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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

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In a study from Tsan et al. the clinical toxicity of dimethylamine borane poisoning of a worker, exposed acutely with this substance without immediately decontamination, was reported. Symptoms including dizziness, nausea, limb numbness, slurred speech, irritable mood, and ataxia were noted. A nerve conduction study revealed polyneuropathy with motor-predominant axonal degeneration. Further cases of DMAB exposure were reported by Tsan et al., where 4 workers were exposed with DMAB, but decontaminated immediately by drinking water or take a shower. In these cases, minor intoxication without any residual neurologic sequelae occurred.

A further poisoning incident was reported by Hung et al. In this report the axonal neuropathy after acute DMAB exposure was studied. The study indicates that acute exposure to Dimethylamine borane (DMAB) may induce axonal polyneuropathy. This is in line with the findings of Tsan et al.

In another study, a worker acutely exposed with DMAB was studied on long-term neurotoxic effects. The study showed that DMAB intoxication lead to long-lasting CNS toxicity on the cognitive dysfunction, parkinsonism and an impaired metabolic activity of the brain.

 

Based on these studies it can be concluded that acute DMAB exposure without immediate decontamination leads primarily to neurotoxicity and polyneuropathy with motor-predominant axonal degeneration and cause long-lasting CNS toxicity.

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