|
Items in cart [0] |
Questions? Call 888-624-8373 |
| Copyright © 2009. National Academy of Sciences. All rights reserved. Terms of Use and Privacy Statement |
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 564
APPENDIX VITT
Previous Estimates of the Risk Due to Radon
Progeny
Several expert groups and individual investigators have published
estimates of the risk associated with exposure to radon progeny. In this
appendix the committee examines some of the more widely cited studies
both for their underlying assumptions and for the numerical value of the
estimated risk.
Like the committee's lifetime risk estimates develop ea in Chapter 2,
two steps are usually involved in estimating the risks from radon exposure:
the development of an appropriate risk coefficient from epidemiological
studies, and the projection of risks over a defined exposure and follow-
up periods. Table VIII-1 lists risk coefficients developed in a number of
epidemiological studies. Two types of risk coefficients are shown; those
for absolute excess risk, the number of cases per person-years at risk per
working-level month (WLM), and the excess relative risk, the proportional
increase per 100 WLM. Estimates from Annex 2A, using a constant relative
risk model are included in Table VIII-1 in cases in which the same cohorts
were considered by this committee. Except for the Malmberget miners, the
results of the Poisson regressions for internal and external controls used in
Annex 2 are not too different from those obtained by other investigators
using standardized mortality ratios.
As important as the risk coefficients are in estimating the risks as-
sociated with radon exposures, the assumptions in the projection models
often have a larger numerical impact. The committee examines these
assumptions for particular studies in the following sections.
564
OCR for page 565
565
o
so
Pa
o
C.
sir
._
i_
v
o
so
o
so
U.
o
x
U.
_
C)
._
lo:
at:
-
m
C.
._
U)
._
lo:
-
o
U'
._
U'
Cd
m
is>
._ ~
Ct ~
~ g
Cal
CJ
~ ·=
.m em
U.
U)
C) U.
iL1 ~ ~
_ Lo —
ID O
en ~ ~
~ ~ By
ID ~ ~
._ ~ ._
~ ~ P:;
=: ~
ed
V)
~ C. 8
,, 8 ' ~ ~— ·
<~ ~ m ·U~ · - ·— {d —
o ~ ~ ~
,, to, ~ OF o go go go
~ ran ~ ~ ~ ~ ~ P:
4)
I, o
U)
o ~
o
o
04 t4 04 04
- - ~ ~ ~ ~ O~ ~ ~
o o o o ~ ~ ~ o ~ o
· - · - · - · - ce c. ct · - ct · -
t4 oo oo o o o ~o o oe
a, ~ ~ ~ a, ~ ~
~ ~ ~ p: ~ ~ ~ ~ ~ ~:
~ ~ ko ~
. . . .
o ~ ~ - ~
1 _1 1 00 1 1
~ oo ~ ~ - ~ oo ~ ~ ~ ~ ~ ~ ~ o
· · . . . . . . . . . .
o o o ~ ~ o ~ ~ o ~ ~ ~ ~ - oo
~ O ~ oo ~ C~
. · . · . · · -
~ ~ ~ ~ ~ o ~ ~ ~ ~ ~
cr~
'e
. -
~ ~ -.
'e
:: ~ 0 e ~;3 = e B e 3~§ e
cl ~ O ~i :E Z
c~
0
.=
u,
._
c,
_
~o
._
._
s"
u'
c,
._
-
:^
~>
._
CJ
-
c~
o
o
~ x
x ~
O
~ -
c:
.— . u,
~ ~ o
m.= x
s
~ o ed
<~^a
U,
~ O.
Cd
8=
OCR for page 566
566
NCRP REPORT 78
age at exposure.
H~,ALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
Risk estimation in a 1984 reporti° by the National Council on Ra-
diation Protection and Measurements (NCRP) relies on the Harley and
Pasternack Model B of lung-cancer excess due to radon progeny.2 The
following assumptions formed the basis of the model.
· Following a latent period, the tumor rate is an exponentially
decreasing function of the time since exposure.
Disease rate excess associated with a single exposure increases with
Lung cancer is rare before the age of 40 yr.
Median age at lung cancer among miners is about 60 yr in non-
smokers and 50 yr or older in smokers.
.
The minimal time for tumor growth, from initial cell transforma-
tion to clinical detection, is 5 yr.
From these postulated disease patterns, the Harley and Pasternack
model specifies a 5-yr latent period for persons first exposed at the age of
35 yr or older and a (40—u) yr latent period for persons under the age
of 35 yr, where u is age at first exposure. For a single annual exposure at
age a, the excess radiation-associated risk above background at age t > u
(and t > 40) is taken to be
A(t, u) = Re-m(~~U)S(t)/S(u),
where R is the attributable-risk coefficient per WLM, S(t) and Stu) are
the probabilities of survival to the designated age, and m is the rate of
removal of transformed stem cells due to repair or cell death. For risk
projection, the NCRP task group fixed m = ln(2~/20 yr-t, corresponding
to a 20-yr half-life. For ages within the latent period or before initial
exposure, the excess risk is zero. The exponential term allows for the
excess risk to decline with time following exposure, and the survival ratio
adjusts for competing causes of mortality. Given the parameters of this
model, one integrates over t from age 40 to maximal assumed life (age 85)
to obtain lifetime risk due to the single exposure at age a, or over years
of exposure, us, . . . ,u", to obtain the excess risk at t due to an previous
exposure. Lifetime excess risk from all exposures is the integral over t and
a.
This model is extremely important, in that it postulates a modified
effect with time since exposure. In this way, it is related to the TSE
model recommended in Chapter 2 of this report and the latency models
of Lundin et al.6 and Thomas and McNeil, all of which contrast with a
relative-risk model constant in age at risk. Indeed, the distinction between
a constant-relative-risk model and models that modify risk according to
OCR for page 567
ESTIMATES OF THE RISK DUE TO RADON PROGENY
567
time since exposure ~ more fundamental than discrimination among the
latter types, which offer refinements in basically similar models.
The analysis presented in Annex 2A clearly suggests that risk effects
are modulated by time since exposure. This is manifest in the declining pa-
rameter estunates of impact of exposures more distant in time. Therefore,
the distinction between the Harley and Pasternack model and a relative-
risk model that declines with time since exposure is related to the rate
of decline in the relative risk. In light of the complexity of risk arising
from chronic radiation exposure, substantial data would be required for an
adequate evaluation of such subtle patterns of risk. An informal method
of considering this issue is to examine additive excess risk after cessation
of exposure. This committee's analysis indicated that the relative risk
declines with time since cessation of exposure. However, the NCRP risk
model requires that this decline be large enough for the attributable risk
to decrease.
To test this hypothesis, data on observed and expected cancers and
person-years of exposure from the four miner cohorts analyzed in Annex
2A were categorized by age, age at last exposure, and cumulative WLM.
Figure VIII-1 presents for each of the four data sets age-specific attributable
risks, (observed—expected)/person-years, for three age-at-last-exposure
groups. In the figures, the excess risks were smoothed by graphing the
mean of the observed excess and two adjacent values and weighting by the
inverse variance. Data from there four worker populations do not show a
consistent pattern of declining excess risk. In several cohorts, the excess
risks generally increase; in others, the excess declines, but only 20 yr or
more after the mean age at last exposure. The NCRP model would predict
a declining excess shortly after cessation of exposure.
Patterns similar to those shown in Figure VIII-1 were observed after
stratification by two categories of cumulative WLM. In addition, Poisson
regression models were fit to the observed risk, where the attributable
disease rate was postulated to be linear in age at last exposure and
cumulative WLM. For each data set, after adjustment for WLM and age
at last exposure, there was no significant improvement in model fit with
the inclusion of age at risk. Parameter estunates for five age categories
tended to increase, as suggested by Figure VIII-1. However, this effect is
poorly estimated. Model fit did not improve significantly with inclusion of
a continuous age variate, although the coefficients were generally positive.
A difficulty in the application of the NCRP model is the choice of
m, the rate of removal of the transformed cell. Harley and Pasternack
acknowledge the issue and select a 2~yr half-life as representative for
extrapolation, although they cite no formal data analysis or experimental
results. Additional work in this area would be beneficial for refining the
model.
OCR for page 568
568
.~ ~ _
o ~ $ ~
m
of "o To con o 0 c ~ g g 8 8 8 ~ ~ ~ ~
1 O Cot to Or is ·L~ 10
000'001 X~SIU 319~11191~V 000'001 X~SIU 319~1nS1~V ~
~ 1 ~ ~ ~ ~ E
1 1 1 1 1 1 1 1 1 1 1 1 1 1
o o o o o o o o o o o o o o o o ~ ._
10 UD ~ CO Cat _ I ~ ~ ~ ~ I ~ ~
~ CO
000'001 X ASIA 319~11191H ~ ~ 000'001 X ASIA 319~1nS18 ~ ~ ~ ·"
OCR for page 569
ESTIMATES OF THE RISK DUE TO RADON PROGENY
569
Although it does not have much impact on NCRP lifetime risk esti-
mates, their model limits the occurrence of radiation-induced lung cancer
to the age of 40 yr and over, a restriction for which no biological mecha-
nism is readily apparent. In contrast, several studies have observed lung
cancers under the age of 40.7'i5 The failure to observe lung cancer in young
persons In several other studies could be due to the very low background
rates and few person-years. For example, Radford and Regard reported
that the mean age at first exposure of the Swedish miners was 28 yr. With
a ~yr latent period, 1,415 miners would accrue a maximum of some 10,000
person-yr by the age of 40, producing 0.5 expected cases if the population
lung-cancer mortality rate for ages 35-39 were 5.1 x 10-5. With this
expected value, there is a 0.6 probability that no cases will occur before
the age of 40.
A methodological issue concerns the manner in which the attributable
risk is adjusted for competing causes of death. As defined, S(t) is the
probability that a person who is subject to disease rates of the standard
population will survive to age I. For a 1-yr exposure at age u < t,
the competing-cause adjustment S(~/S(u) which is the probability of
survival of someone in the standard population to t, given survival to age
u does not incorporate the increased lung-cancer risk, and thus decreased
survival, of someone exposed. This adjustment error is compounded as risk
is integrated over age t and over yearly exposures but is unlikely to be
important except at high dose rates.
BEIR III REPORT
The National Research Council's Committee on the Biological Effects
of Ionizing Radiations (BEIR III)' ~ assumed a linear relationship between
exposure in WLM and the additive excess risk of lung cancer. The excess
risk was estimated to vary with age at diagnosis, as shown in Table VIII-2.
In addition to the minimal age at expression (similar to that in the NCRP
model), a minimal latent period of 15-20 yr (for those exposed at age
15-34) or 10 yr (for those exposed above age 34) is assumed. Later risk is
independent of latent period.
These risk values were based on the combined estimates from the epi-
demiology studies of U.S.6 and Czechoslovakiani3 uranium miners, Swedish
iron miners,l2 and Newfoundland fluorspar miners.7 The techniques for
combining the epidemiological data were not described and so cannot be
evaluated. It appears that substantial weight was given to the results from
the Swedish, Newfoundland, and Czechoslovakian miner surveys. The Col-
orado Plateau uranium miners had much lower lung-cancer risks, which
the committee thought was due to their high dose rates. The Swedish
metal miners had a higher risk, even with less prevalent cigarette smoking;
OCR for page 570
570
HEALTH RISKS OF RADON AND OTHER ALPNA-EMITT13RS
TABLE VIII-2 Excess Risk Estimated To Vary with
Age and Diagnosis
Age (yr) at Diagnosis
Excess Cases
(per 106 person-years at risk per WLM)
<35
35-49
50-65
>65
o
10
20
50
that difference was attributed to longer follow-up. No data are available
to indicate whether these risk estimates apply to childhood irradiation.
The BEIR III reportit discussed, but did not resolve, the effect of
cigarette smoking on these radiation risks. The BEIR III report states
that if the two exposures are additive, their risk estimates would apply to
both smokers and nonsmokers. But if there is a multiplicative interaction
(i.e., the lung-cancer risk estimates due to radiation are proportional to
the smoking-specific rates), the estimates should be increased by 50% for
smokers and reduced by a factor of 6 for nonsmokers.
REPORT OF THOMAS AND MCNElLL
The report of Thomas and McNeill and c~workerst6~47 reviewed epi-
demiological and anunal data on lung cancer, bone and head sarcomas,
and some other cancers, with an emphasis on lung cancer from radon
progeny. To develop risk estimates, the authors considered data from the
Czechoslovakian, Ontarian, and Colorado Plateau uranium miners; the
Newfoundland {luorspar miners; the Swedish metal miners; and (for infer-
ences regarding the shape of the dose-response curve, but not the mag-
nitude of risk) the Japanese atomic-bomb survivors. Animal data were
used primarily to investigate the effect of modifying factors, as opposed to
estimation of magnitude of risk.
The comprehensive report reached qualitative and quantitative con-
clusions largely in accord with those in Chapter 2. Thomas and McNeill
discussed at length the epidemiological and statistical principles under-
lying selection of a risk model (i.e., relative risk versus additive excess
risk), the shape of the dose-response curve, and the role of modifying and
confounding factors. We support and have repeated their approach of for-
mally combining evidence from various cohorts. This committee concurs
with their argument that simply comparing risk estimates from different
cohorts in relation to average exposure of the cohorts is not suitable for
studying the shape of the dose-response curve. Thomas and McNeill used
a more statistically sound method; that is, they fit a single model to a
OCR for page 571
ESTIMATES OF T7IE RISK DUE TO RADON PROGENY
571
combination of data sets. They allowed the degree of risk to vary among
studies, so that they could adjust for varied confounding factors, but in-
corporated parameters common to the data sets to model nonlinearities in
dose-response relationships. The primary lunitation of this analysis, as ac-
knowledged, was the very [united form of the data that could be extracted
from published reports concerning the various cohorts.
Thomas and McNeill adopted a model with the relative-risk constant
in age and, tentatively, linear in cumulative exposure, except at very high
values. Their analysis indicated an estimated value of 2.28/100 WLM
for the excess relative risk. In selecting this estunate, they discounted a
substantially lower risk among the Colorado Plateau miners; and, to some
extent, by using a cell-killing model, they compensated for the lower risks
per unit exposure at very high levels of cumulative exposure. Inclusion
of an exponential term to represent cell killing resulted in a final model
that was nonlinear in dose; however, the decrease in slope caused by this
cell-killing term was important only at very high doses. However, this
allowance for a decrease in slope at very high exposures was statistically
significant. They also considered models in which excess relative risk was
proportional to an estimated power of dose; such models provide for a more
general nonlinearity in dose. The fitted model, although not providing a
statistically significant improvement over a simple linear model, resulted
in a convex dose-response function, that is, a generally (but only slightly)
decreasing slope of the response with increasing cumulative exposure. As
noted above, however, they felt that a linear dose-response relationship at
moderate to low doses was adequate for extrapolation, with data from very
high doses discounted via the cell-killing model. Their interpretation of
the possible curvilinearity was primarily that one should be less confident
that low-dose extrapolations are conservative than in the case of low linear
energy transfer (LET) radiation, where the curvilinearity is generally held
to be of the opposite type (slope increasing with dose).
Although we emphasize that their conclusions are in accord with
those drawn in this report, we believe that the adoption of a constant-
relative-risk model at all ages for the effect of radon daughters is not well
supported. The data available to Thomas and McNeill on this issue were
sparse. The most relevant evidence was presented in Section 7.2.1 of their
1982 report, where they argued that, with the meager data available,
the additive excess risk increases substantially with age, at a given dose,
whereas the relative risk is more stable. In Section 4.2.1.3 of the same
report, they attempted to discriminate between the Attributable-risk
(i.e., excess-risk) and relative-risk models, solely on the bash of the total
(or average) risk over age (and time). This attempt may have been
inappropriate, because information on age-specific risks was not available
to Thomas and McNeill.
OCR for page 572
572
HEALTH RISKS OF RADON AND OILIER ALPHA-EMITTERS
The present committee was fortunate to have access to much more
detailed data on some populations and can confirm to some extent the
conclusions drawn by Thomas and McNeill. Their average risk coefficient
(2.28/100 WLM) is not very different from that found by this committee
(1.5/100 WLM) using external controls and constant-relative-risk model.
The difference is largely due to their exclusion of results from the Colorado
Plateau cohort, which the committee's analysis includes.
The tentative conclusion of Thomas and McNeill regarding the linear-
ity of the dose-response relationship was supported by the data available to
them. We agree with the statistical approach that they used, and for two
reasons concur with the tentativeness of their conclusion as to the shape of
the dose-response curve. First, at very large doses, there is a suggestion of
nonlinearity in specific cohorts, although it is not consistent enough among
all the cohorts to be statistically significant. More important, there cannot
be enough evidence from epidemiological studies to ascertain the effects at
low doses.
On the critical issue of the interaction of cigarette smoking and ra-
diation effects, Thomas and McNeill concluded that the joint effect
seemed to be `'intermediate between additive and multiplicative, although
on balance ithey] would favor the multiplicative model. The evidence
for this was moderately weak, inasmuch as the effects of other modifying
factors~uch as age at exposure, exposure rate, and time since cessation
of exposure—were not controlled.
In conclusion, the reports of Thomas and McNeilli6~7 provide a
strong discussion of principles and methods, but are limited by the data
available to them. The present report is complementary in its approach,
but more data were accessible to the committee. These were the data
from the four cohorts in Eldorado-Beaverlodge, Ontario, Colorado, and
Sweden described in Annex 2A. Although we disagree with the claim made
in Thomas and McNeill's Appendix Ji6 that grouping of doses tends to
result in underestimation of risks, the general consistency of conclusions,
both qualitative and quantitative, between the two reports is notable.
1981 REPORT OF EVANS ET AL.
In a brief report in the journal Nature in 1981, Evans et al. provided
an upper bound to the lifetime lung-cancer risk associated with radon-
daughter exposure in the general population. The report originated in
an international workshop on radiation protection principles for naturally
occurring radionuclides. The authors primarily considered the epidemim
logical evidence in determining the risks of environmental radon. They
cited a range of lifetime attributable-risk coefficients, developed by other
authors, of 21-54 to 1,000 deaths/106 WLM. In their collective judgment,
OCR for page 573
ESTIMATES OF TUB RISK DUE TO RADON PROGENY
573
the Most defensible upper bound of the lifetime risk to the general popu-
lation is 100 lung cancer deaths per 106 WLM.n This coefficient reflects a
reduction in unit exposure for the general population, in comparison with
miners, because of differing exposure conditions, smoking habits, and age
and sex distributions of the two populations.
Evans et al. acknowledged the informality of their approach for de-
termining a risk coefficient for the general population. They did not use
models directly, either to derive a risk coefficient from the miner data or
to extrapolate from miners to the general population. They also assumed
an attributable-risk model and did not specifically address the effects of
cigarette smoking.
1977 UNSCEAR REPORT
The 1977 report of the U.N. Scientific Committee on the Effects of
Atomic Radiation (UNSCEAR)~8 provided an attributable-risk coefficient
for lung-cancer incidence of 200-450/106 WLM, which described a full, for
example, Satyr, expression of the carcinogenic eBect on lung tissue of radon
and of its daughter products. The report reviewed data from American
uranium miners, Swedish underground miners, Newfoundland lluorspar
miners, iron-ore miners in the United Kingdom, and Czechoslovakian
uranium miners. The upper bound of the attributable-risk range was
clearly derived from analysm of the Czechoslovakian data; the derivation of
the lower limit is unclear, although the Swedish data reported by Snibsi4
apparently were considered. The Colorado Plateau data do not appear to
have been used in setting the range.
The UNSCEAR report emphasized the Czechoslovakian study, be-
cause of long latency after the onset of exposure and the availability of
appropriate mortality rates. The authors cited the dose-response rela-
tionship of excess risk to exposure as 230 x 10-6/WLM; this coefficient,
however, was taken from the 1976 reporti3 that was based on an incorrect
method of analysis. To obtain the upper bound of 450 x 10-6/WLM,
the authors merely doubled the value reported by Sevc et al.~3 That
calculation was justified by assuming that the average follow-up in the
Czechoslovakian study (20 yr) represented the median latency for a 40-yr
complete expression of the eRects of exposure. The report did not provide
evidence to support the biological model that is implicit in the doubling of
the risk coefficient.
The Swedish data were also characterized as appropriate for consid-
eration, although the original report by Snihsi4 did not provide complete
information. The present committee does not regard these data as adequate
for risk estimation. For a 4~yr period, Snihs estimated the attributable
OCR for page 574
574
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
risk as 140 x 10-6/WLM, on the basis of the Swedish data. The deriva-
tion of the lower bound of 200 x 10-6/WLM from this value was not
described. The report did not make firm statements about the effects of
cigarette smoking.
ICRP PUBLICATION 32
Publication 32 by the International Commission on Radiological Pro-
tection (ICRP)5 published in 1981, provided a recommended limit for
inhalation of radon progeny by workers. In developing this limit, ICRP
considered both the epidemiological evidence and the results of a dosi-
metric analysis. This committee has focused on ICRP's epidemiological
approach.
The ICRP group emphasized the findings of the Colorado Plateau
and Czechoslovakian studies. Relying on reports from those studies and
on the 1977 UNSCEARi~ and 1980 BEIR IIIii reviews, it cited a range of
attributable risk of 2-20 cases/106 person-yr/WLM. Because the effect of
exposure was noted to vary with age at exposure, the group considered 5-
15 cases/106 person-yr/WLM as The most probable range,n on the basis of
averaging cover all age periods during occupational work." Over ``a mean
manifestation period of 30 years," the group translated the attributable-
risk range of 5-15 cases/106 person-yr/WLM into a total lifetime risk of
1.5-4.5 excess cases/WLM. With adjustment for the higher breathing rate
of miners, the excess risks were reduced by about 20%. The ICRP group
noted that the risks for miners might be increased by the effects of other
exposures and thus tend to overestimate the effects of radon daughters
alone.
This committee could not fully critique ICRP's epidemiological am
preach, because some procedures were not fully described: the derivation
of the range of 2-20 cases/106 person-yr/WLM, the averaging that re-
duced this range to 5-15 cases/106 person-yr/WLM, and the rationale
for the 30-yr period for calculating lifetime risk. As discussed elsewhere,
this committee finds a modified relative-risk model to be preferable to the
attributable-risk model used by ICRP in 1981.5
SUMMARY
The descriptions of risk estimates given above make it clear that a
number of approaches have been applied to estimating the risks due to
radon-daughter exposure. Some are based largely on expert opinion, while
others depend on analyses of limited data on lung-cancer cases associated
with exposure to radon progeny. Results vary, as indicated in Table VIII-1
above and Table 2-13 in Chapter 2. There are at least three underlying
causes for this lack of agreement between risk estimates.
OCR for page 575
ESTIMATES OF THE: RISK DUE TO RADON !'ROGENY
575
1. As discussed in Chapter 2 and Appendix IV, there is a fair amount
of variability between the results of the individual epidemiological studies.
Although these differences are perhaps no greater than would be antici-
pated on statistical grounds, it is not unreasonable to believe that other
factors enter as well. Since some risks estimators put greater weight on
one setups) of observations than another, differences between risk estimates
are not surprising.
2. A variety of techniques must be used to project lifetime risk to
a general population on the basis of relatively short-term occupational
exposures to underground miners, a topic discussed at length in Chapter 2.
Foremost among these is the modeling of age-specific lung-cancer risk. Risk
projections which use models based on the relative risk depend critically on
the age-specific background rates. As discussed in Chapter 2, differences
in estimated lifetime risks occur if the relative risk is constant or if it is
permitted to vary with tune-related factors. Similarly, lifetime risks that
are derived from models of additive excess risk depend on the modeling of
time-related effects. The different models will produce approximately the
same average risk for populations with similar age structure and follow-up
such as the underground miners. However, projecting beyond the range of
the miner cohort data can produce very different numerical estunates.
3. Finally, several of the risk projections described above seem to
depend more on considerations of biological plausibility rather than data
analyses by standard methods. Some investigators might perhaps argue
that biological plausibility should be the main criteria for risk projections,
but others are less sure. Lung cancers observed in the miner studies age
largely due to two complete carcinogens, smoking and high-LET radiation,
whose joint interaction ~ not well defined. The committee believes that
until underlying processes of ca~cinogenesis are understood, an objective
analysm of observational data ~ a surer path to valid estimates of radon
risks.
REFERENCES
1. Evans, R. D., J. H. Harley, W. Jacobi, H. S. McLean, W. A. Mills, and C. G.
Stewart. 1981. Estimate of risk from environmental exposure to Rn-222 and its
decay products. Nature 290:98-100.
2. Harley, N. H., and B. S. Pasternack. 1981. A model for predicting lung
cancer risks induced by environmental levels of radon daughters. Health Phys.
40:307-316.
3. Howe G. R., R. C. Nair, H. G. Hewcombe, A. B. Miller, and J. D. Abbett.
Lung cancer mortality (1950-1980) in relation to radon daughter exposure in a
cohort of workers in the Eldorado Beaverlodge uranium mine. J. Natl. Cancer
Inst. 77~23:357-362.
OCR for page 576
576
HEALTH RISKS OF RADON AND OTHER A~HA-~I==S
4. Hornung, R. W., and T. J. Meinhardt. 1987. Quantitative risk assessment of
lung cancer mortality in U.S. uranium miners. Health Phys. 52:417-430.
5. International Commission on Radiological Protection (ICRP). 1981. P. 24 in
Limits for Inhalation of Radon Daughters by Workers. ICRP Publication 32.
Oxford: Pergamon.
6. Lundin F. E., J. K. Wagoner, and V. E. Archer. Radon Daughter Exposure and
Respiratory Cancer Quantitative and Temporal Aspects. 1971. Joint Monograph
No. 1. Washington, D.C.: U.S. Public Health Service.
Morrision H. I., D. T. Wigle, and A. J. deVilliere. 1981. Lung cancer mortality
and radiation exposure among the Newfoundland flurospar miners. Pp. 372-376
in Proceedings of the International Conference on Radiation Hazards in Mining:
Control, Measurements, and Medical Aspects, M. Gomes, ed. New York: Society
of Mining Engineers of the American Institute of Mining, Metallurgical, and
Petroleum Engineers, Inc.
8. Morrison, H. I., R. M. Semenciw, Y. Mao, D. A. Corkill, A. B. Dory, A. J.
deVilliers, A. J. Stocker, and D. T. Wigle. 1985. Lung cancer mortality and
radiation exposure among the Newfoundland flurospar miners. Pp. 365-368 in
Proceedings of the International Conference on Occupational Radiation Safety in
Mining, E. Stocker, ed. Toronto: Canadian Nuclear Association.
9. Muller J., W. C. Wheeler, J. F. Gentleman, G. Suranyi, and R. A. Kusiak.
1985. Study of mortality of Ontario miners. Pp. 335-343 in Proceedings of
the International Conference on Occupational Radiation Safety in Mining, A.
Stocker, ed. Toronto: Canadian Nuclear Association.
10. National Council on Radiation Protection and Measurements (NCRP). 1984.
Evaluation of Occupational and Environmental Exposure to Radon and Radon
Daughters. NCRP Report 7B. Washington, D.C.: National Council on Radiation
Protection and Measurements. 204 pp.
11. National Research Council, Committee on the Biological Effects of Ionizing
Radiations (BEIR). 1980. The Effects on Populations of Exposure to Low Levels
of Ionizing Radiation. Washington, D.C.: National Academy Press. 524 pp.
12. Radford, E. P., and K. G. St. Clair Renard. 1984. Lung cancer in Swedish iron
miners exposed to low doses of radon daughters. N. Engl. J. Med. 310:1485-1494.
13. Sevc, J., E. Mung, and V. Placek. 1976. Lung cancer in uranium miners and
long-term exposure to radon daughter products. Health Phys. 30:43~437.
14. Snihs, J. O. 1973. The approach to Rn problems in non-uranium mines in
Sweden. Pp. 90~911 in Proceedings of Third International Congress of the
IRPA. CONF-730907-P2. Technical Information Center, U.S. Department of
Energy. Oak Ridge, Tenn.: Oak Ridge Natural Laboratory.
15. Sun S., X. Yang, Y. Lan, M. Xionyu, L. Shengen, and Y. Zhanyun. 1984. Latent
period and temporal aspects of lung cancer among miners. Radiat. Prot. 4~5)
(English translation).
16. Thomas, D. C., and K. G. McNeill. 1982. P. 23 in Risk Estimates for the Health
Effects of Alpha Radiation. INFO-0081. Ottawa, Canada: Atomic Energy
Control Board.
Thomas, D. C., K. G. McNeill, and C. Dougherty. 1985. Estimates of lifetime
lung cancer risks resulting from Rn progeny exposure. Health Phys. 49:825-846.
18. United Nations Scientific Committee on the Effects of Atomic Radiation (UN-
SCLEAR). 1977. P. 725 in Sources and Effects of Ionizing Radiation. Report
E.77.IX.1., New York: United Nations.
19. Whittemore, A. S., and A. McMillan. 1983. Lung cancer mortality among U.S.
uranium miners: A reappraisal. J. Natl. Cancer Inst. 71:480 499.
Representative terms from entire chapter:
risk estimates
