Fluoride-liberating chemicals are found in some automobile wheel cleaners, rust removers, glass-etching solutions, pesticides, agents used in aluminum production, dietary supplements, products used to prevent dental caries, and voriconazole. It is also found in hydrogen fluoride and hydrofluoric acid, which have additional dermal and inhalational hazards and are discussed separately. When ingested, soluble fluoride salts are rapidly absorbed and are more acutely toxic than poorly soluble compounds (Table II-26). Most toothpaste contains up to 5 mg of fluoride per teaspoon, and tea can contain 0.3-5.1 mg of fluoride per liter. Although low fluoride concentrations added to public drinking water decreases tooth decay, in some parts of the world high concentrations of fluoride contaminating drinking water can cause a number of chronic health problems including skeletal fluorosis.

1. In addition to its direct cytotoxic and metabolic effects, fluoride binds avidly to calcium and magnesium causing hypocalcemia and hypomagnesemia, and it also generates reactive oxygen species. Fluoride toxicity disrupts many intracellular mechanisms including glycolysis, G-protein-mediated signaling, oxidative phosphorylation, adenosine triphosphate (ATP) production, function of Na⁺/K⁺-ATPase, and potassium channels.
2. Pharmacokinetics. Fluoride is a weak acid (pKa = 3.4) that is passively absorbed from the stomach and small intestine. In an acidic environment, more fluoride is present as hydrogen fluoride (HF), which is absorbed more rapidly than ionized fluoride. Fasting peak absorption occurs in 30-60 minutes. Fluoride is also absorbed dermally and by inhalation (see “Hydrogen Fluoride,”). The volume of distribution is 0.5-0.7 L/kg. Fluoride is not protein bound but binds readily to magnesium and calcium in blood and tissues and is deposited in bone. The elimination half-life is 2.4-4.3 hours and is prolonged in patients with renal failure.

Vomiting and abdominal pain are common with acute ingestions of elemental fluoride of 3-5 mg/kg (see Table II-26); hypocalcemia and muscular symptoms appear with ingestions of 5-10 mg/kg. Death has been reported in a 3-year-old child after ingestion of 16 mg/kg and in adults with doses in excess of 32 mg/kg. Prolonged excessive exposure to fluoride (levels as low as 6 mg/d) can cause skeletal fluorosis.

1. Acute poisoning. Nausea and vomiting frequently occur within 1 hour of ingestion. Symptoms of serious fluoride intoxication include skeletal muscle weakness, tetanic contractions, respiratory muscle weakness, and respiratory arrest. Hypocalcemia, hypomagnesemia, hyperkalemia, and increased QT interval can occur. Death due to intractable ventricular dysrhythmias usually occurs within 6-12 hours.
2. Chronic effects. The recommended daily limit for children is 2 mg and for adults is 4 mg. Minor overexposure in children younger than age 8 can cause tooth discoloration. Chronic overexposure can cause crippling skeletal fluorosis (osteosclerosis), increased bone density and ligament calcification.

Usually is based on a history of ingestion. Symptoms of Gl distress, muscle weakness, hypocalcemia, and hyperkalemia suggest acute fluoride intoxication.

1. Specific levels. The normal serum fluoride concentration is less than 20 mcg/L (ng/mL) but varies considerably with diet, water source and renal function. Serum fluoride concentrations are generally difficult to obtain and thus are of limited utility for acute overdose management.
2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, calcium (and ionized calcium), magnesium, and ECG. For evaluation of chronic exposure, parathyroid hormone levels and bone imaging may be considered.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary.
   2. Monitor ECG and serum calcium, magnesium, and potassium for at least 6 hours. Admit patients who have electrolyte abnormalities, ECG abnormalities, or muscular symptoms to an intensive care setting with cardiac monitoring.
2. Specific drugs and antidotes. For hypocalcemia, administer IV calcium gluconate, 10-20 mL (children: 0.2-0.3 mL/kg), monitor ionized calcium levels, and titrate further doses as needed. Treat hypomagnesemia with IV magnesium sulfate, 1-2 g given over 10-15 minutes (children: 25-50 mg/kg diluted to <10 mg/mL). Treat hyperkalemia with IV calcium and other standard measures. Antioxidants have not been evaluated in the treatment of acute poisoning.
3. Decontamination
   1. Prehospital. Do not induce vomiting because of the risk for abrupt onset of seizures and arrhythmias. Administer an antacid containing calcium (eg, calcium carbonate [Tums, Rolaids]) orally to raise gastric pH and complex free fluoride, impeding absorption. Milk, rich in calcium, has been shown to bind small fluoride doses and may be useful in the field if calcium carbonate is not available. There are little data documenting the effectiveness of magnesium or aluminum containing antacids.
   2. Hospital. Administer antacids containing calcium as described above. Consider gastric lavage for large recent ingestions. Activated charcoal does not adsorb fluoride.
4. Enhanced elimination. Because fluoride rapidly binds to free calcium and bone and has a short elimination half-life, the effectiveness of prompt hemodialysis for acute poisoning remains unclear. Hemodialysis may be useful in correcting electrolyte abnormalities including hyperkalemia that is refractory to standard therapies.