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OCR for page 159
Polonium
INTRODUCTION
Polonium was the first radioactive element that Marie and Pierre
Curie separated from the uranium ore pitchblende. It has over 25
isotopes with mass numbers of 192-218. All are radioactive, most
are predominantly alpha-emitters, and many have very short half-
lives. The important isotopes and their nuclear properties are listed
in Table 31 Only 208 To 209po, and Hippo have half-lives long
enough to permit useful biomedical research; of these, Judo has
been used most. Typo and Demo are also important, because they
are daughters of radon and contribute a substantial portion of the
radiation dose from inhaled radon. They have such short half-lives
that no experimental biomedical work can be done with them, and
their effects must be inferred from the effects of isotopes with longer
hal£lives. Echo and Echo are in the thorium-thoron decay chain.
One reason for interest in the alpha particles from polonium is
their existence as radon daughters; indeed, with respect to impor-
tant radiation dose, the radon problem is due largely to polonium.
There are other reasons for interest in polonium; of primary interest
is primarily the isotope Echo, which has a half-life of about 138
days and decays to a stable lead isotope (206 Pb) by almost pure
alpha-particle emission. These properties led to its use in much ex-
perimental work that required an alpha-particle source with useful
energy and a convenient half-life.
159
OCR for page 160
160 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
TABLE 3-1 Selected Polonium Isotopes and Their
Alpha Emissions
Isotope Half-Life Emission ~ Energy (MeV)
tospO 2.93 yr ~ (99~0) 5.114
Typo 103 yr ~ (demo) 4.882
210po 138.4 days ~ 5.305
211po 0.52 s a(99~o) 7.448
2l2mpO 45 s ~ (demo) 11.65
213po 4 x 10-6 s ~ (demo) 8.38
214po 1.6 x 10-4 s a(99~o) 7.69
215po 1.8 x 10-3 s ~ 7.38
216po 0.15 s ~ 6.77
217po < 10 s ~ (demo) 6.55
2l~po 3.05 min ~ 6.11
Polonium has been used extensively as an alpha-particle source
for the production of neutrons by interaction with beryllium. Many
large alpha-particle sources were prepared before plutonium was
available in sufficient quantities to supplant polonium for this appli-
cation. In fact, Hobo was the alpha-particle source in the neutron-
producing initiators of at least the first generation of atomic weapons.
During the Manhattan Project days of World War IT, large quantities
of Hobo were produced at a plant in Dayton, Ohio, and protection
of workers and the environment was needed.
Echo has found wide application in static-eliminator devices,
for example, in paper and textile plants. The high specific ioniza-
tion around such devices is effective in reducing static electricity
buildup. However, polonium is difficult to contain, and there have
been instances of contamination, not only from static-eliminator bars
but from solutions left in the open, because of polonium's marked
tendency to "creep.
Polonium occurs naturally in the environment. Airborne radon
decays into polonium isotopes that can be deposited on terrain and
vegetation, for example, on tobacco leaves. Some have postulated
that the alpha-particle radiation from polonium, volatilized from
smoking tobacco, plays an important role in the genesis of lung
cancer in smokers.37
PROPERTIES
The chemical behavior of polonium was described many years ago
by Haissinskyi~ i9 and others, later by Moyer,33 and in the Russian
OCR for page 161
POLONIUM
161
literature by Moroz and Parfenov.30 It has a complex solution and
electrochemistry. Properties of prime importance for understanding
its behavior in living systems are discussed in a volume prepared by
Stannard and Casarett52 53 and are discussed specifically by Morrow
et al.~3~32 Thomas and Stannard,49 Thomas,5t and Feldman and
Saunor.~2 Subcellular distribution was investigated by Lanzola et
a,.26
Polonium is chemically different from most of the alpha-emitting
elements cliscussed in this report. It has many of the characteristics of
the rare-earth elements, is amphoteric, and tends to form hydroxides
and radiocolloids both in vitro and in viva. As a result of the latter,
polonium is phagocyt~zed readily by cells of the reticuloendothelial
system and deposits substantially in the spleen, lymph nodes, bone
marrow, and liver (in that order) after parenteral administration.
Major deposition also occurs In the kidneys. Tissue distribution is
influenced considerably by the route of administration.
Autoradiographic studies, begun in the 1920s by Lacassagne and
Lattes,25 have characteristically demonstrated the presence of much
aggregated polonium both in solutions at or near neutral pH and
in viva. These aggregates demonstrate the presence of radiocolloids.
They are not seen in vivo after oral administration of polonium,5
and they become disorganized and gradually disappear. In contrast,
nonaggregated (sern~-ionic or ionic) polonium is more uniformly dis-
tributed to tissues and less influenced by the route of administration.
The nonaggregated form, although less striking autoradiographically,
can account for a substantial fraction of the radiation dose.
Polonium has less tendency to form specific complexes with
biomolecules than do radium, plutonium, americium, or other trans-
uranic elements, although relatively loose combinations with numer-
ous moieties are common; for example, polonium combines with the
gIobin portion of hemoglobin and other blood constituents and binds
nonspecifically to proteins. It does not exchange for calcium in bone,
as does radium, nor does it combine with osteoid, as does plutonium.
Polonium Is relatively volatile and is easily vaporized from a solid
source.
The only other major element in the alpha-emitter series with
physical and chemical properties somewhat resembling those of polo-
nium is thorium. However, the situation with thorium isotopes is
much more complex, partly because of the ingrowth of daughter
products and the decay of the parent isotopes.
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162 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
DOSIMETRY
In contrast with many of the alpha-emitters discussed in this
report, memo is at the end of a decay chain and disintegrates to a
stable isotope of leacI. The short-lived isotopes in the radon chain
decay to a long-lived intermediate, 2~0Pb.
Substantial radiation doses from polonium can be expected in
many tissues of the body. Indeed, it supplies a more nearly whole-
body dose than any other alpha-emitter except radon gag, but only
by contrast to the highly localized doses imparted by bone seekers,
such as plutonium and radium. In general, the spleen and kidneys
concentrate polonium more than other tissues except for temporary
deposition in the Jung after inhalation of an insoluble form. Effects
are more common in the kidney than in the spleen, despite a nomi-
nally higher dose in the spleen. The lymph nodes and the liver are
also affected.
A high concentration of polonium is found in blood cells after ore]
administration and long after parenteral administration.~3 43 45 47
Polonium can enter red blood cells in nonaggregate form, but ap-
parently not in aggregate, that is, colloidal, form. Because the polo-
nium that enters the body by intestinal absorption does so largely in
nonaggregate form, a much larger fraction of the dose is found associ-
ated with red blood cells combined with the gibbon of hemogIobin.4 5i
A considerably smaller fraction appears in the cells of the reticuloen-
dothelial system, and colloidal aggregates are notably absent. Thus,
dose distribution after oral administration involves a larger contri-
bution to radiation dose from the circulating blood and from nonag-
gregated polonium. The distribution of polonium after inhalation is
intermediate between those after parenteral and oral administration.
The relative concentration increases over time after intravenous ad-
ministration; by 250 days, a substantial fraction of the body burden
of polonium is associated with red blood celIs.46 However, this shift
occurs long after the major biological elimination and does not alter
the cumulative dose very much. It could be pertinent to calculations
of dose rate over long-term conditions.
These characteristics of dose do not seem to be sufficient to
have a large effect on the early toxicity of polonium. Indeed, for
periods of up to 200 days, a gross plot of toxicity as measured
by lethality in rats shows that it is nearly the same for all routes
of administration.~° This simplifies dosage calculations, but applies
largely to doses considerably higher than those of primary interest.
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POLONIUM
163
Calculations of long-term low to intermediate radiation doses should
consider the differences influenced by route of administration.6 7
Because retention half-times in tissues range from as little as
11 days in liver to 153 days in testes, the relative contribution to
dose rate in different tissues depends markedly on time after a single
administration. The largest part of the alpha dose is delivered over
the first 100 days after a single administration, so these differences
have less effect later on total dose than on the dose rate.
Many situations, even continuous intake, involve a series of doses.
In a large experiment with rats,48 it was shown that the metabolism
of polonium was not the same after a multiple-dose regimen as after a
single-dose regimen. Excretion was slower, effective half-time in the
body rose from about 30 days to nearly 40 days, and other evidence
indicated that a more tenacious retention of polonium was received
in multiple doses. Thus, a somewhat higher radiation dose per mi-
crocurie disintegrating within the body is expected for the important
organs (spleen, liver, and kidney) than after a single dose. Anthony
et al.t discussed the influence of these variations on establishing
maximal permissible exposures to polonium. Long-term pathologic
developments are affected by differences in dosage regime.3
The presence of aggregates of polonium in tissues after parenteral
administration raises the question of whether special account should
be taken of the nominally much larger potential dose surrounding
a large aggregate in a given tissue compared with the dose from a
comparable amount of diffusely distributed polonium. Results of an
investigation of the comparability of the "hot spots problem in bone
and the "hot-particle~ problem for plutonium in the lungs seem to
indicate that the diffuse pattern can be as effective or even more
effective in carcinogenesis. This is because of the cell-killing compo-
nent of the aggregates and because a substantial portion of the dose
is derived from monomeric or weakly polymeric forms. Therefore,
special account need not be taken of the dose from aggregates in
calculating polonium doses; the average dose to tissue is considered
the pertinent quantity.
ANIMAL STUDIES
TISSUE DISTRIBUTION AND EXCRETION
Much effort has been devoted over many decades to animal stud-
ies of the distribution and excretion of polonium.~3 25 30 33 47 49 After
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164 HEALTH RISKS OF RADON AND OTHER ALPHA-E~ITTERS
intravenous administration, most polonium is excreted in the feces.
More appeared in urine in rabbits and consistently less in the urine
of dogs. Except for the contribution of polonium not absorbed from
the gut after oral administration, the effect of route of administra-
tion is not large. There is a tendency for greater urinary excretion
of inhaled polonium and especially of orally administered polonium.
Nevertheless, clearances of polonium from the blood through the kid-
ney are generally low, for example, 0.005 mI/m~n after intravenous
administration in the cat and 0.01 mI/rn~n on absorption from the
cat's stomach.32 (Clearance rates for man are 0.01~.08 mI/min.) In
contrast, clearance rates in the cat for radium are 1 and 2 m} of
plasma per men, and those for strontium and calcium about 0.91
and 0.17 mI/m~n, respectively. The amounts of polonium bound to
protein and in colloidal form are considered sufficient to account for
its low urinary clearance rate.
The role of the liver in removing polonium to the feces by the
bile was confirmed in bile duct ligation experiments in animals by
Finki3 and in the early work of Lacassagne summarized by Fink. It
has also been postulated that the intestinal was has a role.~t
Polonium is secreted in the milk of lactating animals.40 54 Equa-
tions for its concentration in milk as a function of tune after intake
have been developed. The effective half-life for excretion in cows'
milk over a Today period was about 3.7 days, increasing to 33 days
at longer times after uptake. The transfer coefficients to milk (in cows
or goats) depend on the species and the nature of the compound in-
gested, but are always well below 1.0 (maximum, 0.18; minimum,
0.0089).
In the context of the important relative toxicity experiments
with alpha-em~tters, 2~0po has acute toxicity far greater, on a per
microcurie basis, than either plutonium or radium. However, if
lethality is measured at 300 days in rats, polonium is only about
twice as toxic.
Blair2 compared the long-term life-span-shortening effects of sin-
gle doses of memo 239 Pu and 226Ra in rats. Echo administered at
1 ,uCi/kg of body weight shortened the life span of the animals by
4.3 weeks. Comparable life-span shortening was brought about by
239 Pu at 0.9 ,uCi/kg and 226 Ra at 5 ,uCi/kg. Thus, the long-term
life-span-shortening effects of polonium and plutonium appear to be
comparable and about 5 times as great as that of radium. Life-span
shortening with a multiple-dose regimen was almost identical, on the
basis of effective dose.50 That was taken as evidence that most of
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POLONIUM
165
the injury (perhaps about Who) produced by polonium alpha par-
ticles was irreversible. In contrast, life shortening in the mouse by
strontium-89 is much reduced if the dose is divided.~7 Indeed, the ef-
fect of beta particles from 89Sr is comparable with that of x rays and
has been interpreted as being due to the presence of a much higher
fraction of reversible injury caused by low linear energy transfer
radiation.
The increase in effectiveness caused by protraction of the dose
from alpha particles, described elsewhere in this report, has not been
seen with polonium. The female rat shows a tendency toward more
life-span shortening on a multiple-dose regimen, but the male does
not. These findings might arise from the design of the experiments
with polonium and perhaps do not contradict the general observa-
tion, especially inasmuch as these experiments predated those which
stimulated the idea that the alph~emitter effect was increased by
protraction.
HISTOPATHOLOGY AND CARCINOGENESIS
Specific short- and long-term pathologic effects of polonium have
been described by investigators at Argonne National Laboratory, Ar-
gonne, Ill.; the Mound Laboratory, Maimisburg, Ohio; the University
of Rochester, N.Y.; and the USSR. Most follow the sequences of acute
or chronic radiation injury. Most of the reports have been in reason-
able agreement, except for a description of extensive liver damage in
rats in a multiple-dose experiment at the Mound Laboratory. The
liver damage, not seen in other studies, might have been attributable
to a strain difference.
Increases in the incidences of cancer in experimental animals
attributable to polonium were not reported until the early 1950s.
Finke} and Hirschi6 reported the presence of lymphomas in mice by
250 days after injection of polonium at about 1.5 and 0.9 psi/kg.
They also reported a significant increase in bone tumors (presumably
arising from bone marrow deposition, inasmuch as polonium is not a
bone-seeking element) at 8 and 0.46 pCi/kg.~4 i~ 47 Although tumors
appeared in the animals at the Mound Laboratory, the incidence did
not differ significantly between control and experimental animals.
Casarett6~8 has described neoplastic changes in rats that re-
ceived single or multiple oral doses of polonium. Over 40 soft-tissue
tumors appeared in 175 rats (23%) on a single-dose regimen and
only three tumors appeared in 34 controls (who). Some of the tumors
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166 HEALTH RISKS OF RADON AND OTHER ALPHA-~ITTERS
were malignant. Many were primary and there was a considerable
variety. Tumor incidence was maximal at the middle doses (5 and 10
psi/kg). At the highest dose (20 ,uCi/kg), the life span was too short
for much expression of tumor growth. At the lowest dose (1 psi/kg),
there were somewhat fewer tumors. Tumors were both increased in
incidence and advanced temporally by polonium. Neoplastic effects
were present, but in different incidences and distributions. After oral
administration, less hyperplastic change occurred in the hematopoi-
etic organs and testes; this finding was compatible with the lower
concentrations of polonium in these organs after oral administration.
Among the nonneoplastic degenerative effects of polonium ~ the
development of sclerotic changes in blood vessels, which might be
due to bloodborne polonium. This effect was seen particularly in the
testes and the kidneys. In the kidneys, the process could be followed
through proliferation of the arteriolar endothelium to the blocking
of blood vessels and ischemia of portions of the kidney.6 This lesion,
like many others in this and other experiments, depended heavily on
dose and was never as marked in the multiple-dose experiment.
General nonneoplastic changes from polonium administration
included atrophy of the seminiferous epithelium and hyperplasia
of interstitial (L`eydig) cells in the testes. In addition, hypoplasia
and atrophy of lymph nodes, thymus and spleen, and bone mar-
row occurred. There was involution of growing cartilage, arteriolar
nephrosclerosis, vacuolization of adrenal cortical cells, atrophy of
the pancreas, hypoplastic and hyperplastic changes in pulmonary
lymphoid tissue, obstructive pulmonary emphysema with partial oh
struction of bronchioles, and general arterioscIerosis.6 Some of these
changes were direct radiation effects; others were indirect degenera-
tive sequelae.
Nearly all these detailed histopathological findings have occurred
at relatively high doses, well above those of primary interest in this
report. Few of the doses are relevant to possible population or
environmental exposure.
Observations in animals in the USSR30 placed considerable em-
phasis on dogs and on changes in the nervous, the endocrine, and the
immune systems and the general stress syndrome, including changes
in the sympathoadrenal system. Extrapolation of the phenomena to
lower than the experimental doses is important, but cannot readily
be quantitated. The increased incidence of lymphomas, lung cancers,
kidney tumors, and neoplasms of the mammary and sex glands has
been described in the report from the USSR.30
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POLONIUM
F UNCTIONAL CHANGES IN ANIMALS
167
With the evidence of polonium-associated arteriosclerosis and
hypertension, Sprout et al.44 used an indirect noninvasive technique
to measure blood pressure in animals bearing polonium under con-
ditions similar to those in the 10-,uCi/kg histopathology experiment.
Increases in blood pressure were clearly evident and were a func-
tion of time after injection of the polonium. The investigators found
cataracts with a slit-lamp microscope. The incidence was high-
nearly 100~o by 1 yr at some closes. Cataracts might be produced
even at lower doses, but the data are inconclusive.
Other functional studies have appeared in the Russian litera-
ture,30 including changes related to the blood and cardiovascular
systems, such as changes in coagulation times, changes in capillary
strength, increased vascular permeability, and changes in cardiac
function and blood-pressure stability. Disturbances of protein and
nucleic acid metabolisms and impairment of activity of the nervous
system and the immune system were observed.
HUMAN STUDIES
PATIENTS AND WORKERS
In the work of the Manhattan Project during World War IT and
as part of the broad study of distribution and excretion of polonium,
five patients hospitalized with lymphatic cancer or leukemia received
tracer doses of polonium.~3 Excretion rates and partition between
urine and feces in all five patients were comparable with those find-
ings in animal experiments. The tissue distribution of the isotope
measured in one patient who died on the sixth day was also compa-
rable, except for a suggestion that more polonium was deposited in
the liver than was usually seen in animals.
Workers at the Dayton Project in World War IT were tested
weekly for polonium excretion. The effective half-life in the human
body was calculated as about 30 days (an average for 18 employees)
and was comparable with findings in rats and dogs.
Three chemists who had increased urinary excretion of polonium
were studied in some detail.34 35 They were estimated to have received
maximal doses of 10 ,uCi in the body (0.13 psi/kg). These doses were
well above the maximal allowable body concentrations at the time
and the limits imposed after World War IT (0.04 ,uCi in the body). No
evidence of kidney damage was evident, but subclinical depression of
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168 HEALTH RISKS OF RADON AND OTHER ALPNA-I£MITTERS
the hematopoietic system was suspected in association with the two
higher doses. There was no long-term follow-up.
Hematologic changes; impairment of the liver, of the kidney,
and in reproductive organs; and changes in protein, carbohydrate,
and pigment metabolism have been reported in Russian workers who
had incorporated 1-5 psi of 2~0po.24 This result is consistent with
findings in animal experiments and could be the only documented
instance of effects of polonium in man.
A different source of polonium in workers is its gradual ingrowth
from the decay of 226 Ra deposited in the skeleton of {uminous-dial
painters and radium chemists, or as an end product of radon-222
exposure and the deposition of 2~0Pb in bone. In both instances,
the polonium is formed in situ and may or may not be transferred
away from the site of deposition of the precursor. As a result, more
polonium is found in bone in these cases, and the potential for ejects
in bone is greater than that after direct uptake. Hill2t analyzed
both Hobo and 2~0Pb concentrations in tissues of several former
dial painters. The ratio of bone concentrations of polonium to soft-
tissue concentration was much higher than was ever found when it
entered the body directly. In one case, the bone of a former radium-
dial painter contained memo at 1,500 psi/kg and 226Ra at about
4,000 psi/kg. In the absence of exposure to specific precursors, the
2~0Pb concentrations in soft tissues have been found to be quite
Tow. Holtzman22 postulated that normal people acquire only a small
fraction of their memo burden in soft tissues from the decay of skeletal
226Ra or 2~0Pb. The highest concentrations of polonium in any
tissue in the radium-dial painters were found in hair.2: One sample
contained 25 ,uCi/kg. High concentrations in the pelts of animals
have also been reported sporadically.
OTHER EXPERIENCES IN HUMANS
Shantyr and coworkers44 reported on clinical and laboratory in-
vestigations in 10 children who were contaminated accidentally with
hero from a damaged polonium-beryIlium neutron source. Analysis
of excrete indicated body burdens of 0.2-7 psi, which is far above the
existing maximal permissible burden of 0.04 psi. Yet no noticeable
changes in general health, blood, or kidney function were observed
throughout a Month observation period. There was some impair-
ment of protein formation in the liver beginning at about 21 months.
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POLONIUM
169
Experience in man has amply confirmed the metabolic behavior
of polonium as observed in investigations with animals. However,
experience with effects, although consistent with the findings In ani-
mals, is far too sparse to support any direct estimates of health risks
in man at the present time.
POLONIUM IN THE ENVIRONMENT
After decay of radon or its daughters in air, polonium deposits
on plants. Grazing animals take up appreciable amounts of Echo
from the environment. Concentrations above 1,000 psi/kg have
been found In some animal tissues in the Arctic food chain and in ar-
eas of high rainfall. Hill2i presented a summary of the Echo content
of various human and animal foods, largely from the United King-
dom. The amounts ranged from 1 psi/kg in carrots and potatoes
in the United Kingdom to 10,000 psi/kg in a sample of dry lichen
and 16,000 psi/kg in a sample of dried grass, both from the United
Kingdom. These figures are subject to wide variation, but Hill con-
cluded that appreciable amounts of Echo are available to humans in
their diet. Adding the contribution of 2~0Pb, which has a half-life
of 21 yr and which is a precursor of Echo, Hill estimated that the
average Western diet would probably include from 1 to 10 psi of
polonium per day. A check on this amount has been made by analy-
ses of the fecal excretion of these nuclides. Holtzman22 calculated a
dietary intake of 1.8 psi/day for a few otherwise unexposed subjects
on an average American diet, and Hillel calculated 3.2 psi/day for
six people in the United Kingdom.
A more elaborate study of metabolic balances involved 12 unex-
posec! men maintained in a metabolic ward for a month or more.23
Both urine and feces were collected. Mean dietary concentrations
over 5 months were 1.63 ~ 0.05 psi/day of Echo and 1.25 ~ 0.04
psi/day of 2~0Pb. Urinary excretion of Echo was 0.269 ~ 0.033
psi/day and 2~0Pb was 0.275 it 0.026 psi/day. Fecal excretion ac-
counted for 1.89 ~ 0.10 and 1.333 ~ 0.062 psi/day, respectively.
Thus, the mean overall balances showed that ledger amounts were
excreted than were taken in through the diet. Ordinary atmospheric
intake could not account for the differences, but intake from tobacco
smoke, especially from cigarettes, was sufficient to make up the dif-
ferences.
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170 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
The usual dose contribution to humans from polonium in the
natural environment has been estimated by the National Council on
Radiation Protection and Measurements36 to be 4.8~0 mrem/yr.
As evidence accumulated in laboratory research that alpha-
emitters were potent pulmonary carcinogens when inhaled as aerosols
of plutonium or polonium and on the health effects in uranium min-
ers, attention turned to a possible role of naturally occurring polo-
nium in the production of lung cancer in smokers. Radford and
Hunt37 calculated a minimal dose of 36 rem to bronchial epithelium
from Ammo inhaled on particles in cigarette smoke as a result of
smoking two packs of cigarettes per day for 25 yr. Skrable et al.42
used the mathematical mode] of the International Commission on
Radiological Protection and calculated a much lower figure. Rajew-
sky and Stah~hoffen39 considered the doses far too low to cause lung
cancer.
Work done in several laboratories demonstrated that the polo-
nium content of tobacco varies considerably in different types of
tobacco and in different locations. The polonium was largely fo-
liar; that implied deposition from the air rather than uptake from
the soil. Ratios of 2~0Pb to Ammo were used to determine how long
the insoluble particles from cigarette smoke remained on bronchial
epithelium.38 Polonium contents of many plants were measured, and
no large differences in initial contents were found. However, the
2~0Pb activity of tobacco was fixed on insoluble particles by the cur-
ing process. Also, the small trichomes on the surface of the tobacco
leaf entered the smoke stream and were deposited in the lungs,28
where they produced high local alpha-radiation sources by the in-
growth of memo. Furthermore, the same trichomes are covered with
a sticky hydrophobic substance that makes foliar deposits of 2~0Pb
or memo stick to tobacco leaves, whereas they might wash off other
plant leaves.
Moroz and Parfenov30 observed that urinary polonium output
was sometimes higher in tobacco smokers. Little et al.27 showed
little significant difference in general tissue contents of polonium
between smokers and nonsmokers. Blanchard3 measured average
concentrations of polonium in several tissues and found them to
be slightly higher in smokers than in nonsmokers. Only in lung
concentrations were the differences statistically significant. Hill,2i
in contrast, reported a two- to threefold difference in lung-tissue
concentration between smokers and nonsmokers, but this was not
found at bronchial bifurcations.
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POLONIUM
171
Because tumors arise in the bronchi, the research focused on
polonium concentrations in the bronchial epithelium. Not only did
different investigators come up with different findings, but their mod-
els for dose calculation were different. Moroz and Parfenov30 con-
cluded that the smoking of two packs of cigarettes a day leads to
supplementary alpha irradiation of the lungs of the smoker, equal
to a 0.1 to 100 fold absorbed dose rate in comparison with that of
the natural background. The highest dose of this wide range of pos-
sible doses approached potential biological significance, whereas the
lowest dose was far too low to influence the statistics on Jung-cancer
incidence in smokers. Cohen et al.9 and Harley et al.20 reported that
alpha activity in the bronchi from Echo in cigarette-smoke tar might
be about 10 fCi per cigarette. From analyses of human lung tissue,
they concluded that there could be areas of high concentration, but
that the usual concentration was about 1 fCi/m2. That translated
to an average radiation dose of about 1 mrad/yr, with possible hot
spots of up to about 1 rad/yr. Again, the doses cover the range
from probably insignificant to possibly significant, depending upon
the importance of hot spots.
Martell29 explained the postulated effectiveness of a few pic-
ocuries of Echo and 2~0Pb in the lung on the basis of the insolubil-
ity of the compounds inhaled in cigarette smoke, in contrast with the
relative solubility of the deposits from other natural sources and
adopted the hot-particle theory. Martell also proposed that chemical
carcinogens in smoke could potentiate the effects of the low radiation
levels. Martell extended his arguments to other carcinogenic agents,
such as asbestos, and even to a role for polonium in the development
of atherosclerosis.
RISK ESTIMATES
We have no direct measure of risk for most polonium isotopes
based on experience in humans, but its health effects exemplify those
of alpha-particle radiation in soft tissues. Risk estimates for humans
must therefore be based on other alpha-particle emitters with appre-
ciable components of dose to soft tissue. Studies on radon and its
daughters and some thorium compounds may be useful in estimating
polonium risks. A risk evaluation based on radon daughter exposure
is probably that of a risk based on the short-hal£life polonium iso-
topes. However, it would apply only to lung cancer, and it may or
may not apply to the longer-lived Echo.
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172 HEALTH RISKS OF RADON AND OTHER ALPHA-EMITTERS
Risk evaluation based on thorium would introduce much un-
certainty because of the complexities of the thorium decay chain.
Some thorium isotopes are distributed in the body very differently
from polonium. The best candidate is probably a colloidal form of
thorium dioxide caDed Thorotrast, because it seeks the reticuloen-
othelial system and delivers most of its alpha dose to the tissue
of deposition, usually the liver. Risk estimates based on Thorotrast
would be largely those for the development of liver tumors. If these
could be expanded to the reticuloendothelial system in general, there
would be some potential for correlation.
An entirely different approach could be based on the empirical
toxicity ratios among plutonium, polonium, and radium developed in
the large experiments with mice by Finkel.~4 t5 In these experiments
the long-term toxicity of polonium was roughly comparable to that
of plutonium and about 5 times that of radium. However, the time
span for these experiments was still short, relative to the life span of
humans and other long-lived animate. In view of the short radiologic
and effective half-time of polonium, it might be overconservative
to assume that the ratio reported in the animal experiments for
plutonium could apply to long-term risk from polonium in humans.
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~ . ~ ~ ` - ~ ~ . ~ . . ..
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Representative terms from entire chapter:
oral administration
