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OCR for page 445
APPENDIX {V
Epidemiological Studies of Persons
Exposed to Radon Progeny
INTRODUCTION
The mining of radioactive ores in the Erz Mountains in eastern Europe
was the first occupation associated with an increased risk of lung cancer.
Metal ores were mined in Schneeberg, on the German side of the mountains,
beginning in the fifteenth century, and in Joachimsthal, on what is now the
Czechoslovakian side, beginning in the sixteenth century.26~30 Both areas
were later mined for radioactive ores. As early as the sixteenth century,
Agricolai described exceptionally high mortality from respiratory diseases
in miners in this region. The lung-cancer hazard was first recognized by
Harting and Hesset9 and was reported in 1879. Their report provided
clinical and autopsy descriptions of intrathoracic neoplasms in miners,
which they classified as lymphosarcoma. In a work force of about 650 men,
Harting and Hesse counted 150 deaths from Miner's disease" between
1869 and 1877; in retrospect, most of these deaths were probably from
lung cancer. During the early twentieth century, histopathological review
of a series of cases established that the malignancy prevalent among miners
in the Erz Mountains was primary cancer of the lung.5 49
The problem was not recognized in the miners on the Czechoslovakian
side of the Erz Mountains until 1929, when two cases of lung cancer were
reported in Joachimsthal miners. In 1932, Pirchan and Sikl46 described
the autopsy findings in nine miners with lung cancer. These 9 miners were
among 19 miners in Joachimsthal who died during 1929-1930. Formal
epidemiological studies of the Schneeberg and Joachimsthal miners were
not carried out, but published reports documented that about 50% of the
miners eventually died from lung cancer.53 Peller44 calculated lung-cancer
445
OCR for page 446
446
HEALTH RISKS OF RADON A~ OTTO A~HA-~ITT=S
mortality rates for the Schneeberg miners during 1875-1912 and found
that they were about 50 times those in Vienna males during 1932-1936.
Many authors offered explanations of the excess cancer in the Schnee-
berg and Joachimsthal miners (see references 26, 30, and 63 for reviews).
Early theories emphasized dust exposure, metals in the ore (particularly ar-
senic), and increased susceptibility as a result of inbreeding in small mining
communities. In 1924, Ludwig and Lorenser31 reported that radioactivity
could be measured in the air and water in the mines of Schneeberg and
might contribute to the development of lung cancer. Pirchan and Sikl46
suggested in 1932 that radioactivity was the most probable cause of the
Joachimsthal cancers, on the basis of the finding of radioactivity in both
Schneeberg and Joachimsthal mines, the occurrence of lung-cancer in both
locations, and the long exposure of underground miners to radioactivity.
Teleky's opinion in 1937 was similar.63 He could find no other satisfactory
explanation and concluded that the high level of radioactivity, thought
not to be present in other mines, led to the apparently unique lung-cancer
problem of Schneeberg and Joachimsthal miners. In 1944, Lorenz30 argued
that radon alone could not be the cause of lung cancer and proposed that
genetic susceptibility to lung cancer might be unusually high in the miners.
However, during the 1950s and 1960s, as the biological basis of respiratory
carcinogenesis became better understood and additional mining groups
were studied, it came to be accepted that inhaled radon progeny were the
cause of lung cancer in the Schneeberg and Joachimsthal miners and other
exposed minerS.26~33,53
After World War II, several new epidemiological studies were initiated
to determine the safety of exposure to radon progeny in mines. Unlike early
studies, the newer surveys addressed such important biological questions
such as the shape of the dose-response curve, the influence on risk of age
at exposure, the effect of dose rate, the temporal expression of risk after
exposure, and the interaction of radon daughters with other substances
associated with lung cancer. This appendix reviews the epidemiological
literature that is now available for addressing these issues.
COLORADO PLATEAU STUDY
Beginning in the late 1940s, the American uranium industry grew
rapidly in the Colorado Plateau, a mountainous region of southwestern
Colorado and southeastern Utah. In 1949, in response to concerns about
the health hazards to workers in this industry and with awareness of
the high lung-cancer incidence in European miners in Joachimsthal and
Schneeberg,2i the U.S. Public Health Service (PHS) began to investigate
the uranium mines and mills in the Colorado Plateau region. The investi-
gation combined an industrial-hygiene survey with a medical study of the
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EPIDEMIOLOGICAL STUDIES OF PERSONS EXPOSED TO RADON 447
workers. A prospective cohort study of miners and millers was carried out
later, first by the PHS and then by the National Institute for Occupa-
tional Safety and Health (NIOSH). Until recently, this study offered one
of the few epidemiological data bases for estimating the lung-cancer risk
associated with exposure to radon progeny.
Field teams from PHS periodically conducted medical surveys of min-
ers and millers between 1950 and 1960.33 Before 1954, the teams did not
attempt to examine all workers, but during 1954-1960, they tried to at-
tain complete coverage. from among the examined miners, a group was
assembled for follow-up that included miners who had worked at least a
month underground in a uranium mine by January 1, 1964.33 The number
of subjects varied in the reports of this investigation (Table IVES; in 1971,
Lundin et al.33 provided data on 3,366 white and 780 nonwhite subjects.
An exposure data base was developed from diverse sources: PHS, state
agencies, and the mining companies. Holaday (quoted by Lundin et al.33)
has provided a chronology (Table IV-2. During the period 1951-1968, for
which cumulative exposure in working-level months (WLM) was initially
calculated, nearly 43,000 measurements of radon-daughter concentrations
were made in the approximately 2,500 mines that were worked (Table
IV-3.33 In discussing sources of potential inaccuracy in the working-level
(WL) data, Holaday (quoted by Lundin et al.33) pointed out that the
measurements taken after 1960 were primarily for control purposes and
might have led to overestimates of the exposures to miners.
Because coverage was not comprehensive for all mines in all years,
several different estimation procedures were used to fill the gaps in the
exposure data. These estimation procedures were more important in the
earlier years, when exposures to radon daughters were higher and fewer
measurements were available.
To make estimates for missing data in the temporal series of WL
measurements for a particular mine, the investigators interpolated and
extrapolated earlier and later concentrations of radon daughters. When
gaps in the data were too wide, area averages by locality, district, and
state were used. For 1950 and earlier years, WL values were estimated on
the basis of the few available radon measurements and the investigators'
knowledge of the mining conditions. Many of the miners worked in other
types of hard-rock mines before becoming uranium miners. For exposures
to radon daughters in the hard-rock mines, WL values were based on
calendar year: 1.0 WL for years before 1935, 0.5 WL for 1935-1939, and
0.3 WL for years 1940 and later.33
The arithmetic average of the individual WL measurements made
within a mine in a given calendar year was assigned to the mine for that
year. Use of the arithmetic average implicitly weighted all measurements
equally; error would have been introduced if the numbers of workers
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448
HEALTH RISKS OF RADON AND OTBR ALPHA-EAiITTERS
TABLE IV-1 Results of Colorado Plateau Study (Summarized from
Principal Reports) of Male Uranium Miners
No. of Lung-
Followup Cancer Deaths
Cutoff No. of (Observed/
Date Subjects Expected) Comment Reference
1959 2,666 6/3 Increase not statistically significant 2
1959 907 5/1.1a Cohort members with at least 3 yr of
experience 2
1962 3,656 15/4.2a Includes 1,156 workers with surface,
open-pit, or occasional under-
ground work, respectively, through
1960 65
1963 3,415 22/5.7b Response increases with cumulative
BALM 66
1967 3,414 62/10.06 Excess lung cancer in all exposure
categories from < 120 WLM to
3,720 WLM 32
1968 3,366 70/11.7b Most comprehensive report 33
1974 3,366 144/29.8b Response increases with cumulative
VVLM in all smoking groups 4
1977 3,362 185/38.4C WLM not considered in analysis 67
ap < 0.05.
UP < 0.01.
CSMR is 482, 95% lower confidence limit is 425.
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EPIDEMIOLOGICAL STUDIES OF PERSONS EXPOSED TO RADON 449
TABLE IV-2 Chronology of Radon and Radon-
Daughter Measurements in Colorado Plateau Studya
Time Source and Type of Measurement
1956-1958
1959-1960
After 1960
Before 1950 Few radon measurements; earliest 1949
1950 Few radon samples by the PHS and Colorado State
Health Department
Radon and radon-daughter samples by PHS, state
agencies, and U.S. Bureau of Mines
Radon and radon-daughter samples taken by PHS in
attempt to survey all mines
1953-1954 Scant data collection by PHS and states; Utah tried to
survey every mine
Scant PHS coverage; variable among states; mining
companies begin measurements
Mine survey work primarily by companies
Colorado, Utah, and New Mexico conducted surveys;
company measurements continued
State and mining-company programs
aBased on data from Lundin et al.33
exposed at the concentrations indicated by the measurement were not
uniform. The arithmetic average could also be strongly influenced by
outlying high values.
To calculate WLM, the WL estimates were combined with work-
history information obtained from annual censuses of active miners and
from questionnaires. Apparently, a 17~h work month was assumed; and
time for vacations, sick leave, or other absences from work was not sub-
tracted from the number of underground hours estimated from the work
history.52 However, cumulative exposures were also not adjusted for time
worked beyond 170 in/month, a common practice in the early years of the
industry.52 The investigators did not have enough information to consider
work location within a specific mine or job classification, which might have
influenced ventilatory demands.
Because WL measurements were sparse in relation to the numbers
of mines that were worked, the WLMs accumulated by most miners were
based on both measurements and estimates. In fact, WLM totals were
calculated solely from measurements on only 10.3% of the white miners.
For 36.1%0 of the white miners, some type of estimation was involved in the
calculation of all WLM values; for the remainder, some WLM estimates
were based on WL values derived by one of the estimation procedures.33
In reports published to date, the WLM estimates have extended through
September 1969. Information on cigarette smoking was obtained during
the survey examinations, at the annual censuses of miners, and from
mailed questionnaires.33~69 As described by Whittemore and McMillan,69
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450
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
TABLE IV-3 Number of Mines Visited and Number
of Measurements Made in Colorado Plateau Study
No. of
Calendar No. of No. of Measurements/
Year Mines Visited Measurements Mine Visited
1951 5 21 4.2
1952 151 242 1.6
1953 56 474 8.5
1954 33 143 4.3
1955 4 15 3.8
1956 101 1,434 14.2
1957 147 848 5.8
1958 54 475 8.8
1959 281 1,867 6.6
1960 179 1,785 10.0
1961 330 2,952 8.9
1962 336 4,362 13.0
1963 315 2,648 8.4
1964 268 4,196 15.7
1965 268 4,856 18.1
1966 274 5,084 18.6
1967 266 5,696 21.4
1968 259 5,691 22.0
1969 149 1,683 11.3
SOURCE: Dr. Richard W. Hornung, National Institute of Occupa-
tional Safety and Health, Cincinnati, Ohio, personal communication.
information on smoking was obtained on one to four occasions between
1950 and 1960, when the surveys were conducted, and at other times
between 1963 and 1969.
Mortality in the cohort was determined with follow-up techniques that
included records of the Social Security Administration and the Internal
Revenue Service, direct contact, and other approaches.33~67 Only a few
subjects could not be traced, and nearly all death certificates were obtained.
Most published reports are based on analysis with a modified life-table
approach, which is a conventional method for longitudinal studies that
compares observed with expected numbers of deaths by cause. More
recently, several investigators have applied modeling techniques to the
data.23~24 34~69 In cohort analyses based on an external referent population,
expected numbers of deaths were calculated with mortality rates for the
western states where the mines were or with the rates for all U.S. white
males.
Table IV-1 summarizes the principal reports for the white male miners.
At all follow-up intervals, statistically significant excesses of lung-cancer
deaths were reported; the standardized mortality ratios (SMRs), which
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EPIDEMIOLOGICAL SlrUDIES OF PERSONS EXPOSED TO RADON 451
TABLE IV-4 Lung-Cancer Deaths by Cumulative
WLM in White Underground Miners in Colorado
Plateau Studya
No. of Lung-Cancer Deaths
Ratio of
Cumulative WLM Observed Expected Observed/Expected
< 120 1 1.81 0.55
120-359 12 2.57 4.67b
360-839 14 2.95 4.756
840-1,799 12 2.52 4.76b
1,800-3,719 21 1.43 14.69b
2 3,720 10 0.42 23.81b
aBased on data from Lundin et al.33
bp < 0.01.
are age- and calendar-year-adjusted ratios of observed to expected deaths,
ranged from approximately 4 to 6, without an obvious temporal trend.
In several reports, the investigators used stratified analysis to examine
the exposure-response relationship of lung-cancer mortality with cumu-
lative WLM by calculating standardized mortality ratios within strata
of increasing WLM 3 4,32,33,66 In one report,32 the mortality rates were
standardized for cigarette smoking; in another,4 they were stratified by
cumulative WLM and smoking. Lundin ~ al.33 adjusted the expected
numbers of lung-cancer deaths for cigarette smoking. The investigators
usually provided tables stratified by the interval after the start of employ-
· · e ~
ment In uranium mining.
Lundin et al.33 compared observed with expected numbers of lung-
cancer deaths in six strata of lifetime cumulative WLM (Table IV-4. A
statistically significant excess was present in all categories of exposure,
except in the category of less than 120 WLM. Archer et al.4 provided
mortality rates by exposure and cigarette smoking but did not include
expected numbers of deaths.
Mortality from causes other than lung cancer was also examined.
Significant excesses were not observed for cancers at sites other than
the respiratory system.4 33~67 Greater than expected numbers of deaths
occurred from tuberculosis, nonmalignant respiratory diseases, accidents,
and suicides. The 1981 report by Waxweiler et al.67 showed a statistically
significant excess of deaths (SMR, 262) attributable to the grouping of
chronic and unspecified nephritis and renal sclerosis.
The data on the white underground miners have also been analyzed
with other statistical approaches. Lundin and coworkers33~34 developed a
descriptive model for the development of lung cancer after radon-daughter
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452
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
exposure; the model was based on the assumption of a time-latency distri-
bution with the same shape and dispersion as that of leukemia incidence
after a single radiation exposure. They used the model to examine the
ejects of latent period, age at exposure, dose rate, and cigarette smoking
and to compare absolute- and relative-risk models for the effect of radon-
daughter exposure. They found that the relative-risk model was preferable
to the absolute-risk model and that a l~yr latent period gave the best
fit. Effects of age at first exposure and of exposure rate on lung-cancer
risk were not demonstrated. With regard to cigarette smoking, Lundin et
al.33~34 concluded that nonsmokers had much less radiation-induced lung
cancer and that the excess radiation-induced lung cancer in smokers was
not heavily influenced by the extent of smoking.
Assuming an exponential form for the relative hazard, Hornung and
Samuels24 used the Cox proportional-hazards model on data accumulated
through the 1977 follow-up date. They found that a lag period of 6-11 yr
for exposure was most compatible with the data. The modeling also showed
that the exposure-response curve was downward at higher doses; that is,
lower exposure rates led to greater effects. On a multiplicative scale for
assessing the effects of exposures on lung-cancer risk, smoking and radon-
daughter exposure had statistically significant ejects, but a cross-product
term of the two exposures was not statistically significant. These analyses
were limited, however, to examination of only the exponential form of the
relative risk.
More recently, Hornung and Meinhardt23 reported on a proportional-
hazards analysis of data based on follow-up of the cohort through December
31, 1982. A total of 255 deaths from lung cancer was identified by that
date. Hornung and Meinhardt considered exponential, linear, and power-
function models of risk and chose the power-function model, because it
provided the best fit to the data. The model was developed with a
stepwise approach; the data were best fitted by variables for cumulative
WLM, cumulative smoking tin packs), and age at initial exposure. In
the power-function model, the coefficient for the interaction of radon-
daughter exposure and cigarette smoking was negative, although it was
of borderline statistical significance tP = 0.058~. This finding implies a
submultiplicative, rather than purely multiplicative, interaction between
cigarette smoking and radon-daughter exposure.
Hornung and Meinhardt23 assessed the effects of several temporal
factors: exposure rate, calendar year, age at exposure, and cessation
of exposure. They found increasing risk with decreasing exposure rate,
greater risk for more recent birth, greater risk for those first exposed at a
greater age, and decreasing risk with cessation. The last two effects were
thought to suggest a late-stage action of radon daughters, in the context
of a multistage model.
OCR for page 453
13PIDEMIOLOGICAL STUDIES OF PERSONS EXPOSED TO RADON 453
Hornung and Meinhardt23 used their power-function model to de-
velop risk estimates for occupational exposures. Quantitative relative-risk
estimates were made for occupational exposure beyond an assumed back-
ground exposure rate of 0.4 WLM/yr. For a 3~yr working lifetime, risk
estimates were made for exposures of 30-120 WLM (1-4 WLM/yr). The
relative risks ranged from 1.42 at 30 WLM to 2.07 at 120 WLM.
Whittemore and McMillan69 used a case-control approach to examine
additive and multiplicative models for the relationship of lung-cancer mor-
tality to radon-daughter exposure and cigarette smoking. The results of
their analyses are discussed briefly here and more fully in Appendix VII. A
multiplicative linear model, with excess relative risk given by the product
of the risk associated with radon-daughter exposure and that associated
with cigarette smoking, fitted the data better than an excess-relative-risk
model in which excess risks associated with radon and smoking were added.
A series of multiplicative relative-risk models was evaluated by the inves-
tigators. They found a better fit for a model that incorporated the effects
of smoking and WLM on relative risk as simple linear variables than for
one that included exponential representations of these factors. Cumulative
exposure variables fitted the data better than measures of exposure rate.
Risk was not affected by age at the start of underground mining.
The PHS study cohort also includes nonwhite male miners, prunarily
American Indians. These subjects are of particular interest because of
the low incidence of lung cancer in American Indians of the Southwest a
pattern probably attributable to a low prevalence of cigarette smoking.4 50
Less information has been reported on the nonwhite subjects (Table IVES.
No cases of lung cancer among American Indians were observed initially,
but a statistically significant excess was present in the 1974 follow-up.4 In
fact, the expected numbers of cases were probably overestimated because of
the use of mortality rates for all nonwhites rather than for American Indians
alone. In New Mexico during 1969-1977, for example, the average annual
lung-cancer mortality rate in American Indian males was 8.6/100,000,
whereas the rate for non-Hispanic white males was 60.8/100,000.5° Lung-
cancer mortality rates for black males have generally been equal to or
higher than rates for white males.
Two other reports have addressed lung-cancer risks in American In-
dians employed in the Colorado Plateau mines. Gottlieb and Huseni~
reported a case series of 17 Navajo males diagnosed as having lung cancer
at the Shiprock Indian Health Service Hospital. All but one had worked as
a uranium miner, and only two had smoked cigarettes; cumulative WLM
ranged from 59 to 2,125. Samet et al.5t conducted a population-based
case-control study to assess the association between uranium mining and
lung cancer in Navajo males. Of 32 lung-cancer cases diagnosed between
1969 and 1982, 23 had a documented history of uranium mining. None of
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454
HEALTH RISKS OF RADON AN-D OTHER ALPNA-EMITTERS
TABLE IV-5 Data on Nonwhite Male Underground Uranium Miners in
Colorado Plateau Study
No. of Lung-
Followup Cancer Deaths,
Cutoff No. of Observed/
Date Subjects Expected Comment Reference
1959 640 0/a Total of 11 deaths 2
1962 1,103 0/0.8 Comparison rates from state data 65
1974 780 11/2b Comparison with male nonwhite
population of Arizona and New
Mexico 4
aNot reported.
bp < 0.01.
the 64 matched controls had been uranium miners. The results imply an
extremely high relative risk in this nonsmoking population, but individual
WLM estimates were not available for all miners, and the data cannot be
used for quantitative risk estimation.
The Colorado Plateau study was designed and implemented 35 yr ago.
Its strengths include the size of the cohort, the long duration of follow-
up, the estimation of WLM for individual subjects, and the availability
of cigarette-smoking histories. Application of new techniques to the data
set has helped to explore the interaction between cigarette smoking and
radon daughters and the effects of time-dependent factors such as dose rate
and lag tunes. Even though investigators have dealt pragmatically with
the severely limited number of WL measurements in calculating WLM
estimates, the quality of the exposure information must be considered in
interpreting the results of the study. Both random error and systematic
bias might affect WLM estimates. Much of the exposure occurred before
extensive measurement procedures were in place. For example, 36.1% of the
total WLM ultimately accumulated by the cohort of white miners occurred
before 1956 (Richard W. Hornung, NIOSH, personal communication, 1986~.
Few measurements were taken during the early years, when exposure
rates were highest, so the higher exposures were probably estimated less
accurately than later ones. If higher exposures were subject to a greater
misclassification, the risk coefficients that have been calculated for the
higher WLM values might be artificially low. Bias could also have been
introduced by the investigators' decision to rely on measurements taken for
control purposes after 1960, in that such measurements can over-represent
higher exposures. Finally, the cohort had relatively high exposures and
thus provides little information on the results of cumulative exposures of
less than 100 WLM.
OCR for page 455
EPIDEMIOLOGICAL S1TJDIES OF PERSONS EXP0573D TO RADON 455
CZECHOSLOVAKIAN URANIUM MINERS
The retrospective cohort mortality study of the Czechoslovakian ura-
nium miners was initially reported in 1971,55 and periodic updates have
been published 22~2~29~47,s4~56~58 The cohort consisted of miners who be-
gan mining uranium ore in 1948-1957. However, the results in the more
recent reports are limited to 2,433 miners55 who began in 1948-1952. The
selection criteria for the cohort have not been specifically described. The
investigators have not reported whether the study cohort included all eligi-
ble miners in a particular geographic area or only a sample, what procedure
was used and what records were reviewed to identify the cohort, the total
number of miners who died from any causes other than lung cancer, and
the distribution of the cohort members by birth year, age, or age when
first exposed.
Individual work histories were abstracted from payroll cards for all
miners (Langon Swent, personal communication, 1984) from 1948. For
each miner, WLM was estimated from radon gas measurements and the
number of months of employment at each mine in each calendar year. Since
1948, more than 120,000 radon gas measurements were made by measur-
ing ionization current in an ionization chamber by electrometer. Yearly
numbers of radon measurements were not given, but the lowest reported
mean number of measurements for a year was 101 ~ 8/mine. The range
of coefficients of variation of average yearly radon concentrations in mines
was 3.5-20.0%. Radon gas concentrations were converted to WL on the
basis of ventilation conditions and practices, emanation rates from different
types of ores, and after 1959, radon-daughter measurements. Since 1968,
each miner's WLM has been determined from individual personal dosime-
try cards. Assessment of dosimetry errors was based on the magnitudes of
coefficients of variation, which do not provide information on the validity
of the dosimetry data.
The cohort was followed with lung-cancer registrations administered
by the authors in health facilities, the records of the hygiene service in
the uranium industry, and oncology notification cards from throughout
the country. The latter two served as independent follow-up sources after
1960. Until 1960, only 12 deaths due to lung cancer occurred. The success
of this approach for identifying lung-cancer cases is not established, and
the number of persons lost to follow-up is not given in the 1976 report by
Sevc et al.56 Except for a paper on skin cancer, health eRects other than
lung cancer have not been reported.
In analyses of this cohort, observed lung-cancer mortality was com-
pared with that expected on the basis of age- and calendar-period-specific
rates of the male population in Czechoslovakia. In the 1976 report by
Sevc et al.,56 person-years at risk for each subject were classified by the
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478
HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
case-control study, the 29 cases included all men who died from lung can-
cer during 19501976 in the parish surrounding two physically connected
lead-zinc mines. Controls (174) consisted of the first three deaths other
than from lung cancer listed before and after the case in the chronologically
ordered parish registry, but matching was dropped in the analysis. The
authors believed that the registry included fairly complete diagnoses from
the death certificates. The local mining company assessed the underground
work experience of all subjects.
Smoking habits of the miners were learned from medical files and
interviews with two retired foremen. For 2 of 10 subjects on whom smoking
information was independently obtained from more than one source, the
information was conflicting.
The age-standardized rate ratio for lung cancer among lead-zinc miners
was 16.3 (90% confidence interval, 7.8-35.3~. Among underground miners,
those who had never smoked (nine) appeared to have longer work-related
induction latent periods than smokers (nine) (respective medians of 49
versus 37 yr) and to have a greater risk of developing lung cancer.
NORWEGIAN NIOBIUM MINERS
Solli et al.60 followed a cohort of employees at a niobium-mining
company that operated from 1951 to 1965. Niobium itself is not considered
to be carcinogenic, but the ore also contained 238 U (0.3-2 ppm) and 232 Th
(50-300 ppm). Exposure estimates for the cohort were of questionable
quality. The WLM from both radon and thoronium progeny was calculated
for the employees on the basis of measurements of alpha activity during 2
days in 1959. Among the employees, a strong dose-response relationship
was found between lung-cancer risk and cumulative WLM (Table IV-
15~. Poor dosimetry probably resulted in underestimation of exposures
by about a factor of 2, according to the authors. Lifetime occupational
histories indicated that three of the subjects had been previously exposed
to asbestos and one had mined iron. In addition, 75%0 of the employees
were smokers, compared with 60% of the Norwegian population.
FLORIDA PHOSPHATE WORKERS
Some U.S. phosphate ore contains uranium and radium. Workers
involved in the mining and the processing of the ore might be exposed to
radon and radon daughters. Two retrospective cohort studies of mortality
in Florida phosphate workers have been conducted recently; each was
performed because of concern raised by apparent clusters of lung cancer.
OCR for page 479
EPID13MIOLOGIC~ STUDIES OF PERSONS EXPOSE TO CON 479
TABLE IV-15 Lung-Cancer Mortality among Norwegian Niobium Mine
Workersa
Cumulative WLM No. of No. of Lung-Cancer
(Corrected/Twofold Person-Years Deaths Observed/Expected
Underestimate) at Risk Observed Expected Ratio
0 4,622 0 1.73 0
1-38 1,343 3 0.50 6.0
40-158 1,312 4 0.58 6.9
160-238 147 2 0.07 28.6
~ 240 169 3 0.08 37.5
aBased on data from Solli et al.60
Stayner et al.6i conducted a study of 3,199 workers employed at a
phosphate fertilizer plant. Seven samples were taken for radon progeny;
the range was 0.00~.02 WL. Overall respiratory-cancer mortality was not
significantly increased (SMR, 113~. Further analysis did not show trends
of respiratory-cancer mortality with duration of employment or length
of follow-up in white men. In black men, respiratory-cancer mortality
was significantly increased in those with more than 20 yr of employment.
However, only five cases were identified in black men, and two were in the
index cluster.
In a larger study, Checkoway et al.~° examined mortality in 17,601
white and 4,722 nonwhite male employees of the Florida phosphate indus-
try. Lung-cancer mortality was not significantly increased in either group,
in comparison with rates for Florida. When mortality from lung cancer
was examined in the workers considered to have potential exposure to
alpha radiation, a significant excess was apparent (SMR, 1.08~.
These studies do not have sufficiently detailed information on ex-
posure for risk estimation. Individual exposures to radon progeny were
not estimated, and information on cigarette smoking was not collected.
Furthermore, the limited measurements that have been made indicate
radon-daughter concentrations only slightly above background concentra-
tions.
RESIDENTIAL EXPOSURE
Within a building, radon-progeny concentrations are determined by
the strength of the source and the rate of air exchange with the outside.
Most of the radon in buildings enters from the underlying soil and building
materials, although water and utility gas can also contribute radon progeny
to indoor air.43 A wide range of radon-daughter concentrations in dwellings
OCR for page 480
480
HEALlrH RISKS OF RADON AND OTHER AWHA-EMITTERS
has been demonstrated, with different radium concentrations in soil and
building materials and different air-exchange rates largely explaining the
size of the range.
Epidemiological investigations of domestic radon progeny as a risk
factor for lung cancer are still preliminary. Both descriptive and analytical
approaches have been used to examine the association between radon-
daughter exposure in the home and lung cancer. Techniques for estimating
lifetime exposure of people to radon daughters from indoor air are not
yet available, and surrogates based on residence type or a few limited
measurements have been used in the analytical studies. The available
studies are insufficient for the development of quantitative risk estimates
for associating exposure to radon progeny in the home and lung cancer.
In the descriptive studies, incidence or mortality rates for lung cancer
within geographic units have been correlated with measures of exposure for
inhabitants of the units. Edlingi5a compared mortality rates for different
Swedish counties with background gamma radiation, described as being
correlated with indoor exposure to radon and its daughters. For lung-
cancer mortality, the correlation coefficients were 0.46 for males and 0.55
for females. Hess and colleagues20 performed a similar analysis for lung-
cancer mortality during 195~1969 in the 16 counties of Maine. Using
average radon concentrations in water as the measure of exposure, they
calculated correlation coefficients of 0.46 for males and 0.65 for females.
In a study of 28 Iowa towns served by deep wells, lung-cancer incidence
increased with the concentration of 226 Ra, a possible surrogate for the
radon concentration in the water.9 These descriptive studies, which did
not consider the exposures of people to radon daughters and other agents,
provided only suggestive evidence that radon progeny exposure in the home
increases lung-cancer risk.
The association has been more directly tested in case-control and
cohort studies. Axelson et al.8 conducted a case-control study in a rural
area of Sweden. The investigation included 37 cases and 178 controls.
Exposure to radon progeny was inferred from the characteristics of the
subjects' residences at the time of death. Those who lived in stone houses
were assumed to be most heavily exposed to radon daughters, and those
who lived in wooden houses were assumed to be least exposed; other types
of dwellings were considered to be sources of intermediate exposure. In spite
of the crudeness of this exposure classification, residence in stone houses
was associated with a significantly increased odds ratio, in comparison
with the reference category of wooden houses (by Mantel-Haenssel method;
odds ratio, 5.4; 90% confidence interval, 1.5-19~. Data concerning cigarette
smoking and residence history were not obtained.
OCR for page 481
EPIDEMIOLOGICAL STUDIES OF PERSONS 13XPOSED TO RADON 481
Edling and Axelsoni6a conducted a similar case-control study in a
rural area of Sweden. The study subjects were residents of the island of
Oeland who died during 1960 1978. The geological characteristics of this
island were thought to result in strong differences in background radon
concentrations within a small area. Inclusion in the study population
required at least 30 yr of residence at the same address before death; 23
lung-cancer cases and 202 controls who died from causes other than lung
cancer met this criterion. Most of the dwellings were monitored for radon
daughters during 3 months of summer and 1 month of winter. The dwellings
were also classified on the basis of structural characteristics, as in the earlier
study by Axelson et al.,8 and cigarette-smoking information was obtained
from next of kin. Lung-cancer risk was significantly associated with radon-
daughter exposure, as assessed by either the measured concentration or the
characteristics of the dwelling, and both crude and smoking-adjusted risk
estunates were significantly increased. Logistic analysis yielded smoking-
adjusted odds ratio, comparing most with least exposed, of 3.9, and the
90% confidence interval was 1.5-10.0.
Pershagen et al.45 reported the findings of two small case-control
studies in Sweden on domestic radon-daughter exposure, one drawn from
a larger study in northern Sweden and the other from a twin registry.
The investigators assembled each series with 30 case-control pairs, divided
equally between smokers and nonsmokers. Exposure to radon was esti-
mated from information on dwelling type; the investigators attempted to
consider all residences lived in by the subjects. In the study group from
northern Sweden, imputed radon exposures were significantly higher in
smokers than in their smoking controls. Estimated exposures to radon
progeny were similar in the nonsmoking cases and controls in the series
from northern Sweden and in the smoking and nonsmoking cases and
controls in the second series (selected from the twin registry).
In the United States, Simpson and Comstock57 examined the relation-
ship between lung-cancer incidence and housing characteristics. During a
12-yr period in Washington County, Maryland, lung-cancer incidence was
not significantly affected by the type of basement construction or build-
ing materials. No measurements of radon or its daughters were made.
Rather, dwelling-related variables were assumed to be surrogates for radon-
daughter exposure.
SUMMARY
Cause-specific mortality risks for a number of the miner groups dis-
cussed above are listed in Table IV-16. Without exception, these studies
OCR for page 482
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OCR for page 484
484
HEALTH RISKS OF RADON AND O1~R ALPHA-EAlITTERS
indicate an excess probability of death due to lung cancer and, in many
cases, other causes of death as well. Continued follow-up of these miner
groups will provide additional information on the association of radon-
daughter exposure to lung cancer and perhaps other diseases. As discussed
in Chapter 2 and Appendix VII, epidemiological information that in-
cludes the smoking status of each participant is of paramount value. The
committee suggests that every effort be made to collect and report such
information for the studies described in this appendix.
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Representative terms from entire chapter:
uranium miners
