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DISCLAIMER
This report 1s an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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-------
EXECUTIVE SUMMARY
Plutonium Is a transuranlc element with an atomic number 94 and Is a
member of the actlnlde series of the periodic table. Plutonium Isotopes of
mass numbers 232 through 246 have been Identified, and all are radioactive.
The two most Important Isotopes of plutonlum are 238 and 239; both Isotopes
decay with the emission of alpha particles (Welgel, 1982). In addition to
the zero oxidation state for the elemental plutonlum, 1t can exist In five
oxidation states from 4-3 to +7. All but the +7 state are fairly common
(Taylor, 1973). The 4-4 state 1s most common under physiological conditions.
Most plutonlum (+4) compounds are Insoluble In water; the water-soluble
compounds such as plutonlum nitrate will hydrolyze In water to form an
Insoluble polymeric hydroxide (MHO. 1983). Plutonium (+4) can exist In
solution under highly acidic conditions or In strongly complexed forms
(Welgel, 1982). Polyamlnocarboxyllc acids such as TTHA are examples of such
complexlng agents (Taylor, 1973).
Plutonium 1s produced from spent uranium fuel rods from nuclear
reactors. The projected worldwide production of plutonlum from thermal
reactor-spent fuel was >90 kg 1n 1985 and >162 kg 1n 1990. The U.S. supply
was an estimated -25% of the world supply. Plutonlum Isotope 239 1s used to
manufacture nuclear weapons. The Isotope 238 Is used to power small terres-
trial and space-based vehicles (satellites). Plutonlum Isotope 238 was used
as a power source for nadlolsotope-powered artificial hearts and heart
pacemakers. However, this use was discontinued because 1t was not certain
whether complete elimination of penetrating radiation from such devices was
possible (Welgel, 1982).
1v
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The fate and transport of plutonlum In the atmosphere Is not completely
understood. The size distribution of airborne plutonlum particles In
ambient air shows that, on the average, -86% may be associated with
particles of <10 microns 1n aerodynamic diameter (Hlrose and Suglmura,
1984); particles with aerodynamic diameters <5 microns are resplrable. Host
of the airborne plutonlum particles will be Insoluble In water and may exist
In +3 and +4 state (Hlrose and Suglmura, 1984). However, water-soluble
plutonlum was detected In rainwater, 38-89% of H In the +5 and +6 valence
state (Fukal et al., 1987). The removal of plutonlum from the atmosphere
will occur through wet and dry deposition. It has been estimated that the
residence time of stratospheric plutonlum may range from a few months to
over a year and that of tropospherlc plutonlum from a few days to weeks
(Fukal et al., 1987; Buesseler and Sholkovltz, 1987).
Plutonlum released to water Is found predominantly In suspended solids
and sediment. In most freshwaters, plutonlum 1s found 1n the +3 and +-4
states, and these species will primarily hydrolyze to form neutral and
anlonlc hyroxyl complexes. Generally, the anlonlc complexes will be
transported 1n the sorbed form and the neutral hydroxide will be transported
In the precipitated form In suspended solids and sediment (MHO, 1983).
However, a small portion of plutonlum may become mobile through the forma-
tion of soluble catlonlc, anlonlc and neutral complexes (Alberts et al.,
1977; Simpson et al., 1980, 1984; Sanchez et al., 1986). In marine waters
and 1n waters from the Great Lakes In the United States, the soluble pluto-
nlum species In water may be Pu6 complexes rather than Pu4 complexes
(WHO, 1983; Platford and Ooshl, 1986). Typical plutonlum BCFs In edible
portions of aquatic organisms are 10 for fish, 100 for crustaceans and 1000
for molluscs and algae. The BCFs 1n whole organisms may be 10-50 times
-------
higher (WHO, 1983). It has been estimated that the partial residence time
of soluble plutonlum may range from -18 days 1n shallow lakes to "2.5 years
1n the deepest lakes; for particle-bound plutonlum, the values may range
from 4 days to 3 years (Cornett and Chant, 1988).
When plutonlum 1s released to soil, 1t usually remains highly Insoluble
and 1n the top few cm of undisturbed soils, even In areas where rainfall Is
considerable (WHO, 1983). The slight vertical movement of plutonlum In most
soils Is due primarily to physical disturbances, for example, cultivation
and burrowing action of animals. In some Instances, the vertical movement
may be due to solublUzatlon of plutonlum through the formation of complexes
with organic and Inorganic Ugands In soil. This process was postulated to
be responsible for the transport of plutonlum 1n subsurface water at a
low-level radioactive burial site 1n Maxey Flats, KY (Toste et al., 1984).
Ihe lateral transport of plutonlum from soil Is due primarily to windblown
dust and surface water runoff (Markham et al., 1978). The transport of
plutonlum from soil to plant 1s usually expressed as the plant-to-so1l
concentration ratio. This value ranges from 10~a to 10~8, Indicating
that a very small amount of plutonlum 1s transferred from son to plant
(Nlshlta, 1981; Brown, 1979; Bunzl and Kracke, 1987; WHO, 1983). However,
the transfer of plutonlum from soil to plant can be much higher for plants
grown In piutonlum-contamlnated soils (Adrlano et al., 1981; White et al.,
1981).
The concentrations of • «»Pu and ««Pu 1n air 1n Winchester, MA, were
0.149 fC1/m3 and 0.019 fC1/m3, respectively, during 1965-1966 (Hagno et
al., 1967). The mean atmospheric concentration of combined 239Pu and
240Pu 1n Fayettevllle, AR, was 0.037 fC1/m3 during 1971-1973 (Gavlnl and
Kuroda, 1977). In 1982, the mean atmospheric level of combined 239Pu and
2«°Pu 1n Japan was 0.005 fC1/m3 (Hlrose and Suglmura, 1984).
v1
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Few data are available on plutonlum levels 1n drinking water. The
concentration of 239Pu 1n tapwater In Broomfleld, CO, was 17 fCI/l (Poet
and Martell, 1972). The concentrations of 239Pu and 240Pu 1n treated
•^
water from a water-treatment plant 1n Chicago, IL, ranged from 0.12-0.29
fC1/l (Alberts and Wahlgren, 1977).
The total diet samples collected from six regions of the United States
contained plutonlum ranging from 2.7-5.8 fCI/kg. Based on dietary Intake,
It was estimated that the average plutonlum Intake was 7.0 fCI/day (Hagno et
al., 1967). It was estimated that the total dietary Intake of plutonlum In
New York CUy during 1972-1974 was 4.1 fC1/day and 1n a cHy 1n Japan In
1984, 8.4 fC1/day (HUamatsu et al., 1986).
The background 239Pu and-240Pu level 1n soil ranged from 0.003-0.025
pC1/g (Purtymun et al., 1987; Llndeken et al., 1973). Locally contaminated
soils may contain much greater concentrations (Arthur, 1982; Poet and
Kartell, 1972; Johnson et al., 1976; Gudlksen and Lynch, 1975). Because of
the deterioration of containers, the subsurface soil from a radioactive
waste disposal site In southeastern Idaho contained <11,000 pC1/g of Pu
(Arthur, 1982).
In human tissues, the maximum concentrations were found In tracheo-
bronchlal lymph nodes (0.73-3.75 pC1/kg wet wt.) and 1n the liver (0.32-0.96
pCI/kg wet wt.) (Fox et al., 1980; Singh et al., 1983; Hussalo et al., 1980;
Taklzawa et al., 1987; Kawamura et al., 1987). Studies Indicate that Pu
accumulates most In bone and liver (Singh et al., 1983).
Studies on the toxlclty of plutonlum to aquatic organisms were not
located In the available literature. Data regarding uptake of mixed
Isomers, 238Pu and 239Pu, from contaminated sediment by the marine worm,
N. dlverslcolor. showed Increasing tissue concentrations with Increased
-------
duration of exposure (Beasley and Fowler, 1976). Hatkar et al. (1983) noted
Increased tissue concentrations 1n clams, M. meretrlx. exposed to seawater
spiked with piuton 1 urn nitrate solution for the first 15 days. This was
followed by a drop 1n tissue levels at 20 days. The differences 1n these
patterns may be due to animal species variations, or more likely, to the
difference 1n chemical species.
Plutonium Is taken up by marine fauna from both sediment and seawater
(Ballestra et al., 1983; Hatkar et al.. 1983). Data strongly Indicate that
trans-Intestinal absorption of plutonlum occurs In marine forms (Beasley and
Fowler, 1976; Fowler and Guary, 1977; Pentreath and Lovett, 1976).
Plutonlum bloaccumulatlon decreases at successively higher trophic levels
(Ballestpa et al., 1983; Beasley and Fowler, 1976; Fowler and Guary, 1977;
Markham et al., 1988; Hatkar et al., 1983). These animal study data provide
equivocal support for an equilibrium model developed by Thomann (1981). The
model predicts a similar general trend of bloaccumulatlon within the food
chain, as these data describe. However, these data do not support the
model's prediction of animal uptake of plutonlum from water only.
B1oconcentrat1on data on marine algae showed concentrations ranging from
-0.1-20 fC1/g (Cross and Day, 1981; Ballestra et al., 1983). Variations In
levels were attributed to variations In suspended sediment load In the
ambient water or to fluctuations 1n levels released from power plants.
Uptake from plutonlum nitrate solution by the alga, D_. prlmolecta. was not
directly proportional to duration of"exposure (Matkar et al., 1983).
Effects of plutonlum on terrestrial fauna were Investigated by Smith
(1979). H1stopatholog1cal examination revealed no lesions In a steer that
Ingested plutonlum at a radioactivity level of 100 iiC1 of 239Pu over >6
months. Of this amount taken In, 0.0034% was retained In bone, muscle and
liver. Measurable amounts were also detected 1n lungs, blood and kidneys.
-------
A study by Romney et al. (1982) of root uptake of piuton 1 urn by wheat,
bushbeans, carrots and alfalfa Indicated that root uptake of plutonlum Is of
minor Importance compared With plant foliage adsorption, and that laboratory
data may underestimate uptake rates occurring under field conditions.
Terrestrial field study data on plutonlum consist of measurements of
uptake by flora and fauna from soil and air. Measurable quantities of
2a9Pu have been detected In organisms that Inhabit sites contaminated by
products released from nuclear weapons or fuel plants. These organisms
Include L. rldlbundus (Woodhead, 1986), arthropods (Bly and Whicker, 1979),
fescue, grasshoppers, shrews, mice, cotton rats, raccoons, opossums,
woodchucks, rabbits (Garten et al., 1981), rats and guinea pigs (Cataldo and
Wlldung, 1983), grains and leafy vegetables (Slmmonds and Llnsley, 1982),
potatoes (Cooper et al., 1985). Soil processes control the quantity of
plutonlum In plants, and plant processes control uptake by animals that
consume the plants (Cataldo and Wlldung, 1983). Environmentally dispersed
plutonlum accumulates In terrestrial biota like thorium does, and to a
lesser degree than uranium does (Garten et al., 1981). Higher concentra-
tions of radlonucllde were measured 1n grain than 1n leafy plant parts.
Researchers suggest this Is because the Insoluble plutonlum particles are
more efficiently removed by natural loss mechanisms from plant surfaces than
from the seeds (Slmmonds and Llnsley, 1982).
The International Commission on Radiological Protection (ICRP, 1986)
extensively reviewed the •literature"" on the pharmacoklnetlcs of plutonlum.
They determined that humans exhale -37% of the plutonlum to which they are
Initially exposed, and that they retain -25% 1n the lungs. The remainder Is
lodged 1n the upper respiratory tract and eventually cleared by macrophages
or by mucoclllary action and swallowed. Clearance from the alveoli follows
1x
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a miilticompartment model, !>tr by far, most of the 2a»Fu02 clears with a
half-life measured In years. Plutonium nitrate can clear from the |ungs
somewhat more quickly. Plutonium Is not well absorbed from the gastrointes-
tinal tract; estimates for absorption range from 10"« to 10~*. Absorp-
tion of radiation by penetration through the skin Is very unlikely, for
"»Pu has very little gamma radiation associated with It.
Most of the Inhaled plutonlum retained by the lung stays 1n the lung for
many years. The human model developed by the ICRP (1979) and data from
human tissues (Singh et al., 1983, Kathren, 1988) Indicated that It will
eventually be absorbed Into the rest of the body and be translocated to the
skeleton and liver, 1n about equal proportions. It can cross the placenta,
but H does not preferentially accumulate In the fetus (Green et al., 1979).
In the blood, 1t 1s usually bound to the serum protein transferrln (ICRP,
1986).
The major route of excretion.of plutonlum Is through the feces. This
occurs when plutonlum Is swallowed after oral or Inhalation exposure. It 1s
also excreted Into the bile (Ballou and Hess, 1972). Whole body retention
half-lives In humans are an estimated 40-200 years for a*»Pu (ICRP, 1986).
The adverse health effects of «»Pu are from the Ionizing radiation
from hlgh-LET alpha particles that damage nearby cells. The number of alpha
particles emitted by the plutonlum 1s measured In C1, and the amount of
radiation Imparted to cells Is measured In rads. As the plutonlum remains
1n the tissue, the number of rads 1n the tissue Increases. Since plutonlum
can remain 1n tissues for many years, a single Inhalation exposure provides
chronic radiation exposure.
Epldemlologlcal studies and studies of workers exposed to plutonlum have
not shown any adverse health effects In humans from "»Pu. However, dogs
(Park et al., 1987; Howard, 1970; Gullmette et al., 1986; Muggenburg et al.,
-------
1986; Clarke el al.: 1966) and rats (Sanders et a!., 1976, 1977. 1988} given
single Inhalation exposures to 2B»PuO_ developed lymphopenla, pulmonary
flbros's, pneumonHls and lung tumors. Dogs exposed to plutonlum nitrate
developed bone tumors (Dagle, 1987). Intravenous Injections of 2>»Pu
citrate leu to bone sarcomas In dogs (Jee et al.. 1962; Mays et al.t 1987)
and mice (Taylor et al., 1983; Humphreys et al., 1987). Oral administration
1s not associated with adverse health effects, probably because so little 1s
absorbed by this route. Nutagenldty tests performed In vivo showed that
plutonlum causes chromosomal aberrations (Brooks et al., 1976, 1980; LaBauve
et al,., 1980; Beechey et al., 1975). The only evidence of effects on repro-
duction and development Is that Intravenous Injections of plutonlum caused
fetal mortality In rabbits and mice.
Plutonlmum emits Ionizing radiation, which 1s known to cause cancer 1n
animals and humans. Although plutonlum has not been shown to cause cancer
1n humans, other radlonuclldes have been shown to do so. In animals, there
Is abundant evidence that Inhalation of plutonlum causes cancer In rats and
dogs. Ionizing radiation of alpha particles produces Intense regions of
lonlzatlon and once the radlonucllde Is Ingested or Inhaled this radiation
can be emitted within the body. Therefore, by analogy to the structure and
activity of other radlonuclldes and Ionizing radiation 1n. general, plutonlum
can be placed 1n U.S. EPA (1986a) Group A ~ human carcinogen. The U.S. EPA
(1989) has proposed a risk factor of 0.039/yd for Inhalation. The oral
risk factor 1s 3.0xlO~VwC1. The cancer-based RQ 1s 0.01 C1, which 1s
based on the Federal Radiation Protection Guidance of a limit of 500 mrem
exposure for members of the general public. No Inhalation or oral RfD
values for plutonlum were calculated because no appropriate methodology was
available to convert animal Initial alveolar deposition exposures 1n C1, or
biological exposures 1n rads to equivalent exposures or doses In humans.
xl
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER . . . . 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 4
1.3. PRODUCTION DATA 6
1.4. USE DATA 7
1.5. SUMMARY 7
2. ENVIRONMENTAL FATE AND TRANSPORT 9
2.1. AIR 9
2.2. WATER 11
2.3. SOIL 14
2.4. SUMMARY 16
3. EXPOSURE 19
3.1. WATER 20
3.2. FOOD 22
3.3. INHALATION 23
3.4. DERMAL . 23
3.5. SUMMARY 25
4. ENVIRONMENTAL TOXICOLOGY 27
. 4.1. AQUATIC TOXICOLOGY 27
4.1.1. Acute Toxic Effects on Fauna 27
4.1.2. Chronic Effects on Fauna. 27
4.1.3. Effects on Flora. . . 29
4.1.4. Effects on Bacteria 30
4.2. TERRESTRIAL TOXICOLOGY 30
4.2.1. Effects on Fauna . 30
4.2.2. Effects on Flora 31
4.3. FIELD STUDIES. 31
4.4. AQUATIC RISK ASSESSMENT 36
4.5. SUMMARY 37
5. PHARMACOKINETCS . . .' " . 40
5.1. ABSORPTION 40
5.2. DISTRIBUTION 43
5.3. METABOLISM 47
5.4. EXCRETION 47
5.5. SUMMARY 48
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TABLE OF CONTENTS (cont.)
Page
6. EFFECTS 50
6.1. SYSTEMIC TOXICITY 51
6.1.1. Inhalation Exposure . 51
6.1.2. Oral Exposure 55
6.1.3. Other Relevant Information 56
6.2. CARCINOGENICITY 56
6.2.1. Inhalation 56
6.2.2. Oral 60
6.2.3. Other Relevant Information 60
6.3. MUTAGENICITY 62
6.4. TERATOGENICITY 63
6.5. OTHER REPRODUCTIVE EFFECTS 65
6.6. SUMMARY 65
7. EXISTING GUIDELINES AND STANDARDS 66
7.1. HUMAN 66
7.2. AQUATIC ' 67
8. RISK ASSESSMENT 68
8.1. CARCINOGENICITY . . . 68
8.1.1. Inhalation 68
8;1.2. Oral 68
8.1.3. Other Routes 68
8.1.4. Weight of Evidence 69
8.1.5. Quantitative Risk Estimates 69
8.2. SYSTEMIC TOXICITY 72
8.2.1. Inhalation Exposure 72
8.2.2. Oral Exposure 73
9. REPORTABLE QUANTITIES 74
9.1. BASED ON SYSTEMIC TOXICITY 74
9.2. BASED ON CARCINOGENICITY 74
10. REFERENCES. 75
APPENDIX A: LITERATURE SEARCHED 102
APPENDIX B: SUMMARY TABLE FOR PLUTONIUM 105
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LIST OF TABLES
No. . Title Page
1-1 Decay Characteristics of Four Plutonium Isotopes. ...... 2
1-2 Chemical Formulas, Atomic/Molecular Weights and CAS
Registry Numbers of Plutonium and Four of Its Compounds ... 3
1-3 Selected Physical Properties of Plutonium and Selected
Plutonium Compounds .... 5
3-1 Concentrations of Plutonium 1n Selected Uncontamlnated
and Contaminated Surface Waters 21
6-1 Effects of 239Pu on Fetuses of Rabbit Dams Given a
Single Intravenous Dose of 23»Pu Citrate 64
xlv
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LIST OF ABBREVIATIONS
AMAD Activity median aerodynamic diameter
ALI Annual limit Intake
BCF B1oconcentrat1on factor
Bq Becquerel
CAS Chemical abstract service
CHO Chinese hamster ovary
DAC Derived air concentration
dpm Disintegrations per minute
DPTA D1ethylenetr1am1nepentaacet1c add
EDTA Ethylenedlamlnetetraacetlc add
fCI Femtocurle
PEL Frank effect level
GHD Geometric mean diameter
Gy Gray
IAD Initial alueolas deposition
KC1 Kllocurle
LET Linear energy transfer
MCL Maximum contaminant level
MeV Million electron volts
MMAD Mass median aerodynamic diameter
MWe Megawatts electricity
NSA Normalized specific activity
Purex Plutonium uranium reduction extraction
R Roentgen
REM Roentgen-equ1valent-man
RfD Reference dose
RQ Reportable quantity
Sv Slevert
TBP Trlbutyl phosphate
TTHA Tr1ethylenetetram1nehexaacet1c acid
wt. Weight
xv
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1. INTRODUCTION
Plutonium (Pu) 1s a metallic, transuranlc element with an atomic number
94. A member of the actlnlde series of the periodic table, H occurs
naturally 1n very small quantities In uranium ores and Is formed by neutron
capture (neutrons produced by spontaneous fission of uranium) followed by
B-decay (MHO. 1983; Ba1r et at.. 1961):
U238 * n -» U239 ——>ND239 — >Pu239
2.35 mln p 2.33 days
Traces of primordial 244Pu have been Isolated from a natural ore. The
ratio of 239Pu to uranium 1n natural uranium ore Is <1:10" and the
ratio of primordial 244Pu to uranium 1n a natural uranium ore 1s
<1:102S. Therefore, plutonlum Is not commercially extractable from
natural ores (Helgel, 1982).
Plutonlum Isotopes of mass number 232-246 have been Identified, and all
the Isotopes are radioactive. The two most Important Isotopes of plutonlum
are 23»Pu and 238Pu (Welgel, 1982). The decay characteristics of these
two Isotopes and two other common plutonlum Isotopes are given 1n Table 1-1.
The a energies of the Isotopes 239 and 240 shown In Table 1-1 are so close
that they cannot be distinguished by the commonly used analytical technique,
alpha spectrometry; the combined amounts are reported by many Investigators
(WHO, 1983). Mass spectrometry Is commonly used to quantify these two
Isotopes (Buesseler and Sholkovltz, 1-987).
1.1. STRUCTURE AND CAS NUMBER
The chemical formulas, atomic/molecular weights and CAS Registry numbers
for elemental plutonlum and four commonly used compounds are given 1n
Table 1-2.
0217d -1- 08/08/89
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TABLE 1-1
Decay Characteristics of Four Plutonium Isotopes*
Isotope Half-Life
(years)
23epu 87.74
"•Pu 24,110
240Pu 6537
241Pu 14.4
Decay Principal Energy
Mode (MeV)
a 5.5
5.47
5.36
a 5.16
5.14
5.1
a 5.17
5.12
5.02
B . 0.021
Intensity
(X)
71.6
28.3
0.1
73.2
15.1
10.6
73.5
26.4
0.07
>99
*Source: Weast, 1985
0217d
-2-
08/08/89
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TABLE 1-2
Chemical Formulas, Atomlc/Holecular Weights and CAS Registry
Numbers of Plutonium and Four of Its Compounds
Element/Compound
Plutonium
Plutonium
Chemical Formula
Pu
PuF4
Atomic/Molecular
Height
239.05
315.05
CAS Registry
Number3
15117-48-3
13709-56-3
tetrafluorlde
Plutonium nitrate,
.pentahydrate
Plutonium oxalate,
hexahydrate
Plutonium
dioxide
aSource: CAS, 1989
bWe1gel, 1982
Pu(N03)4.5H20
Pu(C204)2.6H20
Pu02
577.15
523.18
271.05
61204-24-85
74280-13-0
12049-95-9
0217d
-3-
08/02/89
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1.2. PHYSICAL AND CHEMICAL PROPERTIES
Selected physical properties of plutonlum and Us compounds listed In
Table 1-2 are given In Table 1-3. Plutonlum exists 1n six allotroplc
modifications under ordinary pressure. The thermodynamlc, electrical,
magnetic and spectroscoplc properties of plutonlum were extensively studied;
some of these data can be found In Melgel (1982).
In addition to the zero-oxidation state (elemental plutonlum), plutonlum
can exist 1n five oxidation states from Pu(+3) to Pu(+7). The four common
oxidation states of Pu are +3, +4, +5 and +6. The +5 and +6 oxidation
states generally occur as oxocatlons, for example, PuOt and Puo!
(Taylor et al., 1983). The +4 state Is most common under physiological
conditions. In physiological fluids, It can exist only as strongly
complexed Ions. Weak complexes of Pu(+4) hydrolyze In weak addle and
neutral solutions to form polymeric hydroxides (WHO, 1983). Even at 1 M
acidity, about 23 wt. % of plutonlum Is hydrolyzed; complete hydrolysis of
plutonlum results In the precipitation of Pu(OH)., which polymerizes to
(Pu(OH)4.)n. Therefore, Pu(+4) exists 1n solution only under highly addle
conditions or as strong complexes. Pluton1um(+4)'s Instability Is shown by
the following equation (Welgel, 1982):
3 Pu* + H20 * 2 Pu» + PuO* + 4 H+
The hydrolysis and precipitation of Pu(+4) In solution 1s retarded by
complexatlon. The complex-forming ability of Pu decreases In the following
order: Pu(+4) > Pu(*3) >• Pu(*6) >~ Pu(+5). Among the mono- and divalent
anlons, fluoride, carbonate and oxalate commonly form complexes, for
example, Na~ PuF, with Pu(+4), acetate, lactate and citrate. Solutions
f. O
of Pu(+4) citrate complex have been widely used for administrating soluble
plutonlum to animals. However, even when great care 1s taken, the solution
0217d . -4- 08/08/89
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rv)
-j
a.
TABLE 1-3
Selected Physical Properties of Plutonium and Selected Plutonium Compounds*
Melting Boiling
Compound Physical State Point Point
CO CC)
Pu(a) silvery white 641 3232
solid
PuF« pale brown 1037 NR
solid
»
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may contain <10% of polymeric material (hydrolysis product). Therefore, It
has been suggested that Pu(+4)c1trate solutions be filtered through
mllHpore filters Immediately before use to remove any polymeric material
(Taylor, 1973).
Plutonium also forms strong complexes with polyam1nocarboxyl1c acids and
other Ugahds. The stability of the these complexes Increases In the follow-
ing order: TTHA > DPTA > EOTA. Because of this chelatlng ability, these
compounds have been used for the elimination of Pu from the body of patients
exposed to Pu. Details concerning other chemical properties of Pu can be
found In Taylor (1973).
1.3. PRODUCTION DATA
Plutonium Is produced from spent uranium fuel rods from nuclear
reactors. After a coollng-off period of >150 days to permit short-lived but
*
highly radioactive Isotopes to decay, the spent fuel 1s dec!added from Al,
and Pu separation 1s started. The principal problem In the production of
Plutonium and Us compounds 1s the separation of small amounts of Pu
(-200-900 yg/g) from a large amount of U and other Intensely radioactive
fission and radioactivity-Induced products. In the Purex process, the
aqueous solution of nitrates Is extracted with 30 wt. X of TBP dissolved In
a kerosene-type diluent, and plutonlum Is extracted as Pu(N03)4.2TBP.
Plutonium 1s then reduced to Pu(+3) by ferrous sulfamate, hydrazlne or
hydroxylamlne and transferred to aqueous phase. Further purification Is
achieved by reoxldatlon to Pu(+4) a*hd reextractlon with TBP. The purified
nitrate 1s converted to oxalate (by addition of oxalic acid to the acidic
solution), which 1s heated to form PuOp. The oxide 1s converted to PuF.
by HF-Op gas and then to metallic plutonlum by thermal reduction with Ca.
Further purification of metallic plutonlum 1s done by electrorefInlng
(Melgel, 1982).
0217d . -6- 08/08/89
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An estimated 200 kg of plutonlum 1s produced/1000 MWe produced 1n
uranium-fueled power reactors. The projected worldwide plutonlum production
from thermal reactor-spent fuel 1s >90 kg In 1985 and >162 kg In 1990. The
U.S. supply from power reactors was estimated at -25% of the world supply
(Welgel, 1982).
1.4. USE DATA
Plutonium Is used to manufacture nuclear weapons. However, weapons-
grade plutonlum requires a 239Pu content of >95 wtX. The Isotope 238Pu
1s also technically Important because of the high heat produced during Us
decay. Therefore, this Isotope Is used to fuel small terrestrial and space-
based vehicles (satellites). Plutonium Isotope 238 was once considered the
most promising power source for radlolsotope-powered artificial hearts and
heart pacemakers. However, this use was discontinued because the complete
elimination of penetrating radiation from such devices Is uncertain (Welgel,
1982).
1.5. SUMMARY
Plutonlum Is a transuranlc element with an atomic number 94 and 1s a
member of the actlnlde series of the periodic table. Plutonlum Isotopes of
mass numbers 232 through 246 have been Identified, and all are radioactive.
The two most Important Isotopes of plutonlum are 238 and 239; both Isotopes
decay with the emission of alpha particles (Welgel, 1982). In addition to
the zero oxidation state for the elemental plutonlum, H can exist In five
oxidation states from +3 -to +7. All but the +7 state are fairly common
(Taylor, 1973). The +4 state 1s most common under physiological conditions.
Most plutonlum (+4) compounds are Insoluble In water; the water-soluble
compounds (for example, plutonlum nitrate) will hydrolyze 1n water to form
»
an Insoluble polymeric hydroxide (WHO, 1983). Plutonlum (+4) can exist In
0217d -7- 08/08/89
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solution under highly addle conditions or In strongly complexed forms
(Welgel, 1982). Polyamlnocarboxyllc adds such as T1HA are examples of such
complexlng agents (Taylor, 1973).
Plutonium 1s produced from spent uranium fuel rods from nuclear
reactors. The projected worldwide production of plutonlum from thermal
reactor-spent fuel was >90 kg In 1985 and >162 kg In 1990. The U.S. supply
was an estimated -25% of the world supply. Plutonlum Isotope 239 Is used to
manufacture nuclear weapons. The Isotope 238 Is used to power small terres-
trial and space-based vehicles (satellites). Plutonium Isotope 238 was used
as a power source for radlolsotope-powered artificial hearts and heart
pacemakers. However, this use was discontinued because H was not certain
whether complete elimination of penetrating radiation from such devices was
possible (Welgel, 1982).
0217d -8- 08/08/89
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2. ENVIRONMENTAL FATE AND TRANSPORT
The understanding of the environmental fate and transport of plutonlum
Is greatly facilitated by a knowledge of environmental sources of plutonlum.
These Include nuclear explosions, nuclear reactors, nuclear fuel fabrication
and reprocessing plants and accidents Involving nuclear weapons, nuclear
reactors, 288Pu-powered vehicles or other devices. Hlnute amounts of
plutonlum occur naturally In uranium ores. The major source of plutonlum 1n
the environment 1s nuclear weapons testing, which releases 238Pu, 239Pu,
24opu> 2«ipu and 242Pu to the atmosphere. According to an estimate of
total mass of plutonlum released worldwide In atmospheric nuclear testing,
the two Isotopes, 23»Pu and 2AOPu were produced In the largest quanti-
ties (3.26 tons and 0.59 tons, respectively). Based on C1 of radioactivity
produced by these tests, the beta-emitter 241Pu produced the most
activity. Host of the alpha activity of plutonlum was produced by 239Pu
and 240Pu. Plutonlum Isotopes 238, 239, 240 and 241 are also produced 1n
nuclear reactors. Both 238Pu and 239Pu are released 1n accidents
Involving 238Pu-powered spacecrafts. Artificial heart or heart pacemakers
powered with 238Pu can be sources of 288Pu In the environment (WHO,
1983).
2.1. AIR
The fate and transport of plutonlum In the atmosphere Is not completely
understood. Most atmospheric plutonlum from nuclear weapons testing,
nuclear weapons and reactor fuel fabrication or processing Is released as
airborne particles (Hlrose and Suglmura, 1984). Since nuclear weapons
contain elemental uranium or plutonlum, high-altitude or surface-based
nuclear detonation Initially produces plutonlum (from the beta decay of
uranium 1n the case of uranium-containing devices) In the elemental state.
0217d -9- 08/08/89
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At high temperatures and 1n the presence of oxldants, elemental plutonlum
oxidizes to higher valency states (for example, Pu+3, Pu+4, Pu+5 and Pu+6).
There Is a paucity of data on the atmospheric chemical transformation
processes that are likely to convert Pu(0) Into higher oxidation states. By
analogy to other metals, plutonlum Is expected to undergo chemical
transformation with the formation of PutL, PuC,3, Pu(SO.)2 and other
species. Bond1ett1 (1985) suggested that more highly oxidized species of
1 2
plutonlum (f5 and 4-6) are formed 1n the same way as U02 and. UCL
species are formed from uranium following thermonuclear explosions.
The particle size of atmospheric plutonlum particles 1s Important
because the residence time of the particles 1n the atmosphere depends on
this factor. The size distribution of plutonlum-bearlng particles 1n the
air of plutonlum oxide and carbide processing plants (Andersen, 1964), In
spent fuel bay areas (Dua et al., 1987) and plutonlum metal conversion
facilities (Sanders, 1978) have been reported. It 1s difficult to express
the particle size In one uniform unit because many different units are used
to express the particle size (AMAD, MM AD and GMD). However, the HMADs for
these particles are apparently <10 microns. Additionally, the MMAD may
Increase as the moisture content of air Increases (Andersen, 1964).
An average 86% of plutonlum 1n ambient airborne particles was associated
with particles <10 microns In aerodynamic diameter (Hlrose and Suglmura,
1984). In an attempt to clarify the characteristics of plutonlum particles
In the atmosphere, Hlrose-and Suglmura (1984) noted that <8% of particles
with aerodynamic diameters <10 microns and <1% of particles with aerodynamic
diameters >10 microns were soluble In distilled water. Assuming that, after
nuclear detonations, plutonlum 1s Injected to the atmosphere 1n the lower
0217d ; -10- 08/08/89
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valency states (Hlrose and Suglmura, 1984), most of the atmospheric pluto-
nlum will be 1n the form Pu02, Pu(S04)2 or other Insoluble plutonlum
compounds In the +3 and +4 states. On the other hand, Fukal et al., (1987)
showed that rainwater contains 38-89% of plutonlum In higher valency
I 2
(PuO, and Pu02) and other water-soluble states. This suggests
that Pu exists In the atmospheric partlculate matter In Pu+3 (PuC.._), Pu+4
I «J
(Pu02, Pu(S04)2), Pu*5 (Pu02) and Pu+6 (Pu02) states.
Plutonlum particles are removed from the atmosphere by wet and dry
deposition. From his study at Woods Hole, MA, Gav1n1 (1978) concluded that
dry fallout constitutes only 7.8% of total deposition. Of course, the
contribution from dry deposition will be much higher In arid areas. The
deposition rate of plutonlum from atmospheric fallout was an estimated 0.5
cm/sec (Jakublck, 1976). At this deposition rate. It will take an estimated
17 days for partlculate plutonlum to deposit on soil from the mld-tropo-
spherlc altitude of 7.5 km. The residence time of plutonlum will depend on
Us source. It has been estimated that the residence time of stratospheric
plutonlum (from tests conducted at high altitude) may range from a few
months to over a year (Fukal et al., 1987; Buesseler and Sholkovltz, 1987).
The residence time of atmospheric plutonlum from surface-based nuclear
testing 1s estimated to range from a few days to weeks (Buesseler and
Sholkovltz, 1987).
2.2. WATER
Plutonium released to.water 1s-found predominantly In suspended solids
and sediment. The concentration ratio of plutonlum 1n suspended solid/sedi-
ment to water may vary from 10* to 105 (WHO, 1983). The removal of
plutonlum from water to sediment occurs as a result of Its sorptlon onto
partlculate matter 1n water; Iron and manganese oxides were found to be good
0217d -11- 08/02/89
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sorbent for plutonlum (Sanchez et al., 1986). More efficient scavenging
occurs by finer-grain particles (Carpenter et al., 1987), which provide a
larger surface area for adsorption compared with larger particles of the
same mass.
Although the concentrations of dissolved plutonlum In water are very
small compared with concentrations 1n suspended solids/sediments, the
concentrations of dissolved plutonlum may vary by >4 orders of magnitude In
different waters. In most freshwater systems (except for the Great Lakes 1n
the United States), plutonlum Is found In the +3 and +4 state (WHO, 1983)
and these species will predominantly hydrolyze with the formation of
Insoluble polymeric hydroxy compounds. However, the mobility of plutonlum
can be enhanced when the water contains suitable complexlng agents.
Higher concentrations of plutonlum 1n water columns were observed In a
few addle and alkaline lakes (WHO, 1983). In alkaline water containing
-2 -1
high concentrations of C03 and HC03 Ions, the formation of
_?
Pu-carbonate complexes (for example, Pu(C03)g ) may Increase the Pu
concentration In the water (Simpson et al., 1980, 1984; Sanchez et al.,
1986). In acidic waters, where sulfate and chloride are the dominant Ions
(Alberts et al., 1977), the formation of anlonlc carbonate complex 1s
unlikely. In such waters, the mobility of plutonlum through solubility may
be enhanced through the formation of neutral complexes with organic matter
In the water, although the nature of these complexes has not been Identified
(Alberts et al., 1977; Sanchez et at., 1986). Soluble catlonlc complexes of
plutonlum were found In water samples from Lake Bank In Georgia and In rain
and snow water samples (Alberts et al., 1977). The nature of the complexes
was not reported, but H seems likely that they are complexes of +5 and +6
1 2
states of plutonlum (for example, PuO~ and PuO-}. Sanchez et al.
0217d . -12- 08/08/89
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(1986) reported that, when plutonlum 1s complexed by carbonate op/dlssolved
organic matter, plutonlum removal by sorptlon 1s decreased,/thus enhancing
Us mobility In water.
In marine waters and water from the Great Lakes 1n the United States,
plutonlum exists primarily In the +3, +4, +5 and 4-6 states (WHO, 1983).
Unlike the case of most freshwaters where the solution species would be
4-4
complexes of Pu state, the predominant solution species In marine and
Great Lakes waters are +5 and +6 states of plutonlum (for example, PuO-
and PuO*) (WHO, 1983; Platford and Joshl, 1986). However, Pu+5
(PuO?) disproportionate* quickly In solution at pHs >5 (Fukal et al.,
1987) to Puf4 and Pu+6 states. The reduction of Pu+5 to Pu+3 and Pu+4 Is
also rapid In the presence of sediments (Davis and Denbow, 1988). 'There-
fore, Puf6 may be the only stable soluble species 1n these waters. As In
freshwaters, Pu*3 and Pu+4 will be present In the partlcle-sorbed states In
suspended solids and sediment. The concentrations of plutonlum In suspended
solids/sediment would be orders of magnitude higher than 1n the dissolved
state (WHO, 1983). Once plutonlum 1s deposited In the sorbed state In
sediment, It may not have an active dlagenetlc chemistry and would not be
significantly mobile In coastal or deep-sea sediments (Sholkovltz and Mann,
1984).
Thomann (1981) reported the transfer of plutonlum from water to aquatic
organisms. Typical BCFs for 239Pu 1n edible portions of aquatic organisms
used for assessment purposes are 10" for fish, 100 for crustaceans and 1000
for molluscs and algae. The BCFs 1n the whole organisms may be 10-50 times
higher, depending on the concentrations 1n sediment (WHO, 1983). The
trophic-level studies show that plutonlum Is not b1omagn1f1ed from lower
tropic to higher tropic aquatic animals. In fish, *3°Pu may have higher
BCFs than 239Pu and 240Pu (Noshkln et al., 1986).
0217d . -13- 08/08/89
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The primary process responsible for the/Toss of plutonlum from water Is
sedimentation. Some loss of plutonlum Will occur as a result of uptake by
aquatic organisms. In the case of some surface waters, plutonlum loss will
occur as a result of discharge to larger bodies of water and overflowing of
banks during heavy rains. Walker et al. (1986) showed that bubble scaveng-
ing 1n the water column, coupled with droplet ejection from bubbles bursting
at the surface, may transfer some of the plutonlum from the aquatic phase to
air. It has been estimated that the partial residence time of soluble
plutonlum may range from -IB-days 1n shallow lakes to ~2.5 years In the
deepest Great Lakes. The range of partial residence time for particle-bound
Pu In lakes 1s an estimated -4 days to 3 years (Cornett and Chant, 1988).
2.3. SOIL
When plutonlum Is released to soil, It usually remains highly Insoluble
(WHO, 1983), either because It enters the soil as Insoluble compounds such
as Pu02 from nuclear fallout or as a result of formation of Insoluble
compounds or strongly sorbed compounds with soil components. For example,
*4
when Pu 1s added to wet soil, H hydrolyzes with the formation of
polymeric hydroxide or Ionic compounds that are strongly sorbed onto oxides
of Iron, silica and humlc materials 1n the soil (Bulman et al., 1984; Vyas
and Mlstry, 1984). Therefore, the diffusion coefficient of plutonlum for
surface soils Is low (-10-7 cmVsec); plutonlum will normally remain In
the top few cm of undisturbed soils, even 1n areas of considerable rainfall
(WHO, 1983). • .
The low mobility of plutonlum 1n most soils 1s due to both physical and
chemical processes. Cultivation of land or transport of soil by burrowing
animals are two physical processes that can transfer plutonlum from the soil
surface to a depth of ~30 cm (plowing depth). However, slight vertical
transport of plutonlum was observed In undisturbed arid soils (WHO, 1983).
0217d -14- 08/08/89
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The transport 1n such cases 1s probably mediated by the physical movement of
particles with which the plutonlum Is associated (WHO, 1983; Alberts et al.,
1980).
Chemical processes that Increase the aqueous solubility of plutonlum can
also Increase Us mobility In soil. The Increase In plutonlum solubility
may be due to formation of sol-uble complexes with organic and Inorganic
Ugands In soil or to chemical transformation of Pu+4 to other oxidation
states where 1t Is less susceptible to hydrolysis and precipitation (WHO,
1983). The mobility of plutonlum that 1s due to formation of soluble
complexes will depend on the stability of the complex which 1s due to
competition with other Ugands or Us chem1cal/m1crob1al degradation
reactions 1n soil (WHO, 1983; Vyas and Mlstry, 1984).
Plutonlum Is tranported from one region to another primarily by wind-
blown dust and surface water runoff. The distance the plutonlum-contalning
particles move will generally depend on the particle size; smaller particles
containing higher concentrations of plutonlum will travel farther (Markham
et al., 1978; WHO, 1983). Although the transport of plutonlum from soil to
groundwater Is not common, such migration has been observed In the Maxey
Flats low-level radioactive burial site. Complexatlon of plutonlum with EDTA
was suggested as the reason for the transport of plutonlum from this soil to
subsurface groundwater (Toste et al., 1984).
The transport of plutonlum from soil to plants has been reported by
several authors. The principal mode of plutonlum transfer to plants from
soil are foliar deposition and root uptake. The translocatlon of plutonlum
to the seeds and roots after deposition on the leaf will depend on the
chemical form, particle size, residence time and the weathering reaction of
the leaf. In the case of soybeans, the transfer ratio Is -10~5 of the
0217d . -15- 08/08/89
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amount deposited (WHO, 1983). However, the primary mode of soU-to-plant
transfer Is root uptake. The plant-to-soU concentration ratio by this
route may range from 10"a to 10"B (Nlshlta, 1981; Brown, 1979; Schulz
and Rugglerl, 1981; Bunzl and Kracke, 1987; Popplewell et al., 1984; Romney
et al., 1981; Schreckhlse and Cllne, 1980). The translocatlon from the root
to the above-ground parts of the plant occurs as a result of uptake of
Plutonium solublUzed through chelatlon of Pu4 with the formation of
catlonlc, anlonlc and neutral complexes (Brown, 1979; WHO, 1983; Upton and
Goldln, 1976).
Evidence also suggests that the distribution of plutonlum as a result of
uptake 1s not uniform In different parts of plants. The concentration of
plutonlum 1s usually highest 1n the roots followed by, In decreasing order,
the stem, leaves, bran, grain and fruit or seed (Romney et al., 1981; Schulz
and Rugglerl, 1981; Bunzl and Kracke, 1987). The concentration ratio (plant
over soil) Is usually lower by a factor of 10 1n fruit, grain and seed parts
than 1n foliage (Romney et al., 1981).
Plants grown .In piutonlurn-contamlnated soil may show higher concentra-
tion ratios (plant to soil) than plants grown 1n uncontamlnated soils; the
ratio 1n contaminated soil may vary between 10~4 and 10~2 1n different
parts of the plant. The uptake of z'»/240Pu may be an order of magni-
tude >23ePu uptake (Adrlano et al., 1981). Vegetative parts of plants
grown 1n contaminated soils contained ~4 times more plutonlum In parts
growing closer to ground than parts "growing further from the ground surface.
About 65% of the radioactivity could be removed by washing. Indicating
surfldal contamination (White et al., 1981).
2.4. SUMMARY
The fate and transport of plutonlum In the atmosphere Is not completely
understood. The size distribution of airborne plutonlum particles 1n
0217d -16- 08/08/89
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ambient air shows that, on the average, -86% may be associated with
particles of <10 .microns 1n aerodynamic diameter (Hlrose and Suglmura,
1984); particles with aerodynamic diameters <5 microns are resplrable. Most
of the airborne plutonlum particles will be Insoluble In water and may exist
In *3 and +4 state (Hlrose and Suglmura, 1984). However, water-soluble
plutonlum was detected In rainwater, 38-89% of 1t 1n the +5 and +6 valence
state (Fukal et al., 1987). The removal of plutonlum from the atmosphere
will occur by wet and dry deposition. It has been estimated that the
residence time of stratospheric plutonlum may range from a few months to
over a year and that of tropospheMc plutonlum from a few days to weeks
(Fukal et al., 1987; Buesseler and Sholkovltz, 1987).
Plutonium released to water Is found predominantly 1n suspended solids
and sediment. In most freshwaters, plutonlum 1s found 1n the +3 and +-4
states, and these species will primarily hydrolyze to form neutral and
anlonlc hyroxyl complexes. Generally, the anlonlc complexes will be
transported In the sorbed form and the neutral hydroxide will be transported
1n the precipitated form 1n suspended solids and sediment (WHO, 1983).
However, a small portion of plutonlum may become mobile through the
formation of soluble catlonlc, anlonlc and neutral complexes (Alberts et
al., 1977; Simpson et al., 1980, 1984; Sanchez et al., 1986). In marine
waters and In waters from the Great Lakes 1n the United States, the soluble
plutonlum species In water may be Pu+6 complexes rather than Pu+4 complexes
(WHO, 1983; Platford and.Josh 1, 1966). Typical plutonlum BCFs In edible
portions of aquatic organisms are 10 for fish, 100 for crustaceans and 1000
for molluscs and algae. The BCFs In whole organisms may be 10-50 times
higher (WHO, 1983). It has been estimated that the partial residence time
of soluble plutonlum may range from -18 days In shallow lakes to ~2.5 years
0217d -17- 08/02/89
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In the deepest lakes; for particle-bound plutonlum, the values may range
from 4 days to 3 years (Cornett and Chant, 1988).
When plutonlum Is released to soil, H usually remains highly Insoluble
and In the top few cm of undisturbed soils, even 1n areas where rainfall Is
considerable (WHO, 1983). The slight vertical movement of plutonlum 1n most
soils 1s due primarily to physical disturbances (for example, cultivation
and burrowing action of animals). In some Instances, the vertical movement
may be due to solub1l1zat1on of plutonlum through the formation of complexes
with organic and Inorganic Ugands In soil. This process was postulated to
be responsible for the transport of plutonlum In subsurface water at a
low-level radioactive burial site 1n Maxey Flats, KY (Toste et al., 1984).
Ihe lateral transport of plutonlum from soil 1s due primarily to windblown
dust and surface water runoff (Markham et al., 1978). The transport of
plutonlum from soil to plant 1s usually expressed as the plant-to-soll
concentration ratio. This value ranges from 10~3 to 10~e, Indicating
that a very small amount of plutonlum 1s transferred from soil to plant
(N1sh1ta, 1981; Brown, 1979; Bunzl and Kracke, 1987; WHO, 1983). However,
the transfer of plutonlum from soil to plant can be much higher for plants
grown In plutonlum-contamlnated soils (Adrlano et al., 1981; White et al.,
1981).
0217d . -18- 08/08/89
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3. EXPOSURE
The major source of plutonlum In the environment Is global fallout from
nuclear testing during the past 3 decades. An accidental destruction of the
SNAP-9A satellite In 1964 scattered -17 kC1 of 238Pu and Increased the
global 23BPu activity, particularly 1n the Southern Hemisphere. Localized
plutonlum contaminations occurred 1n many locations. Examples of such
localized contaminations are the nuclear blast site 1n Nagasaki 1n 1945;
nuclear weapons testing at Nevada Test Site, B1k1n1, Huruloa and other
Islands; accidental crashing of B-52 bombers carrying nuclear weapons In
Palomares, Spain and Thule, Greenland; nuclear facilities at Rocky Flats In
the United States and Wlndscale In the United Kingdom, nuclear fuel repro-
cessing plants and atomic power plants all over the world (Komura et al.,
1984). In monitoring plutonlum, many authors determined the 1sotop1c ratio
of p'lutonlum to Identify the source of plutonlum 1n environmental samples.
The alpha particle energies of 239Pu and 240Pu are so close that
ordinary alpha spectrometry cannot resolve them, and the quantification of
Individual Isotopes requires mass spectrometry or alpha spectrometry using a
high-resolution detector (Komura et al., 1984). Therefore, most authors used
the 2aepu/239pu an(j 24opu to Identify the source of plutonlum. This
ratio depends on the latitude but was -0.024 before and -0.035 after the
1964 SNAP-9A Incident In the Northern Hemisphere. The ratio Is much higher
1n reactor fuel and effluents and" may be <3 In older fuels (the ratio
depends on the age of the reactor and 1s higher for older fuels) (Llnsalata
et al., 1980). Therefore, 1f an environmental sample shows a ratio of
23apu/239pu an(j 24opu > 0.035, the sample may be contaminated by
sources other than global fallout. Those authors with access to Instrumen-
tation capable of separating 239Pu from 240Pu used the 2«opu/239pu
0217d . -19- 08/08/89
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ratio to Identify the origin of plutonlum 1n environmental samples. A
2«opu/239pu ratio of 0.05 usually Indicates weapon-grade plutonlum
contamination; a ratio of "0.18 Indicates contamination by global fallout.
Ratios >0.18 1n fallout Indicate high-yield nuclear devices as the plutonlum
source, because a higher neutron flux at the time of detonation Is expected
to yield heavier Isotopes of plutonlum. On the other hand, ratios <0.18 may
Indicate contamination from nuclear reactors (Komura et al., 1984; Beasley
et al., 1981).
3.1. WATER
The concentration of plutonlum In surface water apparently not contami-
nated by any source of pollution (other than global deposit) does not exceed
1 fC1/i, with the exception of waters from a few lakes and reservoirs In
Colorado. Surface waters with possible sources of contamination may show
higher levels of plutonlum than uncontamlnated waters. The levels of
plutonlum In a few uncontamlnated and contaminated surface waters with their
possible sources of contamination are shown In Table 3-.1. Between 1967 and
1978, seawater near San Clemente Island was used to evaluate the effects of
SNAP (Systems for Nuclear Auxiliary Power); Noshkln et al. (1981) found
evidence of contamination of seawater with 238Pu 1n an area 0.025 km2
around the North Light P1er at San Clemente. Both 238Pu and 239Pu were
detected at levels higher than background 1n monitoring wells and streams 1n
and around the Maxey Flats low-level radioactive disposal site (Meyer, 1976).
Few data are available on plulonlum levels 1n drinking water. The
concentration of 239Pu 1n tapwater 1n Broomfleld, CO, was 17 fC1/l (Poet
and Martell, 1972). The concentration of 239Pu and 2«°Pu In treated
water from a water-treatment plant In Chicago ranged from 0.12-0.29 fC1/l
(Alberts and Wahlgren, 1977).
0217d . -20- 08/08/89
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TABLE 3-1
Concentrations of Plutonium In Selected Uncontamlnated and
Contaminated Surface Waters
Water
Uncontamlnated:
Great. Nhaml River
Lake Michigan
Lake Ontario
Lakes and reservoirs
1n Colorado
Baltic Sea and
Gulf of Finland
Pacific Ocean
Contaminated:
Creek near Argonne
National Laboratory
Surface water near
Rocky Flats
Hudson River near
nuclear reactors
Bikini and Enlwetok
Atolls
Qualified Concentration
For (fC1/l)
239Pu 0.36-1.98
239Pu 0.76
239Pu 0.26
239Pu 1-10
239Pu and 0.06-0.26
239Pu and 0.23-0.31
239Pu 0.41-102.0
239Pu 7-810
*39Pu and - 12.1-19.1
23?Pu and 3.2-85.5
Reference
Singh and
Marshall, 1977
Singh and
Marshall, 1977
Singh and
Marshall, 1977
Poet and
Martell, 1972
Lesklnen
et al., 1987
Noshkln
et al., 1981
Singh and
Marshall, 1977
Poet and
Martell, 1972
Llnsalata
et al., 1985
Nev1ss1 and
Schell, 1975
0217d
-21-
08/08/89
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The concentration of plutonlum 1n the sediments of rivers, lakes and sea
has been measured by many authors. Usually, the concentration of 2"Pu
and 240Pu 1n these sediments varies from <1 to ~360 pC1/kg (Buesseler and
Shollovltz, 1987; Carpenter et al., 1987; Purtymun et al., 1987; Beasley et
al., 1981; Unsalata et al., 1980; Goldberg et al., 1978, 1979; Plato and
Jacobson, 1976). The concentration of 238Pu varies between <1 and 14.5
pCI/kg (Purtymun et al., 1987; Unsalata et al., 1980; Goldberg et al.,
1978; Plato and Jacobson, 1976). Plutonium concentrations In sediments of
contaminated ponds and canyons can be >1000 times higher than those found In
sediments from lakes, rivers and sea (Hakonson et al., 1980; Poet and
Martell, 1972). The concentration of plutonlum In sediment usually
decreases with depth, signifying an Increase In concentration within the
last 3 or 4 decades (Carpenter et al., 1987; Beasley et al., 1981; Goldberg
et al., 1978; Kolde et al., 1975).
3.2. FOOD
The following concentrations of «»Pu and 240Pu were found 1n foods
(In fC1/kg wet weight) 1n 3apan: raw milk, <0.7; polished rice, 1.4;
cabbage, 0.95; radish, 0.61; apple, <1.1; pork, <1; egg, <3; and shellfish,
9.4 (Taklzawa et al., 1987). M1lk collected 1n the United States from July-
December, 1965, did not contain any significant amount of plutonlum (Magno
et al., 1967). The total diet samples collected from six regions of the
United States (Northeast, Northwest, Central, Delta, South and Southwest)
contained plutonlum ranging from 2.1-5.8 fC1/kg. Based on dietary Intake,
1t was estimated that the average plutonlum Intake was 7.0 fC1/day (Magno et
al., 1967). It was estimated that the total dietary Intake of plutonlum In
New York City 1n 1972-1974 was 4.1 fCI/day and 1n a city 1n Japan 1n 1984,
8.4 fC1/day (Hlsamatsu et al., 1986).
0217d . -22- 08/08/89
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3.3. INHALATION
The concentration of plutonlum 1n air will depend on the year and season
the measurements are taken. If the measurements follow the detonation of a
nuclear device, the atmospheric plutonlum concentration may be high. The
concentration of 239Pu measured In Winchester, HA, during 1965-1966 ranged
from 0.047-0.437 fC1/m3, with a mean value of 0.149 fC1/m3. The
corresponding values for aa«Pu were 0.015-0.022 fC1/m3 (range) and 0.019
fC1/m3 (mean) (Magno et al., 1967). The concentration range and mean
concentrations of combined 289Pu and 240Pu In the air over Fayettevllle,
AR, 1n 1971-1973 were 0.009-0.083 fC1/m3 and 0.037 fC1/m3, respectively.
Concentrations of 238Pu were also measured, and the range and the mean
values were 0.001-0.016 fC1/m3 and 0.005 fC1/m3, respectively. These
authors also measured 0.62-26.0 fC1/l of combined 238Pu, 239Pu and
2«°Pu 1n rainwater of Fayettevllle 1n 1973 (Gav1n1 and Kuroda, 1977).
The mean concentrations of combined 239Pu and 2«°Pu In the air of
Japan during 1979-1982 were 0.007 fC1/m3 In 1979, 0.002 fC1/m3 In 1980,
0.007 fC1/m3 In 1981 and 0.005 fd'/m3 1n 1982. These authors observed a
seasonal variation In the concentration of fallout plutonlum; the peak
concentration was found In spring. It was theorized that the spring peak
was due to stratospheric fallout of more small particles containing higher
concentrations of plutonlum (Hlrose and Suglmura, 1984).
The workplace concentration of 239Pu 1n spent fuel bays where fuel Is
transferred, cut, stored -and shipped was 5.8 pC1/m3 (Dua et al., 1987).
This concentration 1s ~106 orders of magnitude higher than the concentra-
tion of 239Pu found 1n the ambient air.
3.4. OTHER MEDIA
Globally, soil contains very small amounts of plutonlum (deposition from
atmospheric fallout). The level of plutonlum In such soils (contaminated by
0217d -23- 08/08/89
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fallout) should decrease as the soil depth Increases. The background
239Pu and 2«°Pu level 1n surface soil ranges from 0.003-0.025 pCI/g
(Purtymun et al., 1987; Llndeken et al., 1973). Plutonium levels In
contaminated soil will be much higher. The subsurface soil from a solid
radioactive waste disposal site 1n southeastern Idaho where piuton1 urn leaked
out from the containers contained <11,000 pC1/g of Pu, with most values In
the range 80-1100 pCI/g. The average background at a nearby site was 0.018
pCI/g for 2"Pu and 0.001 pC1/g for 238Pu (Arthur, 1982). Leaking
barrels of plutonlum-laden cutting oil stored 1n southeastern Rocky Flats,
CO, and two accidental fires 1n the plutonlum plant, (one In 1957 and
another In 1969) contaminated soils around the plant; concentrations <6.1
pC.I/g for 23«Pu were detected, compared with background concentrations In
the Denver area of 0.02-0.05 pC1/g (Krey, 1974; Poet and Kartell, 1972;
Johnson et al., 1976). As a result of nuclear tests conducted during
1948-1958, soil near the test areas In Enlwetok Atoll remained contaminated
for a long time. This 1s Indicated by «9Pu concentrations In soils
collected In the early 1970s, which ranged from 1.1-51 pC1/g near the test
sites, compared with Its lowest concentration of 0.04 pCI/g 1n soils away
from the test areas (Gudlksen and Lynch, 1975).
In both occupationally exposed and normal populations, maximum concen-
trations of plutonlum are found 1n tracheobronchlal lymph nodes and the
liver, followed by the bones (Singh et al., 1983; Mussalo et al., 1980;
Lagerqulst et al., 1973; -Taklzawa "et al., 1987; Kawamura et al., 1987).
Plutonium will accumulate most 1n the bones and liver (Singh et al.. 1983).
The tissues of more than 900 persons In seven geographic regions throughout
the United States were analyzed and the following range of median 23BPu
and 239Pu concentrations were found In different tissues (pCI/kg wet wt.):
0217d . -24- 08/08/89
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lymph nodes, 0.73-3.75; Hver, 0.32-0.96; bones, 0.40-0.68; lungs,
0.04-0.46; kidneys, 0.02-0.17 and gonads, 0-0.45 (Fox et al., 1980). From
studies of tissues from former actlnlde workers, Kathren et al. (1988)
concluded that the partitioning of 23BPu may not be the same as that of
239Pu. While 239Pu partitioned approximately equally In the skeleton
and liver, 230Pu partitioned 1.7 times higher 1n the skeleton than 1n the
11ver.
The urine of occupatlonally exposed workers was also analyzed for
239Pu; no evidence of significantly higher Internal doses was found
(Toohey et al., 1981). From skin absorption studies 1n rats, 1t was
concluded that -8% of subcutaneous piuton 1 urn may be absorbed In 10 days
(Matters and Johnson, 1970). Cigarette tobacco In the early 1980s contained
about 0.13 pC1/kg dry wt. of 239Pu and 240Pu, but the mainstream smoke
contained <0.2% of the amount found 1n the tobacco (Mussalo-Rauhamaa and
Jaakkola, 1985).
3.5. SUMMARY
The concentrations of 239Pu and 238Pu 1n air In Winchester, MA, were
0.149 fC1/m3 and 0.019 fC1/m3, respectively, during 1965-1966 (Magno et
al., 1967). The mean atmospheric concentration of combined 239Pu and
24°Pu In Fayettevllle, AR, was 0.037 fC1/m3 during 1971-1973 (Gavlnl and
Kuroda, 1977). In 1982, the mean atmospheric level of combined 239Pu and
240Pu 1n Japan was 0.005 fC1/m3 (Hlrose and Suglmura, 1984).
Few data are available on plulonlum levels In drinking water. The
concentration of 239Pu 1n tapwater 1n Broomfleld, CO, was 17 fC1/l (Poet
and Martell, 1972). The concentrations of 239Pu and 240Pu In treated
water from a water-treatment plant In Chicago, IL, ranged from 0.12-0.29
»
fCI/l (Alberts and Wahlgren, 1977).
0217d . -25- 08/08/89
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The total diet samples collected from six regions of the United States
contained plutonlum ranging from 2.7-5.8 fC1/kg. Based on dietary Intake,
It was estimated that the average plutonlum Intake was 7.0 fC1/day (Magno et
al., 1967). It was estimated that the total dietary Intake of plutonlum In
New York CHy during 1972-1974 was 4.1 fCI/day and In a city 1n Japan In
1984. 8.4 fd/day (Hlsamatsu et al., 1986).
The background «9Pu and 240Pu level In soil ranged from 0.003-0.025
pCI/g (Purtymun et al., 1987; Llndeken et al., 1973). Locally contaminated
soils may contain much greater concentrations (Arthur, 1982; Poet and
MarteH, 1972; Johnson et al., 1976; Gudlksen and Lynch, 1975). Because the
containers had deteriorated, the subsurface soil from a radioactive waste
disposal site In southeastern Idaho contained <11,000 pC1/g of Pu (Arthur,
1982).
In human tissues, the maximum concentrations were found-In tracheo-
bronchlal lymph nodes (0.73-3.75 pCI/kg wet wt.) and In the liver (0.32-0.96
pC1/kg wet wt.) (Fox et al., 1980; Singh et al., 1983; Mussalo et al., 1980;
Taklzawa et al., 1987; Kawamura et al., 1987). Studies Indicate that Pu
accumulates most 1n bone and liver (Singh et al., 1983).
0217d . -26- 08/08/89
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4. ENVIRONMENTAL TOXICOLOGY
4.1. AQUATIC TOXICOLOGY
4.1.1. Acute Toxic Effects on Fauna. Pertinent data regarding the
effects of acute exposure of aquatic fauna to piuton 1 urn were not located In
the available literature dted In Appendix A.
4.1.2. Chronic Effects on Fauna.
4.1.2.1. TOXICITY -- Pertinent data regarding the effects of chronic
exposure of aquatic fauna to plutonlum were not located 1n the available
literature cited In Appendix A.
4.1.2.2. BIOACCUMULATION/BIOCONCENTRATION — Uptake of plutonlum from
contaminated sediments by the marine polychaete, Nereis dlverslcolor. was
assayed by Beasley and Fowler (1976). Sediment samples contaminated by
nuclear device testing were collected from Bikini Atoll 1n the Marshall
Islands. From 40-100 worms were added to each sample of labelled sediment
after the worms voided their guts of previously Ingested materials. The
worms burrowed Into the mud and were left undisturbed for prescribed
Intervals of time. They were not fed additional food. Uptake of plutonlum
was clearly duration-dependent. Total plutonlum content In 22 worms that
were allowed to Ingest sediment containing 135.5^4 pCI/g of plutonlum for 5
days was 0.25^0.02 pC1/g. Exposure of 25 N. dlverslcolor to the same
concentration of plutonlum for 15 days yielded a tissue concentration of
0.48+0.04 pC1/g dry weight plutonlum. With exposure for 40 days, 23 worms
showed a tissue concentration of "0.64*0.07, and for 225 days, 1 worm
contained 0.8U0.14 pC1/g dry weight plutonlum. These values are for a
combination of 239Pu and 238Pu.
Matkar et al. (1983) studied the uptake of 239Pu by clams from
seawater collected from Juhu (Bombay) and spiked with plutonlum nitrate
0217d . -27- 08/08/89
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solution (10s dpm). Concentration of 23»Pu 1n tissues of clams,
Meretrlx meretrlx. reached the highest level at 15 days (3.36*0.62 pC1/kg),
then declined to 1.99^0.57 pC1/kg at 20 days. The concentration factor of
total plutonlum 1n the organism/total plutonlum 1n sediment was 5.5xlO~4
at 15 days exposure and 4.1xlO~4 at 20 days.
Fowler and Guary (1977) studied the absorption efficiency In crabs fed
labeled polychaete worms, Nereis dlverslcolor. and showed that plutonlum Is
readily absorbed from the gut and Incorporated In the predator's tissues.
Six shore crabs, Carclnus maenas. were fed 2-3 labeled worms that were
thoroughly rinsed, whole-body counted and monitored for retention and
elimination of plutonlum. Crabs were sacrificed at prescribed times and
dissected to determine distribution of residual plutonlum. Two large edible
crabs, Cancer pagurus. were similarly treated and assayed (except for
whole-body counts, which could not be done because of the crabs' large
size). There was an Initial rapid loss (90% of whole-body loss 1n C.
maenas) by gut clearance of unasslmllated plutonlum. Absorption efficiency
was high (-20-60% for C.. maenas). Dissections showed that the largest
fraction (43-85%) was In the hepatopancreas, followed by lesser amounts In
shell (8-43%). and muscle and gill (5-10%). Plutonium was at or below the
detection limit In stomach, gut and hemolymph. Absorption was high for C_.
pagurus; 12-41% was retained 1n the tissues at 3 weeks postexposure. The
tissue distribution patterns resembled that of C_. maenas. Similar experi-
ments with other marine* Invertebrates were conducted In the authors'
laboratory with similar results.
NRPB/CEA (1979) calculated concentration factors for 239Pu, which were
the ratio of quantity per unit weight of organism or material considered
(fish, Crustacea etc.) to quantity of activity per unit volume of filtered
water based on dry weight of sediment and wet weight of edible parts.
0217d . -28- 08/08/89
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Marine concentration factors were 10 for fish, 100 for Crustacea, 1000 for
molluscs and 50,000 for sediments. Those for freshwater were 30,000 for
sediments and 10 for fish.
Some generalizations may be made from the above data. Trans-Intestinal
absorption was clearly demonstrated by several researchers (Beasley and
Fowler, 1976; Fowler and Guary, 1977; Pentreath and Lovett, 1976). High
absorption efficiency was noted for some crabs (Fowler and Guary, 1977), but
Increasing concentration of plutonlum along the food chain from producers to
consumers 1s not suggested by the data (Guary and Fralzler, 1977). Bloaccu-
mulatlon of plutonlum decreases as one moves upward 1n the food chain, a
pattern like that modeled by Thomann (1981). However, these data do not
agree with Thomann's model regarding source of body burden. Thomann's model
Indicates that body burden 1s a result of uptake from water only for
23»Pu, but uptake from sediment was evidenced by Ballestra et al. (1983)
and Matkar et al. (1983). Although marine and aquatic fauna absorb and
retain plutonlum In their tissues, data are equivocal regarding extent of
accumulation over time (Beasley and Fowler, 1976; Matkar et al., 1983). The
latter may be explained by the presence of both 238Pu and 239Pu activity
1n the tissues of N. dlverslcolor (Beasley and Fowler, 1976) as opposed to
only 23»Pu In M. meretrlx (Matkar et al., 1983). Data Indicate that
23aPu may be absorbed more efficiently than 23»Pu (Markham et al., 1988).
4.1.3. Effects on Flora.
4.1.3.1. TOXICITY —-Pertinent" data regarding the effects of chronic
exposure of aquatic flora to plutonlum were not located 1n the available
literature cited 1n Appendix A.
4.1.3.2. BIOCONCENTRATION -- Matkar et al. (1983) studied the uptake
of ;z39Pu by algae In seawater collected from Ouhu (Bombay) and spiked with
0217d . -29- 08/08/89
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Plutonium nitrate solution (10s dpm). The average concentration ratio of
Plutonium contained 1n the alga, Dunallella prlmolecta. to concentration In
the seawater was 5.4x10* after exposure durations ranging from 14-94 days.
Uptake was not directly proportional to duration of exposure.
Concentration factors (ratio of quantity per unit weight of algae to
quantity of activity per unit volume of filtered water) experimentally
derived for "»Pu by NRPB/CEA (1979) were 1000 for marine algae and 50,000
for sediments.
4.1.4. Effects on Bacteria.
Pertinent data regarding the effects of exposure of aquatic bacteria to
Plutonium were not located 1n the available literature dted In Appendix A.
4.2. TERRESTRIAL TOXICOLOGY
4.2.1. Effects on Fauna. Smith (1979) assessed the uptake, tissue
distribution and toxldty of plutonlum In ruminants. Steers with surgically
prepared fistulas of the rumen'provided data on Intake of actlnldes over
specified periods of time and on actlnlde ratios In these Ingesta. Radio-
activity levels 1n rumen contents Indicated that, of the 100 uCI of 239Pu
Ingested over >6 months by an Individual animal, 0.0034% was retained In
bone, muscle and liver. Mean concentrations (as pCI/g ash 239Pu) 1n
tissues of a cow-calf pair were: liver. 97.8; lungs, 323.7; muscle, 3.9;
blood cells, 18.6; bone (femur and vertebrae), 117.7; and kidneys, 16.8.
Incomplete data sets regarding gonadal concentrations prevent direct
comparison with these values, but 'total actlnlde concentrations In these
tissues of study animals were significantly higher than those of blood and
muscle, and approached those of bone. Uptake and retention of 238Pu was
greater than that for 239Pu, a finding opposite to that noted 1n the sea-
weed, F_. veslculosus (Cross and Day, 1981). H1stopatholog1cal examination
and actlnlde analyses revealed no rad1olog1cally significant lesions.
0217d . -30- 08/08/89
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Further data taken from field studies and concerning uptake by fauna
from soil and air are presented 1n Section 4.3.
4.2.2. Effects on Flora. Romney et al. (1982) Investigated the plant
root pathway for Incorporating plutonlum Into the food chain. Soil
collected from the Nevada test sites and Tonopah test range was mixed with
fertilizer treatments and potted In 10 l, closed-bottom containers In
which wheat, bushbeans and carrots were grown. Alfalfa was grown 1n a
long-term cropping study to Investigate changes In root uptake over time.
Data Indicate that the root uptake pathway of plutonlum Is of minor Import-
ance compared with that of plant foliage adsorption. Vegetat1on-to-so1l
concentration ratios for «»Pu and 240Pu varied from 10~* to 10~2.
Concentration ratios for fruit and grain were <1/10 that for plant foliage
parts. Uptake of plutonlum under field conditions was much higher than that
generally reported for laboratory conditions. The authors suggest that this
Is due to resuspenslon of materials onto plant foliage under dusty, windy
field conditions.
4.3. FIELD STUDIES
Pentreath and Lovett (1976) assayed the radlonucUde content In plaice,
Pleuronectes platessa. collected from the northeastern Irish Sea at a site
near a nuclear fuel element reprocessing plant. They found seasonal varia-
tions between tissues In the relative concentrations of plutonlum. The
highest concentration of plutonlum 1n Internal organs of fish was In the
gut. Kidneys and gills also had R1gh plutonlum contents, and there were
measurable amounts In the liver, skin, bone, muscle and gonads. Much of the
radioactivity noted In the gut was contained In Ingested animal tissues
(seasonal range = 540X30-501Oi200 fC1/g wet weight). Gut wall content,
although about two orders of magnitude lower than the gut contents (range =
0217d -31- 08/08/89
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15*5-72*4 fCI/g), Indicates that 239Pu and 2«°Pu readily absorb by this
route In this elasmobranch. Because of fluctuating discharges from the
nuclear plant, a steady-state body burden could not be estimated. The
approximate concentration factor for 239Pu and 240Pu 1n plaice muscle
during July (the time most fishing occurs) Is <1. The authors judged this
to be within safe levels for human consumption.
Ballestra et al. (1983) Investigated the mussel, HytHus galloprovln-
clalls. for uptake of plutonlum from coastal waters and sediments along the
northwestern Mediterranean coast. Concentrations of these same forms of
23»Pu and 240Pu In the soft tissues of M. qalloprovlnclalls ranged from
0.06-0.61 fC1/g. The highest concentrations found In mussels were noted 1n
samples collected at the same site (Banyuls). The authors speculate that
the high concentrations are probably caused, at least In part, by local
conditions such as higher suspended sediment load 1n the ambient water.
Concentrations of 239Pu and 2*°Pu In Mediterranean sediments ranged from
0.7-28 fC1/g.
Guary and Fralzler (1977) studied a littoral ecosystem 1n the Bay of
Ecalgraln and described the relationship between marine species and trophic
level of the organisms. Concentration of plutonlum decreased as the trophic
level of the organism Increased. They conclude that concentration of the
radloelement along the food chain from primary producer to tertiary consumer
Is not necessarily Implied by the data.
Curtis et al. (1984)* assayed "biota collected at a "foul site" In
Massachusetts Bay and detected a mean activity level of 5.8xlO~9 pC1/g.
The samples Included specimens from 17 species of fish and several Inverte-
brates, but data were not reported for Individual species. Sediment
0217d . -32- 08/08/89
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-------
Ballestta et al. (1983) assayed seven species of seaweeds from coastal
waters/and sediments along the northwestern Mediterranean coast. Concentra-
tions of 239Pu and 240Pu In the seaweeds varied from 0.1-13 fC1/g. The
highest concentrations of plutonlum 1n seaweeds were noted In samples
collected at the same site (Banyuls). The authors speculated that the high
concentrations are probably caused, at least In part, by local conditions
such as higher suspended sediment load In the ambient water. Concentrations
of 23»Pu and 2*°Pu In Mediterranean sediments ranged from 0.7-28 fC1/g.
Several field reports are available concerning uptake from soil and
atmosphere by terrestrial plants and animals. Hoodhead (1986) reported data
on the uptake and distribution of 289Pu and 240Pu by the black-headed
gull, Larus Mdlbundus. In the Ravenglass Estuary, Cumbria, UK (near a
British nuclear fuel plant). Radlonucllde concentrations 1n tissues as wet
weight were as follows: pectoral muscle, 2.4xlO~3 Bq/g; equivalent whole
body burden, 6.6xlO~3 Bq/g; and equivalent mean solid tissue concentra-
tion, 2.4xlO'a Bq/g.
Bly and Mhlcker (1979) collected arthropods from three study sites near
Rocky Flats nuclear weapons plant and from a distant control site (110 km
north-northeast of Rocky Flats) and analyzed them for plutonlum content.
Leafhoppers and aphlds (Homoptera) were the predominant species collected
for analysis, followed by representatives from the Insect classes, Coleop-
tera. Orthoptera. Aranae. Hemlptera and Hymenoptera. and the crustaceans,
sowbugs (class Isopoda). -All samples contained detectable 23*Pu activity,
but concentrations of plutonlum In the animals were closely correlated to
that 1n the soil. Since the arthropods were not cleansed of surface
activity prior to the assay, It Is Impossible to determine how much of the
activity was from Ingested plutonlum and not from adsorbed substance.
0217d . -34- 08/08/89
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Arthropods were estimated to harbor ~10~8 of the total plutonlum Inventory
1n the ecosystem.
Uptake of plutonlum by biota Inhabiting the White Oak Creek floodplaln
In Tennessee was compared with that of uranium and thorium by Garten et al.
(1981). The floodplaln was a site of liquid radioactive waste retention In
1944. Fescue (Festuca arundlnacea). grasshoppers of families Tettlgonlldae
and AcMdldae. shrews (Blarlna brevlcauda). mice (Peromyscus leucopus).
cotton rats (Slqmodon hlspldus). a raccoon (Procyon lotor). an opossum
(Dldelphls marsuplalls). a woodchuck (Harmota monax) and a rabbit
(Sylvllagus florldanus) were collected and analyzed for rad1onucl1de
accumulation. Measurable amounts of plutonlum were noted In small mammal
carcasses and In leg bones from the larger specimens. Uran1um/pluton1um
ratios In carcasses of shrews, mice and rats, and bone samples from the
rabbit, woodchuck, opossum and raccoon were significantly greater (p>0.05)
than uranium/ plutonlum ratios 1n soil. There was no significant difference
between thorlum/plutonlum ratios In animals and soil. The relative pattern
of accumulation of these actlnldes from soil was uranium > thorium, =
plutonlum, Indicating that environmentally dispersed plutonlum will not
accumulate 1n terrestrial biota more than these other radlonuclldes.
Cataldo and Wlldung (1983) Investigated the Interactions between soil
and microorganisms, plant processes and uptake of plutonlum In the rat and
guinea pig. M1crob1al metabolism promotes trace element solubility In soil
and facilitates the active accumulation of plutonlum by plant roots. When
rats and guinea pigs were fed plant tissues grown on soils containing
plutonlum, fractions of <13.8xlO~4 were found In bone and liver, while
administration by gavage 1n hydrolyzable and complexed forms resulted only
1n fractions of <6.6xlO~4. These data Indicate that soil processes
0217d -35- 08/02/89
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control the quantity of plutonlum In plants, and that plant processes
control uptake by animals that consume the plants.
Slmmonds and Llnsley (1982) determined the concentration of plutonlum
per unit mass of vegetation to Us dally rate of ground deposition (NSA).
Concentrations reported for samples of grain ranged from 1.69xlO~13 to
9.46x10"" C1/kg wet weight, with NSAs of 0.8-0.44 mVday/kg dry weight.
Concentrations for fresh leafy vegetables ranged from 1.5xlO~ls to
4.3xlO'15 C1/kg wet weight, with NSAs of 0.27-0.78 mVday/kg dry weight.
NSAs for strontium and cesium fallout were 5-10 times higher than for
plutonlum. This difference may be due to the comparatively more efficient
removal by natural loss mechanisms of the Insoluble plutonlum from plant
surfaces.
Total foliar application of 166.7 Bq or 6.17 pC1 (10,000 dpm) plutonlum
citrate over a 9-week period to growing potatoes resulted 1n 0.4% of the
radioactivity being taken up by the tubers (Cooper et al., 1985).
4.4. AQUATIC RISK ASSESSMENT
Lack of pertinent data regarding the effects of exposure of aquatic
fauna and flora to plutonlum prevented the development of a freshwater
criterion (U.S. EPA/OURS, 1986). Available data consist of uptake and
concentration assays. These data Indicate that plutonlum uptake by fresh-
water biota diminishes at successively higher levels of the food chain.
Additional data required to develop a freshwater criterion Include the
results of acute assays -with a saimonld fish species, a warmwater fish
species, a third fish species or an amphibian, planktonlc and benthlc
crustaceans, an Insect, a nonarthropod and nonchordate species and an Insect
or species from a phylum not previously represented. The development of a
0217d . -36- 08/08/89
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freshwater criterion also requires data from chronic toxlclty tests with two
species of fauna and one species of algae or vascular plant and at least one
bloconcentratlon study.
Lack of pertinent data regarding the effects of exposure of aquatic
fauna and flora to plutonlum prevented the development of a saltwater
criterion (U.S. EPA/OWRS, 1986). Available data Indicate that plutonlum
uptake by marine biota diminishes at successively higher levels of the food
chain, that degree of uptake may or may not be duration-dependent (depending
upon chemical species), and that plutonlum 1s taken up through the gut of
marine fauna. Additional data required to develop a saltwater criterion
Include the results of acute assays with two chordate species, a nonarthro-
pod and nonchordate species, a mysld or panaeld crustacean, two additional
nonchordate species and one other species of marine fauna. The development
of a saltwater criterion also requires data from chronic toxldty tests with
two species of fauna and one species of algae or vascular plant and at least
one bloconcentratlon study.
4.5. SUMMARY
Studies on the toxldty of plutonlum to aquatic organisms were not
located 1n the available literature. Data regarding uptake of mixed
Isomers, 238Pu and "9Pu, from contaminated sediment by the marine worm,
N. dlverslcolor. showed Increasing tissue concentrations with Increased
duration of exposure (Beasley and Fowler, 1976). Matkar et al. (1983) noted
Increased tissue concentrations In "clams, M. meretrlx. exposed to seawater
spiked with plutonlum nitrate solution for the first 15 days. This was
followed by a drop In tissue levels at 20 days. The differences 1n these
patterns may be due to animal species variations, or more likely, to the
difference In chemical species.
0217d . -37- 08/08/89
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Plutonium Is taken up by marine fauna from both sediment and seawater
(Ballestra et al., 1983; Matkar et al.( 1983). Data strongly Indicate that
trans-Intestinal absorption of plutonlum occurs In marine forms (Beasley and
Fowler, 1976; Fowler and Guary, 1977; Pentreath and Lovett, 1976).
Plutonium bloaccumulatlon decreases at successively higher trophic levels
{Ballestra et al., 1983; Beasley and Fowler, 1976; Fowler and Guary, 1977;
Markham et al., 1988; Matkar et al., 1983. These animal study data provide
equivocal support for an equilibrium model developed by Thomann (1981). The
model predicts a similar general trend of bloaccumulatlon within the food
chain, as these data describe. However, these data do not support the
model's prediction of animal uptake of plutonlum from water only.
Bloconcentratlon data on marine algae showed concentrations ranging from
-0.1-20 fC1/g (Cross and Day, 1981; Ballestra et al., 1983). Variations In
levels were attributed to variations 1n suspended sediment load 1n the
ambient water or to fluctuations In levels released from power plants.
Uptake from plutonlum nitrate solution by the alga, D. prlmolecta. was not
directly proportional to duration of exposure (Matkar et al., 1983).
Effects of plutonlum on terrestrial fauna were Investigated by Smith
(1979). Hlstopathologlcal examination revealed no lesions 1n a steer that
Ingested plutonlum at a radioactivity level of 100 uC1 of "'Pu over >&
months. Of this amount taken 1n, 0.0034% was retained In bone, muscle and
liver. Measurable amounts were also detected In lungs, blood and kidneys.
A study by Romney et al. (19821 of root uptake of plutonlum by wheat,
bushbeans, carrots and alfalfa Indicated that root uptake of plutonlum Is of
minor Importance compared with plant foliage adsorption, and that laboratory
data may underestimate uptake rates occurring under field conditions.
0217d . -38- 08/08/89
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Terrestrial field study data on plutonlum consist of measurements of
uptake by flora and fauna from soil and air. Measurable quantities of
239Pu have been detected In organisms that Inhabit sites contaminated by
products released from nuclear weapons or fuel plants. These organisms
Include L. Mdlbundus (Hoodhead, 1986), arthropods (Bly and Whicker, 1979),
fescue, grasshoppers, shrews, mice, cotton rats, raccoons, opossums,
woodchucks, rabbits (Garten et al., 1981), rats and guinea pigs (Cataldo and
Wlldung, 1983), grains and leafy vegetables (Slmmonds and Llnsley, 1982),
potatoes (Cooper et al., 1985). Soil processes control the quantity of
plutonlum In plants, and plant processes control uptake by animals that
consume the plants (Cataldo and Wlldung, 1983). Environmentally dispersed
plutonlum accumulates 1n terrestrial biota like thorium does, and to a
lesser degree than uranium does (Garten et al., 1981). Higher concentra-
tions of radlonucUde were measured 1n grain than In leafy plant parts.
Researchers suggest this 1s because the Insoluble plutonlum particles are
more efficiently removed by natural loss mechanisms from plant surfaces than
from the seeds (Slmmonds and Llnsley, 1982).
0217d . -39- 08/08/89
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5. PHARMACOKINETICS
5.1. ABSORPTION
Once Inhaled, plutonlum particles have at least five possible fates,
which may or may not Include absorption; they can simply be exhaled. ICRP
(1988) estimates that, In humans, this Is the fate of 37% of the particles
with an AMAD of 1 ym (BEIR, 1988). In mice, 23-42% of the Inhaled
particles are exhaled (Balr et al., 1961). The particles can be removed
from the upper respiratory tract by mucodllary action and then swallowed.
In humans. It has been estimated that this Is the fate of 38% of the Inhaled
plutonlum particles {AMAD=0.2-10ym), which are cleared at a rate of
0.1%/day (ICRP, 1986). This occurred with 70-80% of 239Pu citrate
deposited In the nasopharynx or tracheobronchlal regions In rats (Stather
and Howden, 1975) and with 52% of the deposited 239PuOp 1n mice (Ba1r et
al., 1961). The plutonlum particles can be phagocytlzed by pulmonary
macrophages, with subsequent deposition 1n respiratory lymph nodes. This Is
estimated to occur at a rate of ~0.035% of the deposited dose/day, based on
beagle data (ICRP, 1986). The macrophages can also transport the plutonlum
particles Into the general circulation. The plutonlum particles can be
deposited and retained 1n epithelial cells at various locations 1n the
respiratory tract. Including the nasopharynx, tracheobronchlal and alveolar
regions. The amount taken up by the tracheobronchlal and bronchlolar
epHhella 1s -1% of the deposited dose (BEIR, 1988). The IAD In humans has
been estimated to be ~25% of the" Intake for particles sized 0.2-10 vm
(ICRP, 1986). In dogs exposed to 239PuO? (AMAD=0.75vm), the IAD was
estimated to be **37% (D1el and Lundgren, 1982) In one experiment and -21% In
another (AMAD= 0.5-0.7 ym) (Balr and Wlllard, 1962). Finally, the
0217d . -40- 08/08/89
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particles can be transported from the alveoli across the alveolar caplllary-
endothellal cell surface Into the blood. This was the fate of -3.7% of the
deposited 239Pu oxide In dogs (Morrow et al., 1967). The absorption of
239Pu nitrate and citrate from the pulmonary region 1s -4 times greater
than from the tracheobronchlal or nasopharyngeal regions (Stather and
Howden, 1975). The absorption of PuO^ Is slow; most of It will remain In
the lung for many years before It 1s absorbed (ICRP, 1986).
Various half-times have been proposed for the retention of 239Pu In
the lungs of humans and animals. For humans and large animals such as dogs,
monkeys and sheep, the clearance apparently follows a multlcompartment model
with component half-times of -1, 30 and 500 days (Watts, 1975; ICRP, 1986;
Morrow et al., 1967; LaBauve et al., 1980). The middle 30-day clearance
time 1s sometimes not seen In dogs. The longest half-time component 1s for
60% of the pulmonary deposition (WHO, 1983). In preparing models for the
distribution of plutonlum 1n humans, the ICRP (1979) uses a half-life for
239Pu In human lungs that 1s measured In years.
Rodents show a two-compartment clearance; the fast 1-day component seen
In dogs Is not apparent In rodents. In mice, the half-life of 96% of
Inhaled 239Pu02 was <20 days and was 469 days for the remainder (Balr et
al., 1961). In rats, reports on the clearance half-life of 239Pu02
from the lungs range from 20-40 days for the first compartment (containing
80%-90% of the IAD), and 150-250 days for the second compartment (Rhoads et
al., 1986; Morgan et al., 1984; Sanders et al., 1976).
The fate of the plutonlum particles depends on several factors Including
1) chemical form, 2) firing temperature, 3) Isotope, and 4) particle size.
The chemical form of the compound affects solubility; PuOp remains 1n the
lung longer (Dlel and Lundgren, 1982; Mann and Klrchner, 1967) than Pu
0217d -41- 08/08/89
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nitrate or Pu citrate, which are more soluble salts that rapidly dissolve 1n
lung fluids (Slather and Howden, 1975; ICRP, 1986). The plutonlum oxide
particles fired at higher temperatures (1000°C) have less surface area/unit
volume and therefore have lower solubility and remain In the lung for longer
periods of time than low-fired particles (350°C) (BEIR, 1988; ICRP, 1986).
The 239PuOp Is translocated from the lung -10 times slower than
238Pu02 (ICRP, 1986; Mewhlnney and Dlel, 1983). This may be due to the
high specific activity of 288Pu, which leads to radlolysls, and the
creation of smaller particles. The 239PuOp particles that have a larger
AMAD (micrometer-sized) are deposited higher In the respiratory tract and
are more likely to be translocated to the digestive system than the smaller
particles, and the smaller particles (nanometer-sized) are more easily
absorbed (ICRP, 1986; BEIR, 1988).
Plutonlum Is not well absorbed through the gastrointestinal tract 1n
humans or animals. The ICRP (1988) estimated that the absorption factor In
humans for Insoluble compounds such as plutonlum oxide may be >lxlO~3.
For more soluble compounds such as plutonlum nitrate, the absorbed fraction
was calculated to be 10~*. The gastrointestinal absorption In humans who
ate plutonlum 1n contaminated reindeer meat In Finland was estimated to be
8-9xlO~4 (Mussalo-Rauhamaa et al., 1984).
The absorption of plutonlum depends on the amount of food 1n the
stomach, age of the animal and particular compound of plutonlum. Absorption
was greater In rats that were fasted (Sullivan et al., 1979) than In rats
that were fed (Sullivan et al., 1980). Neonates show Increased absorption
of many chemicals Including 239Pu; neonatal hamsters (David and Harrison,
1984), dogs (S1kov and Hahlum, 1972) and rats (Sullivan 1980a; Ballou, 1958;
S1kov and Mahlum, 1972) absorbed <100 times more plutonlum than adults to
0217d . -42- 08/08/89
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reach absorption factors of 1.7-3.5%. In rats and mice, absorption was ~4
times greater In a citrate medium than In a nitrate medium (Sullivan et al.,
1985). Little species variation In absorption 1s found 1n adult rats,
guinea pigs and dogs (Sullivan, 1980b). There are conflicting reports on
whether the amount of plutonlum Ingested affects Us absorption (ICRP, 1986;
Katz et al., 1955; Harrison and David, 1987).
Oral absorption factors In rats were estimated to be 0.3-0.001% (Stara
et al., 1971). The highest figure (0.3%) was obtained when the animals were
given a very low dose of plutonlum 1n the citrate form. Rats given gavage
doses of 5 yC1 (80 ^g) 239Pu nitrate absorbed 0.004%, as estimated
from the amounts of radioactivity measured 1n the skeleton, liver and urine
(Sullivan, 1980b). Gastrointestinal absorption In adult hamsters given 16.6
kBq of 239Pu citrate was estimated to be 0.003% (David and Harrison,
1984). The fasted beagle dog retained 0.063% of the 237-pluton1um admin-
istered In a gelatin capsule containing ~5 kBq (130 nC1) of 237Pu and
239Pu (Toohey et al., 1984).
No data are available to Indicate whether plutonlum can be absorbed by
Intact skin. Plutonlum has very low levels of gamma radiation activity, so
absorption of radiation from penetrating rays through the skin 1s negligible.
5.2. DISTRIBUTION
The most Important distribution sites for "»Pu are the lungs,
tracheobronchlal lymph nodes, skeleton and liver. As described above,
Inhaled 239Pu02 that reaches the "alveolar portion of the lungs usually
remains there for an extended period of time; It 1s slowly transported to
the tracheobronchlal lymph nodes by macrophages, slowly absorbed Into the
blood and distributed to the skeleton or liver. The distribution of Inhaled
plutonlum has been studied In humans, dogs, monkeys, mice and rats.
0217d • -43- 08/08/89
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The ICRP extensively reviewed the literature on plutonlum and other
radlonuclldes. This commission developed a model from this data which
predicts the distribution of plutonlum In humans. The ICRP (1979) estimated
that 45% of the absorbed dose eventually reaches the skeleton and 45%
reaches the liver In humans. The retention half-life In humans was
estimated to be 20 years for the liver and 50 years for the skeleton (ICRP,
1986). The ICRP (1986) also estimated that the gonads contain -0.01-0.03%
of the body burden In humans. Data from tissues from humans exposed to
nuclear fallout show that, of the accumulated 238Pu, 239Pu and 2*°Pu,
54-60% was 1n the bone, 34-43% In the liver, 3-6% 1n the lungs and lymph
nodes, and <1% elsewhere (Singh et al., 1983). Other studies show that the
distribution of plutonlum 1n humans 1s -53% 1n the skeleton and 47% 1n the
liver (Kathren, 1988)
Autopsy reports from 16 patients Injected Intravenously with 4-6 yg of
plutonlum citrate (Langham et al., 1980) showed that -66% deposited 1n the
skeleton and 23% In the liver. Very little was 1n the circulating blood or
other organs. Samples were obtained at 4-456 days posttnjectlon.
Studies In long-lived animals such as dogs and primates show that PuO~
Is slowly transported out of the lungs over many years. In dogs exposed to
239Pu02 dusts (AMAD=1.8ym), <99% of the plutonlum remaining 1n the
body after 1 year was In the lungs, and to a lesser extent, the tracheo-
bronchlal lymph nodes (Park et al., 1962). When these dogs were studied 4
years later, 50% of the body burden was In the lungs, and <50% was In the
thoracic lymph nodes (Park et al., 1964). The skeleton contained 1-4% of
the body burden, and the liver contained 2-10%. At 14-15 years post-
exposure, the lung contained only -15% of the final body burden, and the
thoracic lymph nodes contained -64%; the liver contained 25%, the abdominal
lymph nodes contained 4% and the skeleton contained -1% (Park et al., 1987).
0217d . -44- 08/08/89
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Other dog studies of shorter duration showed higher relative concentra-
tions In lung and lymph nodes, reflecting the time needed for the plutonlum
to be translocated out of the lung. In one dog study, the plutonlum was
mainly In bronchial lymph nodes and lungs, which contained 87-99% of the
body burden of Inhaled 239Pu oxide (AMAD=l-5 ym) after 299-450 days
(Morrow et al., 1967). In other dogs, 95% of the IAD- of Inhaled 239Pu02
(AMAD=0.5-0.65 ym) was 1n the lungs 2-14 months postexposure, and 4% was
In the bronchial lymph nodes (Ba1r and Wlllard, 1962).
In baboons exposed to 239Pu02 dust particles, the lungs retained
>50% of the dose after 1100 days (Met1v1er et al., 1978). Plutonium trans-
located from the lungs to the lymph nodes so that the equivalent of 1% of
the lung burden was In the lymph nodes after 150 days, and 10% was trans-
ported to the lymph nodes after 500-1000 days. The skeleton and liver
*
contained <1% of the alveolar-deposited dose each.
Rhesus monkeys were exposed to <2000 nCI of 239PuO? (LaBauve et al.,
1980). One year postexposure, 86-96% of the total body activity was In the
lungs of two monkeys that died. This dropped to 53% In one other monkey 3'
years postexposure. The proportion In the tracheobronchlal lymph nodes
Increased correspondingly. Less than 1% was found In the liver or bone.
Since rats and mice do not live as long as larger animals, plutonlum has
less time to be translocated to other organs. In rats, about half of the
Inhaled 239Pu02 (AMAD=2.5ym) remained In the lungs with an Initial
half-life of 30 days, and the remainder had a half-life of 150-250 days
(Sanders et al., 1976). After 1-2 years, <5% was In the skeleton arid
-------
five mice tested (Morgan et al., 1986). The IAD was estimated to be 33% of
the total amount administered. Less than 1% was translocated from the lung
to other organs. Independent of particle size (AMAD=0.8-2.2vm). The
tracheobronchlal lymph nodes contained 0.2% of the IAD, the liver contained
0.03% and the skeleton contained much more; 0.02% was 1n the femora alone.
In mice 70 weeks after Inhalation of 239Pu02 (AMAD=
-------
Plutonium can cross the placenta Into the fetus. Mice dams were Intra-
venously Injected with 239Pu citrate (2.5 yd/cm3) before mating
(Green et al., 1979). The Individual fetuses each contained -0.02% of the
Injected dose at birth, and the transfer occurred largely between gestation
days 12 and 18. The plutonlum was also present 1n the milk, so that the
Individual pups each contained 0.08X of the Injected dose at weaning.
5.3. METABOLISM
Plutonlum Ions are not likely to exist In an uncomplexed form at physio-
logical pH. The most predominant oxidation state 1n physiological condi-
tions Is likely to be the tetravalent form (ICRP, 1986). In the body,
plutonlum 1s usually found as a polymec, bound to the serum protein
transferrln.
A soluble salt such as plutonlum nitrate rapidly dissolves when It
contacts lung fluids, and the polymerized plutonlum Is then easily phago-
cytosed (ICRP, 1986). When plutonlum 1s complexed with citrate, 1t Is less
likely to form polymers and more likely to remain soluble In the body.
5.4. EXCRETION
Inhaled 239PuO_ particles are quite Insoluble and can remain 1n the
lung and body for many years. Various analyses of data from Intravenous
experiments In humans suggest that the half-life for whole body retention of
plutonlum Is 40-200 years (ICRP, 1986). Other data on biological half-lives
of plutonlum In various specific body organs Is presented In the section on
distribution, above. Studies of humans who have worked with plutonlum have
shown that 1t Is detectable In the body for >37 years postexposure (Voelz et
al., 1985).
One to 2 years after a single exposure to monodlspersed 239PuOp
aerosol (AMAD=0.75ym), whole body retention In dogs was calculated to have
0217d -47- 08/08/89
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a half-life of 1200 days (D1el and Lundgren, 1982) or 400 days (Morrow et
al., 1967). The excretion was primarily through the feces, which accounted
for -100 times more total radioactivity than did the urine. Rats have
faster excretion rates. Following Inhalation exposure, 64% of 239Pu
citrate (AMAD=1.5 ym) was eliminated within 100 days 1n rats (Ballou et
al., 1972). Hlstar rats that Inhaled 239Pu02 (AMAD=2.5ym) excreted
51-55% of the IAD within 30 days (Sanders et al., 1976). Over 90% was In
the feces.
Since plutonlum 1s so poorly absorbed by the gastrointestinal system, a
large amount (99%) of an Ingested dose 1s excreted In the feces (ICRP,
1986). Ballou et al, (1972) found that, 3 days after an oral dose of
2s»Pu citrate 1n dogs, only 0.08% was retained, Implying that the rest was
eliminated. The fraction of the Inhaled dose transported by mucodllary
V
action Into the pharynx and swallowed 1s also eliminated In the feces.
Biliary excretion Into the feces also occurs. Rats fitted with cannulas In
the bile duct that had several sections of the Intestine perfused were
Injected Intravenously with plutonlum citrate (Ballou and Hess, 1972).
About 50% of the plutonlum found 1n the Intestinal perfusate originated In
the bile.
5.5. SUMMARY
The International Commission on Radiological Protection (ICRP, 1986)
extensively reviewed the literature on the pharmacok1net1cs of plutonlum.
Ihey determined that humans exhale ~~37% of the plutonlum to which they are
Initially exposed, and that they retain -25% 1n the lungs. The remainder 1s
lodged In the upper respiratory tract and eventually cleared by macrophages
or by mucoclHary action and swallowed. Clearance from the alveoli follows
a multlcompartment model, but by far, most of the 239PuOp clears with a
0217d . -48- 08/08/89
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half-life measured In years. Plutonium nitrate can clear from the lungs
somewhat more quickly. Plutonium Is not well absorbed from the gastrointes-
tinal tract; estimates for absorption range from 10~« to 10~5. Absorp-
tion of radiation by penetration through the skin Is very unlikely, for
239Pu has very Uttle gamma radiation associated with 1t.
Most of the Inhaled plutonlum stays 1n the lung for many years. The
human model developed by the ICRP (1979) and data from human tissues (Singh
et al., 1983, Kathren, 1988) Indicated that It will eventually be absorbed
Into the rest of the body and be translocated to the skeleton and liver, In
about equal proportions. It can cross the placenta, but 1t does not prefer-
entially accumulate In the fetus (Green et al., 1979). In the blood, It 1s
usually bound to the serum protein transferrln (ICRP, 1986).
The major route of excretion of plutonlum 1s through the\ feces. This
occurs when plutonlum 1s swallowed after oral or Inhalation exposure. It 1s
also excreted Into the bile (Ballou and Hess, 1972). Whole body retention
half-lives 1n humans are an estimated 40-200 years for 239Pu (ICRP, 1986).
0217d . -49- 08/08/89
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6. EFFECTS
The radlonucllde 239Pu decays (disintegrates) primarily by emitting
alpha particles. An alpha particle 1s Identical to a helium nucleus and Is
considered h1gh-LET radiation. Because of Us large size, 1t has very
Uttle penetrating power and can only travel a few micrometers but can do a
great deal of damage to the cell that It contacts. Since alpha particles
cannot penetrate the skin, the element that emits them must be absorbed Into
the body to affect health. The particles can Ionize components of nearby
cells, and thus alter a cell's metabolism and chromosomes, and can even kill
the cell. They are particularly dangerous to cells that multiply rapidly.
Special terminology Is needed to describe some of the radiation prop-
erties of the radlonuclldes. The C1 refers to the specific activity of a
radlonucllde, or the number of disintegrations/second. One C1 = 3.7x10*°
disintegrations/second. In International units, this Is also expressed as
Bq. One Bq = 27 pC1 and 1 kBq = 27 nC1. The rad expresses the absorbed
dose or the mean energy from Ionizing radiation Imparted to the Irradiated
tissue/unit mass (gram of tissue). One rad = 100 erg/gram. The Gy Is the
corresponding International unit. One Gy = 100 rad = 1 J/kg. The rem, or
dose equivalent, expresses the equivalence 1n biological effects between
radiations of differing types and energies. One rem = 1 rad x 0. where Q 1s
a quality factor representing the type of radiation energy (alpha, beta or
gamma). The major type of radiation from 239Pu Is alpha radiation, which
Is assigned a Q value of 20. The International unit 1s the Sv, which equals
100 rem.
It 1s difficult to convert units of C1, which measure levels of pluto-
*
nlum In the environment, to rads or rem, which measure doses within body
0217d . -50- 08/08/89
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tissues or biological effectiveness. For example, the following factors
must be taken Into consideration to determine the rad dose to lungs: the
amount of plutonlum that actually remains In the lungs without being exhaled
or removed by mucoclllary action or macrophages; the length of time the
plutonlum remains 1n the lung; the average energy of alpha radiation 1n MeV;
the mass of the lung tissue (estimated to be 1000 g In a reference human);
and the radiological half-life of the «»Pu (~24,000 years). The number
of rads In an organ following a single exposure to a certain amount of C1 of
plutonlum deposited 1n that organ Increases with time as the plutonlum
remains In that organ and decreases as the plutonlum 1s translocated out of
the organ.
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposure.
6.1.1.1. SUBCHRONIC -- Pertinent data regarding the effects of sub-
chronic Inhalation of plutonlum were not located 1n the available literature
dted In Appendix A.
6.1.1.2. CHRONIC — Ep1dem1olog1cal studies of humans exposed to
plutonlum 1n the workplace have shown no adverse health effects or Increased
mortality from exposure to this radlonucUde (Crump et al., 1987; Hempelmann
et al., 1973; Voelz et al., 1983, 1985; Wilkinson et al., 1987). The mor-
tality rates of the workers were lower than for the standard U.S. citizen,
reflecting the "healthy worker effect." These studies are described In
Section 6.2.1.
Almost all of the animal experiments on ««»Pu involve single Inhala-
tion exposures to aerosols of PuOp lasting 10 minutes to 1 hour, followed
by observation periods that can last the lifetime of the animals (1-2 years
In rodents, <15 years In dogs). Since plutonlum dioxide Is cleared from the
0217d . -51- 08/08/89
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lung very slowly, a single Inhalation exposure will deposit plutonlum
particles In the lung, which will remain there for many years. This means
that the animal Is chronically exposed to alpha particle radiation, which Is
the primary cause of adverse health effects following exposure to 239Pu.
Since the animals continue to be exposed to alpha radiation throughout their
lifetime, these experiments can be considered chronic.
The primary health risk from Inhaled "'PuO- 1n animals 1s death
from diseases of the respiratory system. The early effects Include
flbrosls, which can lead to respiratory failure. If the animal survives the
flbrosls, radiation pneumonltls can develop. A reduction 1n the number of
circulating lymphocytes Is also a major effect of Inhaled PuO». Even-
tually, lung or bone tumors will develop, which will also lead to early
death. Data on tumors are presented In Section 6.2.1.
In an ongoing study, beagle dogs (10-12/sex/group for controls and lower
doses, 3 males and 5 females at the highest dose) given a single exposure- to
239Pu02 (AMAD=1.8 yrn) In 1973 or 1974 had IADs of -0, 3.5, 22, 79,
300, 1100 or 5800 nCI/dog (Park et al., 1987). Mean survival was 10-12
years In the four lower dose .groups and controls, 6 years In the 1100 nCI
group and 2 years 1n the 5800 nC1 group. Cause of death was usually radia-
tion pneumonltls or lung tumors. Dose-related lymphopenla was found 1n the
groups exposed to >79 nCI. No consistent changes were noted In serum chem-
istry. One to 3 years postexposure, nine dogs from the two highest exposure
groups developed radiation* pneumonlfls and were sacrificed. These dogs had
a final body burden of 1-12 yd, which was primarily (55-88%) 1n the
lungs. The radiation pneumonltls was characterized by focal Interstitial
and subpleural flbrosls, Increased numbers of alveolar macrophages, alveolar
epithelial hyperplasla and fod of squamous metaplasia. At IADs of >300 nCI
0217d . -52- 08/08/89
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(2»4r nCI/g lung), there was adenomatous hyperplasla of the liver. At >22
nC1 (0.18 nC1/g lung at autopsy), there was sclerosis of the tracheo-
bronchlal lymph nodes and dystrophlc osteolytlc lesions In the skeleton.
Beagle dogs had a single Inhalation exposure to 239PuCL (AMAD=
0.1-0.5 ym) and were observed <10 years (Howard, 1970). For each animal,
the IAD was 0.5-3.5 yd (500-3500 nC1), and the accumulated radiation dose
was 2500-12,000 rads. Acute respiratory effects Including edema and
flbrosls began to occur 1-12 months postexposure 1n animals with an IAD of
0.1 |iC1/g of lung tissue. An IAD of -5 nCI/gm lung tissue was associated
with decreased Hfespan. Of the 35 animals that died, 22 died of primary
lung neoplasla, 8 died of pulmonary flbrosls and 5 were killed for metabolic
studies. As of 1970, five were still alive.
In an ongoing experiment, beagle dogs were exposed to 239PuO?
(AMAI)=0.75 urn), which resulted 1n an IAD of -0, 0.01, or 0.1 yC1 (0, 10,
100 nC1)/dog (D1el et al., 1986). Some were exposed once (n=24) and others
semlannually for <9 years (n=48). Death from radiation pneumonltls and
pulmonary flbrosls occurred In 11 dogs; cumulative lung doses to these dogs
ranged from 1700-3100 rads. Six other dogs died with pulmonary carcinomas.
Deaths occurred 4-9 years postexposure.
Other Investigators also found that lung carcinomas, radiation pneumo-
nltls and flbrosls are the usual cause of death 1n beagles exposed to
23»Pu aerosols. Lymphopenla was also common (Gullmette et al., 1986;
Huggenburg et al., 1986; Clarke et a"!., 1966; Park et al., 1962, 1964; Yulle
et al., 1970).
Plutonium nitrate 1s translocated out of the lungs faster than plutonlum
dioxide and presents a slightly different pathological picture, since bone
and lung tumors developed. In an ongoing study, Dagle (1987) exposed beagle
0217 d -53- 08/08/89
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dogs once In 1976 or 1977 to 239Pu nitrate. The IADs for each dog were ~0
(20 dogs/sex), 2, 8, 56, 295, 1709 (all 10/sex) or 5445 (3 males and 2
females) nC1, corresponding to 0, 0.02, 0.006, 0.5, 2, 14 or 47 nC1/g lung
tissue. One month postexposure, lymphopenla occurred 1n dogs at the two
highest doses. At the highest dose level, all dogs died from radiation
pneumonltls 14-41 months postexposure. The other dogs are presumably still
alive.
Rhesus monkeys (four groups with three/group) were given IADs of <2000
nCI of 23»Pu02 (AMAD=1.6 vm) (LaBauve et al.. 1980). Radiation
pneumonltls was the cause of death 430 or 443 days postexposure 1n two
monkeys with IADs of 1800 and 1000 nC1, respectively. Death from pulmonary
flbrosls occurred 3 years postexposure In one monkey exposed to an IAD of
1000 nC1. Information on the fate of the other monkeys was not available.
Female Wlstar rats were exposed to a1r-ox1d1zed 239PuOp (AMAD=2.2
vm) (Sanders and Mahaffey, 1979). The IAD was 9.9 or 560 nC1/an1mal. In
the high-dose group, 24/26 died of pneumonltls; mean time to death was 89
days. The low-dose group had a longer mean survival period (594 days).
Lung tumors were also found In the treated rats.
Sanders et al. (1976) exposed Wlstar rats to 239Pu02 fired at high
temperatures (AMAD=2.5 ym). Radiation pneumonltls and flbrosls was seen
In the groups receiving 45 nC1/rat or 180 nCI/rat, but not In controls or
groups receiving 0.18 or 5.0 nC1. The exposure was also calculated In rads
using deposition, half-life for clearance, survival time, lung weight and
specific activity. The rats also had significantly Increased numbers of
lung tumors. Other rats exposed to 288Pu02 developed radiation pneumo-
nltls at IADs of 220 and 890 nC1/rat, but not at 0, 0.14 or 11 nC1/rat
(Sanders et al., 1977).
0217d -54- 08/08/89
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-------
-------
(n=3), prostate (n=8), brain (n=6) and thyroid cancers (n=l) were elevated,
but the confidence limits were very wide. No bone cancer was observed.
Lung cancer rates were actually lower In the group with body burdens of
>2 nC1.
The primary cancer effect associated with Inhalation exposure to 239Pu
1s lung cancer, which was seen 1n the experiments In dogs, monkeys and rats.
Exposure to Pu nitrate also Induced bone sarcomas. These studies were
described 1n Section 6.1.1.2.
In the Park et al. (1987) study where beagle dogs were exposed once to
2»»Pu02 (AMAD=1.8 ym) 1n 1973 or 1974, resulting In IADs of -0, 3.5,
22, 79, 300, 1100 or 5800 nC1/dog, mean survival was 10-12 years In the four
lower dose groups and controls, 6 years 1n the 1100 nC1 group, and 2 years
In the 5800 nCI group. Cause of death was usually radiation pneumonltls or
lung tumors. Incidences of lung tumors 1n dogs reclevlng IADs of 0, 3.5,
22, 79, 300, 1100 or 5800 nC1 were 4/20, 0/24, 2/21, 5/20, 14/22, 20/21 and
8/8, respectively. The lung tumors were primarily bronchlolar-alveolar
carcinomas or adenomas.
In beagle dogs given a single Inhalation exposure to 239Pu02 (AMAD=
0.1-0.5 ym) and observed for <10 years (Howard, 1970), an IAD of -5 nC1/g
lung tissue was associated with decreased Hfespan. Primary lung neoplasla
developed 3-10 years postexposure, when >0.01 yC1/g was found In the lung
at autopsy. Doses In rads were not calculated for Individual animals. The
most common tumors were .bronchloTar-alveolar adenocardnomas, Indicating
that the epithelial cells were the most affected. Of the 35 animals that
died, 22 died of primary lung neoplasla.
In an ongoing experiment where beagle dogs were exposed to 239Pu02
once (n=24) or semlannually for <9 years (n»48) (D1el et al., 1986), six
0217d -57- 08/08/89
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dogs died with pulmonary carcinomas. Two dogs with pulmonary carcinomas
exposed once to PuO? had total pulmonary deposits of 13 and 70 nCI/kg,
with cumulative doses to the lungs of 400 and 1900 rads. Four other dogs
exposed repeatedly had pulmonary carcinomas at 24-145 nC1/kg or 600-2700
rads to the lung. Deaths occurred 4-9 years postexposure. No cancer deaths
were found 1n the controls.
Other Investigators also found that lung carcinomas are a frequent cause
of death In beagles exposed to 2a9Pu aerosols (Gullmette et a!., 1986;
Muggenburg et al., 1986; Clarke et al.. 1966; Park et al., 1962, 1964; Yulle
et al., 1970).
Dagle (1987) exposed beagle dogs once to 239Pu nitrate, resulting In
doses of 0, 2, 8, 56, 295, 1709 or 5445 nC1 and corresponding to 0, 0.02,
0.006, 0.5, 2, 14 or 47 nCI/g lung tissue. At the 295 and 1709 nC1 levels,
the primary cause of death was osteosarcomas occurring 34-92 months post-
exposure In the 1709 nC1 group and 54-106 months postexposure 1n the 295 nCI
group. Lung tumors were also seen In these animals.
Sanders et al. (1976, 1977, 1988) Investigated the carcinogenic prop-
erties of Inhaled 289Pu02 and 288Pu02 In rats. In these experi-
ments, female Wlstar rats had single nose-only exposures to PuO~ for 10-30
minutes and were maintained for lifetime observations. The IAD was calcu-
lated as the sum of the plutonlum In the body and excreta 4-30 days post-
exposure. Control groups were always used, and additional rats were
sacrificed for metabolic studies.
Female Wlstar rats were exposed to a1r-ox1d1zed 239Pu02 (AMAD=2.2
ytn) (Sanders and Hahaffey, 1979). The IAD was 9.9 or 560 nCI/anlmal. In
the high-dose group, 24/26 died of pneumonltls; mean time to death was 89
days. Lung tumors were found 1n 2/26 of these animals. The low-dose group
0217d . -58- 08/08/89
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had a longer mean survival period (594 days), and lung tumors were found 1n
10/35 animals. The controls. (n=68) had no tumors.
Sanders et al. (1976) exposed Wlstar rats to 239Pu02 fired at high
temperatures (AMAD=2.5 ym). The Incidence of lung tumors was 0/48 In
controls, 0/114 at IAD of 0.18 nC1/rat, 6/60 at 5.0 nC1, 34/91 at 45 nC1,
and 16/30 at 180 nC1. When the exposure was expressed In rads, the Inci-
dence of lung tumors was significantly Increased at doses of 75-10,000 rads
to the lung, but tumor Incidences did not occur In a dose-related manner.
The most prevalent tumor types were adenocardnomas, followed by squamous
cell carcinomas. Nonpulmonary tumors, especially mammary gland tumors, were
seen 1n all groups Including controls.
Sanders et al. (1977) found that 298PuOp was less effective In
producing lung tumors 1n rats than 23»PuOp. Incidences of lung tumors
following exposure to 238Pu02 were 0/50 1n controls, 1/118 at 0.14 nC1
IAD/animal, 9/120 at 11 nCI, 18/30 at 220 nCI and 5/26 at 890 nC1. A
significant Increase In lung tumor Incidence was seen with a dose of >1720
rads. More adenocarclnomas were observed at lower doses of «»Pu than
with 23BPu.
Sanders et al. (1988) exposed female Wlstar rats to 10 lung-dose ranges
of 0-15. Dose-related relationships were found In the Incidence of
pulmonary metaplasia and tumors. The most common types of lung tumors were
squamous cell carcinomas followed by adenocarclnomas. Tumors were not found
at other sites. Lung tumor Incidences were 0.6% at 0 rads (n=366), 0.5% at
6 rads (0.06 Gy) (n=205), OX at 11 rads (0.11 Gy) (n=147), 0% at 23 rads
(0.23 Gy) (n=106), 4.5% at 46 rads (0.46 Gy) (n=68), 0% at 84 rads (0.84 Gy)
(n=68), 13.8% at 190 rads (1.9 Gy) (n=29), 18.6% at 350 rads (3.5 Gy)
(n=54), 72.5% at 740 rads (7.4 Gy) (n=40) and 84.9% at 1500 rads (15 Gy)
(n=66).
0217d . -59- 08/08/89
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Hamsters are much less sensitive than rats to radiation-Induced lung
tumors.. Syrian golden hamsters (25 controls, 60-66 In treatment groups)
were exposed to 0, 1400, 3620, 3810 or 3820 nd/l of air of 239PuOp
(AMAD=2-2.4 ym) (Thomas et al., 1981). The long-term lung burdens were
equal to 0, 40 and 96-144 nC1. Survival was longer for the low-dose groups
than for the controls, and slightly shorter for the high-dose group. The
hamsters with the greatest exposure had a median lung dose of 12,080 rads or
38 rads/day/an1mal. Lung tumors were found 1n 8/56 animals at 12,080 rads,
7/58 at 8880 rads, 3/50 at 8530 rads, 2/51 at 3860 rads and 0/50 at 0 rads.
Of these tumors, only four (representing a 2% Incidence) were malignant
adenocardnomas. Historical controls showed a 1% Incidence.
Sanders (1977) exposed Syrian hamsters of both sexes to IADs of 0, 3,
19, 31 or 160 nCI of 239PuOp for each animal (AHAD=l-3 ym). Adenoma-
tous metaplasia occurred 1n control and exposed animals, but lung tumor
Incidence did not differ from controls. Similar results were reported by
Hobbs et al. (1976) and Lundgren et al. (1983). Mice (C57BL/6J) exposed to
aerosols of 239Pu02 every other month for up to six exposures In 10
months had greater Incidences of pulmonary tumors than mice exposed once
(Lundgren et al., 1987).
6.2.2. Oral. Pertinent data regarding the carcinogenic effects of oral
exposure to piuton1 urn were not located 1n the available literature cited 1n
Appendix A.
6.2.3. Other Relevant Information". Numerous reports show that Intra-
venous Injections of 239Pu cause bone cancer In animals. Representative
studies are reviewed below.
Beagle dogs given Intravenous Injections of 239Pu citrate developed
osteogenlc sarcomas (Jee et al., 1962). The Incidence for dogs Injected
0217d - -60- 08/08/89
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wHh 0.096 yCl/kg (326 rads) was 7/8; WHh 0.30 VC1 (720 rads), 12/12;
with 0.90 MC1 (1790 rads), 12/12; and with 2.8 yd (6470 rads), 7/9.
Dogs receiving 0, 0.016 or 0.048 yd/kg had no bone tumors. Host of the
tumors (92/98) arose from spongy bone, and the remainder were from the
compact bone. Dogs that developed tumors survived an average of 3-7 years
postexposure.
Beagle dogs were divided Into 11 groups (8-43/group) and given Intra-
venous doses of «»Pu citrate at 0-106 kBq/kg (1 Bq = 27 pCI; 1 kBq = 27
nC1; 106 kBq = 2862 nC1) (Mays et al., 1987). The Incidence of bone
sarcomas was >77X In dogs receiving >1.76 kBq/kg (48 nC1/kg). These dogs
died 5-10 years postlnjectlon, while the controls lived an average of 13
years. When the dose was calculated 1n rads, the dose-response rate for
tumor formation appeared linear, with Incidences of 76X/Gy (1 Gy = 100
rads). The Incidences were 0 at 0 rads, 1/20 at 2 rads (0.02 Gy), 1/38 at
5 rads (0.05 Gy), 3/23 at 15 rads (0.15 Gy), 3/11 at 27 rads (0.27 Gy), 8/25
at 41 rads (0.41 Gy) and 10/13 at 108 rads (1.08 Gy).
C57BL/Do mice of both sexes were Injected Intraperltoneally with 239Pu
citrate (Taylor et al., 1983). Bone tumor Incidences for 0 yd/kg were
0/94; for 0.016 yd/kg, 0/12; for 0.095, 0/11; for 0.286, 0/12; for 0.875,
3/11, and for 2.85, 7/13. The average rads before death were 532 and 1262
for the two highest groups, respectively.
Female CBA/H mice (36-43/group) were Injected Intraperltoneally with
23»Pu citrate once or every 3.5 days for 16 Injections (Humphreys et al.,
1987). The numbers of animals with fully developed osteosarcomas were 0/36,
0/38, 3/39 and 12/40 1n animals given single Injections of 0, 1.85, 5.55 or
18.5 kBq/kg (0, 50, 150 or 500 nC1/kg). For multiple Injections, the
numbers of animals with fully developed osteosarcomas were 0/45, 1/45, 3/45
and 14/43 for the same exposures.
021 iW -61- 08/08/89
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6.3. HUTAGENICITY
Radiation of all types, Including that from alpha-emitting radlonucHdes
such as 239Pu, Is well known for Us action 1n Inducing chromosomal
mutation and aberrations, Including translocatlon Induction (BEIR, 1988).
In Jm vitro tests In plates, alpha radiation from DTPA 239Pu-1nduced cell
mortality 1n Salmonella typh1mur1um strain TA100 at doses >200 R, but
mutants were not observed at doses <1000 R. Chronic alpha Irradiation for 3
days did not modify cellular proliferation 1n CHO cells or alter sister
chromatld exchanges at doses <23 R/day. Gene mutation In CHO cells was
evidenced by an Increase 1n cells resistant to 6-th1oguan1ne at exposures
>5 R. In a human lymphoblastlc cell line, cell proliferation was Inhibited
In a dose-related manner at doses of >20 R/day (Frltsch et al., 1980). In
cultured human dlplold flbroblasts, alpha particles from 238Pu Induced
mutation at the hypoxanthlne-guanlne phosphorlbosyl transferase locus (Chen
et al., 1984).
In Intravenous Injection and Inhalation tests, pluton.1um caused
dose-related Increases 1n the frequency of chromosomal aberrations 1n Syrian
hamster blood lymphocytes (Brooks et al., 1976). Increased Incidence of
chromosomal aberrations was not observed 1n rhesus monkeys treated by the
same routes of exposure. Chromosomal aberrations In spermatogonla In
Chinese hamsters did not differ significantly from controls when these
animals were Injected Intravenously with "»Pu citrate (6xlO~4 or
2xlO~3 yC1/g) (Brooks et al., 19*79). Rhesus monkeys that had single
Inhalation exposures to 2a9Pu02 and accumulated lung doses of >1000 rads
had significant Increases 1n chromosomal aberrations of blood lymphocytes
(LaBauve et al., 1980). Cynomolgus monkeys had single Inhalation exposures
to 239Pu nitrate for IADs of 0, 0.1, 0.3 or 1.0 yd (Brooks et al..
0217d .. -62- 08/08/89
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1980). There was a significant Increase In lymphocytlc chromosomal aberra-
tions 1n monkeys exposed to the highest lung burden. Male mice Injected
Intravenously with «»Pu citrate (-0.3 yd/mouse) showed Increased
frequencies of reciprocal translocatlons Vn spermatocytes (Beechey et al.,
1975).
6.4. TERATOGENICITY
Seven groups of pregnant New Zealand white rabbits were Injected Intra-
venously (apparently once) with 239Pu citrate or citrate alone (controls),
according to the protocol presented In Table 6-1 (Kelman et al., 1982).
Fetal body weights were slightly but statistically significantly reduced at
the high dose. The apparent reduction 1n fetal body weights In groups 2 and
4 were not attributed to treatment. A significant Increase In fetal
mortality was observed 1n most groups treated at 10 and 40 yd/kg. The
number of Utters with one or more dead fetuses Increased at 40 yd/kg.
Severely malformed fetuses Involved one litter In group 1 (one fetus), one
litter In group 6 (three fetuses) and one litter 1n group 7 (one fetus).
The Investigators did not attribute the malformations to treatment. A
significantly Increased Incidence of minor skeletal variations was reported
In the ribs, sternebrae or fontanelles of fetuses In groups 5, 6 and 7.
Generalized retardation of development was reported 1n group 7.
Female mice [{C3Hxl01)Fl] were Injected Intravenously with 0 (n=54), 10
(n=30) or 20 (n=162) yd/kg of "9Pu citrate (Searle et al., 1982).
Matlngs occurred 6 days af-ter the low dose was given, and 3, 6 or 12 weeks
after the high dose. Postlmplantatlon lethality Increased by 12% after the
12-week exposure period, and this was considered by the authors to represent
dominant lethality. Fewer mice became pregnant after the 6- or 12-week
exposure periods, and this prelmplantatlon loss probably represented oocyte
damage.
0217d . -63- 08/08/89
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o
ro
TABLE 6-1
Effects of 23»Pu on Fetuses of Rabbit Dams Given a Single Intravenous Dose of "»Pu Citrate3
o
CO
o
CO
\
CO
Gestation Day:
Group
1
2
3
4
5
6
7
Number of
Utters
•
7
10
i
8
7
8
9
8
Dose
(yd/kg)
0
10
10
10
10
10
40
Treatment
9
9
15
27
15
9
9
Sacrifice
29
10
16
28
28
28
28
Fetal Body
Weight
(g)
10.0+1.8b
9.2+2.9
10.9+3.8
9.1+5.8
11.5+3.9
10.6+2.4
8.3+3.4
Fetal
Mortality
(X/p value)
3/NA
11 /NS
0/NS
16/<0.01
30/<0.01
19/<0.01
23/<0.01
aSource: Kelman et al., 1982
b+ SO
NA = Not applicable; NS = not stated
-------
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of exposure to
Plutonium were not located In the available literature cited In Appendix A.
6.6. SUMMARY
The adverse health effects of 239Pu are from the Ionizing radiation
from hlgh-LET alpha particles that damage nearby cells. The number of alpha
particles emitted by the plutonlum 1s measured 1n C1, and the amount of
radiation Imparted to cells 1s measured In rads. As the plutonlum remains
In the tissue, the number of rads 1n the tissue Increases. Since plutonlum
can remain In tissues for many years, a single Inhalation exposure provides
chronic radiation exposure.
Ep1dem1olog1cal studies and studies of workers exposed to plutonlum have
not shown any adverse health effects 1n humans from 239Pu. However, dogs
(Park et al., 1987; Howard, 1970; Gullmette et al., 1986; Muggenburg et al.,
1986; Clarke et al., 1966) and rats (Sanders et al., 1976, 1977, 1988) given
single Inhalation exposures to 2a9PuO? developed lymphopenla, pulmonary
flbrosls, pneumonltls and lung tumors. Dogs exposed to plutonlum nitrate
developed bone tumors (Dagle, 1987). Intravenous Injections of 239Pu
citrate led to bone sarcomas In dogs (Jee et al., 1962; Mays et al., 1987)
and mice (Taylor et al., 1983; Humphreys et al., 1987). Oral administration
Is not associated with adverse health effects, probably because so Uttle 1s
absorbed by this route. Mutagenldty tests performed In vivo showed that
plutonlum causes chromosomal aberrations (Brooks et al., 1976, 1980; LaBauve
et al., 1980; Beechey et al., 1975). The only evidence of effects on repro-
duction and development 1s that Intravenous Injections of plutonlum caused
fetal mortality 1n rabbits and mice.
0217d . -65- 08/08/89
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
Host national and International regulatory and advisory agencies set
protective limits for public exposure at 500 mrems. The 500 mrem limit Is a
dose equivalent for the weighted mean. for the whole-body dose equivalent.
The limit concerns man-made radiation only, not background radiation levels
or medical exposures. The limit should protect against nonstocastlc effects
such as radiation sickness syndrome and effects on unborn children and
provide an acceptable risk for stocastlc effects such as cancer and
hereditary effects. It was originally based on effects observed after gamma
radiation.
The Nuclear Regulatory Commission regulations for cumulative annual dose
limits for the general population from nuclear power plant operations Is 500
mrem (NRC, 1988). The ACGIH (1989) recommends the same values as the NCRP
(1982) for Ionizing radiation (500 mrem/year). The Federal Radiation
Protection Guidance Is 500 mrem as an upper limit for exposure of Individual
members of the general 'public. Based on this, the RQ for 239Pu 1s 0.01 C1
(U.S. EPA, 1987a).
The WHO-derlved Intervention level for radlonuclldes In food Is 5 mSv
(500 mrem), which has a notional lifetime risk of 10~4 (WHO, 1988). The
radiation protection guidance to Federal agencies for protection against
occupational exposure Is 5 rems, or 10 times greater than the general
population exposure limits-(U.S. EPA7 1987b).
' fl
The WHO/ICRP occupational ALI for Inhalation of 23»Pu compounds 1n
Class W (compounds with biological half-lives measured In weeks, such as
citrates and nitrates) 1s 200 Bq (5.4 nC1), and for Class Y compounds
(half-lives measured 1n years, such as oxides), 600 Bq (16.2 nC1). The
occupational DAC for these compounds 1s 0.1 and 0.3 Bq/m3 (ICRP, 1988).
0217d . -66- 08/08/89
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Emissions of radlonuclldes to air from Department of Energy (DOE)
facilities shall not exceed those amounts that cause a dose equivalent of 25
mrem/year to the whole body or 75 mrem/year to the critical organ of any
member of the public (U.S. EPA, 1988).
The WHO/ICRP occupational Alls for Ingestlon of 239Pu for compounds
with an oral absorption factor of 10~a, 10"* and 10~5 are 3xlO~4
3xlO"5 and 3xlO~6 Bq, respectively (ICRP, 1988).
Ihe EPA limit for maximum average concentration of alpha-emitting radio-
Isotopes released to groundwater from high-level waste for 1000 years after
disposal Is 15 pCI/l (U.S. EPA. 1988).
Ihe NRC.(1988) regulation for maximum concentration above background
released Into water at the boundary of a power plant Is 5.0 pd/8, of
soluble 23»Pu and 30 pCI/l for Insoluble forms.
*
The Interim MCL for gross alpha activity 1s 15 pC1/l, for.a total dose
equivalent of 4 mrem/year for man-made radioactivity (U.S. EPA, 1986b).
7.2. AQUATIC
'Ihe EPA has established a limit for maximum average concentrations of 15
pCI/a, of alpha-emitting radlolsotopes released to groundwater from
high-level waste for 1000 years after disposal (U.S. EPA, 1988).
0217d • -67- 08/08/89
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
8.1.1. Inhalation. Ep1dem1olog1cal studies of humans exposed to
Plutonium 1n the workplace showed no Increase In deaths from cancer (Crump
et al., 1987; Hempelmann et al., 1973; Voelz et al.. 1983, 1985; Wilkinson
et al., 1987). The overall mortality rates of workers were lower than for
the overall U.S. general population, reflecting the "healthy worker effect"
(Crump et al., 1987; Voelz et ai., 1983; Wilkinson et al., 1987).
Abundant evidence exists to show that dogs (Park et al., 1987; Howard,
1970; Dlel et al., 1986; Gullmette et al., 1986; Muggenburg et al., 1986;
Clarke et al., 1966; Park et al., 1964, 1962; Yulle et al., 1970) and rats
(Sanders and Mahaffey, 1979; Sanders et al., 1976, 1977, 1988) that Inhale
239PuO? develop lung tumors, primarily bronchlolar-alveolar carcinomas
• v
or adenomas. Most of the studies used. AMADs of 0.1-5 ym. 2a8PuO» 1s
less effective than 2"9PuO» In producing lung tumors In rats (Sanders et
al., 1977). For Inhalation of plutonlum nitrate, the more significant
health effect 1s from bone tumors (Dagle, 1987). This may be expected
because Inhaled plutonlum nitrate 1s much more easily translocated out of
the lungs Into the circulating blood and Into the bones than 1s plutonlum
oxide. Monkeys (LaBauve et al., 1980) and hamsters (Thomas et al., 1981;
Sanders, 1977) are much less sensitive than dogs or rats to radiation-
Induced lung tumors.
8.1.2. Oral. Pertinent' data regarding the carclnogenldty of oral
exposure to plutonlum were not located 1n the available literature dted In
Appendix A.
8.1.3. Other Routes. Data from mice and dogs Indicate that 239Pu
citrate 1s carcinogenic when administered parenterally. Beagle dogs given
0217d . -68- 10/04/89
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single Intravenous Injections of 2s»Pu citrate developed Increased
" ' h'
dences of bone tumors from doses >15 rads (Mays et a!., 1987; Oee et al.,
1962},. The tumors caused premature death >3 years pustlnjectlon. nice
receiving Intraperltoneal Injections of «»Pu citrate developed bone
tumors from Injections >0.5 yd/animal (Humphreys et al., 1987; Taylor et
al., 1983). The number of animals with tumors In these four experiments
Increased with Increased exposure to plutonlum.
8.1.4. Height of Evidence. Data from epldemlologlcal studies have not
shown any positive relationship between exposure to plutonlum and develop-
ment of cancer 1n humans. However, the human studies have design limita-
tions that render them Inadequate to definitively refute or demonstrate a
carcinogenic effect. Humans have developed cancers from exposure to other
radlonuclldes, such as radium, radon and thorium, and, by analogy, may be
expected to develop cancer from exposure to plutonlum. In animals, there 1s
abundant evidence that Inhalation of plutonlum causes cancer In rats and
dogs. Ionizing radiation of alpha particles produces Intense regions of
1on1zat1on and once the rad1onuc11de Is Ingested or Inhaled this radiation
can be emitted within the body. The carcinogenic properties of Ionizing
radiation have been extensively reported In detail since the beginning of
the 20th century. This overwhelming body of human epldemlologlcal data for
other radlonuclldes and the unchanging physical properties of Ionizing
radiation preclude accepting an alternate effect from the alpha particles of
plutonlum (U.S. EPA, 1989). Therefore, by analogy to the structure and
activity of other radlonuclldes and Ionizing radiation 1n general, plutonlum
can be placed 1n U.S. EPA (1986a) Group A ~ human carcinogen.
8.1,5. Quantitative Risk Estimates. A variety of methods can be used to
estimate human cancer risks from plutonlum, and a number of factors affect
0217d -69- 10/19/89
-------
the choice of an appropriate risk assessment model. Humans have not been
shown to develop cancer from plutonlum by ep1dem1olbg1cal studies, but
humans developed cancer from other radlonuclldes such as radon, radium and
thorium (BEIR, 1988). Animals, however, developed lung, bone and liver
cancer from Inhaled plutonlum.
The various possible methods -that can be used to estimate cancer risks
from plutonlum are as follows:
1. Use the standard linearized multistage model methodology to
develop a q-j* from data on lung tumors 1n rats or dogs from
Inhalation exposure to Pu02> The problem with this method Is
that It 1s very difficult to estimate the equivalent human dose
In mg/kg/day from data from the animal studies, which give
doses In C1/organ weight. It Is difficult to account, for the
differences In Hfespan, since humans will be exposed to the
alpha radiation dose from a single exposure to Inhaled
plutonlum for a much longer time than laboratory animals.
2. Use data on Incidence of bone tumors Induced by Intravenous
Injections of plutonlum Into animals. The shortcomings of this
approach are that one cannot develop accurate human exposure
equivalents from these data, and the route of exposure Is
Irrelevant to environmentally exposed humans.
3. Use data for development of bone cancer 1n humans by analogy to
Ingested radium. Data from radium dial painters show that
radium causes human bone tumors, and this method of risk
assessment for plutonlum was suggested by Rowland (1979).
Ingested 226-Ra caused 53x10"' bone cancers/rad In humans
(Huggenburg et al., 1983). Plutonium 1s known to emit a much
higher dose of alpha radiation to bone cells than an equal
amount of radium. Using data from Induction of bone cancers In
dogs from Injected or Inhaled plutonlum and radium, Muggenburg
et al. (1983) calculate the risk factors from bone cancers of
Inhaled plutonlum 1n humans to be 1200 bone cancers/million
person-rads. Bayeslan analysis of other human and animal
radium data yields a risk estimate of 80-1100 bone cancer
deaths/million person-rads [BEIR, 1988). One of the problems
In using this approach 1s that Ingested radon may have a
different distribution within the body than Inhaled plutonlum,
particularly Pu02, which Is largely retained In the lungs.
4. Use an analogy to radon from data from miners who developed
lung cancer. Based on the estimate for radon and Us progeny,
the risk estimate for lung cancer Is 700 lung cancer deaths/
million person-rad, which 1s equivalent to a dose of 1.4 mrad,
causing one cancer/1 million persons (BEIR, 1988). This model
0217d -70- 10/04/89
-------
assumes that most of the cancers occur 1n people who smoke
tobacco. The shortcoming of this method 1s that the radon gas
has different properties 1n the lung than do plutonlum
particles.
5. Use an analogy to thorium, as suggested by Hays (1982).
Thorium, Injected Intravenously Into humans as Thorotrast,
accumulates preferentially In the liver and causes liver tumors
In humans. Studies of tissues 1n people exposed to plutonlum
from nuclear weapons testing fallout have shown that the
distribution of plutonlum Is -50% to the bone, 40% to the liver
and 4% to the lung and lymph nodes (Singh et al., 1983). Thus,
there may be a risk to humans for developing liver cancer from
absorbed 2a»Pu nitrate. Analysis of human Thorotrast data
provides risk estimates of 300 liver cancer deaths/million
person-rad (BEIR, 1988). One problem with this approach 1s
that the Injected Thorotrast was bound to colloids, which were
especially well absorbed and retained by the liver. Also,
liver tumors were not observed 1n animals exposed to Pu02 or
Pu nitrate.
6. Use the maximum permissible exposure limit of 500 mrem/year, as
do the ICRP (1988), NRC (1988), NCRP (1982), EPA air quality
standards (U.S. EPA, 1988) and EPA RQ determinations (U.S. EPA,
1987a). This Is the method of risk assessment most consistent
with that used by other International and national agencies.
Federal agencies are required to follow this basic radiation
protection guidance (U.S. EPA, 1983). The U.S. EPA also uses
limits of 25 mrem/year for whole-body exposure to set. regula-
tions for emissions to air from Department of Energy facilities
(U.S. EPA, 1988). This value Is made with the additional
policy that all radiation exposures should be made only with
the expectation that benefits will occur and that all exposures
should be "as low as reasonably achievable." The level of risk
associated with this exposure Is ~10~* to 10"a.
One of the problems with this approach 1s that the standard was
originally designed to protect workers from adverse health
effects associated with x-ray or gamma ray radiation from an
external source. It may not be as useful 1n determining risks
from an Internally deposited alpha emitter such as plutonlum.
The conversion from rems/year to C1 In the environment 1s not
straightforward. Radiation dose and dose equivalent, expressed
In rads and rems,-Indicate "the level of radiation absorbed by
bodily tissues. A rem = rad x Q, where Q Is a quality factor
equal to 20 for alpha emitters such as plutonlum. The conver-
sions from pC1 to rads need to take Into account the following
factors: the Initial amount of radlonucUde 1n the tissue of
Interest; biological half-life 1n the tissue; mass of the organ
Involved; and the radiological half-life of the nucllde.
0217d . -71- 10/04/89
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WHO (1983) estimated that the absorbed dose equivalent commit-
ment/unit of Intake of «»Pu In Sv/Bq for a 50-year period
following Intake to be 3.2xlO"4 In the lung, 2.1xlO"4 1n
the liver and 9.5xlO~4 1n bone lining cells.. The whole body
effective dose equivalent uptake/unit Intake was calculated to
be 8.9xlO~5. Since 1 Sv = 100 rem and 1 Bq = -27 pCI, this
1s equivalent to 0.33 rem/nC1.
7. Use the risk factors proposed 1n the Draft Environmental Impact
Statement for Proposed NESHAPS for 'Rad1onucl1des, prepared by
the Office of Radiation Programs of the U.S. EPA In February,
1989 (U.S. EPA, 1989). The risk factors for «'Pu are
0.039/vC1 for Inhalation and 3.0x!0~VyC1 for 1ngest1on.
These are lifetime risk assessments for lifetime Intake based
on 50-year committed dose equivalents. They are calculated
from a modeling scheme that uses the least mean squares method,
based on a linear model, rather than the linearized multistage
model. For 239-pluton1um, the risk factors assume an Inhala-
tion Class of Y (clears from the lung over a period of years)
and an Ingestlon absorption factor of IxlO"4. The organ dose
equivalent rates are based on the calculated environmental
concentrations by AIRDOS-EPA. Absolute risk projection models
were used for bone cancer and leukemia; relative risk projec-
tions were used for lung and other cancers.
8.1.5.1. INHALATION — The risk factor for "»Pu of 0.039/yd for
Inhalation proposed by U.S. EPA (1989) 1$ appropriate. Alternatively, the
risk assessment could be based on a limit of 500 mrem/year for members of
the general public, as set by the Federal Radiation Protection Guidance
(U.S. EPA, 1983).
8.1.5.2. ORAL — Insufficient data are available to derive a new
quantitative risk assessment for cancer based on oral exposure to 239Pu.
However, the risk factor proposed by the U.S. EPA (1989) of 3.0xlO'VvC1
for Ingestlon would be appropriate.
8.2. SYSTEMIC TOXICITY .
8.2.1. Inhalation Exposure. Ep1dem1olog1cal studies of humans exposed to
Plutonium In the workplace have shown no adverse health effects or Increased
mortality from exposure to this radlonucllde (Crump et al., 1987; Hempelmann
0217d . -72- 10/04/89
-------
et al., 1973; Voelz et al., 1983, 1985; Wilkinson et a!., 1987). The mor-
tality rates of the workers were lower than those of average U.S. citizens,
reflecting the "healthy worker effect." The primary health effects from
Inhaled 239PuO_ are 1n the respiratory system In dogs (Park et al.,
1987; Howard, 1970; Dagle, 1987; Dlel et al., 1986;), monkeys (LaBauve et
al., 1980), rats (Sanders et al., 1976, 1977, 1988) and hamsters (Thomas et
al., 1981; Sanders, 1977; Hobbs et al., 1976; Lundgren et al., 1983). The
early effects Include flbrosls, which can lead to respiratory failure and
death. If the animal survives the flbrosls, radiation pneumonltis can
develop. Eventually, lung tumors will develop.
A reduction In the number of circulating lymphocytes Is also a major
effect of Inhaled PuOp. The effects are due to chronic alpha radiation of
the lung tissue, which can arise from a single Inhalation exposure to
239PuO_. Many of the studies attempted to convert the doses from IADs
calculated In C1 to rad units, which account for the time that the plutonlum
remains 1n the tissues.
As discussed previously, 1t would be very difficult to convert the rad
doses calculated 1n these animal studies Into rad doses In human lungs. No
acceptable model for Interspedes extrapolation exists. Furthermore, all of
the endpolnts seen 1n animals are FELs, making 1t Impossible to determine a
LOAEL In these studies. For these two reasons, no RfD for Inhalation
exposure to plutonlum has been calculated.
8.2.2. Oral Exposure. Insufficient data are available from which to
derive RfD values for oral exposure to plutonlum.
0217d . -73- 10/04/89
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The systemic effects seen 1n animals following exposure to plutonlum
(pneumonltis and pulmonary flbrosls) result from the alpha radiation
associated with this radlonucllde. Although the Initial lung deposition can
be calculated In animals, as well as the absorbed dose In rads, there Is no
model to estimate the human equivalent dose from these animal data. An RQ
based on systemic toxlclty 1s not derived.
9.2. BASED ON CARCINOGENICITY
Ionizing radiation, which would Include plutonlum, has been assigned to
U.S. EPA Group A (U.S. EPA, 1986c).
Ihe usual method of describing RQs In units of pounds Is not appropriate
for radlonucHdes (U.S. EPA, 1987a). The commonly used units for radiation
protection are rad and rem, which Indicate the amount of tissue damage from
radiation, or C1, which Indicates the rate of radioactive decay. The U.S.
EPA (1987a) set standards measured 1n C1 and based on the Federal Radiation
Protection Guidance, which recommends 500 mrem as an upper limit on exposure
of Individual members of the general public. Accordingly, the RQ for
23«pu is 0.01 C1. No new Information 1s available that would suggest that
this RQ should be changed.
0217d . -74- 08/08/89
-------
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0217d -88- 08/02/89
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V
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0217d -92- 08/02/89
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•
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*
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0217d -101- 08/02/89
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APPENDIX A
LITERATURE SEARCHED
This HEED 1s based on data Identified by computerized literature
searches of the following:
CHEMLINE
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXLIT
TOXLIT 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
CAS ONLINE (Chemistry and Aquatic)
HSDB
SCISEARCH
Federal Research In Progress
These searches were conducted In April, 1989, and the following secondary
sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1987. TLVs: Threshold Limit Values for Chemical Substances In the
Work Environment adopted by ACGIH with Intended Changes for
1987-1988. Cincinnati, OH. 114 p.
•
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2B. John Wiley and
Sons, NY. p. 2879-3816.
0217d -102- 08/02/89
-------
Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2C. John WHey and
Sons, NY. p. 3817-5112.
Grayson, H. and D. Eckroth, Ed. 1978-1984. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. IARC, WHO, Lyons, France.
Jaber, H.M., W.R. Mabey, A.T. L1eu, T.W. Chou and H.L. Johnson.
1984. Data acquisition for environmental transport and fate
screening for compounds of Interest to the Office of Solid Waste.
EPA 600/6-84-010. NTIS PB84-243906. SRI International, Menlo
Park, CA.
NTP (National Toxicology Program). 1987. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, I.N. 1984. Dangerous Properties of Industrial Materials, 6th
ed. Van Nostrand Re InhoId Co., NY.
SRI (Stanford Research Institute). 1987. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1986. Report on Status Report 1n the Special Review
Program, Registration Standards Program and the Data Call In
Programs. Registration Standards and the Data Call 1n Programs.
Office of Pesticide Programs, Washington, DC.
USITC (U.S. International Trade Commission). 1986. Synthetic
Organic Chemicals. U.S. Production and Sales, 1985, USITC Publ.
1892, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand.Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0217d -103- 08/02/89
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In addition, approximately 30 compendia of aquatic toxldty data were
reviewed. Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, D. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0217d -104- 08/02/89
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APPENDIX B
Summary Table for Plutonium
•
1
0
tn
i
<
Inhalation Exposure
Subchronlc
Chronic
Carclnogenlclty
Oral Exposure i
Subchronlc
Chronic
Carclnogenlclty
REPORTABLE QUANTITIES
Based on chronic toxlclty:
Based on Carclnogenlclty:
Species Exposure
ID ID
ID . ID
NA NA
ID ID
ID ID
NA NA
ID
0.01 C1
Effect RfD or q]* Reference
ID ID ID
ID ID ID
NA 0.039/pCI U.S. EPA, 1989
ID ID ID
ID ID ID
NA 3xlO~VwC1 U.S. EPA, 1989
ID
U.S. EPA. 1987a
o
CO
o
00
CO
ID = Insufficient data; NA = not applicable
------- |