Hydrogen fluoride

   1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification Numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main Brand Names/Trade Names
   1.6 Main Manufacturers/Main importers
   2.1 Main Risks and Target Organs
   2.2 Summary of Clinical Effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   3.1 Origin of substance
   3.2 Chemical structure
   3.3 Physical properties
   3.4 Other characteristics
   4.1 Uses
   4.2 High risk circumstances of poisoning
   4.3 Occupationally exposed populations
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Other
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life
   6.4 Metabolism
   6.5 Elimination
   7.1 Mode of Action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Animal Data
      7.2.3 In-vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake
   7.3 Carcinogenicity
   7.4 Teratogenic
   7.5 Mutagenicity
   7.6 Interactions
   9.1 Acute Poisoning by:
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parental
      9.1.6 Other
   9.2 Chronic Poisoning
      9.2.1 Ingestion
   9.3 Course, prognosis, cause of death
   9.4 Systematic Description of Clinical Effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological CNS Peripheral nervous system Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and Reproductive
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose and throat
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Fluid and Electrolyte disturbance Acid-base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic Reactions
      9.4.14 Other clinical effects
      9.4.15 Special Risks
   9.5 Others
   10.1 General principles
   10.2 Relevant laboratory analysis and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
   12.1 Availability of Antidotes
   12.2 Specific Preventive Measures
   12.3 Other
    1.    NAME

      1.1   Substance

            Hydrogen Fluoride

      1.2   Group

            Inorganic Corrosive

      1.3   Synonyms

            Hydrogen Fluoride
            Hydrofluoric Acid
            Fluorohydric Acid
            Aqueous hydrogen fluoride
            Acide hydrofluorique
            Acide fluorhydrique
            Acide fluorique

      1.4   Identification Numbers
            1.4.1 CAS number


            1.4.2 Other numbers

                  UN:   1052
                  RTECS       MW7875000

      1.5   Main Brand Names/Trade Names

            Wink Rust Stain Remover 7-10% HF (US)

      1.6   Main Manufacturers/Main importers

            DuPont (US)
            Allied (US)

    2.    SUMMARY

      2.1   Main Risks and Target Organs

            Hydrogen fluoride is highly corrosive to all tissues.
            Skin: Burns, necrosis; underlying bone may be decalcified. 

            Eyes: Burns.  

            Gastrointestinal: After ingestion, the oropharynx and the 
                              oesophagus are the primary sites of injury.  

            Heart:            Systemic absorption occurs following skin 
                              exposure or ingestion; severe and rapid 
                              hypocalcaemia may ensue with cardiac 
                              dysrhythmia and arrest. 
            Lungs:            After inhalation, severe pulmonary injury may 
                              occur with pulmonary oedema and 

            Neuromuscular:    Tetany may occur due to hypocalcaemia after
                              systemic absorption. 

      2.2   Summary of Clinical Effects

            Hydrogen fluoride causes necrosis of any tissue with which it 
            comes into contact.  The effect is primarily mediated by the 
            toxicity of the fluoride ion rather than the effect of the 
            hydrogen ion.  Severe and delayed injury can occur with burns 
            developing after a symptom-free interval of 24 hours.  This is 
            particularly true of exposures to dilute (< 20%) solutions. 
            With concentrated solutions (>40 %), the effects are more rapid 
            and pronounced with immediate pain and skin damage. Ingestion 
            causes severe corrosion of the oropharynx and the oesophagus 
            which may be delayed in onset.  Eye contamination causes 
            similarly severe toxicity. Absorption of fluoride through the 
            skin or from the gastrointestinal tract can result in severe 
            hypocalcaemia with tetany and cardiac dysrhythmias. 

      2.3   Diagnosis

            Fluoride exposure can be confirmed by the determination of 
            fluoride in the urine using a random spot urine collection. 
            However, the determination of urinary fluoride is academic in 
            patients with confirmed exposure.  More important, 
            determination of blood calcium is critical following 
            significant exposure because absorbed fluoride may cause fatal 

      2.4   First-aid measures and management principles

            Any suspected or known skin contact with HF should be 
            aggressively diluted and washed with a flood shower or the 
            nearest available high flow of water.  Decontamination should 
            continue for 15 minutes.  All contaminated clothing must be 
            removed.  Exposed skin surfaces should be soaked in a calcium 
            or magnesium salt solution, gel or paste.  Alternatively, 
            quaternary ammonium compounds (e.g., benzalkonium chloride) may 
            be used.  

            After possible eye contact, the eyes must be thoroughly 
            irrigated with at least 2 l of saline or other appropriate eye 
            wash solution for 10-15 minutes. 

            After oral ingestion, calcium-containing antacids, especially 
            in liquid form, should be given.  Nothing else should be given 
            by mouth after ingestion. 

            Calcium supplementation should be given, intravenously or 
            orally, because severe hypocalcaemia may develop rapidly after 
            a delay of minutes to hours following serious exposure ( >1% 
            body surface area for a concentrated solution, or >5% body 
            surface area for a dilute solution (Grecco, 1988)).  Serial 
            determination of blood calcium should be started as soon as 
            possible and repeated every 6 hours for 24 hours or until 
            stable.  As soon as possible, patients should be placed on 
            continuous electrocardiographic monitoring for signs of 
            hypocalcaemia or dysrhythmia. 


      3.1   Origin of substance

            Hydrogen fluoride is generally derived from the reaction of 
            concentrated sulphuric acid on fluospar (CaF2).  

      3.2   Chemical structure
            Hydrogen Fluoride
            Molecular weight: 10

            HF may exist in complexes, eg H6F6, due to hydrogen binding.  

      3.3   Physical properties

            Boiling point:    gas at over 19°C  
            Autoignition:     not relevant
            Vapour pressure:  150 mm (70% solution at 26.7°C)
                              70 mm (70% solution at 20.0°C)
            Solubility:       aqueous solutions to 70% may be prepared.
            Explosive Limits: not applicable

      3.4   Other characteristics

            Normal state at room temperature:  HF is a gas at room 
            temperature but it is most frequently encountered in aqueous 
            solutions.  Solutions more concentrated than 60% fume in air.  

            In the event of a fire, the combustion of carbon-containing 
            materials in the presence of hydrogen fluoride can produce 
            carbonyl fluoride (the fluorine analogue of phosgene).  

            Environmental:  the effects of fluoride ion on bacterial sewage 
            treatment systems, fish and wildlife are potentially 
            disastrous.  Spills can be rapidly complexed with calcium (e.g. 
            as lime) or magnesium salts, resulting in inactivation of the 
            fluoride ion and precipitation. 


      4.1   Uses

            Etching and glass cleaning in the manufacture of glass,
            semiconductors (computer chips), and ceramics (home and
            industrial applications)

            Rust removal in commercial and home laundry products

            Milling titanium

            Metallurgy laboratories

            Petroleum exploration, refining (in alkylation units), and in 
            the oil fields 

            Dental laboratories (for cleaning porcelain prosthetics)


            Some janitorial products for cleaning tiles, and ceramic

            Aluminum brighteners

            Various chemical industries

            Porcelain painters (at home)

      4.2   High risk circumstances of poisoning

            As this material appears innocuous, its severe effects are not 
            suspected in the untrained user.  Therefore without training or 
            extensive warning labels, any of the above circumstances is 
            likely to lead to injuries. 

      4.3   Occupationally exposed populations

            Computer chip manufacturing workers (etch stations and
            quartz tube cleaners and maintenance personnel)

            Oil field workers (e.g., "roustabouts"), and alkylation 
            refinery workers 

            Workers in the synthesis of fluorinated chemicals

            Laundry workers (only when involved with rust removers)

            Glass etchers


    5.    ROUTES OF ENTRY 

      5.1   Oral

            Hydrogen fluoride is sufficiently well absorbed after oral 
            ingestion to cause life-threatening conditions. 

      5.2   Inhalation

            Hydrogen fluoride is absorbed after inhalation and life-
            threatening complications may ensue. 

      5.3   Dermal

            Hydrogen fluoride is absorbed after dermal contact and can 
            result in life-threatening conditions. 

      5.4   Eye

            No data; probably not a significant route of absorption.

      5.5   Parenteral

            No data available.

      5.6   Other

            A case report of attempted suicide using an enema of hydrogen 
            fluoride solution resulted in severe hypocalcaemia 

    6.    KINETICS

      6.1   Absorption by route of exposure

            The rate of absorption by different routes of exposure has not 
            been adequately assessed in man. In the rat, inhaled hydrogen 
            fluoride is absorbed in the upper airways  without apparent 
            deep lung injury at an inhaled concentration of 63 mg/m3.  With 
            direct ventilation of a lung segment via intubation, 99.7% of 
            inhaled hydrogen fluoride at a concentration of 30 - 176 mg/m3 
            was absorbed (Morris and Smith, 1982). 

      6.2   Distribution by route of exposure

            Hydrogen fluoride would be expected to distribute in body water 
            with high protein binding. 

      6.3   Biological half-life

            About 12-24 h.

      6.4   Metabolism

            Not metabolized.

      6.5   Elimination

            After exposure by any route, the fluoride ion is absorbed into 
            the blood and is principally excreted in the urine.  Some 
            fluoride may be incorporated into bone but this is more 
            relevant to chronic exposures to fluoride salts.  Bone 
            demineralization and fluoride deposition can occur after dermal 
            exposures of bony prominences or digits.  In studies of dietary 
            fluoride, 50% of the dose is excreted in 24 h in man (Sticht, 

    7.    TOXICOLOGY 

      7.1   Mode of Action

            Concentrated solutions (>40%) and anhydrous hydrogen fluoride 
            are sufficiently acidic to cause immediate injury due to the 
            activity of the hydrogen ion.  However, the more significant 
            injury to the tissues and systemic toxicity are mediated by the 
            cellular toxicity and chemical activity of the fluoride ion. 
            Fluoride binds irreversibly to calcium and magnesium resulting 
            in precipitation and much of the cellular and systemic toxicity 
            is mediated via this action.   

            The fluoride ion is the most electronegative element in the 
            periodic table; it is a relatively small ion and therefore 
            diffuses readily; and, because hydrogen fluoride is a weak 
            acid, there are sufficiently uncharged species to allow tissue 
            penetration. The fluoride ion is an inhibitor of glycolysis 
            (Embden-Meyerhoff pathway) and it attacks many different 
            cellular constituents including cell membranes and lipids, 
            destroying cell membranes and producing cell necrosis. Severe 
            hypocalcaemia and hypomagnesaemia are produced by hydrogen 
            fluoride absorption causing tetany and disturbances of cardiac 

      7.2   Toxicity

            7.2.1 Human data


                        Fatal exposures to hydrogen fluoride have been 
                        reported. Tepperman (1980) reported death due to 
                        refractory hypocalcaemia about 12 h after exposure 
                        of 2.5% body surface area to anhydrous hydrogen 
                        fluoride.  Mayer and Gross (1985)  reported death 
                        after about 12 h from a 9 -10% body surface area 
                        burn from 70% hydrogen fluoride. 


                        No data available.

            7.2.2 Animal Data

                  The following maximum tolerated exposures to hydrogen 
                  fluoride have been documented in laboratory animals: 
                        Animal      Duration (min)     LC50* (ppm)

                        Rat         5                  4970
                        Rat         15                 2689
                        Guinea Pig  15                 4327
                        Rat         30                 2042
                        Rat         60                 1307  

                  * lethal concentration for 50% of animals

            7.2.3 In-vitro data

                  None applicable.  

            7.2.4 Workplace standards

                  Machle et al (1934) reported that 30 ppm was tolerable 
                  for several minutes by volunteers, but that 110 ppm was 
                  intolerable within one minute.  The American Conference 
                  of Governmental Industrial Hygienists suggest a threshold 
                  limit value (TLV) of 3 ppm as a ceiling level (ACGIH 
                  1990).  In the United Kingdom, the level is 3 ppm; in 
                  Sweden, 2 ppm; in West Germany, 3 ppm.  

            7.2.5 Acceptable daily intake 

                  No data available.

      7.3   Carcinogenicity

            Not carcinogenic.

      7.4   Teratogenic

            Hydrogen fluoride is not significantly teratogenic after single 
            acute exposures.  However, despite the lack of evidence for 
            hydrogen fluoride teratogenicity, chronic effects of fluoride 
            on the fetus and particularly the skeletal system can be 

      7.5   Mutagenicity

            Not mutagenic.

      7.6   Interactions

            Any other agents causing hypocalcaemia (e.g. oxalic acid) can 
            be expected to produce additive effects.  The effects of 
            calcium channel blockers have not been evaluated but 

            hypocalcaemia could be a serious complication in some of these 
            patients.  Patients with endocrine causes of hypocalcaemia, 
            cardiac arrhythmias and renal insufficiency may be at increased 



      9.1   Acute Poisoning by:

            9.1.1 Ingestion

                  Acute effects include corrosion of the oropharynx and the 
                  oesophagus.  after several hours, severe hypocalcaemia 
                  may result in systemic complications. 

            9.1.2 Inhalation

                  Inhalation of the gas or mist causes irritation or 
                  corrosion of the mucous membranes of the upper airway and 
                  severe hypocalcaemia may occur after systemic absorption. 
                  Higher concentrations may cause deep lung injury with 
                  pulmonary oedema and bronchopneumonia. 

            9.1.3 Skin exposure

                  The course of the skin burns from hydrogen fluoride 
                  depend on concentration; more dilute solutions cause 
                  potentially serious but delayed (24 h) systemic effects. 
                  Absorption of the fluoride ion is a significant hazard 
                  mainly due to hypocalcaemia. 

            9.1.4 Eye contact

                  Hydrogen fluoride burns to the eye are corrosive and 
                  require immediate flushing and ophthalmologic 

            9.1.5 Parental
                  No data but expect local severe injury and rapid severe
                  hypocalcaemia and hypomagnesaemia.

            9.1.6 Other

                  No data available.

      9.2   Chronic Poisoning

            9.2.1 Ingestion
            Although chronic poisoning is a problem with other fluoride 
            salts, it has not been reported with hydrogen fluoride. 

      9.3   Course, prognosis, cause of death

            In lethal cases, cardiac arrest has followed skin exposure 
            affecting 10% and 2.5% of the body surface to concentrated 
            (70%) and anhydrous hydrogen fluoride, and after ingestion of 
            several ounces of 7-10% solutions. In these cases, the skin 
            burn was not the immediate cause of death. There was a period 
            lasting several hours during which there were no systemic 
            symptoms. Patients then developed acidosis (pH about 7.20) with 
            hypotension and cardiac arrhythmias.  An increased QT interval 
            was observed in these patients.  In lethal cases, the mechanism 
            of fatality was not appreciated and therefore systemic 
            augmentation of calcium was delayed, by which time the patient 
            was refractory to treatment. 

      9.4   Systematic Description of Clinical Effects

            9.4.1 Cardiovascular

                  The effects on the heart are due to hypocalcaemia. These 
                  include prolongation of the QT interval, arrhythmias 
                  (ventricular tachycardia, fibrillation) and 
                  electromechanical dissociation.  These effects result in 
                  hypotension and can cause cardiac arrest. 

            9.4.2 Respiratory

                  The effect of hydrogen fluoride on the respiratory tract 
                  is typical of highly water soluble corrosive gases.  The 
                  upper airways are primarily affected by gases and 
                  vapours, with the potential for laryngeal oedema, 
                  bronchospasm and pulmonary oedema with higher 
                  concentrations and mists.  Bronchopneumonia may occur 
                  after a few days as a complication of pulmonary injury.  
                  Pulmonary oedema due to hydrogen fluoride may be delayed 
                  for 24-48 hours after exposure. 

            9.4.3 Neurological

                        Not directly affected.

             Peripheral nervous system

                        Inflammatory response of peripheral nerves 
                        underlying exposed skin, especially superficial 
                        nerves of the distal upper extremities. Several 
                        weeks may be required for resolution of the 
                        inflammation (Edelman, 1986). 

             Autonomic nervous system

                        No direct effect.

             Skeletal and smooth muscle

                        Abnormal function has been observed due to the 
                        secondary hypocalcaemia and hypomagnesaemia. 
                        Specifically, fasciculations and tetany have been 
                        reported and inflammation of tendons underlying 
                        areas of skin contact has been a problem (Edelman, 

            9.4.4 Gastrointestinal

                  Severe corrosive effects of the oropharynx and the 
                  oesophagus may occur. The oesophagus may be affected in 
                  the absence of any oropharyngeal injury.  Corrosive 
                  effects on the stomach are possible but have not 
                  generally been reported. 

            9.4.5 Hepatic

                  One study in the rat has noted centrilobular injury but 
                  this has not been confirmed in man and does not appear to 
                  be of any clinical significance. 

            9.4.6 Urinary


                        Some studies have suggested renal cortical injury 
                        consistent with the effects of other fluoride 
                        salts; however, this does not appear to have any 
                        clinical relevance to acute exposure in man. 


                        None known.

            9.4.7 Endocrine and Reproductive

                  None known.

            9.4.8 Dermatological

                  As with other acids, the onset and severity of the burn 
                  depends on the amount of hydrogen fluoride, its 
                  concentration, and the duration of contact. Hydrogen 
                  fluoride penetrates tissues including the skin and nails 
                  and an apparently minor or mild exposure can cause a 
                  serious burn if not promptly and properly treated.   
                  Although hydrogen fluoride solutions weaker than 50% may 
                  cause first degree burns (redness) which may not become 
                  apparent for up to 24 hours, injuries from solutions over 
                  20% generally induce unrelenting pain within 30-60 
                  minutes. Hydrogen fluoride solutions stronger than 50% 
                  cause pain within 5 - 10 minutes and tissue injury 

                  becomes apparent rapidly.  This is usually manifest as 
                  redness followed within 30-60 minutes by a paleness of 
                  the tissue proceeding to frank skin blanching and finally 
                  a subjacent bluish-black necrotic appearance. At this 
                  time, the pain is usually intense.  The skin becomes hard 
                  and leathery. As the acid is one thousand times less 
                  dissociated than hydrochloric acid, and therefore is a 
                  weak acid, substantial quantities of the uncharged moiety 
                  can penetrate deeply into the tissues.  Tepperman (1980) 
                  reported a fatality due to severe hypocalcaemia resulted 
                  from exposure to a concentrated solution affecting only 
                  2.5% of the total body surface. 

            9.4.9 Eye, ear, nose and throat

                  All of these sites are subject to the local corrosive 
                  effects of hydrogen fluoride. See sections 9.4.8 and 

            9.4.10 Haematological
                  No effect.

            9.4.11 Immunological

                  No effect from acute exposure.

            9.4.12 Fluid and Electrolyte disturbance

            Acid-base disturbances

                        Acidosis has been documented in severe cases.  

            Fluid and electrolyte disturbances

                        Most importantly, absorbed fluoride binds magnesium 
                        and calcium irreversibly resulting in 
                        hypomagnesaemia and severe hypocalcaemia, the 
                        latter of which is the usual cause of death from 
                        cardiac disturbances.  Hyperkalaemia may accompany 
                        widespread cellular injury and this can complicate 


                        No data available.

            9.4.13   Allergic Reactions


            9.4.14  Other clinical effects

                  None known.

            9.4.15 Special Risks

                  Patients with known cardiac disturbances may be at 
                  increased risk from hypocalcaemia; however, no specific 
                  studies are available. 

      9.5   Others


    10.   MANAGEMENT

      10.1  General principles

            Immediate removal from exposure and decontamination is 
            essential. Affected areas should be flooded with water for at 
            least 15 minutes.  In cases of serious exposure ( > 2.5% body 
            surface area to anhydrous hydrogen fluoride; 10% body surface 
            area to 70% hydrogen fluoride, 25% body surface area to more 
            dilute solutions) early calcium supplementation should be 

            Patients with renal or cardiac failure may need close 
            observation to prevent hypercalcemia.  Local treatment of the 
            exposed areas of the skin are aimed at decontamination and 
            inactivation of the fluoride ion by complexing with calcium, 
            magnesium, or quaternary ammonium compounds.  

            In severe cases, aggressive support may be needed with 
            treatment of pulmonary oedema (inhalation), arrhythmias and 
            hypotension (all routes of exposure).  Skin burns may need 
            local or intra-arterial injection with calcium gluconate if 
            water decontamination and other topical calcium (or magnesium) 
            salts have not relieved the pain. 

      10.2  Relevant laboratory analysis and other investigations

            10.2.1 Sample collection

                  Blood and urine studies for fluoride are not clinically 

            10.2.2 Biomedical analysis

                  Monitoring of blood calcium, electrolytes, and magnesium 
                  is essential in serious exposures (Trevino et al, 1983).  
                  Arterial blood gases, and electrocardiographic monitoring 
                  is also necessary. Blood calcium and electrolytes should 
                  be measured serially every 6 h for at least the first 24 
                  h in severe cases.  In the absence of full laboratory 
                  support, semi-quantitative analysis for calcium may be 
                  performed in urine (Sulkowitch Test).  A chest X-ray 
                  should be obtained for any suspected inhalation. 

            10.2.3 Toxicological analysis

                  No data available.

            10.2.4 Other investigations

                  No data available.

      10.3  Life supportive procedures and symptomatic treatment

            Monitoring of developing hypocalcaemia is essential.  Removal 
            or inactivation of the fluoride from the site of contact is 
            important and absorbed hydrogen fluoride must also be 
            inactivated.  The standard assessment should include immediate 
            electrocardiographic monitoring of all serious exposures and 
            immediate assessment of serum calcium and electrolytes. This 
            should be repeated every 6 hours for 24 hours, or as indicated 
            by the clinical course.  

            In known or suspected serious exposures, early administration 
            of intravenous (if unavailable, oral) calcium supplementation 
            should be effected.  In patients with normal renal function, 
            excess calcium will be excreted; however, reports of 
            hypercalcaemia during the course of hydrogen fluoride treatment 
            have been noted.  Calcium gluconate, 10 ml of a 10% solution 
            may be given intravenously over several minutes with 1000 mg in 
            1L of 5% dextrose solution over several hours. 

            With known or suspected ingestions, serious skin exposures or 
            inhalations, it is essential to treat the patient 
            The critical effects of hypocalcaemia may be delayed for 2-24 

            A skin burn of more than 1% body surface area, especially when 
            there has been a delay in decontamination, should require 
            admission of the victim to a burns unit for close monitoring 
            (hypocalcaemia and arrhythmias) and treatment (principally 
            administration of calcium).  All persons with extensive skin 
            burns secondary to hydrogen fluoride gas, aerosol, or 
            concentrated solutions should be evaluated for inhalation 
            injury unless they were wearing respiratory protection at the 
            time of the exposure. 

      10.4  Decontamination

            Skin:  FLUSH COPIOUSLY WITH WATER IMMEDIATELY.  This should be 
            done even in an asymptomatic patient, and it should be effected 
            prior to transport to a medical facility if possible.  Never 
            delay water irrigation in order to locate or use a gel or other 
            topical agent. Continue for at least fifteen minutes under 
            running water.  Flood eyes, nose, and mouth if burned (never 
            place anything into the mouth of an unconscious victim). Remove 
            all contaminated clothing.  Use proper gloves and other 
            protective garments when removing contaminated clothing.  Bag 

            the clothing in plastic containers.    Transport to medical 
            care immediately. 

            Gut:   There are few data on decontamination of the gut.  As 
            hydrogen fluoride is corrosive, it is best left is in situ and 
            complexed by administration of calcium (calcium-containing 
            antacids, milk, etc) or magnesium (Epsom salts).  Careful 
            lavage, preferably with milk, after administration of oral 
            calcium may be done, but the optimal procedure is not known. 

            Eyes:  Irrigate the eyes with at least 2 l of saline or water.

            Inhalation:  Remove from exposure to fresh air.  Give oxygen if 
            short of breath or if patient is disoriented.  Transport to 
            hospital emergency room immediately. 

      10.5  Elimination

            Elimination of fluoride is principally via urinary excretion. 
            Enhancement is not necessary. 

      10.6  Antidote treatment

            10.6.1 Adults

                  The use of prepared calcium gluconate gels, magnesium 
                  oxide pastes, and various other preparations have been 
                  compared in various studies (Harris et al, 1981; Bracken 
                  et al, 1985) without convincing evidence of the superior 
                  nature of any agent.  Typically, a 2.5% calcium gluconate 
                  gel has been used and is marketed in Europe.  Saturated 
                  solutions of other calcium salts, and quaternary ammonium 
                  compounds have been used. 

                  While travelling to the hospital (or if there is a delay 
                  in transport) apply hydrogen fluoride Burn Gel (2.5% 
                  calcium gluconate paste) to the exposed areas.  If the 
                  gel is not available, soak affected skin with 25% 
                  magnesium sulphate solution.  This should be done after 
                  the initial showering of the tissue.  This solution may 
                  be made by adding about 0.5 - 1 cup of epsom salts to 2 
                  pints (1100 ml) of water.  Calcium salt solutions may 
                  also be used.  However, these measures should not delay 
                  transport to medical treatment and evaluation. 

            Treatment of hydrogen fluoride burns can be divided into 
            various categories according to concentration (NIH, 1943) and 
            duration of exposure. 

            For:        dermal exposures to hydrogen fluoride concentration 
                        greater than 20% 

                        when the victim has long delay before treatment of 
                        exposure to a lesser concentration 

                        when a large tissue area has been affected by a 
                        lower concentration   

            Initial Medical Treatment:

            Topical or systemic analgesics are likely to mask the symptoms 
            and should generally be avoided. Thoroughly irrigate with 

            Massage calcium gluconate gel into the burned skin for a 
            minimum of 30 minutes and for as long as the pain persists; at 
            times pain persists up to four hours.  If no gel is available, 
            use a calcium (20g Ca2+ in about 2 l of water) or magnesium 
            solution for soaking. 

            Definitive Medical Treatment:

            The affected area, most often the upper extremity (Blunt, 1964; 
            Iverson et al, 1971),  must be injected (infiltrated) with 
            calcium gluconate 10% solution using a 25 - 30 gauge needle 
            (Edelman 1986; Iverson et al, 1971; MacKinnon 1988; Blunt 
            1964).  Never inject calcium chloride.  Generally, there is 
            mild stinging with the infiltration for a few seconds; when 
            this subsides the original pain from the hydrogen fluoride is 
            generally markedly diminished. Multiple small volume injections 
            into the subcutaneous tissues and deep dermis should be 
            performed.  A long spinal needle may be used for large surface 
            area wounds; after placement under the wound, the needle is 
            slowly withdrawn and the calcium gluconate is injected 
            continuously to infiltrate the entire needle tract. If the pain 
            recurs after a period of several hours, the injections may be 
            repeated and extended over a greater area (Dibbell et al, 

            For a large burn area (>5-10%), intravenous calcium should be 
            given and the patient should be placed on a cardiac monitor 
            (Trevino 1983).  Blood calcium should be measured immediately. 
            The area may be infiltrated with calcium gluconate, even if 
            there is little pain or redness, in an attempt to bind the 
            available fluoride and decrease the likelihood and severity of 
            hypocalcaemia.  The fingers are the part of the body most often 
            affected. Never infiltrate more than 0.5 ml of a solution per 
            phalanx as pressure necrosis may occur.  For other areas, 
            inject 0.5 ml per cm2 of tissue. Injections of calcium 
            gluconate solution into the skin and subcutaneous tissues of 
            the fingers must not be circumferential and must be done only 
            with careful judgment because of the possibility of the 
            injection itself producing vascular impairment.  The use of 
            lidocaine in the calcium infusion is not recommended as it may 
            simply mask the important sign of pain.   

            Alternatively, the patient should be referred for calcium 
            gluconate by arterial perfusion to the affected area (Velvart 
            1983, Thiele 1986).  THIS IS A SPECIALIZED TECHNIQUE AND SHOULD 
            For upper extremity burns, an intra-arterial line may be placed 
            at the radial or brachial artery, depending on which site is 
            more likely to provide adequate perfusion of the affected 
            tissues.  Calcium gluconate (2 g in 250 ml normal saline for 
            radial artery; 3 g in 300 ml normal saline for brachial artery) 
            is infused over four hours using a solution pump. The line is 
            left in place for eight hours, and a repeat treatment is then 
            performed.  For lower extremity burns, the femoral artery may 
            be used with 5 g calcium gluconate in 500 ml normal saline. 
            More distal arteries have also been used with 2 g calcium 
            gluconate in 250 ml normal saline.  The results are usually 
            better with antra-arterial treatment and the finger nails may 
            not need to be removed (Edelman 1990). 

            All bullae (blisters) should be removed and the underlying 
            tissues cleaned; calcium gluconate solution or gel should then 
            be applied.  The blister fluid is generally contaminated and it 
            is contraindicated to leave the blisters intact. Remove the 
            nail if periungual or ungual tissues are involved as evidenced 
            by pain or periungual redness or subungual discoloration.  

            For:        dermal exposure to hydrogen fluoride concentration 
            of less than 20% when only a small surface area is involved: 

            Initial Medical Treatment:

            Remove any contaminated garments while wearing rubber or latex 
            gloves. Place the contaminated articles in double plastic bags. 
            Immediately and thoroughly irrigate the patient with water.   
            Use a 30-50% magnesium sulphate solution to soak the affected 
            skin or to apply as wet soaks.  Alternatively, 2.5% calcium gel 
            can be massaged into the burn area for 30 minutes.  As noted 
            above, calcium solutions or quaternary ammonium compounds are 
            also useful. 

            Definitive Medical Treatment

            If pain persists, then inject with calcium gluconate as 
            described above.  NEVER INJECT CALCIUM CHLORIDE. Remove nails 
            as described previously.  Debride any blisters.  In general, 
            contamination of the skin with dilute solutions which are 
            rapidly washed will not need injection. If injection is deemed 
            necessary, then follow the guidelines provided above.  If the 
            pain resolves after initial treatment with washing and topical 
            agents, further treatment is not necessary (Dibbell et al, 

            Burns to eye

            Initial Treatment:

            Immediate flushing is imperative.  Repeat irrigation with at 
            least 2 liters of saline or tap water is recommended.  Use an 
            eye wash station if available. 

            Medical Treatment:

            Flush the eye thoroughly and examine with fluorescein for 
            injury.  Slit-lamp examination is desirable.    A one per cent 
            (1%) solution of calcium gluconate has been advocated for 
            instillation into the eye, however, its usefulness has not been 
            documented (McCulley et al, 1983). Consult an ophthalmologist. 

            Management of systemic effects

            Systemic effects may occur following exposure to relatively 
            small areas of the body to solutions of hydrofluoric acid 
            greater than 20%. Also burns from more dilute solutions when 
            not rapidly decontaminated and/or when there is a large surface 
            area involved may result in significant and potentially life-
            threatening fluoride absorption.  Electrolyte imbalance and 
            hypocalcaemia can occur and may cause severe cardiac 
            arrhythmia.  Hospitalisation must be considered for these 

            Pulmonary effects 

            Pulmonary oedema may occur after inhalation and patients who 
            may be at risk should be monitored in a critical care setting 
            for at least 24 hours.  The onset of pulmonary oedema may be 
            delayed. Initial and follow-up chest radiographs should be 
            taken as indicated clinically. 

                  Administration of 2 - 3% calcium gluconate by nebulizer 
                  (Trevino 1983, MacKinnon 1988) when treating patients 
                  with lung exposure is possible in hospital although its 
                  efficacy is unproven. Acute upper airway embarrassment 
                  should be anticipated for 24 hours and delayed infection 
                  may occur. Laryngoscopy is recommended and emergency 
                  tracheostomy or endotracheal intubation should be readily 
                  available.  Pulmonary function, arterial blood gases and 
                  diffusing capacity should be monitored appropriately.  
                  The value of corticosteroids is uncertain with this and 
                  other irritant inhalation injuries. 

            10.6.2 Children

                  As adults.

      10.7  Management discussion

            Dermal exposure: general principles

            Treatment requires chemical inactivation (complexing) of the 
            fluoride ion by magnesium or calcium salts or by quaternary 
            ammonium solutions.  The injury is not simply an "acid" burn, 
            that is, the hydrogen ion is not the primary injurious agent.  
            Therefore, simple neutralization with a base is not effective 
            or sufficient.  Silvadene cream is not adequate treatment.   

            Various agents and concentrations of agents have been used for 
            topical application.  There is no definitive evidence which 
            demonstrates the best modality.  However, calcium gluconate 
            2.5% gel, magnesium oxide paste, and magnesium sulphate 
            solutions have all been standard treatment for many years.  
            Some authors have insisted that iced water or alcohol is 
            sufficient for burns, but most of these authors did not study a 
            wide range of burns.  

            It is generally accepted that local infiltration of the 
            persistently painful burn wound is essential, for which calcium 
            gluconate is the standard agent. Intra-arterial perfusion of 
            affected limbs has been successfully undertaken and may more 
            effectively deliver calcium to the tissues.  One study (Zachary 
            et al, 1986) has evaluated dimethyl sulfoxide (DMSO) as a 
            topical carrier for calcium salts. The use of calcium gluconate 
            1% as an eyewash is widely recommended for eye contamination, 
            but thorough evaluations have not been published.  Similarly, 
            nebulized 2-3% calcium gluconate has been advocated for 
            inhalation injuries but its efficacy is uncertain. 

            The need to remove the finger nail when involved is not 
            disputed unless intra-arterial calcium can be given.  Some 
            cases (Buckingham 1988) have demonstrated the need for early 
            excision of the burned tissue to prevent the continuing release 
            of fluoride and the resulting hypocalcaemia in patients with 
            refractory arrhythmias. 

            Most low-concentration, short-duration exposures of limited 
            area will do well with topical treatment or local injection of 
            calcium salts although overzealous use of injections may be 
            harmful.  Most often, with simple splash exposures, immediate 
            washing for 15 minutes is sufficient treatment.œ 



      11.1  Case reports from literature

            A petroleum refinery worker was splashed in the face with 
            concentrated hydrogen fluoride (Tepperman, 1980).  Within 30 
            min he was seen at an emergency room where he was in stable 
            condition but had third degree burns of the face.  He was 
            treated aggressively and was intubated in anticipation of 
            pulmonary injury.  At about 1.5 h after exposure, he developed 
            QT segment prolongation; the serum calcium concentration was 
            reported as 35 mg/l.  After 2 hours, he was taken to the 
            operating theatre for burn excision. After 6 hours, he 
            developed ventricular arrhythmias with repeated episodes over 
            the subsequent 4 hours.  He died 10 hours after exposure. A 
            second serum calcium concentration was 22 mg/l.  

            A woman etching computer chips developed a pin-hole in her 
            glove during the four hours that she was working in a dip tank 
            with 5% hydrogen fluoride.  She went to a doctor's office where 
            a non-specific burn ointment was applied (no calcium was 
            applied).  She continued to have pain during the next four 
            days.  At that time she had severe pain under the finger nail 
            and the subungual tissues were black.  There was mild erythema 
            around the proximal cuticle.  Upon removal of the finger nail 
            at a burn treatment center where she was referred, exposed and 
            necrotic bone was identified. The distal phalanx was 
            demineralized and the patient required distal amputation of the 
            finger (Edelman, 1986). 

            A refinery worker was engulfed in a cloud of anhydrous hydrogen 
            fluoride when the coupling from a delivery truck to a reservoir 
            ruptured.  He developed second and third degree burns of the 
            face, arms, chest and neck.  His eyes were inflamed.  After one 
            day, he had a productive cough and chest pain.  No 
            hypocalcaemia was detected.  He developed a bronchopneumonia 
            which was treated with antibiotics.  He was transferred to a 
            burn treatment unit 36 hours after exposure, when calcium 
            gluconate gel was applied to all burned surfaces.  Nebulized 
            calcium gluconate was administered for pulmonary injury.  After 
            3 months, his lung function returned to normal. 

            A female bookkeeper was at home using 10% hydrogen fluoride to 
            frost glass to make pieces for a glass lampshade.  She used 
            cotton pads soaked with the hydrogen fluoride for several hours 
            without any dermal protection. She developed first and second 
            degree burns of the fingers which resolved readily with calcium 
            gluconate infiltration of the affected tissues.  However, she 
            developed a non-suppurative tenosynovitis of the flexor tendon 
            of the index finger which resulted in a 3-week disability and 
            the use of anti-inflammatory medications for resolution 
            (Edelman, 1986). 

      11.2  Internally extracted data on cases

            A four-year-old boy drank several ounces of a laundry rust 
            remover containing 7-10% hydrogen fluoride.  He was taken to an 
            emergency room where he was evaluated.  No oral or pharyngeal 
            burns were noted.  The skin was clear.  The patient was sent to 
            the radiology suite for chest x-rays. During the hour that the 
            patient was in the radiology department, he rapidly developed 

            hypotension and arrhythmias.  Attempts at resuscitation were 
            unsuccessful and the patient died.  A serum calcium level was 
            4.3 mg per 100 ml.

      11.3  Internal cases


      12.1  Availability of Antidotes

            Calcium gluconate 2.5% burn jelly is available in Canada, 
            Europe and other parts of the world.  However, it is not a 
            recognized, approved formulation in the United States.  Calcium 
            gluconate (or glubionate), magnesium sulfate and benzalkonium 
            chloride are generally available materials.  

      12.2  Specific Preventive Measures

            Appropriate latex or rubber gloves should be used when working 
            with hydrogen fluoride.  Frequent checks of glove integrity or 
            changes of the gloves should be performed. Any suspected 
            exposure should be immediately decontaminated.  Worker 
            education about this issue is essential and has largely reduced 
            the incidence of serious injuries in the US semiconductor 
            industry.  Eye goggles, aprons, sleeves and other protective 
            devices should be used in accord with the conditions of use. 
            Concentrated and anhydrous hydrogen fluoride should only be 
            used in exhausted and properly engineered areas.  

            Glass containers should not be used for storage as hydrogen 
            fluoride will dissolve glass.  Explicit warnings in appropriate 
            languages and graphics should be maintained on all containers 
            and work areas.  Work areas should have flood showers and eye 
            wash stations.  Topical calcium or magnesium salts, gels, etc., 
            should be maintained at any site of routine hydrogen fluoride 
            use.  Hydrogen fluoride is not recommended for use in homes, 
            especially where there may be children.  Its use as a home rust 
            remover seems too risky especially since alternative materials 
            of lower toxicity are available. 

      12.3  Other

            No data available.

    13.   REFERENCES

      ACGIH, Threshold Limit Values and Biological Exposure Indices, 
      American Conference of Governmental Industrial Hygienists, Cincinnati  

      Blunt CP.  Treatment of Hydrofluoric Acid Skin Burns by Injection 
      with Calcium Gluconate. Ind Med 33:869-871, 1964. 

      Bracken WM, Cuppage F, McLaury RL, Kirwin C, Klaassen CD.  
      Comparative Effectiveness of Topical Treatments for Hydrofluoric Acid 
      Burns. J Occ Med 27(10):73339, 1985. 

      Buckingham FM.  Surgery:  A Radical Approach to Severe Hydrofluoric 
      Acid Burns, J Occ Med 30(11):873-875, 1988. 

      Dibbell DG, Iverson RE, Jones W, Laub DR, Madison MS.  Hydrofluoric 
      Acid Burns of the Hand. J Bone Joint Surg 52-A(5):931  1970. 

      Edelman PA.  Hydrofluoric Acid Burns, State of the Art Reviews in 
      Occupational Medicine 1(1):89-103  1986. 

      Edelman PA.  Intra-arterial Calcium Gluconate for Treatment of 
      Hydrofluoric Acid Burns of the Extremities. Proceedings of the 
      American Burn Association, Las Vegas, 178, 1990. 

      Grecco RJ, Hartford CE, Haith LR, Patton ML.  Hydrofluoric Acid-
      induced Hypocalcaemia. J Trauma 28(11);1593-1596, 1988. 

      Harris JC, Rumack BH. Comparative Efficacy of Injectable Calcium 
      Gluconate and Magnesium Salts in the Therapy of Hydrofluoric Acid 
      Burns. Clin Toxicol 18:1027-1032, 1981 

      Iverson RE, Laub DR, Madison MS.  Hydrofluoric Acid Burns. Plastic 
      and Recon Surg 48(2):107-112  1971. 

      McCulley JP et al. Hydrofluoric acid burns of the eye. J Occ Med June

      Machle W et al.  The Effects of the Inhalation of Hydrogen Fluoride. 
      J Ind Hyg 16:129 (1934). 

      MacKinnon MA.  Hydrofluoric Acid burns. Occupational Dermatoses 
      6(1):67-74, 1988. 

      Mayer T, Gross PL.  Fatal Systemic Fluorosis Due to Hydrofluoric Acid 
      Burns. Ann Emerg Med 14:149-153, 1985. 

      McCulley JP et al.  Hydrofluoric Acid Burns of the Eye. J Occ Med 
      25:447-50, 1983. 

      Morris JB, Smith FA.  Regional Deposition and Absorption of Inhaled 
      Hydrogen Fluoride in the Rat. Tox Appl Pharm 62:81-89, 1982 

      NIH Division of Industrial Hygiene, National Institute of Health. 
      Hydrofluoric Acid Burns. Ind Med 12:634  1943. 

      Sticht G.  Fluorine. In: Toxicity of Inorganic Compounds, Seiler HG, 
      Sigel H, (eds). Marcel Dekker. New York, 1988, p. 283-291. 

      Tepperman PB  Fatality Due to Acute Systemic Fluoride Poisoning 
      Following a Hydrofluoric Acid Skin Burn. J Occ Med 22:691-692, 1980. 

      Thiele B et al.  Therapie der Fluss-säure verätzung. Deutsch Med 
      Wschr 111:182-184, 1986. 

      Treviño MA, Herrmann GH, Sprout WL.  Treatment of Severe Hydrofluoric 
      Acid Exposures. J Occ Med 25(12):861-63, 1983. 

      Velvart J.  Arterial Perfusion for Hydrofluoric Acid Burns. Human 
      Toxicol 2:233-238, 1983. 

      Zachary LS, Reus W, Gottlieb J, Heggers JP, Robson MC.  Treatment of 
      Experimental Hydrofluoric Acid Burns. JBCR, 7(1):35-59, 1986. 


      Author:     Philip Edelman, M.D.
                  Chief Toxicology and Poison Control
                  University of California Irvine Medical Center
                  1310 West Stewart Drive
                  Suite 306
                  Orange, CA 92668
                  Tel: 1-714-6395006
                  Fax: 1-714-9974377

      Date:       16 May 1995

      Reviewer:   Per Kulling, M.D.
                  Swedish Poison Information Center
                  Karolinska Hospital
                  Box 60 500
                  104 01 Stockholm

                  Tel: 46-8-7362517
                  Fax: 46-8-

      Peer Review: Strasbourg, France, April 1990

    See Also:
       Toxicological Abbreviations
       Hydrogen fluoride (ICSC)