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EC number: 246-805-2 | CAS number: 25306-75-6
- 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
Administrative data
Description of key information
Key value for chemical safety assessment
Additional information
There is no animal or human information available concerning neurotoxicity for xanthates( CHEMINFO ,2004, ,Chemical Profiles Created by CCOHS , www.ccohs.ca).
Animal studies on the neurotoxicity of carbon disulfide(CAS# 75-15-0)have usually been done in rats and provide histopathologic and neuro-chemical data that that support a neurotoxic effect for the chemical(“Toxicological Profile for Carbon Disulfide” , U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, August 2000)
4 hours exposure to inhaled carbon disulfide(CAS# 75-15-0)1370 ppm in male rats and 2600ppm in female mice cause a 30% inhibition of electrically evoked seizure discharge(Frantik E., et all, Environ Res. 66:173-185) .
Rats exposed for 4 hours a day for 10 days at 642 ppm showed decreased noradrenaline, increased dopamine, and elevated tyrosine in the brain(Magos L., Jarvis J.A., 1970, J. Pharm. Pharmacol. 22:936-938).
Female rats exposed to 777.1 ppm for 12 hours showed swollen brain mitochondria and elevated brain adenosine triphosphate levels compared to controls, but no histopathological changes were noted in brain tissue. Rats exposed for 5 hours, 5 days a week, for 10 month showed biochemical changes that involved uncoupling of oxidative phosphorylation(Tarkowski S. , et all, 1980, Toxicol. Lett. 5:207-212)
Neurological effects of carbon disulfide(CAS# 75-15-0) should be consider because it is a metabolite and the most toxic decomposition product of xanthates.
The nervous system is the main organ for carbon disulfide toxicity. Neuropathology , behavioral changes, neuro-physiological changes have been demonstrated in humans. In an vitro assay was demonstrated formation of protein bond isothiocyanate adducts in carbon disulfide treated peptide and protein, and it was proposed that a direct reaction of carbon disulfide(CAS# 75-15-0)with neurofilament lysineamino moieties was a step in the mechanism of neuropathy.
Most information on neuro-toxic effects of carbon disulfide in humans comes from occupational epidemiology studies.
An examination of 118 male workers exposed for about 15 years to carbon disulfide at an estimated concentration from 10 to 20 ppm, revealed that the carbon disulfide exposed workers had reduced maximal motor conduction velocity of the median,ulnar, deep peroneal, and posterior tribal nerves when compared to the contrl gruop( Sepplainen A.M. ,Tolonem M.T. ,1974, Neurotoxicity of long-term exposure to carbon disulfide in the viscose rayon industry: A neurophysiological study. Work Environ Health 11:145-153)
Overt polyneuropathy aws reported in 9 of 17 male workers exposed to 150 - 300 ppm carbon disulfide for longer than 2 years. 19 workers exposed to 15-150 ppm had symptoms of polyneuropathy(Chu C.C. et all, 1995, Polyneuropathy induced by carbon disulfide in viscose rayon workers. Occup. Environ. Med. 52:404-407).
Cerebral computerized tomography of 16 men exposed to 9.6 to 19 ppm carbon disulfide showed in 13 signs of atrophy and neuropsylogical examination indicated brain organic changes(Aaserud O, et all, 1988, Toxicology 49:2-3).
Cerebral computerized tomography also indicated evidence of brain atropy in 12 of 20 workers exposed to carbon disulfide(CAS# 75-15-0)at 21 ppm for 5 years(Chrostek-Maj J., Czczotko B., 1995, Przegląd Lekarski 52:252-256).
Justification for classification or non-classification
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