English Safety Data Sheet Database 中文版 MSDS

ammoniumperchlorate

CAS No. 7790-98-9 | PubChem CID 24639
Section 1. Identification
Chemical Nameammoniumperchlorate CAS No.7790-98-9
Synonyms Chinese Name过氯酸铵
Molecular FormulaNH4ClO4 Molecular Weight117.50
UN No.0402 Data SourcePubChem (NIH/NLM)
GHS Hazard Classification
Signal Word DANGER
Pictograms GHS01 · Explosive GHS03 · Oxidizer GHS07 · Irritant GHS08 · Health Hazard
Hazard Statements H201H271H319H373H272H303H315H335H302
Precautionary Statements P210P220P230P240P250P280P283P306+P360P370+P378P370+P380P371+P380+P375P372P373P401P420P501P260P264+P265P305+P351+P338P319P337+P317P261P264P271P301+P317P302+P352P304+P340P321P332+P317P362+P364P403+P233P405P270P330

Section 2. Hazards Identification

H201: (Deleted) Explosive; mass explosion hazard [Danger Explosives]

H271: May cause fire or explosion; strong Oxidizer [Danger Oxidizing liquids; Oxidizing solids]

P210, P220, P230, P240, P250, P280, P283, P306+P360, P370+P378, P370+P380, P371+P380+P375, P372, P373, P401, P420, and P501 (click each P-code to see the statement)

H201 (92.4%): (Deleted) Explosive; mass explosion hazard [Danger Explosives]

H271 (100%): May cause fire or explosion; strong Oxidizer [Danger Oxidizing liquids; Oxidizing solids]

H319 (48.6%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H373 (48.6%): May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P210, P220, P230, P240, P250, P260, P264+P265, P280, P283, P305+P351+P338, P306+P360, P319, P337+P317, P370+P378, P370+P380, P371+P380+P375, P372, P373, P401, P420, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 105 reports by companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

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.

Not Classified

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

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]

P210, P220, P230, P240, P250, P261, P264, P264+P265, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P370+P378, P370+P380, P372, P373, P401, P403+P233, P405, and P501 (click each P-code to see the statement)

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P210, P220, P230, P240, P250, P264, P264+P265, P270, P280, P283, P301+P317, P305+P351+P338, P306+P360, P330, P337+P317, P370+P378, P370+P380, P371+P380+P375, P372, P373, P401, P420, and P501 (click each P-code to see the statement)

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

P210, P220, P260, P264+P265, P280, P283, P305+P351+P338, P306+P360, P319, P337+P317, P370+P378, P371+P380+P375, P420, and P501 (click each P-code to see the statement)

Section 4. First-Aid Measures

Fresh air, rest.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again.

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

Rinse mouth. Give one or two glasses of water to drink.

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

Refer to the "General First Aid" section. Specific First Aid: Contaminated clothing may be a fire risk when dry. (ERG, 2024)

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.

Section 5. Fire-Fighting Measures

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

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. Do not get water inside containers: a violent reaction may occur.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Cool containers with flooding quantities of water until well after fire is out. Dike runoff from fire control for later disposal. 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. In case of fire: keep drums, etc., cool by spraying with water. Combat fire from a sheltered position.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Use water spray to cool unopened containers.

If material on fire or involved in fire: Do not fight fires in a cargo of explosives. Evacuate area and let it burn. /Ammonium perchlorate explosives/

For more Fire Fighting Procedures (Complete) data for Ammonium perchlorate (6 total), please visit the HSDB record page.

Explosive decomposition may occur under fire conditions.

Section 6. Accidental Release Measures

· 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.

· Use water spray to reduce vapors or divert vapor cloud drift.

· Prevent entry into waterways, sewers, basements or confined areas.

Small Spill

· Flush area with large amounts of water.

Large Spill

· DO NOT CLEAN-UP OR DISPOSE OF, EXCEPT UNDER SUPERVISION OF A SPECIALIST.

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

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.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

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. (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.

· For highlighted materials: see Table 1 - Initial Isolation and Protective Action Distances.

· For non-highlighted materials: increase the immediate precautionary measure distance, in the downwind direction, as necessary.

· 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.

Evacuate danger area! Consult an expert! Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. If appropriate, moisten first to prevent dusting. Sweep spilled substance into covered containers. Then store and dispose of according to local regulations. Do NOT absorb in saw-dust or other combustible absorbents.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Sweep up and shovel. Contain spillage, and then collect with an electrically protected vacuum cleaner or by wetbrushing and place in container for disposal according to local regulations. Keep in suitable, closed containers for disposal.

Wear full protective clothing and positive pressure self-contained breathing apparatus. Prompt cleanup and removal are necessary in order to prevent contamination with combustible materials.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D003, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits 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.

For more Preventive Measures (Complete) data for Ammonium perchlorate (8 total), please visit the HSDB record page.

Section 7. Handling and Storage

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Use water spray to reduce vapors or divert vapor cloud drift. Prevent entry into waterways, sewers, basements or confined areas.

SMALL SPILL: Flush area with large amounts of water.

LARGE SPILL: DO NOT CLEAN-UP OR DISPOSE OF, EXCEPT UNDER SUPERVISION OF A SPECIALIST. (ERG, 2024)

Fireproof. Separated from combustible substances, reducing agents and metals. See Chemical Dangers. Well closed.

Keep container tightly closed in a dry and well-ventilated place. Storage class (TRGS 510): Strongly oxidizing hazardous materials.

Separate from acids, alkalies, reducing agents, combustible materials. Store in cool, dry, well-ventilated location.

Section 8. Exposure Controls / Personal Protection

· 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.

13 [mg/m3]

140 [mg/m3]

830 [mg/m3]

Chronic Oral: 0.0007 mg/kg/day (L900)

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.

· Do not get water inside containers: a violent reaction may occur.

Fire Involving Tanks, Rail Tank Cars or Highway Tanks

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

· Dike runoff from fire control for later disposal.

· 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.

A harmful concentration of airborne particles can be reached quickly when dispersed.

The aerosol is irritating to the eyes, skin and respiratory tract.

The substance may have effects on the thyroid. This may result in reduced levels of thyroid hormones.

Excerpt from ERG Guide 143 [Oxidizers (Unstable)]:

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. (ERG, 2024)

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

NO contact with combustible substances, reducing agents or organic materials. Do NOT expose to heat, friction or shock.

PREVENT DISPERSION OF DUST!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear safety goggles or eye protection in combination with breathing protection if powder.

Do not eat, drink, or smoke during work.

Section 9. Physical and Chemical Properties

Ammonium perchlorate appears as a white, crystalline solid or powder. Classified as a division 1.1 explosive if powdered into particles smaller than 15 microns in diameter or if powdered into larger particles but thoroughly dried. Does not readily burn, but will burn if contaminated by combustible material. May explode under prolonged exposure to heat or fire. Used to make rocket propellants, explosives, pyrotechnics, as an etching and engraving agent, and in analytical chemistry.

Dry Powder

White solid crystals; [CHRIS]

WHITE HYGROSCOPIC CRYSTALS.

White orthorhombic crystals.

Colorless, crystalline compound

Solid at 15 °C

Odorless

Imparts a bitter and salty taste to water

MP: Decomposes, explodes

In water, 2.0X10+5 mg/L at 25 °C

In water, 2.45X10+5 mg/L at 25 °C

In water, 2.49X10+5 mg/L at 25 °C

Solubilities in organic solvents[Table#1332]

For more Solubility (Complete) data for Ammonium perchlorate (6 total), please visit the HSDB record page.

Solubility in water, g/100ml at 25 °C: 20

1.95 at 59 °F (USCG, 1999) - Denser than water; will sink

1.95 g/cu cm

1.95 g/cm³

1.95 @25 °C

Very low

Stable under recommended storage conditions.

464 °F (USCG, 1999)

Decomposes at 130 °C.

Decomposes violently with shock.

When heated to decomposition it emits toxic fumes of /ammonia and chloride/.

Strong oxidizing agent ... shock sensitive ... ignites violently with combustibles

Starts to decompose at 439 °C; the decomposition may be catalyzed by metallic salts such as iron oxide and copper chromite at a lower temperature. Hygroscopic between ca 75 to 95% relative humidity, and begins to deliquesce above 95%.

Ammonium perchlorate (AP) is one of the most important perchlorates owing to its high (54.5%) O2 content and the absence of residue on decomposition. These properties, along with a long shelf life, make it a useful rocket propellant

Three separate activation energies have been observed for /ammonium perchlorate/ decompositions: an activation energy of 123.8 kJ/mol (29.6 kcal/mol) is found below 240 °C; of 79.1 kJ/mol (18.9 kcal/mol) above 240 °C; and finally, of 307.1 kJ/mol (73.4 kcal/mol) between 400 and 440 °C

For more Other Experimental Properties (Complete) data for Ammonium perchlorate (6 total), please visit the HSDB record page.

Other Classes -> Perchlorates

Reactive agents - 4th degree

Potential endocrine disrupting compound

Pesticide -> EPA IRIS

Section 10. Stability and Reactivity

Water soluble.

Salts, Acidic

Oxidizing Agents, Strong

Explosive

Strong Oxidizing Agent

AMMONIUM PERCHLORATE is a strong oxidizing agent. Decomposes at 130 °C and explodes at 380 °C [Mellor 2 Supp. 1:608 1956]. Explosions have occurred in propellant formulations containing ammonium perchlorate to which ferrocene has been added as a burning rate catalyst. Although the cause was not been definitely established, it was most probably frictional heating from dragging a spatula through the mixture [ASESB Expl. Report 211 1966]. Can explode when mixed with sugar, charcoal or on contact with hot copper pipes. Becomes impact-sensitive when contaminated by powdered carbon, ferrocene, sulfur, or other reducing materials such as organic matter or powdered metals.

Incompatible materials: Strong reducing agents, strong acids.

A very powerful oxidizer that has caused explosions in industry.

When contaminated by powdered carbon, ferrocene, /sulfur/, organic matter, powdered metals, nitryl perchlorate, potassium periodate, potassium permanganate, it becomes impact sensitive. Potentially explosive reactions with carbon (above 240 °C), dichromium trioxide (at 270 °C), cadmium oxide (at 260 °C), zinc oxide (at 200 °C), copper chromite, copper oxide, iron oxide, potassium permanganate, potassium dichromate, mono-, di-, tri-, or tetra-methylammonium perchlorates, metal perchlorates (e.g., lithium perchlorate, zinc perchlorate), nitrophenol-formaldehyde polymer. Mixtures with aluminum or copper burn violently when ignited. Mixtures with ethylene dinitrate ignite when stored at 60 °C.

Explosions have occurred in propellant formulations using dicyclopentadienyliron (ferrocene), as a burning rate catalyst. Although the definite cause has not been established, the most probable cause is the heat of friction between the mixer sidewall and the spatula while the latter was scraping through a mixture of ammonium perchlorate and sublimed recrystallized ferrocenes.

For more Hazardous Reactivities and Incompatibilities (Complete) data for Ammonium perchlorate (15 total), please visit the HSDB record page.

Section 11. Toxicological Information

IDENTIFICATION AND USE: Ammonium perchlorate is a colorless, crystalline compound. The most common uses for ammonium perchlorate are in explosives and rocket propellants, which have been widely used in military munitions items, such as mortars, grenades and flares and solid fuel rocket. It is also used in analytical chemistry, and as etching and engraving agent. It has been tested as an experimental medication in (131)I exposure. HUMAN STUDIES: No perchlorate-attributable effects on thyroid, bone marrow, kidney, or liver function were detected in employees at an ammonium perchlorate production facility in Nevada. The study of workers in China also found no effect on thyroid function from long term, low-level documented exposure to ammonium perchlorate. However, epidemiological study of population drinking ammonium perchlorate contaminated water demonstrated statistically significant association between perchlorate exposure and newborn thyroid-stimulating hormone levels. ANIMAL STUDIES: In rats, exposure to ammonium perchlorate in drinking water resulted in statistically significant changes in thyroid stimulating hormone and other thyroid hormones. In developmental experiments in rats, changes in maternal and neonatal thyroid histopathology were detectable at 1.0 mg/kg-day exposure. Behavioral testing in rats suggested that prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups. Exposure of embryonic and larval Xenopus laevis to high concentrations of ammonium perchlorate salt produced a feminizing effect, resulting in a skewed sex ratio. Ammonium perchlorate (100-10,000 ug/plate) was neither toxic nor mutagenic in S. typhimurium TA98, TA100, TA102, TA104, TA1535, or TA1537 with or without metabolic activation. ECOTOXICITY STUDIES: Ammonium perchlorate exposure caused hypothyroidism in young Japanese quail and affected the expression of thyroid-responsive genes during early posthatch development. Furthermore, in Japanese quail maternal perchlorate exposure led to embryonic hypothyroidism and may have interfered with embryonic development. In X. laevis, ammonium perchlorate inhibited metamorphosis in a concentration-dependent manner as evident from effects on forelimb emergence, tail resorption, and hindlimb growth. It was also inhibiting thyroid activity and altered gonadal differentiation in developing X. laevis.

The primary and most sensitive target of the perchlorate anion (perchlorate) is the thyroid gland. Perchlorate inhibits the transport of iodide (I-) from the blood into the thyroid follicle cells. The inhibition is thought to be accomplished by perchlorate competitively blocking iodide binding to a carrier, or sodium/iodide symporter (NIS), which catalyzes the simultaneous transfer of Na+ and I-across the basolateral membrane of thyroid follicle cells. Perchlorate inhibition of the NIS can limit the availability of iodide needed for the production of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), which in turn, may affect the circulating levels of T4 and T3. All known effects of perchlorate on the thyroid hormone system derive directly or secondarily from the inhibition of the NIS. T3 is essential for normal development of the nervous system and for the regulation of metabolism of cells in nearly all tissues of the body. Disruption in the availability of T3 in target tissues can result in adverse effects on a wide variety of organs and systems (L894).

Perchlorate (ClO4) and Perchlorate Salts

Endocrine

7 x 10 ^-4 mg/kg-day

No indication of carcinogenicity to humans (not listed by IARC).

Adverse effects on a wide variety of organ systems can result from disruption in the availability of T3 to target tissues. Organ systems affected by disturbances in T3 levels include the skin, cardiovascular system, pulmonary system, kidneys, gastrointestinal tract, liver, blood, neuromuscular system, central nervous system, skeleton, male and female reproductive systems, and numerous endocrine organs, including the pituitary and adrenal glands. Such an array of secondary potential targets underscores the need to maintain an adequate level of circulating thyroid hormones. Perchlorate, an environmental contaminant, is known to disturb the hypothalamus-pituitary-thyroid (HPT) axis by blocking iodide accumulation in the thyroid. Iodide deficiency can lead to hypothyroidism and goiter (L894, A267).

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

Inhalation (L894) ; oral (L894) ; dermal (L894) ; eye contact (L894).

Redness. Pain.

Burning sensation. Nausea. Vomiting. Diarrhoea.

Irritating to skin, eyes, and respiratory system, depending on the route of exposure. Esophageal or gastrointestinal tract irritation could occur following exposures (L894).

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

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

IRIS Current

LD50: 4200 mg/kg (Oral, Rat) (T13)

LD50: 1900 mg/kg (Oral, Rabbit) (T13)

LD50 Rat oral 4200 mg/kg

LD50 Guinea pig oral 3310 mg/kg

LD50 Rabbit oral 1900 mg/kg

In case of oral exposure, immediately dilute with 4 to 8 ounces (120 to 240 mol) of water or milk. Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in Trendelenburg and left lateral decubitus position or by endotracheal intubation. Control any seizures first. Maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Following 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 inhaled beta2 agonist and oral or parenteral corticosteroids. In case of acute lung injury, maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Following eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. Following dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. (T36)

Radioactive iodide ((131)I-) protection studies have focused primarily on the thyroid gland and disturbances in the hypothalamic-pituitary-thyroid axis. The objective of the current study was to establish (131)I- urinary excretion profiles for saline, and the thyroid protectants, potassium iodide (KI) and ammonium perchlorate over a 75 hour time-course. Rats were administered (131)I- and 3 hours later dosed with either saline, 30 mg/kg of NH(4)ClO(4) or 30 mg/kg of KI. Urinalysis of the first 36 hours of the time-course revealed that NH(4)ClO(4) treated animals excreted significantly more (131)I- compared with KI and saline treatments. A second study followed the same protocol, but thyroxine (T(4)) was administered daily over a 3 day period. During the first 6-12 hour after (131)I- dosing, rats administered NH(4)ClO(4) excreted significantly more (131)I- than the other treatment groups. T(4) treatment resulted in increased retention of radioiodide in the thyroid gland 75 hour after (131)I- administration. We speculate that the T(4) treatment related reduction in serum TSH caused a decrease synthesis and secretion of thyroid hormones resulting in greater residual radioiodide in the thyroid gland. Our findings suggest that ammonium perchlorate treatment accelerates the elimination rate of radioiodide within the first 24 to 36 hours and thus may be more effective at reducing harmful exposure to (131)I- compared to KI treatment for repeated dosing situations. Repeated dosing studies are needed to compare the effectiveness of these treatments to reduce the radioactive iodide burden of the thyroid gland.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Ammonia and related compounds/

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 signs of pulmonary edema and treat if necessary ... . Monitor for shock and treat if 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 mL of water for dilution if the patent can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize. /Ammonia and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . 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. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Ammonia and related compounds/

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Chlorates and Related Compounds/

For more Antidote and Emergency Treatment (Complete) data for Ammonium perchlorate (6 total), please visit the HSDB record page.

/EPIDEMIOLOGY STUDIES/ The Colorado River below Lake Mead, which supplies drinking water for approximately 20,000,000 people, is contaminated by ammonium perchlorate. We identified populations who were exposed and unexposed to perchlorate-contaminated drinking water and compared median newborn thyroid-stimulating hormone (TSH) levels after adjusting for age in days at measurement and for race/ethnicity. Median newborn TSH levels in a city whose drinking water supply was 100% perchlorate-contaminated water from the Colorado River below Lake Mead were significantly higher than those in a city totally supplied with non-perchlorate-contaminated drinking water, even after adjusting for factors known or suspected to elevate newborn TSH levels. This ecological study demonstrates a statistically significant association between perchlorate exposure and newborn TSH levels. It suggests that even low-level perchlorate contamination of drinking water may be associated with adverse health effects in neonates and highlights the need for both further study and control of human low-level perchlorate exposure.

/EPIDEMIOLOGY STUDIES/ /The study objective was/ to understand the occupational hazards of ammonium perchlorate dust on operating workers and to provide the basis preventive measures for protecting the workers' health. 36 workers exposed to ammonium perchlorate dust and 48 unexposed workers from one factory were selected as the exposure and control groups. Investigations on the general condition, sampling of dust in the workplaces and a special medical examination were conducted for two groups, including occupational history, clinical manifestations, blood routine test, hepatic and renal functions, indexes of thyroid hormone, spirometric test and chest X-ray. The total dust concentration of AP in the batch plant reached to 51.63 +/- 43.27 mg/cu m, exceeding the U.S. Occupational Safety and Health Administration (OSHA) permission exposure limits. The systolic blood pressure in the exposure group was higher than that of the control group (146.14 +/- 21.03 VS 134.67 +/- 18.58), and the difference was statistically significant (P < 0.05). The detection rates of the cumulative total symptoms, short of breath and skin itch symptoms in the exposure group were significantly higher than those in the control group (86.11% VS 66.67%; 30.56% VS 12.50%) (P < 0.05), respectively. FT(3) level in the exposure group significantly lowered than the control group, and the difference was statistically significant (P < 0.01); The pulmonary function result showed that FEV1/FVC% in the exposure group was lower than that in the control group (106.50 +/- 28.99 VS 111.70 +/- 19.72), but the difference was not significant. X-ray examination revealed one case of pulmonary X-ray abnormalities in the exposure group, diagnosis of pneumoconiosis, and one case with about 1.0 x 1.0 small nodules detected on the left of lung donor area in the control group. The systolic blood pressure of workers in the exposure group was significantly higher, which could not exclude related to the exposure to AP dust; The T(3) levels in the exposure workers were lower than those in the control group, which may due to AP exposure, suggesting that long-term chronic exposure to AP dust may affect thyroid function.

/BIOMONITORING/ Perchlorate (ClO(4)(-)) and thiocyanate (SCN(-)) are potent and nitrate (NO(3)(-)) a weak competitive inhibitor of the thyroid sodium-iodide symporter. To determine the effects of long-term, high ClO(4)(-) exposure on thyroid function, /the authors/ conducted a study of 29 workers employed for at least 1.7 yr (50% over 5.9 yr) in an ammonium ClO(4)(-) production plant in Utah. Serum ClO(4)(-), SCN(-), and NO(3)(-); serum T(4), free T(4) index, total T(3), thyroglobulin (Tg), and TSH; 14-hr thyroid radioactive iodine uptake (RAIU); and urine iodine (I) and ClO(4)(-) were assessed after 3 d off (Pre) and during the last of three 12-hr night shifts in the plant (During) and in 12 volunteers (C) not working in the plant. Serum and urine ClO(4)(-) were not detected in C; urine ClO(4)(-) was not detected in 12 of 29 and was 272 ug/L in 17 Pre workers; serum ClO(4)(-) was not detected in 27 of 29 Pre; and serum and urine ClO(4)(-) were markedly elevated during ClO(4)(-) exposure to 868 ug/L and 43 mg/g creatinine, respectively. Serum SCN(-) and NO(3)(-) concentrations were similar in all groups. Thyroid RAIUs were markedly decreased in During compared with Pre (13.5 vs. 21.5%; P < 0.01, paired t) and were associated with an increase in urine I excretion (230 vs. 148 ug I/g Cr; P = 0.02, paired t) but were similar to those in the C group (14.4%). Serum TSH and Tg concentrations were normal and similar in the three groups. Serum T(4) (8.3 vs. 7.7 microg/dL), free T(4) index (2.4 vs. 2.2), and total T(3) (147 vs. 134 ng/dL) were slightly but significantly increased in the During vs. Pre workers (P < 0.01, paired t). Thyroid volumes and patterns by ultrasound were similar in the 29 workers and 12 community volunteers. In conclusion, high ClO(4)(-) absorption during three nights work exposure decreased the 14-hr thyroid RAIU by 38% in ClO(4)(-) production workers compared with the RAIU after 3 d off. However, serum TSH and Tg concentrations and thyroid volume by ultrasound were not affected by ClO(4)(-), suggesting that long-term, intermittent, high exposure to ClO(4)(-) does not induce hypothyroidism or goiter in adults.

/ENDOCRINE MODULATION/ The impact of low level dust on the thyroid function of workers chronically exposed to ammonium perchlorate (AP) is uncertain and controversial. The aim of this study was to examine whether workers in China with long-term (>3 years) occupational exposure to low levels of AP dust had affected thyroid homeostasis. Mean occupational exposures to AP dust ranged from 0.43 to 1.17 mg/cu m. Geometric means of post-shift urinary perchlorate levels were 20.5 ug/L for those exposed and 12.8 ug/L for the controls. No significant differences were found for thyroid function parameters of FT3, FT4, or log TSH or for TPO prevalence or thyroglobulin levels. Additionally, no differences in findings were observed for complete blood count (CBC), serum biochemical profile, or pulmonary function test. Median urinary iodine levels of 172 and 184 ug/L showed that the workers had sufficient iodine intake. This study found no effect on thyroid function from long term, low-level documented exposure to ammonium perchlorate. /This study reports/ both thyroid status parameters and urinary perchlorate, a biomarker of internal perchlorate exposure, in occupationally exposed workers in China.

/ENDOCRINE MODULATION/ Employees at an ammonium perchlorate production facility in Nevada and a larger control population from the same chemical complex without direct AP exposure were monitored extensively for airborne perchlorate exposure. Single-shift and working-lifetime cumulative dose estimates were made using standard breathing-rate estimates and assuming rapid absorption, based upon solubility. Calculated single-shift doses ranged from 0.2 to 436 ug/kg, with an average of 36 ug/kg. Working-lifetime cumulative doses in the higher exposure group ranged from 8,000 to 88,000 ug/kg, with an average of 38,000 ug/kg. Thyroid profiles, including free thyroxine index and thyroid-stimulating hormone level, were obtained both before shift and after shift to assess thyroid-axis perturbation due to single working-shift perchlorate exposure. Thyroid-function data were also analyzed with respect to estimates of cumulative exposure to assess any measurable chronic effects on thyroid gland function. Additionally, standard clinical blood test parameters of liver, kidney, and bone marrow function were evaluated to assess any measurable chronic effects of perchlorate exposure on those organs. Multiple regression was used to assess the effects of exposure variables and demographic variables on organ function parameters. No perchlorate-attributable effects on thyroid, bone marrow, kidney, or liver function were detected.

/LABORATORY ANIMALS: Acute Exposure/ /The study objective was/ to study the injury effect of ammonium perchlorate (AP) to lung and to explore whether AP can cause pulmonary fibrosis. /The method was/ to detect the levels of cell counts, TNF-alpha, MDA, HYP and the synthesis of collagen in BALF or rat lung after a certain time when rats were injected AP by intratracheal instillation. AP could bring about acute lung damage and inflammatory reaction. The levels of TNF-alpha of different groups in different time were obviously higher than the normal control group (P < 0.05). AP could affect the levels of MDA, HYP and the synthesis of collagen. But it had no obviously pathological change of pulmonary fibrosis. There were acute injury effect about AP to lung, but this experiment could not make sure whether AP could cause pulmonary fibrosis.

/LABORATORY ANIMALS: Acute Exposure/ Ammonium perchlorate (AP), an oxidizer, has been used in solid propellants. Although AP exposure has been suspected as a risk factor for the development of pulmonary fibrosis, data are still inconclusive. To evaluate the pulmonary toxicity and the potential pulmonary fibrosis caused by occupational exposure to this compound, 25 male rabbits were randomly allocated into five groups to receive AP or bleomycin or saline by intratracheal injection. All rabbits were sacrificed and total RNA from the lungs was extracted. Expressions of types I and III collagens, transforming growth factor-beta(1) (TGF-beta(1)) and tumor necrosis factor-alpha (TNF-alpha) messenger RNA (mRNA) were measured by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of type I and III collagen mRNA in low, moderate and high dose AP groups were significantly higher (p < 0.01 or p < 0.05) than that in the saline group. There was also a significant increased level of TGF-beta(1) and TNF-alpha mRNA in the three AP groups compared with saline control group (p < 0.01 or p < 0.05). These results reveal that AP can increase gene expressions of types I, III collagens, TGF-beta(1) and TNF-alpha in lung of rabbits exposed to AP. The overexpression of these biomarkers were considered as effective indicator linking to the development of pulmonary fibrosis and finally demonstrated that AP has potential to induce pulmonary fibrosis.

/LABORATORY ANIMALS: Acute Exposure/ ... To evaluate the potential pulmonary fibrosis caused by occupational exposure to /ammonium perchlorate (AP)/, 25 male rabbits were randomly allocated into 5 groups to receive AP or bleomycin or saline by intratracheal injection. All rabbits were sacrificed and lung tissues were removed to prepare hematoxylin and eosin (HE) staining for microscope observation and to perform electron microscopy examine. In microscope observation, AP-instilled lung tissue showed inflammatory infiltrates, alveolar collapse, subpleural thickening, and lymphocyte proliferation. Electron microscopy examination of lung tissue showed massive fibroblast accumulation, collagen fiber hyperplasia, and dense collagen deposition. The histopathological changes were considered as effective indicator linking to the development of pulmonary fibrosis. These results demonstrated that chronic instillation of AP can induce pulmonary fibrosis. And these results revealed that AP has pulmonary toxic effect.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Ammonium perchlorate (AP), mainly used as solid propellants, was reported to interfere with homeostasis via competitive inhibition of iodide uptake. However, detailed mechanisms remain to be elucidated. In this study, AP was administered at 0, 130, 260 and 520 mg/kg every day to 24 male SD rats for 13 weeks. The concentrations of iodine in urine, serum thyroid hormones levels, total iodine, relative iodine and total protein, and malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activity in thyroid tissues were measured, respectively. Our results showed that high-dose perchlorate induced a significant increase in urinary iodine and serum thyroid stimulating hormone (TSH), with a decrease of total iodine and relative iodine content. Meanwhile, free thyroxine (FT4) was decreased and CAT activity was remarkably increased. Particularly, the CAT activity was increased in a dose-dependent manner. These results suggested that CAT might be enhanced to promote the synthesis of iodine, resulting in elevated urinary iodine level. Furthermore, these findings suggested that iodine in the urine and CAT activity in the thyroid might be used as biomarkers for exposure to AP, associated with thyroid hormone indicators such as TSH, FT4.

For more Non-Human Toxicity Excerpts (Complete) data for Ammonium perchlorate (27 total), please visit the HSDB record page.

The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for ammonium perchlorate is available.[Available from, as of March 27, 2018: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of March 27, 2018: http://actor.epa.gov/dashboard/]

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 652060 ug/L for 24 hr

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 396210 ug/L for 48 hr

Section 12. Ecological Information

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 652060 ug/L for 24 hr

LC50; Species: Daphnia magna (Water flea) age <24 hr neonate, clone K6; Conditions: freshwater, static, 20 °C; Concentration: 396210 ug/L for 48 hr

/BIRDS and MAMMALS/ The effects of a wide range of ammonium perchlorate (AP) concentrations in drinking water on thyroid function in bobwhite quail chicks was investigated at 2, 4, and 8 weeks of exposure. ...Plasma thyroid hormones (THs) /were measured/ to evaluate organismal thyroid status, thyroid weights to evaluate hypothalamic-pituitary-thyroid (HPT) axis activation, and thyroidal TH content to assess TH stores. At the highest AP exposures plasma THs were decreased, thyroid glands were hypertrophied, and thyroidal TH content was decreased. As in ...previous studies, thyroidal thyroxine (T(4)) content was the most sensitive indicator of decreased thyroid function; plasma T(4) and thyroid weight were much less sensitive. The lack of sensitivity of these variables appears to result from cyclic patterns of thyroid responses involving the HPT axis and intermittent release of stored THs from the thyroid gland. With sustained AP exposure (8 weeks), at the lowest range of AP concentrations used, chicks showed adaptation in thyroid function that fully compensated for the initial (2 week) effects of AP. At the intermediate AP concentrations there was partial compensation for the initial AP effects. At the highest AP exposures used, thyroid function was very low throughout the study, with no indication of compensatory responses. The capability of chicks to increase some aspects of their thyroid function adaptively in response to some levels of sustained AP exposure is contrary to the common generalization that developing animals are most vulnerable to environmental contaminants.

/BIRDS and MAMMALS/ Ground-dwelling birds in perchlorate-contaminated areas are exposed to perchlorate ion, a known thyroid disruptor, and might be vulnerable to the developmental effects of perchlorate-induced hypothyroidism. ...Perchlorate-induced hypothyroidism would alter the expression of thyroid-responsive genes involved in thyroid hormone (TH) regulation and in the development of target organ function. Japanese quail chicks were exposed to 2000 mg/L ammonium perchlorate in drinking water for 7.5 weeks beginning on day 5 posthatch. Hypothyroidism was evident after 2 weeks of exposure as lower plasma THs and lower TH content in exposed chicks than in controls. The degree of hypothyroidism was increased at 7.5 weeks, as indicated by significant thyroid gland hypertrophy and sustained changes in thyroid function. After 2 weeks of exposure, hypothyroidism increased type 2 5'-deiodinase (D2) mRNA level and decreased Spot 14 (SP14) mRNA level in the liver, whereas D2 mRNA and RC3 mRNA levels in brain were not affected. After 7.5 weeks of exposure, mRNA levels in the exposed group did not differ from those in controls in either the liver or brain, suggesting the responsiveness of these genes to THs decreased during development. These results suggest that the brain, but not the liver, was protected from the effects of hypothyroidism, probably by changes in D2 activity at the protein level and/or regulation of TH entry and exit from the brain. ...Perchlorate exposure caused hypothyroidism in young Japanese quail and affected the expression of thyroid-responsive genes during early posthatch development.

/BIRDS and MAMMALS/ Perchlorate, a known thyroid disruptor, is deposited in eggs of exposed female birds, raising concerns that the embryos from these eggs may become hypothyroid, which may in turn affect the development and function of thyroid-dependent organs. /It was/ hypothesized that exposure to ammonium perchlorate (AP) would decrease hen and embryonic thyroid function and affect the expression of thyroid-responsive genes in embryonic brain and liver. Laying Japanese quail hens were treated with 2000 mg/L or 4000 mg/L AP in drinking water. Thyroid status and expression of thyroid-responsive genes were examined in the embryos from eggs of exposed hens. Perchlorate exposure led to hypothyroidism in hens from both treatment groups; egg production was decreased in the high dosage group only. Embryos from eggs of perchlorate-exposed hens had hypertrophied thyroid glands and significantly lower thyroidal hormone storage, indicating hypothyroidism in these embryos. The embryonic hypothyroidism was associated with decreased embryonic growth, delayed hatching and greater mortality during hatching. The mRNA level of type 2 deiodinase (D2) in the liver of embryos from eggs of perchlorate-exposed hens was increased compared to the control embryos, a compensatory response that increases the production of metabolically active T(3). However, the mRNA levels of D2 and RC3 in the brain were not affected. These results suggest that the embryonic brain is protected from hypothyroidism by other mechanisms known to influence hormone entry into and exit from the brain. ...Maternal perchlorate exposure led to embryonic hypothyroidism and may have interfered with embryonic development.

/BIRDS and MAMMALS/ Bobwhite quail chicks were used to investigate ammonium perchlorate (AP; NH4ClO4) effects on thyroid function and growth. Beginning at 3 to 4 days posthatch, ...organismal thyroid status (circulating hormones), activation of the hypothalamic-pituitary-thyroid axis (thyroid wt) and thyroidal hormone content /were evaluated/ over a wide range of AP concentrations (50 ug/L-4,000 mg/L) in drinking water, for relatively short (2-week) and longer (8-week) exposures. Thyroidal thyroxine (T4) content, the most sensitive index of decreased thyroid function, decreased markedly in response to increasing perchlorate exposure. Thyroid weight and plasma T4 were less sensitive indicators and similar in their ability to detect thyroid changes. Growth measurements (body wt and skeletal growth) were very insensitive indices. Because thyroids contain large hormone stores, with low exposures or short time periods, these stores can be used to maintain circulating hormones, at least temporarily. Most depletion of thyroidal T4 occurred during the first two weeks of AP exposure. Subsequent decreases were at a slower rate presumably because thyrotropin stimulation of the thyroids at least partially compensated for some of the perchlorate effect. Additional studies of the interactions between AP concentration and exposure time are needed for understanding the complex nature of thyroid responses to perchlorate.

For more Ecotoxicity Excerpts (Complete) data for Ammonium perchlorate (11 total), please visit the HSDB record page.

5.50e+01

8.20e+02

1.40e+01

4.00e-03

7.00e-04

Volatile

1.60e+02

2.50e+03

4.20e+01

This substance may be hazardous to the environment. Special attention should be given to crustacea.

Ammonium perchlorate's production and use as in explosives, pyrotechnic compositions, jet and rocket propellants, and in analytical chemistry, may result in its release to the environment through various waste streams. Perchlorate salts such as ammonium perchlorate are expected to exist as a solid aerosol or be absorbed to suspended particulate matter. Therefore, removal from the atmosphere is expected to occur by both wet and dry deposition. Perchlorates are not expected to undergo direct photolysis in air. If released in soil, the perchlorate ion is only weakly absorbed to mineral surfaces of moderate ionic strength. The ion exhibits high aqueous solubility and together these properties contribute to its ability to readily migrate in groundwater systems. The ion is not expected to volatilize from soil to the atmosphere as perchlorates exhibit very low vapor pressures. If released to water, ammonium perchlorate readily dissolves and dissociates to the perchlorate ion. Perchlorate is an ion and, therefore, volatilization from water surfaces is not expected to be an important fate process. Hydrolysis does not occur for inorganic salts such as ammonium perchlorate that ionize in aqueous solution. Occupational exposure to ammonium perchlorate may occur through inhalation of dust and dermal contact with this compound at workplaces where ammonium perchlorate is produced or used. The general population is exposed to perchlorate ion via ingestion of contaminated food and drinking water. (SRC)

Perchlorate has been identified in some fertilizer components such as phosphate rock and Chilean nitrate, which contains 0.1% perchlorate(1,2). It has also been identified as occurring naturally in rain and snow(2). /Perchlorate/

Ammonium perchlorate's production and use in explosives, pyrotechnic compositions, jet and rocket propellants(1), as a solid oxidant in space shuttles and intercontinental ballistic missiles(2) and in analytical chemistry(3) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). The perchlorate ion is only weakly absorbed to mineral surfaces of moderate ionic strength(1). Perchlorate ion also exhibits a high aqueous solubility; together these properties contribute to its ability to readily migrate in groundwater systems(2).

AQUATIC FATE: When released to water, ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). Perchlorates are readily soluble in water. In dilute aqueous solutions, the ion is very stable and inert and therefore may persist for decades under normal conditions in groundwater and surface water systems(2). Hydrolysis does not occur for inorganic salts such as ammonium perchlorate that ionize in aqueous solution(1). Perchlorates are not expected to undergo direct photolysis in water(1).

ATMOSPHERIC FATE: Perchlorate salts such as ammonium perchlorate are expected to exist as a solid aerosol or be absorbed to suspended particulate matter(1). Therefore removal from the atmosphere is expected to occur by both wet and dry depostion(1). Perchlorates are not expected to undergo direct photolysis in air(1).

ANAEROBIC: Microorganisms isolated from soil have been found to reduce perchlorates under anaerobic conditions using laboratory tests(1). Perchlorate applied to Yolo loam at a concentration of 180 mg/L and incubated anaerobically under flooded conditions was completely biodegraded after 30 days(1). No loss was observed using a Columbia loam soil(1). The facultative anaerobes belonging to the genera Riemerella, Acidovorax and Azoarcus together may be capable of perchlorate reduction(2). However, nitrate does interfere with perchlorate reduction(3). Using sediment and soil samples obtained from two Texas sites associated historically with perchlorate discharge, anaerobic microcosms studies indicate that rapid perclorate degradation did not occur until nitrate was degraded to a relatively low level(3).

Perchlorates of almost all electropositive metals are known. Solid perchlorates containing the tetrahedral CLO4(-) ion are often isomorphous with salts of other tetrahedral ions. A particular important property of the perchlorate ion is its slight tendency to serve as a ligand in complexes(1). Perchlorate is inert to reduction despite the high oxidation state of the chlorine, +7(2). In dilute aqueous solutions, the ion is very stable and inert and therefore may persist for decades under normal conditions in groundwater and surface water systems(3).

When released to water, ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). Hydrolysis does not occur for inorganic salts such as ammonium perchlorate that ionize in aqueous solution(1). Perchlorates are not expected to undergo direct photolysis in air or water(1). Perchlorate is inert to reduction despite the high oxidation state of the chlorine, +7(2). In dilute aqueous solutions, the ion is very stable and inert and therefore may persist for decades under normal conditions in groundwater and surface water systems(3).

Using a plant-mediated treatment of perchlorate-contaminated water, perchlorate uptake occurred in eastern cottonwoods (Populus deltoides and hybrid populus), Eucalyptus cineria, and willow (Salix nigra) in sand bioreactors. Perchlorate uptake in willows was found initially rapid at a rate that was linear with the volume of water evapotranspired by the tree until a plateau was reached. From an initial application of 88.8 mg (96.4 mg/L), the total amounts of perchlorate in root, lower stem, upper stem, and leaf after 26 days were 0.04, 0.18, 0.34 and 0.48 mg, respectively. 11% of the perchlorate was not accounted for and believed to be degraded in the leaves(1).

Ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). The perchlorate ion is only weakly absorbed to mineral surfaces of moderate ionic strength(1). The ion exhibits high aqueous solubility and together these properties contribute to its ability to readily migrate in groundwater systems(2).

Ammonium perchlorate readily dissolves and dissociates to the perchlorate ion(1). The ion is not expected to volatilize from soil to the atmosphere as perchlorates exhibit very low vapor pressures(1).

The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of both ground and surface waters, particularly in the western US(1). In 1997, low-level perchlorate contamination, <50 ng/mL, was discovered in the western United Stated and since then, has been detected in sites scattered throughout the Nation(2). Affected regions include southern California (metropolitan Los Angeles), Nevada (especially greater Las Vegas), northwestern Arizona, and parts of Utah(2).

DRINKING WATER: The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of groundwater, particularly in the western US(1). 40 surface water drinking water supplies in 11 states surveyed in 1997 and 1998 (CT, IL, IN, IO, KY, MA, MO, NJ, OH, TN, WV) tested negative for perchlorate ion(2). Of the 367 groundwater wells tested in 17 states (AZ, CA, CT, IL, IN, IO, MD, MA, MI, MO, NH, NJ, NM, OH, PA, VA, WV), the presence of the compound was positive in nine wells (approximately 2.5% of the samples); these were located in New Mexico (not detected to 7.1 ug/L) or California (not detected to 6.7 ug/L)(1). Perchlorate concentration ranged from <4 to 7 ug/L(2).

SURFACE WATER: The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of surface water, particularly in the western US(1). Perchlorate ion concentration in stream water sampled from June 2001 through October 2002 near the Naval Weapons Industrial Reserve Plant in McGregor, TX ranged from below the detection limit of 1 ug/L to average concentration of 281 ug/L(2).

RAIN/SNOW: Perchlorate ion was identified at concentrations ranging from not detected to 0.6 ug/L in rain samples. The concentration range in snow ranged from not detected to 0.4 ug/L. Sampling was conducted in Lubbock TX from April through November, 2004(1). /Perchlorate/

Over time, ammonium perchlorate, which is used as a solid oxidant and energetics booster, decomposes and must be replaced. Replacement sites as well as ordnance storage areas are known to suffer from perchlorate contamination(1), believed to be the legacy of years of legal dumping of wastewaters dating back several decades; the original salt was probably ammonium perchlorate(1). Perchlorate has been detected in wells in areas where aerospace material and munitions development, manufacture and testing occur, where explosives and fireworks are manufactured and near facilities that discharge the unregulated material(2). It has been speculated that some fertilizer imported from Chile may contain low levels of the compound(2,3). Perchlorate concentrations in fertilizer components were as follows: phosphate rock (western), 0.10%; phosphate rock (Florida), 0.11%; potash (commercial), 0.29%; potash (muriate), 0.36%; dihydrogen ammonium phosphate, 0.46%; urea, 0.25%; langbenite, 1.86%; Chilean nitrate, 3.64%(3). Concentrations in commercial fertilizers were as follows: ammonium nitrate, 0.22%; Lesco, 0.57%; Procare, 0.20%; fallfeed winterizer, 0.15%; STA-Green, 0.84%; Scotts winterizer, 0.51%; Vigaro, 0.55%; premium lawn, 0.33%; Pennington, 0.61%(3).

SEDIMENT: The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of the environment(1). Perchlorate contamination of sediment and soil has been reported at twenty-seven Department of Defense facilities and at two other federal agency facilities in AL, AZ, CA, IN, MA, MD, NJ, NM, TX, UT, WA and WV as of March, 2005(1). Maximum concentrations in sediment were reported as follows: Aberdeen Proving Ground, MD, 17 ppb; Naval Surface Warfare Center, MD, 230 ppb; Lone Star Army Ammunition Plant, TX, 186 ppb; Alleghany Ballistics Laboratory, WV, 190 ppb(1). It was detected in 93% of 93 sediment samples from Lake Mead, NV at an average concentration of 12.8 mg/kg, max of 56.0 mg/kg(1).

SOIL: The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of the environment(1). Perchlorate contamination of sediment and soil has been reported at twenty-seven Department of Defense facilities and at two other federal agency facilities in AL, AZ, CA, IN, MA, MD, NJ, NM, TX, UT, WA and WV as of March, 2005(1). Maximum perchlorate concentration in soil ranges from 32 to 2,000,000 ppb(1). The concentration of perchlorate underneath the foundation of a former propellant mixing facility at McGregor Texas Navel Weapons Industrial Reserve Plant ranged from 23 to 1,800,000 ug/kg(1). It was detected in 38% of 113 soil samples from Lake Mead, NV at an average concentration of 57.7 mg/kg, max of 1,470 mg/kg(1). Perchlorate concentration of 340 ug/kg was measured in a soil collected in December 1999 from a tobacco field previously treated that summer with fertilizer derived from Chilean caliche (perchlorate level of 35,800 and 1,544,000 ug/kg)(1).

The large-scale disposal of explosives containing ammonium perchlorate salts has resulted in perchlorate contamination of the environment(1). Perchlorate ion concentration was observed to vary seasonally in a stream-side willow tree sampled from October 2001 through October 2002 near the Naval Weapons Industrial Reserve Plant in McGregor, TX(2). Perclorate concentrations were as follows (ug/kg dry wt, DL = 300 ug/kg dry wt): October 2001, 15,800; April 2002, <DL; May 2002, <DL; June 2002, 300; August 2002, 1,200; October 2002, 14,600(2).

Perchlorate ion concentration in aquatic and stream-side plants sampled from June 2001 through October 2002 near the Naval Weapons Industrial Reserve Plant in McGregor, TX, which used ammonium perchlorate; detection limit = 300 ug/kg dry weight in plants(1).

Table: <DL [Table#1330]

Perchlorate was unambiguously detected by ion chromatography-suppressed conductivity (IC-CD) and/or ion chromatography-electrospray mass spectrometry (IC-MS) in seven of seven supermarket milk samples bought randomly in Lubbock, TX. Quantitation by IC-MS and IC-suppressed conductivity detection in conjunction with a preconcentration-preelution method provided comparable results. With a sample cleanup procedure that involved protein removal by ethanol and sequential passage though activated alumina and C-18 silica, the limit of detection for perchlorate in milk was 0.5 ug/L. The levels found ranged from 1.7 to 6.4 ug/L. An evaporated milk sample contained perchlorate at 1.1 +/- 0.6 ug/L level, while we did not find detectable levels in a reconstituted powdered milk sample. /Perchlorate/

Section 13. Disposal Considerations

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D003, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

Section 14. Transport Information

/GUIDE 143 OXIDIZERS (Unstable)/ Fire or Explosion: May explode from friction, heat or contamination. These substances will accelerate burning when involved in a fire. May ignite combustibles (wood, paper, oil, clothing, etc.). Some will react explosively with hydrocarbons (fuels). Containers may explode when heated. Runoff may create fire or explosion hazard.

/GUIDE 143 OXIDIZERS (Unstable)/ Health: TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors, dusts or substance may cause severe injury, burns or death. Fire may produce irritating and/or toxic gases. Toxic fumes or dust may accumulate in confined areas (basement, tanks, hopper/tank cars, etc.). Runoff from fire control or dilution water may cause pollution.

/GUIDE 143 OXIDIZERS (Unstable)/ 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, uphill and/or upstream. Ventilate closed spaces before entering.

/GUIDE 143 OXIDIZERS (Unstable)/ 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 provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

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

UN 0402; Ammonium perchlorate

UN 1442; Ammonium perchlorate

IMO 1.1D; Ammonium perchlorate

IMO 5.1; Ammonium perchlorate

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 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. Ammonium perchlorate is included on the dangerous goods list.

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. Ammonium perchlorate is included on the dangerous goods list.

Oxidizer Explosive 1.1D

Symbol: O; R: 9-44; S: (2)-14-16-27-36/37; Note: G

UN Hazard Class: 5.1; UN Pack Group: II

Source: PubChem CID 24639 (NIH/NLM, public domain). Retrieved from PubChem, a public-domain chemistry database maintained by the U.S. National Library of Medicine. Last updated: 2026-08-02 09:06:47.
Disclaimer: This information is compiled for reference only and does not replace the manufacturer's official Safety Data Sheet. Always consult the supplier's SDS before handling any chemical.