Aqueous hydrogen fluoride
1.4 Identification Numbers
1.4.1 CAS number
1.4.2 Other numbers
1.5 Main Brand Names/Trade Names
Wink Rust Stain Remover 7-10% HF (US)
1.6 Main Manufacturers/Main importers
2.1 Main Risks and Target Organs
Hydrogen fluoride is highly corrosive to all tissues.
Skin: Burns, necrosis; underlying bone may be decalcified.
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
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.
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
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. PHYSICOCHEMICAL PROPERTIES
3.1 Origin of substance
Hydrogen fluoride is generally derived from the reaction of
concentrated sulphuric acid on fluospar (CaF2).
3.2 Chemical structure
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. USES AND HIGH-RISK CIRCUMSTANCES
Etching and glass cleaning in the manufacture of glass,
semiconductors (computer chips), and ceramics (home and
Rust removal in commercial and home laundry products
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
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
Workers in the synthesis of fluorinated chemicals
Laundry workers (only when involved with rust removers)
5. ROUTES OF ENTRY
Hydrogen fluoride is sufficiently well absorbed after oral
ingestion to cause life-threatening conditions.
Hydrogen fluoride is absorbed after inhalation and life-
threatening complications may ensue.
Hydrogen fluoride is absorbed after dermal contact and can
result in life-threatening conditions.
No data; probably not a significant route of absorption.
No data available.
A case report of attempted suicide using an enema of hydrogen
fluoride solution resulted in severe hypocalcaemia
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.
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,
7.1 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
7.2.1 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
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.
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
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
8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS
9. CLINICAL EFFECTS
9.1 Acute Poisoning by:
Acute effects include corrosion of the oropharynx and the
oesophagus. after several hours, severe hypocalcaemia
may result in systemic complications.
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
No data but expect local severe injury and rapid severe
hypocalcaemia and hypomagnesaemia.
No data available.
9.2 Chronic Poisoning
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
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.
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.
Not directly affected.
188.8.131.52 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).
184.108.40.206 Autonomic nervous system
No direct effect.
220.127.116.11 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,
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.
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.
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.
9.4.7 Endocrine and Reproductive
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
No effect from acute exposure.
9.4.12 Fluid and Electrolyte disturbance
18.104.22.168 Acid-base disturbances
Acidosis has been documented in severe cases.
22.214.171.124 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
9.4.15 Special Risks
Patients with known cardiac disturbances may be at
increased risk from hypocalcaemia; however, no specific
studies are available.
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
conservatively DESPITE THE POSSIBLY BENIGN INITIAL APPEARANCE.
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.
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
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.
Elimination of fluoride is principally via urinary excretion.
Enhancement is not necessary.
10.6 Antidote treatment
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
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
ONLY BE PERFORMED BY PHYSICIANS EXPERIENCED IN THIS PROCEDURE.
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
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
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.
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 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.
10.7 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
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.
11. ILLUSTRATIVE CASES
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
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. ADDITIONAL INFORMATION
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.
No data available.
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
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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
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
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.
14. AUTHOR(S), REVIEWER(S), DATE(S)
Author: Philip Edelman, M.D.
Chief Toxicology and Poison Control
University of California Irvine Medical Center
1310 West Stewart Drive
Orange, CA 92668
Date: 16 May 1995
Reviewer: Per Kulling, M.D.
Swedish Poison Information Center
Box 60 500
104 01 Stockholm
Peer Review: Strasbourg, France, April 1990