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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Key value for chemical safety assessment

Additional information

Toxicokinetic Summary


Mode of Action

The injurious effects of bromine are generally considered to be similar to those of chlorine (Rom WN and Barkman HW, 1983; Broderick A and Schwartz DA, 1992; Schwartz DA, 1987). Due to its potent oxidatising action, bromine liberates nascent oxygen or oxygen free radicals from the water present in mucous membranes. Nascent oxygen is a potent oxidizer, capable of producing tissue damage. The extent of the damage is dependent on the dose of bromine and the availability of water to react with it. In addition, the formation of hydrobromic (HBr) and hypobromic (HOBr) acids will result in acid mediated irritation during the reaction. Contact with the respiratory epithelium produces initial alveolar capillary congestion followed by focal and confluent patches of high-fibrinogen oedematous fluid. The fluid is interstitial at first but can fill the alveoli. Once this occurs, copious frothy, blood-tinged sputum is seen. A granulocyte response may occur several hours after inhalation. Hyaline membrane formation can occur later resulting in clinical deterioration at a time when signs of improvement have occurred. Poor oxygen diffusion, hypoxia and hypercapnia result from development of atelectasis, emphysema and membrane formation. Acute obstructive ventilatory impairment leads to severe hypoxaemia, metabolic acidosis and death usually due to cardiac arrest secondary to the hypoxaemia.



Bromine is a gas and therefore inhalation exposure is the most relevant route of exposure to humans (IPCS, 1999). Other routes of exposure are minimal.

Following inhalation, bromine is absorbed by the lungs and the physical characteristics of bromine determine the depth and site of penetration into the lung tissue and therefore the rate of absorption. Bromine deposition in the lungs is primarily determined by the water solubility of bromine. Bromine is relatively more water soluble than chlorine and thus tends to produce effects on the upper respiratory tract (Broderick A and Schwartz DA, 1992).  However, inhalation of high concentrations, e.g. in confined spaces, may also cause marked irritant effects on the lower airways (IPCS, 1999).


No data could be located regarding the absorption of bromine vapours via the ocular or dermal routes of exposure.


Following ingestion, bromine liquid is rapidly and completely absorbed after reaction ( see above) as bromide ion from the intestine by passive paracellular transport. Bromine can cross blood cell membranes in an electrically neutral form (HC, 1996), but hydrolysis occurs almost instantly.



Bromine is distributed widely into various tissues as bromide and mainly into the extracellular fluid of the body (HC, 1996).



The reactivity of bromine in biological systems makes it difficult to study the pharmacokinetics and to separate the effects of the bromine from those of the bromide metabolite.


There are no data regarding the metabolism of inhaled bromine, however bromine has been known to quickly form bromide in living tissue. Bromide is partitioned in the body similarly to chloride and acts by replacing chloride. Bromide is a CNS depressant and its adverse effects are as a result of overdoses, however, due to the extreme irritant nature of bromine, the duration of exposure is severely limited, reducing any likely body burden of bromide (HC, 1996).


No data could be located regarding the biological half-life of inhaled bromine. The biological half-life of ingested bromine/bromide has been reported to be between 12 and 30 days in humans (Sticht G and Kaferstein H, 1988; IPCS, 1999). The biological half-life in rats is markedly shorter, being approximately 3 days.


Bromine reacts with water resulting in the formation of hydrobromous acid, which slowly decomposes to hydrogen bromide and O2 (EPA, 2009). The mechanism of action of bromine is by liberation of nascent oxygen or oxygen free radicals from the water present in mucous membranes. It is the nascent oxygen, a potent oxidiser, which is responsible for bromine-induced tissue damage (Sticht G and Kaferstein H, 1988; HSDB, 2007; IPCS, 1999).



No data could be located regarding excretion of bromine from the body. It is likely that excretion of any systemically absorbed bromine will be as bromide ion via urine.