Ammonia

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

Wear positive pressure breathing apparatus and full protective clothing.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep cylinder cool by spraying with water.

- Ammonia is flammable.

Fresh air, rest. Half-upright position. Administration of oxygen may be needed. Refer immediately for medical attention.

Rinse skin with plenty of water or shower for at least 15 minutes. ON FROSTBITE: rinse with plenty of water, do NOT remove clothes. Refer immediately for medical attention .

Rinse with plenty of water for several minutes (remove contact lenses if easily possible). Refer immediately for medical attention.

· 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.

· Do not touch or walk through spilled material.

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

Warning: Ammonia is extremely corrosive to the skin, eyes, and mucous membranes. Contact with the liquified gas may cause frostbite. Caution is advised.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

General First Aid:

(General first aid procedures)

Under prolonged exposure to fire or intense heat the containers may rupture violently and rocket.

Presence of oil or other combustible materials will increase the fire hazard.

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

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

303.0 [ppm]

20.0 [ppm]

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.

Firefighting gear (including SCBA) does not provide adequate protection ... If exposure occurs, remove and isolate gear immediately and thoroughly decontaminate personnel. Move container from fire area if you can do it without risk. Vapors are heavier than air and will collect in low areas. Vapors in confined areas may explode when exposed to fire. Vapors may travel long distances to ignition sources and flash back. Storage containers and parts of containers may rocket great distances, in many directions. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. Do not put water on liquid ammonia: will increase evaporation. Small fires: dry chemical or carbon dioxide. Large fires: water spray, fog, or foam. Apply water gently to the surface. Do not get water inside container. From a secure explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increased in volume and pitch, tank discolors or shows any signs of deforming), withdraw immediately to a secure position. Isolate until gas has dispersed.

For more Fire Fighting Procedures (Complete) data for Ammonia (7 total), please visit the HSDB record page.

Keep container tightly closed in a dry and well-ventilated place. Contents under pressure. Storage class (TRGS 510): Gases

Before entering confined space where this chemical may be present, check to make sure that an explosive concentration does not exist. Protect against physical damage. Outside or detached storage is preferred. Inside storage should be in a cool, well-ventilated, noncombustible location, preferably with automatic monitoring systems, away from all possible sources of ignition. Separate from other chemicals, particularly oxidizing gases, chlorine, bromine, iodine, and acids.

SRP: Operations involving entry into tanks or closed vessels, and emergency situations, require consideration of potentially oxygen deficient, or "immediately dangerous to life and health" IDLH environments. This may necessitate use of a self-contained breathing apparatus (SCBA), or a positive pressure supplied air respirator.

Separate from other chemicals, particularly oxidizing materials, acids, and halogens. Store in a cool, dry, well-ventilated location.

For more Storage Conditions (Complete) data for Ammonia (7 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Remove all sources of ignition. Evacuate personnel to safe areas. Beware of vapors accumulating to form explosive concentrations. Vapors can accumulate in low areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Wear a self-contained breathing apparatus, eye protection, laboratory coat, and nitrile rubber gloves (and rubber boots or overshoes if spillage is large). Cover the spill with a 1:1:1 mixture by weight of sodium carbonate or calcium carbonate, clay cat litter (bentonite), and sand. Scoop the mixture into a plastic pail and, in the fume hood, add to a pail of cold water. Neutralize the mixture with 5% hydrochloric acid, let stand overnight, and then pour liquid into the drain. Dispose of any solid with normal refuse. Wash area of the spill with plenty of water.

Spill handling: evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Establish forced ventilation to keep levels below explosive limit. Ventilate area of spill or leak. Stop the flow of gas if it can be done safely. Stay upwind; keep out of low areas. Wear positive pressure breathing apparatus and full protective clothing. If the leak is a cylinder and the leak cannot be stopped in place, remove the leaking cylinder to a safe place in the open air and repair the leak or allow the cylinder to empty. For small liquid spills, neutralize with hydrochloric acid. Wipe or mop or use water aspirator. Drain into sewer with sufficient water. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Contact your Department of Environmental Protection or your regional office of the federal EPA for specific recommendations. Initial isolation and protective action distances: distances shown are likely to be affected during the first 30 min after materials are spilled and could increase with time. If more than one tank car, cargo tank, portable tank, or large cylinder involved in the incident is leaking, the protective action distance may need to be increased ... Small spills (from a small package or a small leak from a large package): First isolate in all directions 100 ft. Then protect persons downwind 0.1 mile (day), 0.1 mile (night). Large spills (from a large package or from many small packages): First isolate in all directions 200 ft. Then protect persons downwind 0.4 miles (day), 1.4 miles (night).

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

Excerpt from ERG Guide 125 [Gases - Toxic and/or Corrosive]:

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

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.

Solutions of ammonia can be highly diluted with water, or alternatively, diluted with water and neutralized with HCl and then routed to the sewer system. The amount released to the receiving stream should not exceed the established limits for ammonia. Limited amounts of gaseous ammonia may be discharged to the atmosphere. Federal, state, and local guidelines should be consulted before disposal. Disposal of liquefied ammonia or of large quantities of gaseous or aqueous ammonia directly into water is not desirable, because of the large amount of heat generated. This generation of heat could increase exposure to personnel involved in the process. Recovery of ammonia from aqueous waste solutions is a viable option for many industries.

For more Disposal Methods (Complete) data for Ammonia (6 total), please visit the HSDB record page.

Acute Exposure: EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration. Chronic Exposure: Intravenous arginine (argininosuccinase deficiency), sodium phenylbutyrate and sodium benzoate (ornithine transcarbamoylase deficiency) are pharmacologic agents commonly used as adjunctive therapy to treat hyperammonemia in patients.

The present study investigated the simultaneous influence of particulate matter (PM10) and ammonia (NH3) on performance, lung lesions and the presence of Mycoplasma hyopneumoniae (M. hyopneumoniae) in finishing pigs. A pig herd experiencing clinical problems of M. hyopneumoniae infections was selected. In total, 1095 finishing pigs of two replicates in eight compartments each were investigated during the entire finishing period (FP). Indoor PM10 and NH3 were measured at regular intervals during the FP with two Grimm spectrometers and two Graywolf Particle Counters (PM10) and an Innova photoacoustic gas monitor (NH3). Average daily weight gain (ADG) and mortality were calculated and associated with PM10 and NH3 during the FP. Nasal swabs (10 pigs/compartment) were collected one week prior to slaughter to detect DNA of M. hyopneumoniae with nested PCR (nPCR). The prevalence and extent of pneumonia lesions, and prevalence of fissures and pleurisy were examined at slaughter (29 weeks). The results from the nasal swabs and lung lesions were associated with PM10 and NH3 during the FP and the second half of the FP. In the univariable model, increasing PM10 concentrations resulted in a higher odds of pneumonia lesions (second half of the FP: OR=8.72; P=0.015), more severe pneumonia lesions (FP: P=0.04, second half of the FP: P=0.009), a higher odds of pleurisy lesions (FP: OR=20.91; P<0.001 and second half of the FP: OR=40.85; P<0.001) and a higher number of nPCR positive nasal samples (FP: OR=328.00; P=0.01 and second half of the FP: OR=185.49; P=0.02). Increasing NH3 concentrations in the univariable model resulted in a higher odds of pleurisy lesions (FP: OR=21.54; P=0.003) and a higher number of nPCR positive nasal samples (FP: OR=70.39; P=0.049; second half of the FP: OR=8275.05; P=0.01). In the multivariable model, an increasing PM10 concentration resulted in a higher odds of pleurisy lesions (FP: OR=8.85; P=0.049). These findings indicate that the respiratory health of finishing pigs was significantly affected by PM10.

Ammonia is metabolized by the liver and has established neurological effects. The current study examined the possibility that ammonia contributes to the neurotoxic effects of methamphetamine (METH). The results show that a binge dosing regimen of METH to the rat increased plasma and brain ammonia concentrations that were paralleled by evidence of hepatotoxicity. The role of peripheral ammonia in the neurotoxic effects of METH was further substantiated by the demonstration that the enhancement of peripheral ammonia excretion blocked the increases in brain and plasma ammonia and attenuated the long-term depletions of dopamine and serotonin typically produced by METH. Conversely, the localized perfusion of ammonia in combination with METH, but not METH alone or ammonia alone, into the striatum recapitulated the neuronal damage produced by the systemic administration of METH. Furthermore, this damage produced by the local administration of ammonia and METH was blocked by the GYKI 52466 [4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodiazepin-5-yl)-benzamine hydrochloride], an AMPA receptor antagonist. These findings highlight the importance of ammonia derived from the periphery as a small-molecule mediator of METH neurotoxicity and more broadly emphasize the importance of peripheral organ damage as a possible mechanism that mediates the neuropathology produced by drugs of abuse and other neuroactive molecules.

Ammonia is a bi-product of protein metabolism in the body. It is able to cross the blood-brain barrier and elevated ammonia levels are toxic to the brain. Rats with hyperammonemia showed impaired learning ability and impaired function of the glutamate-nitric oxide-cyclic guanosine monophosphate (glutamate-NO-cGMP) pathway in the brain. Chronic treatment with sildenafil restored learning ability. We therefore tested the hypothesis that sildenafil has a protective effect on the brains of hyperammonemic rats. Hyperammonemia was induced in male rats by daily intraperitoneal (i.p.) injection of ammonium chloride (100 mg/kg body weight) for 8 weeks. Sildenafil citrate was administered intraperitoneally (10 mg/kg body weight/3 days) for 8 weeks. Treatment with sildenafil resulted in a significant reduction in plasma liver enzymes, lipid profile as well as brain lipid peroxidation and caspase-3 mRNA. Meanwhile, plasma NO as well as cGMP, antioxidants and endothelial nitric oxide synthase (eNOS) gene expression were significantly elevated in the brains of hyperammonemic rats. Our results showed that sildenafil exerts a protective effect on the brain by reversing oxidative stress during hyperammonemia and this could be due to (i) cytoprotective, antioxidant and anti-apoptotic effects (ii) increasing cGMP and enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus preventing oxidative damage in the brain. The exact protective mechanism of sildenafil has to be still investigated ... Consequently, therapeutic modulation of the NO/cGMP pathway might have important clinical applications to improve brain functions in patients with hyperammonemia or clinical hepatic encephalopathy. /Hyperammonemia/

Ammonia is a key toxin in the precipitation of hepatic encephalopathy (HE), a neuropsychiatric disorder associated with liver failure. In response to ammonia, various toxic events are triggered in astroglial cells, and alterations in brain glutamate communication are common. Resveratrol is a polyphenolic compound that has been extensively studied in pathological events because it presents several beneficial effects, including some in the central nervous system (CNS). We previously described that resveratrol is able to significantly modulate glial functioning and has a protective effect during ammonia challenge in vitro. In this study, we addressed the mechanisms by which resveratrol can protect C6 astroglial cells from glutamatergic alterations induced by ammonia. Resveratrol was able to prevent all the effects triggered by ammonia: (i) decrease in glutamate uptake activity and expression of the EAAC1 glutamate transporter, the main glutamate transporter present in C6 cells; (ii) increase of glutamate release, which was also dependent on the activation of the Na(+)-K(+)-Cl(-) co-transporter NKCC1; (iii) reduction in GS activity and intracellular GSH content; and (iv) impairment of Na(+)K(+)-ATPase activity. Interestingly, resveratrol, per se, also positively modulated the astroglial functions evaluated. Moreover, we demonstrated that heme oxygenase 1 (HO1), an enzyme that is part of the cellular defense system, mediated some of the effects of resveratrol. In conclusion, the mechanisms of the putative protective role of resveratrol against ammonia toxicity involve the modulation of pathways and molecules related to glutamate communication in astroglial cells.

For more Interactions (Complete) data for Ammonia (13 total), please visit the HSDB record page.

Dermal (Skin), Neurological (Nervous System), Ocular (Eyes), Respiratory (From the Nose to the Lungs)

Respiratory

Eyes, skin, respiratory system

Acute exposure to high levels of ammonia in air may be irritating to skin, eyes, throat, and lungs and cause coughing and burns. Lung damage and death may occur after exposure to very high concentrations of ammonia. Swallowing concentrated solutions of ammonia can cause burns in mouth, throat, and stomach. Splashing ammonia into eyes can cause burns and even blindness. (L958) Chronically high levels of ammonia in the blood are associated with nearly 20 different inborn errors of metabolism including: 3-Hydroxy-3-Methylglutaryl-CoA Lyase Deficiency, Argininemia, Argininosuccinic Aciduria, Beta-Ketothiolase Deficiency, Biotinidase deficiency, Carbamoyl Phosphate Synthetase Deficiency, Carnitine-acylcarnitine translocase deficiency, Citrullinemia Type I, Hyperinsulinism-Hyperammonemia Syndrome, Hyperornithinemia-hyperammonemia-homocitrullinuria syndrome, Isovaleric Aciduria, Lysinuric Protein Intolerance, Malonic Aciduria, Methylmalonic Aciduria, Methylmalonic Aciduria Due to Cobalamin-Related Disorders, Propionic acidemia, Pyruvate carboxylase deficiency and Short Chain Acyl CoA Dehydrogenase Deficiency (SCAD Deficiency). Hyperammonemia is one of the metabolic derangements that contribute to hepatic encephalopathy.

LC50; Species: Campostoma anomalum (stoneroller); Concentration: 1.72 mg/L for 96 hr /Conditions of bioassay not specified/

LC50; Species: Carassius auratus (goldfish); Concentration: 2-2.5 mg/L for 24-96 hr /Conditions of bioassay not specified/

LC50; Species: Carassius auratus (goldfish); Concentration: 7.2 mg/L for 24 hr /Conditions of bioassay not specified/

LC50; Species: Catostomus commersoni (White sucker); Concentration: 0.79 mg/L for 96 hr /Conditions of bioassay not specified/

For more Ecotoxicity Values (Complete) data for Ammonia (126 total), please visit the HSDB record page.

TERRESTRIAL FATE: In soil, ammonia may either volatilize to the atmosphere, adsorb to particulate matter, or undergo microbial transformation to nitrate or nitrite anions(1). Volatilization of ammonia from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 1.61X10-5 atm-cu m/mole(2). Ammonia is a gas with a vapor pressure of 7500 mm Hg at 25 °C and atmospheric pressure(3), and therefore, is expected to volatilize from dry soil surfaces(SRC). In soil, ammonia can serve as a nutrient source for plants, which can be taken up by plants and microorganisms and converted to organic-nitrogen compounds(1). Ammonia in soil can be rapidly transformed to nitrate by the microbial population through nitrification(1). The nitrate formed will either leach through the soil or be taken up by plants or other microorganisms(1). Ammonia at natural concentrations in soil is not believed to have a very long half-life. If ammonia is distributed to soil in large concentrations (such as following an ammonia-containing fertilizer application), the natural biological transformation processes can be overwhelmed, and the environmental fate of ammonia will become dependent upon the physical and chemical properties of ammonia, until the ammonia concentration returns to background levels(1).

AQUATIC FATE: Ammonia is lost from water by volatilization(1) and volatilization is expected(2) based upon a Henry's Law constant of 1.61X10-5 atm-cu m/mole(3). Using this Henry's Law constant and an estimation method(2), volatilization half-lives for a model river and model lake are 1.4 and 12 days, respectively(SRC). In water, ammonia is in equilibrium with the ammonium ion (NH4+), and the ammonia-ammonium ion equilibrium is dependent on the pH(4). The pKa of ammonia is 9.25(5). The proportion of un-ionized ammonia in water increases with increasing temperature and pH, but decreases with increasing salinity(1). At pH 8.5, the proportion of un-ionized ammonia is approximately 10 times that at pH 7.5 and, for every 9 °C increase in temperature, the proportion of un-ionized ammonia approximately doubles(1). In surface water, groundwater, or sediment, ammonia can undergo sequential transformation by two processes in the nitrogen cycle, nitrification and denitrification, which would produce ionic nitrogen compounds, and from these, elemental nitrogen(4). The ionic nitrogen compounds formed from the aerobic process of nitrification (nitrate and nitrite anions) can leach through the sediment or be taken up by aquatic plants or other organisms(4). Removal of ammonium from water can also occur by adsorption to sediments or suspended organic material(4).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ammonia, which has a vapor pressure of 7500 mm Hg at 25 °C(2), is expected to exist solely as a gas in the ambient atmosphere. Gas-phase ammonia is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 100 days(SRC), calculated from its rate constant of 1.60X10-13 cu cm/molecule-sec at 25 °C(3). Gas-phase ammonia is also degraded in the atmosphere by reaction with nitrate radicals(SRC); the half-life for this reaction in air is estimated to be 54 days(SRC), calculated from its rate constant of 5.99X10-16 cu cm/molecule-sec at 25 °C(3). Ammonia reacts rapidly in the atmosphere with both sulfuric and nitric acids to form fine particles(4). In most of the US the majority of aerosol ammonium is associated with sulfate ion(4). Once released into the atmosphere, ammonia is returned to the surface as either gaseous ammonia or as an ammonium ion(4). The ammonium ion can be associated with nitrate, sulfate, or some other anion and incorporated into an aerosol or as part of the ionic mix found in cloud and raindrops(4). Ammonia can dissolve in the water in the atmosphere and form clouds or fog(5). The half-life for ammonia in the atmosphere has been estimated to be a few days; the reaction with acidic substances in the air results in the formation of ammonium aerosols that can be removed by wet or dry deposition(5). Vapor deposition of ammonia from air to surface (to vegetation, soil, etc) also occurs(4). Ammonia does not absorb at wavelengths >290 nm(6) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The US FDA states that the levels of ammonia and ammonium compounds normally found in food do not pose a health risk(1). Maximum allowable ammonia levels in processed foods are as follows: 0.04-3.2% ammonium bicarbonate in baked goods, grain, snack foods, and reconstituted vegetables; 2.0% ammonium carbonate in baked goods, gelatins, and puddings; 0.001% ammonium chloride in baked goods and 0.8% in condiments and relishes; 0.6-0.8% ammonium hydroxide in baked goods, cheeses, gelatins, and puddings; 0.01% monobasic ammonium phosphate in baked goods; and 1.1% dibasic ammonium phosphate in baked goods, 0.003% in nonalcoholic beverages, and 0.012% in condiments and relishes(1).

The substance can be absorbed into the body by inhalation.

inhalation, ingestion (solution), skin and/or eye contact (solution/liquid)

Ammonia can be absorbed into the body by inhalation, ingestion, eye contact, and skin contact. Ingestion is an uncommon route of exposure. Absorption by eye contact may be limited by severe corrosive injury and/or by significant spasmodic blinking (blepharospasm), even with mild exposures.

Oral (L958) ; inhalation (L958) ; dermal (L958)

The CIR Expert Panel concluded that Ammonia and Ammonium Hydroxide are safe as used in hair dyes and colors and safe in cosmetics applied directly to the skin in the present practices of use and concentration described in the safety assessment when formulated to be non-irritating.

Safe for use in cosmetics, with qualifications

IDENTIFICATION AND USE: Ammonia is a colorless gas or liquid. Ammonia is used in the production of ammonium sulfate and ammonium nitrate for fertilizers; and in the manufacture of nitric acid, soda, synthetic urea, synthetic fibers, dyes, and plastics. Ammonia, or dissociated ammonia, is used in such metal treating operations as nitriding, carbo-nitriding, bright annealing, furnace brazing, sintering, sodium hydride descaling, atomic hydrogen welding, and other applications where protective atmospheres are required. The petroleum industry utilizes anhydrous ammonia in neutralizing the acid constituents of crude oil and in protecting equipment such as bubble plate towers, heat exchangers, condensers, and storage tanks from corrosion. It is also used as medication. Ammonia in an aqueous environment exists in equilibrium between ionized ammonium cation and the non-ionized ammonia. This equilibrium can be affected by buffers, pH, temperature, and salinity. Thus, in many cases it is not possible to assign the associated toxicity to the ionized or non-ionized form of the ammonia-nitrogen. HUMAN EXPOSURE AND TOXICITY: Studies using low levels of ammonia show that inhaled ammonia is temporarily dissolved in the mucus of the upper respiratory tract, and then a high percentage of it is released back into the expired air. Following exposure to 500 ppm ammonia for 10-27 min, healthy male subjects eliminated 70-80% of the inspired ammonia by this route. Short term exposure: eye or skin contact with ammonia can cause irritation, burns, frostbite (anhydrous), and permanent damage. Irritates the respiratory tract causing coughing, wheezing, and shortness of breath. Higher exposure can cause pulmonary edema, a medical emergency, that can be delayed for several hours and is life-threatening. Exposure can cause headache, loss of sense of smell, nausea, and vomiting. Inhalation: nose and throat irritation have been reported at 72 ppm after 5 min exposure. Exposures of 500 ppm for 30 min have caused upper respiratory irritation, tearing, increased pulse rate, and blood pressure. Death has been reported after an exposure to 10,000 ppm for an unknown duration. Skin: Solutions of 2% ammonia can cause burns and blisters after 15 min of exposure. These burns may be slow to heal. Anhydrous ammonia may cause skin to freeze. Eyes: Levels of 70 ppm (gas) have caused eye irritation. If not flushed with water immediately, contact with eye may cause partial or complete blindness. Ingestion: ammonia will cause pain if swallowed and burning of the throat and stomach. May cause vomiting. One teaspoon of 28% aqua ammonia may cause death. Long term exposure: repeated exposure can cause chronic eye, nose, and throat irritation. Repeated lung irritation can result in bronchitis with coughing, shortness of breath, and phlegm. Analysis of blood samples from 22 workers exposed to ammonia in a fertilizer factory and 42 control workers not exposed to ammonia showed increased frequency of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs), increased mitotic index (MI), and increased frequency of CAs and SCEs with increasing length of exposure. ANIMAL STUDIES: Analysis of endogenous ammonia levels in the expired air of rats showed concentrations ranging from 10-353 ppb (mean = 78 ppb) in nose-breathing animals. The quantitative difference between inspired and expired ammonia suggests that small amounts are absorbed across the nasopharyngeal membranes into the systemic circulation. Absorbed ammonia is excreted by the kidneys as urea and urinary ammonium compounds, as urea in feces, and as components of sweat. Toxic levels do not develop as a result of chronic inhalation exposure because the body has multiple effective mechanisms for detoxifying and excreting it. Cardiovascular changes that may be analogous to those observed in humans have been observed in rabbits exposed to high concentrations of ammonia. Bradycardia was seen at 2,500 ppm, and hypertension and cardiac arrhythmias leading to cardiovascular collapse followed acute exposures to concentrations exceeding 5,000 ppm. Pathological correlates for these effects have not been demonstrated. Atrophy of pericardial fat has been observed in mice exposed to 4,000 ppm ammonia. Hepatic effects are usually not seen in animals exposed to ammonia gas. Liver necrosis has been observed following acute lethal exposure of mice to 3,440 ppm ammonia for 1 hour. Levels of 170 ppm of ammonia vapor caused mild changes in the spleens, kidneys, and livers of guinea pigs. Static exposures of cats and rabbits for 1 hr at 7000 mg/cu m resulted in the death of approx 50%. Postmortem exam showed severe effects on the upper respiratory tract. Less severe effects in the lower respiratory tract included damage to bronchioles and alveolar congestion, edema, atelectasis, hemorrhage, emphysema, and fluid. The search for the peripheral toxins responsible for the CNS impairment present in hepatic encephalopathy has shown that the administration of ammonia in normal rats reproduced behavioral and electrophysiological changes similar to those seen in galactosamine induced encephalopathy. No statistically significant differences were noted in ovarian or uterine weights of pigs exposed to about 7 or 35 ppm ammonia for 6 weeks. Female pigs that were continuously exposed to about 35 ppm ammonia from 6 weeks before breeding until day 30 of gestation had no statistically significant differences in age at puberty, number of live fetuses, or fetus-to-corpus luteum ratio compared to pigs exposed to only about 7 ppm. No unexposed controls were included in that study. No statistically significant difference in fetal length was evident at 30 days of gestation in offspring of pig dams that were continuously exposed to about 7 or 35 ppm ammonia from 6 weeks before breeding until day 30 of gestation. The mutagenicity of anhydrous ammonia was investigated in a Ames test in S. typhimurium TA98, TA100, TA1535, TA1537 and TA1538, and in E. coli WP2uvrA. The test method was modified appropriately to investigate a volatile test substance. Studies were performed in duplicate in the presence and absence of an exogenous metabolic activation system. No evidence of mutagenicity was seen under the conditions of this assay. ECOTOXICITY STUDIES: Ammonia is an environmental pollutant that is toxic to all aquatic animals. The major sources for atmospheric NH3 are agricultural activities and animal feedlot operations, followed by biomass burning (including forest fires) and to a lesser extent fossil fuel combustion. Close to its sources, acute exposures to NH3 can result in visible foliar injury on vegetation.

New Active Ingredients ... includes chemicals not previously registered as pesticides, as well as pesticide active ingredients initially registered after November 1, 1984 and that currently have active product registrations. By law, these pesticides must meet new safety standards, such as those described in the Food Quality Protection Act of 1996 and, if new safety standards are met, will be reviewed again on a 15-year cycle. Ammonia is designated by EPA as a New Pesticide Active Ingredient. Active Ingredient Number: 005302; Type of Pesticide: insecticide; Use Site: non-food use; Year: 1994.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Ammonia is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 500 lbs.

Ammonia is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

Ammonia (anhydrous)

1

10000

Toxic chemical that can be released at a facility.

Ammonia (conc. 20% or greater)

20.00

CIR ingredient: Ammonia

About 80% is used in fertilizers; it also is used as a refrigerant gas, and in the manufacture of plastics, explosives, pesticides, detergents, and other chemicals. Small amounts of ammonia occur naturally from decomposition of organic matter. [ATSDR Medical Management] Also used in illicit methamphetamine labs; Anhydrous ammonia is the most commonly reported agent in accidental spill or release incidents. [PMID 19225422]

Molding and Core Making [Category: Foundry]

Lithography printing [Category: Hobbies]

For ammonia (USEPA/OPP Pesticide Code: 005302) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

/Ammonia/ is used in the production of ammonium sulfate and ammonium nitrate for fertilizers; and in the manufacture of nitric acid, soda, synthetic urea, synthetic fibers, dyes, and plastics.

(1972) 6.46 X 10+11 g (anhydrous and aqueous)

(1975) 2.95 X 10+11 g (anhydrous)

(1985) 4.54 X 10+11 g

(1987) 1.80 X 10+3 content ton (aq)

For more U.S. Exports (Complete) data for Ammonia (7 total), please visit the HSDB record page.

(1972) 3.50 X 10+11 g (Anhydrous)

(1975) 7.33 X 10+11 g (Anhydrous)

(1985) 2.27 X 10+12 g

(2000) 3.9 million metric tons

For more U.S. Imports (Complete) data for Ammonia (7 total), please visit the HSDB record page.

2023: 40,000,000,000 - <45,000,000,000 lb

(1972) 1.42 X1 0+13 g (Anhydrous)

(1975) 1.49 X 10+13 g (Anhydrous)

(1985) 1.47 X 10+13 g

(1986) 1.70 X 10+4 metric ton

For more U.S. Production (Complete) data for Ammonia (17 total), please visit the HSDB record page.

Fertilizer, 80%; Polymers, 7%; Exports, 6%; Explosives, 3%; Animal feeds, 2%; Other, 2% (1985)

Chemical Profile: Ammonia. Direct application fertilizer, 27%; urea, 21%; ammonium phosphates, 14%; nitric acid, 11%; ammonium nitrate, 8%; exports, 6%; ammonium sulfate, 3%; other, 10%.

Chemical Profile: Ammonia. Demand: July 1987-June 1988: 16.4 million tons; 1988-1989: 17.7 million tons; 1992-1993 /projected/: 18.4 million tons. (Includes exports, but not imports, which totaled 3.2 million tons in 1987-1988.)

Chemical Profile: Ammonia. Direct application fertilizer, 25%; urea, 25%; ammonium phosphates, 17%; nitric acid, 12%; ammonium nitrate, 8%; acrylonitrile, 3%; ammonium sulfate, 4%; other, 6%.

Chemical Profile: Ammonia. Demand: (1993) 17.2 million tons; (1994) 17.9 million tons; (1998) /projected/: 20.9 million tons. (Includes exports of 507,000 tons in 1993, but not imports, which totaled 2.84 million tons.)

Ammonia is produced as a by-product in coal distillation and by the action of steam on calcium cyanamide, and from the decomposition of nitrogenous materials.

Ammonia is manufactured primarily by a modified Haber reduction process using atmospheric nitrogen and a hydrogen source, for example, methane, ethylene or naphtha, at high temperatures (400 to 6500 °C) and pressures (100 to 900 atm) in the presence of an iron catalyst.

From synthesis gas, a mixture of carbon monoxide, hydrogen, carbon dioxide, and nitrogen (from air) obtained by steam reforming or by partial combustion of natural gas (U.S.). or from the action of steam on hot coke (Haber-Bosch process).

Manufactured from water gas (obtained by blowing steam through incandescent coke) as source of hydrogen, and from producer gas (obtained from steam and air through incandescent coke), as source of nitrogen by the Haber-Bosch process.

Grades: Commercial 99.5%; refrigerant 99.97%.

Aqueous soln of ammonia ... is often referred to & labeled as a soln of ammonium hydroxide /although there is little ammonium hydroxide present/. In commerce, ammonia is avail ... in form of aqueous soln of varying concn, or as anhydrous ammonia furnished in liquefied form ... . Ammonia in household use contains 10% ammonia & is ... known as 16 deg ammonia (referring to density in degrees Baume, a concn term).

Shipping grades or purity: Commercial, industrial, refrigeration, electronic, and metallurgical grades all have purity greater than 99.5%.

Ammonia solution, more than 10% and not more than 35% ammonia.

For more Formulations/Preparations (Complete) data for Ammonia (8 total), please visit the HSDB record page.

Cosmetics product ingredient: Ammonia, Total

Information on 181 consumer products that contain Ammonia in the following categories is provided:

Pesticide, Fertilizer, and Other Agricultural Chemical Manufacturing

Ammonia: ACTIVE

Ammonia in solution ... in varying concentration is used in variety of products such as cleaning agents, liniments, and aromatic spirits. Ammonia solution are sometimes used as fertilizers ... Fresh household ammonia ranges in concentration from 5 to 10% NH3, but a 54% solution is also available commercially. /Ammonium hydroxide/

... Usually marketed in liquefied form in steel cylinders or as ammonia water (aqua ammonia, ammonium hydroxide) in drums and bottles.