Dimethylamine-borane (1:1)

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference

Reference Type:

publication

Title:

Case Report: the Clinical Toxicity of Dimethylamine Borane

Author:

Tsan Y. et al.

Year:

2005

Bibliographic source:

Environ Health Perspect. 2005 Dec; 113(12): 1784–1786

Materials and methods

Study type:

poisoning incident

Endpoint addressed:

neurotoxicity

Test guideline

Qualifier:

no guideline followed

Principles of method if other than guideline:

A case were reported of a man who suffered from work-related exposure to DMAB.

GLP compliance:

not specified

Test material

Test material information

Constituent 1

Reference substance name:

Dimethylamine-borane (1:1)

EC Number:

200-823-7

EC Name:

Dimethylamine-borane (1:1)

Cas Number:

74-94-2

Molecular formula:

C2H10BN

IUPAC Name:

N-Methylmethanamine-borane (1:1)

Method

Type of population:

occupational

Subjects:

- Number of subjects exposed: 1
- Sex: male
- Age: 36
- Race: no data
- Demographic information: no data
- Known diseases: no data

Ethical approval:

not specified

Route of exposure:

dermal

Reason of exposure:

accidental

Exposure assessment:

not specified

Details on exposure:

A 36-year-old, healthy male was accidentally sprayed over the face and trunk with the liquid form of DMAB. He kept on working and did not take a shower until > 1 hr later. The DMAB which the worker were exposed was a liquid sprayed on the patient containing 97% DMAB and 3% decomposed materials including boric acid, borates, hydrogen, dimethylamine. DMAB was the only toxic substance at the workplace.

Examinations:

- blood cell count, electrolytes, blood sugar, hepatic and renal function tests, clinical signs, brain computerized tomogram, physical examinations, urinalysis

Medical treatment:

not specified

Results and discussion

Clinical signs:

The patient developed dizziness, nausea, vomiting, sore throat, limb numbness, slurred speech, slow motion, lack of concentration, and ataxia by the next morning, 13 hr after exposure. He was admitted to a local hospital, where a normal brain computerized tomogram was noted. Because of worsening clinical conditions, including “masked” face, irritability, awkwardness, and rocking from side to side while sitting on the bed, he was transferred to our hospital 3 days later. Physical examination revealed some
abnormal neurologic findings. The patient was oriented as to time and place but was easily distracted. His speech was slurred. Normal muscle power was noted for all four limbs. He could stand on a wide base with assistance but deviated to both sides when attempting a tandem gait. Impairment on finger-tonose and heel-to-knee tests was also noted.

Results of examinations:

Mild hyperventilation, with arterial blood gas of pH 7.510, partial pressure of carbon dioxide 30.6 mm Hg, partial pressure of oxygen 100 mm Hg, and bicarbonate 24.7 mmol/L, was found. No drug history, including use of herbal medicine, was noted for the last 3 months. Urinalysis did not detect any illegal drugs, central nervous system-acting drugs, or other medications. Normal blood and urine lead, mercury, and aluminium levels were also noted.
Eight days after chemical exposure, the patient’s electroencephalogram (EEG) revealed diffuse background slowing, indicative of a mild diffuse cerebral dysfunction. Tests of nerve conduction velocity (NCV) for the left-side limbs were normal. Brain magnetic resonance imaging (MRI) on the eighth day showed a symmetric increase in signal intensity on FLAIR (fluid-attenuated inversion recovery), T2WI (T2-weighted intensity), and DWI (diffusion weighted images), but low signal intensity on T1WI without postcontrast enhancement at bilateral cerebellar periventricular areas. A steroid was prescribed for treatment of the possible acute inflammatory effects on neurons. The patient was discharged with stable neurologic function after 6 days of observation.

Outcome of incidence:

The patient was readmitted to the neurology outpatient clinic 18 days after chemical exposure due to difficulty in walking and climbing. Physical examination revealed that the deep tendon reflexes of both knees were areflexic. Muscle power was mildly decreased in the distal and proximal parts of the upper right leg. Lower leg weakness and drop foot were also found bilaterally with muscle power of grade 2/5 in the right foot and 3/5 in the left foot. A nerve conduction study on the 29th day after poisoning showed decreased NCV and complex muscular action potential (CMAP) amplitudes for the left median, left ulnar, left peroneal, and left tibial nerves. H-reflex was absent bilaterally. Sensory conduction and sensory evoked potential tests of the nerves of the upper left and lower left limbs were normal. A brain MRI on the 37th day after poisoning showed that the previous lesions in the cerebellar
dentate nuclei region had subsided. With active physical therapy, the patient could walk straight on a wide base 2 months after poisoning. No dysmetria was noted on the finger-to-nose test, but heel or toe gait was impaired. The muscle power was grade 3/5 in the flexor and extensor of the right foot; 4/5 in the flexor and extensor of the left foot, and others were all 5/5. Weakness in the flexor and extensor of both feet still remained. A repeat EEG was normal. A repeat NCV study revealed no change in polyneuropathy with motor predominant axonal degeneration. The patient receives regular outpatient follow ups. He still walks with a clumsy gait and has difficulty with hand-grasping activity.

Any other information on results incl. tables

Other information about the patient:

The patient denied any medical problems such as hypertension, diabetes, and neurologic diseases. He smoked one pack of cigarettes per day and drank alcohol occasionally.

Applicant's summary and conclusion

Conclusions:

This case study reported that DMAB is toxic to humans and causes neurotoxicity as polyneuropahthy with motor-predominant axonal degeneration at high concentrations.

Executive summary:

In this case report, a 36 -year-old, healthy male was accidentally sprayed over the face and trunk with the liquid form of Dimethylamine borane (DMAB). The patient did not decontaminate at once, and he suffered from more severe symptoms, including dizziness, nausea, limb numbness, slurred speech, irritable mood, and ataxia 13 hr later. Magnetic resonance imaging showed symmetric lesions with hyperintensity on T2WI and FLAIR in bilateral cerebellar dantate nuclei. This patient was readmitted to the hospital due to difficulty in walking and climbing 18 days after exposure. Lower leg weakness and drop foot were found bilaterally. A nerve conduction study revealed polyneuropathy with motor-predominant axonal degeneration. This patient receives regular outpatient follow ups and still walks with a clumsy gait and has difficulty with hand-grasping activity. This case study demonstrates that DMAB is neurotoxic to humans at high concentrations.