Bromate is a colorless, tasteless, odorless and water-soluble strong oxidizing agent. Poisoning was 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, and it is no longer commercially available. However, 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.

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.

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.

Clinical features include GI symptoms, irreversible bilateral sensorineural hearing loss, and acute kidney injury.

1. Within 2 hours of ingestion, patients develop GI symptoms, including vomiting (occasionally hematemesis), diarrhea, and epigastric pain. This may be accompanied by persistent, 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 is rarely reported.

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).

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary.
   2. Treat coma and 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 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.
3. Decontamination. Sodium bicarbonate (baking soda), 1 teaspoon in 8 ounces of water orally, may prevent formation of hydrobromic acid in the stomach. For large recent ingestions, consider gastric lavage with a 2% sodium bicarbonate solution to prevent formation of hydrobromic acid in the stomach. Activated charcoal may also be administered.
4. Enhanced elimination. Extracorporeal removal techniques can clear bromate from the plasma. Several studies suggest that early application of CRRT reduces bromate-induced hearing loss.