Why this poison is interesting

Hydrofluoric acid is the page in this library where every heuristic a clinician has built from experience of other burns points the wrong way. Acid burns hurt immediately; this one may not hurt for a day. Acid burns are as deep as they look; this one is deeper. Concentrated solutions are the dangerous ones; here the dilute solutions are the ones that catch people out, because they buy time to keep working. And after a dermal exposure, the patient who dies does so from a rhythm disturbance rather than from the wound — though that generalisation has to be route-qualified, and the qualification is the page's own source: "acute exposure to hydrogen fluoride can be fatal and is usually as a result of pulmonary oedema".¹ After significant inhalation the lethal event is the lung, not the electrolytes. Traditional teaching

The mechanism behind all of that is a single division of labour. Hydrofluoric acid contains two poisons and they act at different depths. The hydrogen ion is an ordinary acid — it denatures protein at the surface, it hurts, and the injury it causes is self-limiting because the reaction consumes it. The fluoride ion is not consumed by anything at the surface: it penetrates, and the UKHSA overview is explicit that hydrogen fluoride "readily penetrates intact skin, nails and deep tissue layers"¹ and that "fluoride ions are responsible for the systemic effects".¹

The third reason is the inversion in the timings, which the source states as a gradient. Anhydrous hydrogen fluoride or solutions above 50% may have immediate symptom onset. Solutions between 20 and 50% may take up to 8 hours. Solutions under 20% may take up to 24 hours.¹ The weaker the solution, the longer the delay before anybody knows anything is wrong — and a domestic rust remover or wheel cleaner is a weak solution used without gloves by somebody who will not present until the middle of the night.

A poison is a drug whose kinetics have escaped its pharmacology.

The toxic principle

Hydrogen fluoride is a weak acid, and that fact — which sounds reassuring — is the beginning of the problem. A strong acid dissociates completely, so its hydrogen ions react at the surface and its anion is left behind as an inert spectator. A weak acid remains substantially undissociated, and an undissociated, uncharged molecule crosses lipid membranes far more readily than an ion does.

So hydrogen fluoride penetrates as a neutral molecule, dissociates once it is inside the tissue, and releases fluoride where nothing can wash it off. The overview records that "fluoride ions are readily released from water soluble fluoride compounds including hydrogen fluoride and are almost completely absorbed", and that hydrogen fluoride "readily penetrates intact skin, nails and deep tissue layers".¹ Intact skin is not a barrier to it, which is the single sentence that separates this from every other acid.

What the fluoride ion actually does once it is inside

Fluoride has a high affinity for divalent cations — calcium and magnesium — and forms insoluble salts with them. The consequences follow directly and are all documented as a group in the source: "systemic effects caused by exposure to hydrogen fluoride include hypocalcaemia, hypomagnesaemia, metabolic acidosis and hyperkalaemia".¹ Calcium is precipitated out of the tissue and out of the circulation, magnesium with it, and cellular potassium handling is disturbed so that potassium rises. The tissue destruction that makes these burns so deep is partly this: cells stripped of the calcium their membranes and enzymes require. The burn and the electrolyte disturbance are not two diseases — they are the same reaction happening at two scales. Established

One further mechanism explains the eye injury, and it is the general principle of the whole page in miniature. The overview states that the severity of eye burns "is due to the pH and the toxicity of the F- ion", and that "the initial damage caused by the acidity of the hydrogen fluoride enables the fluoride ion to penetrate into deeper layers of tissue where it causes severe eye lesions".¹ The acid is the ion's delivery system.

Toxicokinetics

The unusual feature of this table is that the most important kinetic variable is not a property of the patient at all — it is the concentration of the solution, because it determines both how fast the injury declares itself and, through contact time, how much fluoride is delivered.

Hydrofluoric acid — kinetics governed by the concentration on the label
Parameter	Therapeutic	In overdose	Why it changes
Dermal absorption	Most acids do not cross intact skin	"Hydrogen fluoride readily penetrates intact skin, nails and deep tissue layers"¹	The row that makes this a poisoning rather than a wound. Undissociated hydrogen fluoride crosses as a neutral molecule and dissociates on the far side, which is why washing the surface late achieves so little.
Inhalational absorption	—	"A study in rats reported that the majority of inhaled hydrogen fluoride was absorbed by the lining of the upper respiratory tract"¹	An animal finding, flagged as one. It predicts an upper-airway-predominant injury of the kind seen with the highly soluble gases — see chlorine and ammonia — while the South Korean release also produced gastrointestinal symptoms attributed to absorption from the lower respiratory tract at very high concentration.¹
Onset — the concentration gradient	—	Over 50% or anhydrous: onset "may" be immediate. 20–50%: "up to 8 hours". Under 20%: "up to 24 hours"¹	The single most useful row on the page, and it runs backwards. Weaker solutions are less immediately painful, so contact is prolonged and presentation delayed — and "solutions as low as 2% may cause burns if they remain in contact with the skin for long enough".¹ The dilute product is more dangerous because it is weaker.
Distribution	Fluoride distributes to extracellular fluid and to bone	Sequestered by calcium wherever it finds it, including bone	"Decalcification of underlying bone can occur."¹ The ion is removed from the circulation by the same reaction that constitutes the poisoning — so a falling fluoride concentration is not evidence of recovery.
The systemic consequence	—	"Hypocalcaemia, hypomagnesaemia, metabolic acidosis and hyperkalaemia"¹	Two cations removed and one released. Hypocalcaemia and hyperkalaemia together are a far more dangerous combination than either alone, because they act on cardiac conduction in the same direction while the usual protective effect of calcium against hyperkalaemia is exactly what has been lost.
Elimination	"The main route of excretion of fluoride ions is via the urine"; small amounts in faeces and sweat¹	Unchanged	Renal clearance is real but slow relative to the arrhythmia risk. The clinical race is not against elimination — it is against how much calcium can be replaced and how quickly.
Dialysability	—	Never assessed. EXTRIP has published no recommendation covering hydrofluoric acid or fluoride²	This is the one EXTRIP absence in Band D that is arguably a genuine gap rather than an incoherent question. Fluoride is a small, water-soluble, poorly protein-bound ion — physically an excellent dialysis candidate — and severe poisoning is a metabolic emergency lasting hours. The question has simply not been addressed, and this page notes that without recommending anything.

Metabolism and the metabolites

There is no metabolism. Fluoride is an element and is not transformed into anything — the chemistry on this page is precipitation rather than biotransformation, and the reaction that constitutes the poisoning is the same reaction that eventually removes the ion from circulation.

Two ions, two depths — how one liquid produces a burn and an arrhythmia

Hydrofluoric acid on the skinA weak acid, therefore substantially undissociated — and an uncharged molecule crosses membranes
Hydrogen ion reacts at the surfaceOrdinary acid burnSelf-limiting — the reaction consumes the ion. This is the part that behaves like every other acid
Undissociated HF penetrates intact skin, nails and deep tissueFluoride released in deep tissue"Readily penetrates intact skin, nails and deep tissue layers"¹ — washing the surface no longer reaches it
Precipitates calcium locallyCellular calcium stripped; liquefactive tissue destructionThe deep, disproportionately painful, poorly healing wound¹
Absorbed into the circulationHypocalcaemia and hypomagnesaemiaBoth named as systemic effects¹ — two divalent cations precipitated by one anion
Disturbed cellular potassium handlingHyperkalaemiaNamed alongside the others¹. The combination with hypocalcaemia is the dangerous part
Decalcification of underlying bone"Decalcification of underlying bone can occur"¹ — the injury does not stop at soft tissue
Cardiac conduction abnormality, arrhythmia, tetany, convulsions"Secondary to electrolyte disturbances"¹ — the cause of death, and not the burn

Elimination and accumulation

Fluoride is cleared by the kidney¹ and it is also removed from the circulation by the very reaction that causes harm — precipitation with calcium in tissue and bone. That makes a falling plasma fluoride an unreliable sign of anything, because the ion may have left the blood by being deposited rather than by being excreted.

The latent phase that lengthens as the danger becomes less obvious

Most latent phases in this library are fixed properties of a mechanism. This one is set by the concentration of the product, and it runs in the direction that catches people out. "Anhydrous or hydrogen fluoride or hydrofluoric acid solutions of greater than 50% may have immediate symptom onset. For solutions between 20 to 50% onset of symptoms may take up to 8 hours, while solutions less than 20% onset may take up to 24 hours."¹ A concentrated industrial exposure announces itself and gets treated. A dilute domestic one does not — and "solutions as low as 2% may cause burns if they remain in contact with the skin for long enough".¹ The patient who presents at three in the morning with a painful finger and a normal-looking nail bed, having cleaned alloy wheels the previous afternoon, is the presentation this paragraph exists for.

There is a second, less familiar accumulation route worth naming. Following dermal contact, patients have experienced concurrent inhalation from off-gassing, and went on to develop "pulmonary oedema, pulmonary haemorrhagic oedema and tracheobronchitis".¹ A skin exposure can become an inhalational one, which is a genuine hazard to the patient and, by implication, to whoever is treating them in an enclosed space.

Where this latent phase sits among the others

Hydrofluoric acid — an ion diffusing far enough to reach a nerve ending — and the thinner the solution, the further it travels before anybody feels it

The other 26 kinds of latent phase in this library

Amphetamines and MDMA — a hormone acting normally on a kidney behaving normally, while the patient supplies the water
Antipsychotics — a physical object in the stomach — extended-release quetiapine forming a pharmacobezoar
Arsenic — a tissue declaring on its own timetable rather than the poison's — the arsenic is excreted within days, but the nail that was growing while it circulated does not show its white transverse line for several weeks
Arsine and stibine — a red cell mass haemolysing faster than a kidney can cope with — the exposure is over, the haemolysis is silent until the urine changes colour, and the renal failure that follows is the cause of death
Beta-blockers — a repolarisation lesion waiting for an ectopic beat to fall inside it — sotalol prolongs the QT and then, for hours, nothing happens
Calcium-channel blockers — a tablet that has not yet dissolved
Carbon monoxide — an inflammatory process continuing after the poison itself has gone
Chlorine and ammonia — paraquat's cause at its shortest — the time an injured alveolar epithelium takes to leak
Cocaine — a package that has not yet failed — the calcium-channel blocker's cause moved outside the tablet, where wrapping integrity cannot be measured
Digoxin — distribution of the drug to its target — which that page argues is not a latent phase in the paracetamol sense at all
Ethylene glycol — paracetamol's cause with a different enzyme — glycolate accumulating behind glycolate oxidase while the patient looks merely drunk
GHB and GBL — not the poisoning but its withdrawal — a half-life under an hour means admission for any reason interrupts round-the-clock redosing
Iron — a true remission — the corrosive injury settling while absorbed iron moves into the cells it will poison, so the patient improves on their way to the dangerous phase
Ketamine — nitrous oxide's cause on a longer clock — urothelial damage accumulating over months to years of repeated exposure
Lead — bone giving lead back — a store with a half-life of 10 to 30 years releasing its contents when pregnancy, lactation, menopause or osteoporosis resorbs it, so the blood concentration rises after the exposure has ended
Lithium — transport across cell membranes
Mercury — distribution on two clocks — tissue concentrations peaking within 24 hours everywhere except the brain, which is not reached until 2 to 3 days, and which then cannot let the poison out again
Methaemoglobin inducers — paracetamol's cause at its shortest — one to four hours manufacturing the toxic species
Methanol — paracetamol's cause again — formate accumulating behind a folate-dependent disposal step that primates perform poorly
Nitrous oxide — damage accumulating to a threshold
Opioids — an antidote wearing off before the poison does — renarcotisation, the only gap in this set that treatment creates rather than reveals
Organophosphate insecticides — a fat store emptying — and, separately, a second and unexplained lesion declaring itself at a neuromuscular junction the first phase had already left
Paracetamol — time spent manufacturing a toxic metabolite
Paraquat — the body responding to an injury that is already complete
Sodium-channel blockade — a gap that cannot be shortened
Thallium — hair on its own clock rather than the poison's — sensory symptoms come first and the alopecia that makes the diagnosis obvious follows them, well after the interval in which treatment is recommended

Target organs — and why those

The target organs divide cleanly into the tissue the liquid touched and the tissues that depend on the ions it removed. The first group is where the injury happens and the second is where the patient dies.

Heart

TargetConduction system and myocardium, via calcium, magnesium and potassium

Why hereThe organ that kills the patient after a dermal or systemic exposure, and it is never touched by the acid. The source lists "cardiac conduction abnormalities and arrhythmias" occurring "secondary to electrolyte disturbances"¹ — hypocalcaemia, hypomagnesaemia and hyperkalaemia simultaneously.¹ The combination is worse than the sum: hyperkalaemia destabilises the membrane, and the calcium that would ordinarily be given to stabilise it is precisely what the fluoride has removed. Established

At the bedsideQT prolongation, conduction abnormality, ventricular arrhythmia and arrest. "Changes in electrocardiograms have been reported following dermal exposure", reversible within three days.¹ A patient with a small hydrofluoric acid burn belongs on a monitor, and this card is the reason.

Skin, nails and deep soft tissue

TargetCells stripped of calcium by penetrating fluoride

Why hereThe acid opens the surface and the fluoride continues into "deep tissue layers".¹ The depth of the injury is a property of the ion's diffusion, not of the acid's contact — which is why the wound is characteristically far deeper than it looks and heals poorly. Subungual exposure is disproportionately severe because the nail traps the liquid against the tissue and "nails" are named among the structures penetrated.¹ Established

At the bedside"Severe and deep burns that are extremely painful and difficult to heal", sometimes with "whitish discoloration, or a blue-grey discoloration to the skin followed by rapid tissue destruction and necrosis".¹ Severe pain with an unremarkable appearance is the classic and most misleading combination.

Bone

TargetBone mineral

Why hereFluoride's affinity for calcium does not stop at the soft tissues: "decalcification of underlying bone can occur".¹ This is the same precipitation reaction operating on the body's largest calcium store — which is both an injury and, in a sense, the ion's ultimate sink. Established

At the bedsideDeep, persistent pain out of proportion to the surface wound, and bony involvement under a small burn — particularly at the fingertips, where there is very little tissue between the skin and the bone.

Eye

TargetCornea and deeper structures

Why hereThe source gives the two-stage mechanism explicitly: severity "is due to the pH and the toxicity of the F- ion", and "the initial damage caused by the acidity... enables the fluoride ion to penetrate into deeper layers of tissue where it causes severe eye lesions".¹ It is the whole page's mechanism in one organ — the acid as the delivery system for the ion. Established

At the bedside"Conjunctivitis, conjunctival oedema, corneal epithelial coagulation and necrosis."¹ An ophthalmic emergency, and one where the initial appearance again understates what will follow.

Respiratory tract

TargetUpper airway predominantly; lower airway at very high concentration

Why hereThis is the organ the source names as the usual cause of death: "acute exposure to hydrogen fluoride can be fatal and is usually as a result of pulmonary oedema"¹ — a fact that route-qualifies the cardiac argument made elsewhere on this page. A rat study reported that "the majority of inhaled hydrogen fluoride was absorbed by the lining of the upper respiratory tract"¹ — an animal finding, flagged here rather than presented as human data. In the 2012 South Korean release, gastrointestinal symptoms were attributed to "large volumes of the gas being inhaled and the hydrogen fluoride being absorbed into the lower respiratory system".¹ Off-gassing from a dermal exposure has itself produced pulmonary oedema and tracheobronchitis.¹ Inferred

At the bedsideUpper airway irritation at moderate exposure; pulmonary oedema, haemorrhagic pulmonary oedema and tracheobronchitis after heavy exposure or off-gassing.¹ In one incident, 13 workers exposed to mist at a "maximum concentration of" 125–170 mg/m³ for two minutes and treated immediately with nebulised calcium gluconate reported no dermal or ocular burns, only minor upper respiratory irritation, and none developed pulmonary oedema.¹

Timeline of effects

Hydrofluoric acid — a timeline set by the number on the bottle

Time

What you seeWhat is happening

Possibly immediate (>50% or anhydrous)Concentrated exposure declares itself
What you seeSymptom onset "may" be immediate.¹ Severe pain and visible injury; systemic effects may follow within hours.
What is happeningEnough undissociated hydrogen fluoride to saturate the tissue at once. This is the exposure that gets recognised and treated, and paradoxically the one with the better trajectory for that reason.
Up to 8 h (20–50%)Intermediate solutions
What you seeLittle or nothing to see or feel initially. Onset of symptoms "may take up to 8 hours".¹
What is happeningFluoride diffusing through tissue toward nerve endings and toward the circulation. The injury is proceeding at full rate throughout the silence — this is not a period of safety.
Up to 24 h (<20%)Dilute solutions — the domestic exposure
What you seeNothing at all, often for a full day. Onset "may take up to 24 hours"¹, and "solutions as low as 2%" can burn given contact time.¹
What is happeningThe lowest fluoride flux, and therefore the longest diffusion time to symptom threshold — and the longest contact time, because nothing prompted the person to wash it off.
Hours after absorptionElectrolyte collapse
What you seeParaesthesiae, tetany, myoclonus, convulsions, arrhythmia — "secondary to electrolyte disturbances".¹
What is happening"Hypocalcaemia, hypomagnesaemia, metabolic acidosis and hyperkalaemia."¹ This phase can arrive while the skin still looks unimpressive, which is the whole clinical problem.
DaysThe wound declares its depth
What you see"Severe and deep burns that are extremely painful and difficult to heal"¹, sometimes with whitish or blue-grey discolouration and necrosis.¹
What is happeningLiquefactive destruction of tissue whose cells have been stripped of calcium. The final extent exceeds the initial appearance in essentially every case.
Weeks–monthsLate structural sequelae
What you seePoor healing, scarring and loss of function; after ingestion, "oesophageal or gastric perforation... may develop over weeks or months".¹
What is happeningDeep tissue and bone injury — "decalcification of underlying bone can occur"¹ — resolving, if at all, on the timescale of structural repair.

What the mechanism predicts at the bedside

Ask the concentration, and treat a low one as more suspicious rather than less. Under 20%, onset may take up to 24 hours¹; as low as 2% can burn given contact time.¹
The appearance of the burn does not measure the exposure. Fluoride penetrates intact skin, nails and deep tissue¹, so a small or unimpressive wound can accompany a systemic poisoning.
Put the patient on a monitor and check calcium, magnesium and potassium. The lethal event is "cardiac conduction abnormalities and arrhythmias... secondary to electrolyte disturbances"¹ — not the burn.
Hypocalcaemia and hyperkalaemia together is the dangerous combination, and it is worse than usual because the calcium that would stabilise the membrane is exactly what has been removed.
Subungual and fingertip exposures are disproportionately severe. The nail traps the liquid and is itself penetrated¹, and there is almost no tissue between the skin and the bone that fluoride decalcifies.¹
Calcium is used two different ways — locally, to give the fluoride something to precipitate with, and intravenously, to replace what has already been lost. Neither replaces the other.
Beware off-gassing. Dermal contact has produced concurrent inhalation with pulmonary oedema and tracheobronchitis¹ — a consideration for the patient and for the treating team in a small room.
Nebulised calcium gluconate has a human precedent: 13 workers exposed to mist at a "maximum concentration of" 125–170 mg/m³ for two minutes, treated immediately, had only minor upper respiratory irritation and none developed pulmonary oedema.¹ That is a 13-patient uncontrolled series, not a trial.
Eye exposure is an emergency in which the initial appearance again understates the outcome, because the acid's damage is what lets the ion reach the deeper layers.¹
Extracorporeal removal has never been assessed², and this is the one absence in this band that looks like a real gap rather than a meaningless question.

The antidote, from the poison's side

This is one of the few pages in the library where the antidote is chemically obvious and mechanistically exact: the poison removes a specific ion, and the antidote is that ion. What makes it interesting is that the same molecule is doing two different jobs at two different sites, and that giving it in one role does not accomplish the other.

Topical and infiltrated calcium: A scavenger, not a replacement. Supplying calcium in the tissue gives fluoride something to precipitate with other than the patient's own cellular and skeletal calcium. It is the only intervention that acts on the injury while it is still happening, which is why it is time-critical in a way that intravenous replacement is not. Inferred
Intravenous calcium: A replacement, not a scavenger. It corrects the hypocalcaemia that has already occurred¹ and stabilises the myocardium against the accompanying hyperkalaemia. It does nothing to stop further fluoride being absorbed from the wound, and a patient can require repeated and substantial replacement while the local injury continues. Established
Magnesium: The second cation the fluoride precipitates: hypomagnesaemia is named alongside hypocalcaemia in the systemic effects.¹ It is easy to correct the calcium and forget the magnesium, and an arrhythmia in this setting has two correctable electrolyte causes rather than one.
Nebulised calcium gluconate: For inhalational exposure. The human evidence is a 13-worker series exposed to mist at a "maximum concentration of" 125–170 mg/m³ for two minutes and treated immediately, who reported no dermal or ocular burns, only minor upper respiratory tract irritation, and none of whom developed pulmonary oedema.¹ An uncontrolled series with no comparison group — the mechanism is sound and the evidence is a precedent rather than a demonstration. Inferred
Copious irrigation: Necessary and insufficient. It removes what is still on the surface and cannot reach fluoride that has already penetrated "intact skin, nails and deep tissue layers".¹ The gap between what irrigation achieves for other acids and what it achieves here is the practical reason this poisoning is mismanaged.
Potassium-lowering measures: Aimed at the hyperkalaemia named among the systemic effects¹. Worth noting that the usual first move — calcium for membrane stabilisation — is here also treating the primary lesion, which is a rare alignment.
Extracorporeal removal: Never assessed.² Fluoride is small, water-soluble and poorly protein-bound, so the physical chemistry is favourable; no recommendation exists and this page makes none.

Critical appraisal

One evidence-tier downgrade appears on this page, and it was added at audit. The claim that the patient who dies of a hydrofluoric acid exposure dies of a rhythm disturbance rather than of the wound is true after dermal and systemic exposure and is contradicted, for the inhalational route, by the page's own source: "acute exposure to hydrogen fluoride can be fatal and is usually as a result of pulmonary oedema".¹ That is a citation for the doubt, in the page's only reference, and an earlier draft of this appraisal asserted that no such citation existed anywhere on the page. The claim is now route-qualified as well as badged.
No other downgrade appears, and that is deliberate. No source found contests the fluoride mechanism, the electrolyte disturbance or the use of calcium. Downgrading the calcium interventions on the grounds that no trial exists would be manufacturing a badge from an absence, which is the failure this library has recorded repeatedly and refuses.
The onset-by-concentration gradient is the page's most load-bearing claim and it comes from a single secondary source¹, which attributes it to three of its own references. It is quoted rather than paraphrased throughout, and the hedging word "may" is preserved in every instance — these are stated maxima, not guarantees, and a patient may declare sooner.
The rat inhalation finding is flagged as animal data on both the kinetics row and the organ card. Describing an animal finding in human terms is a failure shape recorded five times in Band C; this page has exactly one such finding and it is marked in both places it appears.
The nebulised calcium gluconate evidence is 13 workers with no control group¹, and is presented as a precedent rather than as efficacy. The badge on it is inferred for that reason.
The distinction between topical calcium as scavenger and intravenous calcium as replacement is this page's inference, badged as such. It follows necessarily from the chemistry and no cited source frames it that way.
The hyperkalaemia mechanism is not explained on this page, only stated, because the source states it without a mechanism.¹ A confident cellular account would be an invention, and the page declines to supply one.
No lethal dose, no fatal burn area and no minimum lethal concentration appears anywhere. The commonly repeated figure relating a fatal outcome to a small percentage of body surface area was deliberately not printed: it is exactly the shape of number that would be misused, and the clinical point — that a small burn can be a lethal exposure — is made mechanistically instead.
The 2012 South Korean incident is described qualitatively.¹ Five workers died; that number is reported because it is a matter of public record about an industrial accident, and no dose, concentration-at-distance or exposure-response inference is drawn from it.
EXTRIP's silence here is treated differently from elsewhere in this band, and that judgement is open to challenge. For cyanide and hydrogen sulphide the absence is uninformative because the timescale forbids the therapy. For fluoride the physical chemistry is favourable and the emergency lasts hours, so the page calls it a genuine gap² — while recommending nothing, because an unaddressed question is not a positive indication.

References

1
Hydrogen fluoride and hydrofluoric acid: toxicological overview. UK Health Security Agency, Compendium of Chemical Hazards. ("Fluoride ions are readily released from water soluble fluoride compounds including hydrogen fluoride and are almost completely absorbed." "A study in rats reported that the majority of inhaled hydrogen fluoride was absorbed by the lining of the upper respiratory tract." "Hydrogen fluoride readily penetrates intact skin, nails and deep tissue layers." "The main route of excretion of fluoride ions is via the urine." "Systemic effects caused by exposure to hydrogen fluoride include hypocalcaemia, hypomagnesaemia, metabolic acidosis and hyperkalaemia. Myoclonus, tetany, convulsions, CNS depression, cardiac conduction abnormalities and arrhythmias may occur secondary to electrolyte disturbances. Fluoride ions are responsible for the systemic effects of hydrogen fluoride." "Decalcification of underlying bone can occur." Eye: severity "is due to the pH and the toxicity of the F- ion"; "the initial damage caused by the acidity of the hydrogen fluoride enables the fluoride ion to penetrate into deeper layers of tissue where it causes severe eye lesions"; "conjunctivitis, conjunctival oedema, corneal epithelial coagulation and necrosis". Dermal: "severe and deep burns that are extremely painful and difficult to heal", "whitish discoloration, or a blue-grey discoloration to the skin followed by rapid tissue destruction and necrosis"; "hydrofluoric acid solutions as low as 2% may cause burns if they remain in contact with the skin for long enough"; "changes in electrocardiograms have been reported following dermal exposure, which were reversible within 3 days". Delayed onset: "Anhydrous or hydrogen fluoride or hydrofluoric acid solutions of greater than 50% may have immediate symptom onset. For solutions between 20 to 50% onset of symptoms may take up to 8 hours, while solutions less than 20% onset may take up to 24 hours." Off-gassing after dermal contact producing "pulmonary oedema, pulmonary haemorrhagic oedema and tracheobronchitis". Ingestion: "oesophageal or gastric perforation may occur which may develop over weeks or months". Reporting Lee, Wiley and Snyder 1993: 13 workers exposed to hydrofluoric acid mist at "a maximum concentration of 125 to 170mg/m3 for 2 minutes", treated immediately with 4 mL of 2.5% calcium gluconate by nebuliser, reported "no dermal or ocular burns, only minor upper respiratory tract irritation and none developed pulmonary oedema". 2012 South Korean release of 8–12 tons of 100% hydrogen fluoride; five workers died.) gov.uk
2
EXTRIP Workgroup — published recommendations index. Extracorporeal Treatments in Poisoning Workgroup. Cited for the absence of any recommendation covering hydrofluoric acid or fluoride. extrip-workgroup.org/recommendations

Hydrofluoric acid

At a glance