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Nitrogen oxides (nitric oxide and nitrogen dioxide, not nitrous oxide [See Nitrous Oxide]) are gases commonly released from nitrous or nitric acid, from reactions between nitric acid and organic materials, from burning of nitrocellulose and many other products, and as a by-product of explosions. Exposure to nitrogen oxides occurs in electric arc welding (especially gas-shielded), electroplating, and engraving. Nitrogen oxides are found in engine exhaust, and they are produced when grain with a high nitrite content ferments in storage silos. Nitric oxide used as a therapeutic agent can react with oxygen (particularly in the presence of hyperoxia) to form nitrogen dioxide and other oxidants.

  1. Mechanism of toxicity. Nitrogen oxides are irritant gases with relatively low water solubility. Nitrogen oxides cause delayed-onset chemical pneumonitis. In addition, they can oxidize hemoglobin to methemoglobin.

  2. Toxic dose. The OSHA legal exposure limit (permissible exposure limit—ceiling [PEL-C]) for nitrogen dioxide is 5.0 ppm. The ACGIH-recommended workplace exposure limit (threshold limit value–8-hour time-weighted average [TLV-TWA]) for nitrogen dioxide is 3 ppm (5.6 mg/m3) and for nitric oxide is 25 ppm (31 mg/m3). The air levels considered immediately dangerous to life or health (IDLH) are 20 and 100 ppm, respectively.

  3. Clinical presentation. Because of the poor water solubility of nitrogen oxides, there is very little mucous membrane or upper respiratory irritation at low levels (<10 ppm for nitrogen dioxide). This allows prolonged exposure with few warning symptoms other than mild cough or nausea. With more concentrated exposures, upper respiratory symptoms such as burning eyes, sore throat, and cough may occur.

    1. After a delay of up to 24 hours, chemical pneumonitis may develop, with progressive hypoxemia and pulmonary edema. The onset may be more rapid after exposure to higher concentrations. Some cases may evolve to bronchiolitis obliterans in the days after an initial improvement.

    2. After recovery from acute chemical pneumonitis and after chronic low-level exposure to nitrogen oxides, permanent lung disease from bronchiolar damage may become evident.

    3. Methemoglobinemia (See Methemoglobinemia) has been described in victims exposed to nitrogen oxides in smoke during major structural fires.

    4. Inhaled nitric oxide (eg, used for therapeutic purposes as a pulmonary vasodilator, especially in neonates) can have extrapulmonary effects, including reduced platelet aggregation, methemoglobinemia, and systemic vasodilation.

  4. Diagnosis is based on a history of exposure, if known. Because of the potential for delayed effects, all patients with significant smoke inhalation should be observed for several hours.

    1. Specific levels. There are no specific blood levels.

    2. Other useful laboratory studies include arterial blood gases with co-oximetry to assess concomitant methemoglobinemia, chest radiography, and pulmonary function tests.

  5. Treatment

    1. Emergency and supportive measures

      1. Observe closely for signs of upper airway obstruction, and intubate the trachea and assist ventilation if necessary (See Airway and Breathing). Administer humidified supplemental oxygen.

      2. Observe symptomatic victims for a minimum of 24 hours after exposure and treat chemical pneumonia and noncardiogenic pulmonary edema (See Hypoxia) if they occur.

    2. Specific drugs and antidotes

      1. The role of corticosteroids is most clearly indicated for later onset of bronchiolitis obliterans. In acute lung injury from chemical inhalation, including inhalation of nitrogen oxide, a beneficial role of steroids has not been established.

      2. Treat methemoglobinemia with methylene blue (See Methylene ...

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