Ammonia Spills. In an ammonia spill a portion of the liquid ammonia released flashes as ammonia vapor.

This instantaneous flash

is followed by a period of slow
evaporation of the remaining liquid ammonia [1176], [1180]. In a release from a refrigerated tank operating slightly above
atmospheric pressure, the amount of the
initial flash is only a few percent of the total, whereas in a release from a pressure vessel at about 9 bar and 24 C approximately 20
% of the spilled ammonia would
flash. Figures for the proportion flashed as a function of pressure and temperature of the spilled ammonia are given in [1180]. This
reference also provides
quantitative information on temperature development and evaporation rate of small and large ammonia pools at certain wind
velocities and also takes radiation
influences (sunny or overcast sky, day or night) into account.
Spill experiments on land and on water in various dimensions have been carried out by various companies and organizations.
Underwater releases were also studied.
Models have been developed to mathematically describe ammonia dispersion in such events [1182-1187].
A number of real incidents with tank cars, rail cars, tanks, loading/unloading of ships and barges, and pipeline transport in which
major spills occurred is described in
[1222-1229], [1246], [1278] and in an excellent review on safety in ammonia storage [1188]. Training of operating personal for
ammonia handling with special regard
to ammonia spills is important [1208], [1214], [1246].
7.3. Health Aspects and Toxicity of Ammonia
In ammonia production, storage, and handling the main potential health hazard is the toxicity of the product itself. For this reason this
section concentrates on
ammonia only. Other toxic substances such as carbon monoxide or traces of nickel carbonyl (which may be formed during shut down
in the methanation stage) may
be only a risk in maintenance operations and need appropriate protection provisions as well as blanketing or flushing with nitrogen.
Human Exposure. The threshold of perception of ammonia varies from person to person and may also be influenced by
atmospheric conditions, values as low as
0.4 2 mg/m3 (0.5 3 ppm) are reported in [1190], but 50 ppm may easily detected by everybody [1304]. Surveys [1191] found
concentrations from 9 45 ppm in
various plant areas. Though initially irritated, exposed persons may quickly become accustomed to these concentrations. Another
report [1192] gives concentration
limits for short time exposures as follows: 100 ppm (10 min); 75 ppm (30 min) 50 ppm (60 min). The time-weighted average
Threshhold Limit Value (TLV) of the
ACGIH is 25 ppm (or 18 mg/m3) [1193]. This recommendation was supplemented by a value for short-time exposure: 35 ppm for 15
min. The MAK value is 50 ppm.
Exposure to higher ammonia concentration has the following effects: 50 72 ppm does not disturb respiration significantly [1305];
100 ppm irritates the nose and
throat and causes a burning sensation in the eyes and tachypnoe [1305]; 200 ppm will cause headache and nausea, in addition to
the above symptoms [1306]; at
250 500 ppm tachypnoe and tachycardia [1306]; at 700 ppm, immediate onset of burning sensations in the eyes [1307]; 1000 ppm
causes immediate coughing
[1308]. The symptomatology of various exposure levels is also described in [1193-1195]. At 1700 ppm coughing with labored
breathing, sometimes with momentary
inability to breath (coughing of rescued persons may continue for hours). 2500 to 4500 ppm may be fatal after short exposure; 5000
ppm and higher causes death by
respiratory arrest [1188].
The metabolism seems not to be significantly changed after exposure to 800 ppm [1308]. A discussion of metabolism and of acute
and chronic health problems
caused by ammonia can be found in [1196].
Toxicology. Ammonia is a strong local irritant. On mucous membranes alkaline ammonium hydroxide is formed, which dissolves
cellular proteins and causes severe
necrosis (corrosive effect).
The primary target organ is the pulmonary system, and the following symptoms can be observed: pharyngitis, laryngitis,
tracheobronchitis, nausea, vomiting,
increased salivation, reflectoric bradycardia, and life-threatening symptoms, such as edema of the glottis, laryngospasm,
bronchospasm, and interstitial lung edema
[1283].
Ammonia or ammonium hydroxide can penetrate the cornea rapidly, leading to keratitis, damage of the iris, cataract, and glaucoma
[1284].
Oral ingestion of aqueous ammonia can corrode the mucous membranes of the oral cavity, pharynx, and esophagus and cause the
shock syndrome, toxic hepatitis,
and nephritis. Because of its corrosive action constrictions of the esophagus may result.
Ammonia is absorbed rapidly by the wet membranes of body surfaces as ammonium hydroxide, converted to urea, and excreted by
the kidneys [1285]. The capacity
of detoxification via urea is sufficient to eliminate the ammonium ion when ammonia is inhaled in nonirritating concentrations. The
inhaled ammonia is partly
neutralized by carbon dioxide present in the alveoli [1286]. Only a small fraction of the ammonia is exhaled unchanged by the lungs
(12.3 % at an inhalation
concentration of 230 ppm) [1287]. Repeated inhalation can cause a higher tolerance because the mucous membranes become
increasingly resistant [1300].
Additional information on the toxicology of ammonia can be found in [1288-1292], [1295-1299], [1309-1315].
Carcinogenicity. Ammonia failed to produce an increase in the incidence of tumors in Sprague Dawley rats even when the protein
ratio in the diet was increased or
when urea was added [1301].
Lifetime ingestion of ammonium hydroxide in drinking water by mice was without any carcinogenic effects [1302].
Mutagenicity. Ammonia is not mutagenic in the Ames Salmonella system and in Saccharomyces cerevisiae [1303].