Gallium and Semiconductor Compounds - Toxicology of Metals - page 537

9.74 - 16.02 mg/kg along a smelter-damaged landscape
gradient in Sudbury, Ontario. The USGS (2004) reported
sediment concentrations measured in 1998 in the Bear
River basin, Utah, over a range of 1.08-19.4

More recent studies (Wappelhorst et al ., 2002) have
shown that gallium has a high transfer coeffi cient from
ingested food into milk of lactating mothers.

µ g/g.

5.4 Biological Half-Time
The biological half-time of gallium nitrate in
humans with normal renal function has been found
to be biphasic with mean half-times of 1 hour for the
fast, fi rst-phase component and 25 hours for the sec-
ond phase after intravenous injections with colorimet-
ric measurement of gallium (Hall et al ., 1979). Kelson
et al . (1980) performed similar studies in humans and
also obtained a biphasic pattern with mean half-times
of 8.3-26 minutes for the fast phase and 6.3-196 hours
for the second phase component. The intersubject vari-
ations may refl ect differences in renal function among
the test patients.

5 METABOLISM

5.1 Absorption

5.1.1 Inhalation

Absorption of gallium from the lungs after
inhalation exposure partially depends on whether it is
in a particulate form such as GaAs or Ga 2 O 3 (National
Toxicology Program, 2000). Acute intratracheal
instillation studies from a number of investigators
(Rosner and Carter, 1987; Webb et al ., 1984; 1986; 1987)
or intraperitoneal injection (Yamauchi et al ., 1986)
has shown dissociation of the gallium and arsenic
moieties to release both elements. Dose absorption
and dissolution rates also seem to vary with dose level
and duration of exposure. The metabolism of gallium
arsenide has been recently reviewed by Carter and
coworkers (2003).

6 LEVELS IN BIOLOGICAL FLUIDS

Liao and his coworkers (2004) reported gallium con-
centrations in blood and urine from workers in Taiwan
engaged in the production of III-V semiconductors.
The geometric mean values of the gallium blood levels
were 0.57, 0.53, 0.44, 0.48

5.1.2 Ingestion

g/L for workers in fabrica-
tion equipment maintenance, workers in dopants and
thin fi lm, fabrication supervisors and engineers, and
offi ce workers (controls), respectively. Gallium con-
centrations in urine were 0.28, 0.23, 0.23, and 0.15

µ

The absorption of Ga after ingestion of GaAs
particles in experimental animals has been shown to
be very low (Yamauchi et al ., 1986).

g/L
for the same groups of workers. Although blood lev-
els were not consistently higher in “exposed” workers
than offi ce workers, urinary gallium was signifi cantly
higher ( P < .05) in all other workers compared with the
offi cer workers.

µ

5.2 Distribution
Absorbed gallium is distributed to a number of
organs with highest concentrations in the liver, kidneys,
and spleen as a result of its binding to and transport
in the circulation by transferrin. Absorbed gallium is
bound to transferrin in the circulation and distributed
to a number of organ systems with major concentrations
in the liver (Sun et al ., 1998), bone, bone marrow, spleen,
and kidneys (Belozerov, 1966; Collery et al ., 1996), in
humans and in animals (Straw et al ., 1975).

7 EFFECTS AND DOSE-RESPONSE
RELATIONSHIPS

7.1 Animal Studies
Numerous studies regarding the target organ toxic-
ity of GaAs compounds in rodents (Flora et al ., 1998;
2002; Goering and Rehm, 1990; Goering et al ., 1988;
Webb et al ., 1984; 1986) have reported pulmonary, renal,
and effects on the heme biosynthetic pathway. The pul-
monary effects were most marked in rodents given sin-
gle intratracheal instillations of the GaAs. More chronic
exposures to GaAs particles by intratracheal instilla-
tion to hamsters (Tanaka et al ., 2000) or by inhalation
to rats and mice (National Toxicology Program, 2000)
produced marked toxicity and infl ammation in the

5.3 Excretion
The main route of excretion for gallium from the
body is through the urine, with lesser amounts excreted
in the feces (Rosner and Carter, 1987; Webb et al ., 1984;
1986; 1987; Yamauchi et al ., 1986). In humans, 67 Ga has
been reported in the breast milk of nursing mothers
(Paterson et al ., 1976; Rubow et al ., 1991; Tobin and Sch-
neider, 1976; Weiner and Spencer, 1994) treated with
this agent. Studies of the nursing infant showed 67 Ga
in only in the gastrointestinal tract (Rubow et al ., 1991).