AMMONIA
CASRN: 7664-41-7
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAgeaaoB:1
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.
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.
/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.
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.
Inhalation causes ... secretion of saliva and retention of urine.
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.
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.
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.
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.
Therapeutic or normal blood level: 0.05-0.17 mg %; 0.5-1.7 ug/ml
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.
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.
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.
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.
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.
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.
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.
/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.
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.
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.
... 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.
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.
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.
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.
Human Toxicity Values:
LCLo Human inhalation 7,000 mg/cu m/3 hr
Skin, Eye and Respiratory Irritations:
The vapor even in low concn is extremely
irritating to skin, eyes and respiratory passages.
Caution: Potential symptoms of overexposure are eye, nose and throat
irritation; dyspnea, bronchospasm and chest pain; pulmonary edema; pink
frothy sputum; skin burns, vesiculation.
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.
Drug Warnings:
Caution: Irritating to skin and mucous
membranes. /Ammonia water-10%/
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.
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.
Persons with corneal disease, and glaucoma, or chronic respiratory
diseases may suffer increased risk.
Probable Routes of Human Exposure:
Routes of entry: Inhalation of gas,
ingestion, skin and eye contact.
WHEN AMMONIA IS USED AS DEVELOPER IN PHOTOCOPYING
PROCESSES ... BLUEPRINT & DIAZO, IT MAY BE RELEASED INTO WORKPLACE.
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.
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.
NIOSH estimates that approximately half a million USA workers have
potential exposure to ammonia.
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.
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.
... 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.
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.
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.
/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.
... 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/ ...
SWINE EXPOSED FOR 2 TO 6 WK AT 100 PPM DEVELOPED CONJUNCTIVAL IRRITATION
& THICKENING OF NASAL & TRACHEAL EPITHELIUM WITHOUT INJURY TO
BRONCHI OR ALVEOLI.
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.
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.
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.
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.
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.
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.
... 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.
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.
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.
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.
/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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
... 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. ...
... 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 dehydrogenase complex.
Ammonia is a toxic molecule that is the principal by-product of
amino acid metabolism. The transport of ammonia
in a nontoxic form protects the brain against high circulating levels. The
liver is the central organ of ammonia metabolism,
but other organs play a key role in the interorgan exchange of this
molecule. Alterations in ammonia metabolism occur
during critical illness.
Absorption, Distribution & Excretion:
AMMONIA IS
ABSORBED BY INHALATION, INGESTION, & PROBABLY PERCUTANEOUSLY AT CONCN
HIGH ENOUGH TO CAUSE SKIN INJURY. DATA ARE NOT AVAIL ON ABSORPTION OF LOW
CONCN THROUGH SKIN. ... EXCRETION IS PRIMARILY BY WAY OF KIDNEYS, BUT A
NOT INSIGNIFICANT AMT IS PASSED THROUGH SWEAT GLANDS.
... The average nasal retention of ammonia by
human subjects was found to be 83%.
Levels of exhaled (nasal) ammonia were measured
in rabbits at different times on the same day, on different days, and in
rabbits in a normal fed state, or in a fasted or fed state in which the
teeth were brushed and the mouth cleansed. The variability of ammonia
levels within any individual rabbit was found to be of the same order as
the variability found between different animals. In addition, rabbits
which were fasted and had their teeth brushed exhaled significantly less ammonia
than did fed animals. Levels in the former group ranged from 2 to 236 ug/cu
m, while those in the latter group ranged from 10 to 758 ug/cu m. Although
brushing the teeth of fed animals compressed the observable range of ammonia
levels (22-404 mg/cu m), this was not a significant reduction compared to
fed, unbrushed animals. Thus, fasting likely minimized foodstuff in the
mouth; the latter may contribute to ammonia
formation through bacterial degradation, which appears to be a significant
source of ammonia exhaled through the nose.
Mechanism of Action:
SRP: 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.
PRIMARY MECHANISM OF AMMONIA TOXICOSIS APPEARS TO
BE INHIBITION OF /CITRIC/ ACID CYCLE. THERE IS INCR IN ANAEROBIC
GLYCOLYSIS, BLOOD GLUCOSE, & BLOOD LACTATE ... ACIDOSIS IS MANIFESTED.
EXACT MEANS BY WHICH AMMONIA BLOCKS CITRIC ACID
CYCLE IS NOT KNOWN.
Rates of glutamate formation & of carbon dioxide production (as
indication of oxidative deamination of glutamate) were determined in
primary cultures of astrocytes exposed to 50 uM labeled glutamate in
absence or presence of added ammonia (0.1-3 mM).
Glutamine formation (1.7 nmol/min/mg protein) was unaffected by all concn
of added ammonia. Pathophysiological concn of ammonia
does not incr formation of glutamine from exogenous glutamate. Carbon
dioxide production rate was 5.9 nmol/min/mg protein, ie, 3 to 4 times
higher than the rate of glutamine formation. It was significantly reduced
(to 3.5 nmol/min/mg protein) in presence of 1 mM or more of ammonia.
This is an indication that toxic levels of ammonia
affect oxidative metabolism.
Acute & sustained hyperammonemia in mice resulted in decr of
transition temperature of Arrhenius plots of synaptosomal (sodium-potassium)ATPase.
This seems to indicate that ammonia alters
physical properties of synaptosomal membranes.
Ammonia disrupts primarily the Krebs cycle. The adverse effects on
the central nervous system and ATP deficiency during the intoxication
often result in animal death.
The irritation to mucous membranes becomes noticeable at about 100 ppm.
Concentrations above 400 ppm may destroy mucous surfaces upon prolonged
contact by dissolving or emulsifying keratin, fat, and cholesterol.
Interactions:
The combined effects of ammonia
and carbon particles inhaled by rats were reportedly much greater than
those from ammonia (or carbon) alone.
... /AMMONIA/
ACCENTUATED RESP PARALYSIS & COMA DUE TO EXPOSURE TO METHANETHIOL. ...
/IT IS/ CONCLUDED THAT THESE AGENTS SYNERGISTICALLY AFFECT CERTAIN ENZYME
SYSTEMS WHICH ARE ACTIVATED UNDER PATHOLOGICAL CONDITIONS.
Pent-4-enoic acid inhibited urea
synthesis approx 90% in rat hepatocytes incubated with pyruvate, ammonia,
& ornithine. The addn of ammonia led to
drastic dose dependent inhibition of ureagenesis by pent-4-enoate.
Half-max effect of ammonia was observed at 0.2 mM
concn. Concommitant cellular concn of N-acetylglutamate were modified by
addn of ammonia as was accumulation of citrulline.
Ammonia may interfere with metabolism of
pent-4-enoic acid & lead to dramatic potentiation of its toxicity.
Sodium benzoate lowers serum ammonia
concn by the activation of a non-urea cycle pathway of ammonia
removal. The disposition of sodium benzoate was monitored in four
hyperammonemic newborn infants, using a simple and newly developed assay
for benzoate and hippurate, to assess (1) the metabolic capability of
patients of this age to utilize this pathway for nitrogen removal, (2) the
potential risks of benzoate toxicity at clinically acheived serum benzoate
concn, and (3) the value of routine monitoring of serum benzoate concn in
this patient population.
Sodium benzoate potentiation of ammonia
toxicity and inhibition of urea synthesis in vitro, has been confirmed and
the mechanism by which benzoate increases mortality and the levels of
blood ammonia in mice given ammonium acetate are
studied. Urea production and N-acetylglutamate levels were decreased by
sodium benzoate. Pretreatment of mice with L-carnitine suppressed
mortality following ammonium acetate plus sodium benzoate administration.
L-carnitine lowered blood ammonia and increased
urea production and N-acetylglutamate levels.
Six epileptic patients are described to
whom the addition of valproic acid to a previously unsatisfactory
antiepileptic treatment caused a toxic encephalopathy. This was
characterized by alterations of the state of consiousness in all patients
a few days after the beginning of treatment with valproic acid. These
ranged from a marked drowsiness to coma and were often associated with
gastrointestinal and neurobiological (ataxia, asterixis) symptoms. In all
cases very high blood levels of ammonia were
found and the EEG's showed a diffuse slowing down of the activity. After
the discontinuation of the drug the toxic symptoms quickly ceased and ammonia
values returned to the normal values. It is hypothesized that the
interference of valproic acid on the metabolism of ammonia
could play an important role in the pathogenesis of the valproic acid
induced toxic encephalopathy.
Drug Warnings:
Caution: Irritating to skin and mucous
membranes. /Ammonia water-10%/
Interactions:
The combined effects of ammonia
and carbon particles inhaled by rats were reportedly much greater than
those from ammonia (or carbon) alone.
... /AMMONIA/ ACCENTUATED RESP PARALYSIS &
COMA DUE TO EXPOSURE TO METHANETHIOL. ... /IT IS/ CONCLUDED THAT THESE
AGENTS SYNERGISTICALLY AFFECT CERTAIN ENZYME SYSTEMS WHICH ARE ACTIVATED
UNDER PATHOLOGICAL CONDITIONS.
Pent-4-enoic acid inhibited urea synthesis approx 90% in rat hepatocytes
incubated with pyruvate, ammonia, & ornithine.
The addn of ammonia led to drastic dose dependent
inhibition of ureagenesis by pent-4-enoate. Half-max effect of ammonia
was observed at 0.2 mM concn. Concommitant cellular concn of N-acetylglutamate
were modified by addn of ammonia as was
accumulation of citrulline. Ammonia may interfere
with metabolism of pent-4-enoic acid & lead to dramatic potentiation
of its toxicity.
Sodium benzoate lowers serum ammonia concn by the
activation of a non-urea cycle pathway of ammonia
removal. The disposition of sodium benzoate was monitored in four
hyperammonemic newborn infants, using a simple and newly developed assay
for benzoate and hippurate, to assess (1) the metabolic capability of
patients of this age to utilize this pathway for nitrogen removal, (2) the
potential risks of benzoate toxicity at clinically acheived serum benzoate
concn, and (3) the value of routine monitoring of serum benzoate concn in
this patient population.
Sodium benzoate potentiation of ammonia toxicity
and inhibition of urea synthesis in vitro, has been confirmed and the
mechanism by which benzoate increases mortality and the levels of blood ammonia
in mice given ammonium acetate are studied. Urea production and N-acetylglutamate
levels were decreased by sodium benzoate. Pretreatment of mice with L-carnitine
suppressed mortality following ammonium acetate plus sodium benzoate
administration. L-carnitine lowered blood ammonia
and increased urea production and N-acetylglutamate levels.
Six epileptic patients are described to whom the addition of valproic acid
to a previously unsatisfactory antiepileptic treatment caused a toxic
encephalopathy. This was characterized by alterations of the state of
consiousness in all patients a few days after the beginning of treatment
with valproic acid. These ranged from a marked drowsiness to coma and were
often associated with gastrointestinal and neurobiological (ataxia,
asterixis) symptoms. In all cases very high blood levels of ammonia
were found and the EEG's showed a diffuse slowing down of the activity.
After the discontinuation of the drug the toxic symptoms quickly ceased
and ammonia values returned to the normal values.
It is hypothesized that the interference of valproic acid on the
metabolism of ammonia could play an important
role in the pathogenesis of the valproic acid induced toxic encephalopathy.
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
Routes of entry: Inhalation of gas,
ingestion, skin and eye contact.
WHEN AMMONIA IS USED AS DEVELOPER IN PHOTOCOPYING
PROCESSES ... BLUEPRINT & DIAZO, IT MAY BE RELEASED INTO WORKPLACE.
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.
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.
NIOSH estimates that approximately half a million USA workers have
potential exposure to ammonia.
Natural Pollution Sources:
Toxic concn ... can be liberated from
decomposing manure that is confined to a slurry pit or chicken house.
Ammonia is the first complex molecule to be identified in
interstellar space; it has been observed in galactic dust clouds in the
Milky Way, and is believed to constitute the rings of the planet Saturn.
Artificial Pollution Sources:
/Manmade/ Combustion Sources: Amount of
emission: coal 2 lb/ton, fuel oil 1 lb/1,000 gal, natural gas 0.3 to 0.56
lb/1x10+6 cu ft, butane 1.7 lb/1x10+6 cu ft, propane 1.3 lb/1x10+6 cu ft,
wood 2.4 lb/ton, forest fires 0.3 lb/ton.
Ammonia discharged daily in metropolitan areas of 100,000 persons
using each heating system: domestic heating fuel: coal: 2,000 lb NH3, oil:
800 lb NH3, /natural/ gas 0.3 lb NH3.
Environmental Fate:
ATMOSPHERIC FATE: It is assumed that ammonia
combines with sulfate ion in the atmosphere or in washout by rainfall
resulting in a rapid return of ammonia to the
soil.
Environmental Biodegradation:
When ammonia
appears in water under the normal conditions (aerobic), it is rapidly
converted to nitrate by nitrification; the principal water contaminant
normally being nitrate. The pH in water is increased by the presence of ammonia
ion, in the form of hydroxide ions. ... Bacteria convert the ammonia
to nitrate creating an oxygen demand (BOD) several days after the
introduction of ammonia. The bacteria that
oxidize ammonia to nitrate are largely of the
genus Nitrosomonas; conversion of nitrite to nitrate is carried out
primarily by the genus Nitrobacter. Temperature, oxygen supply, and pH of
the water are factors in determining the rate of oxidation.
Characteristics of leachate from a major
co-disposal landfill were presented. The leachate is typical of a
stabilized situation where acid fermentation is in balance with methane
formation. No evidence was found of contamination by hazardous components
of the industrial wastes deposited at the site. Aerobic biological
treatment completely nitrified NH3 in the leachate.
Environmental Abiotic Degradation:
Wastewater Treatment: ammonia
is oxidized by ozone; the reaction is first order with respect to the
concn of ammonia and is catalyzed by hydroxide
ion over the pH range 7-9.
Some of the ammonium ions in the
atmosphere are oxidized to oxides of nitrogen and nitrate ion, which
represents a significant contribution to the total acidity of rainfall.
AQUATIC FATE: The proportion of ammonia
(NH3) and ammonium ion found in water used for production is considered an
important indicator of quality in agriculture. In highly populated fish
breeding plants, where feed left overs, excrement and metabolic waste
cause growth disturbances and deficiencies, even though there is an
adequate supply of oxygen, nitrogen cmpd are the decisive factor. A
significant role is played by the undissociated NH3 molecule. ...
Experiments were carried out both with and without ventilation and using
varying amounts of fish feed. The concn of NH3, which depends on pH and
temperature, was investigated to determine the extent of the oxidative
change of NH3 through NO3- during the mineralization process of the feed
leftovers. Under the conditions used in the 2 sets of experiments there
was hardly any tendency for the pH values in the unventilated experiments
to alter and become more alkaline from an ammonification of left over
feed. In the experiments using ventilation, the proteins underwent an
especially intensive process of decomposition, ie, they became completely
mineralized, and considerable amounts of NH4-N and NH3 N were released.
Due to the lack of organic acids, these could not be neutralized and, as a
result, the pH value increased.
Environmental Bioconcentration:
Plants have a high affinity for gaseous ammonia
when leaf stomata are open in daylight.
Soil Adsorption/Mobility:
Ammonia is
strongly adsorbed on soil, and on sediment particles and colloids in
water. This adsorption results in high concentrations of sorbed ammonia
in oxidized sediments. Under anoxic conditions, the adsorptive capacity of
sediments is less, resulting in the release of ammonia
to either the water column or an oxidized sediment layer above.
In clay, the ion tends to be adsorbed on the negative adsorption sites of
clay colloids. It may substitute for potassium in the lattice structure of
a clay mineral.
Environmental Standards & Regulations:
CERCLA Reportable Quantities:
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;
In the Washington D.C. metropolitan area (202) 426-2675. 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.
Clean Water Act Requirements:
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.
Allowable Tolerances:
The fungicide ammonia
is expempted from the requirement of a tolerance when used after harvest
on the raw agricultural commodities grapefruit, lemons, oranges, and corn
grain for feed use only.
Chemical/Physical Properties:
Molecular Formula:
H3-N
Molecular Weight:
17.03
Color/Form:
Colorless gas [Note Shipped as a
liquefied compressed gas. Easily liquefied under pressure].
Odor:
Sharp, cloying, repellent
... Pungent, suffocating odor ...
Sharp, intensely irritating odor
Very pungent odor, characteristic of
drying urine
Boiling Point:
-33.35 DEG C
Melting Point:
-77.7 DEG C
Corrosivity:
CORROSIVE, ALKALINE GAS
Liquid ammonia will attack some forms of
plastics, rubber, and coatings.
Critical Temperature & Pressure:
CRITICAL TEMP: 132.4 DEG C; CRITICAL
PRESSURE: 111.5 ATM
Density/Specific Gravity:
0.7710 G/L @ 760 MM HG (GAS)
Dissociation Constants:
pKa = 9.25 @ 25 deg C
Heat of Combustion:
-7992 Btu/lb= -4440 cal/g= -185.9x10+5
J/kg
Heat of Vaporization:
5.581 KCAL/MOLE
pH:
pH of 1.0N aqueous solution 11.6; 0.1N
aqueous solution 11.1; 0.01N aqueous solution 10.6.
Solubilities:
47% IN WATER AT 0 DEG C
38% IN WATER AT 15 DEG C
34% IN WATER @ 20 DEG C
31% IN WATER @ 25 DEG C
28% IN WATER @ 30 DEG C
18% IN WATER AT 50 DEG C
15% IN 95% ALCOHOL AT 20 DEG C
11% IN ALCOHOL AT 30 DEG C
20% IN ABSOLUTE ETHANOL AT 0 DEG C
10% IN ABSOLUTE ETHANOL AT 25 DEG C
16% IN METHANOL AT 25 DEG C
SOL IN CHLOROFORM & ETHER
531,000 mg/l in water at 20 deg C;
895,000 mg/l in water at 0 deg C; 444,000 mg/l in water at 28 deg C
water solubility = 482,000 mg/l @ 25 deg
C
Soluble in water forming alkaline
solutions; soluble in oxygenated solvents.
Spectral Properties:
INDEX OF REFRACTION: 0.817 @ -79 DEG
C/D; 1.325 @ 16.5 DEG C/D
Surface Tension:
23.4 dynes/cm at 11.1 deg C; 18.1
dynes/cm at 34.1 deg C
Vapor Density:
0.59 (Air= 1)
Vapor Pressure:
vapor pressure = 7,510 mm Hg @ 25 deg C
(from experimentally derived coefficients)
Viscosity:
0.475, 0.317, 0.276 & 0.255
CENTIPOISE AT -69, -50, -40 & -33.5 DEG C, RESPECTIVELY
Other Chemical/Physical Properties:
DENSITY OF LIQ NH3: 0.6818 AT -33.35 DEG
C, 1 ATM; 0.6585 AT -15 DEG C, 2.332 ATM; 0.6386 AT 0 DEG C, 4.238 ATM;
0.6175 AT 15 DEG C, 7.188 ATM; 0.5875 AT 35 DEG C, 13.321 ATM
VAPOR PRESSURE: 2, 5, 10, 20, 40 &
60 ATM AT -18.7, 4.7, 25.7, 50.1, 78.9 & 98.3 DEG C, RESPECTIVELY
Liquified by compression
Specific gravity 0.817 at 79 deg C
Specific gravity at -33.4 deg C (liquid)
0.682
Dipole moment, gas: 4.9x10-30 C m; 1.47
D
HEAT CAPACITY 8.38 CAL/MOL/DEG AT 25 DEG
C
1 mg/cu m= 1.414 ppm; 1 ppm= 0.707 mg/cu
m
AQUEOUS AMMONIA:
pKb 4.767, Kb 1.710X10-5 at 20 deg C; pKb 4.751, Kb 1.774X10-5 at 25 deg
C; pKb 4.740, Kb 1.820X10-5 at 30 deg C
Ionization potential= 10.5 eV
vapor pressure = 1 MM, 10 MM & 40 MM
HG AT -109.1, -91.9 & -79.2 DEG C, RESPECTIVELY, (SOLID); 100 MM &
400 MM AT -68.4 & -45.4 DEG C (LIQUID)
Density/Specific gravity: Density of
aqueous solutions @ 20 deg C/4 deg C: 0.9939 (1%), 0.9811 (4%), 0.9651
(8%), 0.9362 (16%), 0.9229 (20%), 0.9101 (24%), 0.8980 (28%)
Lighter than air; easily liquified by
pressure
Mixtures of ammonia
and air will explode when ignited under favorable conditions: Angew. Chem
43: 302 (1930), but ammonia is generally regarded
as nonflammable.
Freezing point of aqueous solutions, deg
C: -2.9 (4%), -8.1 (8%), -23.1 (16%), -34.9 (20%), -44.5 (24%), -69.2
(28%)
One liter of the gas weighs 0.7714 g
Vapor pressure (kPa) = 152, 429, 1003,
2033, 3709, 6253, and 9963 at -25, 0, 25, 50, 75, 100, and 125 deg C,
respectively
Henry's Law constant = 1.61X10-5 atm
cu-m/mole at 25 deg C
Chemical Safety & Handling:
Hazards Summary:
The major hazards encountered in the use
and handling of ammonia stem from its toxicologic
properties and reactivity. Exposure to this colorless gas (liquid, if
compressed or in aqueous solution) may occur from its use as a fertilizer,
chemical intermediate, alkalizer, metal treating/extraction agent, and
common household cleaner. Ammonia is hazardous by
all routes (ie, dermal, ingestion, inhalation), with the liquid capable of
burning the skin, causing permanent eye damage, or corroding the digestive
tract upon contact; and the gas capable of causing severe eye damage,
pulmonary edema, and even death from spasm, inflammation, and edema of the
larynx. OSHA has established an ammonia
Permissible Exposure Level (PEL) of 50 ppm as an 8-hr time-weighted
average (TWA). The ACGIH recommends an 8-hr TLV-TWA of 25 ppm. Ammonia
levels should be controlled through process enclosure and the use of local
exhaust and dilution ventilation, as necessary. While its offensive odor
may serve as a warning, to assure against ammonia
exposure, workers should wear chemical protective clothing composed of
butyl rubber, natural rubber, neoprene, nitrile rubber, or polyvinyl
chloride (not Viton), gloves, face protection, and, in emergency
situations, a self-contained breathing apparatus. Facilities for
quick-drenching the body, as well as eye-wash fountains, should be
immediately at hand for the worker. Clothing that becomes wet with liquid ammonia
should be placed in closed containers until it can be discarded. While
this substance does not burn or ignite readily (autoignition temp: 1204
deg F), containers of ammonia may explode in the
heat of a fire. For small fires involving ammonia,
extinguish with dry chemical or CO2, and for large fires, use water spray,
fog, or foam, taking care to prevent fire control or dilution water from
causing pollution. More hazardous than its fire potential is ammonia's
reactivity with halogens, interhalogens, and oxidizers. These reactions
may be violent and/or may form explosive products. Ammonia
should be stored in a cool, well-ventilated location, away from sources of
ignition, and separate from other chemicals, particularly oxidizing gases
(chlorine, bromine, and iodine) and acids. Aqueous ammonia
is commonly containerized in steel drums. Anhydrous ammonia
is stored and shipped (prohibited in passenger planes) in pressurized
containers, fitted with pressure-relief safety devices, and bearing the
label, "Nonflammable Compressed Gas". For small spills of ammonia,
isolate 80 feet in all directions from the spill, ventilate the area, and
allow vapor or gas to disperse. For large spills, evacuate the area for
160 feet in all directions, and dike to contain the spill for later
recovery or disposal and to prevent runoff from causing pollution. Stay
upwind and wear positive-pressure breathing apparatus and full protective
clothing, as necessary.
DOT Emergency Guidelines:
Health: TOXIC; may be fatal if inhaled.
Vapors are extremely irritating and corrosive. Contact with gas or
liquefied gas may cause burns, severe injury and/or frostbite. Fire will
produce irritating, corrosive and/or toxic gases. Runoff from fire control
may cause pollution. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Fire or explosion: Some may burn, but
none ignite readily. Vapors from liquefied gas are initially heavier than
air and spread along ground. Some of these materials may react violently
with water. Containers may explode when heated. Ruptured cylinders may
rocket. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least
100 to 200 meters (330 to 660 feet) in all directions. Keep unauthorized
personnel away. Stay upwind. Many gases are heavier than air and will
spread along ground and collect in low or confined areas (sewers,
basements, tanks). Keep out of low areas. Ventilate closed spaces before
entering. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Protective clothing: Wear positive
pressure self-contained breathing apparatus (SCBA). Wear chemical
protective clothing which is specifically recommended by the manufacturer.
It may provide little or no thermal protection. Structural firefighters'
protective clothing is recommended for fire situations ONLY; it is not
effective in spill situations. /Ammonia,
anhydrous; Ammonia, anhydrous, liquefied; Ammonia
solution, with more than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Evacuation: ... Fire: If tank, rail car
or tank truck is involved in a fire, ISOLATE for 1600 meters (1 mile) in
all directions; also, consider initial evacuation for 1600 meters (1 mile)
in all directions. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Fire: Small fires: Dry chemical or CO2.
Large fires: Water spray, fog or regular foam. Move containers from fire
area if you can do it without risk. Do not get water inside containers.
Damaged cylinders should be handled only by specialists. Fire involving
tanks: Fight fire from maximum distance or use unmanned hose holders or
monitor nozzles. Cool containers with flooding quantities of water until
well after fire is out. Do not direct water at source of leak or safety
devices; icing may occur. Withdraw immediately in case of rising sound
from venting safety devices or discoloration of tank. Always stay away
from the ends of tanks. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Spill or leak: Fully encapsulating,
vapor protective clothing should be worn for spills and leaks with no
fire. Do not touch or walk through spilled material. Stop leak if you can
do it without risk. If possible, turn leaking containers so that gas
escapes rather than liquid. Prevent entry into waterways, sewers,
basements or confined areas. Do not direct water at spill or source of
leak. Use water spray to reduce vapors or divert vapor cloud drift.
Isolate area until gas has dispersed. /Ammonia,
anhydrous; Ammonia, anhydrous, liquefied; Ammonia
solution, with more than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
First aid: Move victim to fresh air.
Call emergency medical care. Apply artificial respiration if victim is not
breathing. Do not use mouth-to-mouth method if victim ingested or inhaled
the substance; induce artificial respiration with the aid of a pocket mask
equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult. Remove and isolate
contaminated clothing and shoes. In case of contact with liquefied gas,
thaw frosted parts with lukewarm water. In case of contact with substance,
immediately flush skin or eyes with running water for at least 20 minutes.
Keep victim warm and quiet. Keep victim under observation. Effects of
contact or inhalation may be delayed. Ensure that medical personnel are
aware of the material(s) involved, and take precautions to protect
themselves. /Ammonia, anhydrous; Ammonia,
anhydrous, liquefied; Ammonia solution, with more
than 50% ammonia; Anhydrous ammonia;
Anhydrous ammonia, liquefied/
Initial Isolation and Protective Action
Distances: Small Spills (from a small package or small leak from a large
package): First, ISOLATE in all Directions 30 meters (100 feet); then,
PROTECT persons Downwind during DAY 0.2 kilometers (0.1 miles) and NIGHT
0.3 kilometers (0.2 miles). LARGE SPILLS (from a large package or from
many small packages): First, ISOLATE in all Directions 95 meters (300
feet); then, PROTECT persons Downwind during DAY 0.3 kilometers (0.2
miles) and NIGHT 0.8 kilometers (0.5 miles). /Ammonia,
anhydrous; Ammonia, anhydrous, liquefied;
Anhydrous ammonia; Anhydrous ammonia,
liquefied/
Initial Isolation and Protective Action
Distances: Small Spills (from a small package or small leak from a large
package): First, ISOLATE in all Directions 30 meters (100 feet); then,
PROTECT persons Downwind during DAY 0.2 kilometers (0.1 miles) and NIGHT
0.2 kilometers (0.1 miles). LARGE SPILLS (from a large package or from
many small packages): First, ISOLATE in all Directions 60 meters (200
feet); then, PROTECT persons Downwind during DAY 0.2 kilometers (0.1
miles) and NIGHT 0.3 kilometers (0.2 miles). /Ammonia
solution, with more than 50% ammonia/
Odor Threshold:
WATER: 1.5 MG/L; AIR: 5.2 UL/L; ODOR
SAFETY CLASS C; C= LESS THAN 50% OF DISTRACTED PERSONS PERCEIVE WARNING OF
TLV.
Odor recognition of pure ammonia
in air is 4.68x10+1 ppm.
Sharp, cloying, repellent; low threshold
= 0.0266 mg/cu m; high threshold = 39.60 mg/cu m; irritating concn = 72.00
mg/cu m.
Low threshold= 0.0266 mg/cu m; High
threshold= 39.6 mg/cu m; Irritating concentration= 72 mg/cu m.
Skin, Eye and Respiratory Irritations:
The vapor even in low concn is extremely
irritating to skin, eyes and respiratory passages.
Caution: Potential symptoms of
overexposure are eye, nose and throat irritation; dyspnea, bronchospasm
and chest pain; pulmonary edema; pink frothy sputum; skin burns,
vesiculation.
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.
NFPA Hazard Classification:
Health: 3. 3= Materials that, on short
exposure, could cause serious temporary or residual injury, including
those requiring protection from all bodily contact. Fire fighters may
enter the area only if they are protected from all contact with the
material. Full protective clothing, including self-contained breathing
apparatus, coat, pants, gloves, boots, and bands around legs, arms, and
waist, should be provided. No skin surface should be exposed.
Flammability: 1. 1= This degree includes
materials that must be preheated before ignition will occur, such as Class
IIIB combustible liquids and solids and semi-solids whose flash point
exceeds 200 deg F (93.4 deg C), as well as most ordinary combustible
materials. Water may cause frothing if it sinks below the surface of the
burning liquid and turns to steam. However, a water fog that is gently
applied to the surface of the liquid will cause frothing that will
extinguish the fire.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions,
and that do not react with water. Normal fire fighting procedures may be
used.
Flammable Limits:
LOWER 16%; UPPER 25%.
Autoignition Temperature:
1204 DEG F (651 DEG C)
Fire Fighting Procedures:
DRY CHEM OR CARBON DIOXIDE ARE
RECOMMENDED EXTINGUISHING MEDIA.
STOP FLOW OF GAS BEFORE EXTINGUISHING
FIRE. USE WATER SPRAY TO KEEP FIRE-EXPOSED CONTAINERS COOL. EXTINGUISH
FIRE USING AGENT SUITABLE FOR SURROUNDING FIRE.
Combustible. Wear goggles,
self-contained breathing apparatus, and rubber over clothing (including
gloves). Stop flow of gas, or liquid if possible. Cool exposed containers
and protect men effecting shutoff with water. Let fire burn.
If material involved in fire: Extinguish
fire using agent suitable for type of surrounding fire. (Material itself
does not burn or burns with difficulty.) Cool all affected containers with
flooding quantities of water. Apply water from as far a distance as
possible. Use water spray to knock-down vapors. Solid streams of water may
spread fire. Do not use water on material itself. Do not apply water to
point of leak in tank car or container.
Firefighting Hazards:
Presence of oil or other combustible
materials will increase the fire hazard.
HORIZONTAL FLAME PROPAGATION.
Explosive Limits & Potential:
CRITICAL TEMP OF 133 DEG C IS EASILY
EXCEEDED IN FIRES SO THAT CONTAINERS OF LIQUEFIED AMMONIA
MAY EXPLODE UNLESS THEIR RUPTURE STRENGTH IS SAFELY IN EXCESS OF 112 ATM.
Hazardous Reactivities & Incompatibilities:
Air and hydrocarbons: Explosion limits
have been estimated for mixtures containing C1-C3 hydrocarbons.
Boron halides: The boron halides react violently with ammonia.
With calcium: At ambient temp, ammonia gas reacts
exothermally with calcium, but if warmed the latter becomes incandescent.
The metal dissolves unchanged in liquid ammonia,
but if the latter evaporates, the finely divided metal is pyrophoric.
With 1-chloro-2,4-dinitrobenzene: During the preparation of
2,4-dinitroaniline by a well-established procedure involving heating the
reactants in a direct-fired autoclave (170 deg C and 40 bar were typical
conditions), a sudden incr in temp and pressure preceded a violent
explosion.
With chloroformamidinium nitrate: It is powerfully explosive, and also an
oxidant which reacts violently with ammonia or
amines ...
With 2-chloronitrobenzene: During the
large-scale preparation of 2-nitroaniline at 160-180 deg C/30-40 bar in a
jacketed autoclave, several concurrent processing abnormalities (excess
chloro compound, too little ammonia solution,
failure to apply cooling or to vent the autoclave and non-failure of a
disk-rupture) led to a runaway reaction and pressure-explosion of the
vessel.
Chlorine azide: It gives an explosive
yellow liquid with liquid ammonia.
With 1,2-dichloroethane: Liquid ammonia
and the solvent may explode when mixed. (It is possible this was a
liquefied gas (physical) explosion, rather than an exothermic chemical
reaction).
With magnesium perchlorate: Intensive
drying of ammonia gas by passing it over the
desiccant in a steel drying tube led to an exotherm, followed by a violent
explosion. (An amine derivative may have been formed).
With heavy metals: Ammonia
is capable of reacting with some heavy metal compounds (silver, gold,
mercury) to produce materials, some of uncertain constitution, which may
explode violently when dry.
Action of ammonia
or ammonium salts on gold (III) chloride, oxide or other salts under a
wide variety of conditions gives explosive or "fulminating"
gold. Of uncertain composition but containing Au-N bonds, this is a heat-,
friction- and impact-sensitive explosive when dry, similar to the related
mercury and silver compounds.
With halogens or interhalogens: Ammonia
either reacts violently, or produces explosive products, with all four
halogens and some of the interhalogens.
With iodine and potassium: During the
reductive cleavage of cyclopolyenes with potassium in liquid ammonia,
the intermediate anionic species are quenched with iodine-pentane
mixtures. The possibility of formation of the highly explosive nitrogen
triiodide and the need for precautions are stressed.
With nitrogen trichloride: Contact above
0 deg C of excess chlorine or a chlorinating agent with aqueous ammonia,
ammonium salts ... produces the endothermic ... and explosive nitrogen
trichloride as a water-insoluble yellow oil.
With potassium chlorate: High
concentrations of ammonia in air react so
vigorously with potassium chlorate as to be dangerous.
With nitryl chloride: Interaction of the
chloride with ammonia ... is very violent, even
at -75 deg C ...
With chromyl chloride: Contact with ammonia
causes incandescence.
With chromium trioxide: Gaseous ammonia
leads to incandescence, and the aqueous solution is oxidized very
exothermically.
With trioxygen difluoride: ... Solid ammonia
... reacts with ignition and/or mild explosion.
With selenium difluoride dioxide:
Interaction is violent and many of the products and derivatives are both
shock- and heat-sensitive explosives. These include the ammonium,
potassium silver and thallium salts of the "triselenimidate" ion
...
With nitric acid: A jet of ammonia
will ignite in nitric acid vapor.
Hydrogen peroxide: Ammonia
dissolved in 99.6% peroxide gave an unstable solution which exploded
violently.
With nitrogen oxide: Violent explosions
which occurred at -100 to -180 deg C in ammonia
synthesis gas units were traced to the formation of explosive addition
products between dienes and oxides of nitrogen, produced from interaction
of nitrogen oxide and oxygen.
With dinitrogen tetraoxide: Liquid ammonia
reacts explosively with the solid tetraoxide at -80 deg C, while aqueous ammonia
reacts vigorously with the gas at ambient temperature.
With oxygen and platinum: In school
demonstrations of oxidation of ammonia to nitric
acid over platinum catalysts, substitution of oxygen for air causes fairly
vigorous explosions to occur.
With silver chloride: Exposure of
ammoniacal silver chloride solutions to air or heat produces a black
crystalline deposit of "fulmination silver", mainly silver
nitrate, with disilver imide and silver amide also present. Attention is
drawn to the potential explosion hazard in a method of recovering silver
from the chloride by passing an ammoniacal solution of the chloride
through an ion exchange column to separate the Ag(NH3)+ ion, prior to
elution as the nitrate. It is essential to avoid letting the ammoniacal
solution stand for several hours, either alone or on the column.
With thiocarbonyl azide thiocyanate: The
unstable (endothermic) compound reacts explosively with ammonia
gas, and violently with concentrated hydrazine solutions.
With sulfinyl chloride: Addition of a
solution of 4-nitrobenzoyl chloride (1 g) in a large excess (10 mL) of
sulfinyl chloride to ice-cold concentrated ammonia
solution caused a violent explosion. This may certainly be attributed to
the instantaneous hydrolysis of the excess sulfinyl chloride by the
aqueous ammonia with production of several of
unneutralized acid gases in a test tube.
With thiotrithiazyl chloride: The dry
chloride, which explodes on heating in air, will rapidly absorb ammonia
gas and then explode. The structure of the cation is now known to be a
seven membered ring with only two adjacent sulfur atoms. Thiotrithiazyl
salts other than the chloride are also explosive.
With tetramethylammonium amide: During
the preparation, the liquid ammonia used as
solvent must be removed completely at -45 deg C. The compound decomp
explosively at ambient temp in presence of ammonia.
With tellurium tetrachloride:
Interaction with liquid ammonia at -15 deg C
forms tellurium nitride which explodes at 200 deg C.
With tellurium tetrabromide: Intraction
gives a mixture of tritellurium tetranitride and tellurium bromide
nitride, which explodes on heating.
With stibine: A heated mixture explodes.
With silver (I) oxide: The clear
solution, obtained by centrifuging a solution of the oxide in aqueous ammonia
which had been treated with silver nitrate until precipitation started,
exploded on two occasions after 10-14 days storage in closed bottles in
the dark. This was ascribed to slow precipitation of amorphous disilver
imide, which is very explosive even when wet. When silver oxide is
dissolved in ammonia solution, an extremely
explosive precipitate (probably Ag3N4) will separate. The explosive
behavior is completely inhibited by presence of colloids or ammonium salts
(acetate, carbonate, citrate or oxalate).
With dichlorine oxide: The heat
sensitivity /of dichlorine oxide/ ... may explain the explosions which
occur on contact of many readily oxidizable materials with this powerful
oxidant. Such materials include ammonia. ...
Mixtures with hydrogen detonate on ignition.
With mercury: A mercury manometer used
with ammonia became blocked by deposition of a
grey-brown solid, which exploded during attempts to remove it mechanically
or on heating. The solid appeared to be a dehydration product of Millon's
base and was freely soluble in sodium thiosulfate solution. This method of
cleaning is probably safer than others, but the use of mercury manometers
with ammonia should be avoided as intrinsically
unsafe. Although pure dry ammonia and mercury do
not react even under pressure at 340 kbar and 200 deg C, the presence of
traces of water leads to the formation of an explosive compound, which may
explode during depressurization of the system. Explosions in mercury-ammonia
systems had been reported previously.
With silver nitrate: A bottle containing
Gomari tissue staining solution (ammoniacal silver nitrate), prepared 2
weeks previously exploded when disturbed. The solution must be prepared
freshly each day, and discarded immediately after use with appropriate
precautions. A large quantity of ammoniacal silver nitrate solution
exploded violently when disturbed by removing a glass rod. However, it has
now been shown that neither the solid precipitated during addition of ammonia
to the nitrate, nor the redissolved complex, is sensitive to initiation by
very severe shocks. This was so for fresh or aged solutions. The solids
produced by total evaporation at 95 deg C or higher would explode only at
above 100 kgcm shock force. A pH value above 12.9 is essential for
separation of explosive precipitates, and this cannot be attained by
addition of ammonia alone.
With ethylene oxide: Accidental
contamination by aqueous ammonia of an ethylene
oxide feed tank containing 22 t caused violent polymerization which
ruptured the tank and led to a devastating vapor cloud explosion. The
close similarity to other base-catalyzed incidents was stressed.
Strong oxidizers, acids, halogens, salts
of silver and zinc [Note: corrosive to copper and galvanized surfaces].
With picric acid: Forms explosive salts.
AMMONIA
/REACTS/ WITH ACETALDEHYDE, ACROLEIN, BORON BORON TRIIODIDE, BROMINE,
BROMINE PENTAFLUORIDE, CHLORIC ACID, CHLORINE MONOXIDE, CHLORINE
TRIFLUORIDE, CHLORITES, CHLOROSILANE, CHROMIC ANHYDRIDE, ETHYLENE
DICHLORIDE, ETHYLENE OXIDE, FLUORINE, GOLD, HEXACHLOROMELAMINE, HYDRAZINE
AND ALKALI METALS, HYDROGEN BROMIDE, HYPOCHLOROUS ACID, MAGNESIUM
PERCHLORATE, NITROGEN PEROXIDE, NITROGEN TRIFLUORIDE, OXYGEN DIFLUORIDE,
PHOSPHORUS TRIOXIDE, POTASSIUM AND ARSINE, POTASSIUM AND PHOSPHINE,
POTASSIUM AND SODIUM NITRITE, POTASSIUM FERRICYANIDE, POTASSIUM
MERCURICYANIDE. SODIUM AND CARBON MONOXIDE, STIBINE, SULFUR, SULFUR
DICHLORIDE, TELLURIUM HYDROPENTACHLORIDE AND TRICHLOROMELAMINE.
SEVERE FIRE HAZARD WHEN MIXED WITH
BROMINE PENTAFLUORIDE, CHLOROSILANE, CHROMYL CHLORIDE & FLUORINE. AMMONIA
GAS BURNS IN ATMOSPHERE OF NITRIC ACID. POTASSIUM & PHOSPHINE REACT IN
LIQ AMMONIA TO FORM POTASSIUM DIHYDROPHOSPHIDE, A
SPONTANEOUSLY FLAMMABLE SOLID.
MAGNESIUM PERCHLORATE WAS CONTAINED IN
SMALL STEEL REFRIGERATION-TYPE DRYING TUBE & AMMONIA
WAS PASSED THROUGH IT (AFTER SYSTEM WAS EVACUATED) IN SMALL INCREMENTS IN
ATTEMPT TO FURTHER DESICCATE IT. IT WAS NOTED THAT OUTSIDE OF ... TUBE WAS
WARM TO TOUCH. SHORTLY ... TUBE EXPLODED VIOLENTLY.
Mixtures of ammonia
and air will explode when ignited under favorable conditions ... but ammonia
is generally regarded as nonflammable.
Other Hazardous Reaction:
Poisonous, visible vapor cloud is
produced /from contact with water/.
Prior History of Accidents:
An explosion at the Dixie Cold Storage
Company in Shreveport, LA occurred as two firemen attempted to isolate an
anhydrous ammonia leak in a cold storage
warehouse. The men were badly burned when their protective clothing
ignited in the ensuing fire, and one died within 36 hr. ... Several days
prior to the accident, employees noted a smell of ammonia
and located a leak in the refrigeration system. Steps were taken to
isolate the system and repair a leaky valve at the evaporator unit. As
they were working, ammonia continued to
accumulate in the room. The crew tried to absorb the gas using a 50 lb
cylinder of carbon dioxide. This has been effective for small amounts of ammonia
but was not recommended for large leaks. The carbon dioxide contacted
moist room air and condensed. Ammonia also
condensed, greatly reducing visibility. The room became untenable for
anyone not wearing full protective equipment and workers were using only
industrial type filter masks or chemical respirators. They left the room
and called the fire department to borrow full protective gear. When
firemen arrived, they were told that the leak had been isolated, that it
had not been prolonged, and that only residual gas remained. Water was
sprayed in the room to absorb the ammonia, and a
fan was set up. After considering various alternatives, the firefighters
decided to use an electric fork lift truck to replace the valve located 17
ft above the floor. The floor was very slippery, and the truck slid into
an interior wall and the concrete curb at its base. Explosion occurred
immediately. One firefighter was unable to escape or remove his burning
suit. /The situation indicated that/ the warehouse workers' failure to
reduce the possibility of hazardous anhydrous ammonia
levels, the firefighters' lack of awareness of hazardous gas levels, and
ignition of the gas are major factors in loss of life in this accident.
Immediately Dangerous to Life or Health:
300 ppm
Protective Equipment & Clothing:
EMPLOYEES SHOULD BE PROVIDED WITH &
REQUIRED TO USE IMPERVIOUS CLOTHING, GLOVES, FACE SHIELD (8-INCH MIN),
& OTHER APPROPRIATE PROTECTIVE CLOTHING NECESSARY TO PREVENT ... SKIN
CONTACT ... /THEY/ SHOULD BE PROVIDED WITH & REQUIRED TO USE
SPLASH-PROOF SAFETY GOGGLES ...
Ammonia:
Chemical protective clothing composed of butyl rubber, natural rubber,
neoprene, nitrile rubber, and polyvinyl chloride may be used since data
suggest that breakthrough times are approximately an hour or more. Vitron
is not recommended for use since data (usually from immersion tests)
suggest that breakthrough times are less than one hour.
Wear appropriate personal protective
clothing to prevent skin contact.
Wear appropriate eye protection to
prevent eye contact.
Eyewash fountains should be provided in
areas where there is any possibility that workers could be exposed to the
substance; this is irrespective of the recommendation involving the
wearing of eye protection. />10%/
Facilities for quickly drenching the
body should be provided within the immediate work area for emergency use
where there is a possibility of exposure. [Note: It is intended that these
facilities provide a sufficient quantity or flow of water to quickly
remove the substance from any body areas likely to be exposed. The actual
determination of what constitutes an adequate quick drench facility
depends on the specific circumstances. In certain instances, a deluge
shower should be readily available, whereas in others, the availability of
water from a sink or hose could be considered adequate.]
Recommendations for respirator
selection. Max concn for use: 250 ppm. Respirator Class(es): Any chemical
cartridge respirator with cartridge(s) providing protection against the
compound of concern. May require eye protection. Any supplied-air
respirator. May require eye protection.
Recommendations for respirator
selection. Max concn for use: 300 ppm. Respirator Class(es): Any
supplied-air respirator operated in a continuous flow mode. May require
eye protection. Any powered, air-purifying respirator with cartridge(s)
providing protection against the compound of concern. May require eye
protection. Any chemical cartridge respirator with a full facepiece and
cartridge(s) providing protection against the compound of concern. Any
air-purifying, full-facepiece respirator (gas mask) with a chin-style,
front- or back-mounted canister providing protection against the compound
of concern. Any self-contained breathing apparatus with a full facepiece.
Any supplied-air respirator with a full facepiece.
Recommendations for respirator
selection. Condition: Emergency or planned entry into unknown concn or
IDLH conditions: Respirator Class(es): Any self-contained breathing
apparatus that has a full facepiece and is operated in a pressure-demand
or other positive pressure mode. Any supplied-air respirator that has a
full facepiece and is operated in pressure-demand or other positive
pressure mode in combination with an auxiliary self-contained breathing
apparatus operated in pressure-demand or other positive pressure mode.
Recommendations for respirator
selection. Condition: Escape from suddenly occurring respiratory hazards:
Respirator Class(es): Any air-purifying, full-facepiece respirator (gas
mask) with a chin-style, front- or back-mounted canister providing
protection against the compound of concern. Any appropriate escape-type,
self-contained breathing apparatus.
MAC 100 ppm. Eye protection, respiratory
apparatus, and cotton clothing. Be sure equipment is not aluminum, copper,
lead, or tin. Protective clothing over a cotton layer is recommended.
Preventive Measures:
PROCESS ENCLOSURE; LOCAL EXHAUST
VENTILATION & GENERAL DILUTION VENTILATION. ... WHERE THERE IS ANY
POSSIBILITY OF EXPOSURE OF EMPLOYEE'S BODY ... FACILITIES FOR QUICK
DRENCHING OF BODY SHOULD BE PROVIDED WITHIN IMMEDIATE WORK AREA ...
CLOTHING WET WITH LIQ ANHYD AMMONIA ... SHOULD BE
PLACED IN CLOSED CONTAINERS ... UNTIL IT CAN BE DISCARDED ... AN EYE WASH
FOUNTAIN SHOULD BE PROVIDED WITHIN IMMEDIATE WORK AREA ...
Each vehicle transporting ammonia
in bulk except farm applicator vehicles shall carry a container of at
least 5 gal of water and shall be equipped with a full face mask.
Contact lenses should not be worn when
working with this chemical. /Soln/liquid/
SRP: The scientific literature for the
use of contact lenses in industry is conflicting. The benefit or
detrimental effects of wearing contact lenses depend not only upon the
substance, but also on factors including the form of the substance,
characteristics and duration of the exposure, the uses of other eye
protection equipment, and the hygiene of the lenses. However, there may be
individual substances whose irritating or corrosive properties are such
that the wearing of contact lenses would be harmful to the eye. In those
specific cases, contact lenses should not be worn. In any event, the usual
eye protection equipment should be worn even when contact lenses are in
place.
Water carried on farm vehicles should be
protected from freezing by an external source of heat. Antifreeze
chemicals must not be used. A means of applying the water to the skin
and/or eyes in large quantities must be available. The container should
have an opening large enough for easy access, should be covered to prevent
entry of dirt. ... A plastic squeeze bottle containing at least 8 ounces
of water should be carried by each individual to allow immediate
irrigation of the eyes. /SRP: Workers should know this is for eye safety,
not drinking./ This may provide a few additional seconds in which to reach
the larger container before irreversible eye damage results.
Use care in handling strong ammonia
solution because of caustic nature of solution & irritating properties
of its vapor. Cool container well before opening, & cover closure with
a cloth or similar material while opening.
... GREATEST HAZARD OF WORKING WITH
ALKALINE MATERIALS IS FROM SPLASH OR SPLATTER OF PARTICLES OR SOLN OF
STRONGER ALKALIES ENTERING EYES OF WORKMEN. THIS CAN BE PREVENTED BY USE
OF EYE PROTECTION THAT IS EFFECTIVE AT ALL ANGLES. PROPER PROVISIONS
SHOULD ... BE AVAIL FOR IMMEDIATE & PROLONGED WASHING WITH WATER
SHOULD ... EYE CONTAMINATION OCCUR. /AMMONIA GAS/
SRP: Contaminated protective clothing
should be segregated in such a manner so that there is no direct personal
contact by personnel who handle, dispose, or clean the clothing. Quality
assurance to ascertain the completeness of the cleaning procedures should
be implemented before the decontaminated protective clothing is returned
for reuse by the workers.
The worker should immediately wash the
skin when it becomes contaminated. /Solution/
Work clothing that becomes wet or
significantly contaminated should be removed and replaced. /Solution/
If material not involved in fire: Keep
material out of water sources and sewers. Attempt to stop leak if without
undue personnel hazard. Use water spray to knock-down vapors.
Personnel protection: Avoid breathing
vapors. Keep upwind. ... Avoid bodily contact with the material. ... Do
not handle broken packages unless wearing appropriate personal protective
equipment. Wash away any material which may have contacted the body with
copious amounts of water or soap and water. If contact with the material
anticipated, wear appropriate chemical protective clothing.
Evacuation: If material leaking (not on
fire) consider evacuation from down wind area based on amount of material
spilled, location and weather conditions.
Shipment Methods and Regulations:
No person may /transport,/ offer or
accept a hazardous material for transportation in commerce unless that
person is registered in conformance ... and the hazardous material is
properly classed, described, packaged, marked, labeled, and in condition
for shipment as required or authorized by ... /the hazardous materials
regulations (49 CFR 171-177)./
The International Air Transport
Association (IATA) Dangerous Goods Regulations are published by the IATA
Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and
constitute a manual of industry carrier regulations to be followed by all
IATA Member airlines when transporting hazardous materials.
The International Maritime Dangerous
Goods Code lays down basic principles for transporting hazardous
chemicals. Detailed recommendations for individual substances and a number
of recommendations for good practice are included in the classes dealing
with such substances. A general index of technical names has also been
compiled. This index should always be consulted when attempting to locate
the appropriate procedures to be used when shipping any substance or
article.
Storage Conditions:
Separate from other chemicals,
particularly oxidizing materials, acids, and halogens. Store in a cool,
dry, well-ventilated location.
... MAY BE STORED UNDER HIGH PRESSURE,
REFRIGERATED AT LOW PRESSURE, OR AS AQUEOUS AMMONIA
IN LOW PRESSURE TANKS.
Storage temperature: Ambient for
pressurized ammonia: low temperature for ammonia
at atmospheric pressure.
Permanent storage containers shall be
located at least 50 feet from a dug well or other sources of potable water
supply, unless the container is a part of a water-treatment installation.
Cleanup Methods:
1) VENTILATE AREA OF SPILL OR LEAK TO
DISPERSE GAS. 2) IF IN GASEOUS FORM, STOP FLOW OF GAS. IF SOURCE OF LEAK
IS A CYLINDER & LEAK CANNOT BE STOPPED IN PLACE, REMOVE LEAKING
CYLINDER TO SAFE PLACE IN OPEN AIR & REPAIR LEAK OR ALLOW CYLINDER TO
EMPTY. 3) IF IN LIQ FORM, ALLOW TO VAPORIZE.
Environmental considerations -- air
spill: Apply water spray or mist to knock down vapors. Vapor knockdown
water is corrosive or toxic and should be diked for containment.
Environmental considerations -- water
spill: Neutralize with dilute acid. use mechanical dredges or lifts to
remove immobilized masses of pollutants and precipitates.
Environmental considerations -- land
spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid
material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or
holding areas should be sealed with an impermeable flexible membrane
liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or
foamed concrete. Absorb bulk liquid with fly ash or cement powder.
Neutralize with vinegar or other dilute acid.
Disposal Methods:
SRP: At the time of review, criteria for
land treatment or burial (sanitary landfill) disposal practices are
subject to significant revision. Prior to implementing land disposal of
waste residue (including waste sludge), consult with environmental
regulatory agencies for guidance on acceptable disposal practices.
Dilute with water, neutralize with
hydrogen chloride and discharge to sewer. Recovery is an option to
disposal which should be considered for paper manufacture, textile
treating, fertilizer manufacture, and chemical process wastes.
Pour into large tank of water,
neutralize, and route to sewage plant ... Contact local sewage authority.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1
8-hr Time Weighted Avg: 50 ppm (35 mg/cu m).
Vacated 1989 OSHA PEL STEL 35 ppm (27
mg/cu m) is still enforced in some states.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 25 ppm;
Short Term Exposure Limit (STEL) 35 ppm
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 25 ppm (18 mg/cu m).
Recommended Exposure Limit: 15 Min
Short-Term Exposure Limit: 35 ppm (27 mg/cu m).
Immediately Dangerous to Life or Health:
300 ppm
Other Occupational Permissible Levels:
Emergency Response Planning Guidelines (ERPG):
ERPG(1) 25 ppm (no more than mild, transient effects) for up to 1 hr
exposure; ERPG(2) 200 ppm (without serious, adverse effects) for up to 1
hr exposure; ERPG(3) 1000 ppm (not life threatening) up to 1 hr exposure.
Manufacturing/Use Information:
Major Uses:
MFR NITRIC ACID, EXPLOSIVES, SYNTHETIC
FIBERS, FERTILIZERS; IN REFRIGERATION & CHEM INDUSTRY
PREHARVEST COTTON DEFOLIANT
CHEM INT FOR UREA, AMMONIUM NITRATE,
AMMONIUM SALTS, ADIPIC ACID FOR NYLON, HEXAMETHYLENEDIAMINE FOR NYLON,
ACRYLONITRILE FOR FIBERS & PLASTICS, CAPROLACTAM FOR NYLON,
ISOCYANATES FOR PLASTICS; DIRECT APPLICATION FERTILIZER; NUMEROUS MISC
APPLICATIONS
USED IN MFR OF HYDRAZINE, PESTICIDES
& DETERGENTS
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.
Dissociated ammonia
is used as a convenient source of hydrogen for the hydrogenation of fats
and oils. Through the controlled combustion of dissociated ammonia
in air, a source of pure nitrogen is achieved.
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.
Ammonia is used
in the rubber industry for stabilization of raw latex to prevent
coagulation during transportation and storage.
Ammonia is used
as a catalyst in the phenol-formaldehyde condensation and also in the
urea-formaldehyde condensation to make synthetic resin.
AMMONIA MAY BE
ADDED TO WATER BEFORE (PREAMMONIATION) OR AFTER (POSTAMMONIATION) ADDITION
OF CHLORINE. PREAMMONIATION CAN PREVENT FORMATION OF TASTES & ODORS
THAT ARE CAUSED BY REACTION OF CHLORINE WITH PHENOLS & OTHER
SUBSTANCES. POSTAMMONIATION IS MOST OFTEN USED AMMONIA-CHLORINE
WATER TREATMENT PROCESS.
USED ... ON GRAPEFRUIT, LEMONS &
ORANGES TO CONTROL FUNGAL GROWTH DURING WAREHOUSING. USDA HAS NOW
REQUESTED THAT AMMONIA USED AS PRESERVATIVE IN
HIGH MOISTURE CORN BE EXEMPTED FROM REQUIREMENT OF A TOLERANCE.
MEDICATION (VET)
Fertilizers; manufacture of nitric acid,
hydrazine hydrate, hydrogen cyanide, urethane, acrylonitrile, and sodium
carbonate (by Solvay process); refrigerant, nitriding of steel;
condensation catalyst; synthetic fibers; dyeing; neutralizing agent in
petroleum industry; latex preservative; explosives; nitrocellulose;
urea-formaldehyde; nitroparaffins; melamine; ethylene diamine; sulfite
cooking liquors; fuel cells; rocket fuel; yeast nutrient; developing diazo
films
Methods of Manufacturing:
AMMONIA IS MFR
PRIMARILY BY A MODIFIED HABER REDUCTION PROCESS USING ATMOSPHERIC NITROGEN
& A HYDROGEN SOURCE, FOR EXAMPLE, METHANE, ETHYLENE OR NAPHTHA, AT
HIGH TEMP (400 TO 6500 DEG C) & PRESSURES (100 TO 900 ATM) IN 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 (USA) or from the
action of steam on hot coke (Haber-Bosch used in South Africa).
Manufactured from natural gas
AMMONIA IN SOLN
... IN VARYING CONCN IS USED IN VARIETY OF PRODUCTS SUCH AS CLEANING
AGENTS, LINIMENTS & AROMATIC SPIRITS. AMMONIA
SOLN ARE SOMETIMES USED AS FERTILIZERS. ... FRESH HOUSEHOLD AMMONIA
RANGES IN CONCN FROM 5 TO 10% NH3, BUT A 54% SOLN IS ALSO AVAIL
COMMERCIALLY.
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.
Formulations/Preparations:
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).
Analytic Laboratory Methods:
AIR SAMPLES /SRP: COLLECTED BY IMPINGER/
ANALYZED BY AMMONIA SPECIFIC ELECTRODE; RANGE:
17-68 MG/CU M.
(Air) Sampling and analysis: Second
derivatives spectroscopy; min det limit: 1 ppb; Photometry: min full
scale: 1,800 ppm; IR spectrometry: detection limit: 0.22 ppm; non
despersive IR: detection limit: 250 ppm; detector tubes: UNICO: detection
limit: 20 ppm; AUER: detection limit : 5 ppm; DRAGER: detection limit: 5
ppm; impinger, 800 1 air/30 min; VLS: detection limit : 5 ug/cu m/30 min
Nessler reagent.
The concentration of ammonia
in air can be determined with the Matheson Kitagawa Toxic Gas Detector
Model 8014KA, which gives accurate, dependable, and reproducible results.
Colorimetric: Ambient air containing 14
to 220 ug NH3/cu m (0.02 to 0.3 ppm). Sampled at 1 to 2 l/min for one hour
may be analyzed using this method. Ammonia is
determined colorimetrically with an azo dye. Precision is + or - 1.6
percent for the analytical method. Nitrite, hydrolyzable amino cmpd, and
other N-compounds may interfere. For higher concn, an aliquot of the
solution may be analyzed.
Colorimetric: The range of concn that
can be determined by this method is 20 to 700 ug/cu m (0.025 to 1 ppm) in
air with a sampling time of one hour. Ammonia is
determined colorimetrically using indophenol.
Analyte: ammonium ion; Matrix: air;
Procedure: ion chromatography, conductivity detection; Range: 2-110 ug ammonia
per sample; Precision: 0.043 range: 2-110 ug ammonia
per sample;
M417E Ammonia -
Selective Electrode Method This method is applicable for the measurement
of 0.03-1400 mg nitrogen ammonia/l in potable and
surface waters and domestic and industrial wastes. The ammonia-selective
electrode uses a hydrophobic gas-permeable membrane to separate the sample
solution from an electrode internal solution of ammonium chloride. Ammonia
diffuses through the membrane and changes the internal solution pH, which
is sensed by a pH electrode. In an inter-laboratory study (12
laboratories) using effluent water samples at 0.04, 0.10, 0.80, 20, 100,
and 750 mg/l, mean recovery was 100, 470, 105, 95, 97, and 99%
respectively.
M417B Nesslerization Method (Direct and
Following Distillation) for the Determination of Ammonia
Nitrogen. Direct Nesslerization is used for purified drinking waters,
natural water, and highly purified wastewater effluents. This colorimetric
method is sensitive to 20 ug/l. Interferences such as turbidity, color,
and precipitates are corrected through distillation. At ammonia
nitrogen concentrations of 200, 800, and 1500 ug/l, relative standard
deviation is 38.1, 11.2, and 11.6%, respectively and relative error is 0,
0, and 0.6%, respectively.
APHA Method 4500-NH3: Ammonia
in Water by Colorimetry; Ammonia in Water by
Colorimetry Using an Automated Phenate Method; Colorimetry, water, minimum
detection limit fall within 0.02 mg/l.
NIOSH Method 6015: Ammonia;
Determination of Ammonia by Visible Absorption
Spectrophotometry; Spectrophotometry workplace, detection limit of 0.0050
mg/cu-m.
AREAL Method IP-9: Reactive Acidic and
Basic Gases; Determination of Reactive Acidic and Basic Gases and
Particulate Matter in Indoor Air (Annular Denuder Technique); Annular
denuder, indoor ambient air, detection limit of 0.25 ug/cu-m.
Sampling Procedures:
In air: Detector tubes Model 1055A are
used for high concentrations (1-25%) and Model 105SC for low (5-260 ppm)
concentration ranges of ammonia. A color stain is
produced in the detector tube which varies in length with the
concentration of the sample being measured.
/Air/ Sampler: gas washing bottle:
medium 200 ml water; sampling rate: 0.12 cu ft/min; test concn: 162 ppm;
absorption efficiency: 84%.
The concentration of ammonia
in air can be ... determined by titration. A known volume of the air is
passed through two bubblers in series containing a known volume of
standardized 0.02 N sulfuric acid, the solution in each bubbles combined
quantitatively, and the excess acid titrated with standardized 0.02 N
sodium hydroxide, using methyl red indicator.
Special Reports:
Visek WJ; J Dairy Sci 67 (3): 481-98
(1984). The physical, chem properties of ammonia,
its sources & detoxification, its effects in biological systems, its
influence upon insulin action & glucose metabolism, & its possible
effects on reproduction are discussed.
Environment Canada; Tech Info for
Problem Spills: Ammonia (Draft) (1984).
NIOSH; Criteria Document: Ammonia
(1974) DHEW Pub. NIOSH 74-136.
USEPA/ECAO; Ammonia
(1980) EPA 600/1-77-054.
Brands A; HdbK Toxicol 472-503 (1987).
Studies on the effects of accidental exposure to asphyxiant gases
occurring in occupational settings are reviewed.
DHHS/ATSDR; Toxicological Profile for Ammonia
(1990) ATSDR/TP-90/03
Synonyms and Identifiers:
Related HSDB Records:
Synonyms:
R 717
**PEER REVIEWED**
AM-FOL
**PEER REVIEWED**
AMMONIA,
ANHYDROUS
**PEER REVIEWED**
AMMONIACA (ITALIAN)
**PEER REVIEWED**
AMMONIAC (FRENCH)
**PEER REVIEWED**
AMMONIA GAS
**PEER REVIEWED**
AMMONIAK (GERMAN)
**PEER REVIEWED**
AMONIAK
(POLISH)
**PEER REVIEWED**
Liquid Ammonia
**PEER REVIEWED**
NITRO-SIL
**PEER REVIEWED**
Formulations/Preparations:
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.
Ammonia
solution, more than 35% and not more than 50% ammonia.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1005; Ammonia,
anhydrous, liquified; Ammonia solutions with more
than 50% ammonia.
IMO 2.3; Ammonia,
anhydrous, liquified.
Standard Transportation Number:
49 042 10; Anhydrous ammonia
RTECS Number:
NIOSH/BO0875000
Administrative Information:
Hazardous Substances Databank Number:
162
Last Revision Date: 20020118
Last Review Date: Reviewed by SRP on 1/31/1998
http://www.nycwasteless.com/gov-bus/citysense/edefinitions.htm
Acute Health Effects:
Can cause headache, loss of sense of smell, nausea, and vomiting. Can
irritate skin and eyes, leading to permanent damage. Can irritate nose,
mouth, and throat, causing coughing and wheezing. Can irritate lungs,
causing coughing and/or shortness of breath; higher exposures can cause a
build-up of fluid in the lungs.
Chronic Health Effects:
Repeated exposure can cause chronic irritation of the eyes, nose, throat,
and lungs. Repeated exposures may cause bronchitis, with cough, phlegm,
and/or shortness of breath.
http://www.atsdr.cdc.gov/tfacts126.html
Ammonia occurs naturally in the
environment. Ammonia is irritating to the skin, eyes, nose, throat, and
lungs. Exposure to high concentrations can cause serious burns and high
blood pressure, and can stop the heart from beating. Ammonia has been
found at 23 of the 1,177 National Priorities List sites identified by the
Environmental Protection Agency (EPA).
Exposure to high concentrations of ammonia in the air may cause severe burns on your skin, eyes, throat, and lungs. It can also cause high blood pressure. In extreme cases, blindness, lung damage, heart attack, or death could occur. Breathing lower concentrations will cause coughing and nose and throat irritation.
If you swallowed ammonia, you could get burns in your mouth, throat, and stomach. Concentrated ammonia spilled on the skin will cause burns. Animal studies show effects similar to those observed in people, including irritation to the nose and lungs, lung damage, increased heart rate, and high blood pressure. We do not know if ammonia causes reproductive effects or birth defects.
The EPA has determined that the level of ammonia in lakes and streams that might cause health effects from drinking water or eating fish contaminated with ammonia depends on the pH and temperature of the water. Therefore, it is not possible to establish a safe limit that applies to all bodies of water. Any release to the environment greater than 100 pounds of ammonia or 1,000 to 5,000 pounds of ammonium salts must be reported to the EPA.
The Occupational Safety and Health Administration (OSHA) has set a limit of 50 parts per million (50 ppm) over an 8-hour workday, 40-hour workweek.
The National Institute of Occupational Safety and Health (NIOSH) recommends that workplace air should not exceed 25 ppm ammonia averaged over an 10-hour workday or 40-hour workweek. A short-term exposure limit (up to 15 minutes) of 35 ppm is recommended
http://www.ccohs.ca/oshanswers/chemicals/chem_profiles/ammonia/health_ammonia.html
Ammonia gas is a severe respiratory tract irritant. It is noticeable by
smell at 0.6 to 53 ppm. Volunteers have first noticed nose and throat
irritation at concentrations as low as 24 ppm after 2-6 hours exposure. A
10-minute exposure to 30 ppm was considered faintly irritating by 2/6
volunteers, while 50 ppm was considered moderately irritating by 4/6.
Irritation of the nose and throat was noticeable in 5/10 and 10/10
volunteers after a 5-minute exposure to 72 or 134 ppm. At 500 ppm,
immediate and severe irritation of nose, and throat occurs. Brief exposure
to concentrations above 1500 ppm can cause pulmonary edema, a potentially
fatal accumulation of fluid in the lungs. The symptoms of pulmonary edema
(tightness in the chest and difficulty breathing) may not develop for 1-24
hours after an exposure. Numerous cases of fatal ammonia exposure have
been reported, but actual exposure levels have not been well documented.
If the victim survives, complete recovery may occur depending on the
extent of injury to the respiratory tract and lungs. However, long-term
respiratory system and lung disorders have been observed following severe
short-term exposures to ammonia.
People repeatedly exposed to ammonia may develop a tolerance (or acclimatization) to the irritating effects after a few weeks. Tolerance means that higher levels of exposure are required to produce effects earlier seen at lower concentrations.
http://www.nsc.org/library/chemical/ammonia.htm
Exposure to ammonia can cause lacrimation, burning sensation, swelling
of larynx, spasm of glottis, asphyxia, conjunctivitis, laryngitis, severe
pulmonary and gastrointestinal irritation, nausea, vomiting, diarrhea,
abdominal pains, pulmonary edema, dyspnea, bronchospasm, chest pain,
vesiculation, wheezing, cold and clammy skin, convulsions, collapse, coma,
and even death from acute laryngeal edema. Milder exposure may predispose
to bronchopneumonia following a chemical pneumonitis.
Because is it highly water-soluble, ammonia can cause extensive damage to mucous membranes of the eyes, nose, oropharynx, larynx, and tracheobronchial tree. When ingested, ammonia can cause corrosive esophagitis, sometimes with an associated gastritis. Inhaling ammonia can cause secretion of saliva and retention of urine. Inhaling anhydrous ammonia gas can produce acute, chronic respiratory disease; diffuse tracheobronchitis with severe bronchoconstruction; and bronchorrhea.
Anhydrous liquid ammonia produces second-degree burns on the skin and extensive destruction of the anterior chamber in the eye. If extensive, these lesions can cause edema and sloughing of the airway epithelia, which result in acute upper airway obstruction. Massive exposures can override the absorptive surface area of the upper respiratory tract and result in extensive injury to the lower airways and alveoli. Liquid ammonia can freeze the surface of the skin, causing thrombosis of surface vessels, ischemia, and necrosis.
Ammonia gas releases heat as it dissolves and can cause thermal injury. Exposure to high concentrations of ammonia produces severe burns of the cornea and upper airway, respiratory distress, blood-tinged sputum, and stridor.
Toxic doses of ammonia acutely affect cerebral energy metabolism, localized at the base of the brain.
Ammonia toxicity is a major factor in the pathogenesis of hepatic encephalopathy associated with chronic liver disease.
Populations at special risk of exposure to ammonia include individuals with reduced liver function, corneal disease, glaucoma, or chronic respiratory diseases.
http://www.penweb.org/issues/sludge/health-odor.htm
ABSTRACT. Complaints of health symptoms from ambient odors have become
more frequent in communities with confined animal facilities, wastewater
treatment plants, AND BIOSOLIDS RECYCLING OPERATIONS.
The most frequently reported health complaints include eye, nose, and throat irritation, headache, nausea, diarrhea, hoarseness, sore throat, cough, chest tightness, nasal congestion, palpitations, shortness of breath, stress, drowsiness, and alterations in mood...
Continuous exposure to compounds such as AMMONIA or H2S can lead to odor fatigue and/or tolerance, and this reduced sensitivity may jeopardize health when the warning signal is not adequately perceived...
Some reactive inorganic gases such as AMMONIA and H2S can also be odorants.
Odorants can also stimulate free nerve endings of four other cranial nerves (trigeminal, vagus, chorda tympani, and glossopharyngeal nerves) to induce sensations of irritation.
Sensory neurons of the trigeminal nerve innervate the eyes, nose, anterior 2/3 of the tongue, gums, and cheeks. The trigeminal nerve responds to five different classes of stimuli: (1) chemical, (2) mechanical (such as dust particles that touch the mucous linings of the nose, eye, or mouth), (3) thermal (temperature), (4) nociceptive (pain), and (5) proprioceptive (movement/position).
Trigeminal stimulation by odorous chemicals and dust induces sensations such as irritation, tickling, burning, stinging, scratching, prickling, and itching.
Free nerve endings of the vagus nerve transmit information on irritation in the throat, trachea, and lungs. Free nerve endings of the chorda tympani nerve (along with the trigeminal nerve) medicate irritation on the anterior tongue during mouth breathing; free nerve endings of the glossopharyngeal nerve transmit information about irritation on the posterior tongue.
Almost any airborne chemical can, in sufficient concentration, stimulate chemosensory trigeminal receptors in the nose and eyes, damage tissue, or cause toxic effects.
Administration of irritant compounds to the upper and/or lower airway in laboratory studies produces many systemic responses including: (1) changes in respiratory rate, depending upon the primary level of irritation (upper versus lower), (2) reduced respiratory volume, (3) increased duration of expiration, (4) alterations in spontaneous body movements, (5) contraction of the larynx and bronchi, (6) increased epinephrine secretion, (7) increased nasal secretion, (8) increased nasal airflow resistance, (9) increased bronchial tone, (10) decreased pulmonary ventilation, (11) bradycardia, (12) peripheral vasoconstriction, (13) increased blood pressure, (14) closure of the glottis, (15) sneezing, (16) closure of the nares, (17) decreased pulmonary blood flow, (18) decreased renal blood flow and clearance, and (19) lacrimation or tearing.
Irritants can also induce hoarseness of voice and impair mucociliary clearance functioning.
These physiological responses suggest that the respiratory system may be at risk from harmful substances. Reflexive breath stoppage (apnea) subsequent to stimulation of the trigeminal nerve in the upper airway is probably a defensive device to prevent inhaling chemicals in the air that might damage the lungs or respiratory tract.
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http://www.ammonia-safety.com/health_effects.htm
More Results From: www.ammonia-safety.com
http://www.health.state.nd.us/healthalert/anhydrous.htm
Anhydrous ammonia is a colorless, highly irritating gas with a sharp,
suffocating odor. People will notice the pungent odor at levels
ranging from 5 – 50 parts per million (ppm). Irritating effects
generally begin at levels between 25-50 ppm. More serious effects
generally will not occur until levels are greater than 100 ppm.
Symptoms include burning of the eyes, nose, and throat after breathing even small amounts. With higher doses, coughing or choking may occur. Exposure to high levels of anhydrous ammonia can cause death from a swollen throat or from chemical burns to the lungs.
Eye exposure to concentrated gas or liquid can cause serious corneal burns or blindness.
Most people recover from a single low exposure to anhydrous ammonia without any delayed or long-term effects. After a severe exposure, injury to the eyes, lungs, skin, or digestive system may continue to develop for 18 to 24 hours, and delayed effects primarily to the respiratory system or the eyes are possible
If a severe exposure has occurred, blood and urine analyses, chest x-rays, pulmonary function testing and other tests may show whether the lungs have been injured. Testing is not needed in every case. Special eye examinations may also be conducted.
http://www.ohd.hr.state.or.us/dwp/docs/fact/...
Ammonia in air is an irritant and causes burning of the eyes, nose, throat and
lungs. At levels in air greater than 100 ppm it can cause serious injury
to such tissues. Ammonia is toxic to some fish and other aquatic organisms
at concentrations below 1 mg/l (ppm) in water. Human beings and higher animals
are less sensitive to ammonia in water, but long-term ingestion of water
containing more than 1 mg/l (ppm) ammonia may be damaging to internal
organ systems. Solutions having concentrations greater than 1000 mg/l (ppm) can
cause severe burns and scarring of sensitive skin and mucous membranes.
Household cleaning solutions usually contain between 3% and 30% ammonia, and
pose severe hazard if ingested. As little as one teaspoonful of 10% ammonia
solution can be lethal. Splashing into eyes can cause temporary or permanent
blindness.