(See also Pulmonary Chemical Warfare Agents.)
Irritant gases are those which, when inhaled, dissolve in the water of the respiratory tract mucosa and cause an inflammatory response, usually due to the release of acidic or alkaline radicals. Irritant gas exposures predominantly affect the airways, causing tracheitis, bronchitis, and bronchiolitis. Other inhaled agents may be directly toxic (eg, cyanide, carbon monoxide) or cause harm simply by displacing O2 and causing asphyxia (eg, methane, carbon dioxide).
The effect of inhaling irritant gases depends on the extent and duration of exposure and on the specific agent. Chlorine, phosgene, sulfur dioxide, hydrogen chloride or sulfide, nitrogen dioxide, ozone, and ammonia are among the most important irritant gases. Hydrogen sulfide is also a potent cellular toxin, blocking the cytochrome system and inhibiting cellular respiration. A common exposure involves mixing household ammonia with cleansers containing bleach; the irritant gas chloramine is released.
Acute exposure to high concentrations of toxic gas over a short time is characteristic of industrial accidents resulting from a faulty valve or pump in a gas tank or occurring during gas transport. Many people may be exposed and affected. The release of methyl isocyanate from a chemical plant in Bhopal, India in 1984 killed > 2000 people.
Respiratory damage is related to the concentration of the gas and its solubility.
More water-soluble gases (eg, chlorine, ammonia, sulfur dioxide, hydrogen chloride) dissolve in the upper airway and immediately cause mucous membrane irritation, which may alert people to the need to escape the exposure. Permanent damage to the upper respiratory tract, distal airways, and lung parenchyma occurs only if escape from the gas source is impeded.
Less soluble gases (eg, nitrogen dioxide, phosgene, ozone) may not dissolve until they are well into the respiratory tract, often reaching the lower airways. These agents are less likely to cause early warning signs (phosgene in low concentrations has a pleasant odor), are more likely to cause severe bronchiolitis, and often have a lag of ≥ 12 h before symptoms of pulmonary edema develop.
The most serious immediate complication is acute respiratory distress syndrome (ARDS), which usually occurs within 24 h. Patients with significant lower airway involvement may develop bacterial infection.
Ten to 14 days after acute exposure to some agents (eg, ammonia, nitrogen oxides, sulfur dioxide, mercury), some patients develop bronchiolitis obliterans progressing to ARDS. Bronchiolitis obliterans with organized pneumonia can ensue when granulation tissue accumulates in the terminal airways and alveolar ducts during the body's reparative process. A minority of these patients develop late pulmonary fibrosis.
Symptoms and Signs
Soluble irritant gases cause severe burning and other manifestations of irritation of the eyes, nose, throat, trachea, and major bronchi. Marked cough, hemoptysis, wheezing, retching, and dyspnea are common. The upper airway may be obstructed by edema, secretions, or laryngospasm. Severity is generally dose-related. Nonsoluble gases cause fewer immediate symptoms but can cause dyspnea or cough.
Patients who develop ARDS have worsening dyspnea and increasing O2 requirements.
Diagnosis is usually obvious from the history. Patients should have a chest x-ray and pulse oximetry. Chest x-ray findings of patchy or confluent alveolar consolidation usually indicate pulmonary edema. Spirometry and lung volume testing are done. Obstructive abnormalities are most common, but restrictive abnormalities can predominate after exposure to high doses of chlorine.
CT is used to evaluate patients with late-developing symptoms. Those with bronchiolitis obliterans that progresses to respiratory failure manifest a pattern of bronchiolar thickening and a patchy mosaic of hyperinflation.
Most people recover fully, but some have persistent lung injury with reversible airway obstruction (reactive airways dysfunction syndrome) or restrictive abnormalities and pulmonary fibrosis; smokers may be at greater risk.
Management does not differ by specific inhaled agent but rather by symptoms. Patients should be moved into fresh air and given supplemental O2. Treatment is directed toward ensuring adequate oxygenation and alveolar ventilation. Bronchodilators and O2 therapy may suffice in less severe cases. Severe airflow obstruction is managed with inhaled racemic epinephrine, endotracheal intubation (see Tracheal Intubation) or tracheostomy, and mechanical ventilation. The efficacy of corticosteroid therapy (eg, prednisone 45 to 60 mg once/day for 1 to 2 wk) is unproved, but it is frequently used.
Because of the risk of ARDS, any patient with respiratory tract symptoms after toxic inhalation should be observed for 24 h.
After the acute phase has been managed, physicians must remain alert to the development of reactive airways dysfunction syndrome, bronchiolitis obliterans with or without organized pneumonia, pulmonary fibrosis, and delayed-onset ARDS.
Care in handling gases and chemicals is the most important preventive measure. The availability of adequate respiratory protection (eg, gas masks with a self-contained air supply) for rescuers is also very important; rescuers without protective gear who rush in to extricate a victim often succumb themselves.
Low-level continuous or intermittent exposure to irritant gases or chemical vapors may lead to chronic bronchitis, although the role of such exposure is especially difficult to substantiate in smokers.
Chronic inhalational exposure to some agents (eg, bis[chloromethyl]ether, certain metals) causes lung and other cancers (eg, liver angiosarcomas after vinyl chloride monomer exposure).
Last full review/revision May 2014 by Lee S. Newman, MD, MA
Content last modified May 2014