected (Socialstyrelsen, 1990). There has been a tendency to relate rapidity of action
to the level of radon. National authorities should be aware that such schemes may result
in procrastination, or even inaction, on the part of some occupiers of dwellings where
the radon concentrations are not markedly above the action level.
(76) Attention was drawn in Section 3.3 to the concept of radon-prone areas. A
radon-prone area might be defined as one in which about 1% of dwellings had a radon
concentration of more than ten times the national average value. In any particular case,
18 REPORT OF A TASK GROUP OF COMMITTEE 4
both the country-wide distribution and the choice of action level will influence the
definition. General quantitative advice can be no more than indicative. The spatial
clustering of buildings requiring action because of geological circumstances is
advantageous: it facilitates the establishment of programmes of measurement and
intervention. Furthermore, it helps to order priorities in a national scheme. In setting
priorities, it is prudent to take action more urgently in areas of high radon concentration
while not necessarily basing the urgency of action on the concentrations found in each
individual house.
4.2.3. Application to new dwellings
(77) The emphasis in the preceding sections has been on existing dwellings, but the
approach adopted is also relevant to future dwellings. Differences in the action levels set
by some authorities for the two circumstances are not large and not all authorities have
regarded the differentiation between old and new dwellings as helpful, partly because
such refinement may prove difficult to explain and partly because the figure for new
dwellings cannot be applied rigorously until the dwelling is completed and occupied.
(78) The aims in imposing restrictions on the construction of new dwellings in
radon-prone areas are to keep the radon concentrations in the finished buildings as low
as can reasonably be achieved and to provide for the easy introduction of further
remedial measures if the initial construction fails to achieve concentrations below the
action level for existing buildings. These aims are best achieved by issuing guidance on
construction practices. Particularly careful consideration should be given to
developments on made-up ground if there are indications that radium-bearing wastes
have been dumped there. A thorough quantitative assessment will be needed in this
circumstance, possibly supported by measurements in a temporary structure on the
proposed site.
(79) When new buildings are to be erected in a radon-prone area, it will be advisable
to modify the design of the foundations so as to prevent elevated radon levels. There
are two types of modified foundation, those that readily permit later remedial measures
and those that are resistant to radon, or, more correctly, to soil-gas. In some
circumstances, elevated radon concentrations could be caused by the use of ground fill
or building materials with elevated radium-226 content. As such materials can be
readily detected by the gamma-ray emission, consideration should be given to
identifying them and preventing or limiting their use.
(80) The radon-resistant approach requires bigger changes in foundation design and
construction to prevent soil gas from entering the building by passive means. It then has
no further costs. The simpler solution is the ready-remedy approach, in which a low-
resistance fill layer with a low radium content is provided under the floor slab so that
the radon may be extracted. Space may also be left for an interior exhaust duct for the
extracted air.
(81) Either approach will reduce radon exposure. The approach favoured by
national authorities will depend on local building styles, the extent and severity of
radon-proneness, and the regulatory regime. In the initial phase of a national radon
programme, the authorities will need to monitor closely the outcome of preventive and
remedial procedures to ensure that they are reliable and durable. The most effective
option may prove to be a combination of the two approaches.
PROTECTION AGAINST RADON-222 19
5. THE APPROACH TO PROTECTION IN WORKPLACES
(82) Radon is present in all workplaces. In some, such as uranium mines, it is a
recognised source of exposure and is already subject to control. In others, such as
buildings and non-uranium mines, it is widely ignored. As indicated in Section 1.5, there
is some difficulty in distinguishing between radon concentrations that should be treated
as being due to a practice and those that should be regarded as being due to an existing
situation. The Commission now recommends the use of action levels to clarify the basis
for this choice.
(83) In the first place, an action level is needed to define workplaces, including
mines, in which intervention should be undertaken to reduce radon exposures.
Secondly, it is necessary to define the workplaces in which the Commission’s system of
protection for practices should be applied to radon exposures, with other workplace not
being subject to this system. This definition can also be expressed as an action level.
5.1. The Selection of Relevant Workplaces
(84) It is likely that elevated levels of radon will occur in buildings used as
workplaces in radon-prone areas defined for dwellings. However, such areas may have
been defined only for residential areas. When defining radon-prone areas, national
authorities ought also to take into account non-residential areas.
(85) It would be advisable for regulatory or supervisory agencies to ensure that a
systematic survey is conducted in places of work in radon-prone areas. It would also be
prudent to make additional measurements in a representative sample of workplaces
throughout the country to ensure that no geographical area of importance is being
overlooked. If reliance is being placed on measurements in dwellings to define the areas
of concern for workplaces, care must be taken to ensure that any systematic differences
in the two types of building are taken into account. There is, however, a strong
argument in favour of the same boundaries of radon-prone areas for dwellings and
workplaces. The confusion likely to be caused by different boundaries would then be
avoided. Underground workplaces, and other workplaces such as spas, should be
considered separately.
5.1.1. Workplaces in which intervention is needed
(86) Workers who are not regarded as being occupationally exposed to radiation are
usually treated in the same way as members of the public. It is then logical to adopt an
action level for intervention in workplaces at the same level of effective dose as the
action level for dwellings. The action levels for intervention in workplaces can be most
easily derived from the range of action levels for dwellings by multiplying by 7000/2000
(the ratio of the occupancy) and by 3.88/5.06 (the ratio of the dose conversion
coefficients). The resulting range (rounded) is 500-1500 Bq per rnm3. When selecting
action levels for dwellings and workplaces, authorities should choose values that are
similarly located within the two ranges. In some mines, the equilibrium factor may be
significantly different from 0.4. National authorities may then wish to use a different
action level in terms of radon concentration in such mines.
.MIcRP 23:2-c
20 REPORT OF A TASK GROUP OF COMMITTEE 4
5.1.2. Workplaces in which the system of protection for practices should be applied
(87) For workplaces, the Commission recognises in ZCRP Publication 60 the ubiquity
of radiation and the need to avoid the conclusion that all workers should be subject to a
regime of radiological protection. To avoid unrealistic and unnecessary protective
measures, the Commission has concluded that its system of protection for practices
should be applied at work only when the exposures incurred at work are a result of
situations that can reasonably be regarded as being the responsibility of the operating
management.
(88) To some extent, radon in workplaces can be so regarded. Nevertheless, the
Commission recognises (Paragraph 135) that
I‘ . . . there is some exposure to radon in all workplaces, and it is important not to
require the use of a formal system of separate decisions to exempt each individual
workplace where controls are not needed. They should be excluded from the control of
occupational exposure by some general system. Considerable knowledge and judgement
is needed to define such a system.”
The Commission goes on to recommend that exposure to radon should be excluded
from its system of protection and treated separately, unless the relevant regulatory
agency has ruled otherwise, either in a defined geographical area or for defined practices,
Guidance is offered in this section on the basis for such a ruling.
(89) There are clearly advantages in adopting the same action level for requiring the
application of the system of protection and for instituting remedial measures. The
Commission therefore recommends the adoption of an action level within the range of
500-1500 Bq rnd3 for both purposes. The corresponding range of annual effective dose
is 3-10 mSv. When simple countermeasures do not reduce the radon concentrations
below the action level, the Commission’s system of protection should be applied to the
practice.
(90) The control of radon may also need to be considered in workplaces where there
is already a need for controls on the exposures directly associated with the work, that is
to say, from artificial sources. For such circumstances, the Commission recommends
that ‘it will be sufficient to take account of the exposures to natural sources if, and only if,
they would be controlled in their own right. . . . Elsewhere, they would not need to be
included in radiation monitoring results, or in statistical reports of occupational
exposures” (Paragraph 137).
5.1.3. Workplaces used by members of the public
(91) Some workplaces are also used by members of the public. If the public
occupancy is low, e.g. in offices, libraries and theatres, these workplaces need no special
treatment. If the occupancy is high, e.g. in hospitals, residential institutions and schools,
the premises should be treated as dwellings for the purpose of setting an action level for
remedial measures. Workers should be subject to the Commission’s system of protection
for practices on the same basis as in any other workplace.
5.2. Practical Protection in Workplaces
(92) Having adopted an action level, the regulatory agency or the employer will need
to determine what is to be done with a workplace where the radon concentration
PROTECTION AGAINST RADON-222 2:1
exceeds that level. It would seem most sensible to start by taking whatever remedial
measures are necessary to reduce the radon concentration to a value well below the
action level. In many buildings, there will be little difficulty in taking such measures, but
this may not be so in large complex structures. Preventive measures should be
incorporated in new buildings in radon-prone areas.
(93) Should it prove unreasonably difficult, either in all or some parts of a building
or an underground workplace, to reduce the radon below the action level, the system of
radiological protection should be the same as when workers are exposed to artificial
airborne activity at work. If radon concentrations vary widely in different parts of the
workplace, the action level may be based on the annual time-weighted average
concentration in the different parts of the workplace.
5.2.1. The choice and application of exposure limits
(94) The dose limit recommended by the Commission for effective dose is 20 mSv
per year averaged over a period of 5 years with the proviso that the effective dose
should not exceed 50 mSv in any single year (ICRP, 1991). For workers on short term
contracts, the regulatory agency might consider an averaging period not exceeding the
period of the contract of employment. The selection of the corresponding figure for
exposure to radon progeny can best be done with the help of the convention, based on
equal detriment, for the equivalence of radon exposure and effective dose. As indicated
in Section 2, the Commission has decided to base its risk estimates primarily on the
results of the radon epidemiology. The dosimetric estimate of the effective dose per unit
exposure to radon progeny has therefore not been used in selecting the exposure limit.
(95) From the conversion coefficient of 1.43 mSv per (mJ h mm3), 20 mSv
corresponds to 14.0 mJ h me3 (4.0 WLM) and 50 mSv corresponds to 35.0 mJ h mm3
(10.0 WLM). The corresponding figures for radon are thus:
14 mJ h mm3 per year (4 WLM per year), averaged over 5 years and
35 mJ h me3 in a single year (10 WLM in a single year).
(96) Even if all the l-year exposure is incurred in a short period, the absorbed doses
to lung tissues will not be sufficiently high to cause deterministic effects. The derived air
concentration for radon (occupancy of 2000 hours per year, equilibrium factor of 0.4)
would be about 3000 Bq me3 (average over 1 year). The exposure limits and the
derived air concentrations are not the primary basis of control. The whole of the
Commission’s system of protection for practices should be applied, with emphasis on
the optimisation of protection, which includes the use of any constraints on the choice
of options.
5.2.2. The application of the system ofprotection
(97) The system of protection for practices recommended by the Commission
applies to radon in workplaces where the radon concentration exceeds, or may exceed,
the action level in the same way as it does in any workplace where radioactive
substances are handled in unsealed forms. The issues relating specifically to mines were
set out by the Commission in ZCRP Publication 47 (ICRP, 1986). They are still valid.
More general guidance is given in the following paragraphs and stems directly from the
recommendations of ZCRP Publication 60. This guidance relates only to workplaces in
which it has been decided to apply the Commission’s system of protection.
22 REPORT OF A TASK GROUP OF COMMITTEE 4
(98) Designation of areas, Areas of workplaces where the radon is not directly
associated with the operations in the workplace will need to be treated as supervised
areas in which periodic measurements may be needed to confirm that concentrations
have not increased with time. Exceptionally, the concentrations may be high enough to
require special operating procedures and therefore to require the use of controlled
areas. If the radon concentration is largely due to the operations, it is more likely that
controlled areas will be needed with special working procedures adopted to control the
exposure to radon.
(99) Monitoring of individual exposures. Employers will need to ensure that exposure
of their workers in controlled areas is monitored in a systematic fashion (see Section 7.5
of ICRP Publication 60). It will sometimes be sufficient to use workplace, rather than
individual, monitoring. Devices such as track-etch detectors may be used for either
purpose, provided that workplace monitoring is related to working periods. Gross
exposures rather than net values above the action level should be determined. The
action level is merely the device for deciding to apply the system of protection to the
radon exposures, all of which are then regarded as being the responsibility of the
operating management.
(100) Additivity of exposures. It is possible that workers may be exposed both to
radon above the action level, and to other sources, such as an x-ray machine, to which
the system of protection for practices applies. In mines, there will often be exposures to
radioactive ore dusts and gamma radiation. In such circumstances, it will be necessary
to aggregate the doses for comparison with the dose limit. To do so, the dose conversion
convention should be employed to translate the radon exposure into effective dose,
which should then be added to the other effective doses for overall assessment. More
generally, where workers are exposed to radon above the action level and to other
sources, either internal or external, the conventional procedure of summing the
quotients of the separate annual exposures and limits for comparison with unity should
be followed to check for compliance with the recommended dose limits. The
Commission recognises that no allowance has been made for exposures other than to
radon in interpreting the epidemiological data. The requirement to add the dose from
these sources for control purposes therefore errs somewhat on the side of caution.
6. SUMMARY
(101) The Commission has used an epidemiological basis for the assessment and
control of radon exposure in this report. Since all the available epidemiological studies
use the quantity inhaled potential alpha energy, this has been used as the primary
quantity in this report. The Commission does not recommend the use of the dosimetric
human respiratory model (ICRP, 1994) for the assessment and control of radon
exposures.
(102) The Commission sees practical advantages in the delineation of radon-prone
areas where more buildings than usual have elevated radon levels. For dwellings, it is
suggested that areas with more than 1% of buildings with radon concentrations
exceeding ten times the national average concentration might be designated as radon-
prone, but the choice will depend on local conditions. A similar approach might be
adopted in non-residential areas. Action against radon should be focused on such
radon-prone areas.
PROTECTION AGAINST RADON-222 2.3
(103) The imperatives of intervention against adventitious exposure to radon in
buildings are clear. Above appropriate action levels, intervention is practicable and
usually more cost-effective than other investments in radiological protection.
(104) Two types of building need to be considered, dwellings and workplaces. In
both cases, radon concentrations are most likely to be elevated by the ingress of soil gas
from the subjacent ground. Preventive and remedial measures to avoid this
circumstance are recommended. The action levels adopted should fall within the
recommended range of values given in Table 7.
(105) Proven measures against radon are readily available. For remedial work, the
technical procedure that is most likely to maintain the radon level to a value well below
the action level should be adopted from the outset. Intervention should take place soon
after the discovery of elevated levels, especially if the concentrations are substantially
above the action levels adopted by the competent authority. For preventive work,
construction codes and building guides should be devised that will consistently achieve
low concentrations of radon in the completed buildings.
(106) In workplaces, both in buildings and underground, where the radon
concentrations remain above the recommended action level after any appropriate
remedial measures have been taken, the Commission’s system of protection should be
applied and radon should be treated in the same way as any other radioactive material
at work.
(107) The relevant data on conversion coefficients are given in Table 6 and the main
quantitative recommendations are summarised in Table 7. Corresponding values in
historical units are given in Table 8.
Table 6. Summary of conversion coefficients
Quantity Unit Value Section
Exposure and radon gas conversions (mJ h me3) per WLM 3.54 1.4
(equilibrium factor 0.4) (mJ h mm3) per (Bq h me3) 2.22 x 10-h
WLM per (Bq h rne3) 6.28 x lo-’
Annual exposure per unit radon concentration”
at home (mJ h m-)) per (Bq m-l) 1.56~ IO-’ I .4
at work (mJ h me3) per (Bq mm31 4.45 x lo-”
at home WLM per (Bq m-9 4.40x 10-J
at work WLM per (Bq m-? 1.26 x lo-’
a Assuming 7000 hours per year indoors or 2000 hours per year at work and an equilibrium factor of 0.4.
24 REPORT OF A TASK GROUP OF COMMITTEE 4
Table 7. Summary of values recommended in this report
Quantity Unit
Recommended
value Section
Nominal fatality and detriment coefftcient
at home and at work
Dose conversion convention, effective dose
per unit exposure:
at home
at work
Action level (dwellings)
Radon concentration
Annual effective dose
Action level (workplaces)
Radon concentration
Annual effective dose
Occupational annual limit on exposure
(n-d h me3)-’
mSv per (mJ h rne3)
mSv per (rnJ h m-“)
‘Wvv- 3,
(B%3)
(mJ h me3) per year,
averaged over 5 years
(ml h rnT3) in a single year
8x 1O-5 2.2.2.
2.2.3.
2.2.4.
1.1 2.2.5.
1.4
200-600” 4.2.1.
3-10
500-1500’ 5.1.
3-10
14 5.2.1.
35
a Assuming 7000 hours per year indoors or 2000 hours per year at work and an equilibrium factor of 0.4.
Table 8. Summary of quantities in historical units corresponding to those in Table 7
Quantity Unit
Recommended
value Section
Nominal fatality and detriment coefficient
at home and at work
Dose conversion convention, effective dose
per unit exposure:
at home
at work
Action level (dwellings)
Radon concentration
Annual effective dose
Action level (workplaces)
Radon concentration
Annual effective dose
Occupational annual limit on exposure
(WLM) - ’
mSv per WLM 4 2.2.5.
mSv per WLM 5
(Bqm~m ‘)
‘“9,~~- 3,
WLM per year, averaged
over 5 years
WLM in a sinale year
3 x 10-d 2.2.2.
2.2.3.
2.2.4.
200-600” 4.2.1.
3-10
500-1500” 5.1.
3-10
4 5.2.1.
10
B Assuming 7000 hours per year indoors or 2000 hours per year at work and an equilibrium factor of 0.4.
PROTECTION AGAINST RADON-222 25
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PROTECTION AGAINST RADON-222 27
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ANNEX A. AN ILLUSTRATIVE EXAMPLE OF EPIDEMIOLOGY OF
MINERS EXPOSED TO RADON AND ITS PROGENY
NOTE: This annex is a summary of a study done in 1992. It is used here only to
illustrate the methodology of combining studies and of interpreting the combined finding
in terms of the lifetime risk of chronic exposure.
(Al) This annex summarises the epidemiological findings of several studies that are of
importance for the assessment of exposure limits.
(A2) One general uncertainty in all these studies stems from the estimates of the
miners’ exposure to radon and its progeny. This concerns particularly those miners who
received their exposure at earlier times when no radon measurements were carried out in
these mines. Among the more reliable exposure estimates for this earlier mining period
are those available for the Bohemian uranium miners. This study cohort comprises
4042 miners who started underground work between 1948 and 1957 at a mean age of
32 years (mean duration of employment 8.2 years) and were followed-up from 1953-
1985. The mean annual number of radon measurements per mine-shaft in this mining
district increased from about 100 in 1948 to about 700 in 1970 (Sevc et al., 1993).
A.l. The Principal Study Groups
(A3) Characteristics of the seven more quantitative cohort studies of underground
miners are summarised in Table A.l. For the Beaverlodge (Eldorado) miners, a mean
cumulative exposure of 22 WLM was previously estimated (Howe et al., 1986). A re-
analysis of the exposure conditions and the working history of these miners is still in
hand, but early results indicate that their real exposure was probably, on average, about a
factor of two higher (SENES, 1991; Chambers et al., 1992).
(A4) The cohort studies listed in Table A.1 comprise in total about 31,500
underground miners with a mean age at the start of exposure of about 30 years. The
mean employment period of the uranium miners was about 8 years, averaged over all
cohort studies. The weighted mean value of their cumulative exposure during their
underground work, weighted by the number of miners in each group, was about
120 WLM. The mean follow-up period of these epidemiological studies varies from 14 to
32 years; the mean period, weighted by the person years at risk in each study, is about
20 years.
A.2. Exposure-Risk Relationship
(A5) In general, the cohort studies of miners listed in Table A.1 yield a monotonic
increase of the excess relative lung cancer risk with the cumulative exposure to radon
progeny. Taking into account the statistical confidence range of the excess relative risk,
the data can be fitted by a proportional exposure-risk relationship up to cumulative
exposures of a few hundred WLM (NRC, 1988).
29
30 REPORT OF A TASK GROUP OF COMMITTEE 4
Table A.1. Characteristic data of seven study cohorts of underground miners
Mean Number of lung
Number Person cumulative cancer deaths
of years exposure
Cohort study follow-up period miners at risk (WLM) Obs Exp
Uranium miners
Colorado, USA, 1951-1982, cumulative 2915 66 237 510 157 48.7
exposure <2000 WLM”
New Mexico, USA, 1957-1985 3469 66 500 111 68 17
Ontario, Canada, 1955-1981 11 076 217 810 37 87 57.9
Beaverlodge, Saskatchewan, Canada,
1950-1980 6847 114 170 44 (22)b 65 28.7
Bohemia, 1953-1985 4042 97 913 227 574 122
France, 1946-1985 1785 44 005 70 45 21.1
Iron miners
Malmberget, Sweden, 1951-1976 1292 27 397 98 51 14.9
Total, all studies 31486 635 022 120’ 1047 310
a The higher exposures were eliminated because of the likelihood of the effect of cell killing on the incidence
of lung cancer.
b Original value (Howe er aZ., 1986). See Paragraph (A7).
c Weighted by number of miners in each study.
(A6) Furthermore, the analysis of the excess risk data as a function of time since
exposure indicates some correlation with the baseline risk, R,,, of lung cancer without
radiation exposure. This supports the use of the multiplicative risk projection model.
(A7) Table A.2 shows the mean values of the excess relative risk of lung cancer per
unit exposure that follow from the cohort studies listed in Table A.2. These relative risk
Table A.2. Mean excess relative risk of lung cancer per unit cumulative exposure to radon progeny resulting
from the different cohort studies of underground miners; the values are averaged over the follow-up period
and all exposure cohorts”
Excess relative risk per J h mV3
(282 WLM)h
Study group, follow-up period Mean value 95% confidence interval
Uranium miners
Colorado, USA, 1951-1982, exposure < 2000 WLM
New Mexico, USA, 1957-1985
Ontario, Canada, 1955-1981
Beaverlodge, Saskatchewan, Canada, 1950-1980
Bohemia, 1953-1985
France, 1946-1985
Iron miners
Malmberget, Sweden, 1951-1976
Weighted mean. all studiesd
1.7 0.85-4.0
5.1 2.0-15.4
4.0 1.7-9.4
3.7’ 1.7-8.5
4.8 3.4-6.8
1.7 O-4.6
4.0
3.19
0.85-27
2.3-6.0
a Referring to the studies listed in Table A.1. For references see text.
h To obtain the risk coefficient per 100 WLM, the values have to be divided by a factor 2.82.
c Revised value taking into account new exposure estimates for these miners (SENES, 1991).
d Weighted for person years at risk.
PROTECTION AGAINST RADON-222 31
coefficients are averaged over the follow-up period and all exposure cohorts of each
study; in the case of the Colorado miners the cohort with exposures above 7 J h mm3
(2000 WLM) was excluded. The data for the Colorado, Ontario, and Malmberget miners
are based on the BEIR IV study (NRC, 1988). The values for the uranium miners in
Bohemia, in New Mexico, and in France were taken from new or updated publications
(Sevc et al., 1993; Samet et al., 1991; Tirmarche et al., 1992a,b). In the case of the
Beaverlodge miners, in addition to the previous value (Howe et al., 1986), a revised value
is given, based on the new exposure estimates for these miners (SENES, 1991).
(A8) The excess relative risk coefficients that follow from the different cohort studies
in Table A.2 do not differ significantly. Summing over all these studies results in a
weighted mean value of the excess relative risk coefficient, averaged over the follow-up
period, of
3.79 (2.3 to 6.0) per (J h me3)
or 1.34 (0.8 to 2.1) per 100 WLM
(95% confidence interval in brackets).
(A9) The studies of non-uranium miners that are referred to in this section but not
listed in Table A.l, provide only qualitative or weak quantitative information about the
link between radon exposure and the excess relative risk of cancer. The quantitative
results are consistent with those in Table A.2.
(AlO) In addition, the statistical analysis of the Bohemian uranium miners leads to the
suggestion that the excess relative risk coefficient might be somewhat higher at exposures
below 100 WLM compared with the mean value listed in Table A.2 (Sevc et af., 1993).
However, owing to the absence of an internal control group, the possibility that this
tendency may be due to other confounding factors such as smoking cannot be excluded.
The same is true for the observed tendency of a somewhat higher effectiveness per unit
exposure at protracted exposures. A similar exposure-rate effect has been derived from
the data of the Colorado miners (Hornung and Meinhardt, 1987). However, the analysis
of the data sets from four cohort studies of uranium miners, carried out by the BEIR IV
Committee, yields no consistent pattern on this issue. Another factor that could account
for higher risk coefficients at low exposures might be the presence of other carcinogens,
the exposures to which were not correlated with the radon exposures. The lack of
information about exposures in dwellings may also play a part.
(All) Dosimetric models lead to the conclusion that the bronchial dose per unit of
exposure increases as the fraction of the radon progeny attached to condensation nuclei
decreases. The bronchial dose per unit exposure then increases with increasing
ventilation of working areas in mines or with decreasing dust concentration (NRC,
1991). Following these dosimetric arguments, a higher excess lung cancer risk per unit
exposure in well ventilated mines would be expected compared with that in poorly
ventilated ones. This tendency may go some way towards explaining the finding that the
excess risk per unit exposure is larger at lower exposures. The results of the Swedish
case-control study in dwellings (Pershagen, 1993) suggest that the effect does not
influence the risk estimates of Table A.2, but the statistical limitations prevent a
categorical conclusion.
(A12) Finally, it should be recognised that the primary data on the excess risk of lung
cancer in radon-exposed miners include the risk contribution from external radiation and
from inhaled, long-lived, emitters in mines. Under the exposure conditions of the
considered cohorts of uranium miners, the relative contribution from these other
32 REPORT OF A TASK GROUP OF COMMITTEE 4
occupational radiation sources was probably small. In ZCRP Publication 50 (ICRP,
1987), a relative risk correction of about lo-20% was assumed. For reasons set out in
Annex B, the Commission no longer makes any correction for these factors. There may
also have been some exposure to other carcinogens. Quantitative estimates are available
only in a few studies, so no account has been taken of their contribution to the observed
mortality, all of which has been assigned to the radon exposures.
(A13) In summary, the epidemiological findings from these studies provide no firm
conclusion on the real shape of the exposure-risk relationship, particularly at low
cumulative exposures. They are broadly consistent with a proportional relationship.
They are also consistent with other dose-response relationships, including both
threshold relationships and those with enhanced risk coefficients at low exposures. The
proportional relationship leads to a central estimate of the excess relative risk of fatal
lung cancer per unit exposure at work of
3.79 per (J h me3)
or 1.34 per 100 WLM.
This central estimate of the excess relative risk coefficient refers to a follow-up period
of 20 years, taking into account a time lag (minimum latency) of 5 years.
(A14) To obtain estimates of the lifetime risk of chronic exposure it is necessary to
postulate a projection model. The Commission uses a multiplicative projection model
for this purpose. Three different versions of this model are used in this annex:
(a) The multiplicative model used in ZCRP Publication 50 (ICRP, 1987) which uses
a persistent (excess) relative risk (PRR model).
(b) The modified projection model proposed in the BEIR IV study (NRC, 1988)
which takes into account the variation of the excess relative risk with time since
exposure (TSE) and with attained age (BEIR IV model).
(c) The modified projection model which has been developed at the GSF (Jacobi et
aZ., 1992) which considers the age-specific excess rate of lung cancer as function
of age at exposure and of time since exposure (GSF model).
These models and their original input parameters are summarised at the end of this
annex. The GSF model was developed primarily for the evaluation of the probability of
causation for lung cancer among the uranium miners in Saxonia and Thuringia in
eastern Germany.
(A15) The original models used an excess relative risk coefficient of 1.6 X lo-* per
WLM, reduced in the case of the ICRP model to 1 x lo-* per WLM because of the
expected overestimate due to the use of a constant excess relative risk coefficient. In this
report, the excess relative risk coefficient is lower by a factor of 1.33/1.6, or 0.83.
(A16) Although the three models show some differences in the age specific excess
risks, the estimate of the attributable lifetime risk of lung cancer is much less sensitive to
the choice of model.
(A17) The input parameters of these risk projection models are based on the
epidemiological data from male miners. In ZCRP Publication 50 (ICRP, 1987) and in the
BEIR IV study (NRC, 1988), it was assumed that, at the same exposure to radon
progeny, the relative excess of the age-specific lung cancer rate in females would be
equal to that in males. The validity of this assumption, which implies a purely
multiplicative influence of smoking, is questionable.
PROTECTION AGAINST RADON-222 33
(A18) The lifetime values of the excess relative risk and of the excess absolute risk
of fatal lung cancer from occupational exposure to radon progeny that follow from these
projection models are listed in Table A.3. These central estimates refer to a chronic
exposure at constant annual levels of 3.5, 7 and 14 mJ h m-3 per year (1, 2 and 4 WLM
per year).
Table A.3. Excess lifetime relative risk and lifetime probability of fatal lung cancer for
the ‘Male Reference Worker’, attributable to chronic occupational exposure to radon
(222Rn) progeny from age 18 to 64 (baseline risk R, = 0.042)
Risk quantity
Annual
exposure
mJ h rnvLI
(WLM)
Projection model a
PRR model TSE model TSE model
ICRP 50 BEIR IV GSF
(1987) (1988) (1992)
Excess relative risk 3.5 (1.0) 0.35 0.29 0.31
7.0 (2.0) 0.68 0.56 0.62
14.0 (4.0) 1.33 1.12 1.19
Excess absolute risk 3.5 (1.0) 0.015 0.012 0.013
7.0 (2.0) 0.029 0.024 0.026
14.0 (4.0) 0.056 0.047 0.050
a The excess relative risk coefficients underlying these models have been modified by a
factor of 0.83 from the original values used in the models (see text).
(A19) The nominal fatality probability coefficient for occupational exposure to
radon progeny can now be derived giving the results shown in Table A.3. Of the three
models available, the original ICRP model is unsatisfactory because the constant excess
risk factor is not appropriate. The BEIR IV model and the GSF model give similar
results, but the smooth variation of the excess relative risk factor in the GSF model is
more plausible biologically. The basis adopted in this annex is the attributable
probability of fatal cancer for an exposure of 7 mJ h m- 3 per year of working life using
the GSF projection model. This leads to a probability coefficient (fatality) of
0.026/(7.0 x 47) = 7.90 x 10d5 per (mJ h rnv3)
(2.80 x 10d4 per WLM).
These values have been derived for a male workforce with a working lifetime from age
18 to 64 years, inclusive (47 years). They are assumed also to apply to a similar female
workforce.
A.3. Risk Projection Models
(A20) This section summarises the form of the risk projection models used in this
annex. All the models are multiplicative risk projection models, assuming a correlation
between the excess age-specific lung cancer rate il,, caused by a preceding exposure,
and the normal baseline rate of lung cancer, A, at the attained age a (age at risk). This
implies a multiplicative influence of smoking. Furthermore, all these models proceed
from a proportional relationship between the exposure Pp, received at an age r, (age at
exposure) and the attributed excess rate of lung cancer in the subsequent years, taking
into account a time lag z (minimum latency) between exposure and expression of lung
34 REPORT OF A TASK GROUP OF COMMITTEE 4
cancer. As originally used, all the models used the same excess relative rate, il,llz,, for
males and females. All these projection models proceed from the general equation:
I,(a) =L,(a)f(f,,a)P, (t,) for a 2 (t,+ t).
Besides the inserted age-specific baseline rate, the models apply different functions
f(f,,a) which express the variation of the excess relative rate with time since exposure,
T = a - t,, and with the attained age a.
A.3.1. The model used in ICRP Publication 50 (ICRP, 1987)
(A21) The relative model used in ZCRP Publication 50 proceeds from a mean, time-
averaged, relative risk coefficient and a persisting excess relative risk factor until the
end of life (PRR model):
A,( a)/&( a) =fP,( t,) for a > t, + t,
with r = 5 years.
A.3.2. The BEIR IV model
(A22) The model proposed by the BEIR IV Committee (NRC, 1988) is based
essentially on an analysis of the lung cancer data from uranium miners in Canada and
the U.S.A. It is a modified multiplicative projection model that takes into account the
time since exposure as well as the attained age. The finally recommended model is given
by the relationship:
&(a)/&(a) = sy(a)[P, + 0.5 Pz]
with y(a) = 1.2 for a< 55 years
r(a) = 1.0 for a = 55-64 years
and y(a) = 0.4 for a = 65 years
s is a constant of proportionality with exposure, taken by the original BEIR IV model to
be 0.025. P, is the potential a energy exposure, in WLM, incurred between 5 and
15 years before the age a, and P2, in WLM, is the exposure incurred 15 years or more
before this age.
Thus, this model leads to a stepwise reduction of the age-specific excess rate.
A.3.3. The GSF model
(A23) The primary objective of this recently developed model (Jacobi et al., 1992)
was the evaluation of the probability of causation of lung cancer among the previous
uranium miners in eastern Germany.
(A24) Like the BEIR IV model, this is a modified multiplicative projection model.
Its main variable is the time since exposure, T = a - te. The basic equation of this model,
referring to a single potential energy exposure, Pp, is:
~,(a)/~,(a)=s(t,)P,(r,)~(T)fora>r,+t
where t = 4 years.
The function $ (T ), with T in years, characterises the relative latency distribution,
PROTECTION AGAINST RADON-222 35
which is normalised to one at its maximum. Beyond this maximum a decrease of the
excess relative rate with a half-life of 10 years is assumed.
#(T)=O for TS4 years
$(T)=0.25(T-4) for 4 years < T < 8 years
#(T)=l for 8 years I T I 12 years
and #(T ) = exp[ - (ln2/10)( T - 12)] for T> 12 years.
The function s(t,) is a function of proportionality with exposure taking into account the
decreasing carcinogenic susceptibility of the lung with increasing age r, at time of
exposure. In the original model it decreased from 0.036 WLM-’ for an age at exposure
of 20 years, to 0.017 WLM-’ for age at exposure of 60 years.
Compared with the BEIR IV-step model the GSF model provides a monotonic
variation of the excess relative lung cancer with age or time since exposure.
A.3.4. Excess lifetime risk
(A25) Assuming a proportional exposure-risk relationship, all these relative risk
models proceed from the following general equation for the age specific excess rate of
lung cancer, A,, at an attained age a. The baseline rate at this age is &(a);
(1-z
Ua,P) =&(a) j f,(a,tJ?&)d~~
18~
This relationship refers to a chronic exposure starting at an age t, (age at time of
exposure) of 18 years. P(t,) is the exposure rate at age t,. f,(a,t,) is the attributed excess
relative risk at the attained age a per unit of exposure at age te. The integration
considers a time lag z (minimum latency) between exposure and the expression of lung
cancer from inhaled radon progeny.
(A26) Taking into account a survival probability p(a) from start of exposure until
the considered age a, the excess lifetime risk up to an age of 90 years becomes
90>
K= j- p(a%(d=)da
18.~
ANNEX B. THE MAGNITUDE OF POSSIBLE CORRECTIONS TO
THE EXPOSURE LIMITS
(Bl) Three possible corrections to the exposure limits are considered. The first
relates to the estimation of the total detriment associated with a fatal lung cancer caused
by exposure to radon and its progeny. The other two are concerned with the possible
contribution to the incidence of the observed lung cancers from exposures other than
that due to radon progeny.
B.l. Detriment Other than from Lung Cancer
(B2) In assessing the total detriment associated with a fatal lung cancer attributable
to radon progeny, it is necessary to assess the contributions to the effective dose due to
radon dissolved in tissues other than the lung and due to the direct inhalation of radon
JAIUIP 23:2-D
36 REPORT OF A TASK GROUP OF COMMITTEE 4
progeny. The effective dose equivalent rate from continued exposure to a radon
concentration of 1 Bq mm3 with no contribution from radon progeny except that from
the decay of radon after inhalation has been estimated (Peterman and Perkins, 1988).
Table B.l is based on their data, with some increase in the contributions from organs
with a high fat content. The tissue weighting factors of ZCRP Publication 60 have been
used.
Table B.l. The effective dose from exposure of tissues other than lung due to the
inhalation of unit concentration of radon free of progeny
Organ or tissue
Equivalent dose per Tissue
unit exposure weighting
lo-i0 Sv per (Bq h mV3) factor
Contribution to
effective dose
lo-‘0 sv
Gonads
Bone marrow8
Colon
Stomach
Bladder
Breast b
Liver a
Oesophagus c
Thyroid
Bone
Skin c
Remainder c
0.38
2.00
0.66
0.66
0.33
1.50
1.30
0.66
0.66
0.15
0.66
0.66
0.2
0.12
0.12
0.12
0.05
0.05
0.05
0.05
0.05
0.01
0.01
0.05
0.076
0.24
0.079
0.079
0.165
0.075
0.065
0.033
0.033
0.0015
0.0066
0.033
Total (rounded) 0.74
a Approximately twice the value from Peterman and Perkins (1988).
b Approximately five times the value from Peterman and Perkins (1988).
c Taken as “vessel rich” from Peterman and Perkins (1988).
(B3) For the exposure of workers to radon and its progeny with an equilibrium
factor of 0.4 and an occupancy of 2000 hours, a concentration of radon of 500 Bq me3
is equivalent to an annual effective dose of about 3 mSv, i.e. 1 Bq h me3 is equivalent to
3 x 10e6 mSv. The effective dose from the inhalation of 1 Bq h rnb3 of radon alone
(Table B.l) is 0.74 x lo-’ mSv, or about 2% of the total effective dose.
(B4) It is difficult to estimate the effective dose from tissues other than the lung due
to directly inhaled radon progeny because the estimate depends critically on the rates of
transfer from the point of deposition to other organs and tissues. Preliminary estimates
suggest that the contribution will be a few percent of the total effective dose.
(B5) For lung cancer alone, the detriment coefficient is 0.95 times the fatality
coefficient. On the basis of the two additional contributions to the effective dose, and
thus to the total detriment, the Commission has adopted a total detriment coefficient
equal to the fatality coefficient.
B.2. Lung Cancer due to External Radiation and Ore Dust in the Study Groups
(B6) A typical level of exposure to radon progeny in the mines for which the
epidemiological data have been obtained is in the region of 10 WLM per year. This
corresponds to an effective dose of about 50 mSv per year, giving a fatality rate of
about 3 X 10e3 per year. Estimates of annual gamma doses in uranium mines were given
PROTECTION AGAINST RADON-222 3’7
by the Commission in ICRP Publications 32 and 47 (ICRP, 1981, 1986). These
estimates were in the region of 5-10 mSv per year. The fatality coefficient for lung
cancer from Table B.20 in ICRP Publication 60 is 8.5 X 10e3 per Sv, giving a lung
cancer fatality rate from external radiation in the region of 1104 per year. This is not
sufficient to justify inclusion in the interpretation of the epidemiology. Any such
correction would tend to decrease the estimated risk coefficient associated with the
radon progeny.
(B7) The possible contribution from the inhalation of ore dust is very uncertain.
Concentrations of respirable dust of the order of 10 mg me3 are not uncommon in
uranium mines. The specific alpha activity of the particles is low and any carcinogenic
effects may be influenced more by the physical and chemical forms of the dust than by
the radioactive content. There seems to be no adequate basis for making an allowance
for possible lung cancer due to the dust. Any such correction would tend to decrease
the estimated risk coefficient associated with the radon progeny.
ANNEX C. GLOSSARY
Action level: The concentration of radon at which intervention is recommended to
reduce the exposure in a dwelling or workplace.
Bronchial tree: The branching airways of the respiratory tract from the trachea to the
entry to the gas exchange or pulmonary region of the lung.
Condensation nuclei: Any small particles or ions capable of serving as a site for the
condensation of vapour.
Dose conversion convention: The method used to relate exposure to radon progeny
expressed in WLM, to effective dose expressed in mSv on the basis of equal detriment.
Equilibrium equivalent concentration, ces: The activity concentration of radon, in
equilibrium with its short-lived progeny which would have the same potential alpha
energy concentration as the existing non-equilibrium mixture.
Equilibrium factor, F: The ratio of the equilibrium equivalent concentration and the
radon gas concentration.
Potential alpha energy concentration, cp: The concentration of short-lived radon
progeny in air in terms of the alpha energy released during complete decay through
polonium-214.
Potential alpha energy exposure, P,(T): The time integral of the potential alpha energy
concentration in air, c,, to which an individual is exposed over a given time period T, e.g.
one year.
Radon progeny: The decay products of radon-222, used herein in the more limited
sense of the short-lived decay products from polonium-218 through polonium-214.
Radon prone: An area in which the characteristics of the ground cause more buildings
than usual to have elevated radon levels.
Reference level: Used to establish values of measured quantities such as recording level
or investigation level, above which some specified action or decision should be taken.
Risk: Terms relating to risk are grouped together here.
Risk. In this report, the probability that a fatal lung cancer will
occur.
38 REPORT OF A TASK GROUP OF COMMITTEE 4
Relative risk. The ratio of the risk in an exposed population to that in
a similar unexposed population.
Excess relative risk. Relative risk - 1.
Absolute risk. The probability that a fatal lung cancer will occur.
Excess or attributable risk. The absolute excess or attributable risk due to an
exposure.
Risk coefficient. The risk per unit exposure.
Risk projection model. A model describing the variation of risk as a function of
the time since exposure. It may be related by a factor to
the age specific baseline risk (multiplicative) or added to
the baseline risk (additive).
Soil gas: A gas in the free space within a volume of soil.
Unattached fraction: The fraction of the potential alpha energy concentration of short-
lived radon progeny that is not attached to the ambient aerosol.
Working level: Any combination of the short-lived progeny of radon in one litre of air
that will result in the emission of 1.3 X 16 MeV of potential alpha energy.
Working level month: The cumulative exposure from breathing an atmosphere at a
concentration of 1 WL for a working month of 170 hours.
THE HISTORY OF THE RADON PROBLEM IN
MINES AND HOMES
W Jacobi
The radon saga is a scientific thriller with tragic features and political confounders.
The historical roots of this saga reach back to the 15th century. It is a field full of
dilemmas, controversies and frustrations, some of which still persist. One should learn
from this history which has been described in part by Schiittmann (1988) and Stannard
(1988).
1. THE ‘SCHNEEBERGER LUNG DISEASE’
About 1470, extensive mining of silver commenced in the region of Schneeberg, a
small city in Saxony/Germany at the northern slope of the “Erzgebirge” (Ore
Mountains). Silver was also mined in the region of Joachimsthal (now Jachymov) at the
southern Bohemian side of the Ore Mountains at about the same time. The mining
techniques which were applied in both of these regions at the beginning of the 16th
century have been described and illustrated by Agricola (1494-1555), referred to as the
father of mineralogy, who worked from 1527-1533 as physician in Joachimsthal
(Agricola, 1556). His most famous book De Re Metallica was translated from Latin to
English by the American mining engineer Herbert C. Hoover (who later became the
president of the United States) and his wife Lou. Agricola indicated that in Jachymov,
the silver ore was mined at or near the surface, whereas in Schneeberg already the ore
was mined at greater depths. Some shafts reached a depth of about 400 m.
An unusually high mortality from lung disease, occurring in younger workers, was
observed among the miners in the Schneeberg region in the early 16th century. The first
report stems from Paracelsus (1493-1541) in his book iiber die Bergsucht und andere
Bergkrankheiten (About the ‘Bergsucht’ and other Miner’s Diseases). The word
Bergsucht is a summary term for the lung diseases observed in miners. Paracelsus had
written this book in the year 1537, but it was printed only after his death (Paracelsus,
1567, new edition 1925).
The frequency of this lung disease, which was later called ‘Schneeberger
Lungenkrankheit’ (‘Schneeberger Lung Disease’), increased in the 17th and 18th
centuries, when the mining of silver, cobalt and copper was intensified (see Rosen,
1943). The disease was eventually identified as lung cancer by Haerting and Hesse
(1879). Originally, it was assumed to be a lymphatic sarcoma, originating from the
bronchial lymph nodes and it was somewhat later classified as bronchial cancer.
Haerting and Hesse mention that at about this time 75% of the miners in the
Schneeberg region died from lung cancer. The available reports indicate that the
percentage was probably lower among the miners of Jachymov.
2. THE SEARCH FOR THE CAUSES
Paracelsus (1567) labelled the ‘Schneeberger Lung Disease’ as “Mala Metallorum”. It
was assumed that the lung cancer was caused by inhaled ore dust containing different
39
40 W. JACOBI
metals. Contributory carcinogenic factors were thought to include tubercular disease
and the presence of arsenic in the dust.
In 1898, Marie and Pierre Curie had extracted radium (226Ra) and polonium (210Po)
from Jachymov ores (Curie, 1898). The so-called radium emanation, later called radon
(222Rn) was identified as a radioactive noble gas produced by the decay of radium.
Starting with the first radon measurements by Elster and Geitel (1901), a high radon
concentration in the air of mines at Schneeberg and Jachymov was subsequently
demonstrated. The first cases of cancer, particularly skin cancer, induced by the x-rays
of radium radiation, were reported at the beginning of the 20th century (Frieben, 1902;
Hesse, 1911).
It was on the basis of these findings, that a relation between lung cancer and the high
radon content in these mines was assumed. Schiittmann (1988) considered that H. E.
Miiller, a mining director in Zwickau, Saxony, was the first person to recognize the
causal link. Miiller concluded that the Schneeberger lung cancer was a specific
occupational disease, caused by the radium content of the ore and the high radon
content of the air in these mines which, when inhaled, initiated a carcinogenic process in
the airways of the lung.
This hypothesis was supported by more precise radon measurements carried out in
the 1920s in the Schneeberg (Lorenser and Ludewig, 1924) and Jachymov mines
(Pirchan and Sikl, 1932). However, the role of radon as a causative factor for the
Schneeberger lung cancer was not generally accepted. In a summary report of a group
of pathologists from Dresden which was published in 1926, the opinion was expressed
that this cancer type might be initiated by the inhalation of toxic ore dusts (Rostosky et
aZ., 1926). Lorenz (1944) later claimed that arsenic and other mine contaminants, as
well as the poor health of the miners, were the primary causes.
A research programme in Germany which was initiated in 1936 by B. Rajewsky from
the Kaiser-Wilhelm-Institute (later Max-Planck-Institute) for Biophysics in Frankfurt,
Main, provided further clarification of the relation between radon concentration and
lung cancer. This comprehensive study involved radon measurements in the mines near
Schneeberg; and measurements of the alpha activity in tissue samples and
histopathological analysis of lung tissues from miners who had died from lung cancer
(Hueck, 1939; Rajewsky, 1940). At that time, the average radon concentration in most
mines at Schneeberg was within the range of 70-120 kBq rnm3. In one mine, however, a
mean value of about 500 Bq mV3 was observed. It was known that most workers in this
mine died from lung cancer; it was called “death mine”. On the basis of these
observations and supporting biological studies, it was concluded that in the Schneeberg
mines, the inhalation of radon must be regarded as a possible cause for the high lung
cancer frequency among the miners in Schneeberg region (Rajewsky, 1940).
This summarises the extent of knowledge in 1945. The available data from
Schneeberg and Jachymov did not enable any quantitative estimate of the relationship
between radon exposure and lung cancer. Furthermore, the possible role of the inhaled
short-lived decay products of radon was not yet realised.
3. URANIUM MINING AND THE ROLE OF THE
RADON DAUGHTERS
The extensive mining and processing of uranium for military purposes started in the
1940s. The main sources at this time were the uranium deposits in the Belgian Congo
THE HISTORY OF THE RADON PROBLEM 41
(now Zaire), Canada and in Colorado, USA. In 1946, the intensive mining of uranium
commenced under a directive of the USSR government in the historical mining region
of Aue, Schneeberg in East Germany. Proceeding from the radium production in
Jachymov, the mining of uranium in Bohemia began in 1948. At the same time, uranium
mining started in France.
During this early phase of uranium mining, little attention was paid to the radiological
protection of workers. It was believed that the radon levels in these new mines were
considerably lower than in the older mines in the Ore Mountains and only a few radon
measurements were reported in this period. In the Colorado mines, radon samples were
not taken before 1950; and in the uranium mines in East Germany, radon data are only
available after 1955 (Jacobi, 1992).
During this period, dosimetric studies and radiobiological research on the possible
effects of the inhaled radon were continuing. However, all attempts failed to explain the
induction of lung cancer by inhalation of radon gas alone, until William F. Bale (Bale,
1951) in Rochester introduced the idea that the decay products of radon might be the
causative agent. John Harley confirmed the presence of high concentrations of these
radon decay products by measurements in air (Harley, 1953). Bale stated in his
memorandum: “In these and other past evaluations of the hazard associated with radon,
the vital fact seems to have been almost entirely neglected that the radiation dosage due
to the disintegration products of radon, present in the air under most conditions
where radon itself is present, conceivably and likely will far exceed the radiation dose
due to radon itself and to disintegration products formed while the radon is in the
bronchi”.
In the following years, experimental studies on the deposition and retention of
inhaled radon and thoron decay products in the lung were carried out at the University
of Rochester (Bale and Shapiro, 1956; Shapiro, 1956); and at the Max-Planck-Institute
for Biophysics in Frankfurt, Main (Schraub et al., 1955; Aurand et al., 1955; Jacobi ef
al., 1956). The results of these studies enabled a quantitative estimate to be made of the
mean alpha dose to the bronchial epithelium from inhaled decay products of radon.
Dosimetric lung models for the evaluation of the activity and dose distribution along the
bronchial airways were also developed (Altschuler et al., 1964; Jacobi, 1964). It was
concluded from these various studies that the maximum alpha dose should be expected
in the target cells of the segmental bronchi of the airways. Lung dosimetry of inhaled
short-lived radon decay products, now called radon progeny, is still an important and
controversial area of research.
As a consequence of these studies, there followed the development of more reliable
methods for the monitoring of radon progeny in mines, In the United States, the
concept of the potential alpha energy concentration of radon progeny in air, the so-
called ‘Working Level Concept’ was created (Holaday, 1957). Practical experience has
confirmed the appropriateness of this simplifying concept for the purposes of
monitoring, and for the evaluation of the exposure of miners to radon progeny.
About the same time, a study on the health status and the relation to radiation
exposure of the uranium miners in Colorado was carried out by the Division of
Occupational Health of the US Public Health Service. The preliminary results indicated
a significant excess of lung cancer among these miners (Wagoner er al., 1964). Following
the hearings before the Joint Committee on Atomic Energy of the Congress of the
United States in 1967, revised guidelines for the control of radiation hazards in uranium
mining were established by the US Federal Research Council (FRC, 1967).
42 W. JACOBI
The first quantitative analysis of the cohort study among the US uranium miners,
covering the period from 1950 through 1967, was published by Lundin et al. (1971).
One year later, the results of a similar study among uranium miners in Czechoslovakia
was reported (Sevc et al, 1972; see also Sevc et al., 1976). Both studies concluded that
the lung cancer risk increased monotonically with the cumulative exposure to radon
progeny. But the resulting slope of this dose-response relationship was considerably
higher for the Czech miners. Several other cohorts of uranium miners have since been
followed up. The available updated results of all these studies, which constitute a
follow-up on about 30,000 uranium miners, are summarised in this issue, ICRP
Publication 65.
Averaging these studies provides an excess relative risk of lung cancer of about three.
It is noteworthy that this excess is appreciably higher than the excess relative risk from
all types of cancer in the life-span study of the atomic bomb survivors in Hiroshima and
Nagasaki. It should be emphasized that the epidemiological cohort studies involve, only
a small fraction of all uranium miners. For example, the available information indicates
that in the uranium mines in East Germany, about 250,000 persons worked underground
during the critical years from 1946-1955. Their average exposure to radon progeny is
estimated to be about 100-200 WLM per year (Jacobi, 1992). So far, no epidemiological
data are available from these studies. Thus, it can be assumed that from 1945 to the
present, a total of about 500,000 persons worldwide have worked in uranium mines.
High radon levels have also been observed in non-uranium ore mines.
Epidemiological surveys of some of these mining cohorts indicate an excess risk of lung
cancer, for example, amongst fluorspar miners in Newfoundland, Canada (Morrison et
al., 1988), Chinese tin miners (Lubin et al., 1990, 1993) and iron ore miners in Sweden
(Radford et aZ., 1984).
4. PERCEPTION OF THE RADON PROBLEM IN HOMES
Compared with the situation in mines, the possible influence of radon on lung cancer
risk to the general public was discovered much more recently. One year after the
discovery of radon, the measurements of Elster and Geitel (1901) revealed that radon
(at that time called ‘radium emanation’) was a ubiquitous constituent of atmospheric air.
In a paper entitled “Some Cosmical Aspects of Radioactivity” presented at a meeting in
Canada in April 1907, Ernest Rutherford said: “We must bear in mind that all of us are
continuously inhaling radium and thorium emanations and their products, and ionising
air. Some have considered that possibly the presence of radioactive matter and ionised
air may play some part in physiological processes” (Rutherford, 1907). It is noteworthy
that the balneological application of radon was started in the following years. The first
‘Radium Inhalatory’ (more appropriately called Radon Inhalatory) was opened in 1912
in Bad Kreuznach, Germany.
Early environmental measurements of radon were largely confined to outdoor air.
The first set of indoor radon measurements which involved 225 houses in Sweden, were
published by Hultqvist (1956). This study, which had been initiated by Rolf Sievert,
indicated rather high radon levels in a few houses built of alum-shale concrete with a
high radium content. Little attention was paid internationally to this finding because it
was believed that this was a local Swedish problem.
About 20 years later, larger surveys on indoor radon were made in several countries.
Their results are summarised in the reports of UNSCEAR (1977, 1982, 1988, 1993).
THE HISTORY OF THE RADON PROBLEM 43
These studies reveal the extremely large variation in the radon level in houses, covering
a range from a few Bq me3 up to 100,000 Bq md3. This means that some members of
the population are being exposed to indoor radon levels comparable to those of
underground uranium miners in the early phase of uranium mining. It was recognised
that in most houses with high radon levels, the main source was not the building
material but the convective radon influx from the soil. This finding has proved to be of
great importance for the planning of efficient intervention techniques to reduce the
radon level.
The mean values of the indoor level of radon progeny from these national studies
cover a range of the equilibrium equivalent concentration from about 5-50 Bq mm3.
UNSCEAR (1988) assumes a global mean value of about 15 Bq mM3 and a mean value
of the attributable equivalent dose to the bronchial epithelium of about 15 mSv per year
which is about a factor of ten higher than the mean dose of extra-pulmonary tissues
from all other natural radiation sources. Consequently, on the basis of a world average,
about half the total effective dose from natural radiation sources is due to the inhalation
of radon progeny in wellings (ICRP, 1987; UNSCEAR, 19881993).
Estimates of the possible lung cancer risk from indoor exposure to radon progeny are
presently based upon the epidemiological data of radon-exposed underground miners
(ICRP, 1987; NRC, 1988). As has been pointed out by Stidley and Samet (1993), direct
geographical or ecological correlation studies seem to be of low value, due to the strong
influence of other confounding factors. One possible exception might be the recently
published findings on the lung cancer frequency in Umhausen, a small community in
Tyrol, Austria (Ennemoser et al., 1993). Of more promise are case-control studies on
indoor radon in several countries (Neuberger, 1992). Preliminary results of some
smaller studies of this type have been published (Schoenberg et aZ., 1990; Pershagen et
al., 1992, 1993). Although these preliminary findings indicate a positive correlation
between indoor radon levels and lung cancer, in agreement with the range from miner’s
data, the statistical error range is large.
In summary, perception of the radon problem in houses has three components: (1) a
large variation in the range of indoor levels; (2) the relatively high equivalent dose to
the sensitive bronchial epithelium; and (3) the convincing epidemiological evidence of
an excess risk of lung cancer in radon-exposed miners. A major uncertainty remaining is
the evaluation of the carcinogenic effects from indoor exposure to radon and its
progeny, including the synergistic influence of smoking. A reliable quantitative answer
to this vital question is still awaited.
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