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EC number: 200-315-5
CAS number: 57-13-6
The effects on terrestrial amphibians are
not clear. Some species react already at 107 kg urea/ha with significant
mortality while other species are unaffected.
It is unclear as to the mechanism of urea
toxicity in amphibians and why some species seem relatively unaffected.
The natural habitat of the affected species
is in North America. Therefore, the relevance of this finding is limited
for the risk assessment for Europe.
The majority of mammalians responded
positively to the fertilization of forest with urea (concentrations up
to 750 kg N/ha; 1600 kg urea/ha). This effect might be secondary due to
improved availability of food. Few mammals showed a decline with is
likely also due to secondary effects.
It may be reasonable to conclude that urea
toxicity in native ungulates could be similar to cattle, goats, or sheep
and might be in the vicinity of 500 mg/kg of body weight.
In Sweden, nitrate concentrations appearing
in plants soon after fertilization with 150 kg N/ha (ammonium nitrate,
corresponding to 321 kg urea/ha) were not toxic to reindeer (Nordkvist
and Erne 1983). However, urea-fertilized areas were avoided by reindeer
for winter grazing which takes place through snow cover (Eriksson and
Nine of 20 P. vehiculum tested were more
often found on the side of the container with urea. The mean number of
observations spent on the side without urea was not significantly
greater than 50% (Wilcoxon signed-ranks test, Z = 0.348, p =0.728, n =
20; Figure 1). However, when salamanders were in the urea side of the
container, they were preferentially found on the walls of the container
(Wilcoxon signed-ranks test, Z = 2.929, p = 0.003, n = 20, Figure 1).
When salamanders were in the control side of the container, they were
found with similar frequency either on the floor or on the walls
(Wilcoxon signed-ranks test, Z = 0.284, p = 0.776, n = 20; Figure 1).
Seventeen of 20 R. variegatus tested were more often found on the
control side of the container. The mean number of observations spent on
the side without urea was significantly greater than 50% (Wilcoxon
signed-ranks test, Z = 2.688, p = 0.01, n = 20, Figure 1). This species
was found with low frequency on the walls of the container (Wilcoxon
signed-ranks test, Z = 2.260, p = 0.036, n = 20). Sixteen of 20 T.
granulosa tested were more often found on the control side of the
container. The mean number of observations spent on the side with urea
was significantly lower than 50% (Wilcoxon signed-ranks test, Z = 3.435,
p = 0.001, n = 20, Figure 1). This species was found with very low
frequency on the walls of the container (Wilcoxon signed-ranks test, Z =
3.800, p = 0.001, n = 20).
No mortality occurred in control tanks. The
observed effects increased with both concentration and time, and there
were significant differences in sensitivity among species (Figures 2 and
3). Both doses of urea had an acute effect on survival of P. vehiculum
and R. variegatus. For the urea doses of 225 kg N/ha and at 48 h, P.
vehiculum and R. variegatus had a mortality of 47%. At 12 h, mortality
at the highest doses of urea was 60% for P. vehiculum and 40% for R.
variegatus. At 48 h and at 450 kg N/ha, 14 of 15 P. vehiculum and 12 of
15 P. vehiculum died. T. granulosa had no mortality at both urea
concentrations after 96 h of exposure. Sensitivity to urea increased
with concentration in P. vehiculum (Chi-square test, x = 46.64, p =
0.001, df = 7) and in R. variegatus (Chi-square test, x = 19.10, p =
0.01, df = 7). Sensitivity to urea at 450 kg N/ha was similar between
the two terrestrial salamanders (P. vehiculum and R.
variegatus)(Chi-square test, x = 4.02, p = 0.78, df = 7, Figure 3), but
sensitivity to urea showed differences between both species at the
concentration of 225 kg N/ha (Chi-square test, x = 17.91, p = 0.012, df
= 7). P. vehiculum was more sensitive during the first hours of
exposure, but after 48 h of exposure R. variegatus was more sensitive
These results from (Marco et al 2001)
suggest that urea-based fertilizers at 482.35 kg urea /ha could be
affecting the survival of two amphibian species Salamander Plethodon
vehiculum, Rhyacotriton variegatusi in fertilized forests within 96
hours of exposure in laboratory experiments. The roughskin newt Taricha
granulosa showed no mortality at 964.7 kg urea/ha. Avoidance experiments
did not correlate between toxicity and avoidance behaviour.
The results are considered to be relevant
and reliable for the risk assessment.
The Starea ration was the only ration
readily consumed. Palatability problems were encountered with the other
3 rations so all grain rations were placed in the rumen through the
fistula. Urea is an unpalatable feed ingredient (8,15). Urea often
segregates in rations containing ground ingredients. Considerable
variation existed in nitrogen contents of the cracked and expanded
rations (Table 2) suggesting some urea segregation. The most uniform
ration was Starea.
The content of the nitrogenous constituents
of the feeds are in Table 2. The nonprotein nitrogen content of the
grain mixtures consisted primarily of urea nitrogen. Since the intake of
the nonprotein nitrogen fraction was more variable among rations than
the protein nitrogen intake, the average rumen ammonia concentration was
adjusted to a common nonprotein nitrogen content of 2.25% (5.0% urea
equivalent) by multiplying the ammonia concentration by 2.25 divided by
the urea nitrogen content of the grain mixture. A composite of daily
feed samples was analyzed each week so it was possible to adjust the
ammonia data for a given week by an analysis value for the feed used
during the week.
The adjusted and unadjusted average rumen
ammonia concentrations by rations for the second and seventh days after
the rations were changed are shown in Table 3. By the second day the
rumen ammonia concentration was lowest (P < .01) for the Starea ration.
The finely ground pelleted and expanded rations had intermediate effects
which were not significantly different from that of the control ration.
By the seventh day the rumen ammonia concentration was lowest for the
Starea ration, but the ammonia concentration for the finely ground and
expanded grain rations approached that of the Starea ration. The Staten,
expanded and finely ground rations were significantly different (P <
.01) from the control ration but not different frmn one another. The
diurnal pattern was similar for both pairs of twins (data not shown).
The fine grinding of grain to produce a flour apparently results in
sufficient damage to starch to provide carbohydrate in a form that
assists urea nitrogen utilization
The results with expanded grain and Starea
are similar to those obtained in vitro by Helmer et al. (7). They
observed that Starea or a mixture of expanded grain plus urea lowered
rumen ammonia concentration and increased microbial protein synthesis in
vitro when compared with a mixture of ground grain plus urea. Starea,
when tested in vitro, was slightly superior to the expanded grain and
urea ration suggesting that the reacting of starch and urea may result
in a product that affects the rate of ammonia release from urea to make
its conversion to microbial protein more efficient. If expansion
processed grain is valuable in urea utilization, it would be more
logical to process the grain with urea (Starea) than to feed expended
grain and urea separately. Starea provides enhanced palatability and
reduced segregation of urea in mixed feed. The recovery of urea nitrogen
in the Starea supplements processed was 98%, indicating little if any
loss of nitrogen during processing.
Results not reported here since not relevant
for hte risk assessment of urea.
The Holstein twins (14-15) which had not
been fed urea for 250 days previous to the trial appeared to be more
susceptible to ammonia toxicity than did the Shorthorn steers (04-05)
which had been adapted to urea (Table 8). The Holsteins exhibited toxic
symptoms when they were fed 60 g of urea (control ration) per 100 kg
body weight. However, that level of urea in Stared did not produce toxic
The steers (04-05) which had been adapted to
urea were less sensitive to high urea. It required 108 g of urea per 100
kg weight to produce toxic symptoms. As was the case with the Holsteins,
urea in combination with rolled grain was toxic whereas greater amounts
of urea in Stared were not. In one trial a steer (05) was given 616 g of
urea in the form of Stared, but toxicity did not occur.
Toxicity developed in Animal 15 on the
second day while she was receiving the control ration. This animal
responded favorably when given 18 liters of 5% acetic acid by way of the
tureen fistula. Similarly Animal 04 (control) was treated on the
eleventh day and responded. However, Animals ~4 (control - 14th day) and
05 (control - 25th day) were treated with acetic but failed to respond.
Perhaps that failure was due to a delay in administering acetic acid
after first signs of toxicity were observed. To be effective it appears
that acetic acid should be administered within 30 rain of the first
signs of toxicity. The symptoms of toxicity were: dullness, muscle
tremors, eyes rolling back into the head, frequent urination, excessive
salivation, muscular incoordination, labored breathing and prostration
at the approach of the terminal stage. In the time preceding the death
of animal 14, the venous circulatory system was in a state of collapse
(determined by venous puncture). The first toxic symptoms were usually
noticed 20 min after urea administration.
The results of the experiment indicate that
urea in Starea is not so toxic to animals as is urea mixed with rolled
sorghum grain. An adaptation to high levels of urea was also illustrated
because animals recently fed urea ingested almost twice as much urea
before toxicity occurred as that ingested by nonadapted animals.
The concentration of ammonia in the 30-min
sample appeared to have a greater bearing on whether toxicity would
result than the concentration in samples taken later. If the ammonia
concentration approached 100 mg/100 mL of rumen fluid in the 30 min
sample, toxicity usually resulted. Ammonia concentration often exceeded
the 100 mg concentration at later times without evidence of toxicity. On
one occasion when Starea was fed, the ammonia concentration rose to 216
mg at 120 min without producing toxicity.
In the study from Stiles et al. (1970) it
was shown that urea is an unpalatable feed ingredient for cattle so that
the experiments were performed in rumen fistulated cattle. The Starea
ration (expansion-processed mixture of grain starch and urea) was the
only ration readily consumed.
For the toxicity tests, the animals were
"fed" with 1.4 kg of alfalfa hay and a quantity of grain mixture
containing 20% urea (i.e., 200 g urea per kg feed).
Deaths occurred in animals administered urea
at dose levels equivalent to 600 and 1080 mg/kg bw. Adaptation was
demonstrated as lower toxicity seen in animals previously administered
Since this formulation of urea is not
relveant for the use of urea other then for feeding purposes of
lifestock this formulation is not relevant for the environmental risk
assessment. However, the finding that urea in feed other than Starea was
unpaptable for cattle can be considered relevant for the risk assessment
of wildlife. Hence, the results of thsi study are considered to have
limited relevance for the environmental risk assessment of urea.
Poisoning by ingestion of excess urea
or other sources of nonprotein nitrogen (NPN) is usually acute,
rapidly progressive, and highly fatal. NPN is any source of nitrogen
not present in a polypeptide (precipitable protein) form. Sources of
NPN have different toxicities in various species, but mature ruminants
are affected most commonly. After ingestion, NPN undergoes hydrolysis
and releases excess ammonia (NH3) into the GI tract, which
is absorbed and leads to hyperammonemia.
Ruminants use NPN by converting it via
the ruminal microflora to ammonia, which is then combined with
carbohydrate-derived keto acids to form amino acids. The most common
sources of NPN in feeds are urea, urea phosphate, ammonia
(anhydrous), and salts such as monoammonium and diammonium
phosphate. Because feed-grade urea is unstable, it is formulated
(usually pelleted) to prevent degradation to NH3. Biuret,
a less toxic source of NPN, is being used less frequently than in
the past. Natural protein sources such as rice hulls, beet or citrus
pulp, cottonseed meal, and straw or other low-quality forages may be
treated with anhydrous ammonia to increase available nitrogen in
supplemented livestock diets. Fermentation byproducts from alcohol
(ethanol) manufacture are a source of NPN that comes from incomplete
proteins, and these products are commonly used in liquid or feed
supplements. Most sources of NPN are provided to ruminants by direct
addition of dry supplement to a complete mixed or blended diet, by
free-choice access to NPN-containing range blocks or cubes, or by
lick tank systems combined with molasses as a supplement. Ammonia or
NPN poisoning is a common sequela of abrupt change to urea or other
NPN in the diet when only natural protein was previously fed;
animals have to be gradually acclimated to NPN so that rumen
microflora can increase in numbers to use the NH3produced.
Also, farm animals sometimes drink liquid fertilizers or ingest dry
granular fertilizers that contain ammonium salts or urea.
Ruminants are most sensitive, because
urease is normally present in the functional rumen after 50 days of
age. Dietary exposure of unacclimated ruminants to 0.3–0.5 g of
urea/kg body wt may cause adverse effects; dosages of 1–1.5 g/kg are
usually lethal. Urease activity in the equine cecum is ~25% that of
the rumen, and horses may receive NPN as a feed additive; however,
horses are more sensitive to urea than other monogastrics, and
dosages ≥4 g/kg can be lethal. Ammonium salts at 0.3–0.5 g/kg may be
toxic in all species and ages of farm animals; dosages ≥1.5 g/kg
usually are fatal. Pigs and neonatal calves are generally unaffected
by ingestion of urea except for a transient diuresis. Wild birds
(silver gulls) reportedly have been poisoned after consuming water
contaminated with urea fertilizer spillage.
Livestock may require days or weeks for
total adaptation before rumen microflora can utilize the gradually
increasing amounts of urea or other NPN in the diets; however,
adaptation is lost relatively quickly (1–3 days) once NPN is removed
from the diet.
Diets low in energy and high in fiber
are more commonly associated with NPN toxicosis, even in acclimated
animals. Highly palatable supplements (such as liquid molasses or
large protein blocks crumbled by precipitation), range cubes, or
improperly maintained lick tanks may lead to consumption of lethal
amounts of NPN.
A related CNS disorder in cattle fed
ammoniated high-quality hay, silage, molasses, and protein blocks is
thought to be caused by formation of 4-methylimidazole (4-MI)
through the action of NH3on soluble carbohydrates
(reducing sugars) in these feedstuffs. Cattle fed dietary components
containing 4-MI develop a syndrome known as the “bovine bonkers
syndrome,” named for the wildly aberrant behavior exhibited. Signs
relate to CNS effects, with stampeding, ear twitching, trembling,
champing, salivating, and convulsions. Because nursing calves are
affected, the toxic principle apparently is excreted in milk.
Ammoniated low-quality forages do not have sufficient concentrations
of reducing sugars to form 4-MI, and thus serve as a relatively safe
nitrogen source for acclimated animals.
Another related disorder involves
accidental excessive exposure of ruminants (cattle and sheep) to raw
soybeans. Soybeans have high concentrations of both carbohydrates
and proteins, as well as urease. Overconsumption can cause acute
carbohydrate fermentation and excessive ammonia release, resulting
in ammonia toxicosis and lactic acidosis. Affected animals have
engorged rumens with a gray, amorphous mass inside.
The period from urea ingestion to onset
of clinical signs is 20–60 min in cattle, 30–90 min in sheep, and
longer in horses. Early signs include muscle tremors (especially of
face and ears), exophthalmia, abdominal pain, frothy salivation,
polyuria, and bruxism. Tremors progress to incoordination and
weakness. Pulmonary edema leads to marked salivation, dyspnea, and
Horses may exhibit head pressing; cattle
are often agitated, hyperirritable, aggressive, and belligerent as
toxicosis progresses; sheep usually appear depressed. An early sign
in cattle is ruminal atony; as toxicosis progresses, ruminal tympany
is usually evident, and violent struggling and bellowing, a marked
jugular pulse, severe twitching, tetanic spasms, and convulsions may
be seen. Affected cattle with belligerent aberrant behavior may have
produced some 4-MI in vivo through reaction of excessive NH3,
released from NPN, with carbohydrates and reducing sugars in the
rumen. The PCV and serum concentrations of NH3, glucose,
lactate, potassium, phosphorus, AST, ALT, and BUN usually are
As death nears, animals become cyanotic,
dyspneic, anuric, and hyperthermic, and blood pH decreases from 7.4
to 7.0. Regurgitation may occur, especially in sheep. Death related
to excess NPN usually occurs within 2 hr in cattle, 4 hr in sheep,
and 3–12 hr in horses. Survivors recover in 12–24 hr with no
Carcasses of animals dying of NPN
poisoning appear to bloat and decompose rapidly, with no specific
characteristic lesions. Gross brain lesions are not usually
reported in NPN-induced ammonia toxicosis, but histopathologic
lesions may include neuronal degeneration, spongy degeneration of
the neuropil, and congestion and hemorrhage in the pia mater.
Frequently, pulmonary edema, congestion, and petechial hemorrhages
may be seen. Mild bronchitis and catarrhal gastroenteritis are
often reported. Regurgitated and inhaled rumen contents are
commonly found in the trachea and bronchi, especially in sheep.
The odor of NH3may or may not be apparent in ingesta
from a freshly opened rumen or cecum. A ruminal or cecal pH ≥7.5
from a recently dead animal is highly suggestive of NPN poisoning.
The ruminal pH remains stable for several hours after death under
most circumstances but continues to rise in NPN toxicosis.
Ammonia or NPN poisoning is suggested by
signs, lesions, history of acute illness, and dietary exposure.
Exposure to excess NPN may be evaluated through laboratory analysis
for the ammonia nitrogen (NH3-N) in both antemortem and
postmortem specimens and for urea or other NPN in suspected feeds
and other dietary sources. Specimens for NH3-N analysis
include ruminal-reticular fluid, serum, whole blood, and urine. All
specimens should be frozen immediately after collection and thawed
only for analysis; alternatively, ruminal-reticular fluid may be
preserved with a few drops of saturated mercuric chloride solution
added to each 100 mL of specimen.
Animals dead more than a few hours in
hot ambient temperatures or 12 hr in moderate climates probably have
undergone too much autolysis to be of diagnostic value.
The amount of urea or the equivalent NPN
in biologic specimens is meaningless; however, urea and NPN should
be determined in representative feeds and other dietary sources.
Values for urea and NPN in feed permit calculation of the protein
equivalent (1 part protein = 0.36 parts urea; 1 part urea = 2.92
parts protein) in feed as well as the total estimated dose of NPN
NH3-N concentrations of ≥2
mg/100 mL in blood, serum, or vitreous humor indicate excess NPN
exposure. Clinical signs usually appear at ~1 mg/100 mL. The
concentration of NH3-N in ruminal-reticular fluid is >80
mg/100 mL in most cases of NPN poisoning and may be >200 mg/100 mL.
Acclimated ruminants fed diets high in legume hay, soybean meal,
cottonseed meal, linseed meal, fish meal, or milk byproducts may
have NH3-N concentrations in rumen fluid approaching 60
mg/100 mL with no apparent toxicity. The pH of ruminal-reticular
fluid should also be determined; a pH of 7.5–8 (at time of death) is
indicative of NPN toxicity.
Differential diagnoses include
poisonings by nitrate/nitrite, cyanide, organophosphate/carbamate
pesticides, raw soybean overload, 4-methylimidazole, lead,
chlorinated hydrocarbon pesticides, and toxic gases (carbon
monoxide, hydrogen sulfide, nitrogen dioxide); acute infectious
diseases; and noninfectious diseases such as encephalopathies (eg,
leukoencephalomalacia, hepatic encephalopathy,
polioencephalomalacia), enterotoxemia or rumen autointoxication,
protein engorgement, grain engorgement, ruminal tympany, and
pulmonary adenomatosis. Nutritional and metabolic disorders related
to hypocalcemia, hypomagnesemia, and other elemental aberrations
should also be considered.
Examination and treatment may be
difficult because of sudden and violent behavior. Animals that are
recumbent and moribund usually do not respond favorably to
If possible, affected animals should be
treated by ruminal infusion of 5% acetic acid (vinegar, 0.5–2 L in
sheep and goats and 2–8 L in cattle). Ruminal-reticular fluid
specimens for analysis should be taken before acetic acid therapy.
Concomitant infusion of iced (0–4°C) water (up to 40 L in adult
cattle, proportionally less in sheep and goats) is also recommended.
Acetic acid lowers rumen pH and prevents further absorption of NH3by
converting uncharged NH3to the charged ammonium ion (NH4+);
administration may have to be repeated if affected animals again
show clinical signs. Acetic acid inactivates existing NH3in
the GI tract and rapidly forms ammonium acetate, which can be used
by rumen microflora but does not release NH3. Cold water
lowers the rumen temperature and dilutes the reacting media, which
slows urease activity. In severely affected valuable animals,
removed rumen contents should be replaced with a hay slurry, and a
transfer of some rumen contents from a healthy animal may serve as
an inoculum to restore normal function. Ruminal tympany should be
corrected if indicated, and a trocar may be installed to prevent
Supportive therapy is indicated and
includes IV isotonic saline solutions to correct dehydration, and IVcalcium
gluconateand magnesium solutions to relieve tetanic seizures.
Convulsions may also be controlled with sodiumpentobarbitalor
other injectable anesthestic agents.
Urea should not be fed at a rate
exceeding 2%–3% of the concentrate or grain portion of ruminant
diets and should be limited to ≤1% of the total diet. Additionally,
NPN should constitute no more than one-third of the total nitrogen
in the ruminant diet. Once the decision is made to feed NPN, animals
must be slowly adapted to, and maintained on, a consistent dietary
NPN content with no significant deviation; cows fed range cubes with
NPN must receive the cubes daily with no interruptions. Temporary
absences of NPN from the diet should be avoided at all costs.
Overconsumption of palatable liquid supplements can be controlled by
the addition of phosphoric acid; 1% phosphorus from phosphoric acid
should restrict consumption of liquid supplement to ~2
lb/animal/day. Although properly adapted adult cattle can tolerate
urea at a rate of up to 1 g/kg body wt/day, a safer feeding rate is
no more than half that amount.
Urea should not be fed at a rate
exceeding 2%–3% of the concentrate or grain portion of ruminant
diets and should be limited to ≤1% of the total diet.
Additionally, NPN should constitute no more than one-third of
the total nitrogen in the ruminant diet. ... Although properly
adapted adult cattle can tolerate urea at a rate of up to 1 g/kg
body wt/day, a safer feeding rate is no more than half that
The publication from Scott 2008 contains
following statement: "Deer and moose are ruminants. No toxicity data
specific to them was found. Given that they are ruminants, it seems
reasonable to conclude that urea toxicity is similar to other ruminants,
therefore in the vicinity of 500mg/kg of body weight."
In the monitoring of field studies no direct toxic effects were found for mammalians (Sullivan and Sullivan, 2017). However, urea-fertilized areas were avoided by reindeer for winter grazing (Sullivan and Sullivan, 2017).
Avoidance of urea in feed was observed for cattle ("Urea is an unpalatable feed ingredient" Stiles et al. 1970). This and the relative low toxicity of about 500 mg urea/kg/day in cattle (Thompson, 2015) might be the reason why no toxic effects were observed on mammals in field trials (Sullivan and Sullivan 2017).
Some amphibians react when exposed to urea while others are relatively insensitive (Marco et al. 2001, Sullivan and Sullivan 2017). It is unclear as to the mechanism of urea toxicity in amphibians and why some species seem relatively unaffected. Sensitive species were reported predominantly for North American forest dwelling amphibians and hence this finding might have limited relevance for risk assessment for European ecosystems. For some of these North American forest dwelling amphibians avoidance behaviour has been described (Hatch et al. 2001).
Calculation of the EC50:
In the study reported by Stiles et al.
(1970) the rumen-fistulated Holstein cows (680 kg) received 60 g urea
per 100 kg=> 408 g urea.
On the day of each trial all animals were
fed 1.4 kg of sorghum grain and 1.4 kg of alfalfa hay at 8 AM. At 1 PM
they were fed 1.4 kg of alfalfa hay and a quantity of grain mixture
containing 20% urea. The quantity of grain mixture fed was based on the
weight of the animal determined that day.
The exact % of urea in the feed was not
provided in the study report. However, when 408 g are considered to be
20 % in the grain, this results in the amount of 2040 g grain for the
application. Adding the this amounts to 3440 g of feed plus 408 g of
urea this summarizes to total 3848 g. Hence, the share of urea is
408/3848 =10.6 % or 106 g urea /kg feed.
Note: Due to poor acceptability, the grain
mixture containing urea was placed in the rumen by way of the fistula
after the first day in amounts to supply the quantities of urea. Hence,
the amount was added within very short time and not in a normal feeding
process. Hence, it represents the worst case.
Information for the EC10/NOAEC for
"Use of low concentrations of urea (up to
3%) as a nitrogen supplement to ruminant feeds serves as an inexpensive
low-toxicity source of protein for domestic animal production (Stanton
and Whittier 2006)", cited from Sullivan and Sullivan (2017).
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