Registration Dossier
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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 939-509-6 | CAS number: -
- 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
Carcinogenicity
Administrative data
Description of key information
Reaction mass of 2,4 -Dichloronitrobenzene and 2,6 -Dichloronitrobenzene is a multiconstituent substance containing
2,4 -Dichloronitrobenzene as main component clear evidence of carcinogenic activity by 2 -year feeding in both rats and mice.
The component 2,5-DCNB produced clear evidence of hepatocarcinogenicity in male rats and male and female mice and equivocal evidence of renal cell tumours and Zymbal gland tumor in male rats. Thus, reaction mass of 2,4-dichloronitrobenzene and 2,6-dichloronitrobenzene has to be evaluated as carcinogen.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- 12.3
Justification for classification or non-classification
Due to the available data on 2,4 -DCNB and 2,5 -DCNB reaction mass of 2,4 -dichloronitrobenzene and 2,6 -dichloronitrobenzene has to be allocated to category 1B(H350) according to Regulation(EC)1272, 2008. According to Regulation (EC) 67548/EWG the substance is classified /lasbelled with Carc Cat 2; R 45 = may cause cancer.
Additional information
Reaction mass of 2,4 -Dichloronitrobenzene and 2,6 -Dichloronitrobenzene is a multiconstituentsubstance containing
(611 -06 -3) 2,4 -Dichloronitrobenzene : 50 -80 %
(601 -88 -7) 2,6.-Dichloronitrobenzene: 10 -50 %
(89 -61 -2) 2,5 -Dichloronitrobenzene 0 -5 %
(541 -73 -1) 1,3 Dichlorobenzene 0 -<1 %
mixture of 4,6 -dichloro-1,3 -dinitrobenzene and 2,4 -dichloro-1,3 -dinitrobenzene 0 -10 %
There are no data on carcinogenicity available with 601 -88 -7, 541 -73 -1 and with the mixture of 4,6 -dichloro-1,3 -dinitrobenzene and 2,4 -dichloro-1,3 -dinitrobenzene
611 -06 -3
Carcinogenicity of 2,4 -dichloro-1 -nitrobenzene (2,4 -DCNB) esd examined by dietary administration to F344/DuCrj rats and Crj:BDF1 mice of both sexes for 2 years. Dietary administration commenced when the animals were 6 weeks old. The dietary concentration of 2,4-DCNB was 0 (control), 750, 1,500 and 3,000 ppm (w/w) for male and female rats; 0, 750, 1,500 and 3,000 ppm for male mice; and 0, 1,500, 3,000 and 6,000 ppm for female mice. In rats, there was a dose-dependent and significant induction of renal cell adenomas and carcinomas in both sexes and of preputial glands adenomas in males. In all the 2,4-DCNB-fed groups of both sexes, the incidence of atypical tubular hyperplasia, a pre-neoplastic lesion in the kidney, in the proximal tubule was significantly increased. In mice, there was a dosedependent and significant induction of hepatocellular adenomas,hepatocellular carcinomas, hepatoblastomas and peritoneal hemangiosarcomas in both sexes. The incidence of acidophilic hepatocellular foci was also significantly increased in female mice.Thus, clear evidence of carcinogenic activity of 2,4 -DCNB by 2 -year feeding was demonstratedin both rats and mice.
89 -61 -2
Carcinogenicity and chronic toxicity of 1,4 -dichloro-2 -nitrobenzene (!,4DC2NB= 2,5-DCNB) were examined by feeding each group of 50 F344 rats of both sexes and by feeding groups of 50 BDF1 mice with diets at a concentration of 0, 320, 800, 2000 ppm of the test item. This study was performed a ccording to OECD TG 453 under GLP conditions.
In rats, incidences of hepatocellular adenomas and carcinomas and their combined incidence were increased in the 2,000 ppm-fed males, together with increased incidence of basophilic cell foci in the 800 and 2,000 ppm-fed males. A dose-related increase in combined incidences of renal cell adenomas and carcinomas was noted. Incidence of Zymbal gland adenomas tended to increase in the 2,000 ppm-fed males. In mice, incidences of hepatocellular adenomas in the 800 and2000 ppm fed females and hepatocellular carcinomasin the 2000 ppm fed males and in the 800 and 2000 ppm fed females were increased.Incidence of hepatoblastomas was increased in all 2,5-DCNB-fed males and in 2000 ppm females.
Thus, 2,5-DCNB produced clear evidence of hepatocarcinogenicity in male rats and male and female miceand equivocal evidence of renal cell tumours and Zymbal gland tumor in male rats
OVERALL CONCLUSION
Reaction mass of 2,4 -Dichloronitrobenzene and 2,6 -Dichloronitrobenzene is a multiconstituent substance containing
2,4 -Dichloronitrobenzene as main component which showed clear evidence of carcinogenic activity by 2 -year feeding in both rats and mice.
The component 2,5-DCNB produced clear evidence of hepatocarcinogenicity in male rats and male and female mice and equivocal evidence of renal cell tumours and Zymbal gland tumor in male rats. Thus, reaction mass of 2,4-dichloronitrobenzene and 2,6-dichloronitrobenzene has to be evaluated as carcinogen. Morover, based on the data on mutagenicity it has to be evaluated as genotocic carcinogen.
Both substances 2.4-DCNB and 2.5 -DCNB are genotoxic carcinogens (Kano 2012, Yamazaki 2006). Both substances develop tumours aleady at the lowest dose applied. This is 800 ppm for 2,5 -DCNB. The lowest dose of 2,4 -DCNB.with hepatocellularadenomas and the combined incidence of total hepatic tumors is 750 ppm. Therefore, it seems legal to subsummarize also 2,5 -DCNB in the non-threshold approach used by Kano et al (2012)
Kano et al (2012) used a non-threshold approach to calculate the benchmark dose associated with 10 % risk over background (BMDL10). Based on the dose–response relationships between 2,4 -DCNB-intake and incidences of tumors obtained in the present study, a 95 % lower confidence limit of the BMDL10 was calculated using the linearized multistage model for total hepatic
tumors of male and female mice with US EPA’s benchmark dose software (Ver. 2.1.1) (US EPA 2009, Benchmark dose software version 2.1 user’s manual. 53 -BMDSRPT-0028, US EPA. Washington, DC ). The BMDL10 value for the endpoint of total hepatic tumors in male mice was 12.3 mg/kg per day and in female mice was 23.5 mg/kg per day.
Carcinogenicity: via oral route (target organ): digestive: liver
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.