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 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


Chapter 6.12 




General Description 


Vanadium (V) is a bright white ductile metal belonging to group V of the periodic system of 

elements. It forms compounds mainly in valence states +3, +4 and +5. In the presence of 

oxygen, air or oxygenated blood, or oxidizing agents, vanadium is always in the +5 oxidation 

state. In the presence of reducing agents, vanadium compounds are in the +4 oxidation state 

(1).  Vanadium forms both cationic and anionic salts, and can form covalent bonds to yield 

organometallic compounds which are mostly unstable. 



Vanadium is an ubiquitous metal. The average concentration of vanadium in the earth’s crust 

is 150 μg/g (2); concentrations in soil vary in the range 3-310 μg/g (3) and may reach high 

values (up to 400 μg/g) in areas polluted by fly ash (4).  The concentration of vanadium in 

water is largely dependent on geographical location and ranges from 0.2 to more than 100 

μg/litre in freshwater (2), and from 0.2 to 29 μg/litre in seawater (3). The ocean floor is the 

main long-term sink of vanadium in the global circulation (4).  The concentrations of 

vanadium in coal and crude petroleum oils vary widely (1-1500 mg/kg) (2). 

The world production of vanadium was about 35 000 tonnes in 1981 (5), the major 

producing countries being Chile, Finland, Namibia, Norway,  South Africa, USSR and the 

United States. 

Most of the vanadium produced is used in ferrovanadiurn and, of this, the majority is used 

in high-speed and other alloy steel (usually combined with chromium, nickel, manganese, 

boron and tungsten). 

It has been estimated that around 65 000 tonnes of vanadium annually enter the 

environment from natural sources (crustal weathering and volcanic emissions) and around 

200 000 tonnes as a result of man’s activities (6). The major anthropogenic point sources of 

atmospheric emission are metallurgical works (30 kg per tonne of vanadium produced), 

followed by the burning of crude or residual oil and coal (0.2-2 kg per 1000 tonnes and 30-

300 kg per 10


 litres) (7). 

Global vanadium emissions into the atmosphere from coal combustion in 1968 were 

estimated to range from 1730 to 3760 tonnes. The contribution of vanadium to the 

atmosphere from residual-fuel combustion was estimated at 12 400-19 000 tonnes in 1969 

and 14  000-22 000 tonnes in 1970. In the production of ferrovanadiurn for alloy additions in 

steel-making, vanadium emission to the atmosphere was estimated at 144 tonnes in 1968 (2). 

The burning of wood, other vegetable matter and solid wastes probably does not result in 

significant vanadium emission. In 1972, about 94% of all anthropogenic emissions of 

vanadium to the atmosphere in Canada (2065 tonnes) resulted from the combustion of fuel oil 

and only 1.2% from metallurgical industries (8). 


Occurrence in air 

Currently the ambient air levels of vanadium are quite low, but it is suspected that air 

concentrations will increase in the future as a function of accelerated fossil-fuel combustion 

in rural areas. 

Concentrations vary from tenths of nanograms to a few nanograms. In the air of big cities 

the annual average was between 50 and 100 ng/m

(8,9) with significant seasonal variations 

Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


(winter averages are more than three times the summer averages). More recent data from a 

five-year study in four Belgian cities show yearly averages of 41-179 ng/m

(10).  A recent 

survey of measurements in Member States of the European Community indicates the 

following concentration ranges: remote areas, 0.001-3 ng/m


; urban areas, 7-200 ng/m




industrial areas, 10-70 ng/m

(11). Concentrations up to 2 μg/m

have been reported in several 

cities in the northeastern USA. A marked decline of vanadium concentration in ambient air 

was reported after the introduction of low-sulfur fuels (4). Air pollution by industrial plants 

may be less than that by power stations and heating equipment. The average concentration in 

the area surrounding a steel-plant site in Pennsylvania, USA, was 72 ng/m

(2).  Vanadium 

pentoxide (V




) was detected near a large metallurgical works in concentrations ranging 

from 0.98 to 1.49 μg/m

in 87% of samples and exceeding 2 μg/m

in 11% of samples (12). 

With combustion of the carbonaceous matrix, vanadium is released to the atmosphere as 

fine fly ash with a long atmospheric residence time. Vanadium concentrates on the surface of 

particulate matter from coal combustion. The concentration of vanadium in fly ash from 

residual fuel-oil burning averages around 8% (range 2-18%), representing 56% (39-74%) of 

the vanadium concentration in fuel. The soluble fraction of fly ash vanadium averages 70% 

(42-96%). About 80% of the vanadium-containing particles have a mass median aerodynamic 

diameter smaller than 0.5 μm at the chimney, representing 10-20% of the total aerosol mass 

of vanadium (13). 

A large number of occupations involve exposure to vanadium. Concentrations in the 

working environment range from 0.01 to 30 mg/m

(14),  with varying particle distribution 

patterns and different degrees of solubility for different vanadium compounds. Very high 

levels of vanadium in the air were reported in boiler cleaning (17-60 mg/m




Routes of Exposure 



Concentrations of airborne vanadium have increased in recent years, probably because of the 

increasing direct combustion of crude oil residues in power plants and community-heating 

systems. The average annual values for urban areas are reported to be in the range of 0.05-

0.18  μg/m


. Maximum concentrations of vanadium as high as 2 μg/m

occur in areas of 

greatest population density, during the coldest part of the year and during the late evening 




Concentrations of vanadium in drinking-water may range from about 0.2 to more than 100 

μg/litre (16); typical values appear to be between 1 and 6 μg/litre (8). The concentration of 

vanadium in drinking-water depends significantly on geographical location. 



The few data on vanadium concentrations in food vary considerably; this may be explained 

by differences in the food itself and in the analytical methods used. The mean vanadium 

concentration in the diet was reported to be 32 μg/kg (range 19-50 μg)  (17)  and the mean 

daily intake was estimated to be 20 μg/day (18). Byrne & Kosta (19) estimated that the daily 

dietary intake of vanadium amounts to several tens of micrograms. 

The concentration of vanadium in human milk was found to be 0.1-0.2 ng/g (18).  An 

infant drinking one litre of human milk per day would thus have a daily vanadium intake of 

0.1-0.2 μg (8). 



Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


Relative significance of different routes of exposure 

According to a pathway analysis (8), an individual living in a rural environment (assumed air 

concentration 8 ng vanadium per m




will have a body-burden of around 100 μg, over 80% of 

which is derived from the diet; an urban dweller (assumed air concentration 70 ng/m


) will 

have a total body-burden of around 200 μg (in the latter case, the inhalation route contributes 

approximately one half of the total burden). 

It was estimated that the daily intake by ingestion is about 20 μg and by inhalation 1.5 μg 

in an urban area and 0.2 μg in a rural area (8). 


Kinetics and Metabolism 



The lungs are a significant site of entry of vanadium in the case of community exposure. The 

distribution pattern of particles and the solubility of vanadium compounds, as well as alveolar 

and mucociliar clearance, are important factors that determine the rate of absorption in the 

respiratory tract. Moreover, the irritative effect of vanadium compounds can significantly 

modify the absorption of vanadium by the lungs. Vanadium accumulates in the human lung 

with age, reaching approximately 6.5 μg/g in the over-65 years age group (3).  The lung 

clearance of vanadium pentoxide is relatively rapid in animals after acute exposure, but 

substantially slower after chronic exposure. The metal is deposited in the lung in relatively 

insoluble forms. Soluble compounds are partly absorbed, but the extent of absorption in the 

respiratory tract has not been determined. 

The absorption rate of vanadium compounds after ingestion depends on their solubility 

and chemical nature. Absorption of cationic vanadium is low, not exceeding 0.1-1% (8). Skin 

is probably a minor route of absorption in man (9). 



Absorbed vanadium is transported mainly in the plasma, bound to transferrin. The average 

value for the distribution of blood vanadium between plasma and cells in rats after an 

intravenous injection of 0.9-30 μg vanadium per kg was found to be 9 : 1 (20). Pentavalent 

vanadium is reduced in erythrocytes to the tetravalent form. This reduction is a glutathione-

dependent process (21). 

Byrne & Kosta (19) reported blood vanadium levels in healthy individuals of below 0.5 

μg/litre. The analytical method used was neutron activation analysis with pre-separation of 


Vanadium is widely distributed in body tissues; principle organs of vanadium retention 

are kidneys, liver, testicles, spleen and bones. A major fraction of vanadium from cellular 

vanadium was found retained in nuclei (22).  In pregnant rats the injected vanadium was 

found in the fetus (23). 



Vanadium is excreted mainly in the urine, but also in the faeces. Bile is probably not an 

important pathway for excretion into the faeces, but the existence of alternative routes for 

excretion into the gut (salivary excretion or direct transfer across the intestinal wall) has been 

suggested (20). When 4.5-9.0 mg vanadium as diammonium oxytetravanadate was fed daily 

to 16 elderly persons, urinary excretion, although quite variable, amounted to a mean of 5.2% 

of the amount ingested (24). 




Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


Health Effects 


Nutritional studies have shown that vanadium is an essential element for the chick and rat (3). 

Its deficiency may result in growth reduction, impairment of reproduction and disturbances in 

lipid metabolism. Vanadium is also essential for soil nitrogen-fixing microorganisms (3). It 

may play a significant role in human nutrition (2). 

Biochemical, physiological and pharmacological properties of vanadium compounds have 

been reviewed (1,25).  It has been suggested that vanadium may be a regulatory agent for 

enzymatic activities in mammalian tissues. Vanadium is a potent inhibitor of many enzymes, 

while it stimulates adenylate cyclase. It has been shown to inhibit cholesterol biosynthesis 

and lower plasma cholesterol levels. Vanadium can also directly influence glucose 

metabolism  in vitro and may play a role in its regulation. Lipid peroxidation of rat lung 

extracts, liver microsomes and mitochondria was induced by sulfite and accelerated by the 

presence of vanadium compounds. 

Vanadium may play a physiological role as part of a control on levels of the endogenous 

antioxidant, glutathione. This may also be important with respect to toxic interactions of 

chemicals (26). 


Effects on experimental animals 

The toxicity of vanadium has been found to be high when it is given parenterally, low when it 

is orally administered, and intermediate in the case of respiratory exposure. Toxicity is 

related to the valency of the vanadium compound (increasing with increasing valency). 

Vanadium is toxic both as a cation and as an anion (16,27). 

Severe acute exposure (tens of mg/m


) is responsible for systemic effects. Most frequent 

findings in animal experiments were in the liver, kidneys, gonads and the nervous, 

haematological and cardiovascular systems (2,3,16).  However, systemic effects at very low 

levels of exposure were also reported (28).  When rats were continuously exposed to an 

aerosol of vanadium pentoxide at levels of 6 and 27 μg/m

(3.4-15  μg vanadium per m



neurotoxic effects appeared 30 days from the start of exposure. Measured chronaxy ratio 

between the flexor and extensor muscles of the tibia returned to normal about 18 days 

following cessation of exposure. Histopathological changes observed in the liver following 

the higher level of inhalation exposure (27 μg/m

for 70 days) included central vein 

congestion with scattered small haemorrhages, and granular degeneration of hepatocytes. The 

kidneys showed marked granular degeneration of the epithelium of the convoluted tubules. In 

the heart, myocardial vascular congestion was observed, with focal perivascular 


Numerous studies reported acute or chronic respiratory effects in laboratory animals 

following exposure to different vanadium compounds. Respiratory effects in rats at relatively 

low levels of vanadium pentoxide aerosol (3-5 mg/m


) for 2 hours every other day for 3 

months, included perivascular oedema, capillary congestion, haemorrhages, and in some 

cases desquamative bronchitis or pneumonia (29). Similar effects were also observed at much 

lower levels. Rats exposed to vanadium pentoxide aerosol of 27 μg/m


 for 70 days developed 

different respiratory effects, such as marked lung congestion, focal lung haemorrhages and 

extensive bronchitis (28). Exposure to 2 μg vanadium pentoxide per m

was considered to be 

without effect. 

Exposure to vanadium oxides may alter alveolar macrophage integrity and function to the 

detriment of pulmonary defence. Cytotoxicity, tested on rabbit alveolar macrophages in vitro, 

was directly related to solubility in the order V



> V



> VO


. Dissolved vanadium 

pentoxide (6 μg/ml) also reduced phagocytosis (3). The effect of vanadium compounds on the 

function of alveolar macrophages may result in an impairment of the lung’s resistance to 

Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


secondary bacterial infection. 

It has been stated that VOCl

is a mutagen for Escherichia coli and VOC1


, V







are capable of damaging DNA (30).  There is no information that vanadium 

compounds have embryotoxic, teratogenic and carcinogenic effects. 


Effects on humans 

Both acute and chronic poisonings have been described in workers engaged in the industrial 

production and use of vanadium. Most of the reported clinical symptoms reflect irritative 

effects of vanadium on the respiratory  

There is insufficient evidence that vanadium causes generalized systemic effects except at 

extremely high concentrations (3). Several observers described only vague, general signs or 

symptoms and reported nervous disturbances, neurasthenic or vegetative symptoms

occasionally tremors, palpitation of the heart, high incidence of extrasystoles, changes in the 

blood picture (anaemia, leukopenia, punctatebasophilia of the erythrocytes), reduced level of 

cholesterol in the blood, etc. (16). 

Numerous studies have reported acute and chronic respiratory effects mainly due to 

exposure to vanadium pentoxide (2,3,16).  Most of the reported clinical symptoms reflect 

irritative effects of vanadium on the upper respiratory tract. Only at high concentrations 

(above 1 mg vanadium per m


) were more serious effects of the lower respiratory tract 

observed, such as bronchitis and pneumonitis. Respiratory effects after acute or chronic expo-

sure to low levels of vanadium are summarized in Table 1. 

Acute changes in lung function in workers exposed to vanadium compounds during 

cleaning of boilers were reported (time-weighted average concentration of respirable dust 523 



, 15.3% of vanadium, giving a value of 80 μg vanadium per m


(31). In spite of the 

fact that the workers wore respirators, the changes in lung function developed within 24 

hours and pre-exposure levels had not returned by the eighth day; however, the efficacy of 

the respirators was low (about 9% leakage). 

Respiratory effects after acute exposure to vanadium pentoxide dust were also observed 

in a clinical study in which healthy volunteers were exposed to levels of 100, 200 and 1000 

μg vanadium pentoxide per m

for 8 hours (32). It was found that 98% of the particles were 

smaller than 5 μm. Coughing, which persisted for several days, was the most characteristic 

symptom at all three levels of exposure. 

Chronic inhalation of vanadium pentoxide dusts in industry has resulted in rhinitis, 

pharyngitis, bronchitis, chronic productive cough, wheezing, shortness of breath and fatigue. 

Pneumonitis and bronchopneumonitis have also been observed (2,3,16). It has been reported 

that vanadium workers are more susceptible to colds and other respiratory illnesses than 


Respiratory effects after chronic exposure to vanadium pentoxide were described in 

refinery workers (33)  at an average level of 300 μg vanadium per m


 and at a maximum 

concentration of about 1 mg vanadium per m


 (92% of the particles were smaller than 0.5 

μm). In comparison to controls, a statistically significant higher incidence of symptoms, 

described as cough with sputum production, eye, nose and throat irritation, injected pharynx 

and green tongue were reported. 

In workers exposed for several months to vanadium-containing dust in the range of 10-40 

μg vanadium per m


 (concentrations were previously higher, 200-500 μg vanadium per m


), a 

macroscopic and microscopic survey of the upper respiratory tract of 63 males was 

performed (34). The results were compared with a control group of workers exposed to inert 

dust only, and matched for age and smoking habits. Microscopic examination of nasal smears 

revealed a statistically significant increase in neutrophils, and biopsies of nasal mucosa 

showed significantly elevated numbers of plasma and round cells. The histological picture 

Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


was characteristic for an irritating effect of vanadium dust on the mucous membranes seen 

earlier in exposed laboratory animals. 

One study described a significant incidence (58%) of injected pharynx in workers 

engaged in the refining of vanadium pentoxide from soot generated by the combustion of 

heavy fuel-oil (35). Concentrations of vanadium in the air at various locations in the work 

environment were all less than 400 μg/m


, with mean values of 1.2-12.0 μg/m


Vanadium compounds appear to be capable of inducing asthma bronchiale in previously 

nonatopic subjects and continuing manifestations of asthmatic symptoms were reported 8 

weeks after subjects had left the industry (vanadium pentoxide refinery) (36). 

Some epidemiological data have shown positive correlations between the vanadium 

content of urban air and mortality from bronchitis, pneumonia, nephritis, cancer (other than 

lung cancer in males) (37) and “heart disease” (38). However, these analyses did not take into 

account important, probably relevant, factors such as exposure to other chemicals, smoking 

habits, etc. (16). In addition, most of these causes of excess mortality have not been reported 

in workers occupationally exposed to vanadium compounds (3)


Evaluation of Human Health Risks 



The natural background level of vanadium in air has been reported to range from 0.02 to 1.9 



 in Canada (2). Vanadium concentrations recorded in rural areas varied from a few 

nanograms to tenths of a nanogram per m


, and in urban areas from 50 to 200 ng/m


. In big 

cities during winter, when high-vanadium fuel-oil was used for heating purposes, 

concentrations as high as 2000 ng/m


 have been reported. Air pollution by industrial plants 

may be less than that caused by power stations and heating equipment. 

The concentrations of vanadium in workplace air (0.01-60 mg/m


) are much higher than 

in the general environment. 


Health risk evaluation 

The acute and chronic effects of vanadium exposure on the respiratory system of 

occupationally exposed workers should be regarded as the most significant factors when 

establishing air quality guidelines. Most of the clinical symptoms reported reflect irritative 

effects of vanadium on the upper respiratory tract, except at higher concentrations (above 1 

mg vanadium per m


), when more serious effects on the lower respiratory tract are observed. 

Clinical symptoms of acute exposure are reported (31) in workers exposed to concentrations 

ranging from 80 μg/m


 to several mg vanadium per m


, and in healthy volunteers (32) 

exposed to concentrations of 56-560 μg vanadium per m


 (Table 1). 


A study of occupationally exposed groups provides data reasonably consistent with those 

obtained from controlled acute human exposure experiments, suggesting that the lowest-

observed-adverse-effect level for acute exposure can be considered to be 60 μg vanadium per 



Chronic exposure to vanadium compounds revealed a continuum in the respiratory 

effects, ranging from slight changes in the upper respiratory tract, with irritation, coughing 

and injection of pharynx, detectable at 20 μg vanadium per m


, to more serious effects such 

as chronic bronchitis and pneumonitis, which occurred at levels above 1 mg/m


. Occupational 

studies illustrate the concentration-effect relationship at low levels of exposure (33-35)

showing increased prevalence of irritative symptoms of the upper respiratory tract; this 

suggests that 20 μg vanadium per m


 can be regarded as the lowest-observed-adverse-effect 

level for chronic exposure (Table 1). There are no conclusive data on the health effects of 

Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


exposure to airborne vanadium at present concentrations in the general population, and a sus-

ceptible subpopulation is not known. However, vanadium is a potent respiratory irritant, 

which would suggest that asthmatics should be considered a special group at risk. 

There are no well documented animal data to support findings in human studies, although 

one study reported systemic and local respiratory effects in rats at levels of 3.4-15 μg/m





Available data from occupational studies suggest that the lowest-observed-adverse-effect 

level of vanadium can be assumed to be 20 μg/m


, based on chronic upper respiratory tract 

symptoms. Since the adverse nature of the observed effects on the upper respiratory tract 

were minimal at this concentration and a susceptible subpopulation has not been identified, a 

protection factor of 20 was selected. It is believed that below 1 μg/m


 (averaging time 24 

hours) environmental exposure to vanadium is not likely to have adverse effects on health. 

The available evidence indicates that the current vanadium levels generally found in 

industrialized countries are not in the range associated with potentially harmful effects. 


Table 1. Respiratory effects after acute and chronic exposures to low levels of vanadium 


Type of exposure 



Concentration in μg/m

Symptoms Reference 



Compound Vanadium  








Boiler cleaning 











Changes in parameters of lung 



Clinical study 

(experimental 8-

hour exposure) 








1000 560 



persistent and frequent cough, 

expiratory wheezes 










Persistent cough (7- 1 0 days) 










Slight cough for 4 days 








Vanadium refinery 






Respiratory irritation: cough, 

sputum, nose and throat 

irritation, injected pharynx 


Vanadium refinery 






Irritative changes of mucous 

membranes of upper 

respiratory tract 













1.2-12.0  Respiratory irritation: injected 








1.  Erdmann, E. et al. Vanadate and its significance in biochemistry and pharmacology. 

Biochemical pharmacology, 33: 945-950 (1984). 

2.  Committee on Biologic Effects of Atmospheric Pollutants.  Vanadium. Washington, 

DC, National Academy of Sciences, 1974. 

3.  Waters, M.D. Toxicology of vanadium. In: Goyer, R.A. & Mehlman, M.A., ed. Advances 

in modern toxicology. Vol. 2. Toxicology of trace elements. New York, Wiley, 1977, pp. 


4.  Bengtsson, S. & Tyler, G. Vanadium in the environment. London, University of London 

Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 


Monitoring and Assessment Research Centre, 1976 (MARC Report No. 2). 

5.  Mineral commodity summaries. Washington, DC, US Department of the Interior, Bureau 

of Mines, Division of Ferrous Metals, 1983. 

6.  Galloway, J.N. et al., ed.  Toxic substances in atmospheric deposition: a review and 

assessment. 1980 (National Atmospheric Deposition Program Report NC-141). 

7.  Anderson, D.  Emission factors for trace substances. Research Triangle Park, NC, US 

Environmental Protection Agency, 1973 (Report No. EPA-450/2-73-001). 

8.  Davies, D.J.A. & Bennett, B.G.  Exposure commitment assessments of environmental 

pollutants. London, University of London Monitoring Assessment and Research Centre, 

1983, Vol. 3 (MARC Report No. 30). 

9.  Scientific and technical assessment report on vanadium. Washington, DC, US 

Environmental Protection Agency, 1977 (Report No. EPA-600/6-77-002). 

10. Kretzschmar, J.D. et al. Heavy metal levels in Belgium: a five-year survey. Science of 

the total environment, 14: 85-97 (1980). 

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Chapter 6.12  Vanadium 


Air Quality Guidelines - Second Edition


 WHO Regional Office for Europe, Copenhagen, Denmark, 2000 



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