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EC number: 220-977-9 | CAS number: 2956-12-9
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Description of key information
Additional information
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has statistically estimated that 45,760 workers (5,834 of these are female) are potentially exposed to carbon disulfide in the US(1). Occupational exposure to carbon disulfide may occur through inhalation and dermal contact with this compound at workplaces where carbon disulfide is produced or used(SRC). Monitoring data indicate that the general population may be exposed to carbon disulfide via inhalation of ambient air, ingestion of fruits and vegetables and other food products containing carbon disulfide(SRC).
Monotoring data
Monitoring for S-allyl O-pentyl dithiocarbonate is not carried out at either the sites of manufacture or end-use.
Monitoring is carried out for carbon dioxide which is expected to be released during manufacture, storage and use of S-allyl O-pentyl dithiocarbonate.
Air monitoring data, although limited and of poor quality, indicate that the atmospheric levels of carbon dioxide; oxides are below 10 ppm in the flotation areas. The risk to workers during the flotation process is considered to be low.
Monitoring is however carried out for CS2,which is considered to be the major hazard during manufacture, storage and use of xanthates.
Xanthates and xanthate ester in the presence of heat/moisture decompose and under the conditions of storage and use the major decomposition product is carbon disulphide.
Routine air monitoring for CS2 is recommended at xanthate manufacturing plants and end-use facilities, particularly in areas where CS2 levels may exceed theexposure standard. In particular, static monitoring should be carried out prior to maintenance activities to as certain CS2 exposure levels, in order to determine the type of personal protective equipment deployed.
The NOHSC occupational exposure standard for CS2 is 10 ppm (31 mg/m3) (time weighted average), with a skin notation (NOHSC 1995). This standard has been adopted from the US ACGIH TLV documentation, which is apparently based on “cardiovascular effects in workers exposed to air concentrations of between 10- 40 ppm CS2 and systemic effects observed following skin absorption” (ACGIH 1998).
This standard is listed in Appendix 3 (substances under review) of the NOHSC Guidance Note (NOHSC 1995) as requiring review due to ‘neurological and cardiovascular effects’.
Table1provides details of known national exposure standards adopted for CS2.
Country |
Exposure limits |
Skin notation |
|||
TWA |
STEL |
||||
|
ppm |
mg/m3 |
ppm |
mg/m3 |
|
US NIOSH |
1 |
3 |
101(500)2 |
30 |
yes |
Hungary |
2 |
5 |
3 |
10 |
yes |
Czechoslovakia |
3 |
10 |
6 |
20 |
|
Denmark |
5 |
15 |
- |
- |
yes |
Sweden |
5 |
16 |
8 |
25 |
yes |
Poland |
6 |
18 |
10 |
30 |
|
Australia |
10 |
31 |
- |
- |
yes |
Finland |
10 |
30 |
20 |
60 |
yes |
France |
10 |
30 |
25 |
75 |
|
Germany (DFG) |
103 |
32 |
- |
- |
|
Japan (JSOH)4 |
10 |
31 |
- |
- |
yes |
Netherlands5 |
10 |
30 |
- |
- |
yes |
Russia |
10 |
30 |
- |
- |
|
Switzerland |
10 |
30 |
20 |
60 |
yes |
United Kingdom |
10 |
32 |
- |
- |
yes |
(HSE) |
|
|
|
|
|
US ACGIH |
10 |
31 |
- |
- |
yes |
US OSHA6 |
20 |
65 |
- |
- |
|
N.B. Source: ACGIH (1998) – Standards current as at Jan 1993 unless otherwise
indicated.
1 = 15-min ceiling concentration
2 = IDLH concentration
3 = Pregnancy Group B (probable risk of damage to developing embryo/foetus)
4 = 1996
5 = Oct 1997
6 = 1995
Currently, the highest TWA exposure limit for CS2 (PEL: 20 ppm) is that set by the US OSHA -TWA (OSHA 1995). This exposure limit reflects the exposure limit that was in effect prior to the issuance of revised limits of 4 ppm (PEL), 12ppm (STEL) and 500 ppm (IDLH) in January 1989, apparently established to“reduce substantially the significant risks of cardiovascular disease, neurologicalimpairment, and adverse reproductive effects associated with exposures to CS2”(OSHA 1989). These revised limits were voided by the US Eleventh CircuitCourt of Appeals on 7 July 1992 (ATSDR 1996).
Levels of carbon disulfide in surface waters
Data on levels of carbon disulfide in surface waters are limited to southern Ontario, Canada. Background levels at remote sites in Ontario, largely due to biogenic production, ranged between about 0.005 and 0.4 µg/litre (Caron & Kramer, 1994). In Lake Ontario, in 1981, a median concentration of 0.4 µg/litre and a maximum of 3.9 µg/litre were measured (Kaiser et al., 1983). The authors considered that the lower levels in the open lake were likely due to biogenic activity, while the elevated levels were due mainly to the influence of nearby urban/industrial areas (B. Scott, personal communication, 1998). The highest measured concentration in surface water, 25.0 µg/litre, was associated with a chemical plant on Thompson Creek in the Niagara region that has since closed (Kaiser & Comba, 1983).
Levels of carbon disulfide in seawater
In seawater, Lovelock (1974) reported concentrations in the open Atlantic of 0.52 and 0.78 ng/litre off the coast of Ireland and 5.4 ng/litre in stagnant bay water near Ireland. Leck & Rodhe (1991) measured levels of carbon disulfide between 0.83 and 1.18 ng/litre in the open Baltic and North seas. Kim & Andreae (1987) reported concentrations of carbon disulfide in surface waters in the North Atlantic ranging between 0.01 and 4.6 ng/litre. Data on levels in groundwater were not identified.
Levels of carbon disulfide in soil
Only limited data on concentrations of carbon disulfide in soils were identified. In a 1985-1986 study of background sites in the general vicinity of petrochemical refinery facilities west of Toronto, Ontario, carbon disulfide was detected at one of five sites in Port Credit at 0.000 11 µg/g, but not at any of six sites from Oakville/Burlington (Golder Associates, 1987). In a 1987 survey of organic compounds in surface soils in background areas in the same municipalities, carbon disulfide was detected at 3 of 30 urban residential and parkland sites in Port Credit, Oakville, and Burlington, at concentrations of 0.10, 0.10, and 0.14 µg/g, respectively (Golder Associates, 1987). However, reported levels were near the method detection limit (0.10 µg/g), and the values were not corrected for the observed contamination of the method blank.
In 1988, carbon disulfide was measured in sedi-ment suspensions taken from Lake Ontario, near Burlington, Ontario, and in Harp Lake, near Huntsville, Ontario. Caron & Kramer (1994), using a sulfur-specific gas chromatographic method, were able to detect 5.9 ng carbon disulfide/litre in Lake Ontario sediments and 9.7 ng carbon disulfide/litre in Harp Lake sediments.
Levels of carbon disulfide in air
Western Mining Corporation submitted data from a review undertaken by Industrial Risk Management Pty Ltd 36 of more than 400 atmospheric samples reported to the Department of Mines. The samples measured carbon disulphide levels at their various mining operations and the results showed that:
• the maximum carbon disulphide level measured was 15 ppm in the mixing
section;
• only two readings were above 10 ppm;
• only 20 readings were at or above 5 ppm and most of these were recorded as being
in the “mixing section”; and
• the average concentration of atmospheric carbon disulphide from 133 samples
taken in the mixing section was less than 2.5 ppm.
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