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Diss Factsheets
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EC number: 930-964-6 | 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
Neurotoxicity
Administrative data
- Endpoint:
- neurotoxicity: acute oral
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: The publication provides information on the effects of chloroacetic acid on the blood-brain barrier function. No data on GLP.
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 1 987
Materials and methods
- Principles of method if other than guideline:
- Preliminary studies had indicated that mice surviving a toxic dose of monochloroacetic acid may develop rigid clasping of the front paws as early as 24 hr after treatment. The present investigation was undertaken to further characterize this rigidity, and to study its association with monochloroacetic acid-induced blood-brain barrier damage in mice.
Male Swiss Webster mice were used in the test. The substance was orally administered with a constant volume (0.2 mL/26 g). The doses tested were 320 and 380 mg/kg bw. Immediately following the treatment the animals were observed for a period between 48 hours and 8 weeks. - GLP compliance:
- not specified
- Limit test:
- no
Test material
Reference
- Name:
- Unnamed
- Type:
- Constituent
- Details on test material:
- - Name of test material (as cited in study report): Monochloroacetic acid
- Analytical purity: approx 99%
Test animals
- Species:
- mouse
- Strain:
- Swiss Webster
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: Perfection Breeders (Douglassville, PA).
- Weight at study initiation: 25- 30 g
- Housing: Animals were housed 20 to a cage in polypropylene "shoebox" cages with zinc-plated wirebar lids and Beta-Chip Hardwood Laboratory Bedding (Northeastern Products Corp., Warrensburg, NY).
- Diet (e.g. ad libitum): Purina Rodent Chow (Ralston Purina Co., St. Louis, MO); ad libitum.
- Water (e.g. ad libitum): tap water; ad libitum.
- Acclimation period: At least 1 week.
ENVIRONMENTAL CONDITIONS
- Temperature (°C): 22 ºC
- Humidity (%): 55 %
- Photoperiod: 12 hrs dark / 12 hrs light.
Administration / exposure
- Route of administration:
- oral: gavage
- Vehicle:
- water
- Details on exposure:
- For oral administration, monochloroacetic acid was dissolved in deionized water, and a constant volume of 0.2 mL/26 g was given.
- Analytical verification of doses or concentrations:
- not specified
- Duration of treatment / exposure:
- A single oral exposure
- Frequency of treatment:
- A single exposure
Doses / concentrationsopen allclose all
- Remarks:
- Doses / Concentrations:
320 mg/kg bw
Basis:
nominal conc.
- Remarks:
- Doses / Concentrations:
380 mg/kg bw
Basis:
nominal conc.
- No. of animals per sex per dose:
- 8-10 male animals per group
- Control animals:
- yes, concurrent vehicle
Examinations
- Sacrifice and (histo)pathology:
- Histological examination of brain tissue: Control mice, as well as 48-hr and 2-, 5-, and 8-week survivors from the acute toxicity studies exhibiting varying degrees of front paw rigidity were anesthetized with methohexital sodium, and perfused via the left ventricle with 20 mL of 10% phosphate-buffered formalin. Brains were removed and fixed in 10% phosphate-buffered formalin for 3 days, then transferred to 70% ethanol for storage. The tissues were later dehydrated, cleared, embedded in paraffin, and 6-µm-thick sections were cut on a rotary microtorne using standard histological techniques (Luna, 1968). Midsagittal sections were utilized so that all areas of the brain could be viewed on one slide. Slides were prepared in triplicate and stained with hematoxylin and eosin for a general cytological stain (Luna, 1968), Luxol Fast Blue G with a eresyl fast violet counterstain to outline the myelin sheath (La Bossiere, 1976), and the Bodian stain for nerve fibers.
- Statistics:
- For experiments with only control and one treatment group, the means of the groups were compared using the Student's t test and a 5% significance level. For experiments with several treatment groups, a one-way analysis of variance (ANOVA) was used to test for differences among treatment groups. If the F value was significant (p < 0.05), Student's t test was employed to compare the means of the groups.
Results and discussion
Results of examinations
- Clinical signs:
- effects observed, treatment-related
- Mortality:
- mortality observed, treatment-related
- Body weight and weight changes:
- not specified
- Food consumption and compound intake (if feeding study):
- not examined
- Food efficiency:
- not examined
- Water consumption and compound intake (if drinking water study):
- not examined
- Ophthalmological findings:
- not examined
- Clinical biochemistry findings:
- not examined
- Behaviour (functional findings):
- effects observed, treatment-related
- Gross pathological findings:
- effects observed, treatment-related
- Neuropathological findings:
- effects observed, treatment-related
- Details on results:
- No significant lesions were observed in the control mice at the light microscopic level. Treated rats, however, had lesions. Two 48-hr brains showed pyknosis of Purkinje cell nuclei, and bright red staining of the cell body was observed in two of the three 48-hr brains. No other lesions were observed. Two weeks following MCA exposure the Purkinje cells were fewer in number as seen by discontinuities in the Purkinje cell layer. Two weeks after MCA there were also more Purkinje cells with damaged nuclei and bright red staining of the perikaryon. RBCs outside capillaries were seen in the molecular layer of the cerebellum. A progression of the damage was seen in MCA-treated animals 5 weeks post-treatment, with fewer Purkinje cells lining the granular
cell layer and fewer pyknotic nuclei, suggesting that all the damaged cells have undergone necrosis and have been removed. RBCs were still present at these later time points and appeared to be undergoing necrosis. This indicated that the presence of the RBCs outside the capilIary was not an artifact caused by perfusion of the brains and dislodging of the RBCS.
Although the pathological changes were first seen almost exclusively in the cerebellum, further examination of these brains revealed damage in other areas. After 2 weeks the brain of one mouse exhibited a necrotic focus in the pons. Pyknotic nuclei were observed in treated animals in the brainstem, hippocampus, and cerebral cortex at 2 and 5 weeks after treatment. There was also an apparent increase in vacuoles in the brains of MCA-treated animals, but it cannot be determined if this was treatment-related or an artifact caused by perfusion of the brains and fixation ofthe tissues.
Effect levels
- Dose descriptor:
- NOAEL
- Sex:
- male
- Basis for effect level:
- other: overall effects
- Remarks on result:
- not determinable
- Remarks:
- no NOAEL identified
Any other information on results incl. tables
Monochloroacetic acid causes front paw rigidity in 10% of mice surviving a single oral toxic dose (320 -380 mg/kg bw). Mice exhibiting front paw rigidity were killed at various times after the treatment and their brains were prepared for histological examination. As early as 48 hr post-treatment, RBCs were found outside capillaries in several brain regions, especially the cerebellum. At time points up to 8 weeks after treatment, extracapillary RBCs were seen to be undergoing lysis, and there was loss of cerebellar Purkinje cells.
Applicant's summary and conclusion
- Conclusions:
- Monochloroacetic acid causes front paw rigidity in 10% of mice surviving a single oral toxic dose (320 -380 mg/kg bw). Mice exhibiting front paw rigidity were killed at various times after the treatment and their brains were prepared for histological examination. As early as 48 hr post-treatment, RBCs were found outside capillaries in several brain regions, especially the cerebellum. At time points up to 8 weeks after treatment, extracapillary RBCs were seen to be undergoing lysis, and there was loss of cerebellar Purkinje cells.
- Executive summary:
Preliminary studies had indicated that mice surviving a toxic dose of monochloroacetic acid may develop rigid clasping of the front paws as early as 24 hr after treatment. The present investigation was undertaken to further characterize this rigidity, and to study its association with monochloroacetic acid-induced blood-brain barrier damage in mice.
Male Swiss Webster mice were used in the test. The substance was orally administered with a constant volume (0.2 mL/26 g). The doses tested were 320 and 380 mg/kg bw. Immediately following the treatment the animals were observed for a period between 48 hours and 8 weeks.
Monochloroacetic acid causes front paw rigidity in 10% of mice surviving a single oral toxic dose (320 -380 mg/kg bw). Mice exhibiting front paw rigidity were killed at various times after the treatment and their brains were prepared for histological examination. As early as 48 hr post-treatment, RBCs were found outside capillaries in several brain regions, especially the cerebellum. At time points up to 8 weeks after treatment, extracapillary RBCs were seen to be undergoing lysis, and there was loss of cerebellar Purkinje cells.
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