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3. HEALTH EFFECTS
1959) and approximately 0.001%/hour following contamination of finger skin with Pu(NO
3
)
4
in 9% HCl
(Lister et al. 1963).
Studies conducted in rodents have shown that dermal absorption of plutonium is
accelerated when
plutonium is applied to the skin in an acid medium and increases with severity of acid burns (ICRP 1986).
Plutonium has been found to migrate down hair follicles (AEC 1955) and into sweat and sebaceous
glands (AEC 1970b).
3.4.2
Distribution
3.4.2.1 Inhalation Exposure
Information on the general pattern of distribution of absorbed plutonium in humans is available from
direct measurements of plutonium in human autopsy tissues. Such measurements generally reflect the
long-term distribution pattern, in some cases being heavily influenced by discrete exposure events that
occurred years before death. Although some uncertainty exists regarding the relative
contributions of
inhalation and oral exposures to the tissue distributions observed in the autopsy studies (in particular,
those of general populations), the finding of substantial amounts of plutonium in thoracic lymph nodes is
considered to be indicative of inhalation exposures to insoluble plutonium compounds.
Much more detailed information on the extra-respiratory distribution of inhaled plutonium derives from
numerous studies that have been conducted in animals, including nonhuman
primates, dogs, and various
rodent species. The dog studies are of particular relevance to our understanding of the toxicology of
inhaled plutonium. Beginning in the early 1950s, the U.S. government initiated several life-span studies
of the toxicology of inhaled plutonium in beagles (DOE 1989). The results of these studies form part of
the basis for our understanding of the toxicity and carcinogenicity of inhaled plutonium (see Section 3.2).
Organ Distribution of Absorbed Plutonium in Humans.
Information on tissue distribution of plutonium
in humans has come from the analysis of plutonium levels in postmortem tissue samples.
Postmortem
studies have included workers exposed occupationally (Filipy and Ford 1997; Filipy and Kathren 1996;
Filipy et al. 1994; James et al. 2003; McInroy et al. 1989, 1991; Suslova et al. 2002), as well as studies of
the populations from the general public (Bunzl and Kracke 1983; Ibrahim et al. 2002; Kawamura and
Tanaka 1983; Mussalo et al. 1981; Mussalo-Rauhamma et al. 1984; Nelson et al. 1993; Popplewell et al.
1985; Singh and Wrenn 1983; Yamamoto et al. 2008a). Collectively, these studies have shown that
approximately 95% of the systemic (i.e., absorbed) plutonium burden is found in skeleton (≈45%), liver
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PLUTONIUM
3. HEALTH EFFECTS
(≈45%), and skeletal muscle (≈5%). A substantial fraction of the total body burden (e.g., 20–70%) has
also been found in the respiratory tract (including associated lymph nodes) in
workers who experienced
inhalation exposures (James et al. 2003; McInroy et al. 1989). Autopsy studies of subjects from the
general public have found respiratory tract plutonium burdens ranging from approximately 3 to 6% of the
combined burdens of respiratory tract, liver and skeleton (Ibrahim et al. 2002; Kawamura and Tanaka
1983; Singh and Wrenn 1983). Yamamoto et al. (2008a) also evaluated the activity ratios of
240
Pu/
239
Pu
in autopsy samples from individuals surrounding the Semipalatinsk Nuclear Test Site in the former Soviet
Union. They determined that both isotopes were present at highest concentrations in liver followed by
lungs and kidney, and that the isotopic ratios ranged from 0.088 to 0.207, which were consistent with
values obtained elsewhere from exposure to atomic weapons fallout.
The highest concentrations of absorbed plutonium are usually found in liver, bone, and spleen (Filipy and
Ford 1997; Filipy et al. 1994; McInroy et al. 1991; Yamamoto et al. 2008a). However,
concentrations of
plutonium in the respiratory tract and associated lymph nodes can exceed that of other tissues when
exposures occur from inhalation (McInroy et al. 1991; Singh and Wrenn 1983). Skeletal:liver
concentration ratios measured in tissues from deceased plutonium workers ranged from approximately
0.05 to 1 (Filipy and Kathren 1996). Tissue:liver concentration ratios in a deceased plutonium worker
were as follows: tracheobronchial lymph node [TBLN], 100; lung, 2.6; pituitary, 1.1; skeleton, 0.23;
spleen, 0.22; and other soft tissues <0.2 (McInroy et al. 1991). An analysis of tissue plutonium levels in a
group of deceased plutonium workers (n=69–137) found the following soft tissue:liver concentration
ratios: skeleton (0.2) and spleen (0.05–0.08); ratios for other tissues were <0.05 (Filipy and Ford 1997;
Filipy et al. 1994).
The above estimates reflect measurements made at autopsy and not initial distributions of absorbed
plutonium or redistribution of plutonium over time. Although processes involved
in the distribution,
initial deposition, and redistribution of absorbed plutonium are not clearly defined, available human and
animal data collectively provide some insight. Inhaled plutonium that has entered the blood appears to be
largely bound to transferrin and becomes associated with iron-binding proteins such as ferritin and
lipofuscin upon entering hepatocytes (Stevens et al. 1968; Stover 1968a; Suslova et al. 2002; Taylor et al.
1991). Based on regression analysis of autopsy data
from Mayak workers, approximately 50 and 38% of
the plutonium entering the blood from the lung initially deposited in the liver and skeleton, respectively
(Suslova et al. 2002). Liver retention decreased linearly from 50% at the beginning of exposure to 42% at
25 years postexposure, during which time skeletal deposition increased from 38 to 50%. This
redistribution of approximately 8% of the total systemic content from liver to skeleton during the 25-year