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EC number: 206-768-5 | CAS number: 373-61-5
- 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
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Carcinogenicity
Administrative data
Description of key information
Key value for chemical safety assessment
Justification for classification or non-classification
No data are availble for dihydrogen bis(acetato-O)difluoroborate. Overall there is sufficient information to conclude on the local and systemic carcinogenic potential of acetic acid and to conclude that at concentration below the threshold for dermal toxicity there is no local or systemic carcinogenic potential. No classification is warranted according to EU directive 67/548/EC and EU regulation (EC) NO. 1272/2008 (CLP).
Additional information
No data are available for this endpoint.
Acetic acid, as an active substance, has been considered under the fourth stage of the re-evaluation programme of the Plant Protection Product Directive 91/414/EEC (provisions of Regulation (EC) No 1112/2002) for use as a herbicide on e.g. pome and stonefruit, ornamental shrubs, paths. The decision has been made that it is included in Annex I of that Directive (Commission Directive 2008/127/EC of 18 December 2008 amending Council Directive 91/414/EEC to include several active substances) and therefore the use of acetic acid as a Plant Protection Product it is therefore regarded as registered under REACh(Article 15 of EC Reg 1907/2006). The toxicology endpoints addressed under Dir. 91/414/EECto conclude on toxicological hazard are directly comparable with those under REACh.
EFSA supported the recommendations by the rapporteur Member State and the result of the examination in accordance with the provisions of Article 24a of Regulation 2229/2004 stating that there are clear indications that it may be expected that this use of acetic acid does not result in any harmful effects on human health.
The Draft Assessment Report (EU DAR, 2008) states that “Long-term toxicity/carcinogenicity studies in animals with oral exposure are not necessary, considering that humans are exposed to orally ingested acetic acid from various food sources and there is no evidence that such exposure is causally related to toxic effects and an increased cancer incidence. Therefore, no new animal toxicity studies conforming to long-term toxicity or carcinogenicity test guidelines are necessary for Annex I inclusion of acetic acid.”
In addition to consideration of the status under EC Dir. 91/414/EEC, it is also approved for use as a food additive by the Joint FAO/WHO Expert Committee on Food Additives (Rome, 11-18 October, 1966). In theUSAacetic acid is affirmed as Generally Recognised as Safe (GRAS) by the US FDA (21CFR184.1005) and has also been exempted from the requirement of a tolerance under the US EPA Federal Food, Drug, and Cosmetic Act (FFDCA).
This current review of the repeat-dose toxicity of acetic acid has and similar overall conclusions have been reached. Below is the discussion of the weight of evidence that has been considered in this review.
Non-human information
A thorough review of the available data concluded that acetic acid has no significant genotoxic activity (CSR section 5.7). No guideline, long-term carcinogenicity studies are available for acetic acid, however two investigative studies, one oral (Alexandrov et al., 1989), and one dermal (Slaga et al., 1975), each of 8 months duration, are available.
In the first of these, a study designed to compare the influence of acetic acid on the carcinogenic effect of N-nitrososarcosin ethylester (NSEE) has been reported (Alexandrov et al., 1989). One group of 20 rats received NSEE (dosed orally 5 times per week) and also received 0.5 mL of commercial vinegar (3% acetic acid in water) intraoesophageally by gavage3 times per week for 6 months and then received the vinegar only for a further 2 months. Another group of 9 rats received vinegar only for 8 months and another group of 18 rats received NSEE only for 6 months. After 8 months animals were autopsied and the oesophagus and forestomach examined histopathologically.
As anticipated, rats treated with the carcinogen NSEE had high incidences of pre-neoplastic lesions and papillomas and carcinomas of the oesophagus and forestomach. Acetic acid administration, alone, did not induce tumours, however hyperplasia of the oesophagus and forestomach were reported. The relevance of the hyperplasia observed in this experimental model could not be determined due to the lack of appropriate controls and the unusual means of dosing. In combination, that is administration of vinegar in addition to treatment with NSEE, increased numbers of tumours of the oesophagus were reported. This finding is again consistent with the hyperplastic response observed in the tissues following intraoesophageal gavage with acetic acid that would be likely to enhance the effects of the carcinogen, NSEE. Other organs were not evaluated.
In the second study, topically applied acetic acid was used as a promoter for tumour development in mice that were initiated with beta-propiolactone or dimethylbenzyl[a]anthracene (Slaga et al., 1975). The concentrated acid (glacial acetic acid) was applied dermally 1-3 times per week (at doses of 1-40 mg/animal) for 32 weeks. Control animals received acetic acid, dermally, once per week. The incidence of papillomas and carcinomas was recorded and lesions were removed at random for histological verification.
A single dermal application of acetic acid at doses of up to 40 mg/animal, in mice initiated with beta-propiolactone or dimethylbenzyl[a]anthracene, did not induce excessive mortality. However, more than one weekly application of 10-40 mg acetic acid caused excessive mortality. 33% of mice died when 10 mg acetic acid/animal was applied dermally 3 times per week and approximately 50% of mice died when 20 mg was applied twice a week. No further details regarding these deaths are available.
Concentrations of glacial acetic acid above 2 mg/mouse, topically applied, induced skin irritation and associated hyperplasia. At 10 mg/mouse, the LOAEL for dermal effects, elevated DNA synthesis was sustained for a period 12-24 hours post-exposure, which is consistent with cell proliferation (EU DAR, 2008). In regard to the promoting activity of acetic acid, in the absence of significant local and systemic toxicity of acetic acid, only a weak promoting activity in mice, pretreated with dimethylbenzyl[a]anthracene or beta-propiolactone, was reported. However under the conditions of this 8-month study, concentrated acetic acid was concluded (EU DAR, 2008) to have no carcinogenic potential
The results of both these studies confirm that acetic acid is an irritant at the site of first entry. This is consistent with the physiochemical properties of an acid which is capable of producing aqueous solutions of very low pH (25% solution of acetic acid has pH less that 2) and the material is labelled under DSD and CLP as corrosive. However, at concentrations below the threshold for sustained local irritation and proliferative response, there is no evidence of any carcinogenic potential at the sites of first contact.
Human information
Although these animal studies consider carcinogenic events at sites where local toxicity was expressed, little information may be added regarding systemic carcinogenic potential. Uptake (pulmonary, oral or dermal) of acetic acid is likely to be the rate-limiting process of its disposition in animals and humans, as high-turnover endogenous metabolic pathways such as the Citric Acid Cycle will efficiently remove excess acetate (~0.5 mg/kg bw acetate per minute) such that high systemic concentrations are unlikely (Smith et al., 2007).
Considering that humans are exposed to acetic acid/acetate from food sources and that it is a key intermediate in critical biochemical processes of living organisms (intermediate in catabolism and in anabolic synthesis, e. g., in the formation of glycogen, fatty acid synthesis as well as cholesterol synthesis, in the acetylation of amines, in the conversion into alanine and subsequent incorporation into proteins of plasma, liver, kidney, gut mucosa, muscle, and brain) (Health Council of the Netherlands, 2004), it seems that systemic carcinogenic potential is rather unlikely. An epidemiological study comparing local food consumption patterns in Japan with geographical distributions of gastro-intestinal cancers, vinegar consumption was reported to be negatively associated with standardised mortality ratios for all cancers of the gastro-intestinal tract, including bile ducts and pancreas (Hara et al., 1985).
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.
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