Ammonia MSDS and Public Health Information
Complete Ammonia MSDS Below
Public Health Statement for Ammonia (Amoníaco)
Contents:
This fact sheet answers the most frequently asked health questions about ammonia. This information is important
because this substance may harm you. The effects of exposure
to any hazardous substance depend on the dose, the duration,
how you are exposed, personal traits and habits, and whether
other chemicals are present.
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Highlights
Ammonia is found throughout the environment in the air, soil, and water, and in plants and
animals including humans. Exposure to high levels of ammonia can cause irritation and serious
burns on the skin and in the mouth, throat, lungs, and eyes. At very high levels, ammonia can
even cause death. Ammonia has been found in at least 137 of the 1,647 current or former National
Priority Sites list identified by the Environmental Protection Agency (EPA).
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What is ammonia?
Ammonia occurs naturally and is produced
by human activity. It is an important source of nitrogen which
is needed by plants and animals. Bacteria found in the intestines
can produce 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.
Ammonia is a colorless gas with a very
distinct odor. This odor is familiar to many people because
ammonia is used in smelling salts, many household and industrial
cleaners, and window-cleaning products.
Ammonia gas can be dissolved in water.
This kind of ammonia is called liquid ammonia or aqueous ammonia.
Once exposed to open air, liquid ammonia quickly turns into
a gas.
Ammonia is applied directly into soil
on farm fields, and is used to make fertilizers for farm crops,
lawns, and plants. Many household and industrial cleaners
contain ammonia.
Ammonia may also be known by the following synonyms: Anhydrous ammonia, Aqua ammonia, Aqueous ammonia [Note: Often used in an aqueous solution], AM-Fol, Ammonia anhydrous, Ammonia gas, Ammoniac [French], Ammoniaca [Italian], Ammoniak Kconzentrierter, Ammoniak [German], Ammoniakgas, Amoniak [Polish], CCRIS 2278, Caswell No. 041, EINECS 231-635-3, EPA Pesticide Chemical Code 005302, HSDB 162, Liquid Ammonia, Nitro-sil, R 717, Spirit of hartshorn, UN 1005 (anhydrous gas or >50% solution), UN 2073 (>44% solution), or UN 2672 (between 12% and 44% solution)
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What happens to ammonia when it enters the
environment?
- Ammonia is found throughout the environment in air, water,
soil, animals, and plants.
- Ammonia does not last very long in the environment. It
is rapidly taken up by plants, bacteria, and animals.
- Ammonia does not build up in the food chain, but serves
as a nutrient for plants and bacteria.
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How might I be exposed to ammonia?
- Everyone is exposed to low levels of naturally-occurring
ammonia in air, food, water, and soil.
- You may be exposed to higher levels during use of cleaning
products containing ammonia.
- You may be exposed to higher levels if you apply ammonia
fertilizers or live near farms where these fertilizers have
been applied.
- You may be exposed to high levels if you go into enclosed
buildings that contain lots of animals (such as on farms).
Industrial Processes with risk of exposure from Ammonia:
- Burning Synthetic Polymers
- Electroplating
- Farming (Dusts, Asphyxiants, etc.)
- Firefighting
- Fur Dressing and Dyeing
- Heat Treating
- Molding and Core Making
- Petroleum Refining
- Photographic Processing
- Pulp and Paper Processing
- Semiconductor Manufacturing
- Sewer and Wastewater Treatment
- Tanning Leather
- Toxic Gas from Spilling Chemical in Water
Activities with risk of exposure to Ammonia:
Household Products listing Ammonia as an Ingredient:
Below is listed the brand, category, form, and percent Ammonia content.
- Blue Magic Liquid Metal Auto Polish Auto products liquid
- Blue Magic Cream Metal Polish Auto products cream
- Parks Adhesive Remover-09/04/1998 Hobby/Craft liquid <1
- SOS Ammonia Glass Cleaner Home inside liquid
- Safeway Window Home inside pump spray
- Mr Clean Top Job with Ammonia Home inside liquid
- Brasso Multipurpose Metal Polish Home inside liquid
- Savogran Dirtex Spray Cleaner Home inside aerosol <1
- Goddards Long Shine Silver Polish Home inside liquid 2
- Giant Pure Power Window Cleaner Trigger Spray Home inside spray 1.00
- Parks Adhesive Remover Home maintenance liquid 2-20
- Parks Pro Liquid Paint Stripper Home maintenance liquid 2-20
- Quikrete Concrete Acrylic Fortifier Landscaping/Yard liquid
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How can ammonia affect my health?
No health effects have been found in
humans exposed to typical environmental concentrations of
ammonia. Exposure to high levels of ammonia in air may be
irritating to your skin, eyes, throat, and lungs and cause
coughing and burns. Lung damage and death may occur after
exposure to very high concentrations of ammonia. Some people
with asthma may be more sensitive to breathing ammonia than
others.
Swallowing concentrated solutions of
ammonia can cause burns in your mouth, throat, and stomach.
Splashing ammonia into your eyes can cause burns and even
blindness.
- Liquid Ammonia causes first degree burns on short exposure
- Ammonia gas and liquid are corrosive to skin.
- Ammonia Solutions of 3-5% = strong irritant
- Ammonia Solutions >5% = corrosive
- Ammonia is listed as one of "major irritant inhalants"
- Ammonia may be released if lithium nitride or magnesium diamide are spilled in water.
- Ammonia solutions with more than 50% ammonia are classified as TIH (Toxic Inhalation Hazard).
- Ammonia inhalation may cause Chronic Bronchitis.
- The Half-life of Ammonia - Whole body (following ingestion)= 1-2 days
Ammonia and Chronic Bronchitis - The American Thoracic Society (ATS) criteria for chronic bronchitis is: cough at least 4 X/day, 4 days/week, 3 months/year for 2 years (sputum production on most days for at least 3 months out of the year). Causes include silica, coal dust, grain dusts, cotton dusts, welding fumes, firefighting, and dust in livestock confinement buildings. The length of exposure necessary to cause chronic bronchitis is probably years or decades, not days or months. Chronic bronchitis has been described in boiler cleaners exposed to vanadium pentoxide. Bronchitis and bronchiectasis are the most common causes of hemoptysis.
Symptoms of Ammonia Induced Chronic Bronchitis:
- cough
- dyspnea, exertional
- hemoptysis
- obstructive defect
- sputum production
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How likely is ammonia to cause cancer?
There is no evidence that ammonia causes
cancer. The Department of Health and Human Services (DHHS),
the EPA, and the International Agency for Research on Cancer
(IARC), have not classified ammonia for carcinogenicity.
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How can ammonia affect children?
Children are less likely than adults
to be exposed to concentrated levels of ammonia because most
exposures occur at work. The effects on children are likely
to be the same as for adults. We do not know if exposure to
ammonia causes birth defects, or if it can pass to the fetus
across the placenta or to infants via breast milk.
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How can families reduce the risk of exposure to
ammonia?
- Keep products that contain ammonia out of the reach of
children.
- Make sure there is adequate ventilation when you use cleaners
that contain ammonia, and wear proper clothing and eye protection.
- Never store cleaning solutions in containers that children
might find attractive, like soda bottles.
- Avoid farm fields after they have been treated with ammonia
or ammonia-containing fertilizers.
- Minimize exposure to ammonia in the workplace by wearing
proper safety clothes and equipment, and by following safety
rules.
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Is there a medical test to show whether I've been
exposed to ammonia?
There are tests to measure ammonia in
blood and urine. These tests can not definitely determine
whether you have been exposed because ammonia is normally
found in our bodies.
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Has the federal government made recommendations to
protect human health from Ammonia exposure?
The Food and Drug Administration (FDA)
has salts typically found in foods do not pose a risk to human
health.
The Occupational Safety and Health Administration
(OSHA) has set an acceptable eight-hour exposure limit at
25 parts of ammonia per one million parts of air (ppm) and
a short-term (15 minutes) exposure level at 35 ppm.
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References
Agency for Toxic Substances and Disease Registry (ATSDR). 2004.
Toxicological Profile for Ammonia. Atlanta, GA: U.S. Department of Health
and Human Services, Public Health Service.
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Where can I get more information?
ATSDR can tell you where to find occupational and environmental health
clinics. Their specialists can recognize, evaluate, and treat illnesses
resulting from exposure to hazardous substances. You can also contact your
community or state health or environmental quality department if you have any
more questions or concerns.
For more information, contact:
Agency for Toxic Substances and Disease Registry
Division of Toxicology and Environmental Medicine
1600 Clifton Road NE, Mailstop F-32
Atlanta, GA 30333
Phone: 1-888-42-ATSDR (1-888-422-8737)
FAX: (770)-488-4178
Email: ATSDRIC@cdc.gov
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Ammonia MSDS Information
SECTION I - Material Identity
| Item Name............................... |
ANHYDROUS AMMONIA |
| Part Number/Trade Name.................. |
ANHYDROUS AMMONIA |
| National Stock Number................... |
6830006169184 |
| CAGE Code............................... |
0EXY4 |
| Part Number Indicator................... |
A |
| MSDS Number............................. |
115526 |
| HAZ Code................................ |
C |
SECTION II - Manufacturer's Information
| Manufacturer Name....................... |
HILL BROTHERS CHEMICAL CO. |
| P.O. Box................................ |
NA |
| Street.................................. |
1675 NORTH MAIN STREET |
| City.................................... |
ORANGE |
| State................................... |
CA |
| Country................................. |
US |
| Zip Code................................ |
92667 |
| Emergency Phone......................... |
CHEMTREC 800-424-9300 |
| Information Phone....................... |
714-998-8800 OUTSIDE CA800-821-7234 |
MSDS Preparer's Information
| MSDS Preparer Name...................... |
NK |
| Street.................................. |
1675 NORTH MAIN STREET |
| City.................................... |
ORANGE |
| State................................... |
CA |
| Zip Code................................ |
92667 |
| Date MSDS Prepared/Revised.............. |
14NOV86 |
| Date of Technical Review................ |
01NOV89 |
| Active Indicator........................ |
N |
| Item Manager............................ |
GSA |
Alternate Vendors
| Vendor #5 CAGE.......................... |
BHDRR |
SECTION III - Physical/Chemical Characteristics
| Specification Number.................... |
NK |
| Specification Type/Grade/Class.......... |
NK |
| NRC License Number...................... |
NK |
| Net Propellant Weight (Ammo)............ |
NK |
| Appearance/Odor......................... |
COLORLESS GAS OR LIQ W/EXTREMELY PUNGENT ODOR |
| Boiling Point........................... |
-33C -28F |
| Melting Point........................... |
-77C -107F |
| Vapor Pressure.......................... |
2327@0C32F |
| Vapor Density........................... |
NK |
| Specific Gravity........................ |
0.68@-33C -28F |
| Decomposition Temperature............... |
NK |
| Evaporation Rate........................ |
NK |
| Solubility in Water..................... |
100% |
| Percent Volatiles by Volume............. |
100% |
| Chemical pH............................. |
13+ |
| Corrosion Rate.......................... |
NK |
| Container Type.......................... |
L |
| Container Pressure Code................. |
4 |
| Temperature Code........................ |
8 |
| Product State Code...................... |
U |
SECTION IV - Fire and Explosion Hazard Data
| Flash Point Method...................... |
NA |
| Lower Explosion Limit................... |
25% BY VOL |
| Upper Explosion Limit................... |
16% BY VOL |
| Extinguishing Media..................... |
WATER SPRAY OR WATER FOG |
| Special Fire Fighting Procedures........ |
STOP FLOW OF GAS.USE WTR FOG TO KEEP FIRE-EXPOSED CNTS COOL & TO PROTECT THE MENEFFECTING THE SHUT-OFF.WEAR SCBA & ENCAPSULATING CHEMICAL PROTECTIVE CLOTHING. |
| Unusual Fire/Explosion Hazards.......... |
IF INVOLVED IN FIRE,16-25% AMMONIA MIXTURE/AIR MAY EXPLODE.KEEP CNT COOL TO PREVENT BURSTING OR RELEASE OF GAS.PRESENCE OF OIL OR COMB WILL INCREASE FIRE HAZARD |
SECTION V - Reactivity Data
| Stability............................... |
YES |
| Stability Conditions to Avoid........... |
HEAT, OPEN FLAMES |
| Materials to Avoid...................... |
CONTACT W/OXIDIZING GASES,CHLORINE,BROMINE,IODINE,HALOGENS,CALCIUM,& STRONG MINERAL ACIDS.CONTACT W/COPPER,SILVER,ZINC* |
| Hazardous Decomposition Products........ |
COMBUSTION WILL YIELD NITROGEN & WATER. |
| Hazardous Polymerization................ |
NO |
| Polymerization Conditions to Avoid...... |
NK |
| LD50 - LD50 Mixture..................... |
NK |
SECTION VI - Health Hazard Data
| Route of Entry: Skin.................... |
YES |
| Route of Entry: Ingestion............... |
YES |
| Route of Entry: Inhalation.............. |
YES |
| Health Hazards - Acute and Chronic...... |
INGESTION:IRRITATION OR ULCERATION OF MOUTH,THROAT & DIGESTIVE.INHALATION:IRRITATION OF NOSE,THROAT & LUNGS.SKIN:IRRITATION OR SEVERE BURNS.EYES:MAY CAUSE TEMPERARY BLINDNESS OR SEVERE EYE DAMAGE. |
| Carcinogenity: NTP...................... |
NK |
| Carcinogenity: IARC..................... |
NK |
| Carcinogenity: OSHA..................... |
NK |
| Explanation of Carcinogenity............ |
NK |
| Symptoms of Overexposure................ |
BURNING OF EYES,CONJUNCTIVITIS,SKIN IRRITATION,SWELLING OF EYELIDS & LIPS,DRY RED MOUTH & TOUNGE,BURNING THROAT & COUGHING.IN MORE SEVERE CASES DIFFICULRTY BREATHING,SIGNS & SYMPTOMS OF LUNG CONGESTION,& ULTIMATELY,DEATH FROM RESPIRATORY FAILURE DUE TO PULMONARY EDEMA MAY OCCUR.IRRITATION & BURNS OF THE SKIN & MUCOUS** |
| Medical Cond. Aggrevated by Exposure.... |
AMMONIA IS A RESPIRATORY IRRITANT.PERSONS W/IMPAIRED PULMONARY FUNCTION MAY BE AT INCREASED RISK FROM EXPOSURE. |
| Emergency/First Aid Procedures.......... |
INGESTION:CONSCIOUS GIVE LARGE QTYS OF WTR OR WEAK ACIDS CITRUS JUICE OR DILUTEDVINEGAR.FOLLOW W/RAW EGGS,CREAM OR OLIVE OIL.DO NOT INDUCE VOMITING.INHALATION: REMOVE TO FRESH AIR.IF NECESSARY START ARTIFICIAL RESPIRATION.SKIN & EYES:IMMEDIATELY FLUSH/WASH W/WTR FOR 15 MINS.REMOVE CONTAMINATED CLOTHING WHILE CONTINUINGTO APPLY WTR,BEING CAREFUL NOT TO TEAR THE SKIN.OBTAIN MEDICAL ATTENTION. |
SECTION VII - Precautions for Safe Handling and Use
| Steps if Material Released/Spilled...... |
DO NOT APPLY WTR ONTO LEAKING TANK.STOP THE FLOW OF GAS OR LIQ.WEAR FULL PROTECTIVE CLOTHING & SELF-CONTAINED BREATHING APPARATUS.EVACUATE THE AREA IMMEDIATELY.ELIMINATE ALL OPEN FLAMES IN VICINITY OFINDOOR SPILLS OR RELEASED VAPORS. |
| Neutralizing Agent...................... |
NK |
| Waste Disposal Method................... |
CONSULT FEDERAL,STATE OR LOCAL AUTHORITIES FOR PROPER DISPOSAL PROCEDURES.IF POSSIBLE,ALLOW SPILLED LIQ AMMONIA TO EVAPORATE,AS IT IS TOO VOLATILE TO ABSORB.DIKING WILL CONTAIN THE LIQ & ALLOW IT TO STABILIZE.DO NOT APPLY WTR DIRECTLY TO AMMONIA LIQ. |
| Handling and Storage Precautions........ |
TECT AGAINST PHYSICAL DAMAGE.OUTSIDE SHADED AREA OR DETACHED STORAGE IS PREFERRED.STORAGE SHOULD BE IN A COOL,DRY,WELL VENT,NONCOMBUSTIBLE LOCATION HI |
| Other Precautions....................... |
HIGHLY TOXIC TO FISH & AQUATIC LIFE.DO NOT CONTAMINATE ANY BODY OF WTR BY DIRECTAPPLICATION,CLEANING OF EQUIP,OR DISPOSAL.SINCE AMMONIA IS A FERTILIZER,IT MAY PROMOTE EUTROPHICATION(HIGH IN NUTRIENTS,LOW IN OXYGEN)IN WATERWAYS. |
SECTION VIII - Control Measures
| Respiratory Protection.................. |
UNLESS VENT IS ADEQUATE TO KEEP AIRBORNE CONCENTRATIONS BELOW THE EXPOSURE STANDARD,WEAR APPROVED RESPIRATORY PROTECTION SUCH AS AN AMMONIA CANISTER MASK OR AN APPROVED AIR SUPPLIED RESPIRATOR.USE SCBA IN AREA ABOVE CANISTER LIMIT. |
| Ventilation............................. |
LOCAL EXHAUST.SPARK PROOF FANS DESIRABLE W/MECHANICAL VENT. DUCTS SHOULD BE LOCATED AT CEILING LEVEL & LEADS UP & OUT. |
| Protective Gloves....................... |
RUBBER & SYNTHETIC CHEMICAL GLOVES |
| Eye Protection.......................... |
GAS TIGHT CHEMICAL SAFETY GOGGLES |
| Other Protective Equipment.............. |
EYEWASH FOUNTAIN & SAFETY SHOWER SHOULD BE AVAILABLE IN WORKAREA.LONG SLEEVED CLOTHING CLOSED AT NECK. |
| Work Hygenic Practices.................. |
COTTON CLOTHING & UNDERWEAR.CHANGE CLOTHING IF CONTAMINATED. |
| Supplemental Health/Safety Data......... |
*MATERIALS TO AVOID:ALLOYS OF SAME.MERCURY,SILVER OXIDE OR HYPOCHLORITE CAN FORMEXPLOSIVE COMPOUNDS. **EFF OF OVEXPO:MEMBRANES.HEADACHE,SALIVATION,NAUSEA,& VOMITING.DIFFICULT OR LABORED BREATHING & COUGH W/BLOODY MUCOUS DISCHARGE.BRONCHITISLARYNGITIS,HEMOPTSIS,&PULMONARY EDEMA OR PNEUMONITIS.DEATH MAY RESULT. |
| Disposal Code........................... |
O |
SECTION IX - Label Data
| Protect Eye............................. |
NO |
| Protect Skin............................ |
NO |
| Protect Respiratory..................... |
NO |
| Chronic Indicator....................... |
UNKNOWN |
| Contact Code............................ |
UNKNOWN |
| Fire Code............................... |
UNKNOWN |
| Health Code............................. |
UNKNOWN |
| React Code.............................. |
UNKNOWN |
SECTION X - Transportation Data
| Container Quantity...................... |
150 |
| Unit of Measure......................... |
LB |
SECTION XI - Site Specific/Reporting Information
| Volatile Organic Compounds (P/G)........ |
0 |
| Volatile Organic Compounds (G/L)........ |
0 |
SECTION XII - Ingredients/Identity Information
| Ingredient #............................ |
01 |
| Ingredient Name......................... |
AMMONIA |
| CAS Number.............................. |
7664417 |
| NIOSH Number............................ |
B0087500 |
| Proprietary............................. |
NO |
| Percent................................. |
100 |
| OSHA PEL................................ |
50 PPM |
| ACGIH TLV............................... |
25 PPM/35 STEL; 9293 |
| Recommended Limit....................... |
NK |
Gasoline MSDS DISCLAIMER
Employers, employees, and anyone else should use this information only as a supplement to other information gathered by them, and should make independent judgement of suitability of this information to ensure proper use and protect health and safety. This information is furnished without warranty, and any use of the product not in conformance with this Material Safety Data Sheet, or in combination with any other product or process, is the responsibility of the user.
|
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Complete Toxicological Profile for AMMONIA
Human Health Effects
Human Toxicity
Excerpts
Human
Toxicity Values
Skin, Eye and Respiratory Irritations
Drug Warnings
Medical Surveillance
Populations at Special Risk
Probable Routes of Human
Exposure
Emergency Medical
Treatment
Emergency
Medical Treatment
Antidote and Emergency Treatment
Animal Toxicity Studies
Non-Human Toxicity Excerpts
Non-Human Toxicity Values
Ecotoxicity Values
Metabolism/Pharmacokinetics
Metabolism/Metabolites
Absorption, Distribution
& Excretion
Mechanism of Action
Interactions
Pharmacology
Therapeutic Uses
Drug Warnings
Interactions
Environmental Fate & Exposure
Probable Routes of Human
Exposure
Natural
Pollution Sources
Artificial Pollution Sources
Environmental Fate
Environmental Biodegradation
Environmental Abiotic Degradation
Environmental
Bioconcentration
Soil Adsorption/Mobility
Environmental Standards & Regulations
CERCLA Reportable Quantities
Clean Water Act Requirements
Allowable
Tolerances
Chemical/Physical
Properties
Molecular Formula
Molecular Weight
Color/Form
Odor
Boiling
Point
Melting
Point
Corrosivity
Critical Temperature & Pressure
Density/Specific Gravity
Dissociation Constants
Heat of Combustion
Heat of
Vaporization
pH
Solubilities
Spectral Properties
Surface Tension
Vapor Density
Vapor
Pressure
Viscosity
Other
Chemical/Physical Properties
Chemical Safety & Handling
Hazards Summary
DOT Emergency Guidelines
Odor Threshold
Skin, Eye and Respiratory Irritations
NFPA Hazard
Classification
Flammable Limits
Autoignition Temperature
Fire Fighting Procedures
Firefighting Hazards
Explosive Limits & Potential
Hazardous Reactivities &
Incompatibilities
Other Hazardous Reaction
Prior History of Accidents
Immediately Dangerous to Life or Health
Protective Equipment &
Clothing
Preventive
Measures
Shipment
Methods and Regulations
Storage Conditions
Cleanup Methods
Disposal Methods
Occupational Exposure Standards
OSHA Standards
Threshold Limit Values
NIOSH Recommendations
Immediately Dangerous to Life or
Health
Other
Occupational Permissible Levels
Manufacturing/Use Information
Major Uses
Manufacturers
Methods of Manufacturing
General Manufacturing Information
Formulations/Preparations
Consumption Patterns
U. S. Production
U. S. Imports
U. S. Exports
Laboratory Methods
Analytic Laboratory Methods
Sampling Procedures
Special References
Special Reports
Synonyms and Identifiers
Related HSDB Records
Synonyms
Formulations/Preparations
Shipping Name/ Number
DOT/UN/NA/IMO
Standard Transportation Number
AMMONIA
CASRN: 7664-41-7
For other data, click on the Table of Contents Human Health Effects:
Human Toxicity Excerpts:
SYMPTOMATOLOGY (AMMONIA GAS & WATER ONLY): 1. Vapors cause irritation of eyes & resp tract. High concn cause conjunctivitis, laryngitis, & pulmonary edema or pneumonitis. Sensation of suffocation ... induced by spasm of glottis or by laryngeal edema. 2. Contact with skin can cause burns & vesication. If squirted into eyes ... rise in intraocular pressure may mimic narrow-angle glaucoma. Corneal edema & semidilated fixed pupils ... /are/ typical. 4. If systemic absorption becomes extensive, coma may arise ... preceded by ... hypertonus & convulsions.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-22]**PEER REVIEWED**
AMMONIA HAS A GREATER TENDENCY THAN OTHER ALKALIES TO PENETRATE & DAMAGE THE IRIS, & TO CAUSE CATARACT /IN SEVERE BURNS/. IRITIS MAY BE ACCOMPANIED BY HYPOPYON OR HEMORRHAGES ... EXTENSIVE LOSS OF PIGMENT & SEVERE GLAUCOMA.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 87]**PEER REVIEWED**
/WORKER/ COMPLAINED OF CHRONIC COUGH & INCR DYSPNEA ON EFFORT. BILATERAL INFILTRATES ... SEEN ON CHEST X-RAY, & LUNG FUNCTION INDICES REFLECTED ... VENTILATORY & DIFFUSION ABNORMALITIES. AFTER THREE YR AWAY FROM AMMONIA EXPOSURE ... WORKER HAD PERSISTENT EVIDENCE OF PULMONARY DAMAGE.
[Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974., p. 208]**PEER REVIEWED**
SIX VOLUNTEERS INHALED AMMONIA AT 21 & 35 MG/CU M FOR 10 MIN. 5 REPORTED FAINT TO MODERATE IRRITATION & 1 REPORTED NO IRRITATION AT 35 MG/CU M. ... ANOTHER GROUP ... WAS EXPOSED FOR 5 MIN TO 22, 35, 50 & 94 MG/CU M. ... THE 94 MG/CU M ... CAUSED EYE IRRITATION WITH LACRIMATION, NOSE & THROAT IRRITATION & IN 1 ... CHEST IRRITATION.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 759]**PEER REVIEWED**
Inhalation causes ... secretion of saliva and retention of urine.
[Braker W, Mossman A; Matheson Gas Data Book 6th ED p.24 (1980)]**PEER REVIEWED**
Exposure to high gas concentrations may cause temporary blindness and severe eye damage. Direct contact of the eyes with liquid anhydrous ammonia will produce serious eye burns.
[Braker W, Mossman A; Matheson Gas Data Book 6th ED p.24 (1980)]**PEER REVIEWED**
Hyperammonemic associated encephalopathy developed in an adult receiving essential amino acids. Evidence that her encephalopathy was related to her hyperammonemia included (1) elevated CSF glutamine and serum ammonia levels, (2) the absence of any other drug or metabolic cause of encephalopathy, and (3) resolution of her encephalopathy and abnormal ammonia levels with discontinuation of the hyperalimentation. The serum ammonia levels of patients receiving essential amino acid fluid should be monitored. If the levels remain elevated or if toxicity develops, consideration should be given to switching to an alternate fluid.
[Grazer RE et al; Arch Intern Med 144 (11): 2278-9 (1984)]**PEER REVIEWED**
The effect of various ammonia concn in an enclosed atmosphere on man's adrenocortical system was investigated in five experiments on 20 young healthy test subjects. The most pronounced changes in the adrenocortical system developed when the ammonia content was 5 mg/cu m.
[Kalandarov S et al; Kosm Biol Aviakosm Med 18 (3): 75-7 (1984)]**PEER REVIEWED**
The effect of addition of ammonia to cultures of ... human ... blood lymphocytes was studied. The concn of ammonia in the lymphocyte cultures represented normal (0.01-0.5 mg/dl), subtoxic (0.5-1 mg/dl), and toxic (1-10 mg/dl) concn of ammonia in blood. Viability of the lymphocytes and their mitogenic reactivity were measured. In general, 1.0 and 10 mg/dl of ammonia (toxic concn) affected viability and mitogenic responsiveness of all lymphocytes.
[Klucinski W, Targowski SP; Immunopharmacol 8 (1): 47-52 (1984)]**PEER REVIEWED**
Therapeutic or normal blood level: 0.05-0.17 mg %; 0.5-1.7 ug/ml
[Winek, C.L. Drug and Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer Scientific, 1985., p. ]**PEER REVIEWED**
6 cases were reported of acute ammonia gas exposure following rupture of a pipe containing ammonia. Varying degrees of symptoms of acute inflammation of the respiratory tract and chemical skin burns were observed. Residual chronic bronchitis was evident in 2 cases. One worker died one month after the accident and the autopsy revealed acute laryngitis, tracheitis, bronchopneumonia, and pulmonary edema. The kidneys showed congestions and early hemorrhagic nephritis, which was attributed to toxemia secondary to chemical skin burns.
[NIOSH; Criteria Document: Ammonia p.26 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
During controlled human exposures at about 500 ppm for 30 minutes the following were observed: irregular minute ventilation with a cyclic pattern of hypernea, increases in blood pressure and pulse rate, variable lacrimation, and general complaints of upper respiratory irritation, some of these persisting for 24 hours following exposure.
[NIOSH; Criteria Document: Ammonia p.56 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
2 cases of ocular injuries with a rise in intraocular pressure and cataract formation after ammonia of unknown concentration had been squirted into the victims' eyes during robberies /were reported/. In both cases, the more severely affected eyes showed marked injection and edema of the conjunctiva; diffuse corneal damage; semidilated, oval, and fixed pupils; and a marked increase of the intraocular pressure which persisted and was controlled only with drugs. Glaucoma was observed to be associated with an open angle. Cataract formation was seen in both cases. Visual acuity was reduced to little more than light perception.
[NIOSH; Criteria Document: Ammonia p.34 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
One human subject /was exposed/ for 4 hours to an ammonia concentration of 530-560 ppm in order to study biochemical and blood pressure changes. Blood urea nitrogen and serum creatinine remained unchanged through the exposure. The carbon dioxide combining power of the blood plasma remained unaltered. Repeated blood pressure readings during the experiment showed a linear drop from 127 mm to 102 mm. No reference /was made/ to postexposure blood pressures, and data were not given on any subjective reactions or pulmonary function during or after exposure. During the exposure period, the serum nonprotein nitrogen gradually increased from 27 mg/100 g blood to 57 mg/100 g blood and the blood ammonia rose from nondetectable levels to values of 36.4 mg/100 g blood.
[NIOSH; Criteria Document: Ammonia p.36 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
700 ppm causes eye irritation, and permanent injury may result if prompt remedial measures are not taken; 5000 ppm can cause immediate death from spasm, inflammation, or edema of the larynx. Contact of the liquid with skin freezes the tissue and then produces a caustic burn.
[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5., p. ]**PEER REVIEWED**
Ammonia toxicity is a major factor in the pathogenesis of hepatic encephalopathy associated with chronic liver disease. Ammonia levels in patients with severe liver disease are frequently elevated both in blood and cerebrospinal fluid. Hepatic encephalopathy results in neuropathological damage similar (Alzheimer type II astrocytosis) to that found in patients with congenital hyperammonemia resulting from inherited urea cycle enzymes defects. Cerebrospinal fluid and brain glutamine are significantly elevated in cirrhotic patients with encephalopathy following portocaval anastomosis. In both cases, glutamine is elevated in a region-dependent manner.
[Butterworth RF et al; Neurochem Pathol 6 (1-2): 1-12 (1987)]**PEER REVIEWED**
The eyes of volunteers were exposed to a range of concentrations of sulfur dioxide, ammonia, butan-2-one, pentan-2-one, formaldehyde, 3-methyl-butan-2-one, or acrolein for up to 15 seconds inside close fitting goggles. The subjects also inhaled 10 breaths of 1 liter of each agent through a mouthpiece while wearing a nose clip. Eye irritancy increased with increasing bronchoconstriction. The bronchoconstrictive response occurred at concentrations below the threshold for eye irritation. The sensitivity of the lung to the irritant gases was estimated to be about 1.5 times greater than that of the eye. /The data indicated/ that although some organs may be relatively more sensitive than others, some irritant gases are specific for certain organs.
[Douglas RB, Coe JE; Annal Occup Hyg 31 (2): 265-7 (1987)]**PEER REVIEWED**
/To investigate/ the etiology of altered mental status following transurethral prostatectomy, serum electrolyte and blood ammonia levels were measured in 33 patients before and immediately after transurethral prostatectemy. The irrigating fluid was 3% sorbitol in 12 patients and 1.5% glycine in 21. Serum electrolyte changes were similar in both groups. Elevated blood ammonia levels were observed in eight of the 21 patients receiving glycine irrigation. Three of these patients demonstrated clinical signs of encephalopathy. Absorption of glycine during transurethral prostatectomy appears to produce hyerammonaemia in some patients and may contribute to the encephalopathy.
[Shepard RL et al; Br J Urol 70 (4): 349-51 (1987)]**PEER REVIEWED**
The relationship between ammonia accumulation during submaximal exercise and altitude acclimatization was investigated in 12 healthy male volunteers with an average age of 20 years. All the subjects lived at sea level and had not been exposed to altitudes greater than 1,500 meters for 6 months prior to the study. The study included 21 days at sea level and 14 days at high altitude (4,300 meters). The subjects were divided into an active group that exercised for a total of 40 minutes daily and a sedentary group. Plasma metabolites and ventilation were studied after three submaximal 30 minute cycling exercise periods. There were no significant differences in maximal oxygen uptake for the active and sedentary groups either at sea level or at high altitude. Values for maximal oxygen uptake decreased by 32% for both groups after 24 hr at high altitude. The maximum oxygen uptake values for the sedentary soldiers decreased another 16% after 13 days at high altitude whereas the values for the active subjects did not change after the first 24 hours at high altitude. Oxygen uptake was significantly higher for both groups at sea level than after acute or chronic high altitude exposure. The respiratory exchange ratio during exercise increased after acute exposure to high altitude, but no between group differences were observed. Resting plasma ammonia levels were comparable at all altitudes. Postexercise plasma ammonia levels were elevated in the sedentary group only after chronic high altitude exposure. No significant group differences were noted at any altitude for resting or postexercise plasma glucose and insulin concentrations or the free fatty acid to glycerol ratio.
[Young PM et al; J Appl Physiol 63 (2): 758-64 (1987)]**PEER REVIEWED**
Exposure to high concn can cause temporary blindness and eye damage; 46.8 ppm recognition odor in air; good warning properties; direct contact with liquid causes severe eye burns and skin burns. Dose effect relationship 100 ppm 8 hr MAC, 300 ppm 1 hr MAC, 408 ppm least concn causing throat irritation; 698 ppm least concn causing immediate eye irritation; 1,720 ppm least level causing cough response; 5,000-10,000 rapidly fatal for short exposure 2: 3% burns on wet skin.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 137]**PEER REVIEWED**
... Irritation of the respiratory tract and conjunctivae /was found/ in workers inhaling 100 ppm ammonia, and 20 ppm caused complaints and discomfort in uninjured workers. Studies of the effect on man of exposures in the 5-20 ppm range are meager; however, general field experience with a large number of workers exposed to ammonia from blueprinting and copying machines indicates a maximum acceptable concentration without severe complaints of 20-25 ppm.
[American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 58]**PEER REVIEWED**
Patients who survive for more than 24 hours are likely to recover. Although complete pulmonary recovery is the usual outcome, residual bronchoconstriction, bronchiectasis, and small airway disease have been reported. Fibrous obliteration of the small airways, thought to be a late stage of bronchiolitis obliterans, is felt to be the cause of the chronic obstructive pulmonary disease that occasionally develops.
[Haddad, L.M., Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia, PA: W.B. Saunders Co., 1990., p. 1272]**PEER REVIEWED**
Eye damage varying in degree to total blindness may be the permanent residual effect of an exposure to ammonia. Cataract formation, permanent corneal ulceration, and lenticular opacification have been reported.
[Haddad, L.M., Clinical Management of Poisoning and Drug Overdose. 2nd ed. Philadelphia, PA: W.B. Saunders Co., 1990., p. 1272]**PEER REVIEWED**
A typical case history illustrates the time course and type of injury following a nonfatal acute ammonia exposure. A 61 year old manager of an anhydrous ammonia company was accidentally sprayed in the face and chest with anhydrous ammonia when a valve malfunctioned. Immediate blepharospasm prevented him from moving away from the jet of ammonia. An employee led him to a water tank where he washed his face and chest for 15 minutes. He was taken to the local emergency room, arriving there 1 hour after the injury. Upon arrival he was aphonic and dyspneic with inspiratory stridor. He was coughing serosanguinous material. An emergency tracheostomy was performed. The chest radiograph was normal. He was treated with bronchodilators, steroids, and empiric antibiotics for treatment of second-degree burns over his thighs and chest. He recovered over a 15 day period with eventual removal of the tracheostomy. Serial chest radiographs were normal. His vision was unimpaired and he had no pulmonary complaints at the time of discharge.
[Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 792]**PEER REVIEWED**
Human Toxicity Values:
LCLo Human inhalation 7,000 mg/cu m/3 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.99 (1981)]**PEER REVIEWED**
Skin, Eye and Respiratory Irritations:
The vapor even in low concn is extremely irritating to skin, eyes and respiratory passages.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-22]**PEER REVIEWED**
Caution: Potential symptoms of overexposure are eye, nose and throat irritation; dyspnea, bronchospasm and chest pain; pulmonary edema; pink frothy sputum; skin burns, vesiculation.
[Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 87]**PEER REVIEWED**
Strong irritant to eyes, skin, respiratory tract. Pungent odor. Liquid produces severe burns. Inhalation of high concn causes violent coughing, severe lung irritation, and pulmonary edema. Death can result if rapid escape is not possible. Swallowing liquid is corrosive to mouth, throat, stomach. Not a systemic poison.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 137]**PEER REVIEWED**
Drug Warnings:
Caution: Irritating to skin and mucous membranes. /Ammonia water-10%/
[Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 87]**PEER REVIEWED**
Medical Surveillance:
The following medical procedures should be made available to each employee who is exposed to ammonia at potentially hazardous levels: (1) A complete medical history and physical examination: the purpose is to detect existing conditions that might place the exposed employee at increased risk, and to establish a baseline for future health monitoring. Examination of the eyes and respiratory tract should be stressed. The skin should be examined for evidence of chronic disorders; (2) 14" x 17" chest roentgenogram: Ammonia causes human lung damage. Surveillance of the lungs is indicated; (3) FVC and FEV (1 sec): Ammonia is a respiratory irritant. Persons with impaired pulmonary function may be at increased risk from exposure. Periodic surveillance is indicated. Medical examinations should be repeated on an annual basis, except that an X-ray is necessary only when indicated by the results of pulmonary function testing, or by signs and symptoms of respiratory disease.
[Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1]**PEER REVIEWED**
Populations at Special Risk:
IN EVENT AN INDIVIDUAL'S LIVER FUNCTION IS GREATLY REDUCED, ANY SOURCE OF AMMONIA, SUCH AS ... INHALATION ... CAN LEAD TO HEPATIC COMA WITH INCREASED CIRCULATING AMMONIA.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 756]**PEER REVIEWED**
Persons with corneal disease, and glaucoma, or chronic respiratory diseases may suffer increased risk.
[Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 46]**PEER REVIEWED**
Probable Routes of Human Exposure:
Routes of entry: Inhalation of gas, ingestion, skin and eye contact.
[Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 46]**PEER REVIEWED**
WHEN AMMONIA IS USED AS DEVELOPER IN PHOTOCOPYING PROCESSES ... BLUEPRINT & DIAZO, IT MAY BE RELEASED INTO WORKPLACE.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 756]**QC REVIEWED**
ACCIDENTAL EXPOSURES OF HUMANS MAY ARISE FROM FAILURE OF EQUIPMENT CONTAINING EITHER LIQ OR GASEOUS AMMONIA. ... LIQ AMMONIA EXPOSURES MAY BE COMPLICATED BY FREEZING OF TISSUES & BY INJECTION OF A LIQ STREAM UNDER HIGH PRESSURE.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 759]**QC REVIEWED**
ANALYSIS OF DATA OBTAINED IN PLANT SURVEYS FOUND THE LIMIT OF DETECTION TO BE BELOW 5 PPM & THE COMPLAINT LEVEL TO BE 20-25 PPM.
[American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 27]**PEER REVIEWED**
NIOSH estimates that approximately half a million USA workers have potential exposure to ammonia.
[NIOSH; Criteria Document: Ammonia p.24 (1974) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
Emergency Medical Treatment:
Emergency Medical Treatment:
For more specific material safety information for Ammonia, please consult the Anhydrous Ammonia MSDS Information above.
Antidote and Emergency Treatment:
Call for medical aid. Vapor poisonous if inhaled. ... Move to fresh air. If breathing has stopped, give artificial respiration. If breathing is difficult, give oxygen. ... Remove contaminated clothing and shoes. Flush affected areas with plenty of water. Do not rub affected areas. If in eyes, hold eyelids open, and flush with plenty of water. If swallowed and victim is conscious, have victim drink water or milk.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 138]**PEER REVIEWED**
Inhalation: Move victim to fresh air and give artificial respiration if necessary. Oxygen may be useful. Observed for laryngeal spasm and perform /SRP: intubation or/ tracheostomy if indicated. Skin or eyes: flood immediately with running water for 15 min. Treat subsequently as thermal burn.
[Prager, J.C. Environmental Contaminant Reference Databook Volume 1. New York, NY: Van Nostrand Reinhold, 1995., p. 138]**PEER REVIEWED**
For immediate first aid: Ensure that adequate decontamination has been carried out. If victim 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 left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep victim quiet and maintain normal body temperature. Obtain medical attention. /Ammonia and related compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 171]**PEER REVIEWED**
For basic treatment: Establish a patent airway. 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 normal saline 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 patient can swallow, has a strong gag reflex, and does not drool. ... Do not attempt to neutralize. /Ammonia and related compounds/
[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 171]**PEER REVIEWED**
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
DEATH MAY RESULT PARTLY FROM ASPHYXIA & PARTLY FROM ELECTROLYTE & CELLULAR METABOLIC ACTION OF AMMONIA. TERMINAL SIGNS INCLUDE CYANOSIS, POSSIBLE VIOLENT STRUGGLING & BELLOWING ... & CLONIC CONVULSIONS.
[Jones, L.M., et al. Veterinary Pharmacology & Therapeutics. 4th ed. Ames: Iowa State University Press, 1977., p. 1134]**PEER REVIEWED**
CLINICAL SIGNS INCLUDE REDDENED MUCOUS MEMBRANES, LACRIMATION, COUGHING, SNEEZING, DECR EGG PRODUCTION IN BIRDS, NASAL DISCHARGE ... & DYSPNEA DUE TO PULMONARY EDEMA. FLUID SOUNDS MAY BE DETECTED IN THE LUNGS.
[Jones, L.M., et al. Veterinary Pharmacology & Therapeutics. 4th ed. Ames: Iowa State University Press, 1977., p. 1133]**PEER REVIEWED**
... CONTINUOUS EXPOSURE FOR SEVERAL WK TO 470 MG/CU M ... TO EYES OF ... RABBITS ... PRODUCED OPACITY OVER 1/4 TO 1/2 OF CORNEA IN RABBITS.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 86]**PEER REVIEWED**
AMMONIA ... CROSSES THE OVINE PLACENTA. THE FETUS CAN ACCUMULATE (& APPARENTLY DETOXIFY) MORE AMMONIA THAN THE DAM BECAUSE FETAL TISSUES HAVE LARGER CONCN THAN THOSE OF THE DAM WHEN THE DAM IS POISONED BY UREA.
[Booth, N.H., L.E. McDonald (eds.). Veterinary Pharmacology and Therapeutics. 5th ed. Ames, Iowa: Iowa State University Press, 1982., p. 1031]**PEER REVIEWED**
STATIC EXPOSURES OF CATS & RABBITS FOR 1 HR ... AT 7000 MG/CU M RESULTED IN DEATH OF APPROX 50% ... POSTMORTEM EXAM SHOWED SEVERE EFFECTS ON UPPER RESP TRACT ... LESS SEVERE EFFECTS IN LOWER RESP TRACT INCL DAMAGE TO BRONCHIOLES & ALVEOLAR CONGESTION, EDEMA, ATELECTASIS, HEMORRHAGE, EMPHYSEMA & FLUID.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 758]**PEER REVIEWED**
/49 & 51/ RATS WERE ... EXPOSED CONTINUOUSLY FOR 90 DAYS AT ... 262 MG/CU M & FOR 65 DAYS AT 455 MG/CU M /RESPECTIVELY/. ... 262 MG/CU M ... /PRODUCED/ MILD NASAL DISCHARGE IN ABOUT 25% ... ALL 51 RATS EXPOSED AT 455 MG/CU M SHOWED MILD DYSPNEA & NASAL IRRITATION. THERE WERE 32 DEATHS BY DAY 25 & 50 BY DAY 65.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 758]**PEER REVIEWED**
... RATS ... /EXPOSED/ TO 470 MG/CU M ... CONTINUOUSLY FOR 90 DAYS ... HISTOPATHOLOGY ... FOUND FOCAL OR DIFFUSE INTERSTITIAL PNEUMONITIS IN ALL ... WITH EPITHELIAL CALCIFICATION IN RENAL TUBULES & BRONCHI, EPITHELIAL PROLIFERATION OF RENAL TUBULES, MYOCARDIAL FIBROSIS & FATTY LIVER /IN SOME/ ...
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 758]**PEER REVIEWED**
SWINE EXPOSED FOR 2 TO 6 WK AT 100 PPM DEVELOPED CONJUNCTIVAL IRRITATION & THICKENING OF NASAL & TRACHEAL EPITHELIUM WITHOUT INJURY TO BRONCHI OR ALVEOLI.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 758]**PEER REVIEWED**
Pullets exposed to 200 ppm atmospheric ammonia for 17 days had reduced feed intake & reduced growth rate when compared to controls. After the ammonia exposure period at point of lay, percent egg production was less & mortality was greater for exposed group than controls.
[Deaton JW et al; Poult Sci 63 (2): 384-5 (1984)]**PEER REVIEWED**
Lesions occurring in resp tract of mice after exposure to 10 sensory irritants (incl ammonia), at concn which elicited a resp decrease of 50% (RD50), were compared with respect to type & severity. The RD50 of ammonia was 303 ppm. Exposure for 6 hr/day for 5 days produced lesions in nasal cavity with distinct anterior-posterior severity gradient. Lesions produced by the irritants ranged from slight epithelial hypertrophy or hyperplasia to epithelial erosion, ulceration, & necrosis with variable inflammation of subepithelial tissues.
[Buckley LA et al; Toxicol Appl Pharmacol 74 (3): 417-29 (1984)]**PEER REVIEWED**
Turkeys were given an aerosol vaccine to determine their ability to clear a virulent inhaled pathogenic strain of Escherichia coli, while maintained in presence of atmospheric ammonia at 2 concn (10 & 40 ul/l of air). More Escherichia coli were found in lungs, air sacs, & livers of turkeys exposed to ammonia. Turkeys not exposed to ammonia had better clearance of Escherichia coli. Vaccination against Escherichia coli improved the rate of clearance of Escherichia coli in birds not exposed to ammonia.
[Nagaraja KV et al; Am J Vet Res 45 (2): 392-5 (1984)]**PEER REVIEWED**
Ammonia intoxication decreases the hyperpolarizing action of postsynaptic inhibition in cat spinal cord. The effect of ammonia intoxication on postsynaptic inhibition can be considered as a cause of the encephalopathy produced because postsynaptic inhibition is altered without a change in tissue energy state, the resting membrane potential, the whole neuron resistance, the action potential & the excitatory postsynaptic potentials.
[Raabe W, Lin S; Res 303 (1): 67-76 (1984)]**PEER REVIEWED**
Symptoms of injury are more variable on herbaceous plants than on woody species, ranging from irregular, bleached, bificial, necrotic lesions to reddish interveinal streaking or dark upper surface discoloration.
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.91 (1981)]**PEER REVIEWED**
Fifty pounds of gas used /as a fumigant/ in two dairy sheds killed starlings, sparrows, mice and pigeons after 7 min of fumigation. ... Rapid dispersal of the gas eliminates danger of milk contamination or adverse residual effects on cattle.
[Devore AL et al; Pest Control 35 (2): 24-6 (1967)]**PEER REVIEWED**
... The search for the peripheral toxins responsible for the CNS impairment present in hepatic encephalopathy has ... shown that the administration of ammonia, mercaptans and octanoic acid in normal rats reproduced behavioral and electrophysiological changes similar to those seen in galactosamine induced encephalopathy. The present report shows that a subacute administration of the above toxins induced a marked alteration of the GABA receptor complex which may account for the CNS derangement of hepatic encephalopathy.
[Barald M et al; Arch Toxicol (Suppl) 7: 130-5 (1984)]**PEER REVIEWED**
Decreased ammonia toxicity with increased salinity may be partially explained, at least for low salinity levels, by the fact that there is a slight decrease in the ammonia fraction of total ammonia as ionic strength increases in dilute saline solutions.
[USEPA; Ambient Water Quality Criteria Doc: Ammonia p.31 (1984) EPA 440/5-85-001]**PEER REVIEWED**
Although total ammonia toxicity was reduced at elevated CO2 levels, the inverse was true when considering non-ionized ammonia alone; more NH3 is required in low CO2, high pH water to exert the same toxic effect as seen in fish in high CO2, low pH water. The explanation presented for the decreased toxicity of NH3 in low CO2 water was that CO2 excretion across the gills would reduce pH, and therefore NH3 concentration, in water flowing over the gills.
[USEPA; Ambient Water Quality Criteria Doc: Ammonia p.30 (1984) EPA 440/5-85-001]**PEER REVIEWED**
In experiments with Potamogeton lucens, /it was/ observed that ammonia, which forms a readily available nitrogen source for the plant, can be toxic when present at high concentrations ... causing appreciable injury to detached branches.
[USEPA; Ambient Water Quality Criteria Doc: Ammonia p.72 (1984) EPA 440/5-85-001]**PEER REVIEWED**
/Results of/ an unstated number of rabbits and cats for 1 hour to initial concentrations of 3.5-8.7 mg/l (approximately 5,200-12,800 ppm) /of ammonia/ with an average concentration of 7.0 mg/l (approximately 10,360 ppm was reported to be the "approximate LC50." The static method of gassing used probably resulted in an average concentration of half the initial concentrations or less. Also evaluated was the gas absorption of the nasobuccopharyngeal section of the respiratory tract. Rabbits /which/ inhaled directly through a tracheal cannula, and a second group inhaled normally through nose, mouth, and throat. The mean survival time in the second group was reported to be almost twice that of the first group, 33 hr versus 18 hr. On microscopic examination, the trachea was congested and edematous. The mucosa was necrotic and sloughed off in 80-90% of the animals in which the upper respiratory tract had been bypassed, while the trachea was normal in appearance in the second group of test animals. Similar differential findings, but to a lesser degree, were shown in the bronchial mucosa. The damage to the bronchioles and alveoli surprisingly appeared to be identical in both groups. It was described as congestion, edema, hemorrhage, and atelectasis with emphysema. The upper respiratory tract acted as a protection only to the trachea and bronchi, and that small airways and alveoli were less resistant to ammonia injury in many cases within 10 minutes. Between the 6th and 10th postexposure days, 7 of the 80 died, compared with no deaths in controls. Autopsies were not performed.
[NIOSH; Criteria Document: Ammonia p.47 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
12 guinea pigs /were exposed/ to about 170 ppm ammonia for 6 hours a day, 5 days a week for up to 18 weeks. Chamber concentrations were monitored and ranged from 140-200 ppm. The exposed animals and 6 controls were weighed weekly. No adverse effects were observed by autopsy of the 4 exposed and 2 control animals killed after 6 weeks or after 12 weeks. In 4 animals exposed for 18 weeks, there was congestion of spleens, livers, and kidneys with early degenerative changes in suprarenal glands. Increased blood destruction was suggested by higher quantities of hemosiderin in the spleens. In the upper tubules of the kidneys there was cloudy swelling with precipitated albumin in the lumen and some casts. These changes were also seen in the lower tubules of 2 animals. The cells of the suprarenal glands were swollen and the cytoplasm in some areas had lost its normal granular structure.
[NIOSH; Criteria Document: Ammonia p.48 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
One pig exposed to 280 ppm of ammonia showed immediate irritation of the nose and mouth and abnormal respiratory patterns, and by the 36th hour of exposure had convulsions and extremely shallow and irregular breathing. Convulsions continued for 3 hours after exposure ended but the animal appeared normal several hours later. In each of 2 trials, 4 exposure groups of 9 pigs each were continuously exposed to ammonia for 5 weeks. Data from both trials were combined for analysis. Concentrations of ammonia were measured daily, and the average exposures of the groups were 12, 61, 103, and 145 ppm. Feed consumption and average daily weight gain were adversely affected by increasing ammonia concentrations. Pigs exposed to the 3 higher concentrations had excessive nasal, lacrymal, and oral secretions, but these were less pronounced in those exposed to 61 ppm. Pigs exposed to 61 ppm appeared to adjust within 3-4 days, so that their secretory rate was only slightly higher than that of animals exposed to 12 ppm. Pigs in the 2 higher concentrations coughed approximately 3 times as much as those in the lower, and coughing at 61 ppm was slightly more frequent than at 12 ppm. Five animals from each exposure group were autopsied and all gross and microscopic findings were normal.
[NIOSH; Criteria Document: Ammonia p.50 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
Arginine administration (5 m moles/kg/day) to albino rats for 7 days, revealed that this vital basic amino acid possesses latent potentiality for the accentuation of urea cycle or at least for arginase activity. The mitigation of ammonia toxicity was observed to be more effective in the gastrocnemius and red vastus as compared to white vastus. Ammonia and lactate levels were decreased in blood by arginine and thereby delayed the onset of fatigue by preventing ammonotoxemia and lactic acidemia.
[Krishna Mohan P et al; Indian J Physiol Pharmacol 31 (1): 63-9 (1987)]**PEER REVIEWED**
The short-term effects of ammonia vapor on mucociliary function in the maxillary sinus of rabbits anesthetized with urethane were investigated by a photoelectric technique. Challenges with 1.5 ml ammonia increased mucociliary activity dose dependently, the maximal response being 26.6 + or - 1.6%. The increase appeared within 1.3 + or - 0.3 seconds after exposure. Atropine and hexamethonium decreased the effects of NH3, indicating that part of the response was mediated by cholinergic effector neurons, but a noncholinergic effect clearly remained. Pretreatment with large doses of capsaicin (13 mg ia) abolished the response, whereas the neuropeptide substance P antagonist (d-Pro2, D-Trp7,9) inhibited the noncholinergic response. Challenges with ammonia vapor decreased respiratory rate. An identical response was noticed during injections with the C fiber stimulant capsaicin. Ammonia vapor trigger a mucociliary protective reflex in the airways, involving capsaicin-sensitive C fibers; the increase of mucociliary activity is probably due to the combined effect on the mucociliary system of both neuropeptide substance P and acetylcholine released from the afferent and efferent part of the reflex arc, respectively.
[Lindbery S et al; Am Rev Respir Dis 135 (5): 1093-8 (1987)]**PEER REVIEWED**
The effects of exposure of animals to ammonia on their delayed type of dermal response, the mitogenic and antigenic responses of their lymphocytes, and the bactericidal and phagocytic activities of their alveolar macrophages were examined. ... The response of normal blood lymphocytes to phytohemaglutinin in medium containing 1 or 10 mg of ammonia/dl was significantly affected. There was no significant difference in the bactericidal or phagocytic activities of alveolar macrophages collected from animals exposed to ammonia and control animals. However, ammonia added to the culture of alveolar macrophages from normal animals significantly inhibited their bactericidal activity.
[Targowski SP et al; Infect Immun 43 (1): 289-93 (1984)]**PEER REVIEWED**
The effect of addition of ammonia into the tissue cultures represented toxic, subtoxic, and normal concn of ammonia in the bovine blood during clinical and subclinical urea toxicosis. ... Viability of the lymphocytes was measured by the trypan blue exclusion test and their mitogenic reactivity by incorporation of (3)H thymidine into DNA of lymphocytes. Approximately 30% bovine lymphocytes were killed by ammonia in medium during 72 hr of incubation. Ammonia also affected the response of lymphocytes to stimulation with PHA or Con A as well as mixed lymphocyte culture reaction. The mitogenic response of lymphocytes was also reduced when lymphocytes were preincubated with ammonia for even 1 hr. The mitogenic response was not restored when the number of lymphocytes preincubated with ammonia was reconstituted to the initial concn to compensate for the killed lymphocytes before stimulation with PHA. Therefore, addition of ammonia to the culture either killed lymphocytes or permanently impaired their function.
[Targowski SP et al; Vet Immunol Immunopathol 5 (3): 297-310 (1984)]**PEER REVIEWED**
Recent studies of dairy cattle provide speculative evidence that, high protein feeding or forms of protein that lead to elevated ammonia concn in tissue, decrease conception rates, and increase the calving to conception intervals of dairy cows.
[Visek WJ; J Daisy Sci 67 (3): 481-98 (1984)]**PEER REVIEWED**
Acute symptoms of ammonia (NH3) toxicity to brown trout sac fry and 12 day old fry were described by researchers, who exposed fry to concn ranging from 0.08 to 50.0 mg/l NH3. Symptoms caused by NH3 exposures were: rapid spasm like movements at concn of 2.0 mg/l NH3 and higher within 16-17 minutes of exposure; after 40 minutes these symptoms were also observed at 0.4 mg/l NH3. After 2.5 hr these abnormal movements ceased, and at 10 hr heart activity was decreased and fish lost movement ability at the higher (> 2.0 mg/l NH3) concn. Other symptoms included inability to react to mechanical stimulation and disorders in rhythm of mouth movements culminating in the mouth's staying rigidly open.
[USEPA; Ambient Water Quality Criteria Doc: Ammonia p.78 (1984) EPA 440/5-85-001]**PEER REVIEWED**
Eight rats and four mice /were exposed/ for 16 hr to an ammonia gas concentration of 1,000 ppm in a continuous flow chamber study. No noticeable effects /were noted/ during exposure. One rat died 12 hr after exposure and showed congestion of the brain, liver, and kidneys, plus large hemorrhages in the lung and pulmonary edema. The other 11 animals showed no gross abnormalities during the subsequent 5 months of observation. Two rats and two mice were killed at that time, and autopsy results were negative.
[NIOSH; Criteria Document: Ammonia p.48 (1979) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
The concn of ammonia fumes in the air of animal rooms from bedding soiled with urine ... is also now recognized as a possible complicating factor in the interpretation of animal studies, particularly when there might be respiratory lesions. ... the effects of ammonia at concn of 25-250 ppm in the air of animal rooms on the characteristics of murine respiratory mycoplasmosis in Sherman and Fischer rats. The prevalence of pneumonia, but not of other respiratory lesions of murine respiratory mycoplasmosis, showed a strong tendency to incr directly with environmental ammonia concn. Exposure to ammonia of rats that had not been infected with the mycoplasma organism caused anatomic lesions that were unlike those of mycoplasmosis and were limited to the nasal passages.
[Hayes, W.J., Jr., E.R. Laws Jr., (eds.). Handbook of Pesticide Toxicology Volume 1. General Principles. New York, NY: Academic Press, Inc., 1991., p. 73]**PEER REVIEWED**
Extensive experiments in eight ureotelic species, including man, show that urinary excretion of orotic acid becomes significantly elevated when the quantity of ammonia presented to the liver exceeds the capacity for normal detoxification.
[Visek WJ; J Dairy Sci 67 (3): 481-98 (1984)]**PEER REVIEWED**
Non-Human Toxicity Values:
RD50 Mouse (Respiratory Rate): 303 ppm
[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983., p. 196]**PEER REVIEWED**
LC50 Rabbit inhalation 7,050 mg/cu m/1 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.101 (1981)]**PEER REVIEWED**
LCLo Rabbit inhalation 4,900 mg/cu m/1 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.101 (1981)]**PEER REVIEWED**
LCLo Cat inhalation 4,900 mg/cu m/1 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LC50 Cat inhalation 746 mg/cu m/1 hr (Dynamic air flow)
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LC50 Cat inhalation 7,050 mg/cu m/1 hr (Static conditions)
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LC50 Rat inhalation 7,600 mg/cu m/2 hr (age and strain not specified)
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LC50 Rat inhalation 5,100 mg/cu m/1 hr (age and strain not specified)
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LCLo Rat inhalation 1,400 mg/cu m/1 hr (age and strain not specified)
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.102 (1981)]**PEER REVIEWED**
LC50 Mouse inhalation 7,105 mg/cu m/10 min
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.103 (1981)]**PEER REVIEWED**
LC50 Mouse inhalation 3,360 mg/cu m/1 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.103 (1981)]**PEER REVIEWED**
LC50 Mouse inhalation 3,310 mg/cu m/2 hr
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.103 (1981)]**PEER REVIEWED**
LD50 Rat oral 350 mg/kg
[Environment Canada; Tech Info for Problem Spills: Ammonia (Draft) p.103 (1981)]**PEER REVIEWED**
Ecotoxicity Values:
LC50 Daphnia magna 24 mg/L/48 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Daphnia magna 189 mg/L/48 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Daphnia pulex 187 mg/L/48 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Ceriodaphnia reticulata 131 mg/L/48 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Simochephalus vetulus 123 mg/L/48 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Fathead minnows 8.2 mg/L (hard water)/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Goldfish 2-2.5 mg/L/24-96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Coho salmon 0.45 mg/L/96 hr /Flow-through bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Guppy fry 74 mg/L/72 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Guppy fry 1.26 mg/L/72 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Cutthroat trout (Salmo clarki) fry 0.5-0.8 mg/L/96 hr /Flow-through bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Rainbow trout fertilized egg >3.58 mg/L/24 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Rainbow trout alevins (0-50 days old) >3.58 mg/L/24 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Rainbow trout fry (85 days old) 0.068 mg/L/24 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Rainbow trout adult 0.097 mg/L/24 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Walking catfish 0.28 mg/L/48 hr /Static bioassay/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salmo aguabonita 0.76 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salmo trutta >0.15 mg/L/18 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Oncorhynchus tschawytscha 0.47 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salvelinus fontinalis 0.96-1.05 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Proposium williamsoni 0.47 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Catostomus platyrhynchos 0.67-0.82 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salmo trutta 0.47 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salvelinus fontinalis >3.2 mg/L/1.8 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Oncorhynchus gorbuscha (late alevins) 0.083 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Oncorhynchus gorbuscha (eyed embryos) >1.5 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Oncorhynchus kisutch 0.55 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Salmo salar 0.28 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Pimephales promelas 0.75-3.4; 0.73-2.3 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Catostomus commersoni 0.79; 1.35-1.4 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 186]**PEER REVIEWED**
LC50 Lepomis macrochirus 0.26-4.6 mg/L/96 hr /Conditions of bioassay not specified/
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. 3rd ed. New York, NY: Van Nostrand Reinhold Co., 1996., p. 187]**PEER REVIEWED**
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
ONCE ABSORBED, AMMONIA IS CONVERTED TO AMMONIUM ION AS THE HYDROXIDE & AS SALTS, ESPECIALLY AS CARBONATES. THE AMMONIUM SALTS ARE RAPIDLY CONVERTED TO UREA ... MAINTAINING AN ISOTONIC SYSTEM.
[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 760]**PEER REVIEWED**
Deamination of amino acids by the liver, metabolic activity of nerve and muscle tissue, as well as activity of enzymes contained in the flora of the gut on substrates derived from the diet and the blood all lead to the production of ammonia.
[Fromm PO; Toxic Action of Water Soluble Pollutants on Freshwater Fish EPA Water Pollution Control Research Series No. 18050 DST (1970)]**PEER REVIEWED**
Ammonium ions are produced in the body as a protein metabolite. Ammonium ions produced by deamination are rapidly converted in the liver into relatively harmless urea and excreted by the kidney or are used to make new amino acids. Ammonium ions are also produced in the kidney, conserving fixed base, thus maintaining electrolyte balance.
[NIOSH; Criteria Document: Ammonia p.25 (1974) DHEW Pub. NIOSH 74-136]**PEER REVIEWED**
Carbamide administration to animals is accompanied by its rapid transformation to carbon dioxide and ammonia in the rumen by the microbial enzyme urease. Therefore, large doses of carbamide can result in very high rumen level of ammonia.
[Khmel'nitskii GA; Veterinariya (Moscow) 1: 64-5 (1984)]**PEER REVIEWED**
... Ammonia production was observed from stimulated nerve. ... Relationship between ammonia production and the muscle activity /was studied/. The immediate source of ammonia from muscle appears to be a result of the deamination of adenosine monophosphate and is more apparent in fast twitch than in slow twitch fibers. More recently, increases in blood ammonia levels have been reported in rats after swimming and in humans after arm work, maximal cycle ergometry, and treadmill exercise. Elevated blood ammonia has also been linked to a surprising variety of functional, metabolic, and neurological disturbances other than exercise and fatigue, including the development of hepatic coma, convulsions from ammonia toxicity precipitated by high pressure oxygen breathing, epileptic seizures, and decreased neuronal excitability. In addition, a number of genetic disorders (inborn errors in metabolism) are characterized by elevated blood ammonia concn. Symptoms of neural disability in all of the above conditions have been related to the concn of ammonia in blood. ...
[Mutch BJ, Banister EW; Med Sci Sports Exerc 15 (1): 41-50 (1983)]**PEER REVIEWED**
... Following administration of (13)N ammonia to rats (via either the carotid artery or cerebrospinal fluid), most metabolized label was in glutamine (amide) and little was in glutamate (plus aspartate). Since blood and cerebrospinal fluid borne ammonia are converted largely to glutamine, it is not possible to predict with certainity the metabolic fate of bulk of endogenously produced ammonia. By comparing the specific activity of L-(13)N glutamate to that of L-amine-(13)N glutatmine following intracarotid (13)N ammonia administration it was concluded that metabolic compartmentation is no longer intact in the brains of rats treated with the glutamine synthetase inhibitor L-methionine-SR-sulfoximine and that blood and brain ammonia pools mix in such animals. In L-methionine-SR-sulfoximine treated animals, recovery of label in brain was low (approximately 20% of controls), and of the label remaining, a prominent portion was in glutamine (amide) (despite an 87% decrease in brain glutamine synthetase activity). The rate of tunrnover of blood derived ammonia to glutamine in normal rat brain is extremely rapid (half-life < or = 3 s), but is slowed in the brains of chronically (12-14 wk portacaval shunted) or acutely (urease treated) hyperammonemic rats (half-life < or = 10 s). The slowed turnover rate may be caused by increased astrocytic ammonia, decreased glutamine synthetase activity, or both. In the hyperammonemic rat brain, glutamine synthetase is the only important enzyme for the removal of blood-borne ammonia. Hyperammonemia causes an increase in brain lactate/pyruvate ratios and decrease in brain glutamate and brainstem ATP, consistent with an interference with the malate-aspartate shuttle. In vitro, pathological levels of ammonia inhibit brain alpha-ketoglutarate dehydrogenase complex and, less strongly, pyruvate dehy |
