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OCR for page 176
4
Radium
INTRODUCTION
Four isotopes of radium occur naturally and several more are
man-made or are decay products of man-male isotopes. Radium is
present in soil, minerals, foodstuffs, groundwater, and many common
materials, including many used in construction. In communities
where wells are used, drinking water can be an important source of
ingested} radium. Radium has been used commercially in luminous
paints for watch and instrument dials and for other luminized objects.
It has also been used for internal radiation therapy.
The primary sources of information on the health effects and
dosimetry of radium isotopes come from extensive studies of 224 Ra,
226Ra, and 228Ra in humans and experimental animals. These studies
were motivated by the discovery of cancer and other debilitating
effects associated with internal exposure to 226 Ra and 228Ra. I`ater,
similar effects were also found to be associated with internal exposure
to 224 Ra. The purpose of this chapter is to review the information
on cancer induced by these three isotopes in humans and estimate
the risks associated with their internal deposition.
All members of the worId's population are presumably at risk,
because each absorbs radium from food and water; as a working
hypothesis, radiation is assumed to be carcinogenic even at the lowest
dose levels, although there is no unequivocal evidence to support this
hypothesis. Before concern developed over environmental exposure,
176
OCR for page 177
RADIUM
177
attention was devoted primarily to exposure in the workplace, where
the potential exists for the accidental uptake of radium at levels
known to be harmful to a significant fraction of exposed individuals.
As the practical concerns of radiation protection have shifted and
knowledge has accumulated, there has been an evolution in the design
and objectives of experimental animal studies and in the methods of
collection, analysis, and presentation of human health effects data.
The first widespread effort to control accidental radium expo-
sure was the abandonment of the technique of using the mouth to
tip the paint-laden brushes used for application of luminous material
containing 226 Ra and sometimes 228 Ra to the often small numerals
on watch dials. This change occurred in 1925-1926 following re-
ports and intensive discussion of short-term health effects such as
"radium jaws in some dial painters. Shortly thereafter, experimen-
tal animal studies and the analysis of case reports on human effects
focused on the determination of tolerance doses and radiation prm
section guides for the control of workplace exposure. These limits
on radium intake or body content were designed to reduce the in-
cidence of the then-known health effects to a level of insignificance.
The question remained open, however, whether the health effects
were threshold phenomena that would not occur below certain ex-
posure or dose levels, or whether the risk would continue at some
nonzero level until the exposure was removed altogether. The is-
sue remains unresolved, but as a matter of philosophy, it is now
commonly assumed that the so-called stochastic effects, cancer and
genetic effects, are nonthreshold phenomena and that the so-called
nonstochastic effects are threshold phenomena. Practical limitations
imposed by statistical variation in the outcome of experiments make
the threshold-nonthreshold issue for cancer essentially unresolvable
by scientific study. For nonstochastic effects, apparent threshold
doses vary with health endpoint. Low-leve! endpoints have not been
examined with the same thoroughness as cancer. There is evidence
that 226 228Ra effects on bone occur at the histological level for doses
near the limit of detectability. Whether these effects magnify other
skeletal problems is unknown, but issues such as these leave the
threshold-nonthreshold question open to further investigation.
Current efforts focus on the deterrn~nation of risk, as a func-
tion of time and exposure, with emphasis on the low exposure levels
where there ~ the greatest quantitative uncertainty. The presen-
tation and analysis of quantitative data vary from study to study,
making precise intercomparisons Circuit. Occasionally, data from
OCR for page 178
178 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
several studies have been analyzed by the same method, and this has
helped to illuminate similarities and differences in response among
224 Ra 226Ra, and 228Ra
Human health studies have grown from a case report phase into
epidem~ological studies devoted to the discovery of all significant
health endpoints, with an emphasis on cancer but always with the
recognition that other endpoints might also be significant. This chap
ter focuses on bone cancer and cancer of the paranasal sinuses and
mastoid air cells because these effects are known to be associated with
224 Ra or 226 228Ra and are thought to be nonthreshold phenomena.
Several general sources of information exist on radium and its
health effects, including portions of the reports from the United Na-
tions Scientific Committee on the Effects of Atomic Radiation; The
Effects of Irradiation on the Skeleton by Janet Vaughan; The Radiobi-
ology of Radium and Thorotrast, edited by W. Gossner; The Delayed
Effects of Bone Seeking Ra`]ionuclides, edited by C. W. Mays et al.;
Volume 35, Issue 1, of Health Physics; the Supplement to Volume 44
of Neatth Physics; and publications of the Center for Human Radio-
biology at Argonne National Laboratory, the Radioactivity Center at
the Massachusetts Institute of Technology, the New Jersey Radium
Research Project, the Radiobiology I,aboratory at the University of
California, Davis, and the Ra~liobiology Division at the University of
Utah.
CHEMISTRY AND PHYSICS OF RADIUM
When injected into humans for therapeutic purposes or into
experimental animals, radium is normally in the form of a solution of
radium chloride or some other readily soluble ionic compound. Little
research on the chemical form of radium in body fluids appears to
have been conducted. The radium might exist in ionic form, although
it is known to form complexes with some compounds of biological
interest under appropriate physiological conditions; it aDDarentlv
does not form complexes with amino acids.
—err
Each isotope of radium gives rise to a series of radioactive daugh-
ter products that leads to a stable isotope of lead (Figure 4-la and
4-lb). In addition to the primary radiation alpha, beta, or both-
indicated in the figures, most isotopes emit other radiation such as x
rays, gamma rays, internal conversion electrons, and Auger electrons.
In the analysis of radiation-effects data, the alpha particles emitted
are considered to be the root cause of damage. This is because of the
OCR for page 179
RADIUM
179
high linear energy transfer (LET) associated with alpha particles,
compared with beta particles or other radiation, and the greater
effectiveness of high-LET radiations in inducing cancer and various
other endpoints, including killing, transformation, and mutation of
cells.
The decay products of radium, except radon, are atoms of solid
materials. Radon is gaseous at room temperature and is not chem-
ically reactive to any important degree. Unless physically trapped
in a matrix, radon diffuses rapidly from its site of production. For
222Rn (whose half-life is very long compared with the time required
for untrapped atoms within the body to diffuse into the blood sup-
ply), this rapid diffusion results in a major reduction of the radiation
dose to tissues.
RETENTION AND DISTRIBUTION
Following entry into the circulatory system from the gut or lungs,
radium is quickly distributed to body tissues, and a rapid decrease
in its content in blood occurs. It later appears in the urine and feces,
with the majority of excretion occurring by the fecal route. Reten-
tion in tissues decreases with time following attainment of maximal
uptake not long after intake to blood. The loss Is more rapid from
soft than hard tissues, so there is a gradual shift in the distribution of
body radium toward hard tissue, and ultimately, bone becomes the
principal repository for radium in the body. The fundamental rea-
son for this is the chemical similarity between calcium and radium.
Because of its preference for bone, radium is commonly referred to
as a bone seeker.
Various radiation effects have been attributed to radium, but the
only noncontroversial ones are those associated with the deposition
of radium in hard tissues. Two compartments are usually identified
in the skeleton, a bone surface compartment in which the Helium is
retained for short periods and a bone volume compartment in which
it is retained for long periods. A third compartment, which is not
a repository for radium itself but which is relevant to the induction
of health effects, consists of the pneumatized portions of the skull
bones, that is, the paranasal sinuses and the air cells of the temporal
bone (primarily the mastoid air cells), where radon and its progeny,
the gaseous decay products of radium, accumulate.
Direct observation in viva of retention in these three compart-
ments is not possible, and what has been learned about them has
OCR for page 180
180 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
MASS
NUMBER
232 1 1 41 x 101° y
1~
228 RADIUM I {3_
(MsThl) 5.75 y
224
MASS i
NUMBER
224 RADIUM
(ThX) 3.62 d
__
220 RADON
(THORON) 55.6
216 POLONIUM
(ThA) 0.15 s
DECAY OF RADIUM-224 AND DAUGHTERS
... . . . _
1 -1
| ACTINIUM L (3_ | THORIUM
(MsTh2) 6.13 h 1 1 (RdTh) 1~91 y
1~
r RADII M |
(ThX) 3.62 d
1 ,
212 LEAD i3 _ | BISMUTH
(ThB) 10.6 h | (ThC) 60~6 m —I (ThC') 0.3 As
36%' r~
1
208
THALLIUM 13_ | LEAD
(ThC") 3.1 m ~ (ThD)
STABLE
FIGURE 4-1 a. Decay series for radium-228, a beta-particle emitter, and
radium-224, an alpha-particle emitter, showing the principal isotopes present,
the primary radiations emitted (a, if, or both), and the half-lives (s = second,
m = minute, h = hour, d = day, y = year). b. Decay series for radium-226
showing the primary radiations emitted and the half-lives.
OCR for page 181
RADIUM
MASS
NUMBER
226 RADIUM
1 620y
222 1 3.82d
_
1
218
214
210
206
181
i:.-:-::--
1 -~-~- - ·.
THE SHORT-LIVED
RADON DAUGHTERS
,POLC~ :;:
' 26.8m · ·-L~ ~
!( ·. · ) 1 | (RADIUM C) | _ I
- CAT
.... ..
POLONIUM .e
0.0001648,
(RADIUM C')
CYi021 % (~|J~
.
| THALLIUM i_| BISMUTH Lit_|
51 1m 1 HI 22y ~ Sd ~
POLONIUM
138d
1 °~% ~10-~013% ~]
MERCURY I ~ ~ ~ THALLIUM I ~ _ 1:
Em ~ __ ~ . ~
been inferred from postmortem observations and modeling studies.
During life, four quantities that can be monitored include whole-
body content of radium, blood concentration, urinary excretion rate,
and fecal excretion rate. These are supplemented by postmortem
measurements of skeletal and soft-tissue content, observations of ra-
dium distribution within bone on a microscale, and measurements of
radon gas content in the mastoid air cells.
For humans and some species of animals, an abundance of data
is available on some of the observable quantities, but in no case
have all the necessary data been collected. In general, the data from
humans suffice to establish radium retention in the bone volume
compartment. Animal data supplemented by models are required
to estimate retention in the human bone surface, and human data
combiner} with models of gas accumulation are applied to the pneu-
matized space compartment.
OCR for page 182
182 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
100 RADIUM IN MAN--WHOLE BODY RETENTION
'_ 10
at
an
`> 1.0
0.1
,6 ^O
616i
6~5 ~
MILL)?iNORRIS (8)
MILLER ~ `~, ~
(5) ~ ~ 4
~5_~ AGE >24
MILLER ~~ _ MODEL (March 31, 1971)
(10) 12~1—it (SL)
AGE SUBJECT
60 G.E.H.
25-55 ELGIN
25-32 ELGIN
80 G.S.P.
40 D.M.
63-83 MIT
I NVESTIGATOR
O HARRISON (1967)
O SCHLUNDT (1933), NORRIS (1955)
MILLER (1965)
MAYS (1963)
~ MAYS (1964)
· MALETOSKOS (1966)
~~4 AGE <24
it_ ~ MILLER
\~ MILLER
~ (8)
l l l I MILLER (10)
1o2 103 104 105
1o1
DAYS AFTER INJECTION (or Last Injection)
FIGURE 4-2 Whole-body radium retention in humans. Summary of virtually
all available data for adult man. The heavy curve represents the new model.
Most of the points lie above the model curve for the first 1-2 days because no
correction for fecal delay has been made. SOURCE: International Commission
on Radiological Protection (ICRP).29
Figure ~2 is a summary of data on the whole-body retention of
radium in humans.29 Whole-body retention diminishes as a power
function of time. This observation has also been made for the reten-
tion of radium and other alkaline earths in animals. Marshall and
Onkelix39 explained this retention in terms of the diffusion charac-
teristics of alkaline earths in the skeleton.
The excretion rate of radium can be determined by direct mea-
surement in urine and feces or by determining the rate of change in
whole-body retention with time. When radium levels in urine and
feces are measured, by far the largest amount is found in the feces. In
people with radium burdens of many years' duration, only To of the
excreted radium exits through the kidneys. The other 98~o passes
out through the bowel.
At high radiation doses, whole-body retention is dose depen-
dent. This observation was originally made on animals given high
doses where retention, at a given time after injection, was found to in-
crease with injection level. The most likely explanation is that tissue
damage to the skeleton, at high doses, alters the retention pattern,
OCR for page 183
RADIUM
183
primarily through the reduction in skeletal blood flow that results
from the death of capillaries and other small vessels and through the
inhibition of bone remodeling, a process known to be important for
the release of radium from bone. A recent examination of data on
whole-body radium retention in humans revealed that the excretion
rate diminished with increasing body burden.70 Absolute retention
could not be studied, because the initial intake was unknown, but
the data imply the existence of a dose-dependent retention similar
to that observed in animals. Subnormal excretion rate can be linked
with the apparent subnormal remodeling rates in high-dose radium
cases.77
Radium has an affinity for hard tissue because of its chemical
similarity to calcium. It does, however, deposit in soft tissue and
there is a potential for radiation effects in these tissues. The data
on human soft-tissue retention were recently reviewed.74 The rate of
release from soft tissue exceeds that for the body as a whole, which
is another way of stating that the proportion of total body radium
that eventually resides in the skeleton increases with time.
Postmortem skeletal retention has been studied in animals and in
the remains of a few humans with known injection levels. Otherwise,
the retention in bone is estunated by models.
Autoradiographic studies37 of alkaline earth uptake by bone soon
after the alkaline earth was injected into animals revealed the ex-
istence of two distinct compartments in bone (see Figure 4-3), a
short-term compartment associated with surface deposition, and a
long-term compartment associated with volume deposition. The up-
take and release of activity into and out of the surface compartment
was studied quantitatively in animals and was found to be closely
related to the time dependence of activity in the blood.65 Mathemat-
ical analysis of the relationship showed that bone surfaces behaved
as a single compartment in constant exchange with the blood.37
This mode! for the kinetics of bone surface retention in animals was
adopted for man and integrated into the ICRP mode! for alkaline
earth metabolism, in which it became the basis for distinguishing
between retention in bone volume and at bone surfaces. This is an
instance in which an extrapolation of animal data to humans has
played an important role.
A mechanistic mode! for alkaline earth metabolism29 was devel-
oped by the ICRP to describe the retention of calcium, strontium,
barium, and radium in the human body and in human soft tissue,
bone volume, bone surfaces, and blood. Separate retention functions
OCR for page 184
~ ~~~ ~ ~ ~~ ~~ O~ as
# ~
FICORE 4-3 Autor~dlogr~ph of bone Tom the data lea Tour of ~ krmer
radlum-dl~1 paster strong hotspots unlock areas] and Valise r~dloact~hy
(gray bread.
are given far each of these compartments. When the model ~ used
far radium, careful sttentlon should be paid to the constraluts plied
on the model ~ dam on radium retention in human soR tlssues/4
Because of the m~bematlc~ complexly of the retention actions
some luvestlgators bye fitted simpler actions to the ICHP model.
OCR for page 185
RADIUM
185
These simpler functions have no mechanistic interpretation, but they
do make some calculations easier.
The kinetics of radon accumulation in the pneumatized air spaces
are determined by the kinetics of radium in the surrounding bone,
the rate of diffusion from bone through the intervening tissue to the
air cavity, and the rate of clearance through the ventilatory ducts
and the circulatory system. Diffusion models for the sinuses have not
been proposed, but work has been done on the movement of 220 Rn
through tissue adjacent to bone surfaces. Clearance through the
ventilatory ducts is rapid when they are open. The eustachian tube
provides ventilation for the Me ear and pneumatized portions of
the temporal bone. This duct is normally closed, and clearance by
this pathway Is negligible. The sinus ducts are normally open but
can be plugged by mucus or the swelling of mucosal tissues during
illness. When these ducts are open, clearance is almost exclusively
through them. Clearance half-times for the frontal and maxillary
sinuses are a few minutes when the ducts are open. Otherwise,
clearance half-times are about 100 min and are determined by the
blood flow through mucosal tissues.73 The radioactive half-lives of
the radon isotopes 55 s for 220Rn and 3.8 days for 222Rn are quite
different from their clearance half-times. In effect, essentially all
the 220 Rn that diffuses into the pneumatized air space decays there
before it can be cleared, but essentially all the 222 Rn that reaches
the pneumatized air space is cleared before it can decay. These
relationships have important dosimetric unplications.
BONE CANCER
F REQUENCY AND C ELL TYPE
Radium deposited in bone irradiates the cells of that tissue, even-
tually causing sarcomas in a large fraction of subjects exposed to high
doses. The first case of bone sarcoma associated with 226 228 Ra expo-
sure was a tumor of the scapula reported in 1929, 2 yr after diagnosis
in a woman who had earlier worked as a radium-dial painter.42 Bone
tumors among children injected with 224 Ra for therapeutic purposes
were reported in 1962 among persons treated between 1946 and
.87
Spontaneously occurring bone tumors are rare. Sarcomas of
the bones and joints comprise only 0.24~o of microscopically con-
firmed malignancies reported by the National Cancer Institute's
OCR for page 186
186 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
TABLE 4-1 Locations of Bone Sarcomas among
Persons Exposed to 224Ra and 226 228Ra for Whom
Skeletal Dose Estimates Are Available
Location
224Raa 226,22eRa
Axial skeleton
Appendicular skeleton
Unspecified or widespread 5
8.5
35.5
58
a One tumor located in the left sacroiliac joint has been assigned half to
the appendicular skeleton and half to the axial skeleton.
Surveillance, Epidemiology, and End Results (SEER) program.52
The chance of contracting bone sarcoma during a lifetime is less than
0.1%o.
Some 87 bone sarcomas have occurred in 85 persons exposed to
226 228Ra among the 4,775 persons for whom there has been at least
one determination of vital status. Multiple sarcomas not confirmed as
either primary or secondary are suspected or known to have occurred
in several other subjects. A total of 66 sarcomas have occurred in
64 subjects among 2,403 subjects for whom there Is an estimate of
skeletal dose; fewer than 2 sarcomas would be expected. Many of
the 2,403 subjects are still alive. Tumor frequencies for axial and
appendicular skeleton are shown in Table ~1. The frequencies for
different bone groups are axial skeleton-skull (3), mandible (1), ribs
(2), sternebrae (1), vertebrae (1), appendicular skeleton-scapulae (2),
humeri (6), radii (2), ulnae (1), pelvis (10), femora (22), tibiae (7),
fibulae (1), legs (2; bones unspecified), feet and hands (5; bones
unspecified).
Some 55 sarcomas of bone have occurred in 53 of 898 224Ra-
exposed patients whose health status is evaluated triennially.46 Two
primary sarcomas occurred in 2 subjects. Locations are shown in
Table 4-1 for 49 tumors among 47 subjects for whom there is an
estimate of skeletal dose.
In Table ~1 note the low tumor yield of the axial compared
with the appendicular skeleton. In an earlier summary for 24 224Ra-
induced osteosarcomas,90 21~o occurred in the axial skeleton. These
percentages contrast sharply with the results for beagles injected with
226Ra, in which osteosarcomas were about equally divided between
the axial and appendicular skeletons and one-quarter of the tumors
appeared in the vertebrae.90
OCR for page 234
234 HEALTH RISKS OF RADON AND OTHER ALPHA-~ITTERS
where F(D) is the lifetime risk, as specified by the analyses of Spiess
and Mays85 and ~ is a coefficient based on the time of tumor ap-
pearance for juveniles and abducts in the 224Ra data analyses. The
hal£life for tumor appearance is roughly 4 yr in this data set, giving
an approximate value for r of O.l8/yr. For t less than 5 yr, M(D,t)
is essentially O because of the minimum latent period. Thereafter,
tumors appear at the rate M(D,t).
The age structure of the population at risk and competing causes
of death should be taken into account in risk estimation. An ideal
circumstance would be to know the dose-response relationships in
the absence of competing causes of death and to combine this with
information on age structure and age-specific mortality for the pop-
ulation at large. With the analyses presently available, only part of
this prescription can be achieved. An approximate approach would
be to take the population as a function of age and exposure and apply
the dose-response relationship to each age group, taking into account
the projected survival for that age group in the coming years. At the
low exposures that occur environmentally and occupationally, expo-
sure to radium isotopes causes only a small contribution to overall
mortality and would not be expected to perturb mortality sufficiently
to distort the normal mortality statistics. Also, mortality statistics
an they now exist include the effect of environmental exposures to
radium isotopes.
Table ~7 illustrates the eject, assuming that one million U.S.
white males receive an excess skeletal dose of 1 red from 224 Ra at
age 40. The excess death rate due to bone cancer for t > 5 yr is
computed from:
M(D, t) = (200 x 10~6/rad) x (0.18/yrjexpt—0.18 it—sit. (4-24)
This assumes the 224 Ra dose-response analyses described above and
further assumes that tumors are fatal in the year of occurrence.
After 25 yr, there would be 780,565 survivors in the absence of
excess exposure to 224 Ra and 780,396 survivors with 1 red of excess
exposure at the start of the follow-up period, a difference of 169
excess deaths/person-red, which is about 15% less than the lifetime
expectation of 200 x 10~6/person-rad calculated without regard to
competing risks.
If there were a continous exposure of 1 rad/yr, the tumor rate
would rise to an asymptotic value. If this were substituted for the
tumor rate caused by 224 Ra exposure in Table 4-7 and the survival
OCR for page 235
RADIUM
TABLE 4-7 Effect of Single Skeletal Dose of 1 red from 224Ra Received
by 1,000,000 U.S. White Males at Age 40a
235
No. of No. of
Natural Natural Survivors Survivors
Age Death Survival without 224Ra 224 Ra Annual 224Ra Annual with 224 Ra
(yr) Rate Rate Exposure Tumor Rate Survival Rate Exposure
40 0.00240 0.998 998,000 0 1 998,000
41 0.00263 0.997 99S,006 0 1 995,006
42 0.00289 0.997 992,021 0 1 992,021
43 0.00319 0.997 989,045 0 1 989,045
44 0.00353 0.996 985,089 0.000036 0.999964 985,054
45 0.00391 0.996 981,148 0.000030 0.999970 981,084
46 0.00434 0.996 977,224 0.000025 0.999975 977,136
47 0.00483 0.995 972,338 0.000021 0.999979 972,229
48 0.00538 0.995 967,476 0.000018 0.999982 967,351
49 0.00601 0.994 961,671 0.000015 0.999985 961,532
50 0.00669 0.993 954,939 0.000012 0.999988 954,790
51 0.00742 0.993 948,255 0.000010 0.999990 948,097
52 0.00820 0.992 940,669 0.0000085 0.9999915 940,504
53 0.00902 0.991 932,203 0.0000091 0.9999919 932,032
54 0.00989 0.990 922,881 0.0000060 0.9999930 922,705
55 0.01083 0.989 912,729 0.0000050 0.9999950 912,551
56 0.01184 0.988 901,776 0.0000041 0.9999959 901,597
57 0.01295 0.987 890,058 0.0000035 0.9999965 889,873
58 0.01416 0.986 877,592 0.0000029 0.9999971 877,412
59 0.01547 0.985 864,429 0.0000024 0.9999976 864,249
60 0.01685 0.983 849,733 0.0000020 0.9999980 849,555
61 0.01835 0.982 834,438 0.0000017 0.9999983 834,261
62 0.02004 0.980 817,749 0.0000014 0.9999986 817,575
63 0.02195 0.978 799,759 0.0000012 0.9999988 799,587
64 0.02407 0.976 780,565 0.0000010 0.9999990 780,396
aU.S. white male mortality rates for 1982 from Statistical Abstract of the United States, 106th
ea., U.S. Department of Commerce, Washington, D.C., 1986.
rate of those exposed to 224Ra were adjusted to the corresponding
value (0.9998), survival in the presence of 224 Ra exposure after 25
yr would be 777,293, with 3,272 deaths attributable to the 224 Ra
exposure.
Calculations for 226 Ra and 228 Ra are similar to the calculation
with the asymptotic tumor rate for 224 Ra. For 226 Ra and 228 Ra the
constant tumor rates given by Rowland et al.68 as functions of sys-
temic intake are computed for the intake of interest, and the results
are worked out with a table such as Table 4-7. For continuous intake
with the dose-squared exponential function for bone sarcoma induc-
tion, it is necessary to decide whether to add the cumulative dose
OCR for page 236
236 HEALTH RISKS OF RADON AND OTHER ALPHA-I£MITTERS
and then take the square or to take the square for each annual incre-
ment of dose. Taking the former choice, it is implied that the doses
given at different times interact; with the latter choice it is implied
that the doses act independently of one another. On the microscale
the chance of a single cell being hit more than once diminishes with
dose; this would argue for the independent action of separate dose
increments and the squaring of separate dose increments before the
addition of risks. In the mode} of bone tumor induction proposed
by Marshall and Groer,38 however, two hits are required to cause
transformation. This argues for the interaction of doses and in the
extreme case for squaring the cumulative dose. Unless bone cancer
induced by 226Ra and 228 Ra is a pure, single-hit phenomenon, some
interaction of dose increments is expected, although perhaps it is
a less strong interaction than is consistent with squaring the total
accumulated intake when intake is continuous.
The advantage of using a tabular form for the calculation of
the effect of radiation is that it provides a general procedure that
can be applied to more complex problems than the one illustrated
above. With environmental radiation, in which large populations are
exposed, a spectrum of ages from newborn to elderly ~ represented.
Knowing the death rate as a function of time for each starting age
then allows the impact of radiation exposure to be calculated for
each age group and to be summed for the whole population. The
use of a table for each starting age group provides a good accounting
system for the calculation. The same goals can be achieved if normal
mortality is represented by a continuous function and radiation-
induced mortality is so represented, as for 224Ra above, and the
methods of calculus are used to compute the integrals obtained by
the tabular method.
SUMMARY AND RECOMMENDATIONS
As documented above, research on radium and its effects has
been extensive. With continued research the full fruits of these labors
in terms of lifetime risk estimates for 226 Ra and other long-half-life
alpha-emitters which are deposited in bone should be realized. In
the case of 224Ra, the relatively short half-life of the material per-
mits an estimation of the dose to bone or one that is proportional
to that received by the cells at risk. Correspondingly, relatively sim-
ple and complete dose-response functions have been developed that
permit numerical estimates of the lifetime risk, that is, about 2 x
OCR for page 237
RADIUM
237
10-2/person-Gy for bone sarcoma following well-protracted expo-
sure. In the case of the longer-half-life radium isotopes, the interpre-
tation of the cancer response in terms of estimated dose is less clear.
The dose is delivered continuously over the balance of a person's
lifetime, with ample opportunity for the remodeling of bone tissues
and the development of biological damage to modulate the dose to
critical cells. Deposition (and redeposition) is not uniform and tin
sue reactions may alter the location of the cells and their number
and radiosensitivity. Therefore, est~rnates of the cumulative average
skeletal dose may not be aclequ ate to quantitate the biological insult.
Investigation of other dosimetric approaches is warranted.
Equally important is ensuring the availability of information on
the rate at which tumors have occurred in the populations at risk.
Hazard functions which consider the temporal appearance of tumors
have shown some promise for delineating the kinetics of radium-
induced bone cancers, and may provide insight into the temporal
pattern of the effective dose. Combining this information with results
observed with 224 Ra may lead to the development of a general mode}
for bone cancer induction due to alpha-particle emitters.
Further efforts to refine dose estimates as a function of time in
both man and animals will facilitate the interpretation of animal data
in terms of the risks observed in humans. As indicated in Annex 7A,
the radium-dial painter data can be a useful source of information
for extrapolating to man the risks from transuranic elements that
have been observed in animal studies. A more complete description
of the radium-dial painter data and parallel studies with radium in
laboratory animals, particularly the rat, would do much to further
such efforts.
The committee believes a balanced program of radium research
should include the following elements.
The bone-cancer risk appears to have been completely ex-
pressed in the populations from the 1940s exposed to 224 Ra and
nearly completely expressed in the populations exposed to 226 Ra
and 228Ra before 1930; the bone-cancer risk data from the two epi-
dem~ological studies should be integrated and analyzed with newer
statistical methods to extend the usefulness of human data. The
committee recommends that these studies continue to include dosi-
metric evaluation, especially at the tissue and cellular level, and
evaluation of uncertainties from all sources.
. The committee recommends that the follow-up studies of the
patients exposed to lower doses of 224 Ra since the 1940s now in
OCR for page 238
238 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
progress in Germany and of similar groups of patients exposed to
226 Ra and 228Ra should continue. The detection of bone cancer or
sinus and mastoid cancer at dose levels comparable to those en-
countered in occupational exposures would significantly reduce the
uncertainties of bone-cancer risk estimation at low dose levels.
. Research should continue on the cells at risk for bone-cancer
induction, on cell behavior over time, including where the cells are
located in the radiation field at various stages of their life cycles,
on tissue modifications which may reduce the radiation dose to the
cells, and on the time behavior and distribution of radioactivity in
bone. Meaningful estimates of tissue and cellular dose obtained by
these efforts will provide a quantitative linkage between human and
animal studies and cell transformation in vitro.
The sinus and mastoid! carcinomas in persons exposed to
226 Ra and 228 Ra are produced largely by the action of 222Rn and its
progeny; continued study may offer insights into the ejects of oc-
cupational and environmental radon. The dosimetry of the mastoid
air cell system is much simpler than the dosimetry of the bronchial
tree; the mastoid mucosa may be the respiratory tissue for which the
epithelial structure may permit accurate target cell dose estimates
so that the risk to epithelial tissues per unit dose and the specific
energy that has an impact on cells can be determined; this may im-
prove our estimation of the carcinogenic risk in the epithelium of the
respiratory tract.
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Representative terms from entire chapter:
health risks
