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EC number: 236-102-9 | CAS number: 13162-05-5
- 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
Endpoint summary
Administrative data
Key value for chemical safety assessment
Additional information
In vitro studies:
N-Vinylformamide was not mutagenic in the Ames test in Salmonella
typhimurium strains TA98, TA100, TA1535, TA1537 and TA1538, both in the
presence and in the absence of S-9 mix from Aroclor 1254 induced rats,
when tested up to the limit dose level of 5000 µg/plate (Air Products
and Chemicals, Inc. 1992, BASF AG 1985). Up to this concentration no
bacteriotoxic effect was observed.
N-Vinylformamide was tested in the CHO/HPRT mutation assay in the
absence and presence of metabolic activation with phenobarbital and β-naphthoflavone-induced
rat liver S-9 (BASF SE 2010). The assay was conducted according to OECD
TG 476 at dose levels of 750, 375.5, 187.5, 93.8 or 750, 500, 250 and
125 μg/ml in non-activated and activated studies. The
cells were exposed for 4 or 24h. No cytotoxicity was observed up to 750
µg/ml. Under the conditions of this mutagenicity test, N-Vinylformamide
was negative in both the absence and presence of exogenous metabolic
activation. Supportingly, N-Vinylformamide was tested in the CHO/HGPRT
mutation assay in the absence and presence of metabolic activation with
Aroclor-induced rat liver S-9 (Air Products and Chemicals, Inc. 1992).
The assay was conducted at dose levels of 5000, 2500, 1250, 625 and 312.5μg/ml
in both the non-activated and activated studies. No cytotoxicity was
observed up to 5000 µg/ml. Under the conditions of this mutagenicity
test, N-Vinylformamide was negative in both the absence and presence of
exogenous metabolic activation.
N-Vinylformamide was tested in the micronucleus assay in V79 cells in
the absence and presence of metabolic activation with phenobarbital andβ-naphthoflavone-induced
rat liver S-9 (BASF SE 2010). The assay was conducted according to draft
OECD TG 487 (version 5, 2009). Dose levels of 750, 375, 187.5, 93.8 and
46.9 µg/ml were used for 4h exposure with and without metabolic
activation and 24 exposure with metabolic activation. Exposure for 4h
with and without S9 was also tested at dose levels of 750, 500, 375 and
187.5 µg/ml. No cytotoxicity was observed up to 750 µg/ml. Under the
conditions of this mutagenicity test, N-Vinylformamide was negative in
both the absence and presence of exogenous metabolic activation.
Conclusion: In vitro, N-Vinylformamide was negative in bacterial
(Ames test), mammalian (CHO/HGPRT) mutation, mammalian (CHO/HPRT)
mutation, and mammalian micronucleus assays both in the presence and in
the absence of metabolic activation.
In vivo studies:
Supporting to the negative result in the in vitro micronucleus
assay (BASF SE 2010), N-Vinylformamide has been tested in an in vivo micronucleus
assay (Air Products and Chemicals, Inc. 1992). Male ICR mice were
exposed to 19, 38, or 75 mg/kg and female ICR mice to 29, 58, or 115
mg/kg of the test substance which was administered in a total volume of
10 ml/kg as a single intraperitoneal injection. No reduction in the
ratio of polychromatic erythrocytes (PCE) to total erythrocytes was
observed in the test article-treated groups relative to the vehicle
control suggesting that the test substance did not induce bone marrow
toxicity. N-Vinylformamide was negative in the induction of micronuclei
in anin vivomouse micronucleus test.
Conclusion: In vivo, a micronucleus test using intraperitoneal
injection of N-Vinylformamide in ICR mice was negative.
Short description of key information:
In vitro, N-Vinylformamide was negative in bacterial (Ames test) and
mammalian mutation assays (CHO/HGPRT and micronucleus test in V79 cells)
both in the presence and in the absence of metabolic activation. In
vivo, a micronucleus test using intraperitoneal injection of
N-Vinylformamide in ICR mice was negative.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
GHS classification according to Annex I 1272/2008 CLP (EU GHS):
no classification required
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