Education on HF

1. HF Overview
• By Dr. Ashok Laddha
• Occupational health physician

2. Content
• General Information
• Utilization of AHF and HF in industry
• Classification
• Physico – Chemical Properties
• General Hazards
• Physiopathology & Toxicology
• Treatment of injuries
• Decontamination
• First Aid
• Medical treatment

3. Background
• The history of hydrofluoric acid is linked to the
history of fluorine because hydrogen fluoride was
synthesized for the first time by C.W. Scheele
from fluoride and concentrated acid, while trying
to isolate the fluorine atom. On the industrial
level, hydrofluoric acid results from the following
reaction between calcium fluoride (molecular
formula CaF2) and concentrated sulfuric acid, at
250 °C
• CaF2 +H2SO4=2HF + CaSO4

4. Synonyms
• Hydrogen fluoride (gaseous state)
• Anhydrous hydrofluoric acid (other name of the
gaseous state)
• Hydrofluoric acid (name of aqueous solutions)
• Fluorhydric acid
• Fluoric acid
• HF (using the molecular formula to name the
substance)

5. Why HF is weak acid?
• Bond between Flourine and Hydrogen is very
strong because of very high electro negativity
difference. That is why Flourine doesn't let
Hydrogen go easily. So extent of donating H+
in is low in HF that is why it is
considered weak acid. It is classified
as weak based upon its dissociation when in
solution with water.

6. Most corrosive acid in world
• HF-SbF5 is extremely corrosive, toxic, and
moisture sensitive. Like most strong
acids, fluoroantimonic acid can react violently
with water, owing to the exothermic
hydration.

7. INTRODUCTION
• Hydrofluoric acid (HF) is an inorganic acid commonly used in many
domestic and industrial settings.
• HF was first used for etching glass due to its corrosive properties,
but currently is also widely used in cleaning agents, rust removers,
in the semiconductor industry, and for manufacturing fertilizer,
pesticides and some plastics.
• Technically, HF is a weak acid when compared with other hydrogen
halide acids, meaning the molecule does not strongly dissociate
into hydrogen and fluorine ions when dissolved in water. In fact,
after being dissolved in water, HF becomes much less dangerous
and less acidic at low concentration (≤20%) . However, at high
concentrations (>20%), small quantities of HF can cause life-
threatening burns, and if the diagnosis is missed or the treatment
delayed, the consequences may be devastating for the patient.

8. Utilization of AHF/HF
Industry Uses
Petrochemical As catalytic agent when alkylising petrol
Glass Glass etching
Medicine Propellant for medication, anaesthetic gases, production of antibiotics,
production and coating of surgical prostheses, production of medicines
Agrochemical Pesticides
Metallurgy Metal cleaning/aluminium production
electronics Production of microchips, cleaning agents for electronic circuits
Cleaning Agent Rust removers, outer wall cleaners
Nuclear Processing of uranium ore
coolants AC, Refrigerators
Fluoro-chemistry Production of Fluoride salts, and Fluoro plastics
Extinguishing Agent Fire extinguishers

9. Effect of Concentration
• Low concentration solutions (8-15%) cause little or no pain
on exposure, but can cause delayed onset of severe pain
and after 12-24 hours can develop signs of tissue corrosion.
• Intermediate concentration solutions (20-40%) cause pain
after exposure and may cause deep tissue injury.
• High concentration solutions (50-70%) produce pain
immediately after contact and result in severe tissue injury
and systemic effects.
• The Occupational Safety and Health Administration HF
workplace permissible exposure limit is 3 ppm in air, while
30 ppm concentrations are considered dangerous to life
and health.

10. Classification
Concentration Toxicity
AHF + HF >85% ACUTE TOXICITY (oral, dermal and
inhalation) Cat. 1 and 2
SKIN CORROSION Cat 1
HF <60% AND >85% ACUTE TOXICITY (oral, dermal and
inhalation) Cat 1 and 2
SKIN CORROSION Cat 1A
HF <60% HYDROFLUORIC ACID with not more than
60% of hydrogen fluoride Fatal if
swallowed : Fatal in contact with skin
Fatal if inhaled
Causes severe skin burns and eye
damage

11. Physical Properties
• Hydrogen fluoride is a colorless gas with a
density of 1.15 g/L at room temperature, or a
colorless liquid (below 20°C) with a density of
0.99 g/mL. Hydrofluoric acid (solution of HF in
water), is a colorless solution. Its exact
physical properties (boiling point, melting
point and density) depend on the
concentration of HF in the aqueous solution.

12. Chemical Properties
• Hydrofluoric acid is a very strong, reactive and
corrosive acid. It readily reacts with bases,
acids, and oxidants. One of its best known
reactions is its corrosive, dissolving effect on
glass and ceramics (called etching). Due to
reactivity towards glass and metals, it is
typically stored in plastic containers.

13. Hazardous Reactions-1
• Risk of explosion in contact with: cyanogen fluoride
(polymerization)
methanesulfonic acid -> oxygen difluoride release
nitric acid + glycerol
Risk of explosion in contact of hydrofluoric acid with:
potassium permanganate
metals
potassium
sodium
The substance can react dangerously with:
ammonia
organic substances
sulfuric acid
acetic anhydride; aminoethanol; ammonium hydroxide;
dry paper; silicon compounds; vinyl acetate

14. Hazardous Reaction-2
• Anhydrous hydrogen fluoride may react
dangerously with:
arsenic(III)oxide; calcium oxide; metal oxides
hydrofluoric acid may react dangerously with:
metal silicides; phosphorus pentoxide; bismuth
acid -> oxygen release
fluorine
sodium hydroxide
Glass or quartz get etched.

15. Interesting Fact-1
• There is no concentration of HF which can be
relied upon as safe!
• There is no material that is completely
resistant to HF degradation.

16. Interesting Facts-2
• HF is extremely corrosive
• HF is extremely systemic toxic
• HF is highly reactive

17. Routes of Exposure
• Dermal
• Ingestion
• Inhalation
• Mucous Membrane
• Ocular

18. Target Organs-Toxicity
• Bone
• Teeth
• Skin
• Mucous Membrane
• Respiratory System
• Cardiovascular System
• GIT
• Neuromuscular

19. High Risk Group
• 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 Electroplaters
• Pesticide workers
• Agro workers

20. Bio Transformation
• Once absorbed into the blood, fluoride is rapidly distributed throughout the
organs. Adult persons rapidly eliminate approximately 50% of the amount taken in.
• The excretion proceeds mainly within 24 hours with the urine and to a minor part
via other pathways (with the feces, sweat, saliva and also mother’smilk).
The proportion which remains in the body long-term is almost exclusively (up to
approximately 99%) deposited in the bones and teeth. During this, hydroxyl groups
in the carbonate-apatite structure are replaced by fluoride ions.
• The accumulated fluoride can be at least partially remobilized and excreted. The
half life for elimination from the bones was reported to be 8 – 20 years.
Under prolonged steady exposure to fluoride, the fluoride contents in urine and
plasma directly reflect the intensity of actual exposure. After occupational
exposure ceases, the amount remaining in the body could be higher than what
would be expected from the current level of exposure because of the slow
mobilization of the part in the bones. [

21. Main Toxic Effects
• Acute:
Corrosive action to the mucous membranes
and skin, danger of serious damage of the
eyes and lungs,
disturbances to the metabolism,
cardiovascular and nervous system
Chronic:
Irritation to the airways, eyes and skin;
damage to the bones (skeletal sclerosis)

22. Mechanism of Action-2 primary
mechanisms
• At concentrations >50%, HF acidity increases dramatically and it then behaves like
a strong acid. The hydrogen ion causes a corrosive burn similar to other acid burns
– this damage occurs immediately and results in visible tissue destruction.
However, for low-concentration HF burns – which represent the large majority of
HF burns – immediate corrosive destruction does not occur in any significant
manner and there may be no immediate pain or tissue destruction.
• The second, more significant mechanism of tissue destruction is caused by fluoride
ions. Liquefaction necrosis of deeper tissues is unique to HF because the acid is
highly lipophilic and readily penetrates deep into tissue . The molecule then
wreaks havoc as it releases its acidic hydrogen ion and fluoride ion in the presence
of cations such as calcium and magnesium. This often-delayed reaction is
responsible for the ‘pain out of proportion’ to physical examination findings, a
result believed to be related to the local hyperkalemia effect secondary to calcium
binding. Cell membrane permeability to potassium is increased by local calcium
depletion; in addition, fluoride ions are believed to directly inhibit Na+K+ pumps.
Both result in local hyperkalemia, neuronal depolarization and intense pain.

23. Mechanism of skin penetration

24. Systemic Effect
• The systemic effects are primarily related to electrolyte
disturbances – mainly hypocalcemia – but also hypomagnesemia,
acidosis, fluorosis and hyperkalemia, which can lead to disturbances
of renal, hepatic and cardiac function .
• Fluoride ions bind calcium and magnesium, and this process may
occur at a rate exceeding the body’s ability to mobilize calcium and
magnesium in the serum. In the majority of cases, clinical evidence
of hypocalcemia is absent; therefore, high-risk patients must be
evaluated by electrocardiography for prolonged QT interval and
arrhythmias and placed on cardiac monitoring . In addition to
causing hypocalcemia, fluoride ions are believed to be directly toxic
to myocardial cells by inhibiting adenylate cyclase. For severe HF
burns, serum electrolyte levels should be obtained urgently and
then frequently monitored as dictated by the degree of clinical
exposure and systemic involvement.
• .

25. Prolonged QT Interval

26. framework for risk of systemic toxicity
• HF burns with a high risk to develop lethal
electrolyte imbalances
• 1% BSA burn with anhydrous HF
• 5% BSA burn with >70% concentrated HF
• 7% BSA burn with 50–70% concentrated HF
10% BSA burn with 20–50% concentrated HF
20% BSA burn with 5%
• Inhalation of HF at concentrations >5%

27. Symptoms of serious intoxications
• Symptoms of serious intoxications include:
• Hypocalcaemia (low calcium level in the blood)
• Hypotension (very low blood pressure),
• Tetany and/or laryngospasm (involuntary contraction of
muscles either muscles or vocal cords)
• Respiratory failure (possibly due to pulmonary oedema)
• Ventricular tachycardia (abnormal high pulse cardiac rate)
=> Ventricular fibrillation (heart quivers) => Cardiac arrest.
• Renal and hepatic functions may be impaired and muscular
damage may be secondary to tetany
• Prolonged Q-T intervals in ECG/EKG as a result of
hypocalcemia

28. Cutaneous Burn Management
• Apply 2.5% calcium gluconate gel to the affected area.
If the proprietary gel is not available, constitute by
dissolving 10% calcium gluconate solution in 3 times
the volume of a water-soluble lubricant (eg, KY gel).
For burns to the fingers, retain gel in a latex glove.
• If pain persists for more than 30 minutes after
application of calcium gluconate gel, further treatment
is required. Subcutaneous infiltration of calcium
gluconate is recommended at a dose of 0.5 mL of a 5%
solution per square centimeter of surface burn
extending 0.5 cm beyond the margin of involved tissue
(10% calcium gluconate solution can be irritating to the
tissue).

29. Inhalation Burn
• Patients with inhalation burns may develop
acute lung injury presenting with the
following:
• Hypoxemia
• Stridor
• Wheezing
• Rhonchi
• Ocular burns may present with severe pain.

30. Inhalation Burn
• Exposures to the head and neck should arouse
suspicion of pulmonary involvement. If any doubt
is present, admission for observation is advised.
Specific treatment includes the following:
• Provide 100% oxygen by mask, 2.5% calcium
gluconate by nebulizer with 100% oxygen,
continuous pulse oximetry, ECG, and clinical
monitoring.
• Acute lung injury is treated along conventional
lines, as needed.

31. Ocular Burn
• Generously irrigate with sterile water or saline for at
least 5 minutes. Local anesthetic may be required.
• If pain persists, irrigate with a 1% solution of calcium
gluconate, which is made by diluting the 10% solution
in 10 times the volume of normal saline.
• Do not use undiluted 10% calcium gluconate.
• Calcium salts are very irritating to the eye, and urgent
ophthalmologic consultation should be requested prior
to the irrigation with 1% calcium gluconate solution.

32. Complications-1
• Severe burn with scaring
• Bone loss
• Electrolyte imbalance
• Renal Failure
• Hypotension
• Respiratory Failure
• Cardiac arrhythmia
• Ventricular Tachycardia
• Pulmonary edema
• .

33. Complication-2
• Myocardial infraction
• Lingering chronic Lung Disease
• Eye exposure to hydrogen fluoride may cause
prolonged or permanent visual defects,
blindness, or total destruction of the eye.
• Swallowing hydrogen fluoride can damage the
esophagus and stomach. The damage may
progress for several weeks, resulting in gradual
and lingering narrowing of the esophagus
• Skeletal Sclerosis

34. Warning
• Burns with concentrated HF are usually very
serious, with the potential for significant
complications due to fluoride toxicity.
Concentrated HF, liquid or vapor, may cause
severe burns, metabolic imbalances,
pulmonary edema, and life threatening
cardiac arrythmias. Even moderate exposures
to concentrated HF may rapidly progress to
fatality.

35. Pre -Hospital care-1
• Treatment of hydrofluoric acid burns includes basic life support and
appropriate decontamination, followed by neutralization of the acid
by use of calcium gluconate or hydrofluoric-specific agent such as
Hexafluorine, if available. If exposure occurs at an industrial site,
obtain and transport any available treatment literature.
• Assess and manage acute life-threatening conditions in the usual
manner. Emergency Medical Services (EMS) personnel should use
gloves, masks, and gowns, if necessary.
• Remove soiled clothing. Initially decontaminate by irrigation with
copious amounts of water.
• Ice packs on the affected area may alleviate symptoms by retarding
diffusion of the ion.

36. Pre-Hospital care-2
• If calcium gluconate gel or specific agent (eg,
Hexafluorine) is available, apply liberally to the affected
area.
• For digital burns, if calcium gluconate gel is not
available, the fingers may be soaked in magnesium
hydroxide–containing antacid preparations (eg,
Mylanta) en route to a medical facility. Retain
gel/antacid in a latex glove if practicable, and the
gloved hand may be immersed in iced water.
• Treat inhalation injuries with oxygen and 2.5% calcium
gluconate nebulizer.
• Control pain with opioid agents

37. IMPORTANT GUIDE TO THE SUCCESS OF TREATMENT
• HF skin burns are usually accompanied by
severe, throbbing pain that is thought to be
due to irritation of nerve endings by increased
levels of potassium ions entering the
extracelluar space to compensate for the
reduced levels of calcium ions, which have
been bound to the fluoride. RELIEF OF PAIN IS
AN IMPORTANT GUIDE TO THE SUCCESS OF
TREATMENT

38. Important Safety Precaution
• FIRST AID RESPONDERS AND MEDICAL
PERSONNEL MUST WEAR RUBBER (2 pairs of
NEOPRENE OR POLYVINYL CHLORIDE [PVC])
GLOVES WHEN TREATING HF BURNS TO AVOID
HAND BURNS!

39. Investigations
• Complete blood count
• Serum Calcium
• Serum Magnesium
• ECG
• PFT
• Renal function test
• Cardiac Markers
• Serum Electrolytes
• X-ray chest
• ABG
• Fluorides in urine
• Urine R/M
• Serum Fluoride level

40. 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 hypocalcaemia.

41. Antidote
• 2.5% Calcium Gluconate Gel
• Calcium Gluconate Gel
• Diphorterine HF solution

42. Guidelines for calcium Replacement
• Guidelines advocate calcium replacement in high-risk groups even
before the serum calcium level is determined . Proven
hypocalcemia warrants calcium gluconate infusion parenterally and
frequent serum calcium monitoring. Rapid urinary excretion and
alkalization of urine have been described as effective means of
fluoride ion removal. Hemodialysis has been reported to reduce
both fluoride and potassium levels, and to treat persistent
hypocalcemia despite calcium infusion. Some authors advise that if
severe systemic toxicity develops despite intravenous calcium
infusion and intensive care resuscitation, immediate surgical
excision of the burn should be considered to remove the tissue
source of the fluoride ions . This scenario is extremely rare and
carries a poor prognosis. The use of urgent surgery in this setting is
controversial because there are no controlled studies
demonstrating any benefit over continued resuscitation.

43. Quaternary Ammonium Compounds
• Most HF burns can be satisfactorily treated by
immersion of the burned part in an iced, aqueous
solution of a quaternary ammonium compound.
The most experience is with a solution of 0.13%
benzalkonium chloride.
• The solutions should be cooled with ice cubes.
Shaved or crushed ice may cause excessive
cooling, with the danger of frostbite.
• Iced quaternary ammonium compound solutions
offer several advantages over topical calcium
gluconate gel:

44. Advantage Of QAC
• Ability to treat burns on multiple surfaces, such as the
hand, more efficiently;
• Reduction of local pain due to the cooling effect of ice;
• Possible slowing of the passage of the fluoride ion into
deeper tissues and into the bloodstream due to local
vasoconstriction;
• Does not require continuous massaging
• Important Note:-Quaternary ammonium compounds
should not be used for burns on the face, ears or other
sensitive areas due to their irritating nature. It is
preferable to use calcium gluconate gel or calcium
gluconate injection in these areas.

45. Safe work Practice
• Anyone using HF must be trained in its use and a second person must be in
attendance, aware of the use of HF and be prepared to assist in the event of an
emergency. Training in the use of HF is provided by OHS.
• Tasks involving HF must be undertaken in a fume cupboard.
• Specimen storage areas must be marked as containing HF solutions.
• Solutions containing HF must be stored in polyethylene or Teflon containers. HF
reacts with glass and, therefore, solutions containing HF are incompatible with
glass storage vessels and equipment.
• Eyewash stations, emergency showers and hand washing facilities must be
available in each work area.
• A first aid kit, which includes the HF module, must be available in each work area.
• Laboratory space and placement of equipment should not create a crowded
working environment nor inhibit cleaning.
• All skin and eye contact must be avoided.
• Restriction of laboratory access is important.
• Waste containers for the safe disposal of acids must be provided.

46. TLV
• Irritation to nose and throat at 3 parts per
million (ppm)
• Time-weighted average (TWA) of 0.5 ppm
• Short-term exposure limit (STEL) 15 min - 2
ppm
• 30 ppm is considered immediately dangerous
to life and health (IDLH)

47. Exposure Limit
• The Permissible Exposure Limit (PEL) set by the U.S. Occupational Safety
and Health Administration (OSHA) is a time weighted average exposure for
8 hours of 3 ppm.
• The American Conference of Governmental Industrial Hygienists (ACGIH)
recommends a ceiling level of 2 ppm (1.53 mg/m³) with a 0.5 ppm TLV-
TWA.
• The National Institute for Occupational Safety and Health (NIOSH) has
established the level that is immediately dangerous to life and health
(IDLH) at 30 ppm.
• The American Industrial Hygiene Association (AIHA) has published an
Emergency Response Planning Guideline setting 50 ppm as the maximum
level below which nearly all individuals could be exposed for one hour
without experiencing or developing life-threatening health effects (ERPG-
3),
• 20 ppm as the maximum level below which nearly all individuals could be
exposed for one hour without

48. Caution
• Industrial experience indicates that prompt
treatment, as described, will prevent the
development of serious injury
• Therefore, speed is essential.
• Delays in decontamination, first aid care or
medical treatment or improper medical
treatment will likely result in greater damage or
may, in some cases, result in a fatal outcome.
• Relief of pain is an important guide to the success
of the treatment; therefore local anesthesia
should be avoided

49. Take home message
Be careful!
ANY EXPOSURE OF AHF / HF
MUST BE TREATED
IMMEDIATELY
AND
SPECIFIC
TO AHF/HF!