Toxicology – Chlorine

Core concept

Chlorine (Cl₂) is a highly reactive, water-soluble pulmonary irritant gas that primarily damages the eyes, upper airway, and lungs.

The classic exposure syndrome is:

Chlorine inhalation → immediate eye/throat burning + cough → bronchospasm/chest tightness → chemical pneumonitis ± noncardiogenic pulmonary edema/ARDS

The most important treatment is:

Remove from exposure + airway/oxygenation support + inhaled bronchodilators for bronchospasm

There is:

No specific antidote

Most mild exposures resolve completely, but significant exposures can cause progressive lung injury over several hours and occasionally persistent reactive airways dysfunction syndrome (RADS). Current CDC guidance notes that lung function usually returns toward baseline within about 7–14 days after uncomplicated exposure, although more serious exposures can produce prolonged respiratory problems.

Physical Properties

Chlorine is:

• Chemical formula: Cl₂
• Greenish-yellow gas at room temperature
• Pungent, highly irritating odor
• Approximately 2.5 times heavier than air
• Shipped industrially as a liquefied compressed gas
• Nonflammable, but a powerful oxidizing agent

It can accumulate in:

• Basements
• Pits
• Low-lying areas
• Poorly ventilated enclosed spaces

and may react dangerously with many combustible or reducing materials.

Important Terminology

Chlorine Gas ≠ Household Bleach

These are related but distinct exposures.

Chlorine gas

Cl₂

Primary toxicity:

Inhalational pulmonary injury

Household bleach

Usually contains:

Sodium hypochlorite (NaOCl)

Primary toxicity:

• Local irritation
• Caustic injury if concentrated
• Generation of toxic gases if mixed with other cleaners

Therefore, a patient who “drank chlorine” usually ingested hypochlorite solution, not gaseous molecular chlorine.

How Household Mixing Produces Toxic Gas

This is one of the most important practical chlorine toxicology points.

Bleach + Acid

For example:

• Toilet-bowl cleaner
• Hydrochloric-acid cleaner
• Vinegar

can produce:

CHLORINE GAS

Hypochlorite + acid → Cl₂ release

Bleach + Ammonia

Mixing hypochlorite bleach with ammonia-containing products produces:

CHLORAMINES

rather than simply molecular chlorine.

Chloramine gases are also respiratory irritants and can produce:

• Eye burning
• Cough
• Dyspnea
• Bronchospasm
• Pulmonary injury

Practical rule

Never mix bleach with another household cleaner.

Sources and Uses

Important exposure settings include:

• Water-treatment facilities
• Sewage treatment
• Swimming-pool maintenance
• Chemical manufacturing
• Pulp/paper and textile bleaching
• Plastics and synthetic-material production
• Cleaning accidents
• Industrial chlorine-cylinder leaks
• Accidental mixing of household cleaning agents

Chlorine has also historically been used as a chemical warfare agent.

Routes of Exposure

Inhalation

By far the most important route.

Eyes

Gas or liquid splashes can produce significant injury.

Skin

Concentrated chlorine gas, liquid chlorine, or chlorine-generating solutions can cause chemical injury.

Ingestion

Elemental chlorine is a gas at room temperature, so ingestion typically refers to:

Sodium/calcium hypochlorite solutions

rather than Cl₂ itself.

Toxic Dose / Concentration

Toxicity is determined by:

Concentration × duration of exposure

There is no single clinically reliable toxic dose.

Historical human observations suggest:

• Approximately 1–10 ppm can produce irritation
• Concentrations above roughly 15 ppm can cause significant respiratory distress
• Very high concentrations can produce rapidly fatal pulmonary injury

ATSDR historically estimated a lowest lethal concentration around 430 ppm for 30 minutes, but such numbers should not be interpreted as safe/unsafe cutoffs.

A far more useful occupational emergency threshold is:

NIOSH IDLH = 10 ppm

meaning 10 ppm is considered immediately dangerous to life or health.

Pathophysiology

Chlorine readily reacts with water present on moist respiratory surfaces.

A simplified reaction produces:

Cl₂ + H₂O → hydrochloric acid + hypochlorous acid

This initiates:

• Oxidative injury
• Chlorination reactions
• Free-radical formation
• Direct epithelial damage

The older concept that chlorine toxicity is simply due to formation of hydrochloric acid and hypochlorous acid is incomplete.

Modern understanding emphasizes:

Oxidative injury + epithelial disruption + inflammatory signaling

as major contributors to pulmonary damage.

Airway and Lung Injury

Chlorine causes:

Epithelial injury → increased permeability → inflammation → bronchoconstriction + alveolar-capillary leak

This can produce:

• Bronchospasm
• Airway edema
• Chemical pneumonitis
• Noncardiogenic pulmonary edema
• ARDS

The degree of water solubility means much of the gas is absorbed in the upper respiratory tract, but sufficiently high exposure reaches and injures distal bronchioles and alveoli.

Why Symptoms Can Worsen Later

Severe chlorine injury does not always peak immediately.

The sequence may be:

Exposure → irritation/cough → transient improvement → increasing dyspnea/hypoxemia → pulmonary edema

Pulmonary injury in symptomatic patients can progress for several hours after exposure.

Therefore:

A normal early chest radiograph does not exclude evolving serious lung injury.

Risk Factors for Severe Toxicity

Greater risk occurs with:

• High concentration
• Longer exposure
• Enclosed-space exposure
• Delayed escape
• Preexisting asthma
• COPD
• Other chronic pulmonary disease

Children may be especially vulnerable because:

• Smaller airway diameter
• Greater minute ventilation per kilogram
• Short stature may place them closer to heavier-than-air chlorine concentrations near ground level.

Clinical Features

Mild Exposure

Typical findings:

• Eye irritation
• Lacrimation
• Rhinorrhea
• Burning nose/throat
• Sore throat
• Cough
• Mild chest burning
• Headache

Symptoms usually begin rapidly.

Moderate Exposure

Possible findings:

• Persistent cough
• Chest tightness
• Dyspnea
• Wheezing
• Hoarseness
• Tachypnea
• Bronchospasm
• Hypoxemia

A patient may describe:

“Burning in the chest”

which is characteristic of significant irritant-gas exposure.

Severe Exposure

High-dose exposure can cause:

• Severe bronchospasm
• Upper-airway edema
• Stridor
• Hemoptysis
• Diffuse crackles
• Severe hypoxemia
• Noncardiogenic pulmonary edema
• ARDS
• Respiratory failure
• Cardiovascular collapse

Severe hypoxia can cause:

• Confusion
• Syncope
• Seizures
• Cardiac arrest

HEENT

Common findings include:

• Blepharospasm
• Conjunctival injection
• Tearing
• Nasal irritation
• Pharyngeal irritation

Severe exposure can cause:

• Corneal epithelial injury
• Corneal burns

Upper Airway

Warning findings include:

• Hoarseness
• Drooling
• Stridor
• Progressive respiratory distress
• Inability to manage secretions

Significant laryngeal edema can make later intubation difficult.

Therefore:

Progressive upper-airway obstruction → secure the airway early.

Pulmonary

Common respiratory findings include:

• Cough
• Wheezing
• Rhonchi
• Crackles
• Tachypnea

More severe toxicity:

• Hemoptysis
• Hypoxemia
• Pulmonary edema
• ARDS

Current systematic reviews find that the dominant clinical features of civilian chlorine exposures are cough and dyspnea; the majority recover completely, although severe exposures can be fatal.

Cardiovascular

Cardiac abnormalities are usually secondary to:

• Hypoxemia
• Severe pulmonary injury
• Physiologic stress

Possible findings:

• Tachycardia
• Initial hypertension
• Later hypotension
• Cardiovascular collapse in profound exposure

Chlorine does not characteristically cause a primary cardiotoxic dysrhythmia syndrome.

Neurologic

Mild:

• Headache
• Dizziness
• Lightheadedness

Severe:

• Confusion
• Syncope
• Seizures/coma secondary to major hypoxia

Marked altered consciousness should prompt consideration of:

• Severe hypoxemia
• Additional toxicant
• Trauma
• Alternative diagnosis

Acid–Base Effects

Massive inhalation can occasionally produce:

Hyperchloremic metabolic acidosis

although metabolic acidosis in critically ill patients may also reflect:

• Hypoxia
• Shock
• Lactate accumulation

Skin

Gas exposure usually causes mild irritation.

More concentrated exposure may cause:

• Burning
• Erythema
• Blistering
• Chemical burns

Liquefied chlorine

Contact with liquefied compressed chlorine can additionally produce:

Frostbite

because of rapid evaporative cooling.

Ocular Exposure

Possible findings:

• Immediate burning
• Tearing
• Blepharospasm
• Conjunctivitis

Severe exposure:

• Corneal epithelial injury
• Corneal burn

Persistent:

• Pain
• Photophobia
• Visual change

requires formal ophthalmologic evaluation.

Household Bleach Ingestion

Low-concentration household sodium hypochlorite exposures are generally much less dangerous than concentrated industrial hypochlorite.

Small accidental swallows commonly cause:

• Oral irritation
• Nausea
• Vomiting
• Abdominal discomfort

More concentrated products can cause:

True caustic injury

including:

• Odynophagia
• Dysphagia
• Esophagitis
• Gastric injury
• Hematemesis
• Perforation in extreme cases

Modern household products vary in concentration; some are more concentrated than the traditional 3–6% bleach formulations.

Diagnosis

Diagnosis of chlorine inhalation is primarily:

Clinical

based on:

• Exposure history
• Characteristic odor/event
• Immediate mucosal irritation
• Respiratory findings

There is no clinically useful:

• Serum chlorine concentration
• Urinary chlorine assay

for routine emergency diagnosis.

Differential Diagnosis

Other pulmonary irritant exposures include:

• Ammonia
• Bromine
• Phosgene
• Nitrogen dioxide
• Sulfur dioxide
• Acrolein
• Smoke inhalation
• Chloramine gases

Also consider:

• Asthma exacerbation
• Anaphylaxis
• Pneumonia
• Pulmonary edema
• Aspiration

In structure-fire patients, also consider:

• Carbon monoxide
• Cyanide
• Multiple combustion products

Investigations

Mild Exposure

No laboratory testing is usually needed when symptoms:

• Are minor
• Resolve quickly
• Have a reliable low-level exposure history

Respiratory Evaluation

For significant respiratory symptoms obtain:

• Continuous pulse oximetry
• Serial lung examination

Consider:

• Blood gas
• Chest radiograph

for:

• Persistent dyspnea
• Hypoxemia
• Severe cough
• Crackles
• Hemoptysis
• Significant exposure

Chest Radiograph

Possible abnormalities include:

• Diffuse infiltrates
• Pulmonary edema
• Patchy chemical pneumonitis

However:

An early normal CXR does not exclude later pulmonary edema.

Clinical observation remains important.

Laboratory Tests

Moderate/severe exposures may warrant:

• Electrolytes
• Bicarbonate
• BUN
• Creatinine
• Glucose

For critical illness:

• Blood gas
• Lactate

CBC may be obtained when:

• Serious pulmonary injury
• Infection differential
• Critical illness

is present.

Pulmonary Function

Peak expiratory flow or spirometry can be useful in patients with:

• Bronchospasm
• Persistent respiratory symptoms
• Suspected RADS

but is not required in every acute exposure.

Bronchoscopy

Routine bronchoscopy is not necessary.

It may be considered for:

• Severe airway injury
• Persistent unexplained respiratory failure
• Suspected inhalational mucosal injury
• Airway obstruction requiring direct assessment

Treatment

1. Rescuer Safety

Do not enter a high-concentration chlorine environment without appropriate respiratory protection.

For unknown or dangerous concentrations:

Positive-pressure self-contained breathing apparatus (SCBA) is required.

Because chlorine is heavier than air:

Move upwind and to higher ground when practical.

2. Remove From Exposure

The single most important immediate intervention is:

Fresh air

Move the patient rapidly away from the contaminated environment.

A patient exposed only to chlorine gas without contaminated clothing or liquid chemical generally does not remain a significant secondary contamination hazard once removed from the source.

3. Airway

Assess for:

• Hoarseness
• Stridor
• Progressive edema
• Severe respiratory distress
• Altered consciousness

If airway compromise is evolving:

Intubate early

Use direct visualization/video laryngoscopy or other controlled techniques.

Severe edema can make delayed airway management extremely difficult.

4. Oxygen

Give supplemental oxygen for:

• Dyspnea
• Hypoxemia
• Significant respiratory distress

Patients with severe toxicity may require:

• High-flow oxygen
• Noninvasive support in carefully selected cases
• Endotracheal intubation/mechanical ventilation

Current systematic evidence supports exposure cessation and oxygen as core supportive therapies.

5. Bronchospasm

Inhaled β₂ agonists are standard treatment.

Examples:

• Albuterol
• Salbutamol

Ipratropium may be added for severe bronchospasm according to standard obstructive-airway management.

Systematic review evidence supports inhaled bronchodilators as standard therapy for chlorine-associated bronchoconstriction.

6. Pulmonary Edema / ARDS

Treat according to standard supportive critical-care principles:

• Oxygen
• Appropriate PEEP
• Lung-protective ventilation
• Conservative fluid strategy once shock is corrected

Chlorine-induced pulmonary edema is generally:

Noncardiogenic

so routine diuretics are not an antidote and should not be automatically administered unless there is an independent indication.

7. Corticosteroids

Important modernization

The older text recommends prednisone or methylprednisolone rather broadly after chlorine inhalation.

Modern evidence does not support routine corticosteroids for every chlorine exposure.

Human studies are limited and confounded because steroids are usually administered together with:

• Oxygen
• Bronchodilators
• Other therapies

Systematic reviews conclude that the independent benefit of corticosteroids remains uncertain.

Reasonable use

Steroids may be considered when there is:

• Significant asthma/reactive-airway exacerbation
• Persistent bronchospasm consistent with usual asthma indications

But:

Routine prophylactic steroids to prevent pulmonary edema or fibrosis are not evidence-based.

Nebulized Sodium Bicarbonate

This requires correction from the older text.

The older chapter states that sodium bicarbonate is ineffective and may itself cause chemical pneumonitis.

Current evidence is more nuanced.

A randomized human study using nebulized bicarbonate in chlorine-induced RADS found modest improvement in FEV₁ at 2 and 4 hours, but no evidence that it prevents major outcomes such as:

• Intubation
• Pulmonary edema
• Long-term lung disease
• Mortality

Therefore:

Nebulized sodium bicarbonate is not established first-line therapy.

It may be considered as an adjunct in selected symptomatic patients after consultation with a poison center/medical toxicologist.

It should never replace:

• Fresh air
• Oxygen
• Bronchodilators
• Airway management

No Specific Antidote

There is no antidote for chlorine gas toxicity.

Current CDC and NIOSH guidance emphasizes supportive respiratory care.

Skin Decontamination

For liquid/chlorine-generating chemical contamination:

• Remove contaminated clothing
• Rinse exposed skin/hair with copious tepid water
• Wash with mild soap
• Rinse again

Patients exposed only to gas and without skin/eye irritation usually do not require full decontamination.

Liquefied Chlorine Frostbite

If liquefied chlorine causes frostbite:

• Do not rub
• Remove constricting items
• Rewarm in water approximately 40–42°C

until tissue perfusion returns.

Eye Decontamination

Immediately:

Irrigate with copious water or saline for at least 15 minutes

Remove contact lenses when easily possible.

Then assess:

• Visual acuity
• Cornea

Persistent:

• Pain
• Photophobia
• Vision change
• Corneal injury

requires urgent ophthalmology assessment.

Hypochlorite Ingestion

Do NOT induce vomiting

Never induce emesis.

This risks:

• Re-exposure of the esophagus
• Aspiration

CDC/ATSDR guidance specifically advises against induced vomiting.

Activated Charcoal

Do not routinely give activated charcoal for hypochlorite ingestion.

It provides little benefit and may:

• Promote vomiting
• Increase aspiration risk
• Complicate subsequent endoscopic assessment

Gastric Lavage / Aspiration

The older recommendation for nasogastric aspiration after a large ingestion is not modern routine practice.

Routine gastric lavage is not recommended.

Potential complications include:

• Perforation
• Aspiration
• Additional mucosal trauma

ATSDR specifically notes that gastric lavage is generally not recommended for hypochlorite ingestion.

Oral Dilution After Bleach Ingestion

Older guidance recommends 4–8 oz of milk or water.

Modern practice is more conservative.

After a small recent lower-concentration household bleach exposure, an alert patient who can swallow normally may rinse the mouth and take a small amount of water.

However:

Do not force oral dilution in a symptomatic patient or significant caustic ingestion.

Avoid oral fluids with:

• Drooling
• Dysphagia
• Repeated vomiting
• Airway compromise
• Severe pain
• Suspected perforation

The patient’s airway and GI injury assessment take priority.

Endoscopy After Hypochlorite Ingestion

Routine endoscopy is unnecessary after an uncomplicated small household bleach exposure.

Consider GI/endoscopic evaluation with:

• Concentrated product
• Intentional large ingestion
• Persistent vomiting
• Drooling
• Odynophagia/dysphagia
• Chest or abdominal pain
• Hematemesis
• Other evidence of caustic injury

Severe hypochlorite ingestion should be managed according to general caustic-ingestion principles.

Antibiotics

Routine prophylactic antibiotics have no established role after isolated chlorine inhalation.

Use antibiotics only when there is evidence of:

• Bacterial pneumonia
• Aspiration infection
• Another infectious process

Chemical pneumonitis alone is not an indication for antibiotics.

Monitoring

Symptomatic patients should be monitored for:

• Respiratory rate
• Oxygen saturation
• Work of breathing
• Bronchospasm
• Progression of chest symptoms

Continuous cardiac monitoring is reasonable in:

• Severe hypoxemia
• Critical illness
• Significant coexposures

Observation

The older concept of a rigid observation interval is less useful than clinical severity.

Minor exposure

Patients with only:

• Transient throat/eye irritation
• Minimal cough
• Normal oxygenation

who become fully asymptomatic may often be discharged after an appropriate period of observation.

ATSDR notes that minor symptoms commonly resolve within about an hour.

Significant exposure

Patients with:

• Persistent cough
• Dyspnea
• Chest tightness
• Wheezing
• Hypoxemia
• High-concentration exposure

should be observed longer because:

Pulmonary injury may progress over several hours.

Admission

Hospital admission is appropriate for:

• Persistent dyspnea
• Severe/persistent cough
• Significant bronchospasm
• Hypoxemia
• Hemoptysis
• Upper-airway edema
• Stridor
• Abnormal CXR with pulmonary injury
• Noncardiogenic pulmonary edema
• Significant ocular/skin burns
• Significant caustic hypochlorite ingestion

ICU care is appropriate for:

• Progressive hypoxemia
• Respiratory failure
• ARDS
• Mechanical ventilation
• Hemodynamic instability

Discharge

Discharge requires:

• Resolution or clear improvement of respiratory symptoms
• Normal/reassuring oxygenation
• No progressive airway findings
• Ability to ambulate without significant dyspnea
• Reliable return precautions

Patients should return urgently for:

• Increasing cough
• Wheezing
• Dyspnea
• Chest pain
• Hemoptysis

because deterioration can occur after apparent early improvement.

Long-Term Pulmonary Effects

Most patients recover completely.

Systematic civilian data reported full recovery in approximately 90% of cases with available follow-up.

However, significant exposure can produce:

Reactive Airways Dysfunction Syndrome (RADS)

which is irritant-induced asthma developing after a major exposure.

Symptoms may include:

• Persistent cough
• Wheezing
• Exercise intolerance
• Airway hyperreactivity

ATSDR reports that chlorine-induced RADS has occasionally persisted for years.

Pulmonary Fibrosis

Older sources often emphasize interstitial fibrosis as a common sequela.

Persistent structural lung disease can occur after severe exposure, but:

Permanent pulmonary fibrosis is not the expected outcome of most chlorine exposures.

Most patients recover substantially, while persistent airway hyperreactivity/RADS is a more clinically recognized long-term syndrome.

Pregnancy

The older claim that concentrated hypochlorite is clearly teratogenic should not be directly extrapolated to human chlorine-gas poisoning.

Available data are insufficient to establish a specific human teratogenic syndrome from chlorine exposure.

In significant maternal poisoning, the main fetal threats are likely secondary to:

• Maternal hypoxemia
• Respiratory failure
• Hemodynamic instability

Therefore:

Maternal airway and oxygenation are the priorities.

Do not withhold appropriate oxygen, bronchodilators, airway support, or critical care because of pregnancy.

Occupational Exposure Standards – Chlorine

The old workplace values are outdated.

Current NIOSH

REL: ceiling 0.5 ppm (1.45 mg/m³) over 15 minutes

Current OSHA

PEL: ceiling 1 ppm (3 mg/m³)

NIOSH IDLH

10 ppm

Important correction

The older chapter states:

• OSHA TWA 0.5 ppm
• OSHA STEL 1 ppm
• IDLH 25 ppm

Those values should not be used.

Current federal OSHA is a 1-ppm ceiling, while current NIOSH IDLH is 10 ppm.

Chlorine Dioxide Is a Different Chemical

Chlorine dioxide (ClO₂) is not interchangeable with chlorine gas.

Current occupational values:

• NIOSH REL TWA: 0.1 ppm
• NIOSH STEL: 0.3 ppm
• OSHA PEL TWA: 0.1 ppm
• NIOSH IDLH: 5 ppm

Chlorine Trifluoride Is Also Distinct

Chlorine trifluoride (ClF₃) is a highly reactive fluorinating agent with additional extreme chemical hazards.

Current values:

• NIOSH REL ceiling: 0.1 ppm
• OSHA PEL ceiling: 0.1 ppm
• NIOSH IDLH: 12 ppm

It should not be managed as simply another formulation of ordinary chlorine gas.

Important Pitfalls

1. Confusing chlorine gas with bleach

Bleach contains hypochlorite.

The most dangerous household inhalational exposures frequently occur when bleach reacts with another cleaner.

2. Saying bleach + ammonia produces ordinary chlorine

More precisely:

Bleach + ammonia → chloramines

whereas:

Bleach + acid → chlorine gas

3. Trusting an early normal chest radiograph

Pulmonary edema may develop later.

Normal early CXR ≠ safe after a significant exposure.

4. Sending home a persistently symptomatic patient

Persistent:

• Dyspnea
• Severe cough
• Chest tightness

warrants continued observation/admission because lung injury can progress for several hours.

5. Giving steroids routinely

Evidence for corticosteroids specifically preventing chlorine lung injury is weak.

Use primarily when there is a separate clinical indication such as significant reactive-airway/asthma physiology.

6. Calling nebulized bicarbonate useless

Evidence shows a possible modest short-term spirometric benefit, but not proven major outcome benefit.

Therefore:

Possible adjunct—not standard antidote.

7. Forgetting bronchodilators

Bronchospasm is common and:

Inhaled β₂ agonists are standard therapy.

8. Treating pulmonary edema automatically with diuretics

Chlorine pulmonary edema is typically:

Permeability/noncardiogenic edema

Treat primarily with respiratory support.

9. Giving charcoal after bleach ingestion

Activated charcoal is not recommended for hypochlorite ingestion.

10. Performing gastric lavage after concentrated bleach ingestion

Routine lavage is inappropriate and may worsen caustic injury.

11. Missing airway edema

Hoarseness and stridor after major exposure may precede severe airway compromise.

Intubate before edema makes intubation impossible.

12. Ignoring low-lying chlorine accumulation

Chlorine is approximately 2.5 times heavier than air.

Children and incapacitated individuals near floor level can receive greater exposure.

13. Assuming the patient contaminates the ED indefinitely

After gas-only exposure, patients generally pose little secondary contamination risk once removed to clean air.

Liquid chemical contamination is different and requires decontamination.

14. Using the old IDLH

Current:

NIOSH IDLH = 10 ppm

not 25 ppm.

High-Yield Toxicology Pearls

Chlorine = water-soluble pulmonary irritant gas

Think:

Bleach/industrial chlorine exposure → burning eyes/throat + cough + bronchospasm → delayed pulmonary edema in severe cases

Key points:

• Chlorine is:
• Greenish-yellow
• Pungent
• Heavier than air
• Main route of serious exposure: inhalation
• Mechanism:
• Reaction with water
• Hypochlorous/hydrochloric acid formation
• Oxidative epithelial injury
• Main targets:
• Eyes
• Upper airway
• Bronchi
• Lungs
• Household chemistry:
• Bleach + acid → chlorine gas
• Bleach + ammonia → chloramines
• Mild exposure:
• Eye/throat irritation
• Cough
• Moderate:
• Chest tightness
• Wheezing
• Bronchospasm
• Severe:
• Stridor
• Hemoptysis
• Hypoxemia
• Noncardiogenic pulmonary edema
• ARDS
• Symptoms may worsen for several hours
• Normal early CXR does not exclude serious injury
• Treatment:
• Fresh air
• Oxygen when symptomatic/hypoxemic
• Inhaled β₂ agonists for bronchospasm
• Early airway control if progressive edema
• Lung-protective ventilation for ARDS
• Routine corticosteroids are not proven
• Nebulized sodium bicarbonate:
• May modestly improve short-term FEV₁
• Not established first-line therapy
• Consider only as an adjunct
• No specific antidote
• Eye exposure:
• Immediate irrigation ≥15 min
• Liquid chlorine can cause frostbite
• Small household-bleach swallows usually cause GI irritation
• Concentrated hypochlorite can cause caustic esophagogastric injury
• Do not induce vomiting
• Do not give routine activated charcoal
• Routine gastric lavage is not recommended
• Significant bleach ingestion + dysphagia/hematemesis → evaluate as caustic ingestion
• Major long-term complication:
• RADS / irritant-induced asthma
• Occupational chlorine limits:
• NIOSH ceiling: 0.5 ppm / 15 min
• OSHA ceiling: 1 ppm
• NIOSH IDLH: 10 ppm
• Chlorine dioxide and chlorine trifluoride are distinct chemicals with separate exposure limits and hazards