Skip to Main Content

++

Bromate poisoning was most common during the 1940s and 1950s, when bromate was a popular ingredient in home permanent neutralizers. Less toxic substances have been substituted for bromates in kits for home use, but poisonings still occur occasionally from professional products (bromate-containing permanent wave neutralizers have been ingested in suicide attempts by professional hairdressers). Commercial bakeries often use bromate salts to improve bread texture, and bromates are components of the fusing material for some explosives. Bromates previously were used in matchstick heads. Bromate-contaminated sugar was the cause of one reported epidemic of bromate poisoning.

++

  1. Mechanism of toxicity. The mechanism is not known. The bromate ion is toxic to the cochlea, causing irreversible hearing loss, and nephrotoxic, causing acute tubular necrosis. Bromates may be converted to hydrobromic acid in the stomach, causing gastritis. Bromates are also strong oxidizing agents that are capable of oxidizing hemoglobin to methemoglobin.

  2. Toxic dose. The acute ingestion of 200–500 mg of potassium bromate per kilogram is likely to cause serious poisoning. Ingestion of 2–4 oz of 2% potassium bromate solution caused serious toxicity in children. The sodium salt is believed to be less toxic.

  3. Clinical presentation

    1. Within 2 hours of ingestion, victims develop GI symptoms, including vomiting (occasionally hematemesis), diarrhea, and epigastric pain. This may be accompanied by restlessness, lethargy, coma, and convulsions.

    2. An asymptomatic phase of a few hours may follow before overt renal failure develops. Anuria is usually apparent within 1–2 days of ingestion; renal failure may be irreversible.

    3. Tinnitus and irreversible sensorineural deafness occur between 4 and 16 hours after ingestion in adults, but deafness may be delayed for several days in children.

    4. Hemolysis and thrombocytopenia have been reported in some pediatric cases.

    5. Methemoglobinemia (See Methemoglobinemia) has been reported but is rare.

  4. Diagnosis is based on a history of ingestion, especially if accompanied by gastroenteritis, hearing loss, or renal failure.

    1. Specific levels. Bromates may be reduced to bromide in the serum, but bromide levels do not correlate with the severity of poisoning. There are qualitative tests for bromates, but serum concentrations are not available.

    2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, urinalysis, audiometry, and methemoglobin (via co-oximetry analysis).

  5. Treatment

    1. Emergency and supportive measures

      1. Maintain an open airway and assist ventilation if necessary (See Airway and Breathing).

      2. Treat coma (See Coma and stupor) and seizures (See Seizures) if they occur.

      3. Replace fluid losses, treat electrolyte disturbances caused by vomiting and diarrhea, and monitor renal function. Perform hemodialysis as needed for support of renal failure.

    2. Specific drugs and antidotes

      1. Sodium thiosulfate (See Naloxone and Nalmefene) theoretically may reduce bromate to the less toxic bromide ion. There are few data to support the use of thiosulfate, but in the recommended dose, it is benign. Administer 10% thiosulfate solution, 10–50 mL (0.2–1 mL/kg) IV.

      2. Treat methemoglobinemia with methylene blue (See Methylene Blue).

    3. Decontamination (See Decontamination). Sodium bicarbonate (baking soda), 1 tsp in 8 oz of water orally, may prevent formation of ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.