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EC number: 246-805-2
CAS number: 25306-75-6
Biotransformation to CS2
Sodium isobutyl xanthate readily decomposes to carbon disulphide,
especially in the presence of moisture/water. Therefore, the health
effects of carbon disulphide (CS2) need to be considered in the
assessment of sodium isobutyl xanthate.
Xanthates are metabolised in humans and animals to CS2. Animal data for
xanthates indicate that up to 7% of dose may be eliminated
as CS2 in breath. The elimination vs time curves for sodiumisobutylxanthate
in humansand guinea pigs indicate that biotransformation to CS2
is not saturated at dosesstudied (250 mg or 3.5 mg/kg in humans).
It is known that sodium isobutyl xanthate is metabolised to
CS2 due to the presenceof the CS2/cysteine (glutathione) conjugation
product, 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine of exposed
Carbon disulfide and/or its
metabolite 2-thiothiazolidine-4-carboxylic acid (TTCA) have been
measured at part-per-billion levels in virtually all samples of breath,
blood, urine or breast milk of subjects with no known occupational
exposure in a number of studies (Pellizzari et al., 1982; Phillips,
1992; Brugnone et al., 1994). This provides support for the data on
levels in environmental media, which indicate that humans have
environmental exposure to carbon disulfide.
A single metabolism study (in French) published by Merlevede and Peters
(1965)was identified.In this study, humans and guineapigs
were dosed with various xanthate compounds, including sodium andpotassiumisobutylxanthate,
and the amount of expired CS2 monitored.
Following sub-cutaneous injection (70-200 mg/kg) of potassium ethyl
xanthate inguinea pigs, up to 7% of the dose was expired as CS2 after 8
h, with maximumelimination between 1 - 2 h in most animals. The rate of
elimination was doserelated,however the total percentage recovered was
independent of dose. A morerapid rate of elimination was seen following
sub-cutaneous injection (50 and 100mg/kg) of sodium ethyl xanthate, with
CS2 expiration complete after 6 h, withmaximum elimination at 1 h (total
recovery of CS2 was not reported).
Following oral intake in human volunteers, of 150 and 250 mg sodium
ethylxanthate, a maximum rate (13 – 57 μg/m3/h) of CS2 elimination in
breath wasseen between 1-2 h, with complete elimination by 6 h (total
recovery of CS2 wasnot reported).
The effect of alcohol on xanthate metabolism was also studied. In guinea
pigs,concomitant sub-cutaneous injection of sodium diethyl xanthate and
alcoholresulted in an increased rate of elimination, together with a
greater total recoveryof CS2. These increases were directly related to
the dose of alcohol.
An increased rate of elimination was also apparent in humans
administered 250 mg sodium ethyl xanthate, following intake of 200 ml of
alcohol (approximately18% by volume), however, the lack of a suitable
control group preventedquantitative assessment.
It is generally considered that adverse effects from exposure to
xanthates (inhumans and animals) are associated with CS2 toxicity. It is
not known what contribution to human toxicity is likely from
inhalation/dermal absorption of CS2per se, as a xanthate
decomposition product, and CS2 as a xanthate metabolite.
Effects due to the parent xanthate compound or other metabolites might
also contribute to overall toxicity.
If metabolism to CS2 is associated with critical effects, then the
limited data available on xanthate metabolism indicates that similar
toxicological profiles might be expected for animals and humans.
Animal and human studies indicate that the nervous system is the
critical targetorgan for CS2 from inhalation exposure. Apparently only
one chronic inhalation study has been carried out in animals for CS2 and
there are no chronic animal orhuman data pertaining to neurological
effectsfollowing dermal exposure(ATSDR 1996).
Notwithstanding the available epidemiological data, it has generally
been considered that chronic adverse effects in humans from inhalation
exposure toCS2 are associated with levels in excess of 10 ppm2, although
further, morerefined dose-response data is required in order to fully
characterise chronicNOAELs or LOAELs.
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