Vanadium pentoxide

(b)

Studies of workers exposed to vanadium

There is an extensive published literature concerning the development of ‘boiler-

makers bronchitis’ in persons cleaning boilers in which fuel oils containing high concen-

trations of vanadium were used (Hudson, 1964; Levy et al., 1984). The clinical picture is

characterized by dyspnoea which is largely reversible. Levy et al. (1984) studied 100

workers exposed to vanadium pentoxide (0.05–5.3 mg/m

3

) during the conversion of a

utility company power plant and found severe respiratory tract irritation in 74 individuals.

Expiratory flow rates and forced vital capacity were decreased in about 50% of a sub-

sample (35 individuals) of the workers studied. 

Eye irritation has been reported in workers exposed to vanadium (Lewis, 1959; Zenz

et al., 1962; Lees, 1980; Musk & Tees, 1982). Skin patch testing in workforces produced

two isolated reactions (but none in unexposed volunteers; see Section 4.2.1). The under-

lying reason for the skin responses in these workers is unclear (Motolese et al., 1993).

Lewis (1959) investigated 24 men exposed to vanadium pentoxide for at least 6 months

from two different centres, and age-matched with 45 control subjects from the same areas.

Exposure to vanadium pentoxide was between 0.02 and 0.92 mg/m

3

. In the exposed group,

62.5% complained of eye, nose, and throat irritation (6.6% in control), 83.4% had a cough

(33.3% in control), 41.5% produced sputum (13.3% in control), and 16.6% complained of

wheezing (0% in control). Physical findings included wheezes, rales, or rhonchi in 20.8%

(0% in controls), hyperaemia of the pharynx and nasal mucosa in 41.5% (4.4% in controls),

and ‘green tongue’ in 37.5% (0% in controls).

Zenz et al. (1962) reported on 18 workers exposed to varying concentrations of vana-

dium pentoxide dust (mean particle size, < 5

µm) in excess of 0.5 mg/m

3

during a pelle-

tizing process. Three of the men most heavily exposed developed symptoms, including

sore throat and dry cough. Examination of each on the third work day revealed markedly

inflamed throats and signs of intense persistent coughing, but no evidence of wheezing.

The three men also reported ‘burning eyes’ and physical examination revealed slight con-

junctivitis. Upon resumption of work after a 3-day exposure-free period, the symptoms

returned within 0.5–4 h, with greater intensity than before, despite the use of respiratory

protective equipment. After the process had been operating for 2 weeks, all 18 workers,

including those primarily assigned to office and laboratory duties, developed symptoms

and signs to varying degrees, including nasopharyngitis, hacking cough, and wheezing.

This study confirms that vanadium pentoxide exposure can produce irritation of the eye

and respiratory tract.

Lees (1980) reported signs of respiratory irritation (cough, respiratory wheeze, sore

throat, rhinitis, and nosebleed) and eye irritation in a group of 17 boiler cleaners. As there

was no control group and it was unclear whether there was exposure to compounds other

than vanadium, no conclusions can be drawn regarding the cause or significance of these

symptoms. However, the findings are compatible with those of other studies on inhalation

of vanadium pentoxide. 

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Huang et al. (1989) conducted a clinical and radiological investigation of 76 workers

who had worked in a ferrovanadium factory for 2–28 years. In the exposed group, out of

71 workers examined, 89% had a cough (10% in controls), expectoration was seen in 74%

(15% in controls), 38% were short of breath (0% in controls), and 44% had respiratory

harshness or dry sibilant rale (0% in controls). In 66 of the exposed group examined,

hyposmia or anosmia was reported in 23% (5% in controls), congested nasal mucosa in

80% (13% in controls), erosion or ulceration of the nasal septum in 9% (0% in controls),

and perforation of the nasal septum in one subject (1.5%) (0 in controls). Chest radiographs

of all 76 exposed subjects revealed 68% with increased, coarsened, and contorted broncho-

vascular shadowing (23% in controls). [While exposure to vanadium compounds may have

contributed to the clinical findings and symptoms reported, no firm conclusion can be

drawn from this study in this regard, as mixed exposures are likely to have occurred.]

A prospective study (Hauser et al., 1995a) of pulmonary function in 26 boiler workers

exposed to fuel oil ash showed decreased FEV

1

(forced expiratory volume in 1 s) values

which were associated with PM

10

exposure but not with vanadium exposure. There was no

post-exposure change in non-specific airway responsiveness. Hauser et al. (1995b) used

nasal lavage analysis to study upper airway responses in 37 utility workers exposed to fuel

oil ash. Responses were examined in relation to vanadium concentrations and PM

10

particles using personal samplers. A significant increase in polymorphonuclear cells in

nasal lavage was observed in samples from nonsmokers but not in smokers, suggesting that

exposure to vanadium dust is associated with upper airway inflammation. In both non-

smokers and smokers, a dose–response relationship between adjusted polymorphonuclear

cell count and either PM

10

or respirable vanadium dust exposure could not be found.

Woodin et al. (1998) studied the effects of vanadium exposure/PM

10

concentrations

in 18 boilermakers engaged in a utility boiler conversion; 11 utility workers acted as

controls. The nasal lavage technique was used at various time points and interleukins (IL-

6, IL-8), eosinophilic cationic protein (ECP) and myeloperoxidase (MPO) were investi-

gated as biomarkers. Increases were observed in IL-8 and MPO concentrations but not IL-

6 and ECP concentrations, in the exposed workers. The authors concluded that the

changes observed in the upper airways were related to increased PM

10

and upper airway

vanadium concentrations. Subsequent studies in workers exposed to vanadium-rich fuel-

oil ash (Woodin et al., 2000) also demonstrated lower (72% versus 27% for controls) and

upper (67% versus 36% for controls) airway symptoms. 

While the majority of the above studies have noted reversibility of these acute pulmo-

nary effects, asthma [now possibly labelled ‘reactive airways disfunction syndrome’] has

been reported to develop as a sequela to high, acute exposure to vanadium in some exposed

workers (Musk & Tees, 1982). 

(c)

Environmental exposure 

A single epidemiological study has been conducted (Lener et al., 1998) assessing indi-

vidual exposure in the general population to dusts generated by a plant processing vana-

dium-rich slag. It was estimated that an area with a radius of 3 km was exposed to the dust

VANADIUM PENTOXIDE

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