Nitrogen dioxide poisoning

Nitrogen dioxide poisoning is the illness resulting from the toxic effect of nitrogen dioxide (NO2). It usually occurs after the inhalation of the gas beyond the threshold limit value.Nitrogen dioxide is reddish-brown with a very harsh smell at high concentrations, and while still harmful, it is colorless and odorless at lower concentration. Nitrogen dioxide poisoning depends on the duration, frequency, and intensity of exposure.Nitrogen dioxide is an irritant of the mucous membrane linked with another air pollutant that causes pulmonary diseases such as OLD, asthma, chronic obstructive pulmonary disease and sometimes acute exacerbation of COPD and in fatal cases, deaths.Its poor solubility in water enhances its passage and its ability to pass through the moist oral mucosa of the respiratory tract.Like most toxic gases, the dose inhaled determines the toxicity on the respiratory tract. Occupational exposures constitute the highest risk of toxicity and domestic exposure is uncommon. Prolonged exposure to low concentration of the gas may have lethal effects, as can short-term exposure to high concentrations like chlorine gas poisoning. It is one of the major air pollutant capable of causing severe health hazards such as coronary artery disease as well as stroke.Nitrogen dioxide is often released into the environment as a byproduct of fuel combustion but rarely released by spontaneous combustion. Known sources of nitrogen dioxide gas poisoning include automobile exhaust and power stations. The toxicity may also result from non-combustible sources such as the one released from anaerobic fermentation of food grains and anaerobic digestion of biodegradable waste.The World Health Organization (WHO) developed a global recommendation limiting exposures to less than 20 parts per billion for chronic exposure and value less 100 ppb for one hour for acute exposure, using nitrogen dioxide as a marker for other pollutants from fuel combustion. The standards also based on the concentration of nitrogen dioxide that show a significant and profound effects on the function of the pulmonary of asthmatic patients.Historically, some cities in the United States including Chicago and Los Angeles have high levels of nitrogen dioxide but the EPA set a standard values less than 100 ppb for a one-hour exposure and less than 53 ppb for chronic exposure. Nitrogen dioxide poisoning is the illness resulting from the toxic effect of nitrogen dioxide (NO2). It usually occurs after the inhalation of the gas beyond the threshold limit value.Nitrogen dioxide is reddish-brown with a very harsh smell at high concentrations, and while still harmful, it is colorless and odorless at lower concentration. Nitrogen dioxide poisoning depends on the duration, frequency, and intensity of exposure.Nitrogen dioxide is an irritant of the mucous membrane linked with another air pollutant that causes pulmonary diseases such as OLD, asthma, chronic obstructive pulmonary disease and sometimes acute exacerbation of COPD and in fatal cases, deaths.Its poor solubility in water enhances its passage and its ability to pass through the moist oral mucosa of the respiratory tract.Like most toxic gases, the dose inhaled determines the toxicity on the respiratory tract. Occupational exposures constitute the highest risk of toxicity and domestic exposure is uncommon. Prolonged exposure to low concentration of the gas may have lethal effects, as can short-term exposure to high concentrations like chlorine gas poisoning. It is one of the major air pollutant capable of causing severe health hazards such as coronary artery disease as well as stroke.Nitrogen dioxide is often released into the environment as a byproduct of fuel combustion but rarely released by spontaneous combustion. Known sources of nitrogen dioxide gas poisoning include automobile exhaust and power stations. The toxicity may also result from non-combustible sources such as the one released from anaerobic fermentation of food grains and anaerobic digestion of biodegradable waste.The World Health Organization (WHO) developed a global recommendation limiting exposures to less than 20 parts per billion for chronic exposure and value less 100 ppb for one hour for acute exposure, using nitrogen dioxide as a marker for other pollutants from fuel combustion. The standards also based on the concentration of nitrogen dioxide that show a significant and profound effects on the function of the pulmonary of asthmatic patients.Historically, some cities in the United States including Chicago and Los Angeles have high levels of nitrogen dioxide but the EPA set a standard values less than 100 ppb for a one-hour exposure and less than 53 ppb for chronic exposure. Nitrogen dioxide poisoning is not harmful to all forms of life just like 'chlorine gas poisoning' and carbon monoxide poisoning. It is easily absorbed through the lungs and its inhalation result in heart failure and sometimes death in severe and cases. Individual and races may differ in nitrogen dioxide tolerance level and individual tolerance level for the gas may be altered by several factors, such as metabolic rate, barometric pressure, and hematological disorders but significant exposure may result in fatal conditions that could lead to shorter lifespan due to heart failure. Exposure to high level of nitrogen dioxide may lead to inflammation of the mucous membrane and the lower and upper respiratory tracts.The symptoms of acute nitrogen dioxide poisoning is non-specific and have a semblance with ammonia gas poisoning, chlorine gas poisoning, and carbon monoxide poisoning. The symptoms also resembles that of pneumonia or viral infection and other inhalational injuries but common symptoms includes rhinitis wheezing or coughing, conjunctivitis, headache, throat irritation and dyspnea which may progress to nasal fissures, ulcerations, or perforation.The patient is usually ill-appearing and presents with hypoxemia coupled with shallow rapid breathing. Therapy is supportive and includes removal from further nitrogen dioxide exposure.Systemic symptoms include fever and anorexia. Electrocardiography and chest radiography can help in revealing diffuse, bilateral alveolar infiltrates. Chest radiography may be used in diagnosis and the baseline could be established with pulmonary function testing. There is no specific laboratory diagnostic test for acute nitrogen dioxide poisoning but analysis of arterial blood gas level, methemoglobin level, complete blood count, glucose test, lactate threshold measurement and r peripheral blood smear may be helpful in the diagnosis of nitrogen dioxide poisoning.The determination of nitrogen dioxide in urine or tissue does not establish the diagnosis, and there are technical and interpretive problems with these tests. Prolonged exposure to a very high level of nitrogen dioxide in micro meter-size range, may have an inflammatory effect that principally targets the respiratory tracts leading to chronic nitrogen dioxide poisoning which can occur within days or weeks after the threshold limit value is excessively exceeded. This condition causes fever, rapid breathing coupled with rapid heart rate, and severe seizure of breath.Other effects include diaphoresis, chest pain, and persistent dry cough, all of which may result in weight loss, anorexia and may also lead to right-side heart enlargement and heart disease in advanced cases.Prolonged exposure to relatively low levels of nitrogen (II) oxide may cause persistent headaches and nausea.Like chlorine gas poisoning, symptoms usually resolve themselves upon removal from further nitrogen dioxide exposure, unless there had been an episode of severe acute poisoning. Treatment and management vary with symptoms. Patients are often observed for hypoxemia for a minimum of 12 hours if there are no initial symptoms and if the patient is hypoxemic, oxygen may be administered but high-dose steroids are recommended for patients with pulmonary manifestations. Patients may also be hospitalized for 12 to 24 hours or longer for observation if the gaseous exchange is impaired.In a case where gaseous exchange is impaired, mechanical ventilation and intubation may be necessary and if bronchiolitis obliterans develop within 2 to 6 weeks of nitrogen dioxide exposure, corticosteroid therapy such as anticholinergic may be required for 6 to 12 months to lower the body overreaction to nitrogen dioxide gas. Occupational exposures constitute the highest risk of toxicity and it is often high for farmers especially those that deal with food grains. It is equally high for firefighters and military personnel, especially those officers that deal in explosives. The risk is also high for arc welders, traffic officers, aerospace staffs and miners as well as those people whose occupations are connected with the nitric acid. Silo-filler's disease is a consequence of exposure to nitrogen dioxide poisoning by farmers dealing with silos. Food grains such as corn and millet, as well as grasses such as alfalfa and some other plant material, produces nitrogen dioxide within hours due to anaerobic fermentation. The threshold concentrations of nitrogen dioxide are often attained within 1 to 2 days and begin to decline gradually after 10 to 14 days but if the silos is well sealed, the gas may remain in there for weeks. Heavily fertilized silage, particularly the ones produced from immature plants, generate a higher concentration of the gas within the silo.Nitrogen dioxide is about 1.5 times heavier than air and during silage storage, nitrogen dioxide remains in the silage material.Improper ventilation may result in exposure during the leveling of the silage. Nitrogen dioxide is sparingly soluble in water and on inhalation, it diffuses into the lung and slowly hydrolyzes to nitrous and nitric acid which causes pulmonary edema and pneumonitis leading to the inflammation of the bronchioles and pulmonary alveolus resulting from lipid peroxidation and oxidative stress.Mucous membrane is primarily affected alongside with type I pneumocyte and the respiratory epithelium. The generation of free radicals from lipid peroxidation results in irritation of the bronchioles and alveoli that causes rapid destruction of the respiratory epithelial cells.The overall reaction results in the release of fluid that causes pulmonary edema. Nitrogen dioxide poisoning may alter macrophage activity and immune function leading to susceptibility of the body to a wide range of infections, and overexposure to the gas may also lead to methemoglobinemia, a disorder characterized by a higher than normal level of methemoglobin (metHb, i.e., ferric rather than ferrous haemoglobin) in the blood.