Why this poison is interesting

Arsine has a page of its own rather than a paragraph on the arsenic page for one reason: almost nothing on that page is true here. Inorganic arsenic poisons by binding protein thiols and by substituting for phosphate, produces a gastrointestinal illness followed weeks later by a neuropathy, and is treated with dithiol chelators. Arsine does none of that. It is a gas, its target is a cell rather than an enzyme, and the source states its action without ambiguity: "arsine primarily targets the erythrocyte (red blood cell) and rapidly induces intravascular haemolysis".¹ The element is the same and the poisoning is not.

The second reason is that arsine is one of the very few poisons in this library that is essentially always an industrial accident. It is "formed whenever nascent hydrogen is generated in the presence of arsenic or when water reacts with metallic arsenides", which means it appears unbidden in "smelting and refining of metals, plating, galvanising, and soldering".¹ The crucial sentence for anyone assessing a workplace is this one: "Very small amounts of an arsenic impurity can lead to the formation of highly toxic levels of arsine."¹ Nobody has to be working with arsenic for arsine to be produced, and it is also used deliberately as a doping agent in the semiconductor industry.¹

The third is that the poisoning kills through an organ that arsine never touches. The haemolysis is the lesion; the kidney is the casualty. "Renal failure secondary to haemolysis, if left untreated, is often the cause of death following arsine exposure."¹ That makes arsine one of the clearest examples in this library of a poisoning in which the treatment is directed at the consequence rather than at the poison — because there is no antidote for the poison, and there is well-established supportive treatment for the consequence.

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

The toxic principle

Arsine reaches the red cell almost immediately and by design of its physical chemistry. It "is readily absorbed by the lungs and mucous surface of the respiratory tract", and because it is "lipid soluble... it diffuses rapidly across the alveolar and capillary membranes of the lungs and the red blood cell membrane".¹ The distribution that follows is not the even spread of a systemic poison: "following exposure to arsine, the concentration in the blood increases rapidly, where it is preferentially bound to the red blood cell membrane. Distribution to the liver, kidneys, spleen, and other organs is much slower."¹ The target is reached first and everything else is reached late, which is a distribution pattern almost no other poison in this library has.

The mechanism is not known, and the source says so

The page's central event is stated plainly and then immediately qualified: "The exact mechanism by which arsenic causes erythrocytes to rupture is not known, but it is believed to be due to either oxidative damage or reaction with sulphydryl groups."¹ Inferred Two candidate mechanisms introduced by an explicit statement of ignorance is not a mechanism, and the account is badged inferred here rather than traditional. That distinction is deliberate and is argued in the appraisal: a traditional teaching badge in this library requires a citation contesting a taught claim, and what exists here is an honest absence of establishment rather than a contest. The same shape appears on arsenic and thallium and is badged differently on both, because on those pages a source positively contests an account that is widely taught.

The metabolic fate of arsine is worth stating precisely, because it is the source of the confusion this page exists to prevent. "Following absorption, arsine is oxidised to trivalent arsenic as well as pentavalent arsenic. Trivalent arsenic is subsequently methylated to monomethylarsonate and dimethylarsinate."¹ So arsine does become the poison described on the arsenic page — but it becomes it after the haemolysis, not before. The inorganic arsenic is a downstream product, and it accounts for the delayed features the two poisonings share, not for the acute illness that brings the patient in.

Stibine, and the honest limits of what can be said about it

Stibine — antimony hydride — is covered in the same UKHSA overview and behaves similarly, but the evidence behind it is much thinner and the page will not pretend otherwise. "Stibine is a powerful haemolytic agent. There is limited data available on the toxicity of stibine following acute exposure. The toxic effects of acute exposure to stibine are thought to resemble those associated with arsine exposure."¹ It is generated "during lead battery manufacture or... from overcharging of lead storage batteries" and in the semiconductor industry.¹ Human reports are of mixed exposures: headache, nausea, weakness, abdominal and lumbar pain, haematuria and haemolytic anaemia in workers exposed to "a mixture of stibine, arsine and hydrogen sulphide".¹ And the overview states flatly that "there is no data on the effects of chronic exposure to stibine in humans or animals".¹ Two further cautions about provenance. The stibine kinetics in the source are attributed to a proprietary commercial toxicology database that cannot be independently checked; most of what is actually quoted about stibine's acute toxicity traces instead to a 1969 monograph on industrial metals. And a mixed exposure cannot attribute an effect to one of its components.

Toxicokinetics

The kinetics of arsine are short, and the interesting feature is the order in which compartments are reached rather than any rate. The red cell is not one destination among many; it is the first.

Arsine — a distribution that reaches its target before it reaches anything else
Parameter	Therapeutic	In overdose	Why it changes
Absorption	—	"Readily absorbed by the lungs and mucous surface of the respiratory tract"¹	Lipid-soluble and small, so the alveolus is no barrier. Exposure is effectively absorption
Membrane transit	—	"Diffuses rapidly across the alveolar and capillary membranes of the lungs and the red blood cell membrane"¹	The same property that gets it into the blood gets it into the target cell — there is no step between the two
Distribution	—	"Preferentially bound to the red blood cell membrane"; distribution to "liver, kidneys, spleen, and other organs is much slower"¹	The reverse of the usual pattern. The lesion is established before the poison has meaningfully reached anywhere else
Biotransformation	—	Oxidised to trivalent and pentavalent arsenic; trivalent then methylated to monomethylarsonate and dimethylarsinate¹	It becomes the poison on the arsenic page — afterwards. This explains the shared late features and not the acute illness
Excretion	—	Metabolites predominantly urinary; "the highest urinary excretion occurred within the first 5 days following an acute occupational exposure"¹	Consistent with inorganic arsenic's own kinetics.² The window for confirming exposure biochemically is days, not weeks
Stibine	—	"Readily absorbed following inhalation"; detected in "blood, liver, lungs, kidneys, thyroid, adrenals, and pancreas"¹	Distribution described, kinetics not. There are no rates, no half-life and no chronic data at all¹
Dialysability	—	Not addressed by EXTRIP³	The absence is uninformative. Dialysis has a real role here, but for the renal failure and the free haemoglobin — not to remove arsine, which has already acted

Metabolism and the metabolites

Arsine's metabolism is the clearest illustration on this page of why it needed separating from arsenic. The metabolism converts a haemolytic poison into a thiol poison — but by the time the conversion has happened, the haemolytic damage is done and the resulting inorganic arsenic is present in quantities and over a timescale that belong to a different clinical problem. A clinician treating the acute illness is treating arsine's direct effect; a clinician seeing the same patient weeks later, with a neuropathy and white lines on the nails, is seeing arsenic.

Arsine — one poison that turns into another, in the wrong order to be useful

Arsine gas, inhaledLipid-soluble; "diffuses rapidly across the alveolar and capillary membranes"¹
Preferential binding to the red blood cell membrane — reached before liver, kidney or spleen¹
Intravascular haemolysisThe lesion. Mechanism "not known"; either oxidative damage or reaction with sulphydryl groups¹ Inferred
Free haemoglobin, and a falling red cell mass"Haemolytic anaemia, hepatic and renal damage" as secondary effects¹
Oxidation to trivalent and pentavalent arsenic¹The arsenic page begins here — and it begins after the emergency
Renal handling of free haemoglobin — the step that kills
Acute renal failure"Renal failure secondary to haemolysis, if left untreated, is often the cause of death"¹
Methylation of trivalent arsenic to monomethylarsonate and dimethylarsinate¹
Urinary excretion, highest in the first 5 days¹The confirmatory test, and the origin of the delayed neuropathy and Mee's lines¹

Elimination and accumulation

Arsine itself is not accumulated in any meaningful sense — it acts and is converted. What is excreted is inorganic and methylated arsenic, "predominantly... in the urine", with "the highest urinary excretion" occurring "within the first 5 days following an acute occupational exposure".¹ That figure has a practical consequence: the biochemical confirmation of an arsine exposure has a short window, and a urinary arsenic sent a fortnight later may be unremarkable in a patient who was badly poisoned.

Chronic exposure is described as producing essentially the same picture more slowly. "The effects of chronic exposure to arsine are similar to those observed following acute exposure. The main difference from acute exposure is the longer period of latency."¹ The reported features are "shortness of breath on exertion, malaise, headache, nausea, anorexia, paraesthesia and muscle pain", with "peripheral neuropathy, liver and kidney impairment, anaemia and basophilic stippling" in occupationally exposed individuals — and, in one occupational study, "the degree of anaemia in workers chronically exposed to arsine was proportional to the duration of exposure".¹

Where this latent phase sits among the others

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

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
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
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
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

Arsine's gap is paraquat's cause — the body responding to an injury already complete — with the injury being a destroyed red cell mass rather than an injured epithelium. The exposure ends, the haemolysis is silent, and the first visible sign is the urine changing colour at four to six hours.¹ What makes it distinctive in this set is that the gap is filled by a completely normal physiological process: a kidney doing exactly what a kidney does with free haemoglobin, at a volume it was never designed for.

Target organs — and why those

There is one target and two casualties. Arsine acts on the erythrocyte; the kidney and the liver suffer the consequences of what it does there.

Erythrocyte

TargetThe red cell membrane

Why hereThe only true target organ on this page, and it is a cell rather than a tissue. Arsine is lipid-soluble and "diffuses rapidly across... the red blood cell membrane", where it is "preferentially bound" — reaching it before the liver, kidneys or spleen.¹ Why the erythrocyte in particular is not explained by the source, and this page does not invent a reason: the mechanism of rupture itself is "not known".¹ Inferred

At the bedside"Rapidly induces intravascular haemolysis", with "anaemia, leukocytosis, and increased plasma-free haemoglobin, iron, and potassium concentrations".¹ The film shows "basophilic stippling, Heinz bodies, anisocytosis, poikilocytosis, red blood cell fragments and ghost cells".¹ The rising potassium is worth noting separately — it is released from the cells being destroyed, and it is a cardiac problem before it is a laboratory one.

Kidney

TargetThe nephron, handling free haemoglobin

Why hereThe organ that kills, and it is injured by the lesion rather than by the poison. Arsine reaches the kidney only slowly,¹ by which time the haemolysis is established. The renal failure is the consequence of filtering the contents of a destroyed red cell mass — which is why the source calls it "renal failure secondary to haemolysis" rather than arsine nephrotoxicity. Established

At the bedside"Renal failure secondary to haemolysis, if left untreated, is often the cause of death following arsine exposure. In severe cases oliguria or anuria may develop within 2 days after exposure."¹ "Free haemoglobin, erythrocytes, proteins, casts, and methaemoglobin have been found in the urine."¹ Dark red urine at four to six hours is the sign that the kidney is already being loaded,¹ and it precedes the failure rather than announcing it.

Liver

TargetHepatocytes, secondarily

Why hereIncluded because jaundice is a prominent and confusing part of the picture — but the source is careful, and so is this card. Most of the jaundice is haemolytic rather than hepatic. Inferred

At the bedside"Jaundice of the skin and mucous membranes is observed at 24 to 48 hours following exposure. Serum bilirubin and lactate dehydrogenase levels are usually elevated, and the liver is often enlarged and tender. However, severe liver damage has rarely been reported following arsine exposure."¹ The combination of a tender liver, a high bilirubin and a high lactate dehydrogenase in a patient who is not in liver failure is the expected picture, and reading it as hepatic injury overstates it.

Heart

TargetMyocardium and conduction, indirectly

Why hereA consequence of the haemolysis rather than a direct action, and mechanistically under-specified by the source. It earns a card because the abnormalities are common and because one of the mechanisms is treatable. Inferred

At the bedside"Tachycardia and electrocardiogram (ECG) abnormalities, including alterations in the S-T segment and elevation of the T-wave, have been reported", and "in some cases, ECG abnormalities have lasted for several months after exposure".¹ A peaked T wave in a patient with brisk intravascular haemolysis is hyperkalaemia until proved otherwise — the source records raised plasma potassium among the haematological changes.¹ "Toxic pulmonary oedema or acute circulatory failure has been reported as the cause of death in some cases."¹

Peripheral nerve and nail

TargetLong axons, and the nail matrix — weeks to months later

Why hereThese belong to arsine's metabolite rather than to arsine. They are the same findings, from the same chemistry, as on the arsenic page, appearing because "arsine is oxidised to trivalent arsenic as well as pentavalent arsenic".¹ Inferred

At the bedside"Peripheral neuropathy may develop over the first few months following exposure to arsine."¹ "Vertical white lines on the nails (Mee's lines) may appear 2 to 3 weeks after exposure."¹ Neuropsychological symptoms including "confusion, memory loss, agitation and disorientation" have been reported after acute exposure.¹ A survivor of an arsine exposure should be warned about a neuropathy that has not started yet.

Timeline of effects

Arsine — a haemolysis you cannot see, followed by a kidney you cannot save late

Time

What you seeWhat is happening

1–24 h (usually a few hours)Non-specific onset
What you see"Headache, malaise, weakness, dizziness, dyspnoea, red staining of the conjunctiva, abdominal pain, nausea" and vomiting.¹ Only one of those is at all suggestive, and conjunctival staining is easily missed.
What is happening"Symptoms of arsine poisoning develop within 1 to 24 hours (usually within a few hours) after exposure, depending upon the concentration and duration of exposure."¹ Haemolysis is already under way. The clinical picture at this stage is that of an unwell worker, not of a poisoning.
4–6 hThe urine changes colour
What you see"Dark red urine due to the presence of haemoglobin generally develops within 4 to 6 hours post-exposure."¹
What is happeningThe first objective sign, and the one that makes the diagnosis. The gap before it is not a gap in the injury — the red cells have been breaking down since exposure — it is the time taken for enough free haemoglobin to reach the urine to be visible. This is the point at which an industrial illness becomes a recognisable poisoning.
24–48 hJaundice and the failing kidney
What you see"Jaundice of the skin and mucous membranes is observed at 24 to 48 hours", with raised bilirubin and lactate dehydrogenase and a "often enlarged and tender" liver.¹ "In severe cases oliguria or anuria may develop within 2 days after exposure."¹
What is happeningHaemolytic jaundice, and a nephron loaded beyond its capacity. This is the phase that determines survival, and the source is explicit that untreated renal failure is "often the cause of death".¹
2–3 weeksMee's lines
What you see"Vertical white lines on the nails (Mee's lines) may appear 2 to 3 weeks after exposure."¹
What is happeningThe arsenic, not the arsine. The nail matrix was injured while inorganic arsenic — arsine's metabolite¹ — was circulating, and the mark becomes visible as the nail grows. Identical in cause to the finding on the arsenic page.
MonthsThe neuropathy
What you see"Peripheral neuropathy may develop over the first few months following exposure."¹ Some ECG abnormalities "have lasted for several months after exposure".¹
What is happeningAgain the metabolite rather than the parent gas. One exposure has by this point produced two different poisonings in sequence, and the second is indistinguishable from ordinary arsenic poisoning.

What the mechanism predicts at the bedside

Ask about the process, not about arsenic. "Very small amounts of an arsenic impurity can lead to the formation of highly toxic levels of arsine",¹ and it forms "whenever nascent hydrogen is generated in the presence of arsenic or when water reacts with metallic arsenides" — in "smelting and refining of metals, plating, galvanising, and soldering".¹ Nobody in the workplace need have been handling arsenic.
Look at the urine early. Dark red urine "generally develops within 4 to 6 hours post-exposure"¹ and is the first objective sign in an otherwise non-specific illness.
Check the potassium as urgently as the haemoglobin. The source lists "increased plasma-free haemoglobin, iron, and potassium concentrations" among the haematological changes,¹ and separately reports T-wave elevation and ST changes.¹ Haemolysis on this scale is a hyperkalaemia risk with an ECG to match.
Do not interpret the jaundice as liver failure. Bilirubin and lactate dehydrogenase are usually raised and the liver is often tender, but "severe liver damage has rarely been reported".¹
Do not reach for the chelators. They are the treatment for the poison on the arsenic page, and this is a haemolytic lesion in which the arsenic appears downstream of the damage.¹ The element being the same is not a reason.
Send urinary arsenic early. "The highest urinary excretion occurred within the first 5 days following an acute occupational exposure",¹ so a delayed sample can under-represent a serious exposure.
Treat one exposure as two illnesses when counselling the patient. A survivor should be told to expect the possibility of a peripheral neuropathy "over the first few months" and nail changes at "2 to 3 weeks",¹ neither of which they will otherwise connect to the day they were gassed.
Treat stibine as arsine and say that you are doing so. Its effects "are thought to resemble those associated with arsine exposure",¹ which is an inference in the source rather than a finding, and there is no chronic data on it in humans or animals at all.¹
Consider everyone who was in the area. Arsine is a gas, it is not an agent anybody chooses, and an exposure is an incident rather than a case.

The antidote, from the poison's side

There is no antidote to arsine, and this is one of the few pages in the library where that statement is the whole of the section's argument rather than a preface to a workaround. No agent binds arsine before it reaches the red cell membrane, and by the time a patient presents, the binding has already happened. What remains is the management of a haemolysis and of the renal failure that follows it, which is supportive care of a kind that does not belong on this site and belongs firmly with TOXBASE and NPIS.

Why the chelators do not transfer from the arsenic page: Dimercaprol, DMPS and succimer work by offering thiol groups to arsenite, competing for the protein thiols it would otherwise bind.² That is a coherent strategy against a poison that binds thiols. Arsine's lesion is not a thiol lesion — or at least, not demonstrably one: the source offers "either oxidative damage or reaction with sulphydryl groups" and declines to choose.¹ More decisively, the lesion is a destroyed cell, and a chelator cannot un-haemolyse a red cell that has already ruptured. The inorganic arsenic that chelation could address appears downstream, after the emergency.
Why the treatable problem is renal rather than toxicological: The source identifies the mechanism of death directly: "renal failure secondary to haemolysis, if left untreated, is often the cause of death".¹ The phrase "if left untreated" is the important part — it identifies a modifiable cause of death in a poisoning with no antidote, and it points at supportive and renal-replacement therapy rather than at anything toxicological.
Why extracorporeal treatment has a role that is not detoxification: EXTRIP has not addressed arsine,³ and the absence is uninformative here for an unusual reason: the question a dialyser answers on this page is not whether it can remove the poison. Arsine has already acted, and removing it would not restore a lysed erythrocyte. Renal replacement is used for the renal failure and for clearing the products of haemolysis. This is the same distinction as on the iron page, where dialysis is used for the kidney and for the chelated complex rather than for the poison.

Critical appraisal

Where the evidence on this page stops

This page rests almost entirely on one government toxicological overview,¹ and it is a shorter and thinner document than the arsenic, lead and mercury overviews used elsewhere in this band. It is a secondary source citing its own primary literature, and much of that literature is old — its arsine references include a 1969 monograph on industrial metals and a 1974 clinical paper. There is no modern cohort, no trial and no systematic review behind any statement on this page. The stibine material is thinner still: its kinetics are attributed in the source to a proprietary commercial toxicology database that cannot be independently verified, and most of its quoted acute toxicity traces to a 1969 monograph. The page says so where stibine is discussed. It does draw on the proprietary-sourced distribution list in the kinetics table, which is flagged there rather than left implicit.

This page carries no traditional teaching badge, and the decision is deliberate. The obvious candidate is the mechanism of haemolysis, where the source states that the "exact mechanism... is not known" and offers two hypotheses.¹ The mechanism is badged Inferred instead. Arsenic and thallium carry the lower badge on near-identical statements of ignorance, so the distinction has to be stated precisely. It is not about what the world teaches — that would be a claim about the teaching literature, cited to nothing, and unauditable. It is about what the page asserts. Arsenic and thallium each print a detailed, load-bearing mechanistic narrative as their central explanatory frame while their own anchor declines to establish it; the badge marks the gap between what the page teaches and what the source will support. This page prints the ignorance itself and reasons downstream of it, so there is no asserted account for a badge to downgrade. That test is checkable from the documents alone. (Two reviewers at the Band E audit reached opposite conclusions here — one would have kept both badges and rewritten both justifications, which is what was done; one would have downgraded arsenic's to inferred to match this page. The disagreement is recorded rather than resolved silently, because a badge whose reasoning cannot be reconstructed is indistinguishable from a manufactured one.)
The scope decision to give arsine its own page rather than a section on arsenic is recorded here so an auditor finds it deliberately. PLAN.md §6 lists five pages for this band and this is a sixth, exactly as tramadol was a ninth page in Band C. The argument for it is that the mechanism, the target organ, the timeline, the cause of death and the treatment all differ from inorganic arsenic, and folding it into that page would have produced the drug-class-versus-toxidrome overlap this library has avoided elsewhere. The two pages cross-reference each other explicitly in both directions.
Stibine is covered within this page rather than given its own, and the reason is that there is not enough evidence to fill one. The overview states there is "no data on the effects of chronic exposure to stibine in humans or animals",¹ and its acute human evidence is from mixed exposures that included arsine and hydrogen sulphide.¹ A page built on that would have been mostly hedging.
Every exposure concentration in the source is deliberately omitted from this page. The arsine overview carries lethal concentrations for humans and median-lethal-concentration values for three species; lethal-dose and lethal-concentration framing is permanently out of scope for this library. This is the most concentrated set of such figures encountered in any source used so far, and their absence here is a policy decision rather than an oversight.
One group of animal findings is described and flagged rather than translated into human terms: the repeated-exposure studies in rat, mouse and hamster, whose most sensitive endpoint was haemolysis with abnormal red cell morphology and increased spleen weight.¹ They corroborate the direction of the human picture and are not used to support any figure or threshold on this page.
The claim that the delayed neuropathy and Mee's lines are attributable to arsine's arsenic metabolites is an inference, and is badged as one. The source states the metabolism¹ and separately states the delayed findings;¹ it does not explicitly join them. The join is this page's, and it is flagged rather than presented as sourced.
The reproductive data are deliberately not used to support a claim. The overview reports an increased miscarriage rate among women in the semiconductor industry but records that the studies had "several limitations, including small sample size and exposure to multiple chemicals" and that "it was not possible to determine the role of arsine".¹ The source declines to draw the conclusion and so does this page.
EXTRIP has not addressed arsine.³ The absence is uninformative, and unusually so: the question is not whether the poison can be removed but whether removing it would help, and by the time of presentation it would not. This is a different category of absence from the four other Band E pages and is argued rather than asserted.

How this page connects to the rest of the library

Arsine's most important relationship is adversarial: it exists to be contrasted with arsenic, and the two pages are the library's only pair sharing an element while sharing almost nothing else. Structurally it belongs with hydrofluoric acid — a poison producing one lesion while the patient dies of another organ's response — and with paraquat, whose latent phase has the same cause. Its haemolysis makes it a distant relative of the methaemoglobin inducers, the library's other page in which the red cell is the target rather than a bystander, though the lesions are different: one destroys the cell and the other disables its cargo. And it is the only page in this band with no antidote at all, which is worth stating in a band otherwise defined by chelation.

Evidence tier of the mechanisms on this pageEstablishedDemonstrated in humans, or in a model that reproduces the human syndromeInferredConsistent with the biochemistry and widely accepted, but the causal step has not been shown in humansTraditional teachingTaught and repeated but not demonstrated — the source questioning it is cited

References

1
UK Health Security Agency. Arsine and stibine: toxicological overview. Compendium of Chemical Hazards. gov.uk. Supplies essentially the whole of this page: the erythrocyte target and intravascular haemolysis, the explicit statement that the mechanism of rupture is not known, the kinetics and preferential red-cell binding, the metabolism to inorganic arsenic, the timings of haemoglobinuria, jaundice and anuria, the ECG and haematological findings, the delayed neuropathy and Mee's lines, the sources of industrial exposure, and the stibine material. Its lethal-concentration figures are deliberately not reproduced.
2
UK Health Security Agency. Arsenic: toxicological overview. Compendium of Chemical Hazards. gov.uk. Cited here only for the kinetics of inorganic arsenic, arsine's metabolite, and for the contrast the arsenic page draws out in full.
3
EXTRIP Workgroup. Recommendations index. extrip-workgroup.org. Cited for an absence: the published set covers 22 substances and arsine is not among them. Verified against the site's own menu, 7 September 2026.
4
National Poisons Information Service. TOXBASE — NPIS 0344 892 0111. The authoritative UK source for the management of arsine exposure, including transfusion and renal replacement. Login-gated, and deliberately not quoted anywhere on this page.

Last reviewed 2026-09-08 · Author: Dr Nirmalya Hore

Arsine and stibine

At a glance