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Maternal-fetal Transfer of Plutonium.
Absorbed maternal plutonium can be transferred
to the placenta
and fetus (Lund and Tkatchev 1996; Prosser et al. 1994; Russell et al. 2003). Analyses of plutonium
concentration in the placenta from a live birth that occurred 12 years following a work-related accidental
inhalation exposure to plutonium found concentration ratios for placenta:maternal (estimated maternal
body burden per kg body weight) of 0.16–0.27 (Russell et al. 2003). Analyses of plutonium in a sample
of aborted fetuses from the general public found fetal:maternal concentration
ratios to be <0.2 (Prosser et
al. 1994). Studies in which animals received parenteral injections of plutonium (in most cases, as
plutonium citrate) confirm that absorbed plutonium can be transferred to the fetus (Green et al. 1979;
Kubota et al. 1993; Morgan et al. 1992; Paquet et al. 1998; Russell et al. 2003; Weiss and Walburg 1978).
This distribution pathway would be expected after inhalation exposure. In baboons, fetal:maternal whole
body concentration varied with the period of gestation at which the parenteral injection of plutonium
occurred and were highest when plutonium was administered during early gestation: day 22,
fetal:maternal=4; day 38, fetal:maternal=0.13; and day 106, fetal:maternal=0.04 (Russell et al. 2003,
attributed to Andrew et al. 1977). A similar pattern has been observed in other animal species, and is
thought to reflect distribution and dilution of plutonium initially transferred
to the fetal-placental unit, as
fetal growth progresses. A larger fraction of an administered maternal dose of plutonium is transferred to
fetal-placental tissues during late pregnancy. In baboons that received a single intravenous injection of
plutonium citrate during the 5
th
month of pregnancy, approximately 3–4% of the activity was transferred
to the fetus within 7 days postadministration (Paquet et al. 1998). The fetal:maternal whole-body
concentration ratio was approximately 1.3 and the tissue distribution in the fetus was similar to that
observed in adult animals, with the skeleton and liver accounting for most of the plutonium activity in the
fetal body. Fetal-placental burden was approximately 1% of the administered
plutonium dose in guinea
pigs, mice, and rats that received an injection of plutonium citrate during late pregnancy (Kubota et al.
1993; Morgan et al. 1991). Maternal-fetal transfer of plutonium, administered as an intravenous injection
of plutonium citrate on day 16 of pregnancy was dose-dependent in mice, and ranged from approximately
5% of the dose following administration of 0.1 μCi/kg (3.7 kBq/kg) to approximately 1% following
administration of 27 μCi/kg (100 kBq/kg; Weiss and Walburg 1978). The highest concentrations of
plutonium in the fetal-placental unit are found in the yolk sac; however, as organogenesis progresses,
plutonium is also found
in other tissues, with the largest fraction of the fetal burden in liver and bone
(Green et al. 1979; Kubota et al. 1993; Morgan et al. 1991; Paquet et al. 1998).
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3.4.2.2 Oral Exposure
Studies of the distribution of plutonium in humans exposed to plutonium solely through the ingestion
pathway have not been reported. Studies conducted in nonhuman
primates, dogs, and various rodent
species have shown that plutonium absorbed from the gastrointestinal tract is distributed predominantly
(≈90%) to liver and skeleton. A study conducted in fasted adult baboons (n=4) found that, 46 days after a
single gavage dose of
239
Pu(VI) carbonate, approximately 90% of total body burden
was in the skeleton
and liver, and that the skeletal:liver plutonium ratio (total burden) was approximately 1.2 (range: 0.7–1.7;
USNRC 1992). Skeletal:liver ratios ranging from 1 to 4 have been observed in dogs, following oral
exposures to plutonium bicarbonate and nitrate (Sullivan 1980a; Sullivan and Gorham 1983; Toohey et al.
1984), and values ranging from 1 to 8 have been observed in rats and mice (Sullivan et al. 1985).
3.4.2.3 Dermal Exposure
Occupational accidents have resulted in dermal exposures and/or penetration
of plutonium into skin
wounds and subsequent systemic absorption of plutonium (McInroy et al. 1989; Woodhouse and Shaw
1998). In one case involving a plutonium-contaminated finger wound, postmortem measurements of
239
Pu levels in tissues, measured 17
years following the incident, showed that 41 and 49% of the body
burden were contained in the liver and skeleton, respectively; another 6.6% was associated with muscle
tissue (McInroy et al. 1989). In a similar case of a plutonium-contaminated left finger wound (Popplewell
and Ham 1989), postmortem measurements taken 18 years postaccident revealed a total estimated
plutonium body burden of 2.4 kBq. The left arm axillary lymph nodes accounted for approximately 76%
of the total body burden; other sites of deposition included skeleton (13%), left hand (5.5%), liver (4.5%),
and left arm flesh (1%).
3.4.2.4 Other Routes of Exposure
Plutonium tissue distributions (postmortem) have been measured following intravenous injection of
Pu(IV) citrate into subjects suffering from chronic disorders (Langham et al. 1980). Various analyses and
summaries of these data have been published (AEC 1971; Durbin 1972; Kathren 2004; Leggett 1985).
Postmortem tissue plutonium measurements for seven subjects have been reported; data for five of the
subjects were obtained 1 year following exposure, data for the other two subjects were obtained 7 or
21 years after exposure. Approximately 66% of the injected dose was found in skeleton (most of which
appeared to be associated with bone marrow) and 20–40% in liver (Langham et al. 1980).