A. Inhalational injuries may occur due to workplace exposures, natural disasters, or terrorist attacks and result in a variety of syndromes based on the chemical and physical properties of the toxicant involved and the intensity and duration of exposure.

B. Agents may be inhaled as gases, vapors, dust, fumes, or smoke.

C. Disease is caused by asphyxia, direct toxicity, or systemic reactions.

1. Simple asphyxiants include carbon dioxide (CO₂), methane, nitrogen (N₂), natural gas, propane, and acetylene.

2. Chemical asphyxiants are present in the atmosphere in minute amounts or are released by manufacturing processes or combustion; they asphyxiate at low concentration and include carbon monoxide (CO), hydrogen sulfide (H₂S), oxides of N₂, and hydrogen cyanide (HCN).

1. CO and CO₂, the most common asphyxiants, accumulate in sealed or poorly ventilated areas. They are generated during combustion of carbon-containing fuel.

2. HCN is used as inorganic salt in metallurgy, electroplating, and photo processing and in the combustion of N₂-containing polymers.

1. Simple asphyxiants displace or dilute ambient oxygen (O₂) causing tissue hypoxia; chemical asphyxiants interfere directly with O₂ uptake, transport, or utilization.

2. The affinity of CO for hemoglobin is 240 times that of O₂. The formation of carboxyhemoglobin (COHgb) causes a reduction in the total O₂-carrying capacity of the blood, a left shift of the oxyhemoglobin dissociation curve, and an increased affinity for O₂ at the remaining binding sites. Because of the increased affinity of CO for fetal hemoglobin, infants and fetuses are at greater risk for poisoning.

3. The clinical effects of HCN and H₂S intoxications are directly related to inhibition of cellular respiration in the mitochondria and occur rapidly after inhalation.

1. Breathlessness, tachycardia, headache, fatigue, delirium, syncope, coma, and cardiac arrest may suggest exposure to asphyxiants; severity varies on duration of exposure and underlying health of the victim.

2. In CO poisoning, although arterial O₂ tension (PaO₂) is normal or near normal, measured O₂ saturation and content are reduced. Ordinary pulse oximetry is unable to distinguish which specific gas (CO vs. O₂) is bound to hemoglobin; therefore, the more specific co-oximetry is needed to measure COHgb levels. Signs and prognosis of acute poisoning correlate imprecisely with COHgb levels. Generally, levels <10% are usually not associated with symptoms; levels of 10% to 20% may be associated with headache, tinnitus, dizziness, nausea, and mild behavioral abnormalities; levels of 20% to 40% can present with coma and seizures; and levels >40% are associated with increased risk of cardiac arrest.

3. Both HCN and H₂S typically cause metabolic acidosis with an elevated anion gap, an elevated serum lactate, and a mixed venous O₂ saturation higher than normal.

1. The basic management for any asphyxiation scenario includes removal of the source, 100% O₂, and support of cardiorespiratory function.

2. O₂ is the major therapy for CO poisoning. It decreases the half-life of COHgb by competing with CO for hemoglobin binding sites. Patients with COHgb levels >25% (>20% if pregnant), loss of consciousness, and severe metabolic acidosis (pH < 7.10) or who have evidence of possible end-organ ischemia (e.g., electrocardiogram [ECG] changes, chest pain, altered mental status) are candidates for hyperbaric O₂ therapy (strength of recommendation is weak).

3. Treatment of HCN and H₂S is similar (see Section V). Sodium thiosulfate is not necessary for H₂S intoxication, however.

1. Various agents act as toxic irritants to the respiratory tract and cause mucosal edema, impaired mucociliary function, and pulmonary edema with high-concentration exposures.

2. Agents in this class include ammonia (NH₃ and ammonium hydroxide in solution), chlorine (Cl₂), phosgene (COCl₂, which hydrolyzes to form hydrochloric acid [HCl]), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), formaldehyde, cadmium, mercury, and the metal hydrides.

1. NH₃ is found in fertilizer production, chemical, plastic, and dye manufacture.

2. Cl₂ is used in the production of alkali bleaches and disinfectants and in paper and textile processing. Most exposures result from industrial spills and loss of containment during transportation.

3. Firefighters, welders, and paint strippers are exposed to heated chlorinated hydrocarbons, and COCl₂ is released in these settings. Because COCl₂ is less irritating to the eyes and mucous membranes than Cl₂ or HCl and may be inhaled for prolonged periods without discomfort, the risk of serious injury to the lower respiratory tract is greatly increased.

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