Why this poison is interesting

Mercury is the page in this library where the same substance is either almost harmless or a serious neurotoxin depending entirely on the membrane it crosses. Liquid elemental mercury swallowed from a broken thermometer is absorbed at "approximately 0.01%" from the gastrointestinal tract.¹ The identical metal, as vapour from the same spill, is absorbed at "approximately 80%" across the alveolar membrane.¹ That is a four-thousand-fold difference in bioavailability for one element, and it is a difference of physical form and route rather than of dose.

The second reason is a mechanism that is close to elegant, and it is the organising idea of the page. Elemental mercury is lipophilic and uncharged, so it crosses the blood–brain barrier readily. Inside the brain it is oxidised to the divalent ion, which is charged, protein-bound and "does not cross the blood-brain barrier as readily".¹ The source's own phrasing for what follows is the right one: mercury "may be oxidised and thereby trapped".¹ The blood–brain barrier is not keeping mercury out so much as keeping it in, and it becomes an obstacle only after the poison has passed through it. The source hedges both halves of that and so does this page: mercury "may" be oxidised and thereby trapped, and the divalent form "does not cross... as readily" rather than not at all.¹

The third is that mercury's timing is asymmetric in a way that has a bedside consequence. "Peak levels in all tissues are reached within 24 hours of exposure, apart from the brain where peak levels are only reached after 2 to 3 days."¹ The organ that matters most is the last to fill — and, because of the oxidation step above, the first to be unable to empty. Any therapy that depends on catching mercury before it is trapped has a window of days, not weeks, which is exactly what the chelation literature reports.²

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

Which of the four patterns is this?

A minor pathway becoming the major one — the second pattern, running in an unfamiliar direction. On the paracetamol and methanol pages, a metabolic step creates a toxic species out of a harmless one. Here the oxidation of elemental mercury to the divalent ion is not the step that makes the poison toxic — both forms are toxic — it is the step that decides where the poison is stuck. Mercury does not share the band's other pattern, molecular mistaken identity. Lead is handled as calcium, thallium as potassium and arsenate as phosphate — each is admitted because it resembles a required element. Mercury is not mistaken for anything: it binds thiols by affinity, which is arsenite's chemistry rather than arsenate's, and is the half of that page which also falls outside the pattern.

The toxic principle

Mercury poisons by binding sulfhydryl groups. That is the whole chemistry, and it is why mercury has no single target enzyme in the way that lead has δ-aminolaevulinic acid dehydratase: thiol groups are everywhere, in structural proteins, in transporters and in the active sites of a great many enzymes, so a poison that binds them indiscriminately produces a diffuse illness rather than a specific lesion. The overview reflects this — it is a careful descriptive document about what mercury does to organs, and it is largely silent on the biochemistry of how. That silence is worth naming, because this is the least mechanistically evidenced page in the band, and the sulfhydryl account appears in the source only in passing, as the explanation for why liquid metal is poorly absorbed.¹

Three forms, three diseases — and the source separates them for a reason

The UKHSA overview states at the top of its kinetics section that "elemental and inorganic mercury have different biological properties and hence are discussed separately".¹ Elemental mercury is a lipophilic, uncharged liquid metal that matters almost entirely as a vapour: negligible orally, 80% absorbed by inhalation, distributed to all tissues, and able to reach the brain and the fetus.¹ Inorganic mercuric salts are water-soluble, charged, and absorbed after ingestion at "approximately 5 to 10%"; because of "the poor lipid solubility only a small fraction crosses the blood-brain barrier and the placenta", and they go "primarily... to the kidneys".¹ The practical consequence is that the neurological syndrome and the renal syndrome belong to different exposures, and asking which form the patient met is the first diagnostic question rather than a detail.

Within the inorganic salts there is a further distinction that the source draws explicitly and that matters for absorption: "mercuric compounds (Hg2+) are more readily absorbed than mercurous (Hg1+) forms because of their solubility".¹ Solubility is doing the work again — the same principle that makes liquid metal inert in the gut makes the more soluble salt the more dangerous one.

Toxicokinetics

The table separates the two forms, because merging them produces a set of numbers that describes no real patient. The column that repays attention is the last one: almost every entry reduces to lipid solubility and charge.

Mercury — the same element in two forms, and the physical chemistry decides everything
Parameter	Therapeutic	In overdose	Why it changes
Inhalation (elemental vapour)	—	~80% "crosses the alveolar membrane and is rapidly absorbed"¹	Uncharged and lipophilic, so the alveolus is no barrier at all. This is the route that produces the neurological disease
Ingestion (liquid elemental)	—	~0.01%¹	Converted to the divalent ion in the gut and bound to thiols before it can be absorbed.¹ Effectively an inert substance by this route
Ingestion (inorganic salts)	—	5 to 10% of inorganic mercury in food¹; mercuric (Hg2+) absorbed more readily than mercurous (Hg1+)¹	Charged and water-soluble: absorbed poorly, but far better than liquid metal. Solubility ranks the salts
Dermal (vapour)	—	"Approximately 2.6% of the absorbed dose"¹	Small, but not nothing — and it is why a spill in an enclosed room exposes skin as well as lung
Distribution (elemental)	—	"Lipophilic, therefore... distributed rapidly to all tissues"; kidney holds 50 to 90% of the body burden; crosses the blood-brain barrier and placenta "relatively easily"¹	The only form that reaches the brain in quantity. Distribution is unrestricted precisely because the molecule is uncharged
Distribution (inorganic)	—	Distributed to all tissues but "due to the poor lipid solubility only a small fraction crosses the blood-brain barrier and the placenta"; primarily to the kidneys¹	The renal poisoning without the neurological one — the same target organ, a different clinical picture
Time to peak	—	All tissues within 24 h — except the brain, at 2 to 3 days¹	The organ of interest fills last. A patient assessed on day one has not yet reached their peak cerebral concentration
Biotransformation	—	Oxidised to divalent mercury in red cells, liver and lungs, and to a lesser extent in most tissues¹	The one-way door. "In the brain unoxidised mercury may be oxidised and thereby trapped, as the divalent form does not cross the blood-brain barrier as readily"¹
Plasma binding	—	Divalent mercury in plasma exists mainly in a non-diffusible form, "bound to albumin and globulins", in equilibrium with a diffusible fraction¹	Why a dialyser is of no use. The removable fraction is small and is continuously replenished from a bound pool
Elimination	—	Urine and faeces, with sweat, expired air and saliva minor; half-life approximately 1 to 2 months for both forms¹	Slow, unregulated, and long enough that a chronic exposure accumulates. Inorganic mercury clears from blood and brain biphasically¹

Metabolism and the metabolites

Mercury is an element and is not metabolised in the sense of being broken down. What happens instead is a change of oxidation state, and on this page that single reaction carries more clinical weight than any metabolic step in the band. Elemental mercury is oxidised to the divalent ion in red cells, and "oxidation may also occur in the liver and lungs, although it may occur in most other tissues to a lesser extent".¹ The reaction is the same everywhere; its consequences depend entirely on which side of a membrane it happens on.

Mercury — one reaction, and the compartment it occurs in decides the illness

Elemental mercury vapourUncharged and lipophilic. The form that travels; ~80% absorbed across the alveolus¹
Alveolar membrane — no barrier to an uncharged lipophilic atom
Dissolved in blood, still elemental"Some remains unchanged"¹ — and while it is unchanged it can go anywhere
Oxidised in the red cell, liver or lungDivalent mercury, mostly non-diffusible, bound to albumin and globulins.¹ Delivered onward to the kidney, which ends up holding 50–90% of the burden¹
Crosses the blood–brain barrier firstThen oxidised inside the brain — and trapped, because the divalent form "does not cross the blood-brain barrier as readily".¹ Peak cerebral concentrations at 2 to 3 days¹
Binding to sulfhydryl groups — the reaction that is both the toxicity and, in the gut lumen, the reason for its absence¹
Diffuse thiol-dependent dysfunctionNo single target enzyme. This is why the syndrome is broad and the mechanism is under-specified — the source is descriptive here rather than mechanistic

Reading the source's hedge honestly

The trapping mechanism is the central claim of this page, so the exact wording matters. The overview says mercury "may be oxidised and thereby trapped, as the divalent form does not cross the blood-brain barrier as readily".¹ The second half of that sentence is a statement of fact about the two forms; the first half is hedged. The account is coherent, is consistent with the observed 2-to-3-day brain peak and with the very long neurological half-life, and is consistent with the finding that the water-soluble chelators "do not redistribute... mercury to the brain".² But it is not reported as demonstrated, and it is badged Inferred here and everywhere else it appears on this page rather than promoted to established on the strength of how well it explains things.

Elimination and accumulation

Both forms leave slowly and by the same routes — "predominantly... through the urine and faeces, although some may be excreted in sweat, expired air or saliva", with a half-life of "approximately 1 to 2 months".¹ Two months is short compared with lead's skeletal store and long compared with almost everything else in this library, and it sits in the awkward middle: long enough that repeated occupational exposure accumulates, short enough that removal from source is genuinely effective if the brain has not already been loaded.

Accumulation in the kidney is the other half of the picture and is quantitatively the larger one: the kidney holds 50 to 90% of the body burden of absorbed elemental mercury,¹ and inorganic mercury is distributed "primarily to the kidneys".¹ The organ that carries most of the poison is not the organ that produces the most alarming symptoms, which is a recurring shape in this band.

Where this latent phase sits among the others

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

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
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
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

Mercury's gap is digoxin's cause, with an additional twist that no other member of this set has. Both are distribution lags — the poison is in the patient and has not yet reached its target. What is different here is that arrival at the target and inability to leave it are produced by the same event. Digoxin distributes to the myocardium and later redistributes back out; mercury reaches the brain and is then chemically converted into something that cannot make the return journey.¹

Target organs — and why those

Two organs dominate, and which one the patient presents with is largely decided before they arrive, by the form of mercury they met. The lung is a third target, but only for vapour and only acutely.

Kidney

TargetProximal tubular epithelium

Why hereThe organ with the largest burden by a wide margin, for both forms. Absorbed elemental mercury accumulates there to "50 to 90% of the body burden", and inorganic mercury is distributed "primarily to the kidneys".¹ The tubular cell is thiol-rich, metabolically active and concentrates what it reabsorbs, which is the standard explanation for why this is the organ that accumulates — though the source states the accumulation rather than explaining it. Inferred

At the bedside"Nephrotoxicity including proteinuria and increased urinary enzyme excretion" after occupational exposure to elemental mercury.¹ The renal picture is often silent and is found by testing rather than by symptoms — which is why urinary mercury and urinary protein are measured together in surveillance.

Brain

TargetCentral nervous system, reached only by the elemental form

Why hereThe organ that defines the disease, and the only one where the oxidation step matters. Elemental mercury crosses the blood-brain barrier "relatively easily" because it is lipophilic and uncharged; once inside it is oxidised to a divalent ion that "does not cross the blood-brain barrier as readily" and is thereby trapped.¹ Peak cerebral concentrations are reached at 2 to 3 days, later than every other tissue.¹ Inorganic salts largely do not get here at all.¹ Inferred

At the bedsideAcutely, "tremor, irritability, nervousness and hallucinations".¹ Chronically, "decreased psychomotor skills and neuropsychological symptoms, including fatigue, tremor, headaches, depression, irritability and hallucinations".¹ The classical picture is captured in a documented UK case: coarse tremor of the outstretched hands and protruded tongue, "Hatter's shakes" handwriting, slurred speech, impaired heel–toe walking and heel–shin coordination, and constricted visual fields to confrontation.³

Lung

TargetAirway and alveolus, acutely and only from vapour

Why hereThe port of entry, and at high concentration also a target. This is the one organ injured by the physical act of exposure rather than by distribution, and it is therefore the only mercury syndrome that declares itself within hours. Established

At the bedside"Cough, dyspnoea and chest tightness", with "bronchitis and bronchiolitis with interstitial pneumonitis, airway obstruction, and decreased pulmonary function" reported.¹ High-concentration exposure may also produce "'metal fume fever' like symptoms, including fatigue, fever and elevated leukocyte count".¹ A febrile illness with a raised white count after an occupational exposure is a recognised presentation and is easily mistaken for infection.

Mouth and gingiva

TargetOral mucosa

Why hereIncluded because it is one of the few findings that is reasonably specific to mercury and is visible without a test. Mercury is excreted in saliva,¹ which puts the oral mucosa in continuous contact with it. Inferred

At the bedside"Stomatitis, sore gums and ulceration of the oral mucosa" after occupational exposure to elemental mercury,¹ and "stomatitis... and ulceration of the oral mucosa" acutely.¹ Look in the mouth of anyone with an unexplained tremor and an occupational history.

Skin

TargetPeripheral skin, in the acrodynia syndrome

Why hereA distinctive and poorly explained presentation that the source describes consistently across three separate routes — inhalation, ingestion of inorganic salts, and dermal vapour exposure.¹ Its mechanism is not given anywhere in the source, and this page does not supply one. Inferred

At the bedside"Erythematous and pruritic skin rashes, and a reddening and peeling of the skin" on the nose, palms and soles.¹ The associated features are systemic and striking: "severe leg cramps, irritability, fever, tachycardia, hypertension, excessive salivation or perspiration, fretfulness and weakness".¹ An irritable child with peeling palms, hypertension and excessive salivation is the classical description and it is easy to miss if mercury is not considered.

Timeline of effects

Mercury vapour — a timeline in which the brain is reached last and emptied slowest

Time

What you seeWhat is happening

Minutes to hoursThe respiratory phase
What you see"Cough, dyspnoea, chest tightness"; at higher concentration bronchitis, bronchiolitis with interstitial pneumonitis and airway obstruction.¹ Possibly a "'metal fume fever' like" illness with fever and leukocytosis.¹
What is happeningDirect injury from vapour at the alveolar surface, concurrent with ~80% of it being absorbed.¹ The only mercury syndrome that is fast, and it belongs to the lung rather than to the metal's distribution.
Up to 24 hDistribution — everywhere except the brain
What you seeOften little. Gastrointestinal and cardiovascular features may appear — "stomatitis, abdominal pain, vomiting, diarrhoea", "hypertension and tachycardia".¹
What is happening"Peak levels in all tissues are reached within 24 hours of exposure, apart from the brain."¹ The kidney is loading to 50–90% of the eventual burden during this phase,¹ silently.
2–3 daysThe brain fills
What you seeTremor, irritability, nervousness and hallucinations begin to appear.¹
What is happening"Peak levels... in the brain... only reached after 2 to 3 days."¹ Elemental mercury has crossed as an uncharged atom and is now being oxidised in situ to an ion that cannot readily leave.¹ This is the window in which chelation can still act on mercury that is not yet trapped, and it is consistent with the finding that chelator efficacy "declines or disappears as the time interval between metal exposure and onset of chelation increases".²
Weeks to monthsThe neurological and renal syndromes
What you seeEstablished tremor, psychomotor slowing, neuropsychological symptoms, and the renal picture of proteinuria and raised urinary enzyme excretion.¹ Acrodynia in the exposed, particularly children.¹
What is happeningA whole-body half-life of 1 to 2 months¹ against continuing or recent exposure. Removal from source begins to work here; the brain lags behind everything else, and improvement is measured in months.

What the mechanism predicts at the bedside

Ask what form the mercury was in before asking how much. Vapour, liquid metal and a soluble salt are three different exposures with three different bioavailabilities — 80%, 0.01% and 5–10% respectively¹ — and the answer changes the risk assessment more than any quantity will.
Swallowed liquid mercury is not, by itself, a systemic poisoning. Absorption is "approximately 0.01%".¹ The concerns are the spill in the room and any retained metal, not the ingestion.
A broken thermometer or fluorescent lamp is an inhalational problem in an enclosed space. The source notes that an EU scientific committee has judged short peak exposures from a broken compact fluorescent lamp "very unlikely to pose a health risk",¹ but the mechanism to think about is vapour, not ingestion.
Consider skin-lightening creams and traditional remedies. The overview names both: "mercury salts in some traditional herbal preparations", and "the use of illegal skin lighteners containing inorganic mercury compounds can result in significant exposure by dermal absorption".¹ These are unregulated products and the patient may not consider them medicines, so the question has to be asked directly.
A febrile illness with leukocytosis after an occupational exposure may be metal fume fever rather than infection¹ — but it is a diagnosis of exclusion in a patient who may also have pneumonitis.
Expect the neurological examination to be more informative than the history. The documented findings in the UK case were a coarse tremor of the outstretched hands and protruded tongue, characteristic handwriting, dysarthria, impaired heel–toe and heel–shin coordination, mild dysdiadochokinesis and constricted visual fields to confrontation.³ Visual fields are not routinely tested in a patient presenting with tremor.
Look in the mouth. Stomatitis, sore gums and oral ulceration are described for both acute and chronic exposure,¹ and mercury is excreted in saliva.¹
In a child, put acrodynia and hypertension together. Peeling palms and soles, irritability, leg cramps, tachycardia, hypertension and excessive salivation are described as a syndrome,¹ and each component alone is unremarkable.
Do not wait for a concentration before seeking advice about chelation. Efficacy "declines or disappears as the time interval between metal exposure and onset of chelation increases", with prompt treatment described as "within minutes to a few hours" in the acute salt poisonings.² The brain is filling for 2 to 3 days,¹ and that is the window.

The antidote, from the poison's side

The chelators for mercury are the dithiols, and their logic is transparent: mercury poisons by binding sulfhydryl groups on the patient's proteins, so the antidote is a small molecule carrying two sulfhydryl groups of its own, offered as a preferable partner. The family has a history worth knowing, because it explains the differences between its members. Dimercaprol was developed "in wartime Britain as a potential antidote [to] the arsenical warfare agent lewisite"; DMPS (unithiol) and DMSA (succimer) are "dithiol water-soluble analogs of BAL" developed in the Soviet Union and China in the late 1950s, and all three "have remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century".²

Why the water-soluble analogues are preferred: Kosnett's review states it plainly: "DMPS and DMSA, which have a higher therapeutic index than BAL and do not redistribute arsenic or mercury to the brain, offer advantages in clinical practice."² On a page whose whole argument is that the brain is where mercury gets trapped, an antidote that moves mercury towards the brain is close to a contradiction in terms. This is the single strongest reason to prefer DMPS or DMSA here, and it follows directly from the mechanism rather than from a trial.
Why timing matters more than for most antidotes: "Treatment should be initiated as rapidly as possible (within minutes to a few hours), as efficacy declines or disappears as the time interval between metal exposure and onset of chelation increases."² The kinetics explain why: a chelator circulating in blood and extracellular fluid can only intercept mercury that is still in blood and extracellular fluid. Once the metal is intracellular, and in the brain once it has been oxidised, it is out of reach.
What the evidence for acute poisoning actually is: "Controlled animal experiments support a therapeutic role for these chelators in the prompt treatment of acute poisoning by arsenic and inorganic mercury salts", with "animal experiments and in some instances human data" indicating enhanced excretion.² That is a real but animal-weighted evidence base, and the page states it as such rather than upgrading it.
The best UK evidence in vapour exposure is a single case: A 36-year-old jewellery producer with tremor, dysarthria, incoordination and constricted visual fields received four 5-day courses of oral DMPS at 30 mg/kg/day, with "substantial objective clinical improvement and the excretion of 99,406 microg mercury".³ The authors recommend DMPS "be considered in symptomatic patients who have been exposed to mercury vapor and who have supporting analytical confirmation of the diagnosis".³ This is n = 1, uncontrolled, and it is the strongest thing on the page for the neurological syndrome — which is a statement about the field rather than about the case.

Chelation for chronic mercury exposure is not established treatment

The claim that chelation benefits patients with chronic mercury poisoning is not supported by the review that is the standard reference for chelation in this poisoning. "Although chelation following chronic exposure to inorganic arsenic and inorganic mercury may accelerate metal excretion and diminish metal burden in some organs, potential therapeutic efficacy in terms of decreased morbidity and mortality is largely unestablished in cases of chronic metal intoxication."² Traditional teaching The distinction being drawn is precise and is worth preserving: increased urinary excretion of mercury is not the same as clinical benefit, and a treatment can reliably produce the first without anyone having shown the second. This is a treatment-efficacy downgrade under this library's stated exemption — the same move as the glucagon badge on the beta-blocker page and the immunosuppression badge on the paraquat page, where a review searched the literature and reported that the human evidence was not there. It does not apply to acute poisoning by inorganic salts, where the same review does support a therapeutic role.²

Critical appraisal

One evidence-tier downgrade appears on this page, on the efficacy of chelation in chronic mercury exposure. The citation for the doubt is explicit rather than an absence: the review states that therapeutic efficacy in terms of morbidity and mortality is "largely unestablished" in chronic intoxication while simultaneously accepting that excretion is increased.² The downgrade is deliberately confined to chronic exposure, because the same source supports chelation in acute inorganic salt poisoning.
The oxidation-trapping mechanism — the organising argument of the entire page — is badged Inferred and not established, and this is the decision an auditor should test first. The source hedges the trapping with "may be oxidised and thereby trapped" while stating the underlying fact about differential permeability without a hedge.¹ The account explains the 2-to-3-day brain peak, the long neurological recovery and the preference for chelators that do not redistribute to the brain,² but explanatory power is not demonstration, and this library's rule is that a mechanism not shown in humans is inferred however well it fits.
A deliberate non-downgrade: the difference between the three forms of mercury is badged established. The absorption fractions, the distribution differences and the solubility ranking of mercuric over mercurous salts are all stated directly and unhedged by the source,¹ and no source found contests them. Not manufacturing a badge is as much part of this discipline as applying one.
The renal accumulation is badged Inferred because the source states the fraction and not the reason. The 50-to-90% figure is quoted;¹ the thiol-rich, reabsorbing tubular cell explanation is standard but is supplied here rather than by the source, and is flagged as such.
Acrodynia is described and not explained, and the page says so. The source lists it consistently across three routes of exposure¹ and offers no mechanism; none is invented here.
The single UK case of DMPS in vapour exposure is presented as a single case.³ Its figures — four 5-day courses, 30 mg/kg/day, 99,406 µg mercury excreted — are the report's own, and the improvement it describes is uncontrolled. It is included because it is the best available human evidence for the neurological syndrome, and that fact is itself worth reporting.
EXTRIP has not addressed mercury.⁴ The absence is uninformative rather than a genuine gap: divalent mercury in plasma is "mainly... non-diffusible" and bound to albumin and globulins,¹ and the bulk of the burden is intracellular and renal. A dialyser would be removing the small equilibrium fraction of a large bound pool — the same argument that rules it out for digoxin.
No lethal dose, lethal concentration or comparative-lethality statement appears on this page, consistent with the library's boundary. The UK occupational long-term exposure limit of 0.02 mg/m³ as an 8-hour time-weighted average¹ is included as a regulatory figure and is explicitly not a clinical threshold.

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. Elemental mercury and inorganic mercury: toxicological overview. Compendium of Chemical Hazards. gov.uk. Supplies the absorption fractions for all three routes, the tissue distribution and renal burden, the oxidation and trapping account, the 2-to-3-day brain peak, the 1-to-2-month half-life, the organ syndromes and the UK occupational exposure limit. Unlike the arsenic and lead overviews it contains no TOXBASE reference — checked — and no mechanism-of-toxicity section.
2
Kosnett MJ. The role of chelation in the treatment of arsenic and mercury poisoning. Journal of Medical Toxicology 2013;9(4):347–54. PMID 24178900. The origin and comparative properties of the three dithiol chelators; the statement that DMPS and DMSA do not redistribute mercury to the brain; the timing dependence of efficacy; and the statement that efficacy in chronic intoxication is largely unestablished, which carries this page's evidence-tier downgrade.
3
Bradberry SM, Sheehan TM, Barraclough CR, Vale JA. DMPS can reverse the features of severe mercury vapor-induced neurological damage. Clinical Toxicology 2009;47(9):894–8. PMID 19852623. A single UK case (West Midlands Poisons Unit, Birmingham): a 36-year-old jewellery producer, four 5-day courses of oral DMPS 30 mg/kg/day, substantial objective improvement and 99,406 µg mercury excreted. Cited as a case report, which is what it is.
4
EXTRIP Workgroup. Recommendations index. extrip-workgroup.org. Cited for an absence: the published set covers 22 substances and mercury is not among them. Verified against the site's own menu, 7 September 2026.
5
National Poisons Information Service. TOXBASE — NPIS 0344 892 0111. The authoritative UK source for mercury risk assessment, biological monitoring and chelation indications. Login-gated, and deliberately not quoted anywhere on this page.

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

Mercury

At a glance