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OCR for page 157
8
Indoor-Radon Guidelines and Recommendations
National and international agencies operating under different directives
have been responsible for addressing the health risk associated with indoor
radon and for addressing its regulation. This chapter provides a review and
comparison of national and international guidelines and recommendations
regarding radon in dwellings, schools, and workplaces. It also examines the
differences in the scientific information and in risk-management polices used
for developing the guidelines.
In 1970, through the enactment of several statutes, the US
Environmental Protection Agency (EPA) became responsible for the
establishment of environmental protection standards for both radiologic hazards
and chemical agents. Although there is not now a federal regulation for indoor
radon, EPA has issued guidance under the Indoor Radon Abatement Act about
the risk, measurement and remediation of radon in homes and schools (EPA and
DHHS 1994; 1986~. EPA's published guidelines and recommendations for
indoor radon are different from those of other bodies that develop guidance for
radiation exposure of the public.
RADON MEASUREMENT UNITS
Concentrations of radon gas in air are normally given in units of
picocuries per liter (pCi/L) or becquerels per cubic meter (Bq/m3~; and 1 pCi/L
is equal to 37 Bq/m3. Concentrations of radon decay products (RDPs) normally
are expressed in working levels (WL); 1 WL is defined as any combination of
the short-lived RDPs in 1 L of air that results in the ultimate release of 1.3 x 105
MeV (2.1 x 10-s J/m3) of alpha energy about the amount of energy emitted by
the short-lived decay products in equilibrium with 100 psi of radon. In general,
equilibrium does not occur in houses, because ventilation removes some of the
157
OCR for page 158
158
INDOOR-RADON GUIDELINES
radon and its decay products; also, it takes time for the entering radon to
produce its decay products. Because RDPs have a static charge, they plate out
on walls, furniture, and other solid objects; this reduces the equilibrium ratio
(ER) the concentration of radon progeny in air divided by the concentration
that would exist if the progeny were in equilibrium with the radon gas. The ER
ranges between 0.3 and 0.7; an ER of 0.5 is commonly assumed as an average.
At less than equilibrium, 1 WL is equal to the product of ER and the radon
concentration in picocuries per liter divided by 100. A house with 150 Bq/m3 (4
pCi/L) is likely to have 4 x 10-7 J/m3 (0.02 WL). A working level month (WLM)
is a measure of time-integrated exposure and is the product of time in working
months, which is taken to be 170 hours, and working levels (WL). Thus, 1
WLM is equal to the product of average WL and hours of exposure divided by
170. Under full occupancy conditions (8,760 h/y), residence in a house at 150
Bq/m3 results in about 1.0 WLM per year of exposure. In SI units, 1 WLM is
approximately 3.5 mJh/m3.
PATEIWAYS OF HUMAN EXPOSURE
Inhalation is the principal route of radon exposure of humans. The dose
contribution from the inhaled radon gas itself is small under normal conditions
of exposure. Exposure to radon is due mainly to the inhalation of its short-lived
decay products (polonium-214, polonium-218, lead-214, and bismuth-214),
which deposit nonhomogeneously in the human respiratory tract and irradiate
the bronchial epithelium. Two progeny, Typo and Typo, deliver the most
important alpha-radiation dose to the lung (NCRP 1984c). About 90% of RDPs
can attach initially to airborne particles (ICRP 1993b); tobacco smoke provides
additional attachment sites for RDPs. The unattached fraction (10%) has a
higher rate of deposition and is more efficient in delivering a dose to the critical
cells (basal and secretory cells) of the lung (I:NSCEAR 1993~; about two-thirds
of the total dose in homes from radon comes from the unattached fraction
(National Research Council 1988~. The assumed health effect end point of high
exposure to indoor radon is radiation-induced lung cancer.
This chapter focuses on the lung-cancer risk associated with inhalation
exposures to RDPs. Although risks to other tissues posed by radon can occur
through ingestion of water with high radon concentrations, they are much
smaller than those associated with inhalation exposure to RDPs. All other
exposure pathways distribute smaller amounts of radon and progeny over a
much larger tissue mass with correspondingly lower doses and risks.
OCR for page 159
GUIDELINES FOR EXPOSURE TO TENORM
159
HEALTH EFFECTS AND RISK EVALUATION OF RADON EXPOSURE
The existence of high mortality among miners in central Europe was
recognized before 1600, and the main cause of death was identified as lung
cancer in the late 19th century. It was suggested in 1924 by Ludewig and
Lorenser that the cancers could be attributed to radon exposure (ICRP 1993b).
EPA classifies radon as a known human carcinogen on the basis of data from
epidemiologic studies of underground miners. That classification is supported
by a consensus of national and international organizations (IARC 1988;
National Research Council 1988; ICRP 1987b; NCRP 1984c). Further
information on the deleterious health effects associated with exposure to radon
has been provided by experimental studies of animals (National Research
Council 1988~.
The main source of quantitative information on the risks posed by
radon exposure is the epidemiologic studies of miners which uses data on
thousands of occupationally related lung cancers among many diverse groups of
miners. The epidemiologic evidence of the induction of lung cancer after
inhalation of radon comes from several cohort and case-control studies of
underground miners, particularly uranium miners. The evidence has been
reviewed and summarized in other reports (ICRP 1993b; National Research
Council 1988; UNSCEAR 1988; UNSCEAR 1986~. Most of the data are
consistent with the assumption of a proportional relationship between risk and
cumulative exposure (linear, no-threshold response model). The exception to
linearity occurs at very high exposures (over 2,000 WLM), where the response
per unit exposure decreases; this exception is attributed partly to the reduced life
expectancy of the miners at such high exposures (ICRP 1987b).
The epidemiologic findings have to be extrapolated to provide risk
estimates for long periods of exposure and for populations other than those
studied. For estimating lifetime risk from data covering shorter periods,
projection models are used. Different types of risk-projection models have been
proposed to estimate the possible lifetime risk of lung cancer posed by inhaled
radon progeny in homes on the basis of the results of the epidemiologic studies
of miners (National Research Council 1988; ICRP 1987b; NCRP 1984c).
The National Council on Radiation Protection and Measurements
(NCRP) model is an attributable-risk projection model based on information
obtained from several groups of underground miners in the United States,
Canada, and central Europe (NCRP 1984c). The model expresses lung-cancer
risk uniformly with time after exposure, with the restriction that tumors do not
occur either before a 5-y latent interval or before the age of 40. The model uses
an initial, age-averaged risk coefficient as derived from data on miners and
assumes a decrease in the initial potential excess rate with time after exposure
according to an exponential function. That functional structure provided an age
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160
INDOOR-RADON GUIDELINES
dependence so that the model would fit the observations of lung-cancer
frequency among radon-exposed miners. The NCRP risk reduction with time
since exposure is supported by the followup studies of underground miners
(National Research Council 1988~.
The International Commission on Radiological Protection (ICRP)
model is a constant relative-risk projection model based on the lung-cancer
incidence data from the uranium miner cohort studies (United States, Canada,
and Czechoslovakia) and on information from the atomic-bomb survivors (ICRP
1987b). The model assumes that the excess risk of lung cancer in miners
associated with a given radon exposure is constant with age and over time after
the end of exposures. ICRP made three modifications to the radon relative risk
coefficients from the miner data to reflect presumed differences in residential
indoor exposures. First, because of potential cocarcinogenic influences that
might be present in the mines but not indoors (such as exposures to diesel
fumes, dust, and other forms of radiation), ICRP assumed that the risk
coefficients for residential indoor exposures would be 80% of those for mine
exposures. Second, because of potential differences in breathing rate and the
unattached fraction between residential and mine exposure conditions, ICRP
assumed that the observed dose of alpha radiation per unit of cumulative radon
exposure for the general population is only 80% of that for miners. Third, on the
basis of findings from studies of the atomic-bomb survivors, ICRP assumed a
risk coefficient for exposure of people under 20 y old that was 3 times the risk
coefficient for people 20 or older; this had the effect of increasing the overall
lifetime risk by about 40°/O. The latest recommendations by ICRP (1993b) retain
the multiplicative risk-projection model as in previous publications (ICRP
1987b).
The BEIR IV committee model (National Research Council 1988) is a
relative-risk projection model based on reanalyses of cohort studies of
underground miners (US and Canadian uranium miners and Swedish iron
miners). The model assumes that the rate of excess lung cancer due to radon
exposures increases with age-specific baseline lung-cancer mortality. The BEIR
IV modified relative-risk model is somewhat different from the ICRP 50 model
(ICRP 1987b) in the added assumptions about the effects of time since exposure
and attained age. It incorporates the BEIR IV finding that excess relative risk in
the miners decreased with time since exposure and attained age. Direct evidence
on the sensitivity of children to radon is sparse. The BEIR IV committee did not
find an effect of age at first exposure after controlling for other correlates with
age (National Research Council 19884. That is consistent with the publication of
the BEIR V report, which found no evidence of dependence of lung-cancer risk
on age at exposure for external radiation (National Research Council 1990~. The
effect of any higher relative risk in the period soon after exposure of children
would probably be offset by the decrease in excess relative risk with time.
OCR for page 161
GUIDELINES FOR EXPOSURE TO TENORM
161
Although each of the above three models incorporates risk coefficients
derived from the studies of miners, the biologic assumptions underlying the
models differ. The different features of these risk-projection models are
summarized in table 8.1 (National Research Council 1991~. The NCRP model
(NCRP 1984c) assumes additivity of the risks posed by radon progeny and the
background risk of lung cancer and a time-dependent decline in risk after
exposure. In contrast, the ICRP model (ICRP 1987b) assumes that the
background rate is multiplied by the additional risk associated with radon
progeny. The model developed by the National Research Council (National
Research Council 1988) is also multiplicative, but it incorporates a time-
dependent decline in risk after exposure. With regard to the relationship
between exposure in the mining environment and exposure in the home
environment, the three models make different assumptions. The BEIR IV model
makes no adjustment, whereas the ICRP model reduces the risk by 20% for
adults in the general population, and the NCRP model increases the risk by 40°/O
for the residential exposures, because of a higher calculated unattached fraction.
In addition, the ICRP model increases risk for exposures before the age of 20 y,
and the NCRP model assumes that risk commences at the age of 40 y. In the
BEIR IV model, risk varies with attained age. With regard to smoking, the
NCRP model is additive, whereas the other two models are multiplicative
(National Research Council 1991~.
The estimate of risk based on chronic occupational exposure to radon
in the BEIR IV report (National Research Council 1988), given as a lifetime
fatality coefficient, is 3.5 x 104 per WLM for a US population. The
corresponding ICRP value is 3 x 10-4 per WLM based on a "reference"
population with somewhat lower baseline cancer mortality. EPA's estimates of
lung-cancer risk posed by radon exposure at 150 Bq/m3 (4 pCi/L) 1.6 x 10-3
for never-smokers and 3 x 10-2 for smokers-are based on the report of the
National Research Council (1988) and an adjustment recommended by the
National Research Council (1991~. EPA has made two adjustments to the BEIR
IV model in estimating radon risks. In the first, age-specific baseline lung-
cancer mortality was adjusted by eliminating projected deaths due to an average
background radon exposure of 0.24 WLM per year, reducing the lifetime risk
estimates by about 10%. The second was based on differences in dose to the
bronchial epithelium per unit of radon-progeny exposure in mines and homes
due to a number of physical and biologic factors that are expected to differ in
the two environments. Among the factors considered in the 1991 National
Research Council report are age, sex, aerosol size distribution, unattached
fraction of radon progeny, breathing rate and route (oral vs. nasal), pattern and
efficiency of deposition of radon progeny, solubility of radon progeny in mucus,
and growth of aerosols in the respiratory tract. This comparison of exposure-
dose relations in the mining and home environments indicated that the dose per
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162
INDOOR-RADON GUIDELINES
Table 8.1 Comparison of principal risk-projection models for radon and lung-cancer
Feature NCRP ICRP BEIR IV
Form of model Attributable-risk Relative-risk Relative-risk
Time-dependent Yes; risk declines No
exponentially after
exposure
Lag Sy toy Sy
Yes; risk declines
as time since
exposure lengthens
Effect of age at No effect of age at Threefold increased No effect of age at
exposure exposure risk for exposures exposure
before age of 20 y
Age at risk Risk commences at
ageof40y
Dosimetry Increased risk for
adjustment indoor exposure
Relative risk does Lower risk at age
not change with age of 55 y and older
Decreased risk for No adjustment
indoor exposure
Risk coefficient 10 x 10-6/y per WLM Excess relative risks: Excess relative risk
1.9%/WLM at ages of 2.5%/WLM but
0-20 years and modified by time
0.64%/WLM for since exposure
ages 21 years and
above
Source: National Research Council (1991).
OCR for page 163
GUIDELINES FOR EXPOSURE TO TENORM
163
unit of exposure to radon progeny is about 30°/O lower in the home environment.
Therefore, in calculating the risks associated with residential exposures, EPA
multiplied the risk coefficient in the BEIR IV model by a factor of 0.7 (EPA
1992c).
The assumption underlying the EPA estimates of radon risk by
smoking category is that radon risk varies in proportion to smoking risk (radon
and smoking act multiplicatively in causing lung cancer). The data source used
by EPA for the prevalence of and relative risks associated with smoking was the
surgeon general's report (DHHS 1989~. The calculated lung-cancer death rates
in each smoking category in the general population were compared with the
average lung-cancer death rate for the general population to obtain radon risk
multipliers. For example, the number of lung-cancer deaths per 100,000 current
smokers in the general population (males and females combined) is 10,329. That
is 2.33 times the 4,433 lung-cancer deaths expected in the general population,
averaged over all smoking categories (EPA 1992c). From the presumed
multiplicative interaction between radon and smoking, the radon risk among
current smokers also would be about 2.33 times the radon risk for the general
population. The risk multipliers were used in conjunction with a standard life-
table analysis based on 1980 vital statistics and the EPA-adjusted BEIR IV
relative-risk model to estimate the lung-cancer risks. As discussed previously,
the risk coefficients used in the BEIR IV risk model were adjusted by a factor of
0.7 to correct for an estimated lower bronchial radon dose per WLM in homes
than in mines (National Research Council 1991~. The lung-cancer baseline risk
was also adjusted for an annual background radon exposure of 0.24 WLM.
Table 8.2 shows the risks for never-smokers and current smokers, with the risks
for the general population, for selected radon exposures (EPA 1992c). The lung-
cancer risk to current smokers associated with exposure to radon progeny is
substantially greater than the radon risk to never-smokers.
The analysis of the effects of smoking on Rn risk is subject to
uncertainty about the nature of Me interaction (multiplicative or
submultiplicative), the variation in the relative risk associated with smoking by
age and gender, the changes in age-specific relative risks for smokers as
smoking habits and types of cigarettes change over time, and the influence of
environmental and passive cigarette smoke on Rn risk (EPA 1992c).
More quantitative information on lung-cancer risks posed by exposure
to radon progeny was provided by a joint analysis of data from 11 studies of
underground miners (Lubin and others 1994~. The authors examined over 2,700
lung-cancer deans that occurred among 68,000 miners. The analyses confirm
the linear relationship between cumulative exposure to radon progeny and lung-
cancer risk and a decrease in excess relative risk (ERR) per WLM with attained
OCR for page 164
164
INDOOR-RADON GUIDELINES
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GUIDELINES FOR EXPOSURE TO TENORM
165
age, with time since exposure, and with time after cessation of exposure. Among
miners first exposed to radon progeny under the ages of 10-20 y, the ERR per
WLM was not related to age at first exposure. The report also noted that for
equal total exposure, exposures of long duration and low rate (typical of
exposures in homes) were more harmful than exposures of short duration and
high rate. Among cohorts with tobacco-use information, the slope of the radon
exposure-response function for never-smokers was 3 times that for smokers,
indicating a much greater risk for never-smokers relative to their background
risk of lung cancer from all causes. Assuming that the miner-based findings
apply to residential radon exposure, the study estimated that about 9% of all
lung-cancer deaths among residents of single-family dwellings in the United
States could be attributable to indoor radon exposure. The estimates are similar
to estimates based on the BEIR IV risk model. On the basis of the relative
differences in ERR per WLM for smokers and never-smokers, it was estimated
that indoor radon-progeny exposure could be responsible for 10-12% of the
lung-cancer deaths among smokers and 28-31% of the lung-cancer deaths
among never-smokers. For the roughly 15,000 estimated lung-cancer deaths in
the United States in 1993 that might be attributable to indoor radon-progeny
exposure, those percentages translate to about 10,000 lung-cancer deaths among
smokers and 5,000 among never-smokers (Lubin and others 1994~.
Several studies have aimed at detecting the correlation between the
incidence of lung cancer and exposure to radon in dwellings. The results are
mixed. A study of radon and lung cancer in women, with 480 lung-cancer cases
and 442 controls, has reported a statistically significant trend with increasing
residential radon concentration after adjusting for smoking and age (Schoenberg
and others 1990~. However, another study showed no statistically significant
association between radon exposure in homes and lung-cancer risk (Blot and
others 1990~. A study of indoor radon and lung cancer in Swedish women, with
210 lung-cancer cases and an equal number of controls, reported increasing
trends of lung-cancer risk with radon exposures exceeding 150 Bq/m3
(Pershagen and others 19923.
Recently, Lubin and Boice (1997) provided additional information on
the risk of lung cancer associated with indoor radon. They conducted a meta-
analysis of eight residential case-control studies that included at least 200 case
subjects each and that use long-term indoor radon measurements. The analysis
included a total of 4,263 lung-cancer cases and 6,612 control subjects. From the
published results of each study, relative-risk (RR) estimates for various
categories of radon concentration were obtained, and weighted linear-regression
analyses were performed. The combined trend in RR was significantly different
from zero, and an estimated RR of 1.14 (95°/O CI, 1.0-1.3) at 150 Bq/m3 was
found. The exposure-response trend was similar to model-based extrapolation
OCR for page 166
166
INDOOR-RADON GUIDELINES
found. The exposure-response trend was similar to model-based extrapolation
from miners and to RRs computed directly from miners with low cumulative
exposures.
A summary of lifetime risk estimates of lung-cancer mortality
associated with chronic exposure to radon progeny estimated by various
organizations is provided in table 8.3.
OVERVIEW OF RADON GUIDELINES AND RECOMMENDATIONS
FOR DWELLINGS
National Council on Radiation Protection and Measurements (NCRP)
One of the earliest recommendations for domestic radon exposure in
the United States was developed by NCRP on the basis of available data on
lung-cancer risk (NCRP 1984c). The NCRP recommendation states that an
excess risk of death from lung cancer of 2% (a doubling of the average
background risk of lung cancer) or more over a lifetime for individuals exposed
to enhanced levels of radon decay products should be avoided. The NCRP
recommendation was based on evaluation of the lung-cancer risk and the
avoidance of an unacceptable exposure and thus risk. The recommendation may
be considered as an "upper bound based on maximum tolerable risk." The
excess risk of 2% corresponds to an annual exposure of 2 WLM (equivalent to
8-10 pCi/L if 0.4 or 0.5 is used for the equilibrium ratio) and is the
recommended NCRP remedial action level for radon exposure. It is about 10
times the average background exposure of 0.2 WLM assumed for the US
population. NCRP recommended that exposure above the remedial action level
be reduced using appropriate actions. It also stated that exposures just below the
remedial action level might not be acceptable to some individuals, who could of
course try to reduce their exposures further.
The assumption by NCRP of an excess risk of death from lung cancer
of 2% posed by a lifetime exposure of 2 WLM was based on the available
underground-miner epidemiologic data at the time and on the attributable-risk
projection model (NCRP 1984b). The NCRP estimate is less than the risk
estimated by more-recent projection models, such as those of BEIR IV (National
Research Council 1988) and ICRP 50 (1987b). The most recent
recommendations of ACRE (1993a) retain the same action level for indoor
radon as previously recommended by NCRP (2 WLM) on the basis of an excess
lifetime risk of no more than 10 times the risk associated with the average
annual background levels found in homes and consideration of the feasibility of
remediation.
OCR for page 167
GUIDELINES FOR EXPOSURE TO TENORM
Table 8.3 Comparison of lifetime-risk coefficient estimates associated with
chronic exposure to radon progeny
Reference
Excess lifetime lung cancers:
Deaths per 106 persons per WLM
ICRP (1993b)
EPA (1992c)
EPA (1989b)
EPA (1989b)
National Research Council (BEIR IV) (1988)
EPA (1987b)
ICRP (1987b)
NCRP (1984c)
300
220a
305b
360C
350
460d
230
130
167
aBased on BEIR IV model adjusted by subtracting projected deaths due to average background
radon exposure of 0.24 WLM/y and adjusting risk factor from occupational exposure to general
public with a factor of 0.7.
bBased on BEIR IV model adjusted by eliminating deaths due to average background radon
exposure of 0.25 WLM/y.
CAverage of BEIR IV and ICRP 50 models.
Based on constant relative-risk model.
OCR for page 172
172
INDOOR-RADON GUIDELINES
· To set a reference level of 400 Bq/m3, above which
consideration should be given to reducing radon concentrations in
existing homes, and a design level of 200 Bq/m3 for all new
dwellings.
· To use annual average radon concentrations as a basis for
radiologic protection decisions and to develop criteria for identifying
regions, sites, and building characteristics likely to be associated with
high indoor radon concentrations.
· To have national authorities provide information to the public on
radon exposure, risk, and available remedial measures.
Other
Various countries' and organizations' current recommendations for
action levels for existing houses and for upper limits (bounds) in new buildings
are summarized in table 8.4. Additional comments and information are also
provided in the tabular summary.
Values for existing dwellings are mostly of an advisory nature. In
Sweden and Switzerland, the levels are legally enforced, and both apply
"recommended" action levels, lower than the regulatory limits, above which
remediation is advised. Although most guidances are not enforced standards for
limiting indoor radon exposures of the public, they are widely used as de facto
standards in the real-estate and insurance industries. For example, in the United
States, lending institutions often require radon concentrations (based on short-
term measurements) less than the EPA action level of 150 Bq/m3 (4 pCi/L) as a
condition for financing home purchases.
Of the 15 member states of the European Union, only Austria and
Finland have adopted the values proposed in EC (1990~. Belgium, Germany,
Ireland, Luxembourg, Sweden, and the United Kingdom have adopted
somewhat different values. In the Netherlands, an approach based on limiting
individual risk has been adopted. Peak radon concentrations in the Netherlands
are relatively low in comparison with those of other countries. The 20-Bq/m3
reference level in the Netherlands reflects Me low indoor radon concentrations
generally found and provides lifetime risks of 10-4 or less.
Australia, Austria, Germany, Ireland, Norway, Switzerland, and the
United Kingdom have set their action levels on the basis of recommendations of
ICRP (1993b) and other considerations regarding cost, risk, and feasibility. In
Canada, cost-benefit analysis was used as a basis for a radon reference level of
800 Bq/m3. A similar approach was initially adopted in Sweden, which has
recently reduced its reference level after We publication of ICRP 65 (1993b).
OCR for page 173
GUIDELINES FOR EXPOSURE TO TENORM
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Similarly, the reference level in Luxembourg was reduced from 250 to 150
Bq/m3 in 1992. The value of 150 Bq/m3 recommended by the US EPA is based
as much on technologic limitations and cost-benefit analyses as on health risks
(EPA 1992c).
Although national and international guidance for radon in dwellings
varies, most values have similar scientific and technical bases and are within
only a factor of about 2 from each other. Most differences are related to policies
and risk-management decisions by the various bodies that develop radon
guidance.
RADON ACTION LEVELS FOR WORKPLACES
Workplaces are defined as ordinary places of work, such as offices,
schools, stores, theaters, libraries, and hospitals (Clarke 1995~. For the purposes
of this discussion, workplaces do not include nuclear fuel-cycle facilities. Radon
is present in all workplaces. In some cases, such as uranium mines, exposure to
radon is already subject to occupational control. Because of the lower
occupancy rate and associated lower accumulated exposure, radon in ordinary
workplaces is widely ignored or of secondary concern compared with radon in
dwellings. Some countries, however, have placed strong emphasis on radon
measurement and remediation in schools (for example, Sweden, the United
Kingdom, and the United States).
Exposure to radon in schools is often viewed separately from that in
other workplaces, to emphasize protection of young people and because large
numbers of people are potentially exposed. Although occupancy rates of schools
are lower than those of dwellings, some countries have adopted the same action
levels for both. In Switzerland, the reference level of 400 Bq/m3 for schools is
lower than the legally enforced 1,000 Bq/m3 limit for dwellings but is equal to
the level above which remediation of homes is recommended. In the United
Kingdom, Finland, Switzerland, and Norway, the values for schools are legally
enforced. The US EPA advisory reference level of 150 Bq/m3 for schools is the
same as for dwellings.
There is considerable diversity in the approach to radon in worl~laces,
and the range of action levels is wider than that for dwellings (table 8.5~. Levels
range from a target value of 20 Bq/m3 in the Netherlands to a statutory limit of
3,000 Bq/m3 in Switzerland.
ICRP (1993b) recommends that intervention levels for exposure to
radon in homes be carried over to workplaces for exposure to radon. The level
at which intervention in the workplace is almost certainly justified is the same as
180
INDOOR-RADON GUIDELINES
Table 8.5 National and international reference (action) levels for radon in workplaces
excluding those linked to the nuclear fuel cycles
Radon Concentration (Bq/m3)b
Country or Aboveground Schools Status
Organization Workplaces
Australia 1,000 1,000 Advisory based on IAEA
recommendations
Austria 400 400 Existing advisory
200 200 New advisory
Canada None 800 Advisory
Finland 400 400 Legally enforced
Germany None 250 Advisory
Ireland None 150 Advisory
Luxembourg 150 150 Advisory
Netherlands 20 20 Advisory
Norway 800 800 Legally enforced
Sweden 400 400 Existing advisor
400 400 Legally enforced, new
Switzerland 3,000 400 Legally enforced
United Kingdom 0.01 WL in any 8-h period Legally enforced
US EPA None 150 Advisoly
IAEA 1,000 1,000 Advisor
ICRP 500-1,500 500-1,500 Advisory
aColgan and Gutierrez (1996).
bl Bq/m3 = 0.027 pCi/L
GUIDELINES FOR EXPOSURE TO TENORM
181
in homes 10 mSv in a year. Because of the different occupancy factor 2,000
h at work and 7,000 h at home each year and an effective dose per unit
exposure of 5 mSv per WLM (ICRP 1993b), one arrives at a radon
concentration in the workplace of about 1,500 Bq/m3 as the level at which action
is almost certainly justified. With optimization, the suggested range within
which an action level should be set is 500-1,500 Bq/m3. The IAEA remedial
action level for chronic exposure involving radon in workplaces is a yearly
average 222Rn concentration of 1,000 Bq/m3 (IDEA 1996a). This guideline
appears to be based on the average range of 500-1,500 Bq/m3 recommended by
ICRP (1993b).
SU1\IMARY AND CONCLUSIONS
· The first recommendations for domestic radon exposure in the United
States were developed by NCRP in 1984. The NCRP recommendations
were based on evaluation of the lung-cancer risk and the avoidance of an
unacceptable risk. A personal avoidance of lifetime lung-cancer risk of 2%
was proposed, that is, avoidance of a continuous exposure to 2 WLM (equal
to radon concentration of about 10 pCi/L). This lifetime risk was compared
with a normal lung-cancer risk in smokers of about 10% and in nonsmokers
of about 1%.
· On the basis of different risk projection models, the BEIR IV
Committee and other major radiation protection organizations (ICRP) have
estimated that higher lung-cancer risks are associated with indoor radon
exposure since the NCRP publication of 1984. Although all three models
(NCRP, BEIR IV, and ICRP) incorporate risk coefficients derived from the
studies of miners, the biologic assumptions underlying the models differ.
· EPA's current estimates of lung-cancer risk associated with indoor
radon exposures are based on the BEIR IV report and later adjustments.
EPA risk estimates related to domestic radon exposure are 1.6 x 10-3 for
never-smokers and 3 x 10-2 for smokers at 1 WLM (equal to 4 pCi/L, which
is recommended as the remedial action level). EPA guidelines are generally
comparable with the recommendations of ICRP.
· The above approaches for estimating lung-cancer risks from the miner
data require numerous adjustments for estimating comparable risks in
homes, and those approaches assume that cancer incidence observed in
miners at high radon levels can be extrapolated linearly to zero exposure.
Other sources of uncertainty include statistical variability in the miner data,
182
INDOOR RADON GUIDELINES
the age dependence of risk, extrapolation to females, the relationship
between radon risk and smoking risk, and the impact of risk extrapolation
of the different levels and types of particles in uranium mines and in homes.
