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EC number: 208-863-7 | CAS number: 544-17-2
- 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
Specific investigations: other studies
Administrative data
Link to relevant study record(s)
Description of key information
Formate is a moderate respiratory chain inhibitor (Ki approx. 6 mM) which may be associated with ocular damage seen when elevated formate levels persist (approx. blod levels 7mM, min. 24 hours). The ocular damage is associated with low hepatic folate levels and, hence, slow formate metabolism. It was demonstrated to occur in vitro, and in vivo in non-human primates (monkeys) and in pretreated rats receiving formate.
Additional information
Experimental animals metabolise formate more rapidly than humans and non-human primates, primarily due to higher hepatic folate levels. As a consequence, formate does not accumulate. It may, however, accumulate in humans and monkeys. Therefore, these species differences obscure potential adverse formate effects in experimental animals but may occur in humans.
After methanol poisoning, irreversible ocular toxicity (retina, optical nerve) is seen in humans but not in rodents, and it is attributable to folate. This was confirmed by experiments in vitro and in vivo where functional and morphological changes of the retina and the optical nerve were demonstrated with formic acid and sodium formate (Emmrich, 2002). Monkeys developed ocular lesions when plasma formate levels were increased over an extended period of time (>550 mg/L [approx. 12 mM], > 24 hours) by means of i.v. infusion of sodium formate (Martin-Amat, 1978). Additionally, a rat model was developed to demonstrate ocular toxicity in rats. Pretreatment with N2O significantly reduces the folate level in rats, and functional and morphological lesions are then obtained in rats receiving methanol or sodium formate (Eells, 2000). Formate-induced retinal toxicity in pretreated, methanol-intoxicated rats was recently demonstrated to occur at 2.6 mM formate after 24 hours (Seme, 1999). According to Hanzlik, blood formate must exceed 7 mM (i.e. 315 mg/L) for at least 24 hours to produce irreversible ocular damage to occur in humans.
Folate is a moderate inhibitor (Kiapprox 6 mM) of cytochrome c oxydase, i.e. it impairs respiratory chain and proper ATP supply of the affected cells, it favours generation of lactic acid and, hence, acidosis on a cellular level (Nicholls, 1976; Erecinska and Wilson, 1980). This pattern was seen in photoreceptor cells and optical nerve cells after in vitro or in vivo formate treatment. However, the exact mechanism of ocular toxicity is still not fully understood. It should be noted that folate treatment in vivo does not lead to acidosis, in contrast to methanol poisoning.
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