Hydrogen fluoride (HF) is an irritant gas that liquefies at 19.5°C; in an aqueous solution, it produces hydrofluoric acid. HF gas is used in chemical manufacturing. In addition, it may be released from fluorosilicates, fluorocarbons, or polyfluorotetraethylene (PTFE, Teflon) when heated to over 350°C. Hydrofluoric acid is widely used as a rust remover, in glass etching, and in the manufacture of silicon semiconductor chips. Hydrofluoric acid events at the workplace were shown to be two times more likely to involve injuries compared with other acids. Poisoning usually occurs after dermal exposure, usually on the hands, although ingestions and inhalational exposure occasionally occur. There has been one case report of chemical colitis due to a hydrofluoric acid enema. Similar toxicity may result from exposure to ammonium bifluoride and sodium fluoride.

HF is a dermal and respiratory irritant. Hydrofluoric acid is a relatively weak acid (the dissociation constant is about 1,000 times less than that of hydrochloric acid), and toxic effects result primarily from the highly reactive fluoride ion.

1. HF is able to penetrate tissues deeply before dissociating into hydrogen and fluoride ions. The highly cytotoxic fluoride ion is released and cellular destruction occurs.
2. Fluoride ion binds strongly to calcium and magnesium, resulting in their systemic depletion. This may cause systemic hypocalcemia, hypomagnesemia, and local bone demineralization.

Toxicity depends on the air concentrations and duration of exposure to HF gas or the concentration and extent of exposure to aqueous HF solutions.

1. HF gas. The recommended workplace ceiling limit (ACGIH TLV-C) for HF gas is 3 ppm (2.5 mg/m³) and 30 ppm is considered immediately dangerous to life or health (IDLH). A 5-minute exposure to air concentrations of 50-250 ppm is likely to be lethal.
2. Aqueous HF solutions. Solutions of 50-70% are highly toxic and produce immediate pain. Concomitant inhalational exposure may occur with exposure to higher concentrations caused by the release of HF gas. Intermediate concentrations (20-40%) may cause little pain initially but result in deep injury after a delay of 1-8 hours. Weak solutions (5-15%) cause almost no pain on contact but may cause serious delayed injury after 12-24 hours. Most household products containing aqueous HF contain 5-8% or less.

Symptoms and signs depend on the type of exposure (gas or liquid), concentration, duration, and extent of exposure.

1. Inhalation of HF gas produces ocular and nasopharyngeal irritation, coughing, and bronchospasm. After a delay of up to several hours, chemical pneumonitis and noncardiogenic pulmonary edema may occur. Corneal injury may result following ocular exposure.
2. Skin exposure. After acute exposure to weak (5-15%) or intermediate (20-40%) solutions, there may be no symptoms because the pH effect is not pronounced. Concentrated (50-70%) solutions have better warning properties because of immediate pain. After a delay of 1-12 hours, progressive redness, swelling, skin blanching, and pain occur owing to penetration to deeper tissues by the fluoride ion. The exposure is typically through a pinhole-size defect in a rubber glove, and the fingertip is the most common site of injury. The pain is progressive and unrelenting. Severe deep-tissue destruction may occur, including full-thickness skin loss and destruction of underlying bone.
3. Ingestion of HF may cause corrosive injury to the mouth, esophagus, and stomach.
4. Systemic, life-threatening hypocalcemia and hypomagnesemia may occur after ingestion or skin burns involving a large body surface area or highly concentrated solution (can occur with exposure to >2.5% body surface area and a highly concentrated solution). Hyperkalemia may occur as a result of fluoride-mediated inactivation of the Na-K ATPase, activation of the Na-Ca ion exchanger, or tissue injury. These electrolyte imbalances, either alone or in combination, may lead to cardiac dysrhythmias, the primary cause of death in HF exposures. Prolonged QT interval may be the initial manifestation of hypocalcemia or hypomagnesemia.

Is based on a history of exposure and typical findings. Immediately after exposure to weak or intermediate solutions, there may be few or no symptoms, even though potentially severe injury may develop later.

1. Specific levels. Serum fluoride concentrations are not useful after acute exposure but may be useful in evaluating chronic occupational exposure. Normal serum fluoride is less than 20 mcg/L but varies considerably with dietary and environmental intake. In workers, pre-shift urine excretion of fluoride should not exceed 3 mg/g of creatinine.
2. Other useful laboratory studies include electrolytes, BUN, creatinine, calcium, magnesium, and continuous ECG monitoring.

1. Emergency and supportive measures
   1. All HF ingestions should be considered potentially life-threatening. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat pulmonary edema if it occurs.
   2. Patients with HF ingestion should be evaluated for corrosive injury with consultation by a gastroenterologist for consideration of endoscopic evaluation.
   3. Monitor the ECG and serum calcium, magnesium, and potassium concentrations; give IV calcium (also see below) if there is evidence of hypocalcemia or severe hyperkalemia; replace magnesium as indicated.
2. Specific drugs and antidotes. Calcium rapidly precipitates fluoride ions and is an effective antidote for dermal exposures and systemic hypocalcemia resulting from absorbed fluoride. In addition, serum magnesium should be monitored and replaced aggressively as appropriate.
   1. Skin burns. For exposures involving the hands or fingers, immediately consult an experienced medical toxicologist, burn surgeon, hand surgeon, or a poison control center (1-800-222-1222). Occasionally, dermal exposure may require administration of calcium gluconate by the intra-arterial route or by intravenous Bier block technique. These interventions may provide significant pain relief. Caution: Do not use calcium chloride salt for subcutaneous, Bier block, or intra-arterial injections; this form contains a larger proportion of calcium ion compared with the gluconate salt and may cause vasospasm and tissue necrosis.
      1. Topical. Apply a gel containing calcium gluconate or carbonate, using an occlusive dressing or a rubber glove to enhance skin penetration. Some experts add dimethyl sulfoxide (DMSO) to enhance skin penetration of the calcium, although evidence is anecdotal. Alternatively, soak in a quaternary benzalkonium chloride solution such as Zephiran (1.3 g/L of water) or a magnesium sulfate solution such as Epsom salt solution. If pain is not significantly relieved within 30-60 minutes, consider subcutaneous, intra-arterial injection, or Bier block.
      2. Subcutaneous. Inject calcium gluconate 5-10% subcutaneously in affected areas, using a 27- or 30-gauge needle and no more than 0.5 mL per digit or 1 mL/cm² in other regions.
      3. Intra-arterial. Injection of calcium by the intra-arterial route may be necessary for burns involving several digits or subungual areas, or if topical therapy fails.
      4. Bier block. This intravenous regional perfusion technique has been reported to be useful.
      5. Surgical excision. Early burn excision has been used in cases of exposures not involving the hands in which pain is uncontrollable despite topical or subcutaneous calcium therapy.
   2. Systemic hypocalcemia or hyperkalemia. Administer calcium gluconate 10%, 0.2-0.4 mL/kg IV, or calcium chloride 10%, 0.1-0.2 mL/kg IV.
3. Decontamination. Rescuers entering a contaminated area should wear self-contained breathing apparatus and appropriate personal protective equipment to avoid exposure.
   1. Inhalation. Immediately remove victims from exposure and give supplemental oxygen if available. Some authorities recommend the use of nebulized 2.5% calcium gluconate.
   2. Skin. Immediately remove contaminated clothing and flood exposed areas with copious amounts of water. Then soak in a solution of magnesium sulfate or calcium. Immediate topical use of calcium or magnesium may help prevent deep burns. Some facilities that frequently manage HF cases purchase or prepare a 2.5% calcium gluconate gel (in water-based jelly). This intervention may be highly effective if applied immediately.
   3. Eyes. Flush with copious amounts of water or saline. The effectiveness of a weak (1-2%) calcium gluconate solution is not established. Consult with an ophthalmologist if there is evidence or suspicion of ocular exposure.
   4. Ingestion
      1. Prehospital. Immediately give any available calcium-containing (calcium carbonate or milk) or magnesium-containing substance by mouth. Do not induce vomiting because of the risk for corrosive injury. Activated charcoal is not effective.
      2. Hospital. Consider gastric suctioning with a nasogastric tube. Administer calcium-or magnesium-containing substance as in Item 4.a above.
4. Enhanced elimination. There is no role for enhanced elimination procedures.