Gas toxicity

Poisoning with toxic gases most commonly occurs in the household and industrial workplace setting with potentially life-threatening consequences. Only the most common sources of gas poisoning are discussed here (with the exception of vinyl chloride, which is discussed under “Polyvinyl Chloride” in “Organic solvent toxicity”). Ammonia is a gas that occurs naturally in the human body but also has a variety of industrial and household uses (e.g., cleaning products); exposure can lead to cough, eye irritation, and mucous membrane and skin burns. Hydrogen sulfide can be naturally found in hot springs and volcanos but also has a variety of industrial and household uses (e.g., cleaning products); exposure can lead to conjunctivitis, headache, fatigue, and, in high concentrations, to life-threatening cardiovascular events. Chlorine is used as a disinfectant as well as cleaning and bleaching agent; exposure can lead to respiratory distress and irritation of the mucous membranes and the autonomic nervous system. Nitrogen oxides develop mainly in the process of organic matter decomposition and engine exhausts; exposure can lead to cough, nausea, and, eventually, to chemical pneumonia and bronchiolitis obliterans. Phosgene occurs in pesticides and plastic production processes; exposure can lead to lacrimation, cough, and respiratory distress. Phosphine is a common component of pesticides; exposure can lead to nausea, paresthesis, respiratory distress, and cardiac shock. Ozone is a natural component of the atmosphere that is toxic at high concentrations, e.g., due to environmental pollution and chemical water purification; exposure can cause sore throat and cough, potentially exacerbating respiratory conditions such as asthma and COPD. Hydrofluoric acid occurs in the production of aluminum and in cleaning products; exposure can lead to life-threatening skin, eye, and mucous membrane burns. Radon is a radioactive gas that occurs naturally in the ground and may accumulate in confined spaces; it is one of the main causes of lung cancer in nonsmokers. In the event of exposure to any toxic gas, the source of toxic gas should be addressed and affected individuals removed from the area immediately; clothing should be decontaminated if necessary. O₂ administration and supportive measures (e.g., support of airway, breathing, or circulation) should be provided as necessary depending on the situation.

• Characteristics: colorless, irritant, pungent smell, highly water-soluble (creation of ions: NH⁺)
• Sources of exposure
  • Industry: e.g., gas leaks, soil fertilization, decaying manure on animal farms
  • Household: e.g., cleaning products
  • Endogenous: hyperammonemia due to, e.g., liver disease, urea cycle enzyme defects, or intestinal infection with ammonia-producing bacteria

• Pathophysiology: highly exothermic reaction of anhydrous ammonia with water molecules in human tissue → thermal injury of the affected tissue
• Clinical features
  • Low-dose exposure: rhinorrhea, scratchy throat, chest tightness, cough, dyspnea, eye irritation
  • Chronic or high-dose exposure: full-thickness skin burns (especially of the face and mouth), corneal damage
  • Ingestion of ammonia solutions
    • Low-dose exposure: oropharyngeal, epigastric, and/or retrosternal pain
    • Chronic or high-dose exposure: abdominal pain, viscus perforation
• Diagnostics
  • Laboratory studies
    • General: ↑ serum lactate, ↑ retention parameters, ↑ liver enzymes
    • Specific: serum ammonia levels
  • Imaging
    • Inhalation: chest x-ray (shows pulmonary edema), bronchoscopy (in cases of prolonged or severe exposure)
    • Ingestion: gastrointestinal endoscopy

References:^[1]

• Characteristics: highly flammable, colorless, rotten-egg smell
• Sources of exposure
  • Industry: e.g., food processing, paper mills
  • Household: e.g. cleaning products
  • Natural environment: e.g., swamps, hot springs, volcanoes
• Pathophysiology: inhibition of mitochondrial cytochrome oxidase → irritation of the mucous membranes, hemorrhagic pulmonary edema, neurotoxic effects
• Clinical features
  • Chronic low-dose exposure
    • Irritation of mucous membranes (e.g., conjunctivitis, pharyngitis, greenish-gray line on gingiva)
    • Headache, dizziness
    • Fatigue, insomnia
  • High-dose exposure
    • Agitation
    • Bradycardia, nausea, vomiting
    • Dyspnea, cough, hemoptysis, pulmonary edema
• Diagnostics
  • Laboratory studies
    • ↑ Lactate
    • ABG: metabolic acidosis
  • Imaging: chest x-ray shows pulmonary edema
• Management: IV sodium nitrite
• Complications
  • Acute myocardial infarction
  • Cardiopulmonary arrest
  • Loss of consciousness
  • Seizures
  • Acute respiratory distress syndrome
  • Delayed neuropsychiatric sequelae (e.g., impaired cognitive function, paresis)

References:^[2]

• Characteristics: green-yellow color, sharp smell, water-soluble
• Sources of exposure
  • Industry: e.g., bleaching paper, textiles, paint
  • Household: e.g., cleaning products, pool disinfectant
• Pathophysiology: dissolution in water → formation of hypochlorous/hydrochloric acid and free oxygen radicals → irritation of mucosa (especially in the respiratory tract and the eyes)
• Clinical features
  • Acute low-dose exposure: lacrimation, nose and throat irritation, excessive salivation
  • Acute high-dose exposure
    • Dyspnea, tachypnea, tachycardia, cyanosis, intercostal retractions, cough, chest pain
    • Dizziness, headache
    • Lacrimation, abdominal discomfort, nausea, vomiting
  • Chronic low-dose exposure: chest pain, cough, hemoptysis, sore throat
• Diagnostics
  • Laboratory studies
    • ↑ Retention parameters
    • ABG: hypoxemia, metabolic acidosis
  • Imaging
    • Chest x-ray
    • Laryngoscopy
    • Bronchoscopy
• Management: supportive treatment depending on the patient's clinical presentation (e.g., support of airway, breathing, or circulation)
• Complications: chemical pneumonitis

References:^[3]

• Definition: any gaseous oxide containing nitrogen; mainly NO and NO₂
• Characteristics
  • Low water solubility
  • NO is a colorless and odorless gas, while NO₂ is a reddish-brown gas with a pungent odor.
• Sources of exposure
  • Industry: engine exhausts, electric arc welding
  • Natural environment: decomposition of silage (silo filler's disease); can be prevented by personal protective equipment and workplace controls (e.g., adequate ventilation, not entering the silo until 3 weeks after filling)
• Pathophysiology
  • NO comes into contact with water in the lungs → production of nitric acid → irritation/burning of distal bronchi and surrounding alveoli
  • NO₂ → formation of toxic free radicals → alveolar damage
• Clinical features
  • NO
    • Early symptoms: cough, nausea
    • Late symptoms (days after exposure): chemical pneumonitis (hypoxemia, pulmonary edema), bronchiolitis obliterans
  • NO₂
    • Phase 1: dyspnea, central chest pain, fever, weakness
    • Phase 2: fewer to no symptoms
    • Phase 3: bronchiolitis obliterans
• Diagnostics
  • Laboratory studies
    • ↑ Methemoglobin levels
    • ABG: hypoxemia
  • Imaging: chest x-ray
  • Pulmonary function tests
• Management
  • Minimum 24 hour monitoring (delayed development of chemical pneumonitis is possible)
  • Treatment of chemical pneumonitis
    • Bronchodilators
    • Inhaled corticosteroids
    • Mechanical ventilation
• Complications
  • ARDS
  • Sepsis
  • Acute heart failure

References:^[4]

• Characteristics: colorless, smell of hay
• Sources of exposure
  • Industry: e.g., plastic production, pesticides
  • Household: e.g., paint removers, dry-cleaning agents
• Pathophysiology: acylation of proteins and formation of hydrochloric acid → inhibition of enzymes and corrosive injury
• Clinical features
  • Irritation of mucous membranes: cough, lacrimation
  • Pulmonary edema, cyanosis, dyspnea
• Diagnostics
  • Laboratory studies: ABG shows hypoxemia.
  • Imaging: Chest x-ray shows pulmonary edema.
• Management
  • Removal from exposure
  • Supportive treatment depending on the patient's clinical presentation (e.g., support of airway, breathing, or circulation)

Reference:^[5]

• Characteristics: colorless, odorless
• Sources of exposure: fumigants in pest control
• Pathophysiology: formation of reactive oxygen species → inhibition of enzymes and DNA damage
• Clinical features
  • Dysrhythmia, cardiac shock
  • Nausea, vomiting, tremor, paresthesia
  • Dyspnea, chest pain, ARDS
• Diagnostics
  • Laboratory studies: ABG shows metabolic acidosis
  • Imaging: Chest x-ray shows diffuse infiltrates.
• Management
  • Melatonin (antioxidant)
  • TNF-α
  • Supportive treatment (e.g., support of airway, breathing, or circulation) depending on the patient's clinical presentation

Reference:^[6]

• Characteristics: bluish, odorless
• Sources of exposure
  • Industry
    • Ground-level ozone: smog (e.g., exhaust gases, fossil fuel burning), industrial processes (e.g., water purification, bleaching)
    • Iatrogenic: overexposure from ozone therapy
  • Natural environment: atmospheric ozone
• Pathophysiology: oxidation of biomolecules (e.g., antioxidants, proteins, carbohydrates) → oxidative damage → inflammatory response
• Clinical features
  • Irritation of the mucous membranes: sore throat
  • Dyspnea, cough, chest pain
• Diagnostics
  • Laboratory: ABG shows hypoxemia.
  • Imaging: Chest x-ray may show multiple opacities.
  • Pulmonary function testing: ↓ lung function
• Management: Budenoside

References:^[7]

• Characteristics: colorless, strong irritating odor
• Sources of exposure
  • Industry: e.g., etching microchips, aluminum production
  • Household: e.g., cleaning products
• Pathophysiology: hydrogen fluoride dissociates into hydrogen cations and fluoride anions → corrosive burning and cytotoxicity of affected tissue
• Clinical features
  • Topical: irritation/corrosive burning of mucous membranes (e.g., sore throat, running nose, ocular lesions), skin, and eyes
  • Systemic
    • Myalgia, fever
    • Dizziness, headache
    • Dyspnea, cyanosis
    • Hypertension
    • Arrhythmias
• Diagnostics
  • Laboratory studies
    • Electrolytes: ↓ Ca²⁺ , ↓ Mg²⁺, ↑ K⁺
    • ABG: metabolic acidosis
  • Imaging: Chest x-ray shows pulmonary edema and/or diffuse infiltrative opacities.
• Management
  • In case of skin contact: rinse mucous membranes and skin with cold, running water (at least 30 min)
  • Calcium gluconate (antidote)

Reference:^[8]

• Characteristics: highly radioactive, colorless, odorless
• Sources of exposure: natural environment
  • Radon is produced by the radioactive decay of radium-226, which occurs naturally in rock and soil.
  • May accumulate to hazardous levels in basements and other confined spaces within the home
• Pathophysiology: emission of α-, β-, and γ-particles, and x-rays → cytotoxicity and DNA damage
• Clinical features
  • Acute exposure: no direct symptoms
  • Repeated exposure: lung cancer
  • For further information, see “Clinical features of lung cancer.”
• Diagnostics: For further information, see “Diagnostics” in “Lung cancer.”
• Treatment: For further information, see “Treatment” in “Lung cancer.”
• Prevention
  • Suctioning radon from rooms and basements (e.g., soil suctioning)
  • Ventilation of rooms and basements
  • Sealing basement cracks

Reference:^[9]