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EC number: 203-564-8 | CAS number: 108-24-7
- 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
There are sufficient data to conclude that at concentrations below the threshold for chronic irritation, there is no evidence of carcinogenic potential of acetic anhydride.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Carcinogenicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Justification for classification or non-classification
Although there are no carcinogenicity studies available for acetic anhydride, a thorough review of the available data concluded that acetic anhydride has no significant genotoxic activity. Systemic effects indicate no carcinogenic potential. Regarding local effects, the intrinsic properties of the acetic anhydride molecule induce severe localized irritation/corrosion effects across species. There is no evidence of any carcinogenic potential below the threshold for irritation. Significant discomfort in humans arising from such corrosive effects, limit chronic exposure to conditions where chronic damage and repair will not occur.
Additional information
Non-human data
A thorough review of the available data concluded that acetic anhydride has no significant genotoxic activity (IUCLID section 7.6). No guideline long-term carcinogenicity studies are available for acetic anhydride.
Local effects of acetic anhydride.
The effects of acetic anhydride at sites of initial contact are initiated by irritation of epithelium. The potential for facile, exothermic, transformation of acetic anhydride to acetic acid are likely to be at least partly responsible for the irritant properties of acetic anhydride. The irritant effect may simply be a consequence of physico-chemical properties of the molecule, and in support of this, there is no evidence of a species-specific response to irritation. Continued exposure to acetic anhydride leads to chronic localised irritation and is likely to induce a proliferative response, which might be expected to act as a promotional stimulus to cells that have already been initiated. However, at concentrations of acetic anhydride below the threshold (1 ppm, 4.18 mg/m3 ) for irritation and proliferation there is no reason to expect any carcinogenic potential.
Human data
Although these animal studies consider carcinogenic events at sites where local toxicity was expressed, little information may be added regarding systemic carcinogenic potential. Conversion of acetic anhydride to acetic acid and its uptake (pulmonary, oral or dermal), although rapid and extensive, 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).
Indeed, considering exposure to acetic anhydride at an atmospheric concentration of 1 ppm (4.18 mg/m3), the proposed NOAEC for local irritation effects (4.2 mg/m3), systemic exposure to acetate at this concentration is insignificant. For an 8 hour day spent at light work, and assuming 100% absorption of acetic anhydride/acid for a worker would be 4.2 mg/m3 * wRV m3/kg bw * [mw acetic anhydride / acetic acid] = 4.2 * 0.144 * [102.09 / 60.05] = 1.03 mg/kg bw. To put this intake into perspective with the known removal of acetate, it has been shown that about ~0.5 mg/kg bw acetate can be removed each minute via endogenous pathways, such as the citric acid cycle, in humans following administration of acetate in a drink (Smith et al., 2007). Daily administration of 40 mg/kg bw/day may be used as a medicinal product (Johnston & Gaas, 2006), and 25 mg/kg bw /day estimated as average human (infant) dietary intake (Ishiwata et al., 2002), with peak excursions up to 240 mg/kg bw /day (EU DAR, 2008).
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).
In addition, 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. 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. ”
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