United States
Environmental Protection
Agency
Environmental Monitoring
Systems Laboratory
Las Vegas NV 89193-3478
Research and Development
EPA/600/S6-88/008 Sept. 1988
SEPA Project Summary
Estimating the Risk of Lung
Cancer from Inhalation of Radon
Daughters Indoors: Review and
Evaluation
Thomas B. Borak and Janet A. Johnson
A review of the dosimetrfc models and
epidemiological studies with regard to
the relation between indoor radon ex-
posure and lung cancer indicates that
the Working Level is an appropriate unit
for indoor radon exposure; that the
uncertainty in applying risk estimates
derived from uranium miner data may be
reduced by determining nose vs. mouth
breathing ratios, residential aerosol
characteristics, and lung cancer risk vs.
age at exposure; that there is persuasive
evidence of an association between
radon exposure Indoors and lung
cancer; and that epidemiological studies
in progress may provide a basis for revi-
sion or validation of current models but
only if experimental designs are
employed that will permit pooling of data
to obtain greater statistical power.
This Project Summary was developed
by ERA'S Environmental Monitoring Sys-
tems Laboratory, Las Vegas, NV to an-
nounce key findings of the research pro-
ject that is fully documented in a
separate report of the same title (see
Project Report ordering information at
back).
Introduction
Inhalation of radon gas was the first situa-
tion in which radiation was implicated as
a cause for cancer. The problem can be
traced back for more than 400 years. In the
sixteenth century, an unusual fatal disease
was occurring among underground miners
in Bohemia. About 100 years ago, this
disease was diagnosed as lung cancer and
at that time about 50 percent of the miners
in the region died from lung cancer.
Around 1924, it was suggested that the
high rate of lung cancer may be attributed
to elevated concentrations of the radioac-
tive noble gas, radon. In many ways it was
difficult to reconcile the fact that an insolu-
ble gas could be responsible for the
disease. However, in 1950 it was recognized
that the true cause of high absorbed doses
to the lung was inhalation of the short lived
radioactive descendants (daughters) of
radon which are initially created by the
decay of radon in air.
It has recently become evident that this
same mechanism could be responsible for
the induction of lung cancer in the general
public. Measurements of radon in dwellings
indicate that 20-60 percent of the dose
commitment from natural background
radiation is due to radon. It is generally
more pronounced in regions where dwell-
ings must be closed and insulated to pro-
tect the occupants from the weather.
The objective of this report is to sum-
marize state-of-the-art methodologies for
deriving risk estimates from this en-
vironmental pathway. It also includes an
evaluation of the uncertainties of each
method and suggestions for improving the
risk estimation process. The report is di-
vided into the following major sections:
• DOSIMETRY
• EPIDEMIOLOGY
• RISK MODELS
Sections on dosimetry and epidemiology
are included since each discipline has con-
tributed to the derivation of risk models
employed to assess public health detriment
due to indoor radon exposure.
Current risk models are based on
epidemiologic data from underground
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miners. The intent of this report is to sum-
marize the epidemiologic data available
from indoor radon studies and investigate
its usefulness as a basis for estimating risk
coefficients or validating those derived from
miner data. In addition, studies in progress
are summarized and their potential con-
tribution to quantitative risk estimation
discussed.
The section describing epidemiologic
risk models is included simply to enhance
the usefulness of this report. No attempt
was made to evaluate the merits and defi-
ciencies of each of the models.
Method
Public concern for the health effects of
exposure to indoor radon has made it
necessary to make risk estimates based on
inadequate and incomplete data. The
challenge to the professional community is
to evaluate available information on oc-
cupational exposure and adapt it to non-
occupational environments using basic
concepts of radiation dosimetry. The results
must then be validated on the basis of
epidemiologic evidence and data on
residential exposures.
To attempt to evaluate the problem, a
literature search was conducted to locate
suitable epidemiological studies and per-
sonal and professional contact were used
to obtain information on unpublished work
and on studies in progress. There were 21
published reports that were suitable and 6
data from unpublished studies were ob-
tained. Finally, interim results were ob-
tained from 14 epidemiological studies now
in progress, 8 in the United States and 6
in other countries.
Discussion
There have been a number of attempts
to model absorbed dose to the lung and
portions of the respiratory tract from inhala-
tion of radon daughters. These have been
summarized by the National Council on
Radiation Protection and Measurement
(NCRP84) and James (Ja87). Three recent
models were the focus of this report, by
Harley (Ha86), Jacobi (Ja80, OECD83) and
James (Ja87).
Dose conversion factors for inhalation of
radon daughters have appeared in the
literature since 1956. They range from
0.7-29 mGy WLM'1 (Ja87), but recently the
range of values has been reduced con-
siderably. The results from the three
models indicate that the spread between
models is greater than the conversion from
occupational to environmental exposures
within each model.
Each model was formulated by
distinguished scientists who have selected
input variables according to their interpreta-
tion of available and often identical data.
At this time, there is no indisputable
evidence that permits ranking or elimina-
tion of any of the computations.
The average of all three models gives a
ratio of dose conversion factors for residen-
tial to occupational exposure of 1.3 + 1.3.
The only conclusion that can be made with
confidence is that the ratio of dose conver-
sion factors is greater than 1. The added
uncertainty of deriving risk coefficients us-
ing data from underground miners may not
be significant.
The concept of cumulative potential
alpha energy is sufficient for describing the
exposure of individuals and there is no
justification for redefining or modifying the
WLM or J h trr3. However, there are several
important factors which influence the con-
version from exposure to dose. Improved
data on the following could reduce the
uncertainty in the risk estimates to the
general public:
• Fraction of time nose breathing vs. mouth
breathing
• Unattached fraction
• Aerodynamic median diameter and
geometric standard deviation of attached
aerosols
• Age dependence
• Location of radiosensitive targets
The common denominator for dose con-
version factors is cumulative exposure to
potential alpha energy (WLM). Most
epidemiological studies of indoor en-
vironments measure radon gas only. It is
important to understand the relationship
between radon gas and radon daughter
concentrations.
James (Ja87) has reported that the con-
version to dose can be related directly to
radon concentrations indoors. The reason
is that for a constant level of radon the
potential alpha energy, WL, increases as
the concentration of room aerosols in-
creases. However, the availability of con-
densation nuclei reduces the unattached
fraction, fp. These compensating factors
tend to dampen variations in the dose con-
version factor for a given concentration of
radon gas. These concepts should be
carefully evaluated in future studies.
Two general types of epidemiologic
studies are represented in this body of
literature: ecological and case-control.
Ecological studies may have an inherent
systematic bias towards showing no
association between lung cancer and in-
door radon due to the effect of population
migration. A second source of bias in such
studies may involve secondary character-
istics of geographic regions studied which
may either dilute or enhance an apparent
association. Due to the inherent problems
with interpretation of ecological studies,
they can be weighted less heavily than
case-control studies in the assessment of
the strength of the evidence for a causative
role of radon daughter exposure in lung
cancer etiology.
The majority of the case-control studies
relied on surrogate measures of radon
daughter exposure. However, at least these
measures were determined on an in-
dividual home basis. The studies are so
diverse in design and execution that the
data cannot be pooled or combined in order
to increase the statistical significance.
However, each of the published studies can
be treated as an independent trial to test
the hypothesis of an association between
radon and lung cancer.
Six of the seven published case-control
studies have indicated a relative risk or
odds ratio greater than one. If there is no
association between indoor radon and lung
cancer and there is no systematic bias
among the studies, it can be assumed that
there would be a 50 percent chance of find-
ing a positive association (relative risk or
odds ratio greater than one) and a 50 per-
cent chance of finding a negative associa-
tion. Using the binomial probability distribu-
tion, the probability of six of seven such
studies showing a positive association if,
in fact, none exists, is approximately 0.06.
This analysis depends on the assumption
that the results of the published studies
represent a random sample from a binomial
population of results of all possible studies.
The question of bias in publication of
studies could invalidate this analysis.
The studies in progress are generally of
case-control design and will use actual
radon measurements. Several also have
common design features. Collectively, they
have the potential to show an association
between indoor radon exposure and lung
cancer which would withstand a more
rigorous statistical analysis if such an
association truly exists. It is much more dif-
ficult to provide definitive evidence that an
association does not exist if, in fact, this is
the case.
Even under the best circumstances, the
exposure data from studies in progress may
not be sufficiently refined to allow for
development of risk models and risk coef-
ficients independent of the information
already obtained from studies of under-
ground miners. It is likely that the studies
in progress will provide a means for
validating the adaptation of risk models
derived from miner data to non-
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occupational exposures among the general
population.
Conclusions
Dosimetric analyses that take into ac-
count differences between underground
miners and members of the general public,
in terms of lung morphometry, breathing
patterns, and environmental aerosol
characteristics, indicate that the dose per
unit exposure to radon daughters may be
marginally higher for non-occupational ex-
posures than for miners. Therefore, there
is no apparent rationale for redefining the
Working Level (WL) for indoor radon ex-
posure simply on the basis of the reduced
volume of air inhaled per unit time.
The uncertainty in applying risk
estimates derived from studies of under-
ground miners to the general public may
be reduced by determining the fraction of
the time persons inhale through the nose
vs. the mouth, the physical characteristics
of residential aerosols which would in-
fluence the unattached fraction, and the
relationship between lung cancer risk and
age at exposure.
The results of epidemiologic studies
dealing with indoor radon provide per-
suasive evidence of an association be-
tween lung cancer and residential radon ex-
posure. However, these data are not suffi-
cient to allow derivation of quantitative risk
estimates specific for indoor radon or
validation of risk estimates derived from
underground miner data.
Epidemiologic research in progress may
provide a basis for revision or validation of
current risk models and coefficients. This
is feasible only if the individual investiga-
tions employ designs which allow for pool-
ing of data to obtain greater statistical power
than that possible for any single study.
References
Ha86 Harley, N. H. and B. S. Cohen. Up-
dating Radon Daughter Bronchial
Dosimetry. In: "Radon and Its Decay Pro-
ducts." P. Hopke, ed., Proceedings of the
American Chemical Society, 1986, pp.
419-429.
Ja80 Jacobi, W. and K. Eisfeld. Dose to
Tissues and Effective Dose Equivalent by
Inhalation of Radon 222 and Radon 220
and Their Short Lived Daughters. GSF-
Report-S-626, Munich, Neuherberg,
West Germany, 1980.
Ja87 James, A. C. Lung Dosimetry for
Radon and Thoron Daughters: A Review
and Reassessment With Emphasis on
Domestic Exposure. In: "Radon and Its
Progeny in Indoor Air," Nazaroff, W. W.
and Nero, A. V, eds., New York: Wiley
Interscience, 1987.
NCRP84 National Council on Radiation
Protection and Measurements. NCRP
Report No. 78: Evaluation of Occupa-
tional and Environmental Exposures to
Radon and Radon Daughters in the
United States, Bethesda, Maryland:
NCRP, 1984.
OECD83 Organization for Economic
Cooperation and Development.
Dosimetry Aspects of Exposure to Radon
and Thoron Daughter Products. Report
by a Group of Experts, OECD, 2 rue
Andre Pascal, 75775.Paris, Cedex 16,
France, 198&
Thomas B. Borak is with Colorado State University, Fort Collins, CO 80523,
and Janet A. Johnson is with Western Radiation Consultants, Inc., Fort Collins,
CO 80523.
Stuart C. Black is the EPA Project Officer (see below).
The complete report, entitled "Estimating the Risk of Lung Cancer from Inhalation
of Radon Daughters Indoors: Review and Evaluation," (Order No. PB 88-218 979/
AS; Cost $19.95, subject to change) will be available only from:
National Technical Information Service
5285 Port Royal Road
Springfield, VA 22161
Telephone: 703-487-4650
The EPA Project Officer can be contacted at:
Environmental Monitoring Systems Laboratory
U.S. Environmental Protection Agency
Las Vegas. NV 89193-3478
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