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EC number: 202-620-9 | CAS number: 97-94-9
- 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
Description of key information
Acute oral toxicity study (Rinehart) gave LD50 235 mg/kg
Acute inhalation toxicity study (Kimmel) gave LC50 738 ppm
No acute dermal toxicity study
Key value for chemical safety assessment
Acute toxicity: via oral route
Link to relevant study records
- Endpoint:
- acute toxicity: oral
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- 1960
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Non-GLP with limited details of the study, however, considered sufficient for classification
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 401 (Acute Oral Toxicity)
- Deviations:
- not specified
- GLP compliance:
- no
- Test type:
- standard acute method
- Species:
- rat
- Strain:
- not specified
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- None provided
- Route of administration:
- oral: gavage
- Vehicle:
- other: Nujol (mineral oil)
- Details on oral exposure:
- Test article was administered by stomach tube and observed for 7 days.
- Doses:
- The assay of the solution was based on boron contest as determined by the method of Hill (Rinehart, 1960).
10 animals were dosed with 50 mg TEB kg. Five animals each were dose with 159, 200, 252, 317 or 468 mg TEB/kg. - No. of animals per sex per dose:
- See above
- Details on study design:
- No additional information provided
- Statistics:
- The LD50 was calculated by the method of Weil.
- Sex:
- male
- Dose descriptor:
- LD50
- Effect level:
- 235 mg/kg bw
- Remarks on result:
- other: no further information
- Mortality:
- There were 0/10, 0/5, 0/5, 4/5, 5/5 and 5/5 for the 50, 159, 200, 252, 317 or 468 mg TEB/kg dose groups, respectively. Death occurred within 2-24 hours.
- Clinical signs:
- other: Anorexia and lassitude (all animals) and tremors and convulsions in animals that died.
- Gross pathology:
- No data
- Interpretation of results:
- Category 3 based on GHS criteria
- Remarks:
- Criteria used for interpretation of results: EU
- Conclusions:
- The acute oral LD50 (rats) was 235 mg TEB/kg.
- Executive summary:
The acute oral LD50 (rats) was 235 mg TEB/kg.
Reference
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LD50
- Value:
- 235 mg/kg bw
- Quality of whole database:
- K2
Acute toxicity: via inhalation route
Link to relevant study records
- Endpoint:
- acute toxicity: inhalation
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Literature article of a non-GLP, non-guideline acute inhalation study with adequate details.
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 403 (Acute Inhalation Toxicity)
- Deviations:
- not specified
- Principles of method if other than guideline:
- "The acute inhalation toxicity of TEB was determined not only as a function of concentration but also as a function of the time after initiation of oxidation as well. At various exposure concentrations animals were exposed for 1 h to TEB oxidation product vapors in which either 36 msec or 4.6 min had elapsed between the initiation of the oxidation process and delivery to the exposure apparatus." (Kimmel et al, 1990)
- GLP compliance:
- no
- Test type:
- other:
- Species:
- rat
- Strain:
- Fischer 344
- Sex:
- male/female
- Details on test animals or test system and environmental conditions:
- "Fischer 344 (F-344) rats of both genders, 12 to 13 weeks of age at exposure, were obtained from Harlan
Industries (indianapolis, IN) for the pilot investigation; and F-344 rats, 11 to 14weeks of age at
exposure, were purchased from Charles River Breeding Laboratories (Kingston, NY) for the second
phase of the investigation. Upon receipt all animals were quarantined for a two-week period and
were committed to study following observ(!tion and random selection of representative animals for
quality control analysis. Prior to the exposures and during a 14-day postt!xposure observational
period, animals were group-housed (two to three per unit) in clear plastic cages with wood chip
absorbent bedding. Housing Linits were maintained in sjngle-pass laminar flow facilities. Food and
water were provided ad libitum with the exception of withholding food for a 12-h period prior to
sacrifice. All animals were maintained on a 12 -hr diurnal cycle." (Kimmel et al, 1990) - Route of administration:
- inhalation: vapour
- Type of inhalation exposure:
- nose only
- Vehicle:
- air
- Details on inhalation exposure:
- "The animals were exposed to either fTEB or aTEB using a 48-port, nose-only exposure
apparatus described by Raabe et ai. (1973)."
"At concentrations below 1150 to 1300 ppm, TEB rapidly oxidizes
to diethylethoxyborane (DEEOB), then ethyldiethoxyborane (EDEOB), and ultimately to
triethoxyborane (TEOB) (Callery Chemical, 1978)"
"Because of the rapid oxidation of TEB in air and the possibility that TEB toxicity might be a
function of the extent to which this oxidation has progressed, the acute inhalation toxicity of TEB was
determined not only as a function of concentration but also as a function of the time after initiation
of oxidation as well. At various exposure concentrations animals were exposed for 1 h to TEB
oxidation product vapors in which either 36 msec or 4.6 min had elapsed between the initiation of the
oxidation process and delivery to the exposure apparatus. For the purpose of clarity, fresh TEB (fTEB)
refers, in actuality, to the mixture of TEB and its DEEDB, EDEOB, and TEOB oxidation derivatives
delivt'red to the exposure chamber 36 msec after initial mixing of pure TEB vapor with oxygen. Aged
TEB (aTE B) vapor refers to the atmosphere resulting from a 4.6-min delay between the initiation of
TEB oxidation and delivery to the exposure chamber." (Kimmel et al, 1990) - Analytical verification of test atmosphere concentrations:
- yes
- Remarks:
- By IR and GC
- Duration of exposure:
- 1 h
- Concentrations:
- approximately 370, 600, or 780 ppm
- No. of animals per sex per dose:
- six
- Control animals:
- yes
- Details on study design:
- "Animals were assigned to experimental groups using a body weight normalized random
selection procedure. For the pilot investigation, 12 animals of each sex were assigned to each of three
experimental groups. One group each was exposed to comparable concentrations (approximately
960 ppm) of either fTEB or aTEB and one group was exposed for approxirnately one hour to air to
serve as controls. Half of the animals in each group were designated for evaluation of acute toxicity
after a 14-day postexposure observation period and half of the animals were scheduled for serial
sacrifice to evaluate the development and recovery from pulmonary insult at 4 h, 24 h, and 7 days
postexposure. Six animals of each sex were assigned to each of seven experimental groups for the
second phase (LC50 determination) of the investigation. No provisions were made to include
subgroups for serial, postexposure pathologic evaluation of potential pulmonary or CNS lesions. In
addition to a control group, animals were exposed to either fTEB or aTES at one of three
concentrations (approxi mately 370, 600, or 780 ppm)." (Kimmel et al, 1990) - Statistics:
- "Comparisons of mean body weights were performed using a multivariate analysis of covariance
for repeated measures test (Barcikowski, 1983). LCso determinations were made using a logistic
regression analysis (Bates and Watts, 1988). Histopathology data from the pilot investigation were
analyzed using a log-linear model, three-way contingency analysis (Dixon, 1990). Histopathology
data from the LC50 study were analyzed using a two-factor analysis of variance and Scheffe's multiple
comparison test (Barcikowski, 1983). Unless othenlVise specified, data reported are mean ±standard
deviation." (Kimmel et al, 1990) - Sex:
- male/female
- Dose descriptor:
- LC50
- Effect level:
- 738 ppm
- Remarks on result:
- other: no further information
- Mortality:
- Pilot study: exposure durations were only 52 min because in the first (fTEB) exposure mortality at the time was 100%.
Of the 24 animals exposed to aTEB, a total of 10 died during the exposure and 2 died within 24 h.
LC50 Study: "The overall LC50 for TEB (both fTEB and aTEB, both genders; calculations did not include pilot
study data) was 738 ppm (692 to 806). The LC50 for fTEB only (both genders) was greater at 766 ppm
(699 to 779) and the LC50 for aTEB only (both genders) was less at 709 (629 to 798). The combined
(both fTEB and aTEB) LC50 for males was 676 ppm (591 to 719), whereas the combined LC50 for
females was >821 ppm. Numbers in parentheses are lower and upper 95% fiducial limits. The
general health of animals surviving exposures, as indicated by body weight maintenance, did not
demonstrate exposure concentration, type of TEB, or gender-specific effects." (Kimmel et al, 1990)
LC50 Determination
"No animals exposed to the lowest concentrations of fTEB and aTEB (33S and 399 ppm, respertively)
expired during the course of the investigation. One animal each expired after midlevel exposure to
fTEB or aTEB (617 and 575 ppm, respectively); interestingly, both were males. The animal exposed to
fTEB died during the exposure and the animal exposed to aTEB died within 24 h of exposure. At
higher levels of fTEB and aTEB (741 and 821 ppm, respectively), 5 of 12 animals expired from fTEB
exposure and 10 of 12 animals expired from aTEB exposure. All 5 animals that died from fTEB
exposure were male, 3 died during the exposure and 2 died within 24 h. Six of the 10 animals that
died from aTEB exposure were male. One male and 2 females died during exposure, 2 males and 2
females died on the day of exposure, and the 3 additional deaths occurred within 2 days of exposure
and all were males." (Kimmel et al, 1990) - Clinical signs:
- other: Pilot Study: Abnormal breathing patterns, hyperactivity and broncospasms LC50 Study: "During exposures (all concentrations, either fTEBor aTEB), the majority of animals exhibited labored, shallow breathing which persisted for up to 24 h in animals surviv
- Other findings:
- Histopathology Pilot study:
Pulmonary edema was the most important histopathologic finding. No respiratory tract lesions
were present in rats exposed to aTEB at 7 and 14 days postexposure. Nasal and tracheal epithelial
necrosis occurred in a few of the rats that were exposed to fTEB and was primarily limited to the
ventral half of the tracheal circumference.
"Other significant findings were centrolobar hepatocytic, cytoplasmic, vacuolar degeneration,
and congestion in animals exposed to both fTEB and aTEB. The vacuoles frequently contained a
homogeneous eosinophilic material suggestive of a proteinaceous cell product. Acute to subacute
multifocal myocarditis was observed frequently in all exposure groups." (Kimmel et al, 1990)
Histopathology LC50 study:
"In this investigation gross observations of vascular engorgement and organ discolorations
suggestive of vascular congestion or hemorrhage were found in all TEB exposure groups, as well as in
some control animals. Hemorrhage was occasionally confirmed by histopathologic examination.
Congestion was histopathologically confirmed for the lung, liver, and kidneys of some animals.
Except for those tissues with concurrent diagnoses of edema (primarily lung), the vascular alterations
were considered agonal rather than exposure-related." (Kimmel et al, 1990) - Interpretation of results:
- Category 2 based on GHS criteria
- Remarks:
- Criteria used for interpretation of results: EU
- Conclusions:
- According to the authors: The overall LC50 (males and females) of fTEB and aTEB was 738 ppm.
The combined (both fTEB and aTEB) LC50 for males was 676 ppm (591 to 719), whereas the combined LC50 for females was >821 ppm. - Executive summary:
This is a summary of a study conducted by Kimmel, E.C. et al. at the Harry G. Armstrong Aerospace Medical Research Laboratory at Wright-Patterson Air Force Base. Source: Govt Reports Announcements & Index (GRA&l), Issue 20, 1991 [NTIS]. The test article was described as a clear liquid with a 99% purity.
The study was conducted to determine the acute inhalation toxicity of TEB. It is reported that TEB rapidly oxidizes to diethylethoxyborane (DEEOB), to ethyldiethoxyborane (EDEOB) and to triethoxyborane (TEOB) at concentrations below 1150-1300 ppm. Since the oxidation occurs within milliseconds after initial contact of TEB with air and is complete within minutes, studies were conducted with fresh TEB (fTEB = mixture of TEB, DEEOB, EDEOB and TEOB oxidation derivaties delivered to the exposure chamber 36 msec after initial mixing of pure TEB vapor with oxygen) and with aged TEB (aTEB = vapor resulting from a 4.6 min delay between the initiation of TEB oxidation and delivery to the exposure chamber).
In the first study, groups of 24 rats were exposed to 956 (fTEB) ppm, 897 (aTEB) ppm or air for 1 hour. Mortality was 21/23, 12/24 0/24 for the fTEB, aTEB and control groups respectively. Clinical signs of toxicity included irregular respiration and hyperactivity. Survivors in the fTEB group exhibited abnormal breathing and were cyanotic following exposure. Pathology findings that were significantly different than control were: autolysis (self-digestion) of the trachea (fTEB males, and fTEB females); necrosis of the trachea, (male and female fTEB and male aTEB); lung edema and congestion (males and females fTEGB); liver cell degeneration (males and females fTEB and aTEB) and liver congestion (male and female fTEB).
In a second study to determine an LC50, 12 rats were exposed for 1 hour to either air, 335 or 399 ppm (fTEB and aTEB), 617 or 575 ppm (fTEB or aTEB) or 741 or 821 ppm (fTEB or aTEB). There were no mortalities in the low concentration group or in the control group. There was one mortality in each mid-fTEB and aTEB exposure group (both males), 5/12 (males only) mortalities in the 741 fTEB ppm group and 10/12 (6 males, 4 females) mortalities in the 821 aTEB ppm group.
The overall LC50 for TEB (both fTEB and aTEB of both genders) was 738 ppm. The LC50 (both genders) for fTEB and aTBE was greater than 766 ppm and 709 ppm, respectively. Female LC50 (fTEG and aTEB) was greater than 821 ppm and for males (fTEB and aTEB) the LC50 was 676 ppm. Clinical signs of toxicity included irregular breathing and tremors during exposusre, cyanosis and decreased activity. Lung congestion and edema were considered dose and gender related. Only high concentration females in the aTEB were effected while high concentration fTEB and aTEB males were effected and at a greater incidence. Significant degeneration of liver cells was observed in high concentration aTEB females and in high concentration fTEB and aTEB males. It should be noted that 50% of the control males also had liver cell degeneration in this portion of the study.
The lung edema due to TEB exposure was attributed to increased vascular permeability and tracheal lesions due to TEB dissolving in the tracheal mucus. The significance of the liver alterations was not known nor was the gender related response.
Reference
"Mean concentrations of the fTEB and aTEB exposures in the pilot investigation were 956 ± 57.8 (n = 26) and 897 ± 14.6 (n = 29) ppm, respectively, and remained stable throughout the exposure with coefficients of variation (CV) of 6.0 and 1.7%, respectively. Pilot study exposure durations were only 52 min because in the first (fTEB) exposure mortality at the time was 100%." (Kimmel et al, 1990)
In the LD50 study:
"Mean fTEB and aTEB concentrations in the low-level exposure group were 335 ± 32.7 (n = 111) and 399 ± 27.8 (n + 111) ppm, respectively, and also were stable with CVs of 9.6 and 7.0 %. Mean concentrations of fTEB and aTEB in the midlevel exposures were 617 ± 133.1 (n = 111) and 575 ± 96.7 (n = 111) ppm, respectively, and were relatively variable with CVs of 16.9 and 21.6%. High-level exposure concentrations for fTES and alES were 741 ± 40.8 and 821 ± 56.9 ppm, and were stable with CVs of 5.5 and 6.9%, respectively. All of these exposures were 1 h in duration." (Kimmel et al, 1990)
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- LC50
- Quality of whole database:
- K2; According to the authors: The overall LC50 (males and females) of fTEB and aTEB was 738 ppm.
The combined (both fTEB and aTEB) LC50 for males was 676 ppm (591 to 719), whereas the combined LC50 for females was >821 ppm.
Acute toxicity: via dermal route
Link to relevant study records
- Endpoint:
- acute toxicity: dermal
- Data waiving:
- study scientifically not necessary / other information available
- Justification for data waiving:
- the study does not need to be conducted because the substance is classified as corrosive to the skin
Reference
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Justification for classification or non-classification
Acute oral toxicity study (Rinehart) resulted in Cat 3
Acute inhalation toxicity study (Kimmel) resulted in Cat 2
No acute dermal toxicity study
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