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Introduction

A vast number of compounds produce irritant effects when inhaled in the gaseous form. The most common source of exposure to irritant gases is industry, but significant exposures may occur in a variety of circumstances, such as after mixing cleaning agents at home, with smoke inhalation in structural fires, or after highway or railroad tanker spills.

Mechanism of Toxicity

Irritant gases often are divided into two major groups on the basis of their water solubility (Table II-29).

  1. Highly soluble gases (eg, ammonia and chlorine) react with water in the upper respiratory tract and moist mucous membranes to rapidly produce their primary effects.
  2. Less soluble gases (eg, phosgene and nitrogen dioxide) do not react with the upper respiratory tract or mucous membranes and are inhaled more deeply into the lower respiratory tract producing delayed onset of pulmonary toxicity.
TABLE II-29. IRRITANT TOXIC GASES
GasTLVa (ppm)IDLHb (ppm)
High water solubility
Ammonia25300
ChloraminecN/AN/A
Formaldehyde0.120
Hydrogen chloride2(C)50
Hydrogen fluoride2(C)30
Nitric acid225
Sulfur dioxide0.25(S)100
Moderate water solubility
Acrolein0.1(C)2
Chlorine0.110
Fluorine0.125
Low water solubility
Nitric oxide25100
Nitrogen dioxide0.213
Ozone0.2d5
Phosgene0.12

aThreshold limit value, ACGIH-recommended exposure limit as an 8-hour time-weighted average for a 40-hour workweek (TLV-TWA). “(C)” indicates ceiling limit, which should not be exceeded at any time (TLV-C). “(S)” indicates short-term exposure limit.

bAir level considered immediately dangerous to life or health (IDLH), defined as the maximum air concentration from which one could reasonably escape within 30 minutes without any escape-impairing symptoms or any irreversible health effects.

cChloramine is formed when chlorine or hypochlorite is added to water containing ammonia. It is usually a mixture of mono-, di-, and trichloramines. (N/A: TLV and IDLH are not established.)

dFor exposure of no more than 2 hours (all workloads).

Toxic Dose

The toxic dose varies with the properties of the gas. Table II-29 illustrates the workplace exposure limits (TLV-TWA) and the levels immediately dangerous to life or health (IDLH) for several common irritant gases.

Clinical Presentation

All these gases may produce irritant effects in the upper and/or lower respiratory tract, but warning properties and the onset and location of primary symptoms depend largely on the water solubility of the gas and the concentration of exposure.

  1. Highly soluble gases. Because of the good warning properties (upper respiratory tract irritation) of highly soluble gases, voluntary prolonged exposure to even low concentrations is unlikely.
    1. Low-level exposure causes rapid onset of mucous membrane and upper respiratory tract irritation; conjunctivitis, rhinitis, skin erythema and burns, sore throat, cough, wheezing, and hoarseness are common.
    2. With high-level exposure, laryngeal edema, tracheobronchitis, and abrupt airway obstruction may occur. Irritation of the lower respiratory tract and lung parenchyma causes tracheobronchial mucosal sloughing, chemical pneumonitis, and noncardiogenic pulmonary edema.
  2. Less soluble gases. Because of poor warning properties owing to minimal upper respiratory tract effects, prolonged exposure to moderate levels of these gases often occurs; therefore, chemical pneumonitis and pulmonary edema are more common. The onset of pulmonary edema may be delayed up to 12-24 hours or even longer.
  3. Sequelae. Although most patients who suffer toxic inhalation injury recover without any permanent impairment, bronchiectasis, bronchiolitis obliterans, persistent asthma, and pulmonary fibrosis can occur.

Diagnosis

Is based on a history of exposure and the presence of typical irritant upper or lower respiratory effect. Arterial blood gases and chest imaging may reveal early evidence of chemical pneumonitis or pulmonary edema. Whereas highly soluble gases have good warning properties and the diagnosis is not difficult, less soluble gases may produce minimal symptoms shortly after exposure; therefore, a high index of suspicion and repeated examinations are required.

  1. Specific levels. There are no specific blood or serum levels available.
  2. Other useful laboratory studies include arterial blood gases or oximetry, chest imaging, spirometry, and peak expiratory flow measurement.

Treatment

  1. Emergency and supportive measures
    1. Immediately assess the airway; hoarseness or stridor suggests laryngeal edema, which necessitates direct laryngoscopy and endotracheal intubation if swelling is present. Assist ventilation if necessary (p 4-8).
    2. Give supplemental oxygen, and treat bronchospasm with aerosolized bronchodilators.
    3. Monitor arterial blood gases or oximetry, chest radiographs, and pulmonary function. Treat pulmonary edema if it occurs.
    4. For victims of smoke inhalation, consider the possibility of concurrent intoxication by carbon monoxide or cyanide.
  2. Specific drugs and antidotes. Generally, there is no specific antidote for these gases.
  3. Decontamination. Remove the victim from exposure and give supplemental oxygen if available. Rescuers should take care to avoid personal exposure; in most cases, self-contained breathing apparatus should be worn.
  4. Enhanced elimination. There is no role for enhanced elimination.