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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

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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 ,

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).

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