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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Description of key information

Oral and dermal acute studies available on TMB are not used for classification or risk assessment, as TMB hydrolyses readily into boic acid and methanol. Acute toxicity of boric acid is low, but methanol is classified as acute toxicity category 3 for all three routes based on human experience. Rodents are less sensitive to methanol acute toxicity so that it would be inappropriate to apply the results of the oral rodent study conducted with TMB.

Key value for chemical safety assessment

Additional information

Acute toxicity key information on the hydrolysis products methanol and boric acid are discussed below:


Animal data - Oral:

In rats, LD50 values after single oral administration range from 1187 to 2769 mg/kg bw, depending on the concentration of the aqueous solution used (BASF 1975, concentrations 15 to 35%, not further specified).

Human data:

Oral ingestion dominates as the most frequent route of poisoning, but percutaneous absorption or inhalation of vapours are as effective as the oral route in producing methanol acute toxic syndrome.

A blood level of 500 mg/L methanol in acutely poisoned patients generally is regarded as requiring hemodialysis. This blood concentration can transiently be achieved in an adult person (70 kg) by ingestion of 0.4 mL methanol/kg bw (Kavet and Nauss, 1990). Generally in humans, transient central nervous system (CNS) effects appear at blood methanol levels of 200 mg/L and serious ocular symptoms appear above 500 mg/L ranging from mild photophobia, misty or blurred vison to markedly reduced visual acuity and total blindness (Kavet and Nauss, 1990; Dethlefs and Naraqi, 1978). Acute methanol intoxication evolves in a well-defined pattern. First, a mild depression of the CNS occurs which is followed by an asymptomatic latent period commonly lasting 12 to 14 hours. Clinical symptoms include headache, dizziness, nausea and vomiting, abdominal pain, and labored, periodic breathing and mag progress to coma and death from respiratory failure (Kavet and Nauss, 1990). The minimal acute methanol dose to humans that can result in death is considered to be 300 to 1000 mg/kg by ingestion. Fatalities have occurred in untreated patients with initial methanol blood levels in the range of 1500 to 2000 mg/L (IPCS/WHO, 1997). In general, coma, seizures and prolonged acidosis were poor prognostic signs (Naraqi et al., 1979). Such high and potentially lethal blood methanol levels are less likely to be achieved from inhalation exposure. Exposure to 0.26 mg/L methanol for 4 hours was without significant physiologic effects in human volunteers (Muttray et al., 2001). In conclusion, formate is considered to be the ultimate toxicant in acute methanol intoxication in humans. Acidosis and ophthalmologic changes are typical effects in primates. They do not occur in rodents or rabbits, which are able to remove formate more efficiently. In these animals, CNS depression, narcosis and death are the leading sysmptoms of intoxication.


LD50 values of >2000 mg/kg were recorded for both oral and dermal routes and > 2 mg/L for the acute inhalation study. The highest attainable inhalation concentrationwas 2.12 mg/L.

Boric acid is of low acute toxicity. Although some of the acute oral studies were not of modern standards and were performed prior to the introduction of GLP, they are reproducible across a number of studies and species and of acceptable quality. For acute dermal and acute inhalation some studies do meet the modern GLP standard.


Considering that at the threshold dose of 2000 mg/kg bw TMB, 1848 mg/kg bw methanol would be released by hydrolysis of TMB, and that the minimal acute lethal dose to humans for methanol is described as 300 -1000 mg/kg bw, it is considered appropriate to apply the methanol acute toxicity conclusions to TMB. The other hydrolysis product, boric acid, is of low acute toxicity.

Justification for classification or non-classification

Due to rapid release of relevant amounts of methanol as a hydrolysis product, TMB will be classified as actue toxicity category 3 for all routes:

Although the lethal dose of methanol is high for most experimental animals ( mostly > 2000 mg/kg bw after single oral administration to rodents), the substance is classified as acutely toxic by oral, dermal and inhalative exposure, and as capable of inducing serious irreversible effects upon single exposure by all of these routes according to human evidence.


Acute toxicity category 3: toxic if swallowed; toxic in contact with skin; toxic if inhaled.

STOT single exposure category 1 (route of exposure: oral, inhalation)