Tungsten - Toxicology of Metals - page 855

performed on 255 workers exposed to hard-metal
dust. This showed only slight changes in several of the
workers and yielded one of the six cases described pre-
viously. Airborne dust concentrations at the time of the
survey were of the order of 0.30 mg/m 3 for particles
less than 5-

was observed in workers manufacturing hard met-
als exposed simultaneously to tungsten carbide and
cobalt, confounding by smoking was considered to be
unlikely (Moulin et al ., 1998).
This excess mortality occurred mostly in workers
exposed to unsintered hard-metal dust (Wild et al .,
2000). Tungsten carbide is bioavailable despite its low
solubility; the bioavailability of tungsten increased in
the order tungsten metal, tungsten carbide, and tung-
stenate, where wet grinding is carried out. In a bio-
logical monitoring study in hard-metal workers, the
highest tungsten concentrations in urine were found in
grinders exposed to tungstenate, with high concentra-
tions also in departments producing tungsten carbide
and heavy alloys (Kraus et al ., 2001).

m projected diameter. Gravimetric sam-
ples taken in the sieving room showed 90% tungsten
and 6% cobalt in the incombustible fraction. It was
concluded that the cause of hard-metal disease was the
inhalation of dust from the working environment, but
that the responsible component was likely to be cobalt
rather than tungsten. The absence of cobalt from the
lungs of hard-metal workers, which contained both
tungsten and titanium, was attributed to the high
solubility of cobalt in plasma. In a later report, Bech
(1974) described a total of 12 cases of hard-metal dis-
ease. Interstitial fi brosis was present in the lungs of all
seven who died; emphysema was found in six of these.
It was suggested that hypersensitivity to cobalt was
involved in the development of the disease and that
in early cases the disease may be arrested by removal
from exposure. Although hard-metal disease was con-
sidered to be related to cobalt exposure, Bech (1974)
suggested that tungsten carbide might enhance the
solubility of cobalt in protein-containing fl uid.
Coates and Watson (1971) described 12 cases, includ-
ing 8 deaths, of diffuse interstitial pulmonary fi brosis
in workers processing tungsten carbide. The clinical
picture was one of nonproductive cough, exertional
dyspnea, and weight loss.
Respiratory function tests showed a restrictive pat-
tern with an abnormality of gas transfer. The radiologi-
cal appearances were characterized by progressive,
bilateral nodular, and linear shadowing involving
major portions of both lungs. Detailed histological
examination of three cases (Coates and Watson, 1973)
showed deposits of collagen and elastic tissue in the
septal areas and alteration of the alveolar lining cells
(modifi ed type-l pneumocytes) with swelling and for-
mation of microvilli. Unidentifi ed, hard, multifaceted
crystals were present in the affected areas of the lung.
These authors, too, attributed the condition to the inha-
lation of cobalt-containing dust.
A cohort of male tungsten miners was included in a
Chinese study. The risk of silicosis at comparable silica
dust exposures, was clearly higher among tungsten
miners (cumulative risk, CR = 0.964) compared with
cohorts of tin miners (CR = 0.901) and pottery workers
(CR = 0.225) (Chen et al ., 2005).
An increased mortality from lung cancer was
observed among the hard-metal workers in three
Swedish factories (Hogstedt and Alexandersson, 1990)
and one French factory (Lasfargues et al ., 1994). Sta-
tistically signifi cant increased lung cancer mortality

µ

7.2 Systemic Effects and Dose-Response
Relationships
Tungsten has not been shown to be an essential trace
metal in either animal or plant metabolism.

7.2.1 Animals

In a series of feeding experiments, young rats were
fed for a period of 70 days with different concentra-
tions of sodium tungstate, tungstic oxide, and ammo-
nium paratungstate mixed in Purina dog chow (Kinard
and Van de Erve, 1941). Sodium tungstate, equivalent
to 2% W, tungstic oxide equivalent to 3.96% W, and
ammonium paratungstate equivalent to 5% W were
markedly toxic, causing initial weight loss followed
by the deaths of all animals in each group within 10
days. In diets having an equivalent of 0.5% W, sodium
tungstate and tungstic oxide produced death in three
quarters of the rats, whereas ammonium paratung-
state produced no fatalities. The same authors (1943) in
similarly designed feeding experiments administered
2, 5, and 10% tungsten metal powder over 70 days and
found no effect on weight gain in male rats, but a 15%
reduction in females.
In an extensive live-term study, Schroeder and
Mitchener (1975) added 5 mg/L as sodium tungstate
to the drinking water of rats. At this dose level, there
was little detectable effect as measured by serum cho-
lesterol, glucose, uric acid, and incidence of tumor for-
mation. However, a slight enhancement of growth was
seen in rats of both sexes, and a small but signifi cant
shortening of longevity was noticed in the tungsten-
dosed male rats.
Tungstic acid has been used to produce experimen-
tal epilepsy in laboratory animals (Kusske et al ., 1974).
In a series of cats, 0.02 mL of tungstic acid gel applied
to the surface of the cortex gave rise to abnormal EEG