Vanadium - Toxicology of Metals - page 888

Söremark et al . (1962) reported that vanadium con-
centrated in the fetuses of mice. Later studies reported
that vanadium was preferentially accumulated in the
placenta rather than in the fetus itself (Hackett and Kel-
man, 1983; Roshchin et al ., 1980). Paternain (1990) found
a dose-related increase of vanadium in the liver, kidney,
spleen, in the whole fetus, and in the placenta of preg-
nant mice administered vanadyl sulfate pentahydrate
on days 6-15 of pregnancy. The highest concentration
was found in placenta (Paternain et al ., 1990). Oberg
et al . (1978) and Roshchin et al . (1980) reported a low-
grade accumulation of vanadium in the testes of rats.
In conclusion, absorbed vanadium (as V 5+ or V 4+ )
is distributed mainly to bone, liver, and kidney (HSE,
2002; Ramanadham et al ., 1991; Roshchin et al ., 1980;
Setyawati et al ., 1998; Sharma et al ., 1980). Three days
after administration, 10-25% of the administered dose
was found in bone, 4-5% in liver and kidney, 0.1% in
spleen, and 0.2% in the testes (IPCS, 2001). Brain levels
of vanadium were found to be considerably lower than
in the other organs, suggesting a blood-brain barrier
for the tested vanadium salts. Vanadium compounds
can pass the placenta, but the levels of the metal are
most often higher in the placenta than in the fetus.

given intravenous and intraperitoneal injections of
sodium metavanadate demonstrated a 5:1 ratio of uri-
nary/fecal excretion; they excreted 61% of the dose
through urine within 24 hours. Intestinal excretion
amounted to 10-12% (Talvitie and Wagner, 1954). These
results were confi rmed in later dog and rabbit experi-
ments (Roshchin, 1968). Conklin et al . (1982) found that
90% of intratracheally instilled 48 V 2 O 5 had cleared
from the lung by day 3, and 40% had been excreted
primarily in the urine. The main part of orally ingested
vanadium is excreted mainly unabsorbed with feces in
a couple of days. Setyawati et al . (1998) reported a fecal
excretion 24 hours after an oral dose of vanadyl sulfate
or BMOV of 75 and 62%, respectively.
Studies in rats and mice showed a three-compart-
ment model for elimination with plasma half-times of
15 minutes, 14 hours, and 8.5 days (Parker et al ., 1980;
Sabbioni and Marafante, 1978). Liver, kidneys, bone,
spleen, and testes had the longest half-times (Parker
and Sharma, 1978; Parker et al ., 1980; Sharma et al .,
1980). Ramanadham et al . (1991) calculated the half-life
to be longer, 12 days, for elimination of vanadium from
the kidney in rats, fed VOSO 4 in the drinking water.
According to IPCS (2001), the pattern of vanadium
distribution and elimination in animals indicates that
there is a potential for accumulation and retention of
absorbed vanadium, particularly in the bone.

5.2.2 Human Studies

Vanadium is found in all body tissues. Byrne and
Kosta (1978) reported concentrations of 3.3, 7.5, and 0.5
ng/g fresh weight in kidney, liver, and muscle, respec-
tively (by NAA). Vanadium has also been found in
the placenta at a concentration of 3 ng/g fresh weight
(Thürauf et al ., 1978). It has been suggested that there is
no cumulative effect of vanadium in human tissue (Byrne
and Kosta, 1978; Naylor et al ., 1984; Schroeder, 1970).
More recent reports on tissue levels of vanadium
are scarce. In a study on autopsy samples from 78 non-
occupationally exposed subjects from NE Spain, the
concentrations of vanadium in brain, bone, kidney,
liver, and lung were all below the detection limit (i.e.,
<0.125

5.3.2 Human Studies

The main route of vanadium excretion is through
the urine. The elimination half-life of absorbed vana-
dium has been estimated to be 15-40 hours (Sabbioni
and Moroni, 1983). In a healthy young man orally
administered sodium metavanadate (12.5 mg/day
for 12 days) was completely recovered, largely unab-
sorbed, in the feces (87.6%) and the remainder (12.4%)
in the urine (Proescher et al ., 1917). Similar results
were obtained by Tipton et al . (1969). Studies on work-
ers exposed to vanadium through worksite air showed
that blood and urinary values of vanadium dropped
to half the initial value within a few days after ces-
sation of exposure (Kiviluoto et al ., 1981a; Thürauf
et al ., 1979). Hauser et al . (1998) reported urine vana-
dium concentrations ranging from 0.19-4.3 mg V/g
creatinine in boiler cleaners exposed to air vanadium
concentrations of 19.1 ± 10.7

g/g wet weight) (Garcia et al 2001). In a study
from Mexico City, the concentrations of vanadium in
lung tissues from the 1960s and 1990s were compared
(Fortoul et al ., 2002). During this period, the mean con-
centrations had increased from 1.04 ± 0.05 in the 1960s
to 1.36 ± 0.08

µ

g/g dry weight, implying increasing
vanadium concentration in ambient air, most likely
caused by an increased number of motor vehicles.

µ

g V/m 3 . In these work-
ers, there was a rapid initial clearance of vanadium
followed by a slow clearance that was not completed
even 38 hours after the end of exposure.
The pharmacokinetics of vanadium has been stud-
ied by Heinemann et al . (2003). Five healthy volun-
teers received an intravenous infusion solution of 20%
commercial albumin containing 47.6

µ

5.3 Elimination and Biological Half-Time
5.3.1 Animal Studies

Parenterally administered vanadium compounds
are rapidly excreted, mainly in urine. Rats and rabbits

g vanadium as
an impurity. Serum concentrations of vanadium were

µ