Sodium O-isobutyl dithiocarbonate

Endpoint summary

Key value for chemical safety assessment

Acute toxicity: via oral route

Link to relevant study records

Reference

Endpoint:

acute toxicity: oral

Type of information:

experimental study

Adequacy of study:

key study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

data from handbook or collection of data

Justification for type of information:

Valid Australian Government assessment report
Toxicity is in the range expected when considering other tests on similar substances in the group
Certain details lacking, but considered suitable to confirm similar results as would be expected for this substances

Qualifier:

equivalent or similar to guideline

Guideline:

OECD Guideline 401 (Acute Oral Toxicity)

GLP compliance:

not specified

Test type:

standard acute method

Limit test:

no

Species:

rat

Route of administration:

oral: unspecified

Dose descriptor:

LD50

Effect level:

500 mg/kg bw

Clinical signs:

other:

Interpretation of results:

Category 4 based on GHS criteria

Executive summary:

Toxicity is in the range expected when considering other tests on similar substances in the group

Certain details lacking, but considered suitable to confirm similar results as would be expected for this substances

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LD50

Value:

ca. 500 mg/kg bw

Quality of whole database:

Note that acute oral toxicity has been assess on the range of substances and with the exception of one mouse study, all are in the Acute Toxic 4 category. The quality of the data base is considered sufficient for the purposes of classification and risk management.

Acute toxicity: via inhalation route

Endpoint conclusion

Endpoint conclusion:

adverse effect observed

Dose descriptor:

LC50

Value:

7 690 mg/m³ air

Acute toxicity: via dermal route

Endpoint conclusion

Endpoint conclusion:

no study available

Additional information

There is very little published and unpublished data available on the adverse health effects of xanthates in general and sodium ethyl xanthate in particular. Toxicological data for other xanthates were also assessed where available, as the adverse effects of the various xanthates are similar.

The acute oral toxicity study indicates that sodium ethyl xanthate as a 10% solution at a pH of 10.5 to 11 has an LD50 of 730 mg/kg in mice. The target sites are the central nervous system, liver and the spleen. The oral LD50 for other xanthates in mice ranges from 411 to 583 mg/kg and in rats from 1000 to 2000 mg/kg.

Acute toxicity via oral route:

Effect level:

LD₅₀= 730 mg/kg b.w. in male mice; as 10% water solution of sodium ethyl xanthate (CAS# 140-90-9)

LD₅₀of various xanthates are similar, ranging from 411 to 583 mg/kg b.w. in mice and from 1000 to 2000 mg/kb b.w. in rats.

Oral administration of potassium butyl xanthate (CAS# 871-58-9) to rats produced increased motor activity , cyanosis, irritability , increased respiration and convulsions with death occurring 1 to 2 hours after administration. Autopsy shoved pervascular and pericellular oedema, multiple haemorrhages in the lungs perivascular subarachnoid heamorrhages and acute swelling of the cells of the cortex, subcortical ganglia and brain stem. Also were observed fatty dystrophy of the liver and protein dystrophy of the kidney

PubliFull Public Report, Sodium Ethyl Xanthate, Priority Existing Chemical No. 5 , May 1995, Canberra , Australia

After ingestion of CS₂, CAS# 75-15-0) victims exhibited spasmodic tremors, prostration, dyspnea, cyanosis, peripheral vascular collapse, hypothermia, mydriasis, convulsions, coma and death in few hours from respiratory paralysis. Only mild gastrointestinal irritation and visceral congestion were noted at autopsy. Women appear to be more sensitive than men to the neurotoxic effects of carbon disulfide. Industrially exposed workers have exhibited neuropsychiatric disorders ranging from irritability to manic-depressive psychosis, clinical manifestations of nerve damage are blindness, and signs of parkinsonism.

 (Toxicological Profile for carbon disulfide. U.S. Department of Health and Human Services . Public Health Service . Agency for Toxic Substances and Disease Registry . August 1996)

Acute toxicity via inhalation route:

Depending upon the concentration of CS₂in repairable air different types of poisoning symptoms are encountered. Most prominent are general neurotoxic and narcotic effects.

NOEC: 500 - 700 mg/m³(160 - 224 ppm) of CS₂

2500mg/m³= 800 ppm for 1.5 - 3 hours: strong headache,

6400 - 10000mg/m³(2048 - 3200 ppm) for 30min. narcotic condition, strong headache. (IUCLID Dataset: Carbon Disulfide, Creation date 19 February 2000, European Commission, European Chemicals Bureau)

An inhalation maximum risk level (MRL) 0.3 ppm (0.9mg/m³) for CS₂was derived based on epidemiological data, concerning public health.

LOAEL= 7.6 ppm, represents the average exposure of workers 8 hour/day, 5 days a week for a mean exposure period of 12 years(ATSDR 1996, Toxicological profile for carbon disulfide. Atlanta, GA, US Department of Health and Human Services, Research Triangle Institute Contract No. 205-93-0606).

Acute toxicity via dermal route:

Application of 1 gm/kg of sodium ethyl xanthate in the form of a paste resulted in the death of ten out of twelve animals within 24 hrs. The surviving animals developed irritant effects including oedema and pigmentation of the skin. The sulphide odour noted during the study suggests that decomposition of sodium ethyl xanthate occurred. The dermal LD50 was < 1000 mg/kg.

Sodium ethyl xanthate (CAS# 140-90-9)or sodium isobutyl xanthate (CAS # 25306-75-6) can be assessed as a substances strongly irritating skin of rabbits – IIPC factor accordingly 6.2 and 7.0.(The Institute of Organic Industry Branch of Pszczyna Toxicology Department, March 1998)

Sodium or potassium xanthates dissolved in water undergoes hydrolysis giving alkaline reaction. When xanthates are produced as a water solutions exes of alkali hydroxide is kept (pH >10) as a decomposition inhibitor.

Human information

Xanthates dust or mist from solution cause irritation to the nose, throat and upper respiratory tract. The solids give carbon disulfide in contact with water, very toxic and extremely flammable vapour. Relatively low concentration of carbon disulfide can harm the central nervous system, may cause headache , dizziness, fatigue, excitement and depression. High concentration of CS₂can cause psychological disturbances and death.

It is known one case reported of acute exposure of an employee who lost consciousness when was opened a tank containing powder sodium ethyl xanthate. The worker was restless, vomited and had convulsive twitching of muscles in arms and legs. He complained of difficulty breathing, eye tearing and hoarseness. the respiratory and eye effects persisted for 3 weeks. No toxic effects were observed 3 month later.(COOH, CHEMINFO Sodium ethyl xanthateupdated July 2010,www.ccohs.ca)

Probable the oral lethal human dose of sodium ethyl xanthate is between 50-500mg/kg(Gosselin R.E., Hodge H.C., Smith R.P., Gleason M.N., Clinical Toxicology of Commercial Products,1979.,p. II-211)

An assessment of acid or alkali reserve

Sodium or potassium xanthates dissolved in water undergoes hydrolysis giving alkaline reaction. When xanthates are produced as a water solutions exes of an alkali hydroxide is kept (pH >10) as a decomposition inhibitor.

Respiratory tract

Sodium isopropyl xanthate(CAS# 140-93-2) irritating to skin, eyes, mucous membrane, respiratory tract(The Merck Index , 9th ed., Merck & Co., Inc., 1976 , p. 1116; http:// toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp )

Xanthates dust or water solution mist is irritating to the nose, throat and upper respiratory track under normal condition of use.(COOH, CHEMINFO Sodium ethyl xanthate updated July 20210,www.ccohs.ca)

Sodium isopropyl xanthate(CAS# 140-93-2)is irritating to skin, eyes, mucous membrane, respiratory tract(The Merck Index , 9th ed., Merck & Co., Inc., 1976 , p. 1116; http:// toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp )