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Boric acid and sodium borate have been used for many years in a variety of products as antiseptics and as fungistatic agents in baby talcum powder. Boric acid powder (99%) is still used as a pesticide against ants and cockroaches. In the past, repeated and indiscriminate application of boric acid to broken or abraded skin resulted in many cases of severe poisoning. Epidemics have also occurred after boric acid was added mistakenly to infant formula or used in food preparation. Although chronic toxicity seldom occurs now, acute ingestion by children at home is more common.

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Other boron-containing compounds with similar toxicity include boron oxide and orthoboric acid (sassolite).

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  1. Mechanism of toxicity

    1. The mechanism of borate poisoning is unknown. Boric acid is not highly corrosive but is irritating to mucous membranes. It probably acts as a general cellular poison. The organ systems most commonly affected are the skin, GI tract, brain, liver, and kidneys.

    2. Pharmacokinetics. The volume of distribution (Vd) is 0.17–0.50 L/kg. Elimination is mainly through the kidneys, and 85–100% of a dose may be found in the urine over 5–7 days. The elimination half-life is 12–27 hours.

  2. Toxic dose

    1. The acute single oral toxic dose is highly variable, but serious poisoning is reported to occur with 1–3 g in newborns, 5 g in infants, and 20 g in adults. A teaspoon of 99% boric acid contains 3–4 g. Most accidental ingestions in children result in minimal or no toxicity.

    2. Chronic ingestion or application to abraded skin is much more serious than acute single ingestion. Serious toxicity and death occurred in infants ingesting 5–15 g in formula over several days; serum borate levels were 400–1600 mg/L.

  3. Clinical presentation

    1. After oral or dermal absorption, the earliest symptoms are GI, with vomiting and diarrhea. Vomit and stool may have a blue-green color. Significant dehydration and renal failure can occur, with death caused by profound shock.

    2. Neurologic symptoms of hyperactivity, agitation, and seizures may occur early.

    3. An erythrodermic rash (“boiled-lobster” appearance) is followed by exfoliation after 2–5 days. Alopecia totalis has been reported.

  4. Diagnosis is based on a history of exposure, the presence of gastroenteritis (possibly with blue-green vomit), erythematous rash, acute renal failure, and elevated serum borate levels (although these are not commonly available in clinical laboratories).

    1. Specific levels. Serum or blood borate levels are not generally available and may not correlate accurately with the level of intoxication. Analysis of serum for borates can be obtained from National Medical Services (1-215-657-4900) or other large regional commercial laboratories. Normal serum or blood levels vary with diet but are usually less than 7 mg/L. The serum boron level can be estimated by dividing the serum borate by 5.72.

    2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, and urinalysis.

  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), seizures (See Seizures), hypotension (See Hypotension), and renal ...

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