Why this poison is interesting

These two gases are on one page because the comparison teaches something neither teaches alone. They are chemically opposite — one becomes a strong base on contact with water and the other becomes an acid and a set of free radicals — and yet they produce clinically similar illnesses distinguished mainly by depth. What decides the depth is not the chemistry at all. It is how readily each gas dissolves in the water lining the airway.

The UKHSA overview states ammonia's case directly: it "is extremely soluble in water and dissolves in the mucus fluid covering the mucous lining of the respiratory system to produce ammonium hydroxide, a strong base", and "following short-term inhalation exposure, ammonia is almost entirely retained in the upper nasal mucosa".¹ A gas that is consumed by the first wet surface it meets never reaches the alveolus. The same document draws the conclusion explicitly: this "protects the lungs from exposure to low concentrations of ammonia".¹

Chlorine is less soluble, so more of it survives the upper airway, and the consequence is the most clinically important sentence on this page: exposure to a sufficiently high dose "may result in pulmonary oedema and respiratory failure, the onset of which may be delayed by up to 36 hours".² The gas that hurts less at the time is the one that can kill you the next day. That contrast is real and it is not absolute: the ammonia document states that "in severe cases pulmonary oedema, breathlessness, wheezing, hypoxia, and cyanosis may take 36 hours to develop after the initial inhalation exposure"¹, and that "lower levels of ammonia exposure that do not result in upper airway obstruction may cause significant alkali burns throughout the tracheobronchial tree".¹ An earlier draft of this page taught that ammonia has no latent phase. Its own source says otherwise, and a clinician who believed the draft would under-observe a severe ammonia exposure.

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

The toxic principle

Neither gas is toxic as a gas. Both are precursors that become corrosive on contact with water, and since the entire respiratory tract is lined with water, the reaction happens wherever the gas happens to be when it meets it.

Ammonia "dissolves in moisture in the air and on tissue or mucous membranes to form ammonium hydroxide"¹ — a strong base. Alkali injury is liquefactive: it saponifies membrane lipids and denatures protein in a way that does not form a limiting eschar, so the injury tends to keep going into the tissue. Chlorine produces the opposite chemistry, with the initial symptoms "caused by free-radicals, hypochlorous or hypochloric acid formed by the reaction of chlorine with water in lung or eye tissues".² One gas makes a base, the other makes an acid and an oxidant, and both destroy epithelium.

The warning property is the protective mechanism, and it can be overwhelmed

A gas that is agonising at low concentration causes people to leave, and that behavioural response is a real part of why ammonia exposures are frequently survivable. It is protection by intolerability. But the source is explicit that the mechanism has a ceiling: "inhalation of high concentrations of ammonia may exceed the capacity of this mechanism, leading to systemic absorption through the lungs"¹, and substantial exposures "can cause burns of all depths in the oral cavity, nasopharynx, larynx, and trachea, together with airway obstruction, respiratory distress and pulmonary oedema".¹ Anhydrous ammonia released into a confined space is not the same event as a cleaning-product exposure in a kitchen, and the protective mechanism is exactly what fails in the first case. Compare hydrogen sulphide, where the warning property fails not by being overwhelmed but by anaesthetising the sense that detects it.

There is a third mechanism specific to chlorine and worth naming because it appears early and is treatable. Sufficient exposure "may induce reflex cholinergic bronchoconstriction with associated signs of coughing, wheezing and dyspnoea".² That is a neural reflex rather than a chemical burn — it is the reason the immediate picture can be an acute wheeze, and it is a different problem from the epithelial injury that may declare a day later.

Toxicokinetics

Almost nothing here is kinetics in the usual sense. There is no volume of distribution, no clearance and no half-life that matters, because both gases are destroyed by the reaction that constitutes the poisoning. The variables that behave like kinetic parameters are solubility, concentration and contact time.

Chlorine and ammonia — a table in which solubility does the work of pharmacokinetics
Parameter	Therapeutic	In overdose	Why it changes
Water solubility	—	*Ammonia: "extremely soluble in water"¹. Chlorine: less so*	The parameter that decides everything downstream. It sets the airway level at which the gas is consumed, and therefore which tissue is injured, how fast symptoms appear, and whether there is a latent phase at all.
Site of deposition	—	Ammonia "almost entirely retained in the upper nasal mucosa" after short-term exposure¹; chlorine reaches the lower airway	Deposition is the organ-selectivity mechanism. No transporter, no enzyme, no differential susceptibility — the gas injures whatever it happens to be touching when it dissolves.
Conversion to the toxic species	—	Ammonia → ammonium hydroxide, "a strong base"¹. Chlorine → "free-radicals, hypochlorous or hypochloric acid"²	Bioactivation by water rather than by an enzyme. There is no hepatic step, no genetic variation in the conversion and no way to block it — which is why no antidote of the fomepizole type is even conceivable here.
Capacity of the upper-airway defence	—	Saturable. "Inhalation of high concentrations of ammonia may exceed the capacity of this mechanism"¹	The one genuinely kinetic idea on the page, and it is a saturation phenomenon. Below the ceiling, ammonia is an upper-airway injury; above it, the lungs are exposed and systemic absorption occurs. A protective mechanism that saturates is the first of the library's four patterns in an unexpected place.
Onset	—	Ammonia: immediate. Chlorine: immediate irritation, but pulmonary oedema "may be delayed by up to 36 hours"²	The two gases separate here more than anywhere else. An asymptomatic interval after a chlorine exposure is not evidence that the exposure was trivial, and the observation period has to be set by the gas rather than by the patient's current comfort.
Systemic absorption	—	Ammonia at high concentration only¹; chlorine essentially not, being consumed at the surface	Neither is a systemic poison in the ordinary case, which is why this page has no organ cards for liver, kidney or brain and why the whole of the illness is where the gas landed.
Elimination	—	Not applicable. Both are consumed by the reaction that injures the tissue	The poison is gone before the patient arrives, and the injury is not. That structure — damage outlasting the agent completely — is shared with paraquat and nitrous oxide, though here the mechanism is a burn rather than a metabolic lesion.
Dialysability	—	Never assessed and incoherent. EXTRIP has published no recommendation covering chlorine or ammonia³	There is no circulating xenobiotic to remove. An absence in the strongest sense in this band — the question cannot be posed about a gas that has already been destroyed by the epithelium it burned.

Metabolism and the metabolites

There is no metabolism in the hepatic sense and there are no metabolites in the usual sense — but both gases are nonetheless bioactivated, by water, at the moment of contact. That is the unusual claim of this section: these are prodrugs whose activating enzyme is the airway lining fluid.

Two gases, one activating step, and a fork decided by solubility

Irritant gas inhaledNeither ammonia nor chlorine is corrosive as a dry gas. Both require water
Extremely water-soluble — dissolves at the first wet surfaceAmmonia retained in the upper nasal mucosa"Almost entirely retained" after short-term exposure¹ — the lungs are protected at low concentration¹
Less soluble — a greater fraction travels onwardChlorine reaches the lower airwayWhere the delayed pulmonary oedema comes from²
Reacts with mucosal waterAmmonium hydroxide — a strong base"A strong base"¹. Alkali injury is liquefactive and keeps penetrating
Reacts with tissue waterHypochlorous and hydrochloric acid, plus free radicals"Free-radicals, hypochlorous or hypochloric acid formed by the reaction of chlorine with water in lung or eye tissues"²
Epithelial destruction at the level where the gas dissolvedThe level, not the chemistry, determines the clinical syndrome
Upper airwayBurns, oedema, airway obstructionAmmonia at high concentration causes "burns of all depths in the oral cavity, nasopharynx, larynx, and trachea"¹
Lower airway — after a delayPulmonary oedema and respiratory failure"The onset of which may be delayed by up to 36 hours"²

Elimination and accumulation

Nothing accumulates and nothing is eliminated, because neither gas persists in the body. What develops over time is the tissue's response to an injury that was complete at the moment of exposure — which is exactly the structure of paraquat's latent phase, arrived at by a completely different route.

The other late consequence is chronic rather than acute, and the chlorine data are more substantial than is generally appreciated. Beyond the historical experience of "survivors of World War I gassing incidents"², a follow-up study in July 1999 of twenty individuals exposed in 1995 found that 75% had residual lung volumes below 80% of their predicted value, and nearly half of those tested for airway reactivity to methacholine showed a greater than 15% decline in FEV.² There is also evidence that a single acute exposure "may cause RADS, also known as irritant-induced asthma".² A one-off exposure to an irritant gas is not always a self-limiting event, and twenty patients is the size of the study that says so.

Where this latent phase sits among the others

Chlorine and ammonia — paraquat's cause at its shortest — the time an injured alveolar epithelium takes to leak

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
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

Target organs — and why those

The target organs are simply the surfaces the gas touched, and the interesting question is which surfaces each gas reaches. That is answered by solubility, which makes this the most mechanically predictable organ section in the library.

Upper airway — nose, pharynx, larynx

TargetMucosal epithelium of the first wet surfaces encountered

Why hereAmmonia's principal target by deposition. "Following short-term inhalation exposure, ammonia is almost entirely retained in the upper nasal mucosa."¹ The alkali chemistry then makes the burn a penetrating one: substantial exposures cause "burns of all depths in the oral cavity, nasopharynx, larynx, and trachea, together with airway obstruction".¹ The lesion is where the solubility put it and as deep as the chemistry took it. Established

At the bedsideImmediate intense nasal, oral and throat pain, lacrimation, stridor and hoarseness. Airway obstruction from laryngeal oedema is the early threat, and it can develop faster than the lower-airway problems the patient is being watched for.

Lower airway and alveolus

TargetBronchiolar and alveolar epithelium

Why hereChlorine's principal target, for the same reason inverted — being less soluble, it is not fully consumed above. Injury to the alveolar epithelium produces a leak, and the leak takes time: pulmonary oedema and respiratory failure with an onset that "may be delayed by up to 36 hours".² Ammonia reaches here only when "high concentrations... exceed the capacity" of the upper-airway defence.¹ Established

At the bedsideCough, wheeze and dyspnoea early — partly "reflex cholinergic bronchoconstriction"² rather than injury — then, after an interval, progressive hypoxaemia and pulmonary oedema. "In extreme cases, pulmonary haemorrhage may also occur."²

Eye

TargetConjunctiva and cornea

Why hereBoth gases reach the eye because it is a wet exposed surface, and the chemistry then diverges. Ammonia is the more dangerous of the two here: ammonia and ammonium hydroxide "are corrosive and can rapidly penetrate the eye and may cause permanent injury", so splashes "should be considered an ophthalmic emergency".¹ Chlorine's ocular symptoms arise from the same acid and radical chemistry as in the lung.² The alkali penetrates and the acid tends to stop at the surface — the general rule of chemical eye injury, illustrated by two gases at once. Established

At the bedsideAmmonia: severe pain, corneal injury and a genuine risk of permanent visual loss — irrigate immediately and involve ophthalmology.¹ Chlorine: burning, lacrimation and conjunctivitis, usually self-limiting.

Aerodigestive tract — after ingestion

TargetOesophagus and stomach

Why hereRelevant to ammonia rather than to chlorine gas, because ammonia solutions are domestic products. Ingestion "causes rapid onset of signs and symptoms including pain in the mouth, throat and chest, excessive salivation and extensive alkali burns to the aerodigestive tract".¹ Liquefactive alkali injury does not form a limiting eschar, which is the mechanistic reason perforation is a real risk. Established

At the bedside"In severe cases perforation of the stomach or oesophagus may occur, which can result in complications such as cardiac injury, mediastinitis and pneumonitis. Aspiration of ammonia following ingestion may also lead to respiratory complications."¹

The airway, months later

TargetBronchial reactivity and lung volumes after a single exposure

Why hereIncluded because the assumption that an irritant gas exposure is self-limiting is not well supported for chlorine. A 1999 follow-up of twenty individuals exposed in 1995 found 75% with residual lung volumes below 80% of predicted, and nearly half of those tested showing greater than 15% decline in FEV on methacholine challenge.² A single acute exposure "may cause RADS, also known as irritant-induced asthma".² Twenty patients is a small study and it is the evidence that exists. Inferred

At the bedsidePersistent breathlessness, exertional wheeze and bronchial hyper-reactivity after apparent recovery. Worth warning survivors about, and worth following up.

Timeline of effects

Two gases on one clock — and only one of them has a gap

Time

What you seeWhat is happening

Seconds — ammoniaImmediate upper-airway agony
What you seeIntense nasal, oral and pharyngeal pain, lacrimation, cough, stridor.¹
What is happening"Extremely soluble in water", dissolving in the mucus film to form ammonium hydroxide and "almost entirely retained in the upper nasal mucosa".¹ The symptom and the protection are the same event.
Seconds — chlorineIrritation and reflex bronchoconstriction
What you see"A burning sensation in the eyes and pain or burning of the lungs during respiration", then "coughing, wheezing and dyspnoea".²
What is happening"Free-radicals, hypochlorous or hypochloric acid formed by the reaction of chlorine with water in lung or eye tissues"², plus "reflex cholinergic bronchoconstriction".² The early wheeze is a reflex, not yet the injury.
Minutes–hoursAmmonia at high concentration overwhelms the defence
What you see"Burns of all depths in the oral cavity, nasopharynx, larynx, and trachea, together with airway obstruction, respiratory distress and pulmonary oedema."¹
What is happening"Inhalation of high concentrations of ammonia may exceed the capacity of this mechanism, leading to systemic absorption through the lungs."¹ A saturable protective mechanism, saturated.
Up to 36 h — ammoniaThe ammonia interval this page originally denied
What you see"In severe cases pulmonary oedema, breathlessness, wheezing, hypoxia, and cyanosis may take 36 hours to develop after the initial inhalation exposure."¹
What is happeningThe same delay as chlorine, from the same source family, in the gas this page had described as having none. Solubility decides where the injury lands at low and moderate exposure; it does not abolish the alveolar injury once the upper airway is overwhelmed — and "lower levels of ammonia exposure that do not result in upper airway obstruction may cause significant alkali burns throughout the tracheobronchial tree".¹
HoursThe chlorine interval
What you seeSymptoms may settle. The early wheeze resolves and the patient feels improved.
What is happeningThe reflex bronchoconstriction has worn off; the alveolar epithelial injury has not been repaired and has not yet leaked. Nothing measurable at this moment predicts what follows.
Up to 36 hChlorine pulmonary oedema
What you seeProgressive hypoxaemia, pulmonary oedema, respiratory failure. "In extreme cases, pulmonary haemorrhage may also occur."²
What is happening"The onset of which may be delayed by up to 36 hours."² The interval is the time an injured alveolar barrier takes to fail, not a time during which the poison was acting — it left long ago.
Months–yearsChronic airway consequences
What you seeReduced FEV; in one small follow-up, 75% of twenty exposed individuals had residual lung volumes below 80% of predicted.² RADS after a single exposure.²
What is happeningAirway remodelling and persistent hyper-reactivity following epithelial destruction. The mechanism is not established by the sources cited here, and the finding is a cohort observation rather than an explanation. Inferred

What the mechanism predicts at the bedside

Ask which gas, and then ask about solubility rather than about toxicity. It predicts the level of the injury, the speed of onset and whether a latent phase exists.
Ammonia hurts immediately and that is partly why people survive it — the exposure is intolerable, so it ends. The absence of that warning is what makes a less soluble gas more dangerous at the same concentration.
In ammonia exposure the early threat is the upper airway. Burns of all depths in the larynx and trachea with airway obstruction¹ can develop faster than any lower-airway problem.
In chlorine exposure the early wheeze is a reflex — "reflex cholinergic bronchoconstriction"² — and its resolution is not evidence that the lung is undamaged.
Chlorine's pulmonary oedema may be delayed by up to 36 hours.² The observation period is set by that number, not by how the patient looks at four hours.
A high-concentration ammonia exposure is a different disease from a low-concentration one, because the protective mechanism saturates.¹ Anhydrous ammonia in a confined space is the scenario where the lungs are exposed.
Ammonia in the eye is an ophthalmic emergency — corrosive, rapidly penetrating, capable of permanent injury.¹ Irrigate immediately.
Ammonia ingestion risks perforation, mediastinitis and cardiac injury¹, and the alkali chemistry is why: liquefactive injury does not form a limiting eschar.
Warn survivors of chlorine exposure about persistent respiratory symptoms, and consider follow-up. Reduced lung volumes and irritant-induced asthma after a single exposure are documented.²
There is no antidote and no role for dialysis³. Removal from exposure, decontamination, airway management and supportive care are the whole of it.
Mixing bleach with ammonia-containing cleaners generates chloramine gas — a common domestic mechanism for producing an irritant gas exposure indoors, and a reason to ask what was being cleaned with what.

The antidote, from the poison's side

There is no antidote to either gas and there cannot be one, and the reason is worth stating precisely because it is different from the reasons on the other antidote-less pages in this band. Paraquat has no antidote because nothing can compete with a catalytic redox cycle. Hydrogen sulphide has none because it clears itself faster than an antidote could act. Here there is no antidote because by the time the patient is a patient, the poison no longer exists — it was destroyed by the reaction that burned the airway.

Removal from exposure: The whole of the specific treatment. Both gases are consumed at the surface they injure, so ending the exposure ends the injury — though not, in chlorine's case, its consequences.
Why no enzyme blocker is possible: The activating step is water. Fomepizole works for methanol because a single enzyme stands between parent and toxin. Here the conversion to ammonium hydroxide or to hypochlorous acid happens on contact with mucosal fluid¹², with no enzyme to inhibit and no genetic variation to exploit.
Why no scavenger is possible: The reaction is complete within a breath, at a surface. A circulating scavenger cannot reach a molecule that no longer exists, and nothing can be given fast enough to intercept it at the epithelium.
Nebulised sodium bicarbonate for chlorine: Proposed on the reasoning that neutralising the acid formed on the airway surface might limit injury. Evidence does exist and it is narrow. A trial of 44 patients with reactive airways dysfunction syndrome after chlorine inhalation, given nebulised sodium bicarbonate or placebo on top of corticosteroids and a beta2-agonist, found significantly higher FEV1 at 120 and 240 minutes and better quality-of-life scores;⁴ allocation was sequential odd-even, so this is quasi-randomisation. A systematic review counts it as the field's one human randomised controlled study and summarises it precisely: "The only additional benefit of sodium bicarbonate was to increase the forced expiratory volume in one second, 2 and 4 h after administration."⁵ An earlier retrospective series of 86 cases found no patient deteriorated and concluded the treatment "appears safe and merits prospective evaluation".⁶ So: a short-lived spirometric benefit in one small quasi-randomised trial, no evidence of harm, and nothing bearing on the outcomes that matter. Inferred The mechanistic objection is that the reaction is essentially instantaneous. It is mentioned because a reader will encounter the proposal. Inferred
Bronchodilators: Directed at the "reflex cholinergic bronchoconstriction" chlorine induces² — treating a reflex rather than the burn, which is a coherent target and a limited one.
Irrigation: The one intervention that is genuinely time-critical, and it applies to eyes and skin rather than to the airway. Ammonia splashes to the eye are an ophthalmic emergency because the alkali penetrates rapidly.¹
Observation: The most important thing done for a chlorine-exposed patient, and it is not a treatment. A 36-hour window for pulmonary oedema² means the clinical decision is about duration of monitoring rather than about drugs.
Extracorporeal removal: Never assessed and incoherent³ — there is no circulating substance to remove.

Critical appraisal

No evidence-tier downgrade appears on this page. No source found contests the solubility mechanism, the chemistry of either gas, or the delayed onset of chlorine's pulmonary oedema. A badge would have to be manufactured to appear here, which is the failure this library is most prone to and explicitly refuses.
The comparative claim that chlorine is 'less soluble' than ammonia is not quoted from either source in those words. Ammonia is described as "extremely soluble in water"¹; the chlorine document makes no comparable statement. The comparison is standard chemistry and is inference on this page, and if it were wrong the whole organising argument would fail. It is flagged here rather than buried.
Phosgene is named in the exam callout as the classic less-soluble delayed-onset gas and is not cited. It is included because it completes the gradient the page is teaching; it is not covered by either source and there is no page for it in this library.
The 36-hour figure carries its source's hedge. Pulmonary oedema "may be delayed by up to 36 hours"² — a stated maximum for a possible event, not a guarantee of a safe interval and not a discharge criterion. This page states no observation period, which is a TOXBASE and NPIS matter.
The chronic-sequelae data are one small follow-up study of twenty individuals², reported four years after their exposure. It establishes that persistent abnormality occurs; it cannot establish how often, and the organ card is badged inferred accordingly. The source itself introduces it as suggesting sequelae "may be more frequent than previously anticipated" — a hedge that is preserved rather than dropped.
Only the alkali-versus-acid comparison is inference. The ammonia half is sourced: the ammonium hydroxide formed "saponifies lipids of the epidermal fats and cell membranes" and "the resultant liquefactive necrosis may appear pale and without charring or blistering and may cause an increased depth of injury".¹ An earlier draft of this bullet said no source stated any of it, which was wrong — the audit found the citation inside a document the page already cites. What remains this page's own inference is the claim that alkali is therefore worse than acid at equal exposure.
The chlorine concentration–effect table in the source was deliberately not reproduced.² The clinical points this page needs are made qualitatively. Printing a table relating airborne concentrations to acute effects would be an occupational-hygiene document repurposed as a clinical dose–response, and this library does not print thresholds of that kind.
No lethal concentration, no exposure limit and no time-to-death figure appears anywhere on this page.
The nebulised bicarbonate paragraph was rewritten after the Band D audit left it open. It previously said that no source cited here established benefit — true as written, because none was cited, but it told a reader the evidence base was emptier than it is. A quasi-randomised trial of 44 patients and a systematic review that counts it as the field's only human randomised study both exist,^4,5 and the benefit they report is real, narrow and spirometric. This is the same failure shape as the paraquat correction in Band D: a null result asserted from a search that was not run. It is included because omitting it would leave a reader to meet the idea without the objection.
Chloramine from mixing bleach with ammonia is named in the bedside list and is not sourced here. It is a well-known domestic mechanism and it is a route of exposure rather than a mechanistic claim, but note that neither cited document covers it.
EXTRIP's silence³ is uninformative in the strongest sense on this page — there is no circulating xenobiotic about which the question could even be asked.

References

1
Ammonia: toxicological overview. UK Health Security Agency, Compendium of Chemical Hazards. ("Ammonia dissolves in moisture in the air and on tissue or mucous membranes to form ammonium hydroxide." "Ammonia is extremely soluble in water and dissolves in the mucus fluid covering the mucous lining of the respiratory system to produce ammonium hydroxide, a strong base. Following short-term inhalation exposure, ammonia is almost entirely retained in the upper nasal mucosa. Inhalation of high concentrations of ammonia may exceed the capacity of this mechanism, leading to systemic absorption through the lungs." "Ammonia is water soluble and is therefore absorbed by the mucosa of the upper respiratory tract, this protects the lungs from exposure to low concentrations of ammonia." "Substantial exposures to concentrated aerosols of ammonium hydroxide, elevated levels of ammonia gas or anhydrous ammonia fumes can cause burns of all depths in the oral cavity, nasopharynx, larynx, and trachea, together with airway obstruction, respiratory distress and pulmonary oedema." "Ammonia and ammonium hydroxide are corrosive and can rapidly penetrate the eye and may cause permanent injury. Therefore, splashes in the eye should be considered an ophthalmic emergency." "Ingestion of ammonia solution (ammonium hydroxide) causes rapid onset of signs and symptoms including pain in the mouth, throat and chest, excessive salivation and extensive alkali burns to the aerodigestive tract. In severe cases perforation of the stomach or oesophagus may occur, which can result in complications such as cardiac injury, mediastinitis and pneumonitis.") gov.uk
2
Chlorine: toxicological overview. UK Health Security Agency, Compendium of Chemical Hazards. ("These initial symptoms are caused by free-radicals, hypochlorous or hypochloric acid formed by the reaction of chlorine with water in lung or eye tissues." "Immediate symptoms following inhalation include a burning sensation in the eyes and pain or burning of the lungs during respiration. Sufficient exposure may induce reflex cholinergic bronchoconstriction with associated signs of coughing, wheezing and dyspnoea. Exposure to a sufficiently high dose may result in pulmonary oedema and respiratory failure, the onset of which may be delayed by up to 36 hours. In extreme cases, pulmonary haemorrhage may also occur." Chronic sequelae: World War I gassing survivors; reduction in forced expiratory volume the most consistently reported chronic effect; a July 1999 follow-up of twenty individuals previously exposed in 1995 found 75% with residual lung volumes below 80% of predicted and nearly half of those tested for methacholine airway reactivity with a greater than 15% decline in FEV; evidence that a single acute exposure "may cause RADS, also known as irritant-induced asthma". The document's Table 1 relating airborne concentration to acute toxic effects was deliberately not reproduced on this page.) gov.uk
3
EXTRIP Workgroup — published recommendations index. Extracorporeal Treatments in Poisoning Workgroup. Cited for the absence of any recommendation covering chlorine or ammonia. extrip-workgroup.org/recommendations
4
Aslan S, Kandiş H, Akgün M, et al. The effect of nebulized NaHCO3 treatment on "RADS" due to chlorine gas inhalation. Inhalation Toxicology 2006;18(11):895–900. PMID 16864407. 44 patients with reactive airways dysfunction syndrome after chlorine inhalation, allocated to nebulised sodium bicarbonate or placebo on top of corticosteroids and a short-acting beta2-agonist. Allocation was sequential odd-even, which is quasi-randomisation rather than true randomisation — a distinction the systematic review below does not draw.
5
Huynh Tuong A, Despréaux T, Loeb T, et al. Emergency management of chlorine gas exposure — a systematic review. Clinical Toxicology 2019;57(2):77–98. PMID 30672349. Three databases, 2007–2017, 45 relevant papers including one human randomised controlled study — the trial above. Its verdict on bicarbonate is quoted on this page.
6
Bosse GM. Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation. Journal of Toxicology: Clinical Toxicology 1994;32(3):233–41. PMID 8007031. 86 retrospective cases treated on a poison-centre recommendation; no patient deteriorated after treatment, and the author concluded it "appears safe and merits prospective evaluation".

Chlorine and ammonia

At a glance