NITROGEN DIOXIDE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
NITROGEN DIOXIDE AZOTE (French) AZOTO (Italian) DINITROGEN TETROXIDE NITRITO NITRO NITROGEN DIOXIDE (LIQUID) NITROGEN OXIDE NITROGEN PEROXIDE NITROGEN PEROXIDE, LIQUID NITROGEN TETROXIDE OXIDES OF NITROGEN RED OXIDE OF NITROGEN STICKSTOFFDIOXID (German) STIKSTOFDIOXYDE (Dutch)
IDENTIFIERS
SYNONYM REFERENCE
- (RTECS , 1991; AAR, 1987; CHRIS , 1990; EPA, 1985; Sax & Lewis, 1989)
USES/FORMS/SOURCES
Nitrogen dioxide is used commercially as a chemical intermediate, catalyst, nitrating agent, oxidizing agent, polymerization inhibitor, oxidizer for rocket fuels, and in bleaching flour (Lewis, 1997; Budavari, 1996).
Nitrogen dioxide is a "criteria air pollutant" (Clayton & Clayton, 1994). It is a reddish-brown gas which condenses to a brown liquid at temperatures below 21.15 degrees C (Budavari, 1996; Lewis, 1997). It can occur at levels as high as 0.45 ppm in polluted urban air (Clayton & Clayton, 1994). Nitrogen dioxide can disproportionate in air to form a mixture of nitrogen oxides, and the commercial pressurized product called nitrogen tetroxide is actually an equilibrium mixture of nitrogen dioxide and N2O4 (Budavari, 1996). Nitrogen dioxide decomposes in water to form NITRIC ACID and NITRIC OXIDE (Budavari, 1996). Oxides of nitrogen can react with AMINES to form carcinogenic and mutagenic N-NITROSAMINES. They can also react with POLYNUCLEAR AROMATIC HYDROCARBONS (PAHs) to form nitro-aromatic compounds, some of which are potent mutagens (Hisamatsu, 1984; Tokowa, 1981; Pitts, 1978). Thus, chemical reactivity may be an important consideration in nitrogen dioxide toxicity. The toxicology of nitrogen dioxide has been reviewed (Morrow, 1984; p 151; Pitts, 1978; NIOSH, 1976). Nitrogen oxides are formed endogenously in the lung and respiratory tract by the enzyme nitric oxide synthetase. They may play a role in airway and smooth muscle relaxation, and nitric oxide inhalation therapy may actually be beneficial in some persons with asthma, adult respiratory distress syndrome (ARDS), or pulmonary hypertension. The interrelationships between endogenous and inhaled nitrogen oxides have been reviewed (Gaston et al, 1994). Nitrogen dioxide at potentially toxic (greater than 5 ppm) concentrations can form spontaneously under certain conditions when nitric oxide is used therapeutically in the ventilator treatment of lung disease (Losa et al, 1997). Most studies of nitrogen dioxide are in reference to air pollution and acid rain, involving mixed exposures with other chemicals. Many occupational exposures to nitrogen dioxide occur as a result of its formation from the decomposition of nitrates, as in silage (silo filler's disease) (ACGIH, 1992). Symptomatic exposures are also reported in indoor ice arenas due to the use of combustion powered ice conditioning equipment (zambonis) (Karlson-Stiber et al, 1996). The odor threshold is in the range of 0.04 to 5 ppm, and this may not be sufficient to protect susceptible individuals (Hathaway et al, 1996; Clayton & Clayton, 1994). In any event, odor alone should never be used to determine if an environment is safe.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- Because nitric oxide and nitrogen dioxide almost always occur together, this review is based on the properties of nitrogen oxides. Nitrogen dioxide forms nitric acid upon contact with water. It is more acutely toxic than nitric oxide.
- Exposure to nitrogen oxides results in acute and chronic changes of the pulmonary system including pulmonary edema, pneumonitis, bronchitis, bronchiolitis, emphysema and possibly methemoglobinemia. Usually, no symptoms occur, except a slight cough, fatigue, and nausea. However, potentially fatal pulmonary edema can occur following minimal early symptoms.
Acute effects may or may not develop within one to two hours after exposure, and include tachypnea, tachycardia, fine crackles and wheezing, and cyanosis. Another acute scenario involves dyspnea and coughing which subside over two to three weeks. The second stage involves abrupt development of fever and chills, more severe dyspnea, cyanosis, and pulmonary edema. There is no correlation between severity of the first and second stages. Recovery may be either complete or may involve some degree of impairment of pulmonary function.
- Nitrogen dioxide exposure does occur with the use of nitric oxide inhalation therapy in infants. Exposure of nurses and respiratory therapists occurs as well, but is generally transient.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
TOXIC; may be fatal if inhaled or absorbed through skin. Fire will produce irritating, corrosive and/or toxic gases. Contact with gas or liquefied gas may cause burns, severe injury and/or frostbite. Runoff from fire control may cause pollution.
ACUTE CLINICAL EFFECTS
- The primary concern in acute nitrogen dioxide exposure is its effects on the respiratory tract; severe pulmonary edema and emphysema can result from both acute and chronic exposures. Nitrogen dioxide can also form methemoglobin and act as an asphyxiant (HSDB , 2000).
- Methemoglobinemia can have an insidious onset and produce symptoms similar to those of hypoxia: headache, vomiting, dizziness, weakness, loss of judgement and coordination, drowsiness, and respiratory arrest. A deep, "chocolate brown" central cyanosis that does not resolve with inhalation of 100 percent oxygen is characteristic of methemoglobinemia (Dabney et al, 1990).
- Levels of 25 ppm are associated with respiratory irritation and chest pain (Clayton & Clayton, 1994). Exposure to 50 ppm can produce chronic lung damage, and 100 ppm can be fatal (Clayton & Clayton, 1994). Exposure to 250 ppm produces coughing, frothy sputum, and increased difficulty in breathing, with non-cardiogenic pulmonary edema developing by 2 hours later, followed by death (Clayton & Clayton, 1994). The fatal complications of significant and symptomatic acute exposure may be delayed by several weeks (Clayton & Clayton, 1994). Delayed fatal non-cardiogenic pulmonary edema may develop 2 to 3 weeks after acute exposure which may have produced relatively mild effects (Hathaway et al, 1996).
- Nitrogen dioxide can react with fats in cell membranes causing damage to the pneumocytes and pulmonary macrophages, resulting in decreased lung function and reduced resistance to pulmonary infections (Clayton & Clayton, 1994). So-called SILO-FILLER'S DISEASE has been attributed to nitrogen dioxide.
- Nitrogen dioxide can be one of the most insidious poisons. It is not particularly acutely irritating to the mucous membranes and gives little warning of dangerously high exposures (HSDB , 2000; Budavari, 1996). After exposure to high concentrations, inflammation of the lungs develops following a delay of 5 to 72 hours (HSDB , 2000). Massive non-cardiogenic pulmonary edema and death may follow.
- Bronchiolitis obliterans can rarely develop in survivors (Hathaway et al, 1996). Sometimes permanent impairment of pulmonary function persists (Hathaway et al, 1996).
- Volunteers exposed to an airborne concentration of 1 ppm of nitrogen dioxide for 2 days experienced no ill effects except for a reduction of pulmonary function (HSDB , 2000). Reduced pulmonary function has been produced by exposure to airborne concentrations as low as 0.05 ppm (Clayton & Clayton, 1994). Low level exposures may also make normal persons more sensitive to bronchoconstricting agents (Clayton & Clayton, 1994). Persons with chronic lung disease had reduced lung function (increase in airway resistance) when exposed to nitrogen dioxide at concentrations as low as 1.6 ppm (Clayton & Clayton, 1994).
- Bronchoconstriction and increased bronchial reactivity have been produced by inhalation of nitrogen dioxide in human volunteers under controlled conditions; concentrations as low as 200 mcg/m(3) may produce an effect in asthmatics (Berglund et al, 1994).
- Exposure to 400 ppb nitrogen dioxide for 6 hours significantly interacted with allergen exposure in human volunteers with seasonal allergic rhinitis, increasing levels of eosinophil cationic protein and mast cell tryptase in nasal lavage fluid (Wang et al, 1995).
- In asthmatics, exposure to 260 ppb nitrogen dioxide for 30 minutes significantly increased airway responsiveness to histamine 5 hours later. Thoracic gas volume was decreased after exposure, but tryptase, eosinophil cationic protein, and myeloperoxidase were not affected in these subjects (Strand et al, 1996).
- Exposure to 600 ppb of nitrogen dioxide for 1 hour significantly increased airway responsiveness in a group of asthmatic adults and children, while 300 ppb did not (Salome et al, 1996).
CHRONIC CLINICAL EFFECTS
- Because acute exposures to nitrogen dioxide can produce chronic effects, there may be no practical distinction between acute and chronic toxicity.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Clothing frozen to the skin should be thawed before being removed. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Keep victim under observation. Effects of contact or inhalation may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
INHALATION EXPOSURE PERSONNEL PROTECTION INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. Treatment of toxic pulmonary edema caused by nitric oxide inhalation should be directed towards reversal of ventilatory failure by using oxygen in assisting ventilation. In patients with toxic bronchiolitis, steroids may be beneficial in decreasing the amount of inflammation. Methemoglobinemia and mild acidosis may be present, but specific treatment for these conditions will probably not be necessary.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy. METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg. Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome. Because pulmonary symptoms may be delayed, all patients with significant exposure should be carefully observed for at least 48 hours.
DERMAL EXPOSURE - Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. All patients with significant dermal exposure should be carefully observed for possible development of delayed clinical signs and symptoms. Follow treatment recommendations in the Inhalation Exposure section where appropriate.
EYE EXPOSURE - Eye exposure to nitric oxide normally does not occur to a significant extent. However, this substance is a strong eye irritant due to the formation of nitric acid, which can permanently alter proteins. Because this reaction is relatively slow, permanent injury may possibly be prevented by immediate decontamination. DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE - Nitrogen dioxide exists as a liquid below 21 degrees C. Ingestion is unlikely at higher temperatures. Gastric decontamination is not likely to be useful, as the toxin will vaporize at body temperature. Emesis should not be induced, because of the corrosive nature of this material. DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Patients who have ingested liquid nitrogen dioxide may be a risk for developing pulmonary edema, due to the possibility of fumes escaping into the pharynx and respiratory system. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy. METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg. Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
Death due to airway obstruction secondary to edema of the glottis has not been well documented, but is estimated to occur at concentrations greater than 100 ppm (Tse & Bockman, 1970). The odor of nitrogen dioxide is perceptible at concentrations as low as 0.11 ppm. Symptoms appear at 13 ppm. A concentration of 200 ppm may be fatal (Budavari, 1996). Exposures in the range of 100 to 150 ppm for a few minutes are dangerous, and 200 to 700 ppm can be fatal after brief exposure (Sax & Lewis, 1989). Although asymptomatic, normal adult human volunteers demonstrated changes in bronchoalveolar lavage findings consistent with inflammatory changes when exposed to 2 ppm nitrogen dioxide for 4 hours (Devlin et al, 1999).
MAXIMUM TOLERATED EXPOSURE
SUMMARY One attempt to arrive at an ambient air standard for nitrogen dioxide, which was based on results of studies since 1966, concluded that the maximal no-effect dose is approximately 0.6 ppm without any safety factor. Applying various safety factors as currently practiced by various regulatory agencies would lead to air standards in the parts per billion range (Morrow, 1975). The lowest effective concentration to produce bronchoconstriction in asthmatics is 200 mcg/m(3), derived from meta-analysis (Berglund et al, 1994).
Death due to airway obstruction secondary to edema of the glottis has not been well documented, but is estimated to occur at concentrations greater than 100 ppm. The odor of nitrogen dioxide is perceptible to most at 0.22 ppm, but some individuals can detect it as low as 0.11 ppm (ACGIH, 1991). Symptoms appear at 13 ppm. Mucous membrane irritation occurs at 1 to 13 ppm (Clayton & Clayton, 1994).
OCCUPATIONAL Workers who were exposed to 30 to 35 ppm nitrogen dioxide for several years showed no apparent ill effects (ACGIH, 1991). Nurses and respiratory therapists had transient exposures to nitrogen dioxide of up to 3.1 ppm, but 15 minute and full shift averages were below the 0.5 ppm detection limit, suggesting transient exposures (Phillips et al, 1999).
ADULT A group of 22 adult volunteers who were exposed to 1 or 2 parts per million nitrogen dioxide under controlled conditions for 2 hours per day over 3 consecutive days had increased frequencies of infection by attenuated influenza A/Korea/82 virus compared to a control group, but the differences were not statistically significant. An outbreak of respiratory illness associated with use of propane powered ice-resurfacing machines was reported among adolescent hockey players. Simulated reenactment produced nitrogen dioxide levels as high as 1250 ppb (Rosenlund & Bluhm, 1999).
An amateur ice hockey team (n=15) was inadvertently exposed to elevated levels of carbon monoxide and nitrogen dioxide in a poorly ventilated ice arena. Of the 15 players, 12 were treated as outpatients while 3 developed pneumonitis. The primary symptoms were cough, dyspnea, chest pain, and hemoptysis. Infiltrates were observed on chest x-ray in 5 of 15 patients and one patient had evidence of peribronchovascular interstitial pattern on chest CT. His diagnostic studies were consistent with severe respiratory failure. In lung function studies, 4 patients developed restrictive ventilatory disorders, one had an obstructive disorder and one patient had a combined disorder. Most patients (n=8) were treated with IV or inhaled corticosteroids, beta2 agonists and antibiotics and several patients required oxygen therapy. In 14 patients, recovery was uneventful and treatment was discontinued within approximately one month. However, one patient required inhaled corticosteroid treatment for another 3 months to treat a persistent, mild-obstructive ventilatory disorder. Emission studies were conducted following exposure and both carbon monoxide (1.95 times for CO) and nitrogen dioxide (more than 10 times the normal limit) exceeded the recommended indoor air quality standards (Brat et al, 2013).
- Carcinogenicity Ratings for CAS10102-44-0 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Nitrogen dioxide ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Nitrogen dioxide EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Nitrogen dioxide IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Nitrogen dioxide MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS10102-44-0 (U.S. Environmental Protection Agency, 2011):
Oral: Inhalation: Drinking Water:
CALCULATIONS
CONVERSION FACTORS mg/m(3) = 1.882 x ppm
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS10102-44-0 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS10102-44-0 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS10102-44-0 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS10102-44-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS10102-44-0 (U.S. Occupational Safety and Health Administration, 2010):
Threshold Quantity, in pounds:250 Threshold Quantity, in pounds:250
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS10102-44-0 (U.S. Environmental Protection Agency, 2010):
Listed as: Nitrogen dioxide Final Reportable Quantity, in pounds (kilograms): Additional Information: Listed as: Nitrogen oxide NO2 Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS10102-44-0 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS10102-44-0 (U.S. Environmental Protection Agency, 2010b):
Listed as: Nitrogen dioxide P or U series number: P078 Footnote: Listed as: Nitrogen oxide NO2 P or U series number: P078 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS10102-44-0 (U.S. Environmental Protection Agency, 2010):
Listed as: Nitrogen Dioxide Reportable Quantity, in pounds: 10 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS10102-44-0 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS10102-44-0 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS10102-44-0 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1067 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1067 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS10102-44-0 (NFPA, 2002):
-HANDLING AND STORAGE
STORAGE
Nitrogen dioxide is corrosive to steel when wet, but may be stored in steel cylinders when the moisture content is 0.1% or less (Budavari, 1989). Protect container(s) against physical damage (NFPA, 1991).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 10102-44-0.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Substance does not burn but will support combustion. Vapors from liquefied gas are initially heavier than air and spread along ground. These are strong oxidizers and will react vigorously or explosively with many materials including fuels. May ignite combustibles (wood, paper, oil, clothing, etc.). Some will react violently with air, moist air and/or water. Cylinders exposed to fire may vent and release toxic and/or corrosive gas through pressure relief devices. Containers may explode when heated. Ruptured cylinders may rocket.
Nitrogen dioxide is noncombustible, but is an extremely strong oxidizing agent; may cause fire in contact with clothing and other combustible materials (ITI, 1988). Does not burn, but supports combustion of carbon, phosphorus, and sulfur (Budavari, 1989).
When heated to decomposition, nitrogen dioxide releases highly toxic fumes of oxides of nitrogen (Sax & Lewis, 1989).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS10102-44-0 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Water only; no dry chemical, CO2 or Halon®. Contain fire and let burn. If fire must be fought, water spray or fog is recommended. Do not get water inside containers. Move containers from fire area if you can do it without risk. Damaged cylinders should be handled only by specialists.
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Do not direct water at source of leak or safety devices; icing may occur. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS10102-44-0 (NFPA, 2002):
- Choose an extinguishing agent suitable for fires in surrounding material (AAR, 1987).
- Water may be used in flooding quantities as fog (AAR, 1987).
When heated to decomposition, nitrogen dioxide releases highly toxic fumes of oxides of nitrogen (Sax & Lewis, 1989). Does not burn, but supports combustion of carbon, phosphorus, and sulfur (Budavari, 1989).
EXPLOSION HAZARD
- Nitrogen dioxide is a very reactive oxidizing agent; the following table lists representative reactants and their interaction type (ITI, 1988):
DUST/VAPOR HAZARD
- When heated to decomposition, nitrogen dioxide releases highly toxic fumes of oxides of nitrogen (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, nitrogen dioxide releases highly toxic fumes of oxides of nitrogen (Lewis, 1996).
- This agent does not burn, but supports combustion of carbon, phosphorus, and sulfur (Budavari, 1996).
- Nitrogen dioxide is a very reactive oxidizing agent; the following table lists representative reactants and their interaction type (ITI, 1988):
EVACUATION PROCEDURES
- Initial Isolation and Protective Action Distances (ERG, 2004)
Data presented from the Emergency Response Guidebook Table of Initial Isolation and Protective Action Distances are for use when a spill has occurred and there is no fire. If there is a fire, or if a fire is involved, evacuation information presented under FIRE - PUBLIC SAFETY EVACUATION DISTANCES should be used. Generally, a small spill is one that involves a single, small package such as a drum containing up to approximately 200 liters, a small cylinder, or a small leak from a large package. A large spill is one that involves a spill from a large package, or multiple spills from many small packages. Suggested distances to protect from vapors of toxic-by-inhalation and/or water-reactive materials during the first 30 minutes following the spill.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 100 meters (330 feet) in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 100 meters (330 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Many gases are heavier than air and will spread along ground and collect in low or confined areas (sewers, basements, tanks). Keep out of low areas. Ventilate closed spaces before entering.
- Downwind evacuation should be considered if this material is involved in a fire or if a large discharge has occurred (AAR, 1987).
- AIHA ERPG Values for CAS10102-44-0 (AIHA, 2006):
Listed as Nitrogen Dioxide ERPG-1 (units = ppm): 1 ERPG-2 (units = ppm): 15 ERPG-3 (units = ppm): 30 Under Ballot, Review, or Consideration: No Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS10102-44-0 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Nitrogen dioxide TEEL-0 (units = ppm): 0.5 TEEL-1 (units = ppm): 0.5 TEEL-2 (units = ppm): 12 TEEL-3 (units = ppm): 20 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS10102-44-0 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
Listed as: Nitrogen dioxide Proposed Value: AEGL-1 10 min exposure: ppm: 0.5 ppm mg/m3: 0.94 mg/m(3)
30 min exposure: ppm: 0.5 ppm mg/m3: 0.94 mg/m(3)
1 hr exposure: ppm: 0.5 ppm mg/m3: 0.94 mg/m(3)
4 hr exposure: ppm: 0.5 ppm mg/m3: 0.94 mg/m(3)
8 hr exposure: ppm: 0.5 ppm mg/m3: 0.94 mg/m(3)
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Nitrogen dioxide Proposed Value: AEGL-2 10 min exposure: ppm: 20 ppm mg/m3: 38 mg/m(3)
30 min exposure: ppm: 15 ppm mg/m3: 28 mg/m(3)
1 hr exposure: ppm: 12 ppm mg/m3: 23 mg/m(3)
4 hr exposure: ppm: 8.2 ppm mg/m3: 15 mg/m(3)
8 hr exposure: ppm: 6.7 ppm mg/m3: 13 mg/m(3)
Definitions: AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.
Listed as: Nitrogen dioxide Proposed Value: AEGL-3 10 min exposure: ppm: 34 ppm mg/m3: 64 mg/m(3)
30 min exposure: ppm: 25 ppm mg/m3: 47 mg/m(3)
1 hr exposure: ppm: 20 ppm mg/m3: 38 mg/m(3)
4 hr exposure: ppm: 14 ppm mg/m3: 26 mg/m(3)
8 hr exposure: ppm: 11 ppm mg/m3: 21 mg/m(3)
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS10102-44-0 (National Institute for Occupational Safety and Health, 2007):
IDLH: 20 ppm Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Fully encapsulating, vapor protective clothing should be worn for spills and leaks with no fire. Do not touch or walk through spilled material. Keep combustibles (wood, paper, oil, etc.) away from spilled material. Stop leak if you can do it without risk. Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact spilled material. Do not direct water at spill or source of leak. If possible, turn leaking containers so that gas escapes rather than liquid. Prevent entry into waterways, sewers, basements or confined areas. Isolate area until gas has dispersed. Ventilate the area.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 124 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
DECONTAMINATION OF SPILLS Spray or sift a thick layer of a (1:1) mixture of dry soda ash and slaked lime behind a shield. After mixing, spray water from an atomizer with great caution. Transfer slowly into a large amount of water (ITI, 1988).
Water spray may be used to reduce or knock down vapor (AAR, 1987). Flue gas NOx is substantially reduced by the novel technique of injection of plasma-treated ammonia and its decomposition products. The results showed that 85 to 90% of the NOx is removed by injecting ammonia radicals at a low plasma power input. Ammonia plasma injection was shown experimentally to be more effective than simple ammonia injection. This technique provides an inexpensive and effective NOx reduction system for stationary sources (Zhou et al, 1992).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and approved personal protection equipment. Get fire-fighting equipment ready (Ford, 1989). In general it would be preferable to detoxify spilled material before absorbing for disposal whenever possible.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- This study evaluated the fluxes of NO and N2O from sandy loam soils and clay loam soils, with and without the addition of NH4NO3 fertilizer. The aeration state of the soil controlled the relative rate of NO and N2O emission. Nitric oxide was the major gas emitted from well aerated soils, a condition that favored nitrification. Nitrous oxide was emitted from less aerated soils, conditions that favor denitrification (Skiba et al, 1992).
- Nitrite concentrations that were continuously measured in orographic cloud and combined with pH measurements were used to estimate the formation of nitrous acid (HONO) in the north of England. The estimated HONO concentrations were up to 0.5 ppbc and approximately 10% of the total NOx measured. The results suggest that dry deposition of HONO may contribute up to 3 kg N/ha/yr in upland forests (Cape et al, 1992).
- A computer simulation model supported the hypothesis that acid-induced leaching of nutrients from the soil is a cause of nutritional imbalance in tree leaves (Vanoene, 1992).
ENVIRONMENTAL FATE AND KINETICS
OTHER Nitrogen oxides react with volatile organic compounds to produce ozone, a principal factor in photochemical smog. Both volatile organics and nitrogen oxides are emitted by transportation and industrial sources (Sullivan, 1987). Visible differential absorption spectrometry, ground based, was used to determine atmospheric NO2 in Antarctica. The measurement taken in the morning showed moderate NO2 vertical column levels of 1.5 to 2.5 times 10(15) molecules/cm, while evening results were 2 to 3 times 10(15) molecules/cm. During spring NO2 was found to be positively correlated with ozone (Gil & Cacho, 1992). A three-year study was done in which denitrification activity was monitored in sandy loam soil and course sandy soil. A simple model was constructed to calculate the denitrification loss. The model predicted an annual loss of 1 to 2 kg N per ha in the course sandy soil, compared to the measured value of 0.6 kg N per ha. Measured nitrogen losses in the sandy loam soil were 1.5, 3.0 and 13.0 kg N per ha, and the model predicted values of 14, 9 and 14 kg N per ha (Vinther, 1992). DENITRIFICATION: N2O is a product of soil denitrification. In a controlled study under greenhouse conditions, the production of nitrous oxide was positively correlated with the carbon content of the test soils. Tests with acetylene showed that denitrification losses were underestimated by measuring only nitrous oxide since N2O is still reduced to N2 after 100 hours continuous exposure to acetylene (Iqbal, 1992). BIOLIGICAL DENITRIFICATION POTENTIAL: A first order kinetics process for denitrification was found with a nitrate concentration decrement rate of 12 percent per day in the first 5 cm of the sediment layer in South American soil (Whitaker & Matvienko, 1992).
ENVIRONMENTAL TOXICITY
- PUBLISHED VALUES (OHM/TADS , 1991)
1. LCLo (INHL) DOG: 123 mg/m(3)/8h 2. LCLo (INHL) MONKEY: 123 mg/m(3)/8h 3. LC50 (INHL) RAT: 88 ppm/4h 4. LC50 (INHL) MOUSE: 1000 ppm/10min 5. LC50 (INHL) RABBIT: 315 ppm/15min 6. LC50 (INHL) GUINEA PIG: 30 ppm/1h
Aquatic toxicity: WATERFOWL TOXICITY: Data not available BIOLOGICAL OXYGEN DEMAND (BOD): None FOOD CHAIN CONCENTRATION POTENTIAL: None
- AIR POLLUTION: Nitrogen dioxide generated from indoor heaters and stoves was monitored for several months. The nitrogen dioxide levels for heating with a kerosene heater and an oil fan heater were calculated at 219 and 474 mcg/m(3), respectively. The nitrogen dioxide levels during cooking were 290 mcg/m(3) (Kawamoto et al, 1993).
- Experimental test, chosen to simulate rural roadside conditions, exposed plants to 60 nL/L of nitrogen dioxide for 37 weeks. The procedure resulted in a 36% reduction in new shoot production, and 46% reduction in old shoots showing new growth. It was concluded that plants growing near roadways could be adversely affected by NO2 pollution (Bell et al, 1992).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
- 46.01 (Clayton & Clayton, 1994)
DESCRIPTION/PHYSICAL STATE
- Nitrogen dioxide is a colorless solid, a yellow liquid, and a brown gas (Weast, 1989).
- It is a reddish-brown gas with an irritating odor. It is a liquid below 21.15 degrees C (Budavari, 1996).
VAPOR PRESSURE
- 400 mmHg (at 80 degrees C) (HSDB , 1991)
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
FREEZING/MELTING POINT
BOILING POINT
- 21.15 degrees C (Budavari, 1989)
SOLUBILITY
OTHER/PHYSICAL
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