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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Link to relevant study record(s)

Description of key information

Several publications and the review by US EPA Health and Environmental Profile for Methylene Bromide (1987).

Key value for chemical safety assessment

Bioaccumulation potential:
low bioaccumulation potential

Additional information

Dibromomethane appears to be absorbed after oral and inhalation exposure in rats and rabbits (concluded based Repeated dose toxicity section) and after dermal exposure(Rodkey and Colloson 1977; McDougal etal., 1985). Dibromomethane was metabolized in vitro to carbon monoxide and inorganic bromide by microsomal enzymes of the liver, lungs, and kidney, but not of the brain or spleen (Kubic and Andreas 1975). The oxidation appears to be catalysed by a cytochrome P-450 dependent system (Kubic and Andreas 1975, 1978, Stevenes et al., 1980). During dermal exposure, the metabolism of dibromomethane was saturable as indicated by the nonlinear increase in plasma bromide ion concentration (McDougal et al., 1985). Intraperitoneal administration of 522 mg/kg dibromomethane to male rats resulted in a peak of carboxyhemoglobin level of 14% of the hemoglobi concentration at 4 hours treatment (Kubic and Andreas 1974). By 10 hours after treatment, the carboxyhemoglobin level was approaching the pre-treatment level. Repeated daily exposure did not result in accumulation of carboxyhemoglobin. The only information regarding the excretion of dibromomethane is that the metabolite carbon monoxide is excreted in the exhaled air (Rodkey and Collison 1977).