Registration Dossier

Data platform availability banner - registered substances factsheets

Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Diss Factsheets

Administrative data

Description of key information

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
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
Strain:
Wistar
Sex:
male
Details on test animals or test system and environmental conditions:
TEST ANIMALS

- Weight at study initiation: 200-265g

- Fasting period before study: Over night

- Water: ad libitum
Route of administration:
oral: gavage
Vehicle:
unchanged (no vehicle)
Doses:
250, 500,1000, 1250, 1700, 2000 mg
No. of animals per sex per dose:
10 male
Control animals:
no
Details on study design:
- Duration of observation period following administration: 14 days

- Frequency of observations and weighing: Regular intervals on the day of dosing and daily thereafter for 14 days.

- Necropsy of survivors performed: yes

- Other examinations performed: clinical signs, body weight,organ weights, histopathology, other: Gross necropsies were performed on all survivors and any animals which died during the observation period. Body weights of survivors were recorded prior to sacrifice.


Sex:
male
Dose descriptor:
LD50
Effect level:
1 250 mg/kg bw
Based on:
test mat.
Remarks on result:
other: oral administration of Sodium Isopropyl Xanthate (SIPX) to rats produced increased motor activity, cyanosis, irritability, increased respiration and convulsions with death occurring 1 to 2 hours after administration.
Sex:
male
Dose descriptor:
LD0
Effect level:
250 mg/kg bw
Based on:
test mat.
Remarks on result:
other: LD0 Lethal dose for 0% of the animal test population
Mortality:
All death occurring 1 to 2 hours after administration.
Clinical signs:
other: Oral administration of Sodium Isopropyl Xanthate (SIPX) to rats produced increased motor activity, cyanosis, irritability, increased respiration and convulsions with death occurring 1 to 2 hours after administration.
Gross pathology:
Autopsy showed perivascular and pericellular oedema, multiple haemorrhages in the lungs, perivascular subarachnoid haemorrhages and acute
swelling of the cells of the cortex, subcortical ganglia and the brain stem. Fatty dystrophy of the liver and protein dystrophy of the twisted canaliculi of the kidneys were observed.
Other findings:
The findings of these studies indicate that Sodium Isopropyl Xanthate (SIPX) produces adverse effects on the central nervous system, liver and kidneys.

Table 3:

Oral toxicity of xanthates (from: Kirk-Othmer, 1984)16

Xanthate

Species

LD0

 (mg/kg)

LD50

(mg/kg)

References

Sodium ethyl

rat

500

17

Potassium ethyl

Rat

 mouse

500

1700

583

17, 18

Sodium isopropyl

rat

250

1250

17

Potassium isopropyl

rat

mouse

— —

1700

 583

18 —

Potassium n-butyl

mouse

411

 465

19,20

Sodium isobutyl

rat

 

500

17

Potassium isobutyl

rat

mouse

— —

1290

 480

18 18

Sodium sec-butyl

rat

>2000

17

Potassium amyl (mixed)

rat

1000

1000–2000

17, 21

Potassium iso amyl

rat

mouse

— —

765

470

18 18

C5-C6 mixture

rat

1500

22

 

 

The LD50 value of 1250 mg/kg in rats were determined for Sodium Isopropyl Xanthate (SIPX). This show that Sodium Isopropyl Xanthate (SIPX) is of slightly order of acute oral toxicity .

 

The LD50 of the various xanthates are similar, ranging from 411 to 583 mg/kg in mice and from 1000 to >2000 mg/kg in rats.

The acute oral toxic effects of one xanthate, potassium butyl xanthate, are providedin two summaries in Chemical Abstracts.

 Similar symptoms and pathology findings were seen in these studies carried out by Babayan.

 

References :

16.Kirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd ed, pp 645-661,John Wiley & Sons, 1984.

17.Dow Chemical Company, 1964, unpublished toxicological data to C.B. Shaffer,American Cyanamid; data from P. Avotin, American Cyanamid, privatecommunication, 1982 as cited in Kirk-Othmer Encyclopaedia of Chemical

18.Babayan, E.A., 1963, “Toxicology of Potassium Butyl Xanthate” Material 2-oi[Vtoroi] Itog. Nauchn. Konf. Inst. Gigieny Truda I Prof. Zabolevan Posvyashch.Vopr. Gigieny Truda I Prof. Patol. Erevan, pp 75-77 (Pub 1964)(Russ)Chem Abstract,64, 8836e (1966).

19.Babayan, E.A., “Toxicological Characteristics of the Flotation Agent PotassiumButyl Xanthate”, Mater. Itogovoi Nauch. Konf. Vop. Gig Tr Profpatol. Khim.Gornorud. Prom., 3rd 1966 (Pub 1968) 97-102 (Russ) inChemical Abstracts,Vol 73,1970.

20.Fronk, N.G., The Dow Chemical Company, private communication, 1982, as cited inKirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd Ed, pp 645-661,John Wiley & Sons, 1984.

21.Buzina, A.Z., Burkhanov, A.I. and Abeuev, Kh.B., 1977 Zdravookhr. Kaz., 88 ascited inKirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd Ed, pp645-661, John Wiley & Sons, 1984.

22.Chemical Abstracts,Vol 64, 1966.

 

Interpretation of results:
other: sligthly toxic
Remarks:
Criteria used for interpretation of results: EU
Conclusions:
The LD50 value of 1250 mg/kg was determined in a reliable study. This show that Sodium Isopropyl Xanthate (SIPX) is of a Slightly order of acute oral toxicity .
Based on the data provided in this review, Sodium Isopropyl Xanthate (SIPX) shall be classified for acute oral toxicity.
Endpoint conclusion
Endpoint conclusion:
adverse effect observed
Dose descriptor:
LD50
Value:
ca. 1 250 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

Link to relevant study records
Reference
Endpoint:
acute toxicity: inhalation
Type of information:
read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
data from handbook or collection of data
Justification for type of information:
Certain details lacking, but considered suitable to confirm similar results as would be expected for this substances
Study provided on similar substance to help build up a weight of evidence demonstrating potential for read-across between the xanthates
The sodium and potassium salt xanthates is considered suitable as a key source of data for the others sodium and potassium salt xanthates
Considered valid for read-across for purposes of classification.
No further vertebrate testing can be justified.
Reason / purpose for cross-reference:
read-across source
Reason / purpose for cross-reference:
read-across: supporting information
Qualifier:
equivalent or similar to guideline
Guideline:
OECD Guideline 403 (Acute Inhalation Toxicity)
Deviations:
not specified
GLP compliance:
not specified
Species:
rat
Strain:
not specified
Sex:
not specified
Route of administration:
inhalation
Type of inhalation exposure:
not specified
Vehicle:
not specified
Duration of exposure:
2 h
Control animals:
not specified
Dose descriptor:
LC50
Effect level:
7 690 mg/m³ air
Clinical signs:
other:
Interpretation of results:
GHS criteria not met
Conclusions:
The sodium and potassium salt xanthates is considered suitable as a key source of data for the others sodium and potassium salt xanthates
Considered valid for read-across for purposes of classification.
No further vertebrate testing can be justified.
Executive summary:

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


Study provided on similar substance to help build up a weight of evidence demonstrating potential for read-across between the xanthates

Endpoint conclusion
Endpoint conclusion:
adverse effect observed
Dose descriptor:
LC50
Value:
7 690 mg/m³ air

Acute toxicity: via dermal route

Link to relevant study records
Reference
Endpoint:
acute toxicity: dermal
Data waiving:
study scientifically not necessary / other information available
Justification for data waiving:
the study does not need to be conducted because the substance is classified as corrosive to the skin
Reason / purpose for cross-reference:
data waiving: supporting information
Clinical signs:
other:
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 Isopropyl Xanthate (SIPX) has an LD50 of 1250 mg/kg in rats and produced increased motor activity, cyanosis, irritability, increased respiration and convulsions with death occurring 1 to 2 hours after administration. 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= 1250 mg/kg b.w. in rats of Sodium Isopropyl Xanthate (SIPX) (CAS# 140-93-2)


LD50 of 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 toxicity


 










































































































Table 3:



Oral toxicity of xanthates (from: Kirk-Othmer, 1984)16



Xanthate



Species



LD0



 (mg/kg)



LD50



(mg/kg)



References



Sodium ethyl



rat



500





17



Potassium ethyl



Rat


 mouse



500



1700


583



17, 18



Sodium isopropyl



rat



250



1250



17



Potassium isopropyl



rat


mouse






1700


 583



18




Potassium n-butyl



mouse





411


 465



19,20



Sodium isobutyl



rat



 



 500



17



Potassium isobutyl



rat


mouse






1290


 480



18 18



Sodium sec-butyl



rat





>2000



17



Potassium amyl (mixed)



rat



1000



1000–2000



17, 21



Potassium iso amyl



rat


mouse






765


470



18 18



C5-C6 mixture



rat





1500



22



 



 



 



 



 



 



 



 



 


The LD50 value of 1250 mg/kg in rats were determined for Sodium Isopropyl Xanthate (SIPX). This show that Sodium Isopropyl Xanthate (SIPX) is of a slightly order of acute oral toxicity .


 


The LD50 of the various xanthates are similar, ranging from 411 to 583 mg/kg in mice and from 1000 to >2000 mg/kg in rats.


The acute oral toxic effects of one xanthate, potassium butyl xanthate, are provided in two summaries in Chemical Abstracts.


Similar symptoms and pathology findings were seen in these studies carried out by Babayan.


 


References :


16.Kirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd ed, pp 645-661,John Wiley & Sons, 1984.


17.Dow Chemical Company, 1964, unpublished toxicological data to C.B. Shaffer,American Cyanamid; data from P. Avotin, American Cyanamid, privatecommunication, 1982 as cited in Kirk-Othmer Encyclopaedia of Chemical


18.Babayan, E.A., 1963, “Toxicology of Potassium Butyl Xanthate” Material 2-oi[Vtoroi] Itog. Nauchn. Konf. Inst. Gigieny Truda I Prof. Zabolevan Posvyashch.Vopr. Gigieny Truda I Prof. Patol. Erevan, pp 75-77 (Pub 1964)(Russ)Chem Abstract,64, 8836e (1966).


19.Babayan, E.A., “Toxicological Characteristics of the Flotation Agent PotassiumButyl Xanthate”, Mater. Itogovoi Nauch. Konf. Vop. Gig Tr Profpatol. Khim.Gornorud. Prom., 3rd 1966 (Pub 1968) 97-102 (Russ) inChemical Abstracts,Vol 73,1970.


20.Fronk, N.G., The Dow Chemical Company, private communication, 1982, as cited inKirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd Ed, pp 645-661,John Wiley & Sons, 1984.


21.Buzina, A.Z., Burkhanov, A.I. and Abeuev, Kh.B., 1977 Zdravookhr. Kaz., 88 ascited inKirk-Othmer Encyclopaedia of Chemical Technology,Vol 24, 2nd Ed, pp645-661, John Wiley & Sons, 1984.


22.Chemical Abstracts,Vol 64, 1966.


 


 


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 – 10000 mg/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 Isopropyl Xanthate (SIPX) (CAS# 140-93-2) 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 )


 

Justification for classification or non-classification