Why this poison is interesting

Iron is the only entry in this library that the body has no way of excreting. Human iron balance is regulated at the point of absorption — the gut decides how much to let in, and once it is in there is no physiological route out except bleeding and the shedding of cells. That single fact generates almost everything else on this page: why an overdose is not self-limiting, why the treatment is a molecule that carries iron out through the kidney, and why iron is one of very few poisonings in which the antidote creates an excretory pathway that did not previously exist.

The second reason is a clinical one, and it is the reason iron has killed children in the era of good supportive care. The poisoning has a phase in which the patient genuinely improves. The ferrous sulfate label describes it plainly: a second phase at 6 to 24 hours "characterised by a temporary remission or clinical stabilisation".² This is not a plateau or an absence of progress. The vomiting stops, the child settles, and the observations normalise — while absorbed iron is distributing into the cells it is about to poison. A clinician who takes improvement as evidence of a trivial ingestion is reading the timeline correctly and drawing the wrong conclusion from it.

The third is that iron demonstrates, more cleanly than any other page here, what happens when a carrier protein runs out. Iron in plasma is not free; it travels bound to transferrin. In overdose transferrin saturates, and the iron that appears beyond that point is a different chemical entity with different behaviour. The remarkable thing is that the UK label frames its own treatment endpoint in exactly those terms — chelate "until the serum iron is within the plasma binding capacity"² — so the toxic species on this page is defined by the therapeutic target rather than argued into existence.

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

The toxic principle

Iron circulates bound to transferrin, and is stored as ferritin and haemosiderin in the reticuloendothelial system, with the great majority of the body's iron in haemoglobin and smaller amounts in myoglobin and the haem enzymes.² Every one of those is a container. There is no plasma pool of unbound iron in health, because unbound iron is chemically reactive in a way that bound iron is not — the entire architecture of iron handling is a set of arrangements for never letting the ion loose.

Why saturation, rather than dose, is the event that matters

A therapeutic dose of a ferrous salt is absorbed, bound to transferrin as it crosses the mucosa² and delivered to the marrow. Nothing about that process is toxic. What changes in overdose is not the identity of the substance but the availability of the carrier. Once the quantity absorbed exceeds what transferrin can hold, the surplus circulates unbound — and the label's chelation endpoint, "until the serum iron is within the plasma binding capacity",² is a direct statement that the free fraction is the thing being treated. This is why serum iron rather than ingested dose is "the best laboratory measure of severity"¹ and why the number is taken at about four hours, when absorption is complete but distribution has not yet emptied the plasma.

There are two distinct injuries, and confusing them is the commonest source of muddle about iron. The first is local and corrosive: concentrated iron salt in contact with gastrointestinal mucosa produces the early vomiting, the diarrhoea, and the "grey or black" vomit and stools the label describes,¹ together with the bleeding that can be severe enough to cause hypovolaemic shock on its own. The second is systemic and cellular, and it happens in the tissues the absorbed iron reaches. The first injury needs no absorption at all; the second is the one chelation addresses.

The cellular mechanism is the least well evidenced claim on this page, and it is fair to say so. Neither UK label offers one: both describe the syndrome in careful clinical detail and are silent on how free iron injures a cell.^1,2 The conventional account — that catalytically active iron drives free-radical chemistry and impairs oxidative phosphorylation, producing the anion-gap acidosis the labels do describe — is consistent with the biochemistry and with the observed pattern of organ injury, but it is inference from the syndrome rather than a demonstration in humans, and it is badged accordingly throughout this page. Inferred

Toxicokinetics

The kinetic story is short because most of the usual parameters are unavailable: neither UK label gives a volume of distribution, a clearance or a half-life for iron in overdose, and there is no meaningful elimination constant to give. What the table below records instead is the set of places where normal iron handling stops being a regulator and starts being a liability.

Iron — a kinetic table in which the important entries are the ones that do not exist
Parameter	Therapeutic	In overdose	Why it changes
Absorption	Regulated at the mucosa; "absorbed most easily in the ferrous state", then bound to transferrin as it enters the blood²	Regulation is overwhelmed; a corrosive dose also injures the mucosa that is meant to be doing the regulating	The control point and the injured tissue are the same tissue. Damaging the gut removes the very mechanism that limits how much gets in
Site of absorption	"Iron is absorbed mainly in the small intestine, but can be absorbed along the entire length of the alimentary canal"²	The whole length of gut is available, and undissolved tablets keep delivering	Why whole bowel irrigation is considered at all¹ — the reservoir is the lumen, not the stomach, and it moves
Plasma binding	Bound to transferrin; effectively no free iron²	Transferrin saturates. The excess circulates unbound	The single event that separates a therapeutic dose from a poisoning, and the endpoint chelation is titrated to²
Peak plasma concentration	Not clinically relevant	Serum iron at about 4 hours is "the best laboratory measure of severity"¹	Earlier is falsely reassuring (absorption incomplete) and later is falsely reassuring (distribution into tissue). The window is the point
Distribution	Directed to marrow, liver and stores	Free iron enters cells that have no mechanism for refusing it	The plasma concentration falls as the patient deteriorates, because leaving the blood is not the same as leaving the patient — the digoxin problem in a different currency
Elimination	None. No physiological excretory route for a surplus	Still none	The defining kinetic fact of this page. Loss occurs only through blood loss and shed cells, which is why chelation is not an adjunct here but the only route out
Dialysability	Not applicable	"Haemodialysis does not remove iron effectively"¹	Iron is not free enough, for long enough, in a compartment a dialyser can reach. Dialysis is used for the kidney, and to clear ferrioxamine¹

Metabolism and the metabolites

There is no metabolism. Iron is an element; it is not transformed into anything, and there is no toxic metabolite to manufacture. What it does instead is change oxidation state and change binding partner, and both of those are reversible physical events rather than biotransformations. This puts iron in a small group in this library — with lithium, hydrofluoric acid and the other metals in this band — where the poison that arrives is the poison that acts.

Iron — a pathway made of containers, and what happens when they are full

Ferrous salt in the gut lumenCorrosive in its own right. The mucosal injury needs no absorption and accounts for the first phase entirely
Absorption, "most easily in the ferrous state"² — normally rate-limited by the mucosa, here overwhelmed
Iron entering the portal blood"Immediately attached to transferrin"² — for as long as there is transferrin left
Bound to transferrinSafe. Delivered to marrow and stores; this is nutrition, not poisoning
In excess of the binding capacityFree iron. The species chelation is titrated against² and the one that reaches the hepatocyte first
Portal delivery — the liver sees the highest concentration before anything else does
Cellular injury and anion-gap metabolic acidosis¹The mechanism is Inferred rather than stated by either label: redox-active iron impairing oxidative phosphorylation, consistent with the acidosis and the pattern of organ injury

A word about the two labels, because they do not read like contemporaries

The two ferrous sulfate SmPCs² and the ferrous fumarate SmPC¹ describe the same poisoning and were both current when this page was written, but they are documents of different vintages. The fumarate label gives a toxic threshold, a sampling time, a chelation trigger with units, a whole-bowel-irrigation option and a statement about dialysis.¹ The sulfate labels give the four-phase description — which is the better clinical picture — and then recommend gastric lavage, desferrioxamine instilled into the stomach, saline cathartics, and "milk and eggs with 5g bismuth carbonate every hour as demulcents".² They are not in conflict; one carries management advice of an older vintage. (Revision dates do not track that difference — the sulfate label has been revised more recently than the fumarate one; it is the content that is dated, not the document.) Both are cited here for what each does well, and this is noted rather than smoothed over because a reader who fetches the sulfate label expecting current management will be misled.

Elimination and accumulation

The heading is close to a joke on this page. Iron does not have an elimination pathway. Losses in health are incidental — desquamated cells, menstrual and other blood loss — and none of them scales up in response to a surplus. There is no renal excretory route — the label's own list of losses, "urine, faeces, hair, skin, sputum, nails, sloughing of mucosal cells, and through blood loss",¹ is a list of shed cells, not of iron being excreted — no biliary route that returns a meaningful quantity to the outside world, and no enzyme that degrades an element. Accumulation is therefore the default state of an iron overdose, and the only questions are where it accumulates and whether anything can be made to carry it out.

There is a second reservoir, and it is mechanical rather than chemical. Iron tablets are radiodense, aggregate, and can persist in the gut for many hours; the fumarate label's suggestion to "consider whole bowel irrigation"¹ exists because the lumen keeps supplying the circulation long after a single-dose decontamination window has closed. This is the same structural problem as the modified-release tablet on the calcium-channel blocker page and the swallowed package on the cocaine page: the reservoir is outside the body, and it moves.

Where this latent phase sits among the others

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

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
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
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

Iron's entry is unusual in one respect worth naming. Most gaps in this set are periods in which nothing observable happens. Iron's is a period in which something observable happens and it is good — the label calls it a "temporary remission or clinical stabilisation".² A latent phase that presents as improvement is more dangerous than one that presents as nothing, because it supplies a positive reason to stop worrying.

Target organs — and why those

The organ list divides on a single question: did the iron have to be absorbed to get there? The gut is injured by contact. Everything else is injured by delivery, and the order in which the organs appear follows the anatomy of that delivery.

Gastrointestinal mucosa

TargetEpithelium in direct contact with dissolving iron salt

Why hereThe only organ injured without absorption, and therefore the only one that can be damaged by a dose too small to poison anything else. Concentrated ferrous salt is corrosive on contact. This is also why the mucosa's role as the regulator of iron entry fails precisely when it is most needed — the control point is made of the tissue being destroyed. Established

At the bedsideNausea, vomiting, abdominal pain and diarrhoea within hours, with vomit and stools that "may be grey or black".¹ In more serious cases "recurrence of vomiting and gastrointestinal bleeding, 12 hours after ingestion",¹ and haemorrhage sufficient to contribute to shock.

Liver

TargetHepatocytes, reached first and at the highest concentration

Why hereThe organ downstream of the portal vein, which is an anatomical accident rather than a chemical preference. Absorbed iron arrives at the liver before it reaches the systemic circulation, so hepatocytes see a concentration nothing else in the body experiences — an inference from anatomy rather than a claim either label makes, since neither describes portal-first delivery. Inferred What is measured is the dose–response: in 73 patients, clinically important hepatotoxicity was "unlikely with a serum iron concentration of < 700 microg/dL (128 micromol/L) within the first 12 hours", while clinically important injury occurred "with values in excess of 1000 microg/dL (182 micromol/L)".³ Established

At the bedsideJaundice, coagulopathy, hypoglycaemia and encephalopathy in the third phase.^1,2 In the cohort above, 13 of 73 patients had transaminases above 150 U/L and nine had values above 1000 U/L.³ Hepatic failure is the usual mode of late death and it is the organ that most justifies chelating a patient who currently looks well.

Circulation

TargetIntravascular volume, and the myocardium directly

Why hereTwo separate causes of shock, and they need different treatment. The label attributes shock to "hypovolaemia or direct cardiotoxicity"¹ — the first from gastrointestinal fluid and blood loss, the second from iron acting on the myocardium itself. A patient who remains hypotensive after adequate volume replacement has the second, and volume alone will not fix it. Inferred

At the bedside"Evidence of hypoperfusion (cool peripheries and hypotension), metabolic acidosis and systemic toxicity".¹ The acidosis is a positive anion gap acidosis,¹ which distinguishes it from the hyperchloraemic picture of pure fluid loss.

Kidney

TargetTubule, through perfusion rather than through iron

Why hereA secondary organ, and the page is careful about that. The label attributes renal failure to "poor tissue perfusion"¹ rather than to a direct nephrotoxic action of iron. It matters because it changes what the treatment is: this is an organ saved by restoring circulation, not by chelation — and yet renal function determines whether the antidote works at all, because ferrioxamine is cleared by the kidney. Inferred

At the bedsideOliguria and acute kidney injury in the third phase.² Dialysis "should be considered on a supportive basis for acute renal failure as this will facilitate removal of the iron-desferrioxamine complex"¹ — the one circumstance in which a dialyser is useful in iron poisoning.

Gastric outlet and pylorus

TargetHealing corrosive injury, weeks later

Why hereThe library's longest structural sequel, and it is scar tissue rather than poison. The iron is long gone. What remains is a mucosal burn healing by fibrosis in a tube whose narrowest point is the pylorus, so the scar presents as obstruction. This is the same class of injury as a caustic stricture — the mechanism is the healing, not the agent. Established

At the bedside"Rarely, gastric scarring causing stricture or pyloric stenosis (alone or in combination) may lead to partial or complete bowel obstruction 2-5 weeks after ingestion."¹ The sulfate label places the same phenomenon "several weeks after ingestion".² A patient vomiting a month after an iron overdose is not relapsing; they are obstructing.

Timeline of effects

Iron — four phases, one of which looks like recovery

Time

What you seeWhat is happening

0–6 hThe corrosive phase
What you seeVomiting, diarrhoea, abdominal pain; vomit and stools "may be grey or black".¹ Hypotension, tachycardia, hyperglycaemia and lethargy in larger ingestions.² "Patients with only mild to moderate poisoning do not generally pass this first phase."²
What is happeningDirect mucosal injury from iron salt in contact with epithelium, plus the beginning of absorption. Severity here reflects local concentration, not systemic dose — which is why a well-looking patient may still have absorbed a great deal.
6–24 hRemission
What you see"A temporary remission or clinical stabilisation."² Vomiting settles, the patient looks and feels better, and observations may normalise.
What is happeningThe corrosive insult has finished and the cellular one has not yet declared. Absorbed iron is leaving the plasma for the tissues, which is why a serum concentration taken now is falling while the patient's total burden is unchanged. Nothing has been eliminated.
From about 12 hThe systemic phase
What you see"Recurrence of vomiting and gastrointestinal bleeding",¹ shock, positive anion-gap metabolic acidosis, hepatocellular necrosis with jaundice, hypoglycaemia, coagulopathy, encephalopathy, oliguria, convulsions and coma.^1,2
What is happeningFree iron in the tissues, and the liver worst affected because it is first in line. Shock from "hypovolaemia or direct cardiotoxicity".¹ This is the phase the second phase concealed.
2–5 weeksThe stricture
What you see"Gastric scarring causing stricture or pyloric stenosis... partial or complete bowel obstruction 2-5 weeks after ingestion",¹ and "possibly late hepatic damage".²
What is happeningFibrosis of a healing corrosive burn. No iron is involved by this stage; the injury is the repair. This is the longest interval between exposure and presentation anywhere in this library, and it presents to a different specialty than the poisoning did.

What the mechanism predicts at the bedside

Ask for elemental iron, not tablet weight. "Ingestion of 20 mg/kg elemental iron is potentially toxic."¹ The elemental fraction differs between salts — a 322 mg ferrous fumarate tablet, a 200 mg ferrous sulfate tablet and a gluconate preparation are not interchangeable arithmetic — so the number on the packet is not the number in the risk assessment.
Time the serum iron rather than simply requesting it. "The serum iron taken at about 4 hours after ingestion is the best laboratory measure of severity."¹ A level before absorption is complete and a level after distribution has begun are both falsely low, and they are falsely low for opposite reasons.
Treat improvement at six to twelve hours as uninformative. The remission is a described feature of the poisoning,² not evidence against it. The question at that point is what the four-hour concentration was, not how the patient looks.
A persistently raised anion gap after fluid resuscitation is a systemic-toxicity finding. The label pairs "metabolic acidosis" with "systemic toxicity" and describes a "positive anion gap" acidosis in the severe phase.¹
Hypotension that does not correct with volume suggests the second mechanism. Shock is attributed to "hypovolaemia or direct cardiotoxicity",¹ and only the first is a filling problem.
Check the glucose. Hyperglycaemia appears in the first phase and hypoglycaemia in the third,^1,2 so the direction of the abnormality carries timing information.
A plain abdominal radiograph can show tablets, but not seeing them proves nothing — dissolved and liquid preparations are not radiodense, and the fumarate label's whole-bowel-irrigation option¹ is aimed at a lumen that may already have moved on.
Do not use dimercaprol. The ferrous sulfate label states it directly: "Dimercaprol should not be used since it forms a toxic complex with iron."² This is the one page in this band where the chelator used on every other metal is explicitly contraindicated, and it is worth knowing before a metal-poisoning reflex supplies it.
Warn the patient or the parents about week four. Obstruction two to five weeks later¹ will not be connected to the overdose by anybody who has not been told to expect it.

The antidote, from the poison's side

Desferrioxamine is the clearest example in this library of an antidote that manufactures an elimination pathway. The poison has none; the chelator binds free iron to form ferrioxamine, and ferrioxamine is cleared by the kidney. The patient acquires, for as long as the infusion runs, a renal route for excreting iron that human physiology does not otherwise provide. Full dosing, dilution, infusion-rate and adverse-effect detail is on the desferrioxamine monograph; what follows is only what the poison's behaviour explains.

Why the trigger is a concentration and a symptom together: The label's criterion is compound: "if the patient is symptomatic (other than nausea), serum iron concentration is between 3-5 mg/L (55-90 micromol/L) and still rising".¹ All three clauses are doing work. Nausea alone is excluded because the corrosive phase produces it at doses that never threaten the liver. "Still rising" matters because a falling concentration means distribution, not clearance. And the concentration is required because symptoms alone cannot distinguish a gastric burn from a systemic load.
Why the endpoint is transferrin rather than a number: The sulfate label titrates chelation "until the serum iron is within the plasma binding capacity".² That is a statement about the toxic species rather than about a target range — treatment stops when free iron ceases to exist, which is the same moment the poisoning stops being a poisoning.
Why the kidney decides whether the antidote works: Ferrioxamine leaves by the renal route. In the patient whose kidneys have failed, the chelator can bind iron and then have nowhere to take it — which is precisely the circumstance in which dialysis becomes useful, not to remove iron ("haemodialysis does not remove iron effectively") but because dialysis "will facilitate removal of the iron-desferrioxamine complex".¹ It is a rare instance in this library of dialysis being used to clear an antidote rather than a poison.
Why dimercaprol is contraindicated here and standard elsewhere: "Dimercaprol should not be used since it forms a toxic complex with iron."² Every other page in this band reaches for a dithiol chelator; iron is the exception, and the label states the reason rather than leaving it to be inferred.

Critical appraisal

No evidence-tier downgrade is applied on this page, and that is a deliberate decision rather than an oversight. The obvious candidate is the four-phase description itself, which is universally taught and rests on the sources the review above describes as case series and expert consensus.⁴ But an absence of strong evidence is not a citation for the doubt, and this library's rule refuses a traditional teaching badge justified only by an absence — the failure mode that produced a manufactured badge in Band B and four struck badges in Band C. No source found for this page contests the staging; the review describes the evidence as thin without disputing the description. If a source is found that genuinely contests the phases, the badge becomes available and should be applied.
The cellular mechanism is badged Inferred wherever it appears, because neither label states one and the account given is reasoning backwards from the acidosis and the organ pattern. This is the weakest link in the page's argument and is the first thing an auditor should attack.
The direct-cardiotoxicity claim rests on five words of a label — shock from "hypovolaemia or direct cardiotoxicity"¹ — with no supporting mechanism given anywhere in the source. It is badged Inferred and it is doing real clinical work on this page, which is an uncomfortable combination.
The two ferrous sulfate labels and the ferrous fumarate label were compared rather than pooled. Their overdose sections differ substantially and the difference is one of vintage, not of substance; both are cited, for different things, and the discrepancy is described on the page. The two sulfate labels (products 3130 and 2623) carry near-identical overdose sections and are cited as one source.
A commonly quoted figure for a fatal iron dose appears on one of these labels and is deliberately not reproduced here. Comparative and lethal-dose framing is permanently out of scope for this library. The toxic threshold of 20 mg/kg elemental iron¹ is reproduced, because it is a treatment threshold and clinicians cannot risk-assess without it.
EXTRIP has not addressed iron. The workgroup's published recommendation set covers 22 substances and iron is not among them.⁵ The absence is uninformative rather than a gap: the label already states that dialysis does not remove iron effectively,¹ and the physical chemistry — an ion held in a high-affinity protein complex and rapidly leaving the plasma — answers the question without a guideline. This is the same category of absence as cyanide's rather than hydrofluoric acid's.

How this page connects to the rest of the library

Iron is the entry point to this band and it is deliberately the least metallic of the metals: it is a nutrient, it is bought in a shop, and it poisons children. Its structural twin elsewhere is paracetamol — an over-the-counter agent with a deceptive early course and a hepatic endpoint — but the mechanism could hardly be more different, since paracetamol must manufacture its poison and iron arrives as one. Within this band it is the odd member in three ways: it is the only one with a UK-licensed antidote pathway of its own, the only one where dimercaprol is explicitly contraindicated,² and the only one whose poisoning is usually a single acute ingestion rather than an exposure. The other five pages are about elements that accumulate; this one is about an element that simply cannot leave.

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
Ferrous Fumarate 322mg Tablets — Summary of Product Characteristics, §4.9 Overdose and §5.2. electronic Medicines Compendium, product 498. The modern of the two UK label vintages: carries the 20 mg/kg elemental threshold, the 4-hour sampling point, the chelation trigger with units, the whole-bowel-irrigation option, the 2–5 week stricture window and the statement on dialysis.
2
Ferrous Sulfate 200mg Coated Tablets and Ferrous Sulfate Tablets 200mg — Summaries of Product Characteristics, §4.9 Overdose, §5.1 and §5.2. electronic Medicines Compendium, products 3130 and product 2623. Overdose sections are near-identical between the two products and were compared before being cited as one source. Supplies the four-phase description, the transferrin binding-capacity endpoint and the dimercaprol contraindication; its management advice is of an older vintage.
3
Robertson A, Tenenbein M. Hepatotoxicity in acute iron poisoning. Human & Experimental Toxicology 2005;24(11):559–62. PMID 16323571. Retrospective 20-year single-centre series, 73 patients aged 1–48; hepatotoxicity unlikely below a serum iron of 700 µg/dL (128 µmol/L) within 12 hours and clinically important above 1000 µg/dL (182 µmol/L).
4
Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatric Emergency Care 2011;27(10):978–85. PMID 21975503. Cited for its characterisation of the evidence base, not for a figure.
5
EXTRIP Workgroup. Recommendations index. extrip-workgroup.org. Cited for an absence: the published recommendation set covers 22 substances and iron is not among them. Verified against the site's own menu, 7 September 2026.
6
National Poisons Information Service. TOXBASE — NPIS 0344 892 0111. The authoritative UK source for iron risk assessment, decontamination and chelation thresholds. Login-gated, and deliberately not quoted anywhere on this page.

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

Iron

At a glance