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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 192
CCOHS Chemical Name: Carbon disulfide

Synonyms:
Carbon bisulfide
Carbon bisulphide
Carbon disulphide
Carbon sulfide
Carbon sulphide
Dithiocarbonic anhydride
Sulphocarbonic anhydride
Sulphuret of carbon
Sulfure de carbone

Chemical Name French: Disulfure de carbone
Chemical Name Spanish: Disulfuro de carbono
CAS Registry Number: 75-15-0
UN/NA Number(s): 1131
RTECS Number(s): FF6650000
EU EINECS/ELINCS Number: 200-843-6
Chemical Family: Sulfur and compounds / inorganic carbon compound / dithiocarbonic acid anhydride
Molecular Formula: C-S2
Structural Formula: S=C=S

SECTION 2. DESCRIPTION

Appearance and Odour:
Commercial carbon disulfide has a yellow colour and a strong disagreeable odour, like decaying cabbage. Pure carbon disulfide is a clear, colourless liquid with a sweet, pleasing, ethereal odour.(5,27)

Odour Threshold:
Reported values vary widely and are not reliable; 0.022 ppm (detection); 0.21 ppm (recognition); 0.016 to 0.42 ppm (methods not specified).(28)

Warning Properties:
NOT RELIABLE - wide range of odour threshold values reported and olfactory fatigue may occur.

Composition/Purity:
Carbon disulfide is available in a number of grades, ranging in purity from about 99.9 to 99.99%. It may contain traces of hydrogen sulfide and other sulfur compounds.(17,27,29) Carbon disulfide is shipped in drums, tank trucks, special portable tanks, and railtank cars.

Uses and Occurrences:
The main use of carbon disulfide is in the manufacture of viscose rayon. It is also used to produce carbon tetrachloride, cellophane films, rubber vulcanization accelerators, xanthates, pharmaceutical intermediates (such as thiocarbanilide and thiocyanates), mercaptoethylamine, and several fungicides, soil fumigants, insecticides and their intermediates, and as a laboratory chemical. Carbon disulfide is used as a solvent for rubbers, waxes, fats, oils, plastics, sulfur, phosphorus, selenium, bromine and iodine; as a solvent for dehydration, extraction, reaction and separation applications; as a spectroscopy and oil well solvent; as a catalyst presulfidation agent; and in the manufacture of electronic vacuum tubes.(5,17,27,29)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Carbon disulfide is either a yellow liquid with a strong disagreeable odour (decaying cabbage)(commercial product) or a clear, colourless liquid with a sweet, ethereal odour (pure). EXTREMELY FLAMMABLE LIQUID AND VAPOUR. Forms explosive mixtures with air over a wide concentration range. Flame is nearly invisible. Liquid can accumulate static charge by flow, splashing or agitation. Vapour can be ignited by a static charge and is heavier than air and may spread long distances. Distant ignition and flash back are possible. Can decompose at high temperatures forming irritating/toxic sulfur oxides. TOXIC. Harmful if inhaled, absorbed through skin or swallowed. Central nervous system depressant. Can cause headache, dizziness, fatigue, excitement or depression. High concentrations can cause serious psychological disturbances. Aspiration hazard. Swallowing or vomiting of the liquid may result in aspiration (breathing) into the lungs). POSSIBLE REPRODUCTIVE HAZARD - may cause embryotoxic and fetotoxic effects, based on animal information.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Carbon disulfide is toxic, easily forms very high vapour concentrations at room temperature and so poses a high inhalation hazard. Relatively low concentrations of the vapour can cause harmful effects on the central nervous system (CNS), based on human and animal information. Initial symptoms may include headache, dizziness, fatigue, excitement or depression. High concentrations can cause serious psychological disturbances and in some cases death.(1)
Psychiatric disturbances (including excitability, confusion, extreme irritability, uncontrolled anger, emotional instability, nightmares, depression) have been observed following episodes of exposure to high concentrations of carbon disulfide. Exposure levels and durations producing these effects are often unspecified. Deaths have reportedly occurred rapidly following exposure to 5000 ppm.(2,3,4)
Technical grade carbon disulfide is typically contaminated with hydrogen sulfide. If applicable, refer to the CHEMINFO record for hydrogen sulfide for additional information.

Skin Contact:
Carbon disulfide liquid can be absorbed through intact skin and may cause harmful effects.(3,5) Effects are similar to those described for inhalation above. Carbon disulfide vapour may also be absorbed through the skin. Significant skin absorption was observed in volunteers exposed to water solutions containing carbon disulfide.(5)
There is no specific information available about the irritating effects of short-term contact. Repeated or prolonged contact may result in blistering and burns, based on human and animal information. Blisters have been reported to occur on the hands of viscose rayon employees.(5)

Eye Contact:
There is no specific information available on short-term contact with the liquid. High vapour concentrations may cause irritation. Eye irritation was reported among employees exposed to high peak concentrations (estimated at 48- 320 ppm (150-1000 mg/m3)).(6)

Ingestion:
Deaths have been reported following ingestion of approximately 15 mL.(2,5) Symptoms include tremors, exhaustion, shortness of breath, peripheral vascular collapse, reduced body temperature, dilation of the pupils, convulsions, coma and death in a few hours.(3)
Based on its physical properties (viscosity and surface tension), it is possible that carbon disulfide can be aspirated (inhaled into the lungs) during ingestion or vomiting. Aspiration of even a small amount of liquid could result in a life threatening accumulation of fluid in the lungs. Severe lung damage (edema), respiratory failure, cardiac arrest and death may result. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

EFFECTS ON THE NERVOUS SYSTEM: Many studies have reported harmful effects on the peripheral nervous system (nerves of the arms, legs, hands and feet) in employees following long-term exposure to carbon disulfide. Symptoms have included muscle weakness, numbness or tingling and loss of sensation in the extremities (legs and, later, hands). These symptoms are often accompanied by central nervous system effects (headache, dizziness, fatigue, insomnia). In most studies, exposures were not well characterized and there was often exposure to hydrogen sulfide at the same time.(1,2) One study found that peripheral nervous system effects were clearly present in 9/17 viscose rayon employees exposed to estimated concentrations of 150-300 ppm during fiber cutting.(7) Another study found peripheral nervous system effects in 30 employees exposed to up to 220 ppm for 10-16 years.(2)
Even when no obvious symptoms are present, mild peripheral and central nervous system effects have been detected by measuring conduction velocity in the nerves of the legs, behavioural tests and electroencephalogram (EEG) recordings. In these studies, exposures were generally less than 20 ppm.(2,8,9) A few studies report that nervous system effects remained 4-10 years after exposure ended.(2,6,9)
Animal studies have also shown significant effects on the nervous system following exposure to carbon disulfide.

EFFECTS ON THE HEART AND BLOOD VESSELS: Many studies have shown that long-term exposure to carbon disulfide can cause harmful effects on blood vessels (increased atherosclerosis, leading to risk of cardiovascular disease). However, due to a lack of exposure information and the many complex factors which can influence cardiovascular health, it is not possible to associate these effects with a specific exposure level.
Harmful effects on the blood vessels (vasoconstriction and mild to moderate sclerotic changes) have been observed in young employees exposed to 64-288 ppm.(2,4) Minor effects such as increased blood cholesterol and changes in blood pressure have also been observed.(2,5)
A recent review has analyzed the many studies which have associated increased deaths due to ischemic heart disease in employees with carbon disulfide exposure. This review concluded that an increased risk of death due to ischemic heart disease is only significant in employees exposed to high concentrations of carbon disulfide for many years. These high exposure concentrations occurred many years ago and are no longer observed in the workplace. It was concluded that exposures of 15-20 ppm would not be associated with an increased risk of ischemic heart disease.(10)

EFFECTS ON THE SKIN: Repeated or prolonged skin contact can result in severe skin injury including blistering and significant skin absorption. Historically, serious blisters were reported in employees exposed to carbon disulfide in the viscose rayon industry.(5)

EFFECTS ON THE EYE: No firm conclusions can be drawn regarding harmful effects on the retina (microaneurysms) observed in several studies involving employees exposed to concentrations as low as 20 ppm.(2) Other studies did not find this effect in employees exposed to similar concentrations.(2) Other effects on the eyes (including effects on the optic nerve) have also been reported.(2,5,11)

Carcinogenicity:

No increase in deaths from cancer was observed in a study of rayon plant employees exposed to carbon disulfide. Exposure levels were approximately 5-30 ppm and had historically been 20-60 ppm.(2,5) Because of limitations in study design and/or lack of statistical significance, no firm conclusions can be drawn from two reports of increased occurrence of lymphocytic leukemia and/or lymphosarcoma observed among rubber industry employees exposed to a number of solvents including carbon disulfide. Exposures were not well characterized.(2,5) There is no relevant animal information available.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not classifiable as a human carcinogen (A4).

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
No firm conclusions can be drawn on the basis of the available human information. Embryotoxic and fetotoxic effects have been observed in one animal study, in the absence of harmful effects on mothers. There is inadequate information available to evaluate a study which reported birth defects in offspring of employees occupationally exposed to low concentrations of carbon disulfide.(5) There is insufficient information available in English to evaluate one study which reported an increased incidence of miscarriage among female employees and the wives of male employees exposed to carbon disulfide in the viscose rayon industry. Other studies have not reported this effect.(2,5,12,13)

Reproductive Toxicity:
No firm conclusions can be drawn from several human studies which have suggested that carbon disulfide may harm the male reproductive system. The available studies are limited by factors such as self-reporting bias, small study population, inadequate control groups and/or poor exposure information. In one study, impotence and/or decreased libido, but no effect on fertility or semen quality, were reported among men employed in the viscose industry and exposed to 0.3-10 ppm or greater than 10 ppm.(14) Inconsistent or inconclusive results were obtained in occupational studies which examined the levels of certain hormones which regulate reproduction.(2,5,12) Earlier studies which reported harmful effects on fertility cannot be evaluated due to the presence of significant other toxicity in the exposed men, as well as design limitations.(2,4,5,12) A few other human studies have not shown harmful effects on fertility or male reproductive function.(2,5) In rats, reproductive effects were observed in the presence of other toxicity following long-term inhalation, but reproductive outcome was not assessed.
Because of limitations in study design, no firm conclusions can be drawn from a number of reports of harmful effects on female reproduction (menstrual disturbances, endocrine alterations) in occupationally exposed groups.(2,5) Carbon disulfide has been measured in breast milk of exposed mothers in the Chinese viscose rayon industry.(15) Effects on fertility cycle length were observed in an animal study.

Mutagenicity:
There is no human information available. Negative results have been obtained in studies using live animals. Positive and negative results have been obtained in cultured mammalian cells. Negative results have been obtain in bacteria.

Toxicologically Synergistic Materials:
Several reports have suggested that the combined exposure to hydrogen sulfide and carbon disulfide be either additive or synergistic. In one study, there was no influence of hydrogen sulfide on carbon disulfide-induced peripheral nerve toxicity (tail nerve conduction velocity) in rats exposed for 25 weeks to 500 ppm carbon disulfide and 50 ppm hydrogen sulfide. In another study, combined exposure to hydrogen sulfide and carbon disulfide had a greater effect on fetal and maternal body weights than carbon disulfide alone.(2)
Exposure to ethanol enhanced the harmful effects on the nervous system following exposure to 256 ppm carbon disulfide for 8 months (species unspecified).(2)
Because carbon disulfide exposure affects one of the main metabolic systems (the mixed function oxidase system), it may alter the rates of metabolism of many drugs and industrial chemicals.(2)
The nervous system responses to carbon disulfide are greatly influenced by the mineral content of the diet, at least in animals. Therefore, a highly mineralized diet may offer protection from these effects.(16)
Exposure to carbon disulfide can speed up the harmful effects caused by an atherosclerotic (cholesterol-rich) diet, based on animal information.(2)

Potential for Accumulation:
Carbon disulfide is quickly absorbed via inhalation, oral and dermal routes and distributed throughout the body. Distribution is greatest in organs such as the brain and liver. About 10-30% of absorbed carbon disulfide is excreted unchanged from the lungs and about 1% is excreted in the urine. The rest of the absorbed carbon disulfide is metabolized to a number of compounds including dithiocarbamates, inorganic sulfate and other sulfur containing compounds, which are excreted in the urine. Some carbon dioxide, which is exhaled, is also formed.(5,17) Although traces of carbon disulfide have been detected in the blood about 80 hours after the end of exposure, about 70% of an inhaled dose is excreted or metabolized within a few hours.(3)


SECTION 4. FIRST AID MEASURES

Inhalation:
Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the buddy system). Remove source of contamination or move victim to fresh air. Remove any contaminated clothing to prevent further inhalation exposure. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Immediately transfer victim to an emergency care facility.

Skin Contact:
Avoid direct contact. Wear chemical protective clothing, if necessary. Remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Wash gently and thoroughly with water and non-abrasive soap for at least 20 minutes or until the chemical is removed. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transfer victim to an emergency care facility. Discard contaminated clothing, shoes and leather goods.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes or until the chemical is removed while holding the eyelid(s) open. Take care not to rinse contaminated water into the non-affected eye. Obtain medical attention immediately.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, or is unconscious or convulsing. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz) of water. If vomiting occurs naturally, have victim lean forward to reduce risk of aspiration. Repeat administration of water. If breathing has stopped, trained personnel should begin artificial respiration or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transport victim to an emergency care facility.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.
Carbon disulfide rapidly forms high vapour concentrations. Significant inhalation exposure should be assumed if any skin or eye contact occurs.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
-30 deg C (-22 deg F) (closed cup) (5,27)

Lower Flammable (Explosive) Limit (LFL/LEL):
1% (2,31); 1.3% (5,31)

Upper Flammable (Explosive) Limit (UFL/UEL):
50% (5,31)

Autoignition (Ignition) Temperature:
90 deg C (194 deg F).(30) Also reported as 100 deg C (212 deg F) (5,31)

Electrical Conductivity:
7.8 x 10(-4) pS/m at 18 deg C (29,32)

Minimum Ignition Energy:
0.009 millijoules (33,34)

Combustion and Thermal Decomposition Products:
Sulfur oxides.(35)

Flammable Properties:

Specific Hazards Arising from the Chemical:
During a fire, irritating/toxic sulfur oxides may be generated. Closed containers may rupture violently and suddenly release large amounts of product when exposed to fire or excessive heat for a sufficient period of time.

Extinguishing Media:
Carbon dioxide, dry chemical powder, inert gas, foam, water spray or fog.(30,35) Fluoroprotein and protein foams are recommended over other types of foam for carbon disulfide. Water may be ineffective except as a blanket.(30) One source has suggested that foam may be ineffective.(31)

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid very toxic carbon disulfide and its decomposition products. Caution should be used in fighting a carbon disulfide fire because the flame is nearly invisible.
Stop leak before attempting to stop the fire. If the leak cannot be stopped, and if there is no risk to the surrounding area, let the fire burn itself out. If the flames are extinguished without stopping the leak, vapours could form explosive mixtures with air and reignite. Water may be ineffective except as a blanket. The water must be gently applied to the surface of the liquid.(30) If possible, isolate materials not yet involved in the fire, and move containers from fire area if this can be one without risk, and protect personnel. Otherwise, fire-exposed containers or tanks should be cooled by application of hose streams and this should begin as soon as possible and should concentrate on any unwetted portions of the container. If this is not possible, use unmanned monitor nozzles and immediately evacuate the area.
If a leak or spill has not ignited, use water spray in large quantities to disperse the vapours and to protect personnel attempting to stop a leak. Water spray can be used to dilute spills to nonflammable mixtures and flush spills away from ignition sources. Solid streams of water may be ineffective and spread material. For a massive fire in a large area, use unmanned hose holder or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire.
Carbon disulfide and it decomposition products are hazardous to health. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective equipment (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical protective suit with positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 3 - Short exposure could cause serious temporary or residual injury.
NFPA - Flammability: 4 - Will rapidly or completely vaporize at atmospheric pressure and normal ambient temperature, or readily disperse in air and burn readily.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 76.14

Conversion Factor:
1 ppm = 3.11 mg/m3; 1 mg/m3 = 0.32 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: -111.5 to -112 deg C (-168.7 to -169.6 deg F) (5,27,29,31)
Boiling Point: 46.3 deg C (115 deg F) at 101.3 kPa (27,29,31)
Relative Density (Specific Gravity): 1.263 at 20 deg C (2,27,32,37); 1.26 at 25 deg C (29) (water = 1)
Solubility in Water: Slightly soluble (210 mg/100 mL at 20 deg C) (27,29)
Solubility in Other Liquids: Soluble in all proportions in ethanol, methanol, diethyl ether, benzene, chloroform, carbon tetrachloride and oils.(5,32)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 1.94 (17). Log P(oct) = 1.84; 2.16 (calculated) (38)
pH Value: Not available
Vapour Density: 2.67 (air = 1) (17,35)
Vapour Pressure: 39.66 kPa (297.5 mm Hg) at 20 deg C (5,27); 47.9 kPa (359 mm Hg) at 25 deg C (17)
Saturation Vapour Concentration: 39.15% (391510 ppm) at 20 deg C; 47.24% (472400 ppm) at 25 deg C (calculated)
Evaporation Rate: 10.9 (n-butyl acetate = 1); 1.8 (diethyl ether = 1) (37)
Critical Temperature: 273 deg C (523.4 deg F) (27,29)

Other Physical Properties:
DYNAMIC-VISCOSITY:0.363 to 0.367 mPaS (0.363 to 0.367 centipoise) at 20 deg C (17,27,32); 0.36 mPa.s (0.36 centipoise) at 25 deg C (29)
VISCOSITY-KINEMATIC: 0.288 to 0.291 mm2/s (0.288 to 0.291 centistokes) at 20 deg C; 0.285 mm2/s (0.285 centistokes) at 25 deg C (calculated)
SURFACE TENSION: 32.3 mN/m (32.3 dynes/cm) at 20 deg C (27,29); 31.58 mN/m (31.58 dynes/cm) at 25 deg C (calculated)(32)
CRITICAL PRESSURE: 7600 to 7700 kPa (75 to 76 atm) (27,29)
DIELECTRIC CONSTANT: 3.0 at -112 deg C; 2.64 at 20 deg C (29,32)


SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable. Exposure to ultraviolet radiation from sunlight may cause carbon disulfide vapour to ignite and explode.(39)

Hazardous Polymerization:
Does not occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


AIR and RUST - may ignite and explode. This reaction may be initiated by rust.(39)
STRONG OXIDIZING AGENTS (e.g. chlorine monoxide, dinitrogen tetraaoxide (nitrogen dioxide), nitrogen oxide, permanganic acid (permanganates and sulfuric acid)) - may explode on contact.(30,39)
REDUCING AGENTS (e.g. hydrogen iodide, lithium aluminum hydride or sodium borohydride)- react violently, with risk of fire and explosion.(34)
CHEMICALLY ACTIVE METALS AND THEIR COMPOUNDS (e.g. aluminum powder, zinc powder) - may ignite in carbon disulfide vapour.(30,39)
ALKALI METALS (e.g. potassium-sodium alloy, potassium, sodium or lithium) - mixtures are capable of detonation by shock and pressure, though not by heating.(30,39)
HALOGENS (e.g. fluorine, chlorine) - may ignite on contact.(30,39)
METAL OXIDES - may form explosive salts.(31)
METAL AZIDES (e.g. cesium azide, lead azide, lithium azide, potassium azide, rubidium azide or sodium azide) - react to form violently explosive metal azidodithioformates which are sensitive to shock or heat.(30,39)
AMINES (e.g ethylenediamine) or IMINES (e.g. ethyleneimine) - mixing in a closed container may cause the temperature and pressure to rise.(30)
MERCURY FULMINATE - decomposes explosively.(39)

Hazardous Decomposition Products:
Sulfurous compounds

Conditions to Avoid:
Heat, open flames, static discharge, friction, sparks, hot surfaces, exposed electric light bulbs, bare steam pipes, and other ignition sources and sunlight (as a source of ultraviolet radiation).

Corrosivity to Metals:
Carbon disulfide is not corrosive to high silicon iron, steel, stainless steels, aluminum, tantalum or titanium.(40,41) Copper and copper alloys are attacked by carbon disulfide.(27) Carbon disulfide liquid and vapour become very corrosive to iron and steel at temperatures above 250 deg C. At elevated temperatures, carbon disulfide is not corrosive to high chromium stainless steels.(27)

Stability and Reactivity Comments:
Can attack some plastics (such as ABS, chlorinated polyether, some polyesters, polyethylene, polystyrene and PVCs), elastomers (such as ethylene- propylene, neoprene, nitrile BUNA, polysulfides, SBR styrene and silicone rubbers), rubbers and coatings.(31,40)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (mouse): 2300 ppm (4-hour exposure), cited as 10 g/m3 (2-hour exposure) (18, unconfirmed)
LC50 (male mouse): approximately 110 ppm (4-hour exposure), cited as approximately 220 ppm (60-minute exposure) (19). NOTE: This value is inconsistent with other toxicity information.
LC50 (rat): 5700 ppm (4-hour exposure), cited as 25 g/m3 (2-hour exposure) (18, unconfirmed)

LD50 (oral, mouse): 3020 mg/kg in corn oil (2,5)
LD50 (oral, guinea pig): 2125 mg/kg (18)

Skin Irritation:

Blisters and ulcers were observed in rabbits on treated areas of the ears following continuous 3-day contact.(2,5)

Effects of Short-Term (Acute) Exposure:

Inhalation:
Signs of depression of the central nervous system (CNS) (reduced performance in behavioural tests) were observed in mice exposed by inhalation to as low as 580 ppm for 1 hour, 194 ppm for 3 weeks, or in monkeys exposed to 200-600 ppm for 2 hours.(2,5) A few inhalation studies have shown minor, largely temporary, effects on the liver, kidney and brain biochemistry following short-term exposure (2-8 hours) to concentrations less than 100 ppm.(2,5)

Ingestion:
Peripheral nervous system effects have been observed in animals exposed to relatively low oral doses. Decreased muscle responsiveness (to noradrenaline) was observed in rats given 12.5 mg/kg/day orally in olive oil for 1-4 weeks.(5) Hindlimb paralysis and a decrease in body weight gain was observed in female rabbits that received 25 mg/kg/day for 14 days during pregnancy. Similar effects were observed in rats with higher exposure.(5) Effects on brain chemistry were observed in rats 2 hours after one-time oral administration of 300 mg/kg.(5) Oral exposure to carbon disulfide does not appear to cause significant liver toxicity, although the information is limited and no firm conclusions can be drawn.(5) No deaths were observed in rats given 253 mg/kg/day orally for 4 weeks or given a single dose of up to 632 mg/kg.(5)

Effects of Long-Term (Chronic) Exposure:

Inhalation:
Harmful effects on the nervous system (slowed nerve function, reduced motor performance, muscle weakness, effects on peripheral nerves, spinal cord and brain) have been observed in animals following long-term exposure (more than one month) to concentrations as low as 256-400 ppm. Effects generally developed over a number of months. When recovery was evaluated, some improvement was observed in some studies, but not in others.(2,5) A few studies have shown that carbon disulfide causes harmful effects on the cardiovascular system. An increase in blood cholesterol and phospholipid levels was observed in rats and rabbits exposed to as low as 176 ppm for up to 8 months. In another study, cardiovascular effects were observed in rats exposed to 16 ppm for 1-6 months, while being fed a high fat diet.(2,5) Harmful kidney effects were observed in rats and rabbits following exposure to concentrations as low as 200 ppm for 6 months or 480 ppm for 6-14 months (rabbits).(2,5) Permanent damage to vision was observed in 4 monkeys exposed to 256 ppm for 5- 13 weeks. A similar effect was observed in 2 monkeys exposed to 256 ppm intermittently for 5 weeks; one recovered somewhat within 16 weeks.(2,5) Liver changes (including increased liver enzyme levels in serum, and vacuolation of hepatocytic cytoplasm) have been observed in rats and rabbits following inhalation of concentrations as low as 200 ppm for more than 5 months.(2) Other harmful effects on the brain, liver, kidneys and intestinal tract have been observed in a study in which small numbers of rats and mice were exposed to 37 ppm. Statistical evaluation of the data was not conducted.(20)

Ingestion:
Harmful effects on the blood (normochromic and normocytic anemia, eosinopenia and an increase in reticulocyte cell numbers) were observed in rats given 25 mg/kg/day orally for 60 days.(5) Harmful effects on the nervous system were observed in rats following oral administration of 303 mg/kg for 8 weeks (twice/week) and 606 mg/kg for 12 weeks.(2)

Carcinogenicity:
Long-term animal studies have not been carried out. No firm conclusions can be drawn from a study in which lung tumours were observed in mice following inhalation of 300 ppm for 6 months. Results were in the same range as those for control groups exposed to 6 other compounds.(2)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
One study has shown embryotoxic and fetotoxic effects in the offspring of rabbits exposed to carbon disulfide, in the absence of harmful effects on mothers.(2,5,21,22)
Harmful effects on the embryo and fetus (decreased body weight and deaths) were observed in the offspring of rabbits following exposure to 600 ppm during pregnancy, in the absence of significant harmful effects on mothers. Teratogenic effects were observed at 1200 ppm, but only in the presence of harmful effects on mothers (decreased body weight gain, incoordination and wheezing). No harmful effects were observed at 60-300 ppm.(22) No firm conclusions can be drawn from some other studies due to factors such as a lack of maternal toxicity information, poor study design or poor reporting.(23,24,25) In other studies, fetotoxic, teratogenic and/or embryotoxic effects were observed in rats or rabbits, in the presence of harmful effects on mothers.(2,5) Other studies have shown no harmful effects on offspring or mothers following exposures to as high as 40 ppm.(2,5)

Reproductive Toxicity:
There is insufficient information available to conclude that carbon disulfide harms fertility, but it has had reproductive effects in animals following inhalation of high concentrations.
In one study, decreased sperm count, reduced sex hormone levels and changes in copulatory behaviour were observed in male rats exposed to 600 ppm for 10 weeks. These effects were observed in the presence of other toxicity (reduced weight gain).(26) Reproductive outcome (e.g. fertility) was not assessed. In another study, a longer fertility cycle was observed in female rats following inhalation of 3 ppm or above for 4 months.(2) The significance of this effect is not well understood.

Mutagenicity:
Negative results have been obtained in various studies using live animals and cultured mammalian cells, including a test for bone marrow chromosomal aberrations in rats and a rat dominant lethal test.(2,5) Positive results were obtained (chromosome aberrations) in cultured rat bone marrow cells.(2) Negative results have been obtained in two tests using bacteria, with metabolic activation.(2,5)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) Lilis, R. Carbon disulfide. In: Environmental and Occupational Medicine. Edited by W.N. Rom. 2nd ed. Little, Brown and Company, 1992. p. 993-998
(2) Carbon disulphide. Health-based recommended occupational exposure limit. Report No. 1994/08E. The Dutch Expert Committee on Occupational Standards, Health Council of the Netherlands, July 1994
(3) Gosselin. R.E., et al. Carbon disulfide. In: Clinical Toxicology of Commercial Products. 5th edition. Williams & Wilkins, 1984. p. III-90 to III- 94
(4) Fielder, R.J., et al. Carbon disulphide. Toxicity Review No. 3. Health and Safety Executive , Her Majesty's Stationery Office, Nov. 1981
(5) Agency for Toxic Substances and Disease Registry. Toxicological profile for carbon disulfide (Update). Public Health Service, US Department of Health and Human Services, Aug. 1996
(6) Aaserud, O., et al. Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers. American Journal of Industrial Medicine. Vol. 18, no. 1 (1990). p. 25-37
(7) Chu, C-C., et al. Polyneuropathy induced by carbon disulphide in viscose rayon workers. Occupational and Environmental Medicine. Vol. 52, no. 6 (June 1995). p. 404-407
(8) Ruijten, M.W.M.M., et al. Verification of effects on the nervous system of low level occupational exposure to CS2. British Journal of Industrial Medicine. Vol. 50, no. 4 (Apr. 1993). p. 301-307
(9) Seppalainen, A.M., et al. Neurotoxicity of long-term exposure to carbon disulfide in the viscose rayon industry: a neurophysiological study. Work- Environment-Health. Vol. 11 (1974). p. 145-153
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Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2000-07-03

Revision Indicators:
WHMIS health effects 2002-04-25
WHMIS proposed classification 2002-04-25
Short-term inhalation 2002-04-25
Emergency overview 2002-04-25
TDG 2002-05-29
PEL transitional comments 2004-01-08
PEL-TWA final 2004-01-08
PEL-STEL final 2004-01-08
PEL final comments 2004-01-08
TLV basis 2004-01-09
Resistance of materials for PPE 2004-04-08
Bibliography 2004-04-08
TLV definitions 2005-02-17
TLV-TWA 2006-02-14
TLV proposed changes 2006-02-14
Carcinogenicity 2006-02-15
WHMIS detailed classification 2006-02-15



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