Hydrogen Bromide

CAS RN:10035-10-6

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: In the past, bromides were widely used both as a sedative and an antiepileptic agent in the United States, and they are still used as sedatives in some areas of the world. It is still found as a bromide salt in many medications. The major source of bromide exposure in humans in the United States is the presence of bromide residues in food. Bromine-containing fumigants are extensively used in horticulture and in post-harvest treatments, but the amounts are too minimal to cause toxicity. Contaminated well water may be a source of bromide exposure.
    • B) PHARMACOLOGY: Bromide ion causes secondary anion potentiation of gamma-aminobutyric acid (GABA) channels in the CNS. GABA receptors are complexed with chloride channels. Available bromide ions, due to their smaller hydrated diameter, diffuse more readily through cellular channels, producing a hyperpolarized post-synaptic membrane, which potentiates the action of GABA, an inhibitory neurotransmitter.
    • C) TOXICOLOGY: With chronic exposure, the bromide ion displaces chloride from plasma, extracellular fluid, and, to some extent, from cells. The kidneys increase the elimination of chloride ions in an attempt to maintain a constant total halide concentration. Central nervous system function is progressively impaired, presumably through a membrane-stabilizing effect. A toxic concentration can be reached very rapidly when the intake of chloride is reduced.
    • D) EPIDEMIOLOGY: Bromide poisoning is rare and, when it does occur, is generally secondary to chronic ingestion rather than acute overdose.
    • E) WITH POISONING/EXPOSURE
      • 1) ACUTE: Bromide poisoning following acute ingestion is rare. Acute effects may include nausea, vomiting, gastric irritation, CNS depression, coma, hypotension, tachycardia, and respiratory distress.
      • 2) CHRONIC: Ingestion of chronic, excessive amounts may produce a toxic syndrome called "bromism", which is characterized by behavioral changes, hallucinations, psychosis, ataxia, irritability, headache, and confusion. Other symptoms of chronic bromide toxicity include: anorexia, weight loss, constipation, slurred speech, anemia, bromoderma (an erythematous, nodular, or acneiform rash over the face and possibly the entire body), bullous or pustular eruptions on the skin, toxic epidermal necrolysis, musculoskeletal pain, lethargy, and liver enzyme abnormalities. Fever may be seen in up to 25% of cases of chronic ingestion. Chronic intoxication usually develops over 2 to 4 weeks or longer.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) Fever may occur with chronic intoxication.
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Pupils may be normal, miotic or mydriatic. Nystagmus is common.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Tachycardia and hypotension have occurred with acute intoxication.
0.2.7 NEUROLOGIC
  • 0.2.7.1 ACUTE EXPOSURE
    • A) Acute intoxication can result in CNS depression and coma.
    • B) Chronic effects may include behavioral changes, irritability, confusion, muscular weakness, anorexia, ataxia, lethargy, abnormal reflexes, and slurred speech.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Nausea and vomiting occur following acute or chronic ingestion. Anorexia and weight loss may occur with chronic intoxication.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Acute renal failure is rare. Incontinence may develop with chronic intoxication.
0.2.12 FLUID-ELECTROLYTE
  • 0.2.12.1 ACUTE EXPOSURE
    • A) Spuriously elevated chloride level and low anion gap are characteristic of bromism, due to laboratory interference by the bromide ion.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Bromide toxicity is associated in about 25% of cases with the development of bromoderma, an erythematous, nodular or acneiform rash over the face and possibly the entire body. One case of toxic epidermal necrolysis has been reported.
0.2.18 PSYCHIATRIC
  • 0.2.18.1 ACUTE EXPOSURE
    • A) Chronic bromism has been associated with toxic psychosis resembling paranoid schizophrenia, personality changes, and mania with paranoid delusions.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Bromides cross the placenta and may be detected in the milk of nursing mothers. Case reports suggest that prenatal exposure may cause growth retardation, craniofacial abnormalities and developmental delay.
0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Household uses include toilet, metal and drain cleaners, rust remover, in batteries, and as a primer for artificial nails. Used in clandestine methamphetamine labs (ie, hydrochloric and sulfuric acid). Industrial uses include: metal refining, plumbing, bleaching, engraving, plating, photography, disinfection, munitions, fertilizer manufacture, metal cleaning, and rust removal.
    • B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars.
    • C) EPIDEMIOLOGY: Inadvertent ingestions occur with moderate frequency in children, and are less common than alkaline exposures. Serious exposures are rare in the developed world (generally only seen with deliberate ingestions), largely because only low concentration acids are available in the home. Serious effects are more common in developing countries.
    • D) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or Grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop Grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema.
      • 2) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because acidic products available in the home are generally of low concentration.
        • a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.
      • 3) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported.
      • 4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
      • 5) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis, and systemic toxicity.
0.2.3 VITAL SIGNS0.2.20 REPRODUCTIVE HAZARDS
  • A) Single doses of dibromoacetic acid has resulted in reductions of sperm and serum testosterone in experimental animals. Repeated or single oral administration of monobromoacetic acid did not produce effects on male rat reproductive organs or sperm.
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