Acute inhalation injury is a common problem that is responsible for 4.9% of workplace deaths. Gas solubility and chemical reactivity are the major explanation for the site of action and severity of a toxic inhalation. Corrosive irritant gases such as ammonia, sulfur dioxide, or methyl isocyanate produce intense upper airway symptoms including severe coughing, substernal burning, burning in the nose and throat, as well as conjunctivitis, and often superficial burning of the facial skin. Intense eye, nasal, and upper airway physical findings and symptoms suggest a severe exposure and the possibility of lower airway damage and the subsequent development of pulmonary edema. Patients with intense upper airway signs and symptoms are also at risk for laryngeal edema and upper airway compromise. The estimation of the severity of exposure is determined not only by duration of exposure and gas concentration but also by gas reactivity and water solubility. Other factors include gas density and the height of the patient, gas temperature, breathing pattern, oronasal versus mouth breathing, and conditions that affect breathing pattern, such as nasal congestion, coughing, preexisting asthma, or chronic obstructive pulmonary disease. Host factors such as orthopedic problems, tripping, or falling may prevent quick evacuation from the area of exposure. The long-term effects of an acute toxic inhalation include chronic bronchitis, bronchiectasis, bronchiolitis obliterans, bronchostenosis, reactive airways dysfunction syndrome, obstructive and restrictive disease, as well as an isolated residual volume. Management for a toxic inhalation is primarily supportive, but treatment strategies vary with specific agents on the basis of the propensity of the toxic inhalant to cause bronchiolitis obliterans and airway damage as well as pulmonary edema. Gases that are chemical asphyxiants require agent-specific therapy.