Potassium Nitrate

This chemical does not meet GHS hazard criteria for 5.9% (131 of 2229) of reports.

H272 (93.9%): May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

H315 (59.4%): Causes skin irritation [Warning Skin corrosion/irritation]

H319 (59.5%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H335 (59.3%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

P210, P220, P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P370+P378, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2229 reports by companies from 21 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 131 of 2229 reports by companies.

There are 20 notifications provided by 2098 of 2229 reports by companies with hazard statement code(s).

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H272: May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

P203, P210, P220, P260, P264, P270, P280, P308+P316, P318, P319, P321, P370+P378, P405, and P501 (click each P-code to see the statement)

H303: May be harmful if swallowed [Warning Acute toxicity, oral]

H315: Causes skin irritation [Warning Skin corrosion/irritation]

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H371: May cause damage to organs [Warning Specific target organ toxicity, single exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P203, P210, P220, P260, P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P308+P316, P318, P319, P321, P332+P317, P337+P317, P362+P364, P370+P378, P403+P233, P405, and P501 (click each P-code to see the statement)

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Refer for medical attention .

Get medical attention.

INHALATION: Remove to fresh air.

EYES: Flush with water for at least 15 min., lifting lids occasionally.

SKIN: Remove contaminated clothing and shoes. Flush with water. (USCG, 1999)

General First Aid:

· Call 911 or emergency medical service.

· Ensure that medical personnel are aware of the material(s) involved, take precautions to protect themselves and avoid contamination.

· Move victim to fresh air if it can be done safely.

· Administer oxygen if breathing is difficult.

· If victim is not breathing:

-- DO NOT perform mouth-to-mouth resuscitation; the victim may have ingested or inhaled the substance.

-- If equipped and pulse detected, wash face and mouth, then give artificial respiration using a proper respiratory medical device (bag-valve mask, pocket mask equipped with a one-way valve or other device).

-- If no pulse detected or no respiratory medical device available, provide continuous compressions. Conduct a pulse check every two minutes or monitor for any signs of spontaneous respirations.

· Remove and isolate contaminated clothing and shoes.

· For minor skin contact, avoid spreading material on unaffected skin.

· In case of contact with substance, remove immediately by flushing skin or eyes with running water for at least 20 minutes.

· For severe burns, immediate medical attention is required.

· Effects of exposure (inhalation, ingestion, or skin contact) to substance may be delayed.

· Keep victim calm and warm.

· Keep victim under observation.

· For further assistance, contact your local Poison Control Center.

· Note: Basic Life Support (BLS) and Advanced Life Support (ALS) should be done by trained professionals.

Specific First Aid:

· Contaminated clothing may be a fire risk when dry.

In Canada, an Emergency Response Assistance Plan (ERAP) may be required for this product. Please consult the shipping paper and/or the "ERAP" section.

Excerpt from ERG Guide 140 [Oxidizers]:

SMALL FIRE: Use water. Do not use dry chemicals or foams. CO2 or Halon® may provide limited control.

LARGE FIRE: Flood fire area with water from a distance. Do not move cargo or vehicle if cargo has been exposed to heat. If it can be done safely, move undamaged containers away from the area around the fire.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: For ammonium nitrate products: Do not fight cargo fire. Withdraw, evacuate and isolate area for at least 1600 meters (1 mile). Treat as an explosive (ERG Guide 112). Do not enter area for 24 hours or until expert advice has been provided. Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from tanks in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

In case of fire in the surroundings, use appropriate extinguishing media.

If material on fire or involved in fire: Flood with water. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible.

If fire becomes uncontrollable--consider evacuation of one-half (1/2) mile radius.

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· Keep unauthorized personnel away.

· Stay upwind, uphill and/or upstream.

· Ventilate closed spaces before entering, but only if properly trained and equipped.

· Keep combustibles (wood, paper, oil, etc.) away from spilled material.

· Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.

· Stop leak if you can do it without risk.

· Do not get water inside containers.

Small Dry Spill

· With clean shovel, place material into clean, dry container and cover loosely; move containers from spill area.

Small Liquid Spill

· Use a non-combustible material like vermiculite or sand to soak up the product and place into a container for later disposal.

Large Spill

· Dike far ahead of liquid spill for later disposal.

Excerpt from ERG Guide 140 [Oxidizers]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

LARGE SPILL: Consider initial downwind evacuation for at least 100 meters (330 feet).

FIRE: If tank, rail tank car or highway tank 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. If ammonium nitrate products are in a tank, rail car or truck and involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, initiate evacuation including emergency responders for 1600 meters (1 mile) in all directions. (ERG, 2024)

Immediate precautionary measure

· Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

· Consider initial downwind evacuation for at least 100 meters (330 feet).

· If tank, rail tank car or highway tank 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.

· If ammonium nitrate products are in a tank, rail car or truck and involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, initiate evacuation including emergency responders for 1600 meters (1 mile) in all directions.

Sweep spilled substance into plastic or glass containers. Wash away remainder with plenty of water.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers.

Personnel protection: Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. Approach fire with caution.

For more Preventive Measures (Complete) data for POTASSIUM NITRATE (6 total), please visit the HSDB record page.

Excerpt from ERG Guide 140 [Oxidizers]:

Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Do not get water inside containers.

SMALL DRY SPILL: With clean shovel, place material into clean, dry container and cover loosely; move containers from spill area.

SMALL LIQUID SPILL: Use a non-combustible material like vermiculite or sand to soak up the product and place into a container for later disposal.

LARGE SPILL: Dike far ahead of liquid spill for later disposal. (ERG, 2024)

Separated from combustible substances and reducing agents.

Separated from combustible and reducing substances.

· Wear positive pressure self-contained breathing apparatus (SCBA).

· Wear chemical protective clothing that is specifically recommended by the manufacturer when there is NO RISK OF FIRE.

· Structural firefighters' protective clothing provides thermal protection but only limited chemical protection.

11 [mg/m3]

120 [mg/m3]

740 [mg/m3]

Small Fire

· Use water. Do not use dry chemicals or foams. CO2 or Halon® may provide limited control.

Large Fire

· Flood fire area with water from a distance.

· Do not move cargo or vehicle if cargo has been exposed to heat.

· If it can be done safely, move undamaged containers away from the area around the fire.

Fire Involving Tanks, Rail Tank Cars or Highway Tanks

· For ammonium nitrate products: Do not fight cargo fire. Withdraw, evacuate and isolate area for at least 1600 meters (1 mile). Treat as an explosive (GUIDE 112). Do not enter area for 24 hours or until expert advice has been provided.

· Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles.

· Cool containers with flooding quantities of water until well after fire is out.

· ALWAYS stay away from tanks in direct contact with flames.

· For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

Threshold limit value for potassium nitrate in the air at the workplace as applied in USSR: 5 mg/cu m /From table/

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed.

The substance is irritating to the eyes, skin and respiratory tract. Ingestion could cause effects on the blood. This may result in the formation of methaemoglobin. The effects may be delayed. Medical observation is indicated.

Full cover clothing and chemical goggles. Use approved respirator to protect against dust. (USCG, 1999)

Wear rubber gloves, safety glasses, protective work gowns.

NO contact with combustible substances or reducing agents.

PREVENT DISPERSION OF DUST!

Use local exhaust or breathing protection.

Protective gloves.

Wear safety goggles.

Do not eat, drink, or smoke during work. Wash hands before eating.

Potassium nitrate appears as a white to dirty gray crystalline solid. Water soluble. Noncombustible, but accelerates the burning of combustible materials. If large quantities are involved in fire or the combustible material is finely divided an explosion may result. May explode under prolonged exposure to heat or fire. Toxic oxides of nitrogen are produced in fires. Used in solid propellants, explosives, fertilizers.

Dry Powder; Large Crystals; Liquid; Dry Powder; Other Solid; Large Crystals; CBI

White crystalline powder or transparent prisms having a cooling, saline, pungent taste

Colorless or white solid; "Cooling, saline pungent taste" [Merck Index] Slightly hygroscopic; [HSDB] White crystalline solid; [Aldrich MSDS]

COLOURLESS-TO-WHITE CRYSTALLINE POWDER.

Colorless, rhombic or trigonal crystals

White granular or crystalline powder

Odorless

Cooling, saline pungent taste

752 °F at 760 mmHg (decomposes) (USCG, 1999)

400 °C (decomp)

633.2 °F (USCG, 1999)

333-334 °C

35g/100ml

Sol in water, glycerol; slightly sol in alcohol

Insoluble in ethanol

1 g/2.8 mL water at about 25 °C; 1 g/0.5 mL boiling water; 1 g/620 mL alcohol

38.3 g/100 g water at 25 °C

For more Solubility (Complete) data for POTASSIUM NITRATE (7 total), please visit the HSDB record page.

Solubility in water, g/100ml at 25 °C: 35.7

2.109 (USCG, 1999) - Denser than water; will sink

2.1 at 25 °C

2.1 g/cm³

2.105 @25 °C

When heated to decomp it emits very toxic fumes of /nitrogen oxides & dipotassium oxide/.

Boiling point 400 °C (decomp)

... /Potassium nitrate/ decomposes on heating producing nitrogen oxides, oxygen, which increases fire hazard.

4,5-8,5 (5 % solution)

Index of refraction: 1.335 (Alpha), 1.5056 (Beta), 1.5064 (Gamma)

Enthalpy of fusion = 11.9 kJ/mol

In contact with air, pure molten potassium nitrate is stable up to about 530 °C. Above 750 °C, the nitrite product decomposes with the formation of nitrogen oxides.

HEAT OF FUSION: 2840 CAL/G MOLE= 28.1 CAL/G

TRANSITION POINT: 129 °C FROM RHOMBIC TO TRIGONAL FORM

For more Other Experimental Properties (Complete) data for POTASSIUM NITRATE (7 total), please visit the HSDB record page.

thermal expansion coefficient

dielectric constant

pyroelectric constant

crystal structure

dielectricity

diffusion

Soluble in water.

Nitrate and Nitrite Compounds, Inorganic

Strong Oxidizing Agent

CSL00099

Decolorizing carbon + POTASSIUM NITRATE

Potentially explosive

Explosive

User-Reported

POTASSIUM NITRATE mixed with alkyl esters may explode, owing to the formation of alkyl nitrates; mixtures with phosphorus, tin (II) chloride, or other reducing agents may react explosively [Bretherick 1979. p. 108-109]. Powdered antimony mixed with potassium nitrate explodes when heated [Mellor 9:282 1946-47]. A mixture of antimony trisulfide and potassium nitrate explodes at a red heat [Mellor 9:524. 1946-47]. Arsenic disulfide forms explosive mixtures when mixed with potassium nitrate, [Mellor 9:270.1946-47]. A mixture of sodium acetate and potassium nitrate may cause an explosion [Pieters 1957. p. 30]. A mixture of potassium nitrate and sodium hypophosphite constitutes a powerful explosive [Mellor 8:881. 1946-47]. A mixture of powdered zirconium and potassium nitrate explodes when heated above the melting point [Mellor 7:116. 1946-47].

A micro Parr calorimeter exploded when the wrong proportions of these ingredients were used. The intended mixture was 4.0 g sodium peroxide, 0.2 g dextrose, and 0.2 g potassium nitrate; actual proportions were 0.35 g, 2.59 g, and 0.2 g respectively. There was insufficient sodium peroxide to dissolve decomposition gases, hence a rapid temp and pressure build-up caused the Parr bomv to burst.

... A mixture of potassium nitrate and sodium hypophosphite constitutes a powerful explosive.

A mixture of arsenic and potassium nitrate explodes when ignited.

A batch of 3,257 g of boron, 9362 g of potassium nitrate, 989 g of laminac, and 500 g of trichloroethylene had been mixing for 5 min, when an explosion occurred.

For more Hazardous Reactivities and Incompatibilities (Complete) data for POTASSIUM NITRATE (26 total), please visit the HSDB record page.

Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613)

Ingested nitrate or nitrite under conditions that result in endogenous nitrosation is probably carcinogenic to humans (Group 2A). (L135)

Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (L1137)

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Oral (L1137) ; inhalation (L1137)

Cough. Sore throat.

Redness.

Redness. Pain.

Abdominal pain. Blue lips, fingernails and skin. Dizziness. Laboured breathing. Confusion. Convulsions. Diarrhoea. Headache. Nausea. Unconsciousness.

Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (L1137)

Methemoglobinemia - The presence of increased methemoglobin in the blood; the compound is classified as secondary toxic effect

LD50: 1901 mg/kg (Oral, Rabbit) (T13)

The lethal dose of potassium nitrate for an adult ranges from 54 to 462 mg/kg.

LD50 Rabbit oral 1901 mg/kg

LD50 Rat oral 3750 mg/kg

LD50 Rabbit oral 1.166 g anion/kg /Nitrate ion/

LD50 Rat oral 3015 mg/kg

Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (L1613)

Nitrates have long been considered as harmful dietary components and judged responsible for deleterious effects on human health, leading to stringent regulations concerning their levels in food and water. However, recent studies demonstrate that dietary nitrate may have a major role in human health as a non-immune mechanism for host defense, through its metabolism to NO in the stomach. NO is a versatile molecule and although evidence exists showing that administration of low doses of exogenous NO protects against gastrointestinal inflammation, higher NO doses have been shown to exacerbate injury. So, the effect of an ingestion of nitrates in doses corresponding to a normal diet in human consumers on an experimental gastritis induced by iodoacetamide in rats was investigated. During gastritis one of the following compounds was given orally: water; potassium nitrate; the NO donor sodium nitroprusside; the NO scavenger haemoglobin given with either water or potassium nitrate. N(G)-nitro-l-arginine methyl ester (l-NAME), a non-specific NO synthase inhibitor, was administered with either water, iodoacetamide alone, or combined with potassium nitrate. After killing, the stomach was resected and microscopic damage scores, myeloperoxidase and NO synthase activities were determined. Iodoacetamide-induced gastritis was significantly reduced by potassium nitrate administration, an effect which was reproduced by sodium nitroprusside and reversed by hemoglobin. l-NAME induced gastric mucosal damage in itself, and potassium nitrate did not prevent the gastritis induced by iodoacetamide associated with l-NAME. In conclusion, dietary nitrate exerts a protective effect against an experimental gastritis in rats by releasing NO in the stomach but such an effect requires the production of endogenous NO. /Nitrates/

Dietary nitrate is reduced to nitrite by some oral bacteria and the resulting nitrite is converted to nitric oxide (NO) in acidic gastric juice. The aim of this study is to elucidate the pathophysiological role of dietary nitrate in the stomach. Intragastric administration of nitrate rapidly increased nitrate and NO in plasma and the gastric headspace, respectively. Water-immersion-restraint stress (WIRS) increased myeloperoxidase (MPO) activity in gastric mucosa and induced hemorrhagic erosions by a nitrate-inhibitable mechanism. In animals that had received either cardiac ligation or oral treatment with povidone-iodine, a potent bactericidal agent, administration of nitrate failed to increase gastric levels of NO and to inhibit WIRS-induced mucosal injury. WIRS decreased gastric mucosal blood flow by a mechanism which was inhibited by administration of nitrate. These data suggested that the enterosalivary cycle of nitrate and related metabolites consisted of gastrointestinal absorption and salivary secretion of nitrate, its conversion to nitrite by oral bacteria and then to NO in the stomach might play important roles in the protection of gastric mucosa from hazardous stress. /Nitrates/

Desensitization of hypersensitive teeth by the combination of dimethyl isosorbide (DMI) and potassium nitrate (potassium nitrate) is more effective than when potassium nitrate is used alone. potassium nitrate/DMI work together to desensitize hypersensitive teeth at a higher, quicker, and more profound and lasting level.

The intestinal transport of D-xylose was studied during subchronic poisoning of male Wistar rats with the oral administration of potassium nitrate and sodium nitrite. The metabolic parameters of small intestine mucosa were determined one hour after xylose administration, i.e., Na+/K(+)-ATPase, alkaline phosphatase, oxygen consumption, and lactic acid level. Nitrite reduced the absorption of xylose and decreased the activity of Na+/K(+)-ATPase and alkaline phosphatase. No effect of sodium nitrite was demonstrated on the aerobic metabolism of intestinal mucosa with an increased lactic acid level. Potassium nitrate did not effect the processes of intestinal absorption of xylose nor the metabolic parameters of small intestine mucosa.

For more Interactions (Complete) data for POTASSIUM NITRATE (7 total), please visit the HSDB record page.

Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Treat hypotension with supine positioning, intravenous crystalloid fluids, and a low dose -pressor if needed. Monitor vital signs and ECG for 4 to 6 hours. Symptomatic methemoglobinemia may be treated with methylene blue. ... Administer activated charcoal. Gastric emptying is not necessary for small ingestions if activated charcoal can be given promptly . Hemodialysis and hemoperfusion are not effective. Severe methemoglobinemia in infants not responsive to methylene blue therapy may require exchange transfusion. /Nitrates and Nitrites/

Decontamination: Remove victim from exposure and administer supplemental oxygen if available. Remove contaminated clothing and wash with copious soap and water. Irrigate exposed eyes with water or saline. /Nitrates and NItrites/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... Anticipate seizures and treat as necessary ... For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 d of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... /Nitrates, nitrites, and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or is in severe respiratory distress. Monitor cardiac rhythm and treat arrhythmias if necessary. Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. If unresponsive to these measures, vasopressors may be helpful. Watch for signs of fluid overload ... Treat seizures with diazepam or lorazepam ... Administer 1% solution methylene blue if patient is symptomatic with severe hypoxia, cyanosis, and cardiac compromise not responding to oxygen. DIRECT PHYSICIAN ORDER ONLY ... Use proparacaine hydrochloride to assist eye irrigation ... /Nitrates, nitrites, and related compounds/

For more Antidote and Emergency Treatment (Complete) data for POTASSIUM NITRATE (9 total), please visit the HSDB record page.

Clinical Evaluation: History. Evaluation of a patient with suspected nitrate/nitrite exposure includes a complete medical history and physical examination. Clues to potential exposure are often obtained by reviewing the following items with the patient or family: location of home (urban, suburban, or rural); drinking water source and supply (if well water: depth, location, type of well construction, and frequency of microbiologic and nitrate testing); surrounding activities (agricultural or industrial) and proximity to drinking-water source; type of sewer system (municipal or septic) and proximity to drinking water source; recent flooding; occupations, avocations, and hobbies of family members; nutritional status (for infants: type of formula, feeding regimen, and source of dilution water); family history, including recent use of medications by infant and mother; and history of recent gastroenteritis with vomiting or diarrhea. /Nitrates and Nitrites/

Physical examination should include special attention to the color of the skin and mucous membranes. If there is a history of gastroenteritis (especially in infants), evaluate the patient for the possible presence of dehydration (poor skin turgor, sunken fontanelle, dry mucous membranes). All cyanotic patients should be assessed for possible cardiac and lung disease (cardiac murmurs, gallops, arrhythmias; rales, rhonchi, wheezes, dullness or hyperresonance in the chest). A central chocolate-brown or slate-gray cyanosis that does not respond to administration of 100% oxygen is indicative of methemoglobinemia. Cyanosis due to cardiorespiratory compromise most often improves with administration of 100% oxygen. In young infants, look for labored breathing, respiratory exhaustion, hypotension, below-average weight gain, and failure to meet developmental markers. Gastroenteritis can increase the rates of production and absorption of nitrites in young infants and aggravate methemoglobinemia. /Nitrates and Nitrites/

Signs and Symptoms Signs and symptoms of methemoglobinemia can be directly correlated with the percentage of total hemoglobin in the oxidized form... The lips and mucous membranes of patients with nitrate/nitrite toxicity usually have more of a brownish than a bluish cast. Dyspnea, especially on exertion, is common. Varying degrees of central nervous system depression might be present. The cardiac and pulmonary examinations are usually normal, but systolic flow murmurs might be detected. Cardiac arrhythmias and hypotension can occur in patients with severe poisoning, although death from methemoglobinemia alone is uncommon, except in infants. /Nitrates and Nitrites/

Laboratory Evaluation Most commonly, a drop of the patient's blood is placed on a piece of filter paper next to a drop of blood from person who does not have methemoglobinemia; when dry, the blood with methemoglobin will turn a deep chocolate-brown or slate-gray color. A tube of methemoglobin containing blood will not turn red when shaken in air or when oxygen is bubbled through it, whereas blood that is dark because of normal deoxyhemoglobin will turn red. Screening Tests: Examination of blood color. Determination of the calculated versus measured arterial saturation gap. Hemoglobin and hematocrit. Serum-free hemoglobin (for hemolysis detection). Serum haptoglobin (for hemolysis detection). Heinz bodies on peripheral blood smear. Urinalysis. Specialized Tests: Determination of methemoglobin level. Tests for causes of congenital methemoglobinemia. Hemoglobin electrophoresis. Activity of NADH-dependent methemoglobin reductase. Tests for Causes of Failure of Methylene Blue Therapy (see Treatment and Management section): Activity of glucose-6-phosphate dehydrogenase (G-6-PD). Activity of NADPH-dependent methemoglobin reductase. Sulfhemoglobin blood level (not readily available for clinical use). /Nitrates and Nitrites/

For more Medical Surveillance (Complete) data for POTASSIUM NITRATE (7 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ Death and severe effects of nitrate ingestion are generally associated with doses above 10 g NO3-. Doses between 2 and 9 g NO3- have been reported to cause methemoglobinemia. These values correspond to 33 to 150 mg NO3-/kg. /Nitrate/[IPCS; Poisons Information Monograph G016: Nitrates and nitrites. (September 1996). Available from, as of October 24, 2006: http://www.inchem.org/documents/pims/chemical/pimg016.htm]

/SIGNS AND SYMPTOMS/ The major acute toxic effect from /nitrate and/ nitrite is development of methemoglobinemia, a condition where more than 10% of the hemoglobin is transformed into methemoglobin. When the conversion exceeds 70% the condition can be fatal ... These effects are reversible. The major concern of possible long-term effects of exposure to nitrate and nitrite is associated with formation of nitroso compounds, many of which are carcinogenic. This formation may take place wherever nitrite and nitrosable compounds are present, but it is favored by acidic conditions or the presence of some bacteria. The gastrointestinal tract and especially the stomach is regarded as the main formation site, but nitrosation reactions can also take place in an infected urinary bladder ... /Nitrate and nitrite poisoning/[IPCS; Poisons Information Monograph G016: Nitrates and nitrites. (September 1996). Available from, as of October 24, 2006: http://www.inchem.org/documents/pims/chemical/pimg016.htm]

/SIGNS AND SYMPTOMS/ Ingestion of large quantities may cause violent gastroenteritis. Prolonged exposure to small amounts may produce anemia, methemoglobinemia, nephritis.[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983., p. 1102]

/SIGNS AND SYMPTOMS/ ... Potassium nitrate ... /is/ rapidly absorbed and excreted unchanged, causing few reactions other than diuresis and perhaps catharsis. Under some circumstances, however, appreciable amounts of nitrate are converted to nitrite.[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-316]

For more Human Toxicity Excerpts (Complete) data for POTASSIUM NITRATE (28 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ ... KNO3 was given in large quantities (1.0 to 1.2 g/kg) to goats to study the in vivo mechanism of acute nitrate poisoning. 1. The fatal dose of orally admin estimated to be 1.0 to 1.5 g/kg. The mean time for death to occur after the admin was 14 hr 4 min. This was not dose related. 2. MHb gradually incr after the admin in all, and in the dead ones it reached a max just before death, 62.6 + or - 9.9%. In the survived goats, MHb gradually incr after admin, reached a max, and then gradually decr and disappeared. However, it varied greatly individually. 3. NO3 in the rumen juice showed a max value in the first admin after admin of KNO3. It was 560 to 3847 ppm. Higher levels were detected in the groups receiving larger doses. And then, part of NO3 was reduced in the rumen juice to NO2. It incr slightly preceding MHb. In the dead animals it reached a max (190.3 + or - 82.5 ppm) just before death. It was noted that the influence of ammonia poisoning had to be considered in goats among the above-described NH3-N in which more that 50 mg/dL was detected. NO3 and NO2 quickly absorbed into the blood and excreted into the urine. Many of the goats maintained high levels of NO3 during the experiment. The behavior of NO2 in the blood and urine varied in parallel with MHb, though the amt detected was very small, ie the max was 18.6 ppm. 4. The blood oxygen pressure showed a very high negative correlation with MHb. In the dead goats the NO2 declined following the incr of MHb showing minimum level (12.8 + or - 3.4 ppm) just before death. Main cause of death by acute nitrate poisoning is concluded to be oxygen shortage.[European Chemicals Bureau; IUCLID Dataset, Potassium nitrate (7757-79-1) (2000 CD-ROM edition). Available from, as of October 25, 2006: http://esis.jrc.ec.europa.eu/]

/LABORATORY ANIMALS: Acute Exposure/ In experimental horses, an oral dose of 1000 mg/kg of body wt of potassium nitrate caused illness but not death. Nitrate has been associated with the death of horses under field conditions ... The acute oral lethal dose of potassium nitrate is 1000 mg/kg /in sheep/.[Booth, N.H., L.E. McDonald (eds.). Veterinary Pharmacology and Therapeutics. 5th ed. Ames, Iowa: Iowa State University Press, 1982., p. 944]

LC50; Species: Daphnia magna (Water flea); Conditions: freshwater; static; Concentration: 900 mg/L for 4.2 days /total/

LC50; Species: Daphnia magna (Water flea); Conditions: freshwater; static; Concentration: 490 mg/L for 24 hr /total/

LC50; Species: Daphnia magna (Water flea); Conditions: freshwater; static; Concentration: 490 mg/L for 48 hr /total/

LC50; Species: Daphnia magna (Water flea); Conditions: freshwater; static; Concentration: 226 mg/L for 72 hr /total/

For more Ecotoxicity Values (Complete) data for POTASSIUM NITRATE (14 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ The intended purpose of /pesticide/ products containing these active ingredients is to kill certain vertebrates and wasp pest species inhabiting burrows. ... Application is subsurface and precludes exposure to avian populations and aquatic organisms. The Agency realizes, however, that any organism in a properly treated burrow will likely be killed and is concerned about potential impact to populations of non-target and endangered species. The open literature indicates that several types of non-target organisms, including burrowing owls, may inhabit the burrows of target pests. ... Due to the potential risk to non-target organisms, the Agency is currently developing more extensive labeling regarding timing of application and observation of signs indicating the presence or absence of target and nontarget organisms. These instructions will be explicit concerning actions users must take before applying the product. The use of these products may also result in a potential impact on endangered species which utilize burrows...

/AQUATIC SPECIES/ /Reproduction rate (numbers of Hydra at a given time) of Hydra attenuata is recorded in control soln and in soln containing 50, 150, 250 mg NO3/L (81.5, 245, 408 mg KNO3/L)/. At 50 mg NO3/L (81.5 mg KNO3/L) and 150 mg NO3/L (245 mg KNO3/L) the growth rate was similar or slightly superior to that of the controls. At 250 mg NO3/L (408 mg KNO3/L) the rate of growth was considerably retarded, but clubbing of tentacles was not observed. Potassium nitrate was found to be the least toxic of the 3 nitrates (KNO3, NaNO3, NH4NO3) tested with a no-effect level of between 150 and 250 mg NO3/L (between 245 and 408 mg KNO3/L). The cation had a considerable influence on toxicity of nitrate soln.

/AQUATIC SPECIES/ /In a/ static /assay,/ ... in soln with a potassium nitrate concn up to 1,035 mg potassium nitrate/L the development of loach (Misgurnus fossilis) /embryos/ up to resorption of the yolk sac was similar to the controls. At 2,068 to 2,586 mg potassium nitrate/L prolarvae hatched but then died. Starting at a concn of 5,171 mg potassium nitrate/L or more no development occurred.

/AQUATIC SPECIES/ Chronic toxicity of potassium nitrate due to a slight incr of KNO3 (8.5 mg K/L or 22 mg KNO3/L) was studied /in Tinca tinca (tench)/ over an exposure period of 2 to 35 days /in a/ flow-through /system/. The effect on blood and tissue parameters such as: plasma glycose, free plasma fatty acids, plasma glycerol, serum lactic acid, amino acids of whole blood and of plasma and of plasma cortisol was studied. Further Na and K were assayed in whole blood, plasma and liver, water content in liver and in muscle was determined together with glycogen levels in the heart, the liver and the muscles ... When Tinca tinca was exposed to a slight incr in the potassium content of the water (from 1.5 mg K/L to 8.5 mg K/L) metabolic and hormonal changes occurred which lasted more than 4 wk. An initial phase of lipolysis was followed by as partial consumption of glycogen reserves, which in turn was followed by a phase of glyconeogenesis. Hypoglycemia persisted through the experiment. The ion distribution in erythrocytes and liver changed relative early, there was no observable change in water content. These changes are similar to those observed during osmoregulation of fish.

... potassium nitrate ... /is/ present in well water contaminated by runoff from nitrogen fertilizers, decaying matter, or sewage treatment plants.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

/GUIDE 140: OXIDIZERS/ Fire or Explosion: These substances will accelerate burning when involved in a fire. Some may decompose explosively when heated or involved in a fire. May explode from heat or contamination. Some will react explosively with hydrocarbons (fuels). May ignite combustibles (wood, paper, oil, clothing, etc.). Containers may explode when heated. Runoff may create fire or explosion hazard.

/GUIDE 140: OXIDIZERS/ Health: Inhalation, ingestion or contact (skin, eyes) with vapors or substance may cause severe injury, burns or death. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may cause pollution.

/GUIDE 140: OXIDIZERS/ Public Safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.

/GUIDE 140: OXIDIZERS/ Protective Clothing: 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 will only provide limited protection.

For more DOT Emergency Guidelines (Complete) data for POTASSIUM NITRATE (8 total), please visit the HSDB record page.

UN 1486; Potassium nitrate

IMO 5.1; Potassium nitrate

49 187 37; Potassium nitrate

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Oxidizer

UN Hazard Class: 5.1; UN Pack Group: III