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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Diss Factsheets

Toxicological information

Additional toxicological data

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Administrative data

additional toxicological information
Type of information:
other: dossier on the toxicological profile of CTC
Adequacy of study:
supporting study
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: secondary surce

Data source

Reference Type:
secondary source
Toxicological profile for carbon tetrachloride
Bibliographic source:
U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry

Materials and methods

Test material

Constituent 1
Chemical structure
Reference substance name:
Carbon tetrachloride
EC Number:
EC Name:
Carbon tetrachloride
Cas Number:
Molecular formula:

Results and discussion

Applicant's summary and conclusion

Executive summary:

summary on interaction between CTC and alcohol as described in the ATDSR dossier (August 2005):

"- Alcohol consumption is an important risk factor for the development of serious toxicological effects following exposure to carbon tetrachloride, since alcohol induces CYP2E1, leading to increased production of reactive metabolites.

- Secondary alcohols can also potentiate carbon tetrachloride hepatorenal toxicity in humans. Potentiation of carbon tetrachloride hepatoxicity in mice by isopropanol far exceeded that caused by an equal dose of ethanol, though both exerted their maximum effect when given 18 hours before carbon tetrachloride. Methanol co-treatment in rats potentiated the hepatotoxicity of carbon tetrachloride by inducing CYP2E1 in rat liver.

- Investigations in rats indicate that ketosis, caused either by diabetes or administration of ketones, can potentiate carbon tetrachloride hepatotoxicity. The bulk of available evidence suggests that elevated levels of ketone bodies induce the enzyme system responsible for biotransformation of carbon tetrachloride to its reactive metabolites.

- Phenobarbital (PB) has been shown to produce a marked increase in carbon tetrachloride hepatotoxicity in rats and it is widely used to provide experimental animal models of carbon tetrachloride-induced cirrhosis.

- DDT increased the sensitivity of rats to carbon tetrachloride poisoning (McLean and McLean 1966), and mice fed 100 ppm polybrominated biphenyls (PBBs) or 200 ppm polychlorinated biphenyls (PCBs) in their diet for 28 days experienced increased carbon tetrachloride hepatotoxicity (Kluwe et al. 1979). Potentiation of renal dysfunction was also found in the PBB-pretreated mice. All of these compounds are broad-spectrum mixed-function oxidase (MFO) inducers.

- Concurrent treatment with methamphetamine at doses between 5 and 15 mg/kg increased hepatotoxicity

in rats treated with carbon tetrachloride

- Certain haloalkanes and haloalkane-containing mixtures have been demonstrated to potentiate carbon tetrachloride hepatotoxicity.

- Nicotine: Treatment of rats for 10 days with nicotine in drinking water increased liver histopathology (fatty change, necrosis, and dark-cell change) caused by an injection of carbon tetrachloride. It was proposed that the increased hepatotoxicity might have resulted from a synergistic effect of the lipid peroxidation induced by both agents.

- Carbon disulfide and other alkyl sulfides: Just as chemicals that serve to stimulate the metabolism of carbon tetrachloride lead to increased toxicity, chemicals that impair carbon tetrachloride metabolism lead to decreased toxicity."