Nitrogen oxides (nitric oxide and nitrogen dioxide, not 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, as a by-product of detonations, and as a breakdown reactant of the rocket fuel dinitrogen tetroxide. Nitrogen oxides are also released in engine exhaust and are a common component of traffic-related air pollution. Occupational exposure occurs in electric arc welding (especially gas-shielded), electroplating, engraving, and in agricultural work when grain with a high nitrite content is filled into 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.

Nitrogen oxides are irritant gases and cause direct injury through free radical generation and acid formation. They cause delayed-onset chemical pneumonitis. In addition, they can oxidize hemoglobin to methemoglobin.

The Federal OSHA legal permissible exposure limit-ceiling (PEL-C) for nitrogen dioxide (NO₂) is 5.0 ppm; California OSHA has a short-term exposure limit of 1 ppm; and the ACGIH-recommended workplace exposure limit (threshold limit value-8-hour time-weighted average [TLV-TWA]) for NO₂ is 0.2 ppm. The OSHA PEL and ACGIH TLV-TWA for nitric oxide (NO) is 25 ppm. Air levels immediately dangerous to life or health for NO₂ and NO are 20 and 100 ppm, respectively.

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 for 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 and symptom onset can be more rapid.

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. Chronic low-level exposures (such as those resulting from engine exhaust) are associated with acute asthma exacerbations and an increased incidence of asthma in children. Such exposures are also associated with cardiac and metabolic disease including myocardial infarction, diabetes and increases in overall mortality.
3. 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) can have extrapulmonary effects, including reduced platelet aggregation, methemoglobinemia, and systemic vasodilation.

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.

1. Emergency and supportive measures
   1. Observe closely for signs of upper airway obstruction, and intubate the trachea and assist ventilation if necessary. Administer humidified supplemental oxygen.
   2. Observe symptomatic victims for a minimum of 24 hours after exposure and treat pneumonitis and noncardiogenic pulmonary edema 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 been suggested but is not established.
   2. Treat methemoglobinemia with methylene blue.
3. Decontamination . Rescuers should wear self-contained breathing apparatus and, if there is the potential for high-level gas exposure or exposure to liquid nitric acid (as a source of nitrogen dioxide), chemical-protective clothing.
   1. Inhalation. Remove victims from exposure immediately and give supplemental oxygen, if available.
   2. Skin and eyes. Remove wet clothing and flush exposed skin with water. Irrigate exposed eyes with copious water or saline.
4. Enhanced elimination. There is no role for enhanced elimination procedures.