PB-244 336
GUIDES FOR SHORT-TERM EXPOSURES OF THE PUBLIC TO
AIR POLLUTANTS. IV. GUIDE FOR AMMONIA
National Research Council
Prepared for:
Environmental Protection Agency
November 1972
DISTRIBUTED BY:
National Technical Information Service
U. S. DEPARTMENT OF COMMERCE
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Guides for Short-Term Exposures of the Public to Air Pollutants
IV. Guide for Ammonia
by
The Committee on Toxicology
of the
National Academy of Sciences - National Research Council
November 1972
-------
BIBLIOGRAPHIC DATA
SHEET
1. Report No.
NAS/ACT/P-628.5
PB 244 336
4. Title and Subtitle
Guides for Short-Term Exposures of 'the Public to Air
Pollutants. IV. Guide for Ammonia.
5. Report Date
November 1972
7. Awhor(s)
&• Performing Organization Kept.
No- NAS/ACT/P-628.5
9. Performing Organization Name and Address
Committee on Toxicology of the National Academy of Sciences
National Research Council
2101 Constitution Avenue, N.W.
Washington. DC 20418
10. Proje.:t/Task/Work Unit No.
11. Comrai-t/Gram No.
CPA 70-57
12. Sponsoring Organization Name and Address
Environmental Protection Agency
4th and M Streets, S.W.
Washington, DC 20460
13. Type of Report fi Period
Covered
Final 1970-71
14.
IS. Supplementary Notes
16. Abstracts
Recommendations are made for limits of air concentrations of ammonia to which
the public may safely be exposed for short periods of time. The scientific
basis and associated literature references for the recommendations are presented.
17. Key Words and Document Analysis. 17a. Descriptors
Air Pollution
Ammonia
Exposure
Sensitivity
Toxictty
17b. Identifiers/Open-Endcd Terms
Air Pollution effects (humans)
Short-Term Public Limits (STPL's)
Public Eraereen'-y Limits (PEL's)
Air poiiution effects (animals)
17e. COSATI Field/Group 13]J
18. Availability Statement
Release unlimited.
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Report)
UNCLASSIFIED
20. Security Class (This
Page
1,'N
,'Nri.ASSIFIFD
21. No. o( Pages
16
22. Price
FORM NTIS-33 (REV. 3*72)
THIS FORM MAY HE REPRODUCED
USCOMM-DC I052-P72
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Committee on Toxicology
Herbert E. Stokinger, Chairman
Arthur B. DuBois, Vice-Chairman
Bertram D. Diniran
Seymour L. Friess
Harold M. Peck
V. K. Rowe
C. Boyd Shaffer
Frank G. Standaert
James H. Sterner
Richard D. Stewart
Subcommittee on Ammonia
Frank G. Standaert, Chairman
David W. Fa.ssett, Reviewer
William G. Fredrick
Joseph F. Msllor
Harold M. Peck
Jac Siegel
• L. M. Roslinski, Staff Officer
Advisory Center on Toxicology
National Academy of Sciences - National Research Council
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Prepared under Contract No. CPA 70-57
between the National Academy of Sciences,
Advisory Center on Toxicology and the
.Environmental Protection Agency.
Contract Monitor:
Dr. Vaun A. Newill
Assistant for Health Effects
Office of Research and Monitoring
Environmental Protection Agency
Washington, D. C. 20460
- ii -
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NOTICE: The study reported herein was undertaken under the aegis of
the National research Council with the express approval of the Governing
Board of the NRC. Such approval indicated that the Board considered
that the problem is of national significance; that elucidation or solution
of the problem required scientific or technical competence and that the
resources of the NRC were particularly suitable to the conduct of the
project.
The members of the study committee were selected for their
individual scholarly competence and judgment with due consideration for
the balance and breadth of disciplines. Responsibility for all aspects of
this report rests with the study committee, to whom sincere apprecia-
tion is expressed. - . .
Although the reports of our study committees are not submitted
for approval to the Academy membership or Council, each report is
reviewed by a second group of appropriately qualified individuals according
to procedures established and monitored by the Academy's Report Review
Committee. Such reviews are intended to determine, inter alia, whether
the major questions and relevant points of view have been addressed and
whether the reported findings .conclusions, and recommendations arose
from the available data and information. Distribution of the report is
approved, by the President, only after satisfactory completion of this
review process.
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INTRODUCTION
The Environmental Protection Agency has focused its initial
concerns on long-term exposures of the public to air pollutants. In
addition to the long-term levels there are occasional circumstances
wherein the public may be exposed briefly to relatively high concentra-
tions. For example, batch-process techniques in industries may result
in pulses of effluent. The testing and launching of rockets releases
exhaust products. Rapidly changing meteorological conditions may result
in short periods of locally high concentration of stack effluents.
Accidental releases of chemicals sorp
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Ammonia
Introduction
Ammonia, a colorless gas at ambient temperatures and pressures,
has the following characteristics:
Molecular weight: 17. 03
Boiling point: -33° C
Solubility: 90 g in 100 ml H20 (at 0° C)
Explosive limits: 16 - 25% by volume in air
Vapor density (air=l): 0. 597 (STP)
Specific gravity of liquid NH^: approximately 0. 6
pH of a 1% solution in H^O: approximately 11. 7
Odor threshold: 5-53 ppm
Ammonium hydroxide, a 28% solution of ammonia in water, and
"household ammonia," normally a 10%aqueous solution, are two common
preparations of this gas.
Ammonia is a naturally occurring substance, the result of protein
metabolism in living organisms. It is readily absorbed. Ruminants use
the ammonia to make amino acids (36) but in man virtually all is
immediately reconverted to urea in the liver. Individuals with severe
liver disease may fp.il to detoxify the ammonia and may manifest
derangements of central nervous system functions (37). Ammonia is
also formed from glutamate by the kidney (35) and in this organ is an
important component of the acid, base, electrolyte balancing system.
In normal man the mean blood level (measured as N) is 0. 08 mg% (34).
The global average of ammonia in the atmosphere has been esti-
mated to be 6 parts per billion of air (ppb)* resulting primarily from natural
sources (5). Sawicki (6) estimates the average concentration in urban
air to be about 20 ppb. The annual U.S. production (synthetic) in 1971
has been reported to be 27.4 billion pounds. '
At 25° C and 760 mm Hg 1 ppm NH3 ~ 0. 7 mg/m3.
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Effects on Animalp
Henderson and Haggard (1) classify ammonia as a primary irritant.
Silver and McGrath (2) exposed white mice to high concentrations of
ammonia for 10-minute periods and reported the LC$Q to be 7, 060 mg/m^
(~10,200 ppm) with 93% of the deaths occurring.during exposure. During
exposure the mice exhibited great excitement, their eyes were closed,
and within one minute they were gasping. Convulsions and deaths began
to occur after the fifth minute. The report does-not include a description
of pathological changes.
Rats exposed to approximately 100 ppm ammonia (70 mg/m ) for
5 hrs/day, 5 days/week for a total of 60 days showed no difference
between the rate of their ciliary activity and that in control animals.
However, histological changes in the epithelium of the trachea of the
exposed animals were greater than in the controls (11).
Coon et aL^ (4) tested rats, guinea pigs, rabbits, monkeys, and
dogs with continuous (65 to 114 days) or repeated (8 hrs/day x 5 days/week
for 6 weeks) exposures to ammonia. Repeated exposure at 155 mg/m^
'(223 ppm) produced no adverse effects. After repeated exposures at 770
mg/m^ (1100 ppm) the authors reported finding ocular and nasal irritation
in rabbits and dogs and inflammatory changes in the lungs of rats and
guinea pigs.
Continuous exposure at 40 mg/m^ (58 ppm) was observed to cause
non-specific inflammatory changes in the lungs of the experimental
animals (114 days of exposure) and, at 127 mg/m^ (183 ppm) and 262 mg/m
(3.77 ppm), similar changes were reported in both the lungs and kidneys
(90 days of exposure). Continuous exposure c.t levels of 445 mg/m-*
(665 ppm) and 470 mg/m^ (677 ppm) for 65 and 90 days respectively
caused 87-98% mortality in exposed rats and marked eye irritation in
rabbits and dogs.
. Weatherby (8) exposed male guinea'pigs to ammonia at a concentra-
tion of 170 ppm (140-200 ppm) for 6 hrs/day, 5 days/week for up to 18
weeks and examined the animals at 6-week intervals. Animals sacrificed
after 6 and 12 weeks showed no abnormalities that could be attributed to
ammonia. Examination of the animals exposed for IK weeks reportedly
revealed considerable congestion of spleens, livers, and kidneys and
early degenerative changes in the adrenal glands. It is interesting to note
that no changes suggestive of chronic intoxication were observed in the
heart, lungs, stomach, or small intestine of the experimental animals.
Because of its high solubility in water,, ammonia would be expected
to act as an irritant primarily on the upper respiratory passages, being
absorbed by the moist membranes lining these passages. Absorption of
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ammonia by the upper respiratory tract may prevent irritation of the
deeper lung structures, Boyd and co-workers (7) demonstrated such a
"Naso-Bucco-Pharyngeal Filter" in rabbits. The authors also concluded
• that the upper respiratory tract is more resistant to the action "of-ammonia
than is the brochiolar-alveolar structure.
Cralley (3) examined the effects of ammonia on mucociliary activity
of sections of excised rabbit trachea. He observed that 500 ppm NH3 for
five minutes or 400 ppm for 10 minutes caused irreversible cessation of
ciliary activity.
Dalhamn and co-workers (9,10,11), in a series of experiments,
examined the effects and absorption of ammonia on the ciliated epithelium
and upper respiratory tract of rabbits and rats. Ammonia concentrations
of 500 ppm caused cessation of ciliary activity on excised rabbit trachea
in 5 to 15 minutes (9). At concentrations below 260 ppm, there was no
discernible effect on ciliary activity through 20 minutes of exposure (10).
These authors concluded that "a concentration of about 100 ppm arnmonia
seemed to be the critical level influencing ciliary beating, and the con-
concentration of NH3 in the air entering the nose should be about 2000
ppm to produce the requisite 100 ppm in the trachea. "
S
It is interesting to note that exposure of rats to about 100 ppm
ammonia along with carbon particles ("3. 5 rng/m^) for 5 hrs/day, 5
days/week for 60 days resulted in a significant decrease in ciliary
activity as well as more pronounced .-histological changes in the tracheae
of the exposed animals. Carbon particles alone at concentrations of
7 mg/m^, did not cause any significant changes in the ciliary activity
or in the histological appearance- of the tracheal epithelium (11).
Absorption of NHj to the carbon particles may have resulted in an
increased carriage of NH^ into the trachea.
Effects on Humans
The odor threshold for ammonia has been variously reported as low
as 5 ppm and as high as 53 ppm (15,17); recent evidence cited in the 1971
T.LV documentation (18) indicates that the odor threshold is in the area
of 5 ppm. Another unpublished inquiry supports this lower level (16). ,
The physiological effects of ammonia on humans appears to be simi-
lar to that observed in experimental animals. Irritation of the mucous
membranes of the upper respiratory tract becomes noticeable at about
100 ppm and concentrations above 400 ppm may destroy mucous surfaces
upon prolonged contact (duration of exposure not given) (12). Weatherby
(8) states that 5 or 6 members of his staff inhaled chamber exhaust air
containing 140-200 ppm ammonia and all were of the opinion that no person
would remain in such an atmosphere voluntarily for any appreciable period
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of time because of the disagreeable odor and respiratory distress.
However, Silverman and co-workers (19) report that subjects voluntarily
inhaled 500 ppm ammonia for 30 minutes. Evidently concentrations
between 140 and 500 ppm are irritating although tolerable for at least
30 minutes. Concentrations in excess of 2500 ppm are reported to be
dangerous for as little as 1/2 hour (12) although fatal inhalation of
ammonia would be expected only when the victim is unable to escape
from the contaminated atmosphere. Death is usually from pulmonary
edema (12-14).
Silverman and co-workers (19) found that the retention of ammonia
in the respiratory passages of humans was considerably less than that
reported by Landahl and Herrmann (20) when exposure time was increased
up to 30 minutes. They exposed seven human volunteers to ammonia at
500 ppm (350 mg/m^) and found that the average retention of ammonia
was 20% with time to equilibrium ranging from 10 to 27 minutes. The
symptoms of the subjects were reported to be nasal dryness and irrita-
tion, excessive lacrimation in two subjects and elevation of the minute
respiratory volume 50% to 250% over control values. No significant
changes in nitrogen metabolism were observed in response to the ammonia
exposures.
Long industrial experience indicates that no permanent injury
occurs from exposure to NH^ throughout a working lifetime at levels
below those that cause intolerable acute effects.
Guide Values for Short-Term Limits
Short-term public exposures are those occurring at predictable
times and arising from single or, occasionally, repeated events. Since
the exposure can be predicted there is no justification for submitting the
public to any appreciable risk (21). The concentrations given below may
be odorous, but are expected to be tolerable. They are considered to be
below the level of irritation and well below the levels that might be
expected to cause injury.
Short-Tcrm Public Limits (STPL's) '
•
10 min 20 ppm (ceiling)
30 min 10 ppm (ceiling)
60 min 10 ppm (ceiling)
5 hrs/day, 3-4 days/mo 5 ppm (Time-weighted averages
with excursions above
average not to exceed
"ceiling" limits)
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Many people find the odor of ammonia objectionable and any con-
centration above their odor threshold may be expected to produce
complaints from these individuals regardless of how short the exposure.
Public Emergency Limits (PEL's)
Public emergency limits apply to situations in which pollutants
escape in an uncontrolled manner at unpredicted times atid places as the
result of accidents such as damage to transportation equipment or fire in
a chemical-storage facility. Although the STPL's require that there be
no adverse effects, the PEL's recognize the possibility of some serious
discomfort, provided that the effect is reversible and that no S3rious
sequelae result from it. The concentrations in the following PEL's are
considered to present a strong odor with possible lacrimation and irrita-
tion of the upper respiratory tract (nose and throat), but no inoapacitation
or prevention of self-rescue.
Public Emergency Limits (PEL's)
10 min 100 ppm
30 min 75 ppm
60 min 50 ppm
The preceding limits are proposed on the basis of studies
examining the effects of NH3 inhalation on healthy animals and humans.
It is suggested that appropriate research be done to determine the effects
of NH3 inhalation on persons having pre-existing pulmonary disease in
order to determine whether such persons art: more susceptible to these
effects.
In recommending the limits the Committee on Toxicology assumed
that NHj was the only contaminant to which the public would be exposed
during any single episode. Mixed exposures to pollutants causing
synergistic effects with NH3 such as those observed with NH3 and carbon
particles (11) might well require more conservative exposure limits.
Effects of Ammonia on Vegetation
The effects of ammonia on plants have not received a great deal
of study possibly because continuous emission from industrial sources
is not sufficiently high to produce acute injury symptoms. Reports of
field injury from gaseous ammonia can be expected as anhydrous
ammonia becomes more and more popular as a fertilizer.
Buckwheat, coleus, sunflower, and tomato foliage have reportedly
been injured upon exposure to 40 ppm NH3 for 1 hour. Slight marginal
injury has been observed in these plants after a 4-hr exposure to 16. 6
ppm NH3 (23).
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Benedict and Breen (24) used weeds as a means of evaluating
potential vegetation damage due to a number of air pollutants. They
found that a 4-hr exposure to an ammonia level of 12 ppm produced some
leaf marking in most of 10 varieties of weeds that were tested. Sunflower
and mustard were the most susceptible having 30% and 22% of the leaf
area "marked. " Dandelion, pigweed, and duckweed were observed to be
the least susceptible. Little effect was observed on the plants after a
4-hr exposure at 3 ppm. Drying the soil in which the plants were growing
before exposing them to ammonia resulted in decreased marking of the
leaves. Middle-aged leaves (those that had been at full size for about one
week) appeared to be the most susceptible to the ammonia, with younger
leaves rarely being marked.
Hutchinson e£ a_l. (25) monitored the ammonia levels in growth
chambers containing single seedlings of cotton, corn, soybean, or sun-
flower, and reported that these seedlings absorb significant quantities
of NH^ even at low atmospheric levels (34-63 ppb). They conclude that
the atmospheric levels might satisfy up to 10% of the total nitrogen
requirement of the plants.
15
Porter e_tal. (26) using levels of 1, 10, and 20 ppm N-labeled
ammonia, reported that up to 43% of atmospheric ammonia was absorbed
and rapidly metabolized to amino acids and protein by corn seedlings
over a 24-hr exposure period. The authors observed no visible damage
to the plants after a 24-hr exposure at these levels.
Ammonia at very high concentrations (15,000 - 45,000 ppm) for
brief periods of time (0.5 sec) has been used as a defoliant for cotton
crops (27). . i
Effects on Materials
Ammonia, in the presence of water or water vapor, will attack
copper, silver, zinc, and all their alloys.. Galvanized surfaces as well
as aluminum and its alloys may alsso be corroded by ammonia in the
presence of moisture. Iron and steel will not react readily with either
dry or moist ammonia (31).
Contact of ammonia with certain other chemicals including mercury,
chlorine, iodine, bromine, calcium, silver oxide, or hypochlorite can
form explosive compounds (31).
An in-depth discussion concerning the corrosivity of metals and
alloys ie beyond the scope of this guide. The corrosive potential of
ammonia on a number of metals is given in Metals Handbook (32).
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Analytical Methods
; Although a number of methods are available fqr measuring NH,
in the air, many of them are only semi-quantitative and serve only as
indicators of the presence of NH3- One such method is the use of moist
litmus paper, which, it is claimed, will turn blue in one second at 100
ppm NHj and in 6. 5 seconds at 10 ppm (28).
Absorption of the NHo in a standard acid and Iteration of the excess
acid using a standard base is a method generally applicable to NH^
determination (29).
The most popular method for NH-j analysis in both air and water
is determination with Nessler's reagent (28, 29, 30). Sensitivity of 3 ppm
in a 50-liter air sample is reported.
A recently developed method for determination of NHj is the
"ammonia electrode," claimed to have a sensitivity down to 20 ppb.
The method is based on the conversion of NH3 in solutions to NH4+
with the production of an OH" which is "sensed" by means of a membrane
electrode. The response time for the instrument is reported to be less
than one minute (33).
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. References
1. Henderson, Y. and Haggard, H. W. Noxious Gases and the '-.'
Principles of Respiration Influencing their Action. New York.
Reinhold Publ. Co. 1943. (p. 124-125).
2. Silver, S. D. and McGrath, F. P. A comparison of acute toxicities
of ethylene imine and ammonia to mice. J. Ind.Hyg. Tox. 30:7-9
1948.
3. Cralley, L. V. The effects of irritant gases upon the rate of ciliary
activity. J. Ind. Hyg. Tox. 24:193-198 1942.
4. Coon, R.A. , Jones, R.A., Jenkins, L. J. ,Jr. , and Siegel, J;
Animal inhalation studies on aiiimonia, ethylene glycol, formalde-
hyde, dimethylamine, and ethano'.. Toxicol. Appl. Pharmacol. 16:
646-655 May 1970.
• 5. Robinson, E. and Robbins, R. C. Gaseous nitrogen compound
pollutants from urban and natural sources. JAPCA 20:(5) 303-306
1970.
6. Sawicki, E. Airborn carcinogen's and allied compounds. Arch.
Environ. Health 14:46-53, 1967.
7. Boyd, E. M. , Maclachlan, M. L. , and Perry, W. F. Experimental
ammonia gas poisoning in rabbits and cats. J. Ind.Hyg. Tox. 26:
29-34, 1944. .
8. Weathe.rby, J. H. Chronic toxicity of ammonia fumes by inhalation.
Proceedings Soc. Exper. Biology and Medicine 81:300-301,1952.
9. Dalhamn, T. and SjOholm, J. Studies on SO£, NO2, and NH3:
Effects on ciliary activity in rabbit trachea of single in vitro
exposure and resorption in rabbit nasal cavity, Acta. physiol.
scand. 58:287-291 1963.
10. Dalhamn, T. , Effects of ammonia alone and combined with carbon
particles on ciliary activity in the rabbit trachea in vivo with
studies of the absorption capacity of the nasal cavity. Intern. J. of
Air and Water Pollution 7:531-539 1963.
11. Dalhamn, T. and Reid, L. Ciliary activity and histologic observa-
tions in the trachea after exposure to ammonia and carbon particles.
IN: Inhaled Particles and Vapors II. Davies, ed. , Pergamon Press,
1967.
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12. Patty, F. A. , ed. Industrial Hygiene and Toxicology, Vol. II, 2nd
ed. New York. Interscience Publs. 1963. (p. 862)
13. Fairhall, L. T. Industrial Toxicology, 2nd ed. Baltimore,
Williams and Wilkins Co. 1957 (p. 14)".
14. Caplin, M. Ammonia-gas poisoning. Forty-seven cases in a
London shelter. Lancet, 241:95-96, 1941.
15. Flury, F. and Zernik, F: Schadliche Case. Berlin. Verlag von
Julius Springer. 1931. (p. 152).
16. Smyth, H. Jr. personal communication.
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Meeting, Air Pollution Control Assoc. , St. Paul. June 23-27,
1968. Paper No. 68-13.
18. Am. Conf. Govern. Ind. Hyg. Documentation of Threshold Limit
Values for Substances in Workroom Air. Cincinnati, Ohio.
Third Ed. 1971.
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response of man to ammonia in low concentrations. J. Ind. Hyg.
Tox. 31:74-78, 1949.
20. Landahl, H. D. and Herrmann, R. G. Retention of vapors and
gases in the human nose and lung. Arch. Ind. Hyg. 1:36-45 1950.
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Committee on Toxicology. Basis for establishing guides for short-
term exposures of the public to air pollutants. June 1971.
22. Dalhamn, T. , Mucous flow and ciliary activity in the trachea of
healthy rats and rats exposed to respiratory irritant gases.
Acta Physiol. Scand.Suppl. 123, pp. .1-161 (1956).
*
23. Heck, W.W. , Daines, R. H.', and Hindawi, I. J. "Other phytotoxic
pollutants. " IN: Jacobson, J. S. and Hill, A. C. , editors.
Recognition of Air Pollution Injury to Vegetation: A Pictorial Atlas.
Air Pollution Control Association Informative Report No. 1.
TR-7 Agricultural Committee. 1970. p. F-l-F-24.
24. Benedict, H. M. and Breen, W. H. The use of weeds as a means of
evaluating vegetation damaged caused by air pollution. Proc. 3rd
Natl. Air Pollution Symp. Pasadena, Calif. 1955. p. 177-190.
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25. Hutchinson, G. L. , Millington, R. J. , and Peters, D. B.
Atmospheric ammonia - Absorption by plant leaves. Science
175:771-772. February 18, 1972.
26. Porter, L. K. , Viets, F. G.,'-Jr.;;.and Hutchinson, G. L. Air
Containing nitrogen-15 ammonia: Foliar absorption by corn
seedlings. Science 175:759-761. February 18, 1972.
27. Fisher, J. B. , and Cazaly, G. W. Defoliation of cotton plants with
ammonia. U.S. Patent No., l^O^^'gv^.une-JS, ,1963.
28.
Hygienic Guide Series - Anfey'dT^ttl^iriini&'ma:. Am. Ind. Hyg. Assoc.
J. 32:139-142 1971. .-fel^^^
29. Elkins, H. B. The Chemistry of .Industrial Toxicology. New York.
John Wiley and Sons,
.
30. ASTM Standards; Industrial Water; Atmospheric Analysis. Part 23.
1965. American Society for Testing.;and Materials, Philadelphia
• . P. 326-331. ':-^;^^'-;;;-.-;;/- :. . " . •
31. Manufacturing Chem. Assb^^^al^^ljftejts^SpS..(anhydrous ammonia,
1960) and SD13 (aqua ammonia'^J947)>i;: liyman,' T. (editor).
32. Lyman, T. Metals Handbook. .Vol. L Properties and Selection of
Metals. Am. Soc. Metals, MeXals,. Pack, Novelty, Ohio. 8th ed.
- ' -~~1"r • '.' ''''"' J -'"**••
33. Orion Res., Inc. Data Sheet Form DS95-10/1711. 1971.
" ' ' 'n ',- &•;'•+ " :.•'.•
34. Diem, K. , editor. Documerita Geigy. Scientific Tables. 6th ed.
Geigy Pharmaceuticals. Ardsley, New York. 1962. (p. 558)
35. Lowenstein, J. M. Ammonia production in muscle and other
tissues: the purine nucleotide cycle. Physiol. Reviews 52:382-
414 April 1972.
36. Chalupa, W. Metabolic aspects of honprotein nitrogen utilization
in ruminant animals. Fed. Proc. 31:1152-1164 May-June 1972.
37. Visek, W. J. Effects of urea: hydrolysis on cell life-span and
metabolism. Fed. Proc. 31:1178-1193 May-June 1972.
• TT- '••=_'•.:•'• **.' T •".-•-
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