Vanadium pentoxide

from the plant in Mnisek in the Czech Republic. The population in this area at the time of

the study was 4850. The two-year study concentrated on three groups of 10–12-year-old

schoolchildren: 15 children (11 boys, four girls) from the localities of Cisovice and Lisnice

(Group A), the area potentially most affected by the emission of vanadium; 28 children

(14 boys, 14 girls) from the locality of Mnisek (Group B), an area of medium exposure; and

32 children (17 boys, 15 girls) from the locality of Stechovive (Group C), a control area not

affected by any emission from vanadium production. Vanadium concentrations in venous

blood, hair and fingernail clippings were determined. The mean vanadium concentration in

blood was 0.10 

± 0.07 µg/L in the exposed Group A (Group B data not given) and 0.05 ±

0.05 

µg/L in the control group. In hair, the concentrations were 96 ± 42 µg/kg and 181 ±

114

µg/kg in the exposed groups A and B, respectively, compared with 69 ± 50 µg/kg in

controls. Concentrations in fingernails were 189 

± 41 µg/kg and 186 ± 38 µg/kg in the

exposed groups A and B, respectively, compared with 109 

± 68 µg/kg in the controls. Vana-

dium concentrations in blood, hair and fingernails were elevated in children living close to

the plant. In group B, those with parent(s) working at the plant had higher vanadium concen-

trations in hair than those whose parent(s) did not, suggesting a secondary exposure in the

home from dust transferred on working clothes.

Health status of the children in the study was assessed based on haematological para-

meters, specific immunity, cellular immunity and cytogenetic analysis. Children from the

exposed groups A and B had lower red blood cell counts and lower concentrations of

serum and salivary secretory IgA than control group, and a seasonal decrease in IgG.

Marked differences between exposed and control groups were seen in natural cell-

mediated immunity, with significantly higher mitotic activity of T-lymphocytes in

children living in the immediate vicinity of the plant. A higher incidence of viral and

bacterial infections was registered in children from the exposed area. However, the study

could not control for confounding by exposures to compounds other than vanadium. Cyto-

genetic analysis revealed no genotoxic effects (see Section 4.4.1). The overall conclusion

was that long-term exposure to vanadium had no negative impact on health; the

differences observed were within the range of normal values in all cases (Lener et al.,

1998).

4.2.2

Experimental systems

(a)

In-vivo studies

(i)

General toxicity

The acute toxicity of vanadium is low when given orally, moderate when inhaled and

high when injected. As a rule, the toxicity of vanadium increases as its valency increases,

with vanadium (V), as in vanadium pentoxide, being the most toxic form (Lagerkvist

et al., 1986; WHO, 1988; National Toxicology Program, 2002). 

Studies in animals have shown that equivalent doses of vanadium pentoxide are better

tolerated by small animals, including rats and mice, than by larger animals, such as rabbits

IARC MONOGRAPHS VOLUME 86

258

pp227-292.qxp  31/05/2006  09:49  Page 258

---

and horses (Hudson, 1964). The LD

50

of vanadium pentoxide is highly species-dependent

(Table 6). Differences in diet and route of vanadium administration may contribute to

these discrepancies. 

Ammonium metavanadate given to six weanling pigs at a dose of 200 mg/kg of feed

(200 ppm) for 10 weeks was found to suppress growth and increase mortality (Van Vleet

et al., 1981). In contrast, ammonium metavanadate was not markedly toxic when

200 mg/kg of feed (200 ppm) (approximately equivalent to 6.6 mg/kg bw) or less were

fed to growing lambs for 84 days (Hansard et al., 1978).

(ii)

Respiratory effects

Inhalation exposure

Male CD-1 mice exposed by inhalation to vanadium pentoxide (0.01-M and 0.02-M

solution as aerosol, for 1 h) developed an increased mitochondrial matrix density and

distorted nuclear morphology in non-ciliated bronchiolar Clara cells (Sánchez et al.,

2001; abstract only).

In rats and mice exposed to vanadium pentoxide at concentrations up to 16 mg/m

3

for

3 months, inflammation and epithelial hyperplasia were observed in the nose and lung of

rats and in the lung of mice at exposures 

≥ 2 mg/m

3

. Non-neoplastic lesions in the nose

VANADIUM PENTOXIDE

259

 

 

Table 6. Acute toxicity values for vanadium pentoxide in experimental animals 

Species 

Route of 

administration 

Dose or concentration/ 

exposure 

Parameter

a

 

Reference 

Mouse 

Oral 

23 mg/kg bw 

LD

50

 

 

Subcutaneous 

10 mg/kg bw 

LD

50 

Lewis (2000)

  

Lewis (2000) 

 

Subcutaneous 

87.5–117.5 mg/kg bw 

LD

 

Hudson (1964)

 

 

Subcutaneous 

102 mg/kg bw 

LD

100 

Venugopal & Luckey (1978) 

Rat 

Oral 

10 mg/kg bw 

LD

50 

 

Inhalation 

70 mg/m

3

/2 h 

LC

LO 

Lewis (2000)

  

Lewis (2000) 

 

Subcutaneous 

14 mg/kg 

LD

50 

Lewis (2000) 

 

Intraperitoneal 

12 mg/kg bw 

LD

50 

Lewis (2000) 

Guinea-pig 

Subcutaneous 

20–28 mg/kg bw 

LD

 

Hudson (1964)

 

Rabbit 

Intravenous 

1–2 mg/kg bw 

LD 

Hudson (1964) 

 

Intravenous 

10 mg/kg 

LD

LO

 

Lewis (2000) 

 

Inhalation 

205 mg/m

3

/7 h 

LC

100

 

Sjöberg (1950) 

 

Subcutaneous 

20 mg/kg 

LD

LO

 

Lewis (2000) 

Cat 

Inhalation 

500 mg/m

3

/23 min 

LC

LO 

Lewis (2000) 

a

 LD

100

: dose which is lethal to 100% of the animals; LD

50

, dose which is lethal to 50% of the animals; 

LC

100

, concentration in air which is lethal to 100% of the animals; LC

LO

, lethal concentration low: the 

lowest concentration in air which is lethal to animals; LD, lethal dose

 

pp227-292.qxp  31/05/2006  09:49  Page 259

---