| 1.1 Substance|
| 1.2 Group|
| 1.3 Synonyms|
| 1.4 Identification numbers|
| 1.4.1 CAS number|
| 1.4.2 Other numbers|
| 1.5 Main brand names, main trade names|
| 1.6 Main manufacturers, main importers|
| 2.1 Main risks and target organs|
| 2.2 Summary of clinical effects|
| 2.3 Diagnosis|
| 2.4 First-aid measures and management principles|
|3. PHYSICO-CHEMICAL PROPERTIES|
| 3.1 Origin of the substance|
| 3.2 Chemical structure|
| 3.3 Physical properties|
| 3.3.1 Colour|
| 3.3.2 State/form|
| 3.3.3 Description|
| 3.4 Hazardous characteristics|
| 4.1 Uses|
| 4.1.1 Uses|
| 4.1.2 Description|
| 4.2 High risk circumstances of poisoning|
| 4.3 Occupationally exposed populations|
|5. ROUTES OF ENTRY|
| 5.1 Oral|
| 5.2 Inhalation|
| 5.3 Dermal|
| 5.4 Eye|
| 5.5 Parenteral|
| 5.6 Others|
| 6.1 Absorption by route of exposure|
| 6.2 Distribution by route of exposure|
| 6.3 Biological half-life by route of exposure|
| 6.4 Metabolism|
| 6.5 Elimination by route of exposure|
| 7.1 Mode of Action|
| 7.2 Toxicity|
| 7.2.1 Human data|
| 22.214.171.124 Adults|
| 126.96.36.199 Children|
| 7.2.2 Relevant animal data|
| 7.2.3 Relevant in vitro data|
| 7.2.4 Workplace standards|
| 7.2.5 Acceptable daily intake (ADI) and other guideline levels|
| 7.3 Carcinogenicity|
| 7.4 Teratogenicity|
| 7.5 Mutagenicity|
| 7.6 Interactions|
|8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS|
| 8.1 Material sampling plan|
| 8.1.1 Sampling and specimen collection|
| 188.8.131.52 Toxicological analyses|
| 184.108.40.206 Biomedical analyses|
| 220.127.116.11 Arterial blood gas analysis|
| 18.104.22.168 Haematological analyses|
| 22.214.171.124 Other (unspecified) analyses|
| 8.1.2 Storage of laboratory samples and specimens|
| 126.96.36.199 Toxicological analyses|
| 188.8.131.52 Biomedical analyses|
| 184.108.40.206 Arterial blood gas analysis|
| 220.127.116.11 Haematological analyses|
| 18.104.22.168 Other (unspecified) analyses|
| 8.1.3 Transport of laboratory samples and specimens|
| 22.214.171.124 Toxicological analyses|
| 126.96.36.199 Biomedical analyses|
| 188.8.131.52 Arterial blood gas analysis|
| 184.108.40.206 Haematological analyses|
| 220.127.116.11 Other (unspecified) analyses|
| 8.2 Toxicological Analyses and Their Interpretation|
| 8.2.1 Tests on toxic ingredient(s) of material|
| 18.104.22.168 Simple Qualitative Test(s)|
| 22.214.171.124 Advanced Qualitative Confirmation Test(s)|
| 126.96.36.199 Simple Quantitative Method(s)|
| 188.8.131.52 Advanced Quantitative Method(s)|
| 8.2.2 Tests for biological specimens|
| 184.108.40.206 Simple Qualitative Test(s)|
| 220.127.116.11 Advanced Qualitative Confirmation Test(s)|
| 18.104.22.168 Simple Quantitative Method(s)|
| 22.214.171.124 Advanced Quantitative Method(s)|
| 126.96.36.199 Other Dedicated Method(s)|
| 8.2.3 Interpretation of toxicological analyses|
| 8.3 Biomedical investigations and their interpretation|
| 8.3.1 Biochemical analysis|
| 188.8.131.52 Blood, plasma or serum|
| 184.108.40.206 Urine|
| 220.127.116.11 Other fluids|
| 8.3.2 Arterial blood gas analyses|
| 8.3.3 Haematological analyses|
| 8.3.4 Interpretation of biomedical investigations|
| 8.4 Other biomedical (diagnostic) investigations and their interpretation|
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations|
| 8.6 References|
|9. CLINICAL EFFECTS|
| 9.1 Acute poisoning|
| 9.1.1 Ingestion|
| 9.1.2 Inhalation|
| 9.1.3 Skin exposure|
| 9.1.4 Eye contact|
| 9.1.5 Parenteral exposure|
| 9.1.6 Other|
| 9.2 Chronic poisoning|
| 9.2.1 Ingestion|
| 9.2.2 Inhalation|
| 9.2.3 Skin exposure|
| 9.2.4 Eye contact|
| 9.2.5 Parenteral exposure|
| 9.2.6 Other|
| 9.3 Course, prognosis, cause of death|
| 9.4 Systematic description of clinical effects|
| 9.4.1 Cardiovascular|
| 9.4.2 Respiratory|
| 9.4.3 Neurological|
| 18.104.22.168 CNS|
| 22.214.171.124 Peripheral nervous system|
| 126.96.36.199 Autonomic nervous system|
| 188.8.131.52 Skeletal and smooth muscle|
| 9.4.4 Gastrointestinal|
| 9.4.5 Hepatic|
| 9.4.6 Urinary|
| 184.108.40.206 Renal|
| 220.127.116.11 Others|
| 9.4.7 Endocrine and reproductive systems|
| 9.4.8 Dermatological|
| 9.4.9 Eye, ears, nose, throat: local effects|
| 9.4.10 Haematological|
| 9.4.11 Immunological|
| 9.4.12 Metabolic|
| 18.104.22.168 Acid-base disturbances|
| 22.214.171.124 Fluid and electrolyte disturbances|
| 126.96.36.199 Others|
| 9.4.13 Allergic reactions|
| 9.4.14 Other clinical effects|
| 9.4.15 Special risks|
| 9.5 Others|
| 9.6 Summary|
| 10.1 General principles|
| 10.2 Life supportive procedures and symptomatic treatment|
| 10.3 Decontamination|
| 10.4 Enhanced elimination|
| 10.5 Antidote treatment|
| 10.5.1 Adults|
| 10.5.2 Children|
| 10.6 Management discussion|
|11. ILLUSTRATIVE CASES|
| 11.1 Case reports from literature|
|12. ADDITIONAL INFORMATION|
| 12.1 Specific preventive measures|
| 12.2 Other|
|14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES|
International Programme on Chemical Safety
Poisons Information Monograph 102
Inorganic carbon compound
solfuro di carbonio,
sulfure de carbone,
1.4 Identification numbers
1.4.1 CAS number
1.4.2 Other numbers
EPA Pesticide chemical code: 016401
UN Hazard class: 3 (flammable liquids)
UN Pack Group: I
UN subsidiary risks: 6.1 (poisonous substance)
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
It is widely produced by many chemical companies.
2.1 Main risks and target organs
Acute toxic effects include central nervous system
depression, peripheral neuropathy and cardiovascular
collapse. Dyspnoea and respiratory failure may occur
following exposure to high concentration. Carbon disulphide
is irritant to eyes and skin and may cause corneal erosions
and chemical burns respectively. Chronic exposure may cause
neuropsychiatric disorders, peripheral neuropathies and
increased risk of atheroma.
2.2 Summary of clinical effects
Acute carbon disulphide poisoning is rare but very
dangerous. Absorption occurs through the skin, by ingestion
or by inhalation. In severe poisoning, the patient rapidly
becomes comatose and death occurs in a few hours, usually due
to respiratory depression and convulsions.
In less severe cases local irritation, nausea, vomiting and
abdominal pain are followed by headache, euphoria,
hallucinations, manic delirium, paranoid reactions and
Chronic occupational exposure is more common. After 10 -15
years it may cause sensory and motor neuropathy,
neuropsychiatric changes and parkinsonism. Atherosclerosis,
in particular coronary heart disease, impaired vision
(perception of coloured rings around lights and retinal
changes), renal and hepatic damage, and permanent impairment
of reproductive function also occur after long-term
exposures. In addition, sleep disturbance, fatigue, anorexia
and weight loss are common complaints among exposed workers.
Local contact may result in irritation, burning sensation,
blistering or deep burns. Conjunctivitis, pain and blurred
vision result from exposure of the eyes to the vapour, and
severe irritation or burns occur after direct contact.
The diagnosis is made on the history of exposure and the
presence of clinical effects. In acute poisoning by
ingestion, there may be nausea, vomiting and abdominal pain
followed by headache, euphoria, hallucinations, manic
delirium, dyspnoea, cyanosis, peripheral vascular collapse,
convulsions and coma.
Carbon disulphide can be measured in blood, urine and breath
but this is not useful in the management of poisoning.
Dithiocarbamine (DTS) may also be measured in urine.
In chronic occupational exposure, the diagnosis is made from
the presence of sensory and motor neuropathy,
neuropsychiatric changes, parkinsonism, renal and hepatic
damage, sleep disturbance, fatigue, anorexia and weight
2.4 First-aid measures and management principles
Remove patient to fresh air if carbon disulphide is
inhaled. In cases of ingestion do not induce vomiting.
Perform gastric aspiration or lavage if the toxin was
recently ingested. Wash contaminated skin with soap and
water. Irrigate contaminated eyes copiously with water.
In case of severe poisoning, support respiration, administer
oxygen and monitor cardiovascular function.
There is no specific antidote. Give symptomatic and
supportive treatment as required.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Carbon disulfide was formerly manufactured by direct
reaction of sulphur vapour and coke in iron or steel retorts
at 750 - 1000°C but, since the early 1950's, the preferred
method of synthesis has been the catalyzed reaction between
sulphur and methane:
CH4 + S CS2 + 2H2S
(Greenwood & Earnshaw, 1984)
Carbon disulfide is a natural product of anaerobic
biodgradation. In nature, minute amounts occur in coal tar
and in crude petroleum (Merck, 1979). Other sources include
animal waste, in particular pig urine and faeces, fish
processing, plastic and refuse combustion, synthetic fibre
and starch manufacture, turbines, natural gas and
3.2 Chemical structure
CS2 S = C = S
Molecular weight: 76.14
3.3 Physical properties
Pure carbon disulfide is a clear colourless,
highly refractive, mobile, volatile, very flammable
liquid. The pure liquid has a rather pleasant
ethereal odour, while the usual commercial and reagent
grades are yellowish and foul smelling (decaying
radishes). Decomposes on prolonged standing.
Boiling point: 46.5°C at atmospheric pressure
Melting point: -111.6°C
Flash point: -30°C (closed cup)
Explosive limits: lower 1.0%, upper 50.0% vol/vol
Carbon disulfide is spontaneously flammable at
Can be ignited by hot steam pipes (Merck)
It burns with a blue flame to carbon dioxide and
Density (liquid): 1.2632 at 20°C
Vapour density: 2.67 (air = 1)
Solubility in water at 20°C: 0.294 g/100 ml
Solubility of water in carbon disulfide: 0.005%
Miscible with anhydrous methanol, ethanol, ether,
benzene, chloroform, carbon tetrachloride, oils.
Azeotrope with water, boiling point 42.6°C, contains
97.2% carbon disulfide
Can be stored in iron, aluminium, glass, porcelain,
Teflon (Merck, 1989).
Fats and lipids are soluble in carbon disulfide and it
is also a solvent for waxes, lacquers, camphor, resins
and vulcanized rubber.
Carbon disulfide undergoes slow decomposition in
3.4 Hazardous characteristics
The vapour is denser than air and therefore sinks to the
ground. Carbon disulfide dissolves phosphorous, sulphur,
selenium, bromine, iodine, fats, resins and rubber (Merck)
(check limit in detection and development on
The principal industrial uses of carbon
disulfide are the manufacture of viscose rayon,
cellophane film, carbon tetrachloride and
xanthogenates and electronic vacuum tube (Greenwood &
Earnshaw, 1984 & Merck Index 1989).
Carbon disulfide is also used as an insecticide for
the fumigation of grains, nursery stock, in fresh
fruit conservation and as a soil disinfectant against
insects and nematodes (British Crop Protection
Council, 1987).Carbon disulfide is a solvent for
phosphorous, sulfur, selenium, bromine, iodine, fats,
resins, rubber (Merck, 1987).
Used for fumigation in airtight storage warehouses,
airtight flat storages, bins, grain elevators,
railroad box cars, shipholds, barges and cereal
4.2 High risk circumstances of poisoning
Accidental ingestion or inhalation of carbon disulfide
occurs usually in an industrial setting.
4.3 Occupationally exposed populations
Carbon disulfide is typically an industrial chemical and
exposure is almost exclusively confined to occupational
situations. In theory, any worker engaged in processes using
carbon disulfide may be exposed to some degree. However, in
practice, only workers in the viscose rayon industry are
exposed to concentrations high enough to have deleterious
effects on health.
For every kilogram of viscose used, about 20 - 30 g of carbon
disulfide and 4 - 6 g of hydrogen sulfide will be emitted.
About 0.6 - 1.0 kg of viscose is used per hour in the
different processes involved in the production of textile
yarn. However, exposure to carbon disulfide is usually
highest in connection with the production of staple fibre and
cellophane, where the equivalent amounts of viscose used are
approximately 70 - 100 kg and 1,800 - 2,000 kilograms per
hour respectively (WHO, 1979).
Some cases of acute exposure have occurred during the process
of tank cleaning, in spills and fires involving the product
5. ROUTES OF ENTRY
Poisoning by ingestion is uncommon.
Inhalation is the commonest route of absorption of
carbon disulphide in man.
Skin contact is a significant route of absorption,
although much less important than inhalation.
No data available.
No data available.
No data available.
6.1 Absorption by route of exposure
Inhalation represents the main route of absorption; in
man, an equilibrium between the carbon disulphide
concentration in inhaled and exhaled air is reached during
the first 60 minutes of exposure. The percentage retained at
equilibrium appears to be about 40 - 50% of the amount of
carbon disulphide in the inhaled air and depends on both the
concentration of carbon disulphide in the air and the
partition coefficient between blood and tissues. This
percentage is lower in continuously exposed workers than in
volunteers exposed for the first time to carbon disulphide
Concentrations of 1 - 1.2 mg/L (320 - 390 ppm) are bearable
for several hours, but headaches and unpleasant feeling
appear after 8 hours. At 3.6 mg/L (1,150 ppm) giddiness sets
in, and mild intoxication occurs after exposure for 30 min -
1 hour to 6.4 - 10 mg/L (2,000 - 3,200 ppm). At
concentrations over 15 mg/L (4,800 ppm) unconsciousness
occurs after several inhalations (ILO, 1983).
Carbon disulphide can be absorbed through the skin and this
has been confirmed in a number of studies. The rate of
absorption is proportional to its the concentration. It was
estimated that immersion of one hand for one hour in a
washing bath solution containing 0.1 mg/L carbon disulphide
at a viscose rayon plant resulted in the absorption of 17.5
mg of carbon disulphide (CEC, 1988).
Ingestion is rare, but may cause serious toxicity.
6.2 Distribution by route of exposure
Carbon disulphide is distributed in the blood stream;
and the erythrocyte:plasma ratio is 2:1. It is rapidly
cleared from the blood compartment and because of this the
determination of carbon disulphide in blood is not a useful
test in exposure.
Carbon disulphide can exist in both "free" and 'bound' forms
to plasma proteins, the bound form is the fraction that has
reacted with amino acids to give thiocarbamates (in a
reversible reaction). "Free" carbon disulphide is rapidly
eliminated and is usually undetectable.
These two forms of carbon disulphide and different tissue
affinities may explain the conflicting clinical reports (WHO,
6.3 Biological half-life by route of exposure
Carbon disulphide disappears very rapidly from the
blood. The partition coefficient is 2.8 (air:blood). The
plasma elimination half-life is about 1 hour (WHO,
Around 70 - 90% of the retained carbon disulphide is
metabolized and excreted in the urine. Carbon disulphide
undergoes microsomal hepatic metabolism, with subsequent
conjugation. Some of the metabolites detected in the urine
are thiourea (the most important) and mercaptothiazoline and
2-mercapto-thiazoline-4-carbonic acid, but there appears to
be a poor correlation between the amount of metabolites and
the degree of exposure.
6.5 Elimination by route of exposure
Exhalation is the primary route of excretion of
unmetabolized carbon disulphide; 10 - 30% of the amount
absorbed is exhaled. Less than 1% is excreted unchanged in
the urine and 70 - 90% undergoes metabolism and excretion
(CEC, 1988). Respiratory elimination takes place in 3 phases:
a first phase of rapid elimination of the carbon disulphide
absorbed on the mucosa of the lungs and upper respiratory
tract; secondly, a slower phase, with exhalation of carbon
disulphide released from the blood, and thirdly, a very slow
phase, where carbon disulphide released from tissues and
organs is exhaled. Animal studies show that carbon disulphide
undergoes desulphuration and the released carbon is exhaled
as carbon dioxide.
Small quantities of carbon disulphide are excreted in saliva,
sweat and through the skin of exposed workers. Elimination of
carbon disulphide in faeces is negligible (WHO, 1979).
7.1 Mode of Action
Carbon disulphide reacts with a variety of nucleophilic
compounds in the body, characterized by the presence of a
functional group with a free pair of electrons in the
molecule (mercapto-, amino-, hydroxyl-). The majority of
biochemically important compounds (e.g. pyridoxamine,
cerebral monoamine oxidases, dopamine carboxylases, amino
acids, biogenic amines and sugars) contain nucleophilic
groups and may react with carbon disulphide. Thus, a number
of possible mechanisms for the effects of carbon disulphide
have been postulated:
- acute CNS toxicity and peripheral neurotoxicity may be
attributed to the formation of dithiocarbamates (CEC,
- non-enzymatic reaction of carbon disulphide with free
amino groups indicates possible reaction with
macromolecules such as enzymes, structural proteins,
polypeptides and nucleic acids (CEC, 1988).
- the chelating effect of carbon disulphide metabolites
(dithiocarbamates) on various essential metals,
required for the functioning of enzymes (e.g. zinc and
copper); the neurotoxic action of carbon disulphide
could easily be explained by chelating effects on both
metals (WHO, 1979).
- an effect of carbon disulphide on enzymatic systems:
acute oral chronic exposures of animals to carbon
disulphide result in changes of mitochondrial
respiration and oxidative phosphorylation (WHO,
- disturbance of vitamin metabolism: carbon disulphide
alters the metabolism of vitamin B6 and nicotinic acid
- impairment of catecholamine metabolism: there is a
decrease in the level of noradrenaline and increase in
the level of dopamine. Brain dopamine B-hydroxylase
is inhibited and unable to convert dopamine into
noradrenaline. The inhibition of the enzyme occurs
through the conversion of carbon disulphide to
diethylthiocarbonate which chelates the cupricions
essential for the enzyme function (CEC, 1988).
- disturbances in lipid metabolism, which lead to
elevated total and esterified cholesterol levels in
serum. Changes in the lipid metabolism may lead to
development of atheromatous changes in the aorta (WHO,
- interaction with microsomal drug metabolism: an
important feature of the liver toxicity caused by
carbon disulphide seems to be the deactivation of
cytochrome P450. This effect is due to the oxidative
desulfuration of carbon disulphide by mixed-function
oxidases (De Matteis & Seawright, 1973). The
resulting highly reactive sulphur becomes covalently
bound to the microsomal protein, mainly to the
apoprotein of cytochrome P450. It is possible that
the liberated sulphur is the real toxic agent in liver
toxicity arising from carbon disulphide exposure (WHO,
7.2.1 Human data
Lethal doses by ingestion are 30-60
ml, but an early report suggests that 15 ml
may be fatal in an adult (Davidson & Feinleb,
1972). Mild intoxication, paraesthesia and
irregular breathing occur within 30-60
minutes exposure to 6.4 to 10 mg/l
(2,000-3,200 ppm). A concentration of 15 mg/l
(4,800 ppm) has proven lethal after 30
minutes, and at higher concentrations,
unconsciousness occurs after several
inhalations (ILO, 1983).
Prolonged exposures to vapour concentrations
at lower concentrations resulted in
significant health effects (CEC, 1988).
Women appear to be more sensitive than men to
the neurotoxic effect of carbon disulphide
(Gosselin et al., 1984).
No data available.
7.2.2 Relevant animal data
Numerous studies of the toxicokinetics and
metabolism of carbon disulphide, have been carried out
in rats, mice, rabbits, cats and dogs. Rats are the
most resistant and dogs the most sensitive species to
neurotoxicity. In acute exposure studies,
neurological signs prevail and many biochemical
changes have been demonstrated, such as inhibition of
microsomal mixed-system oxidases, destruction of
cytochrome p 450 in the liver, disturbances of
catecholamine metabolism and enzymatic changes (WHO,
1981). With phenobarbital pre-treated rats, the
decline of cytochrome p 450 is greater and
centrilobular hydropic degeneration occurs in the
Data provided by RTECS (1986) are:
oral LD50 - rat 3,188 mg/kg
oral LD50 - mouse 2,780 mg/kg
oral LD50 - rabbit 2,550 mg/kg
oral LD50 - guinea pig 2,125 mg/kg
Most of the experimental studies have shown that
carbon disulphide can directly affect the CNS and
peripheral nervous system, resulting in axonal damage
7.2.3 Relevant in vitro data
Available from RTECS
7.2.4 Workplace standards
Minimum Alveolar Concentration (MAC): 20ppm
expressed in parts of air. The threshold limit value
(TLV) in Britain was reduced to 10 ppm in 1980 whereas
the U.S. National Institute of Occupational Safety and
Health recommends a level of 1 ppm.MAC level
recommended by group of WHO experts: 60 mg/m3 (no
more than 15 minutes). MAC (men workers) 10 mg/m3
MAC (women workers) 3 mg/m3 (ppm)
7.2.5 Acceptable daily intake (ADI) and other guideline
No data available.
Both animal and human data are inconclusive. Carbon
disulphide has been associated with bone marrow hyperplasia,
lymphatic leukaemia and lymphosarcoma but the data available
are very limited (CEC, 1988).
There is a weak teratogenic effect in the rat following
low-level exposure to a combination of hydrogen sulphide and
carbon disulphide. There was evidence of embryotoxicity in
the cat. Embryonic alterations were induced in cats exposed
to carbon disulphide during gestation (WHO, 1979).
Studies on Salmonella typhimurium, Drosophila, human
fibroblasts, cultures of human blood leucocytes and rats have
been inconclusive and further investigation is needed (CEC,
Repeated exposure to a concentration of carbon
disulphide of 3,900 units for 2 hours per day over a period
of 20 - 30 days prolonged both the hexobarbital sleeping time
and alcohol retention time in rats and mice (Lazarev et al.,
1965). Carbon disulphide caused reversible inhibition of the
oxidative drug metabolism in human liver endoplasmic
reticulum. The treatment led to a rapidly reversible but
significant decrease in the oxidative N-demethylation of the
There seems to be synergy between alcohol and carbon
disulphide. The age factor and simultaneous exposure to
hydrogen sulphide may also be synergistic (CEC, 1988).
8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
188.8.131.52 Toxicological analyses
184.108.40.206 Biomedical analyses
220.127.116.11 Arterial blood gas analysis
18.104.22.168 Haematological analyses
22.214.171.124 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
126.96.36.199 Toxicological analyses
188.8.131.52 Biomedical analyses
184.108.40.206 Arterial blood gas analysis
220.127.116.11 Haematological analyses
18.104.22.168 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
22.214.171.124 Toxicological analyses
126.96.36.199 Biomedical analyses
188.8.131.52 Arterial blood gas analysis
184.108.40.206 Haematological analyses
220.127.116.11 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
18.104.22.168 Simple Qualitative Test(s)
22.214.171.124 Advanced Qualitative Confirmation Test(s)
126.96.36.199 Simple Quantitative Method(s)
188.8.131.52 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
184.108.40.206 Simple Qualitative Test(s)
220.127.116.11 Advanced Qualitative Confirmation Test(s)
18.104.22.168 Simple Quantitative Method(s)
22.214.171.124 Advanced Quantitative Method(s)
126.96.36.199 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
188.8.131.52 Blood, plasma or serum
184.108.40.206 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
8.5 Overall Interpretation of all toxicological analyses and
Relevant laboratory analyses and other
Collect blood and urine for biomedical and toxicological
Depending on the clinical condition of the patient
appropriate investigations may include: blood gases, full
blood count, electrolytes and urea, and liver function
In chronic exposure the following may be required:
cholesterol, glucose tolerance and thyroid function
Urine and breath levels of carbon disulphide may be
evaluated. Because of the poor correlation with carbon
disulphide concentrations in air as well as for analytical
reasons, the concentration of carbon disulphide in blood is
not a useful test of exposure. Dosage of mercaptothiozolinone
in urine may be useful.
Other investigations that may be appropriate include:
Blood pressure measurement
Full clinical neurological investigation
Electroneuromyographic studies and nerve conduction
studies (for early detection of peripheral
Optic fundus study and photography
Dexterity tests, simple reaction time, Wechsler Adult
Intelligence Scale For the detection of
9. CLINICAL EFFECTS
9.1 Acute poisoning
After ingestion of sublethal doses, symptoms
may develop several hours after ingestion. Vomiting,
nausea and numbness of lips, are followed by abdominal
pain, brisk reflexes, tachycardia and
electrocardiographic changes. Dyspnoea, cyanosis,
peripheral vascular collapse, convulsions, coma and
respiratory paralysis can occur. Dizziness and ataxia
are common. Illusions, delusions and neuropsychiatric
changes can appear between the 2nd and 5th day.
Acute poisoning is associated with psychiatric and
neurological signs and symptoms such as extreme
irritability, uncontrolled anger, rapid mood changes
including manic delirium and hallucinations, paranoid
ideas and suicidal tendencies, and memory defects.
Convulsions, coma, and cardiac and respiratory arrest
may occur in severe poisoning.
Acute inhalation produces rapid onset of both
local irritation and CNS symptoms ranging from
pharyngitis, nausea, vomiting, dizziness, headache,
delirium, hallucination, convulsions, coma and death
(Ellenhorn and Barceloux, 1988). Inhalation of
concentrations over 4,800 ppm may produce coma or
death after a few inhalations. If consciousness is
regained motor agitation and disorientation may
follow. Direct irritant effects on the lungs are
frequent and characterized by cough, shortness of
breath and chest pain. Subtle changes in pulmonary
function are transient.
Psychiatric disturbances and disturbances of the
central and peripheral nervous systems are often late
sequelae following apparent recovery (ILO, 1983).
In less severe exposures local irritation, nausea,
vomiting and abdominal pain are followed by headache,
euphoria, hallucinations, manic delirium, paranoid
reactions and suicidal tendencies.
9.1.3 Skin exposure
Local contact causes reddening, erythema and
pain, cracking and peeling of skin. Blistering and
chemical burns may result from severe exposure.
Contact dermatitis may result from prolonged exposure
to liquid or concentrated vapour.
9.1.4 Eye contact
Splashes of carbon disulphide in the eye cause
mmediate and severe irritation that may lead to
chemical burns of the cornea.
9.1.5 Parenteral exposure
No data available.
No data available.
9.2 Chronic poisoning
No data available.
The initial feature may include: headache,
malaise, visual disturbances, anaemia, fatigue,
anorexia, dysesthesia or paraesthesiae and trigeminal
neuralgia. This may be followed by weight loss,
psychosis, and a polyneuropathy characterised by
diminished or absent Achilles and atellar reflexes,
sensory disturbances in a glove-stocking distribution,
peripheral nerve conduction defects. Other
disturbances included myopathy of the calf muscle.
Optic neuritis and impairment of other cranial nerves
such as VIIth pair may also occur. Hyper- and
hypoacidic gastritis and duodenal ulceration are a
common finding (WHO, 1979).
The classification of different syndromes quoted by
WHO (WHO, 1979) includes:
Atherosclerotic vasculoencephalopathy; the principal
forms being bulbar-paralytic, hemiplegic, or
The typical mental deterioration has been called an
organic psychosyndrome, which may be due to general
cerebral atherosclerosis, to direct toxicity. or to
The adverse effects on the vascular system is
widespread,involving cerebral, ocular, coronary and
renal vessels, myocardial infarction, nephrosclerosis
and retinal microaneurysm may be present.
Arterial hypertension, elevation of serum cholesterol
(not cholesterol esters) and renal damage may occur
Impaired sexual function and cases of hypothyroidism
have been reported.
The classical picture of carbon disulphide poisoning
with encephalopathy, psychosis, polyneuritis is very
seldom observed nowadays.
9.2.3 Skin exposure
Carbon disulphide liquid may be absorbed
through the skin but there are no reports of chronic
poisoning by this route of exposure.
9.2.4 Eye contact
Only local irritation may occur.
9.2.5 Parenteral exposure
No data available.
No data available.
9.3 Course, prognosis, cause of death
After acute severe poisoning there may be rapid onset of
coma followed by death due to respiration failure.
Neurological sequelae are common in patients who survive.
Chronic carbon disulphide poisoning is more common than cute
poisoning, and occurs after prolonged exposures to
concentrations usually over 30 units. Neuropsychiatric
disorders, hyperaesthesiae, parkinsonism and polyneuropathy
follow the initial symptoms of skin "formication" (crawling
sensation), weakness and malaise, although the most marked
variety of neurological signs and symptoms may occur
(Gosselin et al., 1984).
Neurological complications are usually irreversible.
Chronic intoxication has been strongly associated with
increased cardiovascular mortality, early arteriosclerosis
9.4 Systematic description of clinical effects
Coronary heart disease is one of the main
concerns in workers exposed for years to 10 - 30 ppm.
Increased mortality due to ischaemic heart disease has
been reported in exposed workers (CEC, 1988).
Relatively modest exposure to carbon disulphide may
raise low density lipoprotein-cholesterol
concentration and diastolic blood pressure (Egeland et
Carbon disulphide causes vasoconstriction (especially
in the arteries of the upper and lower
Hypertension has also been observed.
Carbon disulphide is an irritant to the
respiratory system. Transient inflammation in small
airways causes mild ventilation-perfusion alterations
and air trapping (changes in vital capacity and
arterial pO2 are observed). Pulmonary changes are
usually transient (CEC,1988).
In acute poisoning, CNS symptoms may
range from headache, dizziness, agitation,
euphoria, and aggressive behaviour to
unconsciousness, and even death resulting
from respiratory failure.
In chronic poisoning the first signs are
psychological: restlessness, excitation and
loss of temper, mood changes, lethargy.
Gradually, the patient becomes depressed,
anxious, paranoid with suicidal tendencies.
Nightmares and apathy are also present.
Illusions and delusions may appear and there
may be daytime somnolence and nocturnal
In the further course of chronic
intoxication, neurological signs become more
prominent. Both diffuse cortical and focal
symptoms from damage to the subcortical grey
matter and extrapyramidal system are typical.
Symptoms of Parkinsonism appear:
bradykinesia, bradylalia, muscle rigidity,
tremor and increased elementary postural
In chronic intoxication, statokinesiometry
has shown postural stability disorder in 73%
of a group of 37 patients studied. Balance
disorders detected by means of this test
showed high compatibility with results of
electronystagmography which confirmed damage
of the central part of vestibular system due
to carbon disulphide intoxication (Sulkowski
et al., 1992).
220.127.116.11 Peripheral nervous system
The earliest clinical signs are
distal sensory abnormalities, numbness and
mild anaesthesia (CEC, 1988). The typical
sign of carbon disulphide intoxication in man
is a toxic polyneuropathy. Distribution of
the abnormalities is mostly symmetrical, and
objectively there is hyporeflexia.
A decrease in conduction velocity of slow
motor fibres occurs at low levels of exposure
to carbon disulphide (Ruijten et al.,
Cranial nerves are affected. Optic neuritis
with visual disturbances, changes in colour
perception, scotomata, and constriction of
the visual fields have been observed.
Exposure to carbon disulphide can also impair
hearing ability. Audiometric examinations in
workers shows evidence of nerve deafness and
also a decreased ability to distinguish sound
intensity within the range 1.5-3.0
18.104.22.168 Autonomic nervous system
Neurasthenic syndrome with autonomic
nervous system disturbance is
22.214.171.124 Skeletal and smooth muscle
Amyotrophy has been described in the
triceps sural and quadriceps muscles of the
legs, as well as in the small muscles of the
hand, the thenar, the hypothenar and in the
interosseal muscles (WHO, 1979).
In acute poisoning nausea, vomiting and
abdominal pain occur. In chronic poisoning dyspepsia
and gastritis (atrophic), and duodenal ulceration
have been described (Gosselin et al., 1984).
Liver damage is not a prominent feature but an
enlarged, tender liver may be observed (Gosselin et
al., 1984). Chronic exposure may produce
centrilobular hepatic necrosis (Ellenhorn and
Some reports have drawn attention to
nephrosclerosis in autopsies of patients but
this could be ascribed to a general
atherosclerotic process induced by carbon
Chronic renal dysfunction with abnormal
creatinine clearances may be seen after
long-time, low-level occupational exposure
(Gosselin et al., 1984).
No data available.
9.4.7 Endocrine and reproductive systems
Carbon disulphide causes several disturbances
of the endocrine system (WHO, 1979):
- a reduction of adrenal activity
- a reduction of the endocrine activity of the
testis and impairment in spermatogenesis
possibly due to direct gonadal damage, with
decreased libido and potency. There is
decreased in 17-ketosteroids,
17-hydroxycorticosteroids and androsterone in
the urine. Urinary excretion of testosterone
and gonadotropin luteinizing hormone is also
- hormonal disturbances in women, resulting in
menstrual irregularities, spontaneous
abortion and premature births
- impairment of thyroid function, which could
be primary or due to a deficiency in TSH or
the TSH-releasing factor or both.
The most common complaints are loss of libido and
menstrual disorders (Gosselin et al., 1984).
Liquid carbon disulphide is a severe irritant
of both the skin and mucosa. Blisters and more severe
burns have been observed in viscose rayon workers.
Degenerative changes in the local peripheral nerves
has been observed after skin contact (Davidson &
9.4.9 Eye, ears, nose, throat: local effects
Chronically exposed workers have an increased
incidence of retinal microaneurysms (Gosselin et al.,
Retinopathy, eye damage with blind spots, narrowing of
vision and decreased ability to see in the dark may
occur as early effects of exposure (CEC, 1988).
Contact lenses should not be worn when working with
carbon disulphide (OSHA, 1978).
A moderate decrease in the haemoglobin
concentration and erythrocyte count was reported in
workers exposed to carbon disulphide. Increased
platelet aggregationand increase in thromboplastin has
been reported (EHC, 1979).
No data available.
126.96.36.199 Acid-base disturbances
May be secondary to severe respiratory
or cardiovascular disturbances.
188.8.131.52 Fluid and electrolyte disturbances
May result from respiratory and
Carbon disulphide causes decreased
glucose tolerance and may also elevate
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Pregnancy: In a study of women exposed to
carbon disulphide (30 ppm) there was a higher
incidence of spontaneous abortion and premature births
than in the control group.
Breast feeding: Carbon disulphide has been found in
the breast milk of mothers occupationally exposed to
levels up to 12.3 mg/m3 (cited in CEC, 1988).
There is an inborn error of metabolism manifesting
itself as an abnormal iodine-azide reaction in subjects
working under a high or moderate carbon disulphide exposure.
This test is used to screen workers exposed to carbon
With increasing occupational exposure to carbon
disulphide,low density lipoprotein(LDL)-cholesterol and
apolipoproteins A1 and B rose, while high density
A1 and LDL-cholesterol/apolipoprotein B ratios decreased
significantly (Vanhoorne et al., 1992).
10.1 General principles
The patient should be removed from exposure and
decontaminated. Clothing should be removed and the skin
thoroughly washed with soap and water. In the case of eye
contact irrigate thoroughly with water. Give appropriate
symptomatic and supportive measures.
Provide symptomatic treatment.
There is no specific antidote.
Because of the risk of delayed sequelae adequate follow up
should be provided.
10.2 Life supportive procedures and symptomatic treatment
In all acute exposures, maintain a clear airway, give
oxygen and assist respiration if necessary.
If carbon disulphide has contaminated lips or mouth, or
has been ingested, rinse lips and mouth thoroughly with
water. Following recent ingestion do not induce vomiting but
perform gastric aspiration and/or lavage.
In the case of skin contamination, remove contaminated
clothing, wash with copious amounts of water.
If eyes are contaminated, irrigate for at least 15 minutes
with room-temperature water and seek ophthalmologist's
advice. Contact lenses may be affected by the solvent and
impede eye decontamination (CEC, 1988).
10.4 Enhanced elimination
No measures are known to be effective in enhancing
elimination of carbon disulphide.
10.5 Antidote treatment
10.6 Management discussion
Many management recommendations such as large doses of
vitamin B6 and I.V. urea (1.5 mg/kg) are based on the
findings of old studies. However, their efficiency in carbon
disulphide poisoning has not been established and further
research is needed.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Tolonen studied 97 men exposed to carbon disulphide at
levels of 60 - 125 mg/m3 over 15 years. He compared the
incidence of heart disease, psychological impairment and also
the nerve conduction velocity with those in 96 controls.
Twice as many exposed men had abnormalities and combined
disorders occurred more frequently in the exposed group e.g.
a combination of 3 abnormalities was 3 times more frequent in
the exposed group than in controls.
Spyker et al (1982) reported the symptoms found in 27
individuals who had to manage a railway tank-car which caught
fire. Seven appeared to be severely ill and four had
shortness of breath and chest pain.
The symptoms found were: headache (59%), dizziness (59%),
nausea (52%), burning of throat, lips or skin (40%),
shortness of breath or chest pain (15%), impotence (7%) and
vomiting (4%). Headache and dizziness were the predominant
signs, indicative of CNS effects. Vital capacity studies and
pO2 measurements showed a mild ventilation-perfusion
abnormality and air trapping.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Exposure should be avoided by pregnant or lactating
women and by subjects with a history of psychiatric
disturbance, neurological, cardiac, renal, pulmonary, liver
and endocrine disorders.
Since screening of workers normally involves the iodine azide
reactions, workers with a positive test under control
conditions should generally not be occupationally exposed to
No data available.
ACGIH - American Conference of Governmental Industrial
Hygienists (1986). "Documentation of the threshold limit values
for chemical substances in the workroom environment".
British Crop Protection Council (1987). The Pesticide Manual, a
World Compendium, 8th Ed.
Commission of the European Communities (CEC) (1988). Solvents in
Davidson M, Fenliebs M (1972). Carbon disulphide poisoning: a
review. Am Heart J 83(1); 100-114.
De Matteis E, Seawright AA (1973). Oxidative metabolism of carbon
disulphide by the rat. Effect of treatments which modify the
liver toxicity of carbon disulphide. Chem Biol Interact
Egeland GM, Burkhart GA, Schnorr TM et al (1992) Effects of
exposure to carbon disulphide on low density lipoprotein
cholesterol concentration and diastolic blood pressure. Br. J.
Ind. Med. 49: 287 - 293.
Ellenhorn MJ, Barceloux DG (1988). Medical Toxicology, Diagnosis
and Treatment of Human Poisoning. Elsevier, Amsterdam.
Environmental Health Criteria No.10: Carbon Disulphide (1979).
Gosselin RE, Smith RP, Hodge HC (1984). Clinical Toxicology of
Commercial Products, 5th Ed. Williams & Wilkins; III: 90-94.
Greenwood NN, Earnshaw A (1984). Chemistry of the Elements,
International Labour Office (ILO) (1983). Encyclopedia of
Occupational Health and Safety, 3rd Ed.
Lazarev et al (1965). On possible adverse reactions following use
of some drugs by persons handling carbon disulphide. Gig Tr Prof
Zabol; 9: 24-27.
National Institute of Occupational Safety and Health (NIOSH)
(1986). Registry of toxic effects of chemical substances (RTECS).
Publ. N 84-101-6, US Dept Health & Human Sciences.
OSHA (1978). Occupational Safety and Health Association. OSHA,
Ruijten MWMM, Salle HJA, Verberk MM, Muijser H (1990) Special
nerve functions and colour discrimination in workers with long
term low level exposure to carbon disulphide. Br. J. Ind. Med.
47: 589 - 595.
Spyker DA et al (1982). Health effects of acute carbon disulphide
exposure. J Toxicol & Clin Toxicol 19(1): 87
Sulkowski WJ, Kowalska S, Sobczak Z, Jozwiak Z (1992) The
statokinesiometry in evaluation of the balance system in persons
with chronic carbon disulphide intoxication. Pol. J. Occup. Med.
Environ. Health. 5: 265 - 276.
Vanhoorne M, De Bacquer D, De Backer G (1992) Epidemiological
study of the cardiovascular effects of carbon disulphide. Int. J.
Epidemiol. 21: 745 - 752.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
Authors: Dr Patricia Dorfman and Dr Julia Higa de Landoni
Servicio de Toxicologia
Hospital de Clinicas "José de San Martin"
1120 Buenos Aires
Date: April 1990
Reviewer: Dr A. Nantel
Centre de Toxicologie du Québec
Centre Hospitalier de l'Universite Laval
2705 bld. Laurier
Québec G1V 4G2
Tel: 1 418 654 2254
Fax: 1 418 654 2754
Date: November 1990
review: Adelaide, Australia, April 1991
Update: Dr R. Fernando, June 1993