HYDROGEN BROMIDE
Flammability | 0 | |
Toxicity | 3 | |
Body Contact | 4 | |
Reactivity | 1 | |
Chronic | 3 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Manufacture of organic and inorganic bromides, hydrobromic acid, as a reducing agent and
as catalyst in controlled oxidations, in the alkylation of aromatic compounds, in the
isomerisation of conjugated diolefins. Regeant
HBr, BrH, "anhydrous hydrogen bromide", "anhydrous hydrobromic acid", "hydrobromic acid,
anhydrous", "hydrobromic acid"
Toxic by inhalation.
Causes severe burns.
Risk of serious damage to eyes.
Risk of explosion if heated under confinement.
The material can produce severe chemical burns within the oral cavity and gastrointestinal tract following ingestion. Ingestion of acidic corrosives may produce burns around and in the mouth. the throat and esophagus. Immediate pain and difficulties in swallowing and speaking may also be evident. Swelling of the epiglottis may make it difficult to breathe which may result in suffocation. More severe exposure may result in vomiting blood and thick mucus, shock, abnormally low blood pressure, fluctuating pulse, shallow respiration and clammy skin, inflammation of stomach wall, and rupture of esophageal tissue. Untreated shock may eventually result in kidney failure. Severe cases may result in perforation of the stomach and abdominal cavity with consequent infection, rigidity and fever. There may be severe narrowing of the esophageal or pyloric sphincters; this may occur immediately or after a delay of weeks to years. There may be coma and convulsions, followed by death due to infection of the abdominal cavity, kidneys or lungs. Not normally a hazard due to physical form of product. Considered an unlikely route of entry in commercial/industrial environments.
The material can produce severe chemical burns to the eye following direct contact. Vapors or mists may be extremely irritating. If applied to the eyes, this material causes severe eye damage. Direct eye contact with acid corrosives may produce pain, tears, sensitivity to light and burns. Mild burns of the epithelia generally recover rapidly and completely. Severe burns produce long-lasting and possibly irreversible damage. The appearance of the burn may not be apparent for several weeks after the initial contact. The cornea may ultimately become deeply opaque resulting in blindness. Not considered to be a risk because of the extreme volatility of the gas.
The material can produce severe chemical burns following direct contactwith the skin. Skin contact with acidic corrosives may result in pain and burns; these may be deep with distinct edges and may heal slowly with the formation of scar tissue. Skin contact with the material may damage the health of the individual; systemic effects may result following absorption. Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.
If inhaled, this material can irritate the throat andlungs of some persons. Inhalation of vapors or aerosols (mists, fumes), generated by the material during the course of normal handling, may produce toxic effects. Corrosive acids can cause irritation of the respiratory tract, with coughing, choking and mucous membrane damage. There may be dizziness, headache, nausea and weakness. Swelling of the lungs can occur, either immediately or after a delay; symptoms of this include chest tightness, shortness of breath, frothy phlegm and cyanosis. Lack of oxygen can cause death hours after onset. Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo. Material is highly volatile and may quickly form a concentrated atmosphere in confined or unventilated areas. Vapor is heavier than air and may displace and replace air in breathing zone, acting as a simple asphyxiant. This may happen with little warning of overexposure. Symptoms of asphyxia (suffocation) may include headache, dizziness, shortness of breath, muscular weakness, drowsiness and ringing in the ears. If the asphyxia is allowed to progress, there may be nausea and vomiting, further physical weakness and unconsciousness and, finally, convulsions, coma and death. Significant concentrations of the non-toxic gas reduce the oxygen level in the air. As the amount of oxygen is reduced from 21 to 14 volume %, the pulse rate accelerates and the rate and volume of breathing increase. The ability to maintain attention and think clearly is diminished and muscular coordination is somewhat disturbed. As oxygen decreases from 14-10% judgement becomes faulty; severe injuries may cause no pain. Muscular exertion leads to rapid fatigue. Further reduction to 6% may produce nausea and vomiting and the ability to move may be lost. Permanent brain damage may result even after resuscitation at exposures to this lower oxygen level. Below 6% breathing is in gasps and convulsions may occur. Inhalation of a mixture containing no oxygen may result in unconsciousness from the first breath and death will follow in a few minutes. Inhalation of quantities of liquid mist may be extremely hazardous, even lethal due to spasm, extreme irritation of larynx and bronchi, chemical pneumonitis and pulmonary edema.
Repeated or prolonged exposure to acids may result in the erosion of teeth, swelling and or ulceration of mouth lining. Irritation of airways to lung, with cough, and inflammation of lung tissue often occurs. Chronic exposure may inflame the skin or conjunctiva. Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems. There is some evidence that human exposure to the material may result in developmental toxicity. This evidence is based on animal studies where effects have been observed in the absence of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not secondary non-specific consequences of the other toxic effects. Principal route of occupational exposure to the gas is by inhalation. Chronic intoxication with ionic bromides, historically, has resulted from medical use of bromides but not from environmental or occupational exposure; depression, hallucinosis, and schizophreniform psychosis can be seen in the absence of other signs of intoxication. Bromides may also induce sedation, irritability, agitation, delirium, memory loss, confusion, disorientation, forgetfulness (aphasias), dysarthria, weakness, fatigue, vertigo, stupor, coma, decreased appetite, nausea and vomiting, diarrhoea, hallucinations, an acne like rash on the face, legs and trunk, known as bronchoderma (seen in 25-30% of case involving bromide ion), and a profuse discharge from the nostrils (coryza). Ataxia and generalised hyperreflexia have also been observed. Correlation of neurologic symptoms with blood levels of bromide is inexact. The use of substances such as brompheniramine, as antihistamines, largely reflect current day usage of bromides; ionic bromides have been largely withdrawn from therapeutic use due to their toxicity. Several cases of foetal abnormalities have been described in mothers who took large doses of bromides during pregnancy.