How is oxides of nitrogen dangerous

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Establish intravenous access in seriously symptomatic patients. Continuously monitor cardiac rhythm. Administer supplemental oxygen by mask to patients who have respiratory symptoms. Some clinicians recommend high doses of corticosteroids for seriously symptomatic patients, especially with severe bronchospasm; in patients with acute respiratory failure without bronchospasm, the value of steroids is unproven.

If the skin was in contact with liquid nitrogen oxides or their solutions, chemical burns may occur; treat as thermal burns. Continue irrigation for at least 20 minutes. If liquid nitrogen oxides or nitric acid has been splashed in the eyes, irrigate until the pH of the conjunctival fluid has returned to normal.

Test visual acuity. Examine the eyes for corneal damage and treat appropriately. Immediately consult an ophthalmologist for patients who have severe corneal injuries. Consider endoscopy to evaluate the extent of gastrointestinal tract injury. Extreme throat swelling may require endotracheal intubation or cricothyroidotomy. Gastric lavage is useful in certain circumstances to remove caustic material and prepare for endoscopic examination.

Consider gastric lavage with a small nasogastric tube if: 1 a large dose has been ingested; 2 the patient's condition is evaluated within 30 minutes; 3 the patient has oral lesions or persistent esophageal discomfort; and 4 the lavage can be administered within 1 hour of ingestion. Care must be taken when placing the gastric tube because blind gastric tube placement may further injure the chemically damaged esophagus or stomach. Because children do no ingest large amounts of corrosive materials, and because of the risk of perforation from NG intubation, lavage is discouraged in children unless intubation is performed under endoscopic guidance.

Toxic vomitus or gastric washings should be isolated, e. There are no antidotes for nitrogen oxide poisoning. Cyanosis alone does not require treatment. Methylene blue may not be effective in patients who have G6PD deficiency and may cause hemolysis.

Clinical response to methylene blue treatment is usually observed within 30 to 60 minutes. Side effects include nausea, vomiting, abdominal and chest pain, dizziness, diaphoresis, and dysuria.

Consider exchange transfusion in severely poisoned patients who are deteriorating clinically in spite of methylene blue treatment. Intravenous ascorbic acid administered to severely poisoned patients has not proved to be effective.

Administration of steroids is thought by some physicians to reduce the likelihood of the development of bronchiolitis obliterans by reducing inflammation and therefore lung damage. Steroids should be started soon after exposure and continued for 8 weeks, then tapered gradually. The data on steroid use to prevent late sequelae bronchiolitis obliterans is anecdotal and somewhat controversial. The diagnosis of acute nitrogen oxide toxicity is primarily based on respiratory symptoms and establishing a history of exposure to nitrogen oxides.

Routine laboratory studies for all exposed patients include CBC, glucose, and electrolyte determinations. Additional studies for patients exposed to nitrous oxides include determination of methemoglobin levels. The condition of victims who have respiratory complaints should be evaluated with pulse oximetry or ABG measurements , chest radiography, spirometry, and peak flow measurements.

Pulse oximetry is not reliable if methemoglobin is present. The levels of these urinary metabolites are not medically useful but may be helpful in documenting exposure. Consider hospitalizing patients who have histories of significant inhalation exposure and are symptomatic. Symptomatic patients should be observed in a controlled setting for 48 hours for delayed noncardiogenic pulmonary edema. All patients determined to have been exposed to nitrogen oxides should be advised that life-threatening symptoms may develop as late as several weeks after the exposure.

Patients who have been observed for several hours after minimal exposure and remain asymptomatic may be treated as outpatients.

They should be advised to seek medical care promptly if symptoms develop see Nitrogen Oxides-Patient Information Sheet. A patient whose symptoms resolve within 24 to 36 hours may be released with a follow-up appointment to assess pulmonary status. Obtain the name of the patient's primary care physician so that the hospital can send a copy of the ED visit to the patient's doctor.

Close outpatient follow-up should be continued in patients who experienced significant respiratory compromise because these patients are at high risk of developing bronchiolitis obliterans within several weeks. If a work-related incident has occurred, you may be legally required to file a report; contact your state or local health department. Other persons may still be at risk in the setting where this incident occurred.

If the incident occurred in the workplace, discussing it with company personnel may prevent future incidents. If a public health risk exists, notify your state or local health department or other responsible public agency. This handout provides information and follow-up instructions for persons who have been exposed to nitrogen oxides. Print this handout only.

Nitrogen oxides are a mixture of gases that each contain nitrogen and oxygen. Nitrogen oxides are formed naturally when fossil fuels e. They are also formed during electric arc welding, electroplating, and engraving.

They are part of airborne smog and are partly indirectly responsible for the burning eyes, nose, and throat caused by air pollution, through formation of the intensely irritating compound peroxyacetylnitrate, PAN.

Breathing low levels of nitrogen oxides may cause brief, nonspecific symptoms such as cough, shortness of breath, tiredness, and nausea. Nitric oxide NO is not considered to be hazardous to health at typical ambient conditions. However, excess nitric oxide and its products may cause respiratory ailments, hematologic side effects, metabolic disorders, low blood pressure, nausea, vomiting and diarrhoea.

Nitrogen dioxide NO 2 at high concentrations causes inflammation of the airways. Breathing in high levels of NO 2 can increase the likelihood of respiratory problems: wheezing, coughing, colds, flu and bronchitis. People with asthma are prone to have more intense attacks. Prolonged exposure to high levels of NO 2 can cause irreversible damages to the respiratory system.

High levels of NOx can have a negative effect on vegetation by making it more susceptible to disease and frost damage. When NOx reacts with other pollutants in the presence of sunlight, it forms ozone.

Ozone at high concentrations also damage vegetation. Air pollution occurs when gases, dust particles, fumes or odour are introduced into the atmosphere which has harmful or poisonous effects. The common air pollutants are also known as criteria pollutants :. The amount of nitrogen oxides emitted into the atmosphere as air pollution, from both man-made sources, can be quite significant. While NO 2 is a primary pollutant, it is also a contributing component for secondary pollutants formed from a chemical reaction.

The most common is ozone. Photochemical smog, most common in sunny, dry locations, is created when NO 2 from gas combustion is exposed to sunlight, splits and releases an oxygen ion O.

The released O combines with oxygen molecule O 2 forming ozone O 3. Ozone is one of the major secondary pollutants. You can read more about ozone pollution in our blog: Why do I have an ozone pollution problem and what can I do about it? Indoor NO 2 levels are a result of both indoor and outdoor sources. While indoor NO 2 is produced by unvented heaters and gas stoves, high outdoor NO 2 levels originating from local traffic and other combustion sources can influence indoor levels. Long term exposure can decrease lung function, increase the risk of respiratory conditions and increases the response to allergens.

NOx also contributes to the formation of fine particles PM and ground level ozone, both of which are associated with adverse health effects. High levels of NOx can have a negative effect on vegetation, including leaf damage and reduced growth. It can make vegetation more susceptible to disease and frost damage. A study of the effect of nitrogen dioxide and ammonia NH3 on the habitat of Epping Forest has revealed that pollution is likely to be significantly influencing ecosystem health in the forest.

The study demonstrated that local traffic emissions contribute substantially to exceeding the critical levels and critical loads in the area. NOx also reacts with other pollutants in the presence of sunlight to form ozone which can damage vegetation at high concentrations. Notes: Critical Level is the threshold level for the atmospheric concentration of a pollutant above which harmful direct effects can be shown on a habitat or species.

Critical Load is the threshold level for the deposition of a pollutant above which harmful indirect effects can be shown on a habitat or species. In some instances the limits were exceeded by significant amounts.