This report contains the collective views of an international group of
    experts and does not necessarily represent the decisions or the stated
    policy of the United Nations Environment Programme, the International
    Labour Organisation, or the World Health Organization.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    World Health Orgnization
    Geneva, 1986

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
    International Labour Organisation, and the World Health
    Organization. The main objective of the IPCS is to carry out and
    disseminate evaluations of the effects of chemicals on human health
    and the quality of the environment. Supporting activities include
    the development of epidemiological, experimental laboratory, and
    risk-assessment methods that could produce internationally
    comparable results, and the development of manpower in the field of
    toxicology. Other activities carried out by the IPCS include the
    development of know-how for coping with chemical accidents,
    coordination of laboratory testing and epidemiological studies, and
    promotion of research on the mechanisms of the biological action of

        ISBN 92 4 154194 6  

         The World Health Organization welcomes requests for permission
    to reproduce or translate its publications, in part or in full.
    Applications and enquiries should be addressed to the Office of
    Publications, World Health Organization, Geneva, Switzerland, which
    will be glad to provide the latest information on any changes made
    to the text, plans for new editions, and reprints and translations
    already available.

    (c) World Health Organization 1986

         Publications of the World Health Organization enjoy copyright
    protection in accordance with the provisions of Protocol 2 of the
    Universal Copyright Convention. All rights reserved.

         The designations employed and the presentation of the material
    in this publication do not imply the expression of any opinion
    whatsoever on the part of the Secretariat of the World Health
    Organization concerning the legal status of any country, territory,
    city or area or of its authorities, or concerning the delimitation
    of its frontiers or boundaries.

         The mention of specific companies or of certain manufacturers'
    products does not imply that they are endorsed or recommended by the
    World Health Organization in preference to others of a similar
    nature that are not mentioned. Errors and omissions excepted, the
    names of proprietary products are distinguished by initial capital




    1.1. Properties and analytical methods
    1.2. Sources in the environment
    1.3. Environmental transport, distribution and transformation 
    1.4. Environmental levels and human exposure
    1.5. Kinetics and metabolism
         1.5.1. Uptake and absorption
         1.5.2. Distribution
         1.5.3. Metabolic transformation
         1.5.4. Excretion and turnover
         1.5.5. Plant metabolism of ammonia
    1.6. Effects on aquatic organisms
    1.7. Effects on experimental animals and  in vitro test systems
         1.7.1. Single exposures
         1.7.2. Short-term exposures
         1.7.3. Skin and eye irritation; sensitization
         1.7.4. Long-term exposure
         1.7.5. Reproduction, embryotoxicity, and teratogenicity
         1.7.6. Mutagenicity
         1.7.7. Carcinogenicity
         1.7.8. Mechanisms of toxicity
    1.8. Effects on man
         1.8.1. Organoleptic effects
         1.8.2. Clinical, controlled human studies and accidental 
         1.8.3. Endogenous ammonia
    1.9. Evaluation of the health risks for man and effects on the 
    1.10. Conclusions


    2.1. Physical and chemical properties of ammonia and ammonium 
         2.1.1. Gaseous and anhydrous liquid ammonia
         2.1.2. Aqueous solutions
         2.1.3. Chemical reactions
         2.1.4. Ammonium compounds
    2.2. Sampling and analytical methods
         2.2.1. Air and water samples
         2.2.2. Soil samples
         2.2.3. Blood and tissue samples


    3.1. Production and use
    3.2. Sources releasing ammonia into the air

    3.3. Sources discharging ammonia into water
         3.3.1. Point sources of ammonia
         3.3.2. Non-point sources of ammonia
         3.3.3. Comparison between point and non-point sources


    4.1. Uptake and transformation in atmosphere
    4.2. Transport to the earth's surface
         4.2.1. Wet and dry deposition
         4.2.2. Contribution to acid rain
    4.3. Transformation in surface water
    4.4. Uptake and transformation in soils


    5.1. Environmental levels
         5.1.1. Atmospheric levels
         5.1.2. Levels in water
         5.1.3. Levels in soil
         5.1.4. Food
         5.1.5. Other products
    5.2. General population exposure
         5.2.1. Inhalation
         5.2.2. Ingestion from water and food
         5.2.3. Dermal exposure
    5.3. Occupational exposure
    5.4. Exposure of farm animals
         5.4.1. Oral exposure
         5.4.2. Inhalation exposure


    6.1. Microorganisms
    6.2. Plants
         6.2.1. Terrestrial plants
         6.2.2. Aquatic plants
         6.2.3. Fresh-water plants
         6.2.4. Salt-water plants
    6.3. Aquatic invertebrates
         6.3.1. Fresh-water invertebrates: acute toxicity
         6.3.2. Fresh-water invertebrates: chronic toxicity
         6.3.3. Salt-water invertebrates: acute and chronic toxicity
    6.4. Fish
         6.4.1. Ammonia metabolism in fish
        Ammonia production and utilization
        Ammonia excretion
         6.4.2. Fish: acute toxicity
        Salt-water fish
         6.4.3. Factors affecting acute toxicity
        Dissolved oxygen
        Carbon dioxide
        Prior acclimatization to ammonia

         6.4.4. Fish: chronic toxicity
    6.5. Wild and domesticated animals
         6.5.1. Wildlife
         6.5.2. Domesticated animals
        Oral exposure
        Inhalation exposure


    7.1. Absorption
         7.1.1. Respiratory tract
         7.1.2. Gastrointestinal tract
         7.1.3. Skin and eye
    7.2. Distribution
         7.2.1. Human studies
         7.2.2. Animal studies
    7.3. Metabolic transformation
    7.4. Reaction with body components
    7.5. Elimination and excretion
         7.5.1. Expired air
         7.5.2. Urine and faeces
    7.6. Retention and turnover
    7.7. Uptake and metabolism in plants


    8.1. Single exposures
         8.1.1. Inhalation exposure
         8.1.2. Oral exposure 
        Effects of metabolic acidosis induced by 
                         ammonium chloride  
        Organ effects following oral 
        Influence of diet on the effects of 
         8.1.3. Dermal exposure 
         8.1.4. Effects due to parenteral routes of exposure  
        Central nervous system effects  
        Effects on the heart  
    8.2. Short-term exposures 
         8.2.1. Inhalation exposure 
         8.2.2. Oral exposure 
        Histopathological effects 
        Effects of ammonium as a dietary nitrogen 
         8.2.3. Dermal exposure 
    8.3. Skin and eye irritation; sensitization 
    8.4. Long-term exposures  
         8.4.1. Inhalation exposure 
         8.4.2. Oral exposure 
    8.5. Reproduction, embryotoxicity, and teratogenicity
    8.6. Mutagenicity
    8.7. Carcinogenicity

    8.8. Factors modifying effects  
         8.8.1. Synergistic effects 
         8.8.2. Antagonistic effects  
    8.9. Mechanisms of toxicity 


    9.1. Organoleptic aspects 
         9.1.1. Taste 
         9.1.2. Odour 
    9.2. Clinical and controlled human studies  
         9.2.1. Inhalation exposure 
         9.2.2. Oral exposure   
        Effects of acute oral exposure  
         9.2.3. Endogenous hyperammonaemia  
        Inborn errors of metabolism 
        Hepatic features


    10.1. Atmospheric exposure and effects
          10.1.1. General population exposure
          10.1.2. Occupational exposure
    10.2. Exposure through food and water
    10.3. Ocular and dermal exposure
    10.4. Accidental exposure
    10.5. Evaluation of risks for the environment
          10.5.1. The aquatic environment
          10.5.2. The terrestrial environment
    10.6. Conclusions  
          10.6.1. General population
          10.6.2. Sub-populations at special risk
          10.6.3. Occupational exposure
          10.6.4. Farm animals
          10.6.5. Environment


    11.1. Research needs







Professor E.A. Bababunmi, Department of Biochemistry, University of 
   Ibadan, Ibadan, Nigeria  (Chairman)

Dr J.R. Jackson, Albright and Wilson, Ltd., Occupational Health and 
   Hygiene Service, Warley, United Kingdom  (Rapporteur)

Professor I. Kundiev, Research Institute of Labour, Hygiene, and 
   Occupational Diseases, Saksaganskogo, Kiev, USSR

Dr M. Piscator, Department of Environmental Hygiene, Karolinska 
   Institute, Stockholm, Sweden

Professor D. Randall, Department of Zoology, University of British 
   Columbia, Vancouver, British Columbia, Canada

Dr V.R. Rao, Department of Toxicology, Haffkine Institute, Parel, 
   Bombay, India

Dr J.A.A.R. Schuurkes, Laboratory of Aquatic Ecology, Faculty of 
   Natural Sciences, Catholic University, Nijmegen, The Netherlands

Dr J.R. Stara, Office of Research and Development, US Environmental 
   Protection Agency, Cincinnati, Ohio, USA

Dr H. Suzuki, Department of Hygiene, Fukushima Medical College, 
   Fukushima, Japan

Dr R.V. Thurston, Fisheries Bioassay Laboratory, Montana State
   University, Bozeman, Montana, USA

Dr E. Weisenberg, Institute for the Standardization and Control of 
   Pharmaceuticals, Ministry of Health, Jerusalem, Israel 


Dr E. Smith, International Programme on Chemical Safety, World
   Health Organization, Geneva, Switzerland  (Secretary)

Mrs I.-M. Linquist, Occupational Safety and Health Branch,
   International Labour Office, Geneva, Switzerland

Dr C. Xintaras, Office of Occupational Health, World Health
   Organization, Geneva, Switzerlanda

a Attended half day only.


    Every effort is made to present information in the criteria 
documents as accurately as possible.  In the interest of all users 
of the environmental health criteria documents, readers are kindly 
requested to communicate any errors that may have occurred to the 
Manager of the International Programme on Chemical Safety, World 
Health Organization, Geneva, Switzerland, in order that they may be 
included in corrigenda, which will appear in subsequent volumes. 

                        *    *    *

    A data profile and information on the various limits set by 
countries can be obtained from the International Register of 
Potentially Toxic Chemicals, Palais des Nations, 1211 Geneva 10, 
Switzerland (Telephone No. 988400 - 985850). 

    Concentrations in this document are expressed in the terms used 
in original references. 

    1 mmol is equivalent to 14 mg ammonia-nitrogen/litre
                            17 mg NH3/litre
                            18 mg NH4+/litre

    1 mg ammonia-nitrogen is equivalent to 1.21 mg NH3
                                           1.29 mg NH4+

    In air, 1 mg/m3 is equal to about 1.42 ppm, depending on the 
temperature and pressure. 


    Following the recommendations of the United Nations Conference 
on the Human Environment held in Stockholm in 1972, and in response 
to a number of resolutions of the World Health Assembly and a 
recommendation of the Governing Council of the United Nations 
Environment Programme, a programme on the integrated assessment of 
the health effects of environmental pollution was initiated in 
1973.  The programme, known as the WHO Environmental Health 
Criteria Programme, has been implemented with the support of the 
Environment Fund of the United Nations Environment Programme.  In 
1980, the Environmental Health Criteria Programme was incorporated 
into the International Programme on Chemical Safety (IPCS), a joint 
venture of the United Nations Environment Programme, the 
International Labour Organisation, and the World Health 
Organization.  The Programme is responsible for the publication of 
a series of criteria documents. 

    A WHO Task Group on Environmental Health Criteria for Ammonia 
was held in Geneva on 8-13 July, 1985.  Dr E.M. Smith opened the 
meeting on behalf of the Director-General.  The Task Group reviewed 
and revised the draft criteria document and made an evaluation of 
the health risks of exposure to ammonia. 

    The original draft of this document was prepared by THE UNITED 
ASSESSMENT OFFICE under the direction of DR J.F. STARA.  Additional 
contributions were made by DR J.R. JACKSON, PROFESSOR D. RANDALL, 

    The efforts of these contributors and of all who helped in the 
preparation and finalization of the document are gratefully 

                            * * *

    Partial financial support for the publication of this criteria 
document was kindly provided by the United States Department of 
Health and Human Services, through a contract from the National 
Institute of Environmental Health Sciences, Research Triangle Park, 
North Carolina, USA - a WHO Collaborating Centre for Environmental 
Health Effects. 


1.1.  Properties and Analytical Methods

    Ammonia (NH3) is a colourless acrid-smelling gas at ambient 
temperature and pressure.  It can be stored and transported as a 
liquid at a pressure of 10 atm at 25 C. 

    Ammonia dissolves readily in water where it forms, and is in 
equilibrium with, ammonium ions (NH4+).  The sum of ammonia and 
ammonium concentrations is termed "total ammonia" and, because of 
the slightly different relative molecular masses, may be expressed 
as "total ammonia-nitrogen (NH3-N)".  In most waters, NH4+ 
predominates, but increases in pH or temperature or decreases in 
ionic strength may materially increase levels of non-ionized 

    Ammonia will adsorb on various solids.  At concentrations of 
between 16 and 27% by volume, it can form explosive mixtures with 
air.  Catalytic oxygenation is an important reaction in the 
manufacture of nitric acid.  Ammonia dissolves in dilute acids to 
form ionized ammonium salts, which are similar in solubility to 
alkali metal salts, and can be crystallized.  Some of these salts 
are found in nature.  Heating solutions or crystals of the salts 
yields gaseous ammonia.  Ammonia forms chloramines in water 
containing hypochlorous acid. 

    There are difficulties in sampling media for the determination 
of ammonia, and in preventing contamination and losses before 
analysis.  A variety of analytical techniques are available; many 
have interactions.  For measurements, the flourescent 
derivatization technique has advantages. 

1.2.  Sources in the Environment

    Ammonia is present in the environment as a result of natural 
processes and industrial activity, including certain types of 
intensive farming.  Atmospheric ammonia is volatilized from the 
earth's surface in quantities of about 108 tonnes/year, mostly from 
natural biological activity.  Industrial activity may cause local 
and regional elevations in emission and atmospheric concentrations.  
Surface waters receive ammonia from point sources, such as effluent 
from sewage treatment and industrial plants, in quantities 
estimated in the USA to be about half a million tonnes annually.  
Much more significant quantities arise from non-point sources, such 
as atmospheric deposition, the breakdown of vegetation and animal 
wastes, applied artificial fertilizers and urban runoff, and these 
are significant, even in industrial areas. 

1.3.  Environmental Transport, Distribution, and Transformation

    Ammonia in the environment is a part of the nitrogen cycle.  It 
volatilizes into the atmosphere where it may undergo a variety of 
reactions.  Photolytic reactions destroy some of the ammonia and 
reactions with sulfur dioxide or ozone produce aerosols, most 

importantly of ammonium sulfate or nitrate, which return to the 
earth's surface as wet or dry deposition.  In surface waters, 
ammonium may undergo microbiological nitrification, which yields 
hydrogen and utilizes oxygen so that, in certain systems, 
acidification and oxygen depletion may result.  In one study, one-
third of the acidifying effect of precipitation was attributed to 
ammonium deposition.  Ammonia may be assimilated by aquatic plants 
as a nitrogen source or transferred to sediments or volatilized.  
In soil, major sources of ammonia are the aerobic degradation of 
organic matter and the application and atmospheric deposition of 
synthetic fertilizers.  The ammonium cation is adsorbed on 
positively charged clay particles and is relatively immobile.  Most 
ammonium undergoes nitrification; the nitrate ion is mobile and is 
removed by leaching, plant root uptake, or denitrification. 

1.4.  Environmental Levels and Human Exposure

    Atmospheric concentrations vary according to underlying land 
usage.  Urban concentrations are typically in the range of 5 - 
25 g/m3 and rural concentrations, 2 - 6 g/m3.  Areas with 
intensive manure production or use may produce concentrations of 
100 - 200 g/m3.  Particulate ammonium concentrations above oceans, 
remote from land, have been found to be 10 - 115 ng/m3.  In most 
situations, atmospheric particulate ammonium concentrations are 
comparable to gaseous ammonia concentrations. 

    Surface waters contain concentrations of total ammonia that 
vary both regionally and seasonally.  In the USA, most surface 
waters contain less than 0.18 ng/litre, though those near large 
metropolitan areas may contain 0.5 ng/litre, as total ammonia.  In 
hydrologically isolated acidified small lakes, concentrations may 
reach 3 mg NH4+-N/litre, and values near intensive farms of 12 mg 
NH4+-N/litre have been recorded.  Ground water usually contains low 
concentrations of ammonia, because of ammonium adsorption and/or 
nitrification; this, and the conversion of ammonia to chloramines 
on chlorination, results in low levels of ammonia in most treated 

    Ammonia in soil is largely fixed; that in solution is in 
dynamic equilibrium with nitrate and is not directly available to 
plants.  Ammonia occurs in unprocessed foods, but ammonium salts 
are added to processed foods.  Acceptable Daily Intakes (ADIs), 
where specified, relate to the anion.  Cigarette smoking and 
certain medicines may contribute to intake, in some cases, but the 
intake from all sources is small in comparison with endogenous 
intestinal ammonia production. 

    Occupational exposure to low levels of ammonia is common, but, 
in certain occupations, work-place concentrations may exceed 
100 mg/m3.  At such levels, the daily ammonia intake is small in 
relation to endogenous production, but it is significant, since 
inhaled ammonia enters the systemic circulation. 

1.5.  Kinetics and Metabolism

1.5.1.  Uptake and absorption

    At low concentrations, inhaled ammonia dissolves in the mucous 
fluid lining the upper respiratory tract and little reaches the 
lower airways.  Initial retention is about 80% in both the dog and 
man, but, in man, it falls to less than 30% in less than 27 min.  
In rats, increases in blood-ammonia were measured following short-
term exposure to ammonia at 220 mg/m3 but not at 23 mg/m3.  The 
increases were less marked with longer exposure.  Calculated blood-
ammonia increases with exposure to air containing 18 mg/m3 are 
about 10% of fasting levels. 

    Ammonia is formed in the human intestinal tract by the 
biological degradation of nitrogenous matter, including secreted 
urea, in quantities of about 4 g/day.  Nearly all of this is 
absorbed (mainly passively) and is metabolized in the liver on 
first passage, so that only small amounts reach the systemic 

1.5.2.  Distribution

    Ammonia is normally present in all tissues constituting a 
metabolic pool.  Its distribution is pH dependent, since NH3 
diffuses more easily than NH4+.  Oral administration of ammonium 
chloride to healthy male and female volunteers at 9 mg/kg body 
weight produced transient increases in blood-ammonia in about half 
of the subjects.  Patients with cirrhosis showed a greater and more 
prolonged increase over a higher baseline.  This confirms 
substantial first pass metabolism in the liver. 

    Administration of 15N-labelled ammonium compounds to 
experimental animals indicated that the initial distribution of 15N 
depended on the route of administration and that, after parenteral 
administration, more was distributed to organs other than the 

1.5.3.  Metabolic transformation

    Ammonia is taken up by glutamic acid in many tissues, and this 
will take part in a variety of transamination and other reactions, 
the nitrogen being incorporated in non-essential amino acids.  In 
the liver, ammonia is used in the synthesis of protein by the 
Krebs-Henseleit cycle. 

1.5.4.  Excretion and turnover

    The principal means of ammonia excretion varies between phyla.  
Mammals excrete urea and secrete ammonium in the kidney tubules as 
a means of hydrogen ion excretion.  Faecal and respiratory 
excretion are insignificant.  Exhaled air may contain volatilized 
ammonia from the microfloral degradation of salivary urea.  In man, 
on a 70 g protein/day diet, 70% of administered ammonium 15N is 
lost in a week; on a 20 g protein/day diet, 35% is lost. 

1.5.5.  Plant metabolism of ammonia

    Ammonia is toxic in plants and cannot be excreted.  It is 
detoxified by combination with carbon skeletons, and so excess 
ammonia may strain carbohydrate metabolism.  Some plants have 
special means of handling ammonia, enabling them to tolerate it or 
use it preferentially. 

1.6.  Effects on Aquatic Organisms

    Concentrations of ammonia that are toxic for aquatic animals 
are generally expressed as non-ionized ammonia (NH3), because, in 
the environment, NH3 and not the ammonium ion (NH4+) has been 
demonstrated to be the principal toxic form of ammonia. 

    Concentrations of ammonia, acutely toxic for fish, can cause 
loss of equilibrium, hyperexcitability, increased breathing, 
cardiac output, and oxygen uptake, and, in extreme cases, 
convulsions, coma, and death.  At lower concentrations, ammonia 
produces many effects in fish including a reduction in egg hatching 
success, a reduction in growth rate and morphological development, 
and pathological changes in the tissue of the gills, liver, and 

    Several factors have been shown to modify acute ammonia 
toxicity in fresh water.  Some factors alter the concentration 
of NH3 in the water by affecting the aqueous ammonia equilibrium, 
while other factors affect the toxicity of NH3 itself, either 
ameliorating or exacerbating its effects.  Factors that have been 
shown to affect ammonia toxicity include dissolved oxygen 
concentration, temperature, pH, previous acclimatization to 
ammonia, fluctuating or intermittent exposures, carbon dioxide 
concentration, salinity, and the presence of other toxic 
substances.  The best studied of these is pH; the acute toxicity 
of NH3 has been shown to increase as pH decreases.  Data on 
temperature effects on acute NH3 toxicity are limited and 
variable, but there are indications that NH3 toxicity is greater 
at low (< 10 C) temperatures. 

    Data concerning concentrations of NH3 that are toxic for fresh-
water phytoplankton and vascular plants, although limited, indicate 
that fresh-water plant species are appreciably more tolerant to NH3 
than invertebrates or fish. 

    (a)   Fresh-water organisms

    Mean 48- and 96-h LC50 values reported for fresh-water 
invertebrates and fish ranged from 1.10 to 22.8 mg NH3/litre for 
invertebrate species, and from 0.56 to 2.48 mg/litre for fish 
species.  Mean 96-h LC50 values ranged from 0.56 to 2.37 mg 
NH3/litre for salmonid fish and from 0.76 to 2.48 mg/litre for non-
salmonids.  In terms of LC50, Percidae and Salmonidae are 
considered to be the most sensitive families and walleye and 
rainbow trout are the most sensitive species within these families. 

    For fresh-water organisms, the families most sensitive in terms 
of chronic toxicity are Salmonidae and Catostomidae, pink salmon 
and white sucker being the most sensitive species within these 
families.  Limited chronic toxicity data for invertebrates, mostly 
cladocerans and one insect species, indicate that they are 
generally more tolerant than fish, although the fingernail clam 
appears to be as sensitive as salmonids. 

    (b)   Salt-water organisms

    Available acute and chronic ammonia toxicity data for salt-
water organisms are very limited.  Mean LC50 values for marine 
invertebrate species range from 0.94 to 18.3 mg NH3/litre and, for 
marine fish species, from 0.32 to 1.31 mg/litre.  The prawn, 
 Macrobrachium rosenbergii, appears to be the most sensitive 
invertebrate species tested, and the red drum, the most sensitive 
fish species. 

1.7.  Effects on Experimental Animals and  In Vitro Test Systems

1.7.1.  Single exposures

    There have been many estimates of inhalational toxicity in 
which the theoretical relationship between concentration, duration 
of exposure, and lethality has been observed.  Typical results are 
LC50 values in rats ranging from 31 612 mg/m3 for a 10-min exposure 
to 11 620 mg/m3 for a 60-min exposure.  The corresponding value for 
a 2-h exposure was 7600 mg/m3.  Exposed mice exhibited avoidance 
behaviour at concentrations above 350 mg/m3, and ciliary activity 
was arrested above this level in  in vitro studies on rabbit 
tracheal epithelium.  Other effects of exposure include bradypnoea 
and bradycardia, changes in various serum-enzyme levels, and 
histological changes in the lung.  At high concentrations, 
convulsions occurred. 

    There have been a number of studies on the oral toxicity of 
various ammonium salts, some of which have been complicated by the 
acidity or alkalinity of the preparations used.  Median lethal 
doses for ammonium sulfamate or sulfate were in the range 3 - 
4.5 g/kg body weight in both rats and mice.  Ammonium chloride 
causes substantial acidosis and has been reported to produce 
pulmonary oedema by a different mechanism by gavage, but not by 
intraperitoneal injection.  There is also evidence that ammonium 
ions exert a direct effect on the appetite by their effect on 
prepyriform cortical areas.  Ammonium chloride, even after 
administration for periods of a few days, produces hypertrophy of 
the kidney, but the extent to which this results from acidosis, a 
solute load, or a direct effect of the ammonium ion is not clear.  
Diet and the clinical condition of the liver are important 
modulators of ammonia toxicity, and it has been shown that the 
administration of ornithine, aspartic acid, or adenosine 
triphosphate (ATP) exerts a protective effect against ammonia 

    No information is available regarding systemic toxicity from 
single dermal exposures to ammonia or ammonium compounds. 

    Symptoms after intravenous injection of ammonium salts are 
characterized by immediate hyperventilation and clonic convulsions, 
followed by either fatal tonic extensor convulsion or the onset of 
coma, in which tonic convulsions and death can occur at any time.  
After 30 - 45 min, surviving animals recover rapidly and 
completely.  After injection, neurological symptoms commenced when 
the blood-ammonia concentration doubled above basal values.  Brain-
ammonia levels did not increase until blood levels reached 20 times 
basal values; at this stage, brain levels suddenly increased to 
about 100 mg ammonia-nitrogen/kg wet weight.  However, immediate 
increases in brain-ammonia after intravenous injection have also 
been observed, and it has been suggested that there is no critical 
blood-ammonia concentration for diffusion of ammonia through the 
blood-brain barrier.  Some workers have demonstrated the induction 
of ventricular fibrillation of the heart following injections of 
ammonium salts. 

1.7.2.  Short-term exposures

    Ninety-day inhalation exposures of rats to 127 mg/m3 and 
262 mg/m3 did not produce any, or only minimal, changes.  Continuous 
exposure to 455 mg/m3 was fatal for 50 out of 51 rats by the 69th 
day of exposure.  Similar results were obtained in guinea-pigs.  
The principal pathological findings were eye irritation, corneal 
opacities, and diffuse lung inflammation.  Similar results have 
been published by a number of authors.  Concentration-dependent 
increases in susceptibility to infection during ammonia exposure 
have been reported.  Blood-ammonia levels increased with 
inhalational exposure to increasing concentrations of ammonia above 
70 mg/m3, for periods of 1 - 7 days. 

    Studies on the effects of ingestion of ammonium chloride 
(10 g/litre drinking-water - about 1 g/kg body weight per day) 
and ammonium sulfamate (5 g/kg body weight per day for 6 days 
per week) did not show any significant toxic effects.  Cyclical 
administration of various ammonium salts, at moderate doses, for 3 
weeks out of 4 affected the reproductive system of virgin female 
rabbits.  Ammonium salts have been given as a dietary supplement to 
animals on diets deficient in non-essential amino acids, with 
resultant increases in weight gain.  Ammonium salts can prevent and 
reduce the weight loss associated with 10% and 20% reduction of the 
crude protein content of the diet of pigs. 

    There is no information regarding the systemic effects of 
short-term dermal exposure. 

1.7.3.  Skin and eye irritation; sensitization

    There is little information on animals to complement the 
extensive human experience.  In rabbits, ammonia has been shown to 
penetrate the cornea rapidly and to cause corneal burns.  Ammonium 
persulfate is a recognized skin sensitizer in man.  No data on 
sensitization potential in animal models are available. 

1.7.4.  Long-term exposure

    Inhalation exposure studies did not extend beyond 130 days.  A 
130-day study demonstrated congestion of parenchymatous organs at 
18 weeks, but not at 12 weeks, in guinea-pigs exposed to about 
119 mg/m3 for 6 h/day, 5 days/week.  Long-term studies have not 
been carried out according to modern protocols, and observed 
effects have mainly been related to changes in acid-base balance. 

1.7.5.  Reproduction, embryotoxicity, and teratogenicity

    There have not been any formal studies based on modern 
protocols, but studies have been undertaken to investigate the 
effects of ammonia in hen-houses on the egg-laying performance of 
intensively reared poultry.  No systematic conclusions could be 

1.7.6.  Mutagenicity

    Ammonium sulfate has been reported non-mutagenic in  Salmonella
and  Saccharomyces test systems, but mutagenic in  E. coli at toxic 
levels and may affect mutagenic responses to other agents.  Various 
workers have described effects on  Drosophila, which were minimal 
or achieved only at toxic levels.  There is no evidence that ammonia 
is mutagenic in mammals. 

1.7.7.  Carcinogenicity

    There is no evidence that ammonia is carcinogenic, though it 
can produce inflammatory lesions of the colon and cellular 
proliferation, which could increase susceptibility to malignant 
change.  There was no evidence that ammonia was responsible for the 
increased incidence of tumours with increased dietary protein 
intake.  Ammonia did not either cause tumours or increase the 
spontaneous incidence of tumours in life-time studies on mice. 

1.7.8.  Mechanisms of toxicity

    Although there are a number of hypotheses, there is no 
established mechanism for the toxicity of ammonia or ammonium 

1.8.  Effects on Man

1.8.1.  Organoleptic effects

    Ammonia can be tasted in water at levels above about 35 
mg/litre.  Odour thresholds have been variously reported according 
to the definition used and technique of measurement.  Most people 
can identify ammonia in air at about 35 mg/m3 and can detect it at 
about one-tenth of this level. 

1.8.2.  Clinical, controlled human studies and accidental exposure

    Exposure to ammonia in air at a concentration of 280 mg/m3
produced throat irritation; 1200 mg/m3 produced cough; 1700 mg/m3
was life-threatening, and more than 3500 mg/m3 caused a high 
mortality.  Respiratory symptoms were usually reversible, but 
chronic bronchitis has been reported to develop.  Volunteers 
exposed by oro-nasal mask experienced irritation and increased 
minute volumes.  Retention of inspired ammonia decreased 
progressively to about 24% after about 19 min of exposure.  The 
blood chemistry remained normal.  Respiratory indices were 
insignificantly altered at concentrations up to 98 mg/m3 (which was 
tolerable).  Other studies have demonstrated a high incidence of 
symptoms at this level.  Irritation occurred at 35 mg/m3, which was 
neither discomforting nor painful.  Industrial exposure at 88 mg/m3 
was described as "definitely irritating". 

    Ingestion of ammonia solutions has produced caustic burns of 
the upper gastrointestinal tract.  Ingestion of ammonium chloride 
produces metabolic acidosis and diuresis and is administered for 
these effects. 

1.8.3.  Endogenous ammonia

    Ammonia plays a key role in nitrogen metabolism, and its level 
in the body may be increased as a result, either of in-born errors 
of metabolism, or, as a result of impaired liver function.  The 
role of hyperammonaemia in causing the encephalopathy associated 
with the latter is not completely clear, but there is sufficient 
evidence to indicate a significant contribution. 

1.9.  Evaluation of the Health Risks for Man and Effects on the

    Atmospheric exposure of the general population is toxicologically 
insignificant.  Occupational exposure can give rise to symptoms, 
particularly in occupations exposed to decaying organic matter.  
Accidental exposure to ammonia in any of its forms produces 
irritant or caustic effects. 

    Exposure to ammonia in the water supply and food is 
insignificant in comparison with the nitrogen intake through the 
diet which becomes available as metabolic ammonia. 

    The most significant effects of ammonia are in the aquatic and 
terrestrial environments where, as a result of urbanization, 
industry, and farming and as a result of deposition to sensitive 
environments, significant toxic effects of ammonia may arise. 

1.10.  Conclusions

    Ammonia does not present a direct threat to man except as a 
result of accidental exposure, particularly in industry.  Farm 
animals may be adversely affected when reared intensively in closed 
conditions.  Localized effects of point-source emissions of ammonia 
and of deposition in sensitive environments is a cause of concern. 


2.1.  Physical and Chemical Properties of Ammonia and Ammonium Compounds

2.1.1.  Gaseous and anhydrous liquid ammonia

    Ammonia (NH3) is a colourless gas at atmospheric pressure, 
which is lighter than air and possesses a strong penetrating odour.  
Some of the relevant physical properties of ammonia are summarized 
in Table 1. 

    The vapour pressure of ammonia gas over pure ammonia liquid can 
be calculated using the equation (NRC, 1979): 

    log10P = 9.95028 - 0.003863T - 1473.17/T,

    where P = partial pressure in mm Hg, and T = temperature at K.

    Ammonia may be liquefied under pressure at about 10 atm and is 
stored and transported in this state. 

2.1.2.  Aqueous solutions

    Ammonia dissolves readily in water where it ionizes to form the 
ammonium ion. 
    NH3 + H2O ========= NH4+ + OH-

    The solubility of ammonia in water is influenced by the 
atmospheric pressure, temperature, and by dissolved or suspended 
materials.  Solubility values at moderate concentrations and 
temperatures can be obtained from the graphic (Sherwood, 1925) and 
tabular (Perry et al., 1963) compilations, and from empirical 
formulae (Jones, 1973). 

    The total ammonia content of water is the sum of non-ionized 
(NH3) and ionized (NH4+) species.  Ammonia is readily soluble in 
aqueous systems (Table 1) and, at the pH of most biological 
systems, exists predominantly in the ionized form.  At low 
concentrations, the molarity of total dissolved ammonia is given by 
(Drewes & Hales, 1980): 

    [NH3] + [NH4+] = H[NH3(gas)] + KbH[NH3(gas)],

where [NH3(gas)] is the molar concentration of gas-phase ammonia, 
Kb is the dissociation constant given by: 

         [NH4+] [OH-]
    Kb = ------------ = 1.774 x 10-5 (at 25C)

and H is a Henry's law constant given by (NRC, 1979): 

           log10H = 1477.8/T - 1.6937

Table 1.  Physical properties of ammoniaa
Properties                               Values
Boiling point at one atm                 -33.42 C

Melting point                            -77.74 C

Density (liquid) at -33.35 C and 1 atm  0.6818 gm/cm2

Density (gas)                            0.7714 g/litre

Viscosity at -33 C                      0.254 centipoise

Viscosity at 20 C                       9.821 x 109 poise

Refractive index at 25 C                1.325

Dielectric constant at 25 C             16.9

Surface tension at 11 C                 23.38 dyn/cm

Specific conductance at -38 C           1.97 x 10-7 cm-1

Thermal conductivity at 12 C            5.51 x 10-5 gcal/cm

Vapour pressure at 25 C                 10 atm

Critical temperature                     132.45 C

Critical pressure                        112.3 atm

Critical density                         0.2362 g/cm3

Solubility in water, 101 kPa

    at  0 C                             895 g/litre
       20 C                             529 g/litre
       40 C                             316 g/litre
       60 C                             168 g/litre
a From:  Jones (1973) and Windholz et al., ed. (1976).

The pKa for the ammonia/ammonium equilibrium  can be calculated at 
all temperatures, T(K), between 0 and 50 C (273 < T < 323) by 
the equation (Emerson et al., 1975): 

     Ka = [NH3] [H+]/[NH4+],
     pKa = 0.09018 + 2729.92/T

Theoretically, the fraction (f) of total ammonia that is non-
ionized depends on both water temperature and pH, according to the 

preceding and the following equations (Emerson et al., 1975): 

     f = 1/[10        + 1]

Thus, in water at 0 C and a pH of 6, less than 0.01% of the total 
ammonia present is in the non-ionized form, whereas, at 30 C and a 
pH of 10, 89% of total ammonia is non-ionized. 

    The above relationship holds in most fresh waters.  However, 
the concentration of non-ionized ammonia will be lower at the 
higher ionic strengths of very hard fresh waters or saline waters.  
Using the appropriate activity coefficients, in sea water of ionic 
strength = 0.7, the above relationship can be restated as follows 
(API, 1981): 

              (pKa-pH + 0.221)
     f = 1/[10                + 1]

    At 25 C, the pKa can be calculated to be 9.24, from the 
equation of Emerson et al. (1975).  Therefore, at pH 8, and at a 
temperature of 25 C, the above equation shows that 3.31% of the 
total ammonia in sea water exists in the non-ionized form.  The 
corresponding value in fresh water can be calculated to be 5.38%.  
Thus, at this pH and temperature, sea water with an ionic strength 
of 0.7 would contain 62% as much non-ionized ammonia as fresh 

2.1.3.  Chemical reactions

    Gaseous ammonia is readily adsorbed on certain solids.  The 
adsorption characteristics of ammonia on metal surfaces are 
important in its synthesis and other catalytic reactions (Cribb, 
1964).  Because of the adsorption of ammonia on charcoal, acid-
impregnated charcoal masks are used for protection against ammonia 

    Ammonia can form explosive mixtures with air at atmospheric 
temperature and pressure, if present in concentrations of 16 - 27% 
by volume.  The products of combustion are mainly nitrogen and 
water, but small traces of ammonium nitrate (NH4NO3) and nitrogen 
dioxide (NO2) are also formed. 

    Another important reaction involving the oxidation of ammonia 
is its catalytic oxidation to nitric oxide (NO) and nitrous oxide 
(N2O) (Miles, 1961; Matasa & Matasa, 1968).  This reaction is an 
important step in the manufacture of nitric acid. 

    Under normal atmospheric conditions, ammonia does not undergo 
any primary photochemical reactions at wavelengths greater than 
290 nm. 

    When exposed to radicals or other photochemically excited 
species, ammonia undergoes secondary decomposition: 

    NH3 + -OH  ->  -NH2 + H2O

    NH3 + O  ->  -NH2 + -OH

Some of these reactions may be important in the balance of 
atmospheric nitrogen. 

    Ammonia also undergoes decomposition to nitrogen and hydrogen, 
when exposed to an electric discharge (Jones, 1973).  It reacts 
with sulfur dioxide gas to form ammonium sulfate in the atmosphere 
(Kushnir et al., 1970). 

    Aqueous ammonia can take part in substitution reactions with 
organic halide, sulfonate, hydroxyl, and nitro compounds, and, in 
the presence of metallic catalysts, it is used to produce amino 
acids from keto acids.  Ammonia reacts with hypochlorous acid 
(HOCl) to form monochloramine, dichloramine, or nitrogen 
trichloride (Morris, 1967; Lietzke, 1978).  The formation of these 
 N-chloramines depends on the pH, the relative concentrations of 
hypochlorous acid and NH3, the reaction time, and the temperature.  
When pH values are greater than 8, and when the molar ratio of HOCl 
to NH3 is 1:1 or less, the monochloramine predominates.  At higher 
Cl2:NH3 ratios or, at lower pH values, dichloramine and 
trichloramine are formed.  These, and various organic chloramines, 
are produced during the chlorination of water containing NH3 or 
organic amines.  The presence of these chloramines may contribute 
to the taste and odour of drinking-water, and to various 
associated health problems (Morris, 1978). 

2.1.4.  Ammonium compounds

    Ammonium compounds comprise a large number of salts, many of 
which are of industrial importance; ammonium chloride, ammonium 
nitrate, and ammonium sulfate are produced on a large scale.  With 
the exception of metal complexes, the ammonium salts are very 
similar in solubility to the salts of the alkali metals, but differ 
in that they are completely volatilized on heating or ashing. 

    Ammonium salts undergo slight hydrolysis in aqueous solution.  
Most dissociate at elevated temperatures to give ammonia and the 
protonated anion.  The physical and chemical properties of ammonium 
compounds of environmental importance are discussed below, and some 
of their physical properties are summarized in Table 2. 

    Ammonium chloride [NH4Cl] occurs naturally in volcanic
crevices as a sublimation product.  When it sublimes, the
vapour is completely dissociated into hydrogen chloride and
ammonia.  Like other ammonium salts of strong acids, the
chloride hydrolyses in aqueous solution to lower the pH of the
solution.  The solid tends to lose ammonia during storage.  Aqueous 
solutions of ammonium chloride have a notable tendency to attack 
ferrous metal and other metals and alloys, particularly copper, 

bronze, and brass.  Ammonium chloride can be oxidized to nitrosyl 
chloride and chlorine by strong oxidizing agents, such as nitric 

    Ammonium nitrate [NH4NO3] does not occur in nature.  It is 
soluble in water and liquid ammonia and slightly soluble in 
absolute ethyl alcohol, methanol, and acetone.  Although ammonium 
salts of strong acids generally tend to lose ammonia during 
storage, ammonium nitrate can be considered a very stable salt.  It 
undergoes decomposition at elevated temperatures or under extreme 
shock, as in commercial explosives.  Ammonium nitrate acts as an 
oxidizing agent in many reactions, and, in aqueous solution, it is 
reduced by various metals.  Solutions of ammonium nitrate attack 
metals, particularly copper and its alloys. 

    Ammonium sulfate [(NH4)2SO4] is found naturally in volcanic 
craters.  It is soluble in water and insoluble in alcohol and 
acetone.  The melting point of ammonium sulfate is 230 C.  On 
heating in an open system, the compound begins to decompose at 
100 C, yielding ammonium bisulfate (NH4HSO4) that has a melting 
point of 146.9 C. 

    Ammonium acetate [CH3COONH4] is a deliquescent material that is 
highly soluble in cold water and in alcohol.  Solubility does not 
increase greatly with increasing temperature, at least up to 25 C.  
In aqueous solution at atmospheric pressures, ammonium acetate 
readily loses ammonia, especially in alkaline conditions. 

    Ammonium carbonate [(NH4)2CO3] and ammonium bi-carbonate 
[NH4HCO3] have long been known because of their occurrence in 
association with animal wastes.  Ammonium bicarbonate is the more 
readily formed and the more stable.  It decomposes below its 
melting point (35 C), dissociating into ammonia, carbon dioxide, 
and water.  Ammonium bicarbonate reacts with, and dissolves, 
calcium sulfate scale.  Ammonium carbonate decomposes on exposure 
to air with the loss of ammonia and carbon dioxide, becoming white 
and powdery and converting into ammonium bicarbonate.  Ammonium 
carbonate volatilizes at about 60 C.  It dissolves slowly in water 
at 20 C, but decomposes in hot water. 

2.2.  Sampling and Analytical Methods

2.2.1.  Air and water samples

    Measurement of ammonia levels in air is difficult.  Atmospheric 
levels are low, and samples can be contaminated by emissions from 
man; thus, the analyst should remain remote from the sampling 
device.  In addition, air samples are bubbled through acid media to 
form an aqueous solution of ammonia, predominately in its ionic 
form.  The extraction of ammonia is variable and both gaseous 
ammonia and that contained in aerosols will be extracted.  In some 
instances filters are used to remove aerosols from the gas stream 
so that only ammonia gas is sampled.  There are, however, some 
problems with aerosol filters as they may interact with gaseous 
ammonia when the aerosol is collected on the filter (NRC 1979). 

Table 2.  Physical properties of some ammonium compoundsa
Property        Ammonium       Ammonium       Ammonium       Ammonium      Ammonium         Ammonium
                chloride       nitrate        sulfate        acetate       carbonate        bicarbonate
Synonyms        ammonium       ammonium       ammonium       ammonium      ammonium         ammonium bicarbonate;
                chloride;      nitrate        sulfate;       acetate       carbonate;       ammonium hydrogen
                sal ammoniac                  mascagnite                   monohydrate      carbonate

Colour          colourless     colourless     colourless     white         colourless       colourless

Physical state  cubic          rhombic        rhombic        crystals,     cubic            rhombic or monoclinic
(25 C, 1 atm)  crystals       crystals       crystals       hygroscopic   crystals         crystals

Formula         NH4Cl          NH4NO3         (NH4)2SO4      CH3COONH4     (NH4)2CO3 x H2O  NH4HCO3

Relative        53.49          80.04          132.14         77.08         114.10           79.06
molecular mass

Melting point   340 sublimes   169.6          230            114           58               35
(C)                                          decomposes                   decomposes       decomposes

Boiling point   520            > 210                         decomposes                     sublimes
(C)                           decomposes

Density         1.527 (20 C)  1.725 (25 C)  1.769 (50 C)  1.17 (20 C)                   1.58 (20 C)

Refractive      1.642                         1.533                                         1.423, 1.555
index, nb20

Solubility in   370 (20 C)    1920 (20 C)   754 (20 C)    1480 (4 C)   1000 (15 C)     217 (20 C)
a From:  Dean (1979) and Weast (1979).
    Air samples collected by liquid impinger yield aqueous 
solutions.  Fabric filters used for collecting aerosols may be 
extracted with water for analysis.  Generally, air and water 
samples are analysed using similar techniques, which are summarized 
in Table 3. 

    Various methods for preventing interference can be used, but 
distillation at pH 9.5 is often carried out.  Care must be taken 
with water samples to prevent oxidation, volatilization, or 
microbiological assimilation of ammonia.  Thus, samples should be 
acidified and refrigerated in sealed containers (and may be treated 
with reagents) and analysed within 24 h (APHA, 1976; NRC, 1979; US 
EPA, 1979b; ASTM, 1980; API, 1981; Analytical Quality Control 
(Harmonised Monitoring) Committee, 1982). 

2.2.2.  Soil samples

    Soil samples are usually collected by the grab method.  To 
inhibit microbial activity during transport and storage, reagents 
(e.g., mercury (II) chloride) can be added to the soil (NRC, 1979).  
Rapid drying at 55 C, then sealing the samples in air-tight 
containers is a more satisfactory method of preservation for 
ammonium determination (NRC, 1979), but even this may not prevent 
erroneous results, and samples should be analysed soon after sample 
collection (NRC, 1979).  Analytical methods for the determination 
of ammonia and ammonium in soils have been reviewed by NRC (1979). 

2.2.3.  Blood and tissue samples

    The various techniques used for the determination of ammonia in 
blood and tissues ultimately incorporate the ammonia detection 
methods described in Table 3, but with various conditions, such as 
distillation, aeration, and diffusion to minimize interference 
(NRC, 1979).  Because of the higher protein concentration in 
tissues, determination of ammonia is subject to greater glutamine-
caused error than in body fluids (NRC, 1979). 

Table 3.  Ammonia detection methods
Medium  Particular      Method            Principle                  Interferants         Sensitivity  Reference
Air     silo air NH3    alkalimetric      air is drawn through       other acidic or      70 - 700     Elkins (1959);
                                          sulfuric acid until        alkaline             mg/m3        Leithe (1971)
                                          bromophenol indicator      contaminants                      
                                          changes colour; volume                                       
                                          of air is inversely
                                          proportional to 
                                          ammonia concentration

Water   high            titrimetric       NH3 in water is distilled                       1 - 25       API (1981)
        concentrations                    off into distilled water                        mg/litre
                                          which is titrated with
                                          acid to a methyl red/
                                          methylene blue end-point

Air                     Nesslerization    NH3/NH4 in dilute          amines, cyanate,     14 - 95      Leithe (1971);
                                          sulfuric or boric acid     alcohols, aldehyde,  mg/m3 air    NIOSH (1977)
                                          is reacted with alkaline   ketones, colour,                  
Water                                     mercuric and potassium     turbidity, residual  1 - 25       Stern (1968);
                                          iodide solution (Hg I2 x   chlorine             mg/litre     API (1981)
                                          KI); absorbence at 440 nm                       water        
                                          is compared with a
                                          standard curve; distil-
                                          lation can preceed

Air     low             indophenol        NH3 in solution is         monoalkyl amines,    7 - 7000     Leithe (1971)
        concentrations  reaction          reacted with hypochlorite  formaldehyde         g/m3        
                                          and phenol (slow-warm

Water                                                                turbidity, colour    10 - 2000    API (1981)
                                                                     salt (sea water)     g/litre

Air     measurement     ammonia           measurement of ionization  mercury, volatile    14 - 2100    Sloan & Morie
        of tobacco      electrode         potential of NH3 -->       amines               g/m3        (1974)
        smoke           (potentiometric)  NH+4                                                        

Table 3.  (contd.)
Medium  Particular      Method            Principle                  Interferants         Sensitivity  Reference
Water                                                                                     0.05 - 1400  API (1981)

Air     continuous      chemiluminescent  air is passed through                           3.5 - 3500   Spicer (1977)
        measurement                       high- and low-temperature                       g/m3        
                                          catalytic converters,
                                          which respectively
                                          measure NOx + NH3 and
                                          NOx; NH3 is obtained by

Air     tobacco         gas chromato-     gas chromatography with                         7 - 70       Sloan & Morie
        smoke           graphy            thermal conductivity                            mg/m3        (1974)

Air     continuous      UV spectro-       NH3(gas) exhibits several                       0.7 - 7      Leithe (1971)
        measurement     photometry        strong absorption bonds                         mg/m3        
                                          between 190 and 230 nm;
                                          absorption in 10 cm 
                                          quartz cells at 204.3 nm
                                          has been used (molecular
                                          extinction coefficient =

Air     continuous      Fluorescent       1-phthaldehyde                                  0.07 g/m3   Abbas & Tanner
        measurement     derivatization    derivatization                                  upwards      (1981)
        high            technique                                                                      

    Ammonia is present in the environment as a result of natural 
processes and through the industrial activities of man.  It is 
generally accepted that, of the ammonia present in the atmosphere, 
99% is produced by natural biological processes.  Ammonia is 
continually released throughout the biosphere by the breakdown or 
decomposition of organic waste matter.  Thus, any natural or 
industrial process that concentrates and makes nitrogen-containing 
organic matter available for decomposition represents a potential 
source of high local concentrations of ammonia in water, air, and 
soil.  Industrially-produced ammonia, from non-biological nitrogen, 
also represents an environmental source, by release through 
agricultural fertilization and industrial emissions.  Coal 
gasification or liquefaction may provide a major local source of 
ammonia.  The natural occurrence of ammonia compounds is indicated 
in section 2.1.4. 

3.1.  Production and Use

    Ammonia is one of the most widely-used industrial chemicals.  
It is ranked fourth in production volume in the USA after sulfuric 
acid, lime, and oxygen (Chemical and Engineering News, 1980).  
Total production of ammonia-nitrogen in the USA increased from 
5.8 x 106 tonnes in 1964 to 11.5 x 106 tonnes in 1974 (Keyes, 
1975), and had further increased to 17.6 x 106 tonnes by 1979 
(Chemical and Engineering News, 1980).  The demand in the USA for 
the production of ammonia is projected to reach 25 x 106 tonnes by 
1990 (Mai, 1977). 

    Ammonia is mainly produced industrially by the Haber-Bosch 
process in which nitrogen and hydrogen are combined under high 
pressure in the presence of a catalyst (Harding, 1959; Matasa & 
Matasa, 1968).  Prior to the Haber-Bosch process, ammonia was 
produced by the hydrolysis of cyanamides or cyanides.  A smaller 
scale method for ammonia production is regeneration from ammonium 
salts by heating with a base.  Alkaline earth metal oxides and 
hydroxides have been used with the naturally-occurring ammonium 

    Most of the ammonia produced in the USA is consumed as 
fertilizers (80%), fibres and plastics (10%), and explosives (5%) 
(Chemical and Engineering News, 1980).  It is also used in the 
production of animal feed (1.5%), pulp and paper (0.6%), and rubber 
(0.5%) (Keyes, 1975) and in a variety of other chemical production 
processes.  Ammonia and ammonium compounds are used as cleaning 
fluids, scale-removing agents, and in food as leavening agents, 
stabilizers, and for flavouring purposes.  A survey by the US Food 
and Drug Administration (US FDA) indicated that about 6000 tonnes 
of ammonium compounds were used in food in 1970 (FASEB, 1974) 
comprising ammonium bicarbonate, 317 tonnes; ammonium carbonate, 
24 tonnes; ammonium hydroxide, 535 tonnes; monobasic ammonium 
phosphate, 52 tonnes; dibasic ammonium phosphate, 434 tonnes; and 
ammonium sulfate, 1468 tonnes.  Information for ammonium chloride 
was not available.  The use of ammonium compounds in food nearly 
doubled during the period 1960 - 70. 

3.2.  Sources Releasing Ammonia into the Air

    Ammonia is released into the atmosphere by agricultural, waste-
disposal, and industrial activities.  Ammonia global release has 
been estimated at 113 - 244 x 106 tonnes ammonia-nitrogen/year 
(Sderlund & Svensson, 1976).  In the USA, industrial emissions 
from ammonia and fertilizer production (anhydrous ammonia, aqueous 
ammonia, ammonium nitrate, ammonium phosphates, urea), from 
petroleum refineries, coke ovens, and sodium carbonate manufacture, 
and loss of anhydrous ammonia during distribution, handling, and 
application have been estimated to be approximately 328 x 103 
tonnes, annually (NRC, 1979; US EPA, 1981).  This figure does not 
include volatilization of ammonia after soil applications of 
nitrogen fertilizer, which may amount to 5 - 10% of the ammonia and 
urea fertilizer applied.  These losses were estimated to comprise 
another 285 x 103 tonnes, annually (US EPA, 1981). 

    Combustion processes release ammonia as a by-product in amounts 
that are dependent on the substance being burned and the conditions 
of combustion.  Assuming that 2% of the municipal wastes generated 
in the USA are incinerated, about 0.8 x 103 tonnes of ammonia would 
be emitted annually from this source.  On the other hand, fossil 
fuel combustion in the USA is estimated to release 783 x 103 
tonnes/year (US EPA, 1981). 

    On the basis of the number of cattle in the USA and an average 
excretion of 31 kg urea per animal per year, it has been estimated 
that 3400 x 103 tonnes/year of ammonia are produced by cattle in 
the USA (API, 1981).  Similar calculations made in the Netherlands 
on the basis of the manure production of cattle, pigs, and poultry 
give a figure of 114 x 103 tonnes/year (Buysman, 1984).  Estimates 
of atmospheric emissions from the Netherlands and the USA are shown 
in Table 4. 

    It must be emphasized that substantial uncertainties are 
associated with these estimates, which are given for rough 
comparison only.  Ammonia from sources that cannot be quantified 
includes that which volatilizes from livestock wastes or polluted 
water, and emissions from the combustion of wood.  These sources 
must be considered in perspective with natural sources, especially 
the microbial fixation of nitrogen and the mineralization of 
nitrogenous organic matter.  Emissions from these natural sources 
far outweigh those from man-made sources, on a global scale; 
however, man-made sources can result in locally elevated 
atmospheric concentrations. 

Table 4.  Estimated atmospheric emissions of 
ammonia in the USA and the Netherlands
Source                     Annual emission 
                           (103 tonnes NH3)
                           USAa  the Netherlandsb
animal manure              3400  114 (1)

fertilizer volatilization  285   6.1 - 10.6

industrial activities      1111  7.6

other sources              0.8   0.5
a From:  US EPA (1981).
b From:  Buysman (1984).

    The very high contribution to ammonia emission from animal 
manure production in the Netherlands is remarkable.  More than 80% 
of the annually emitted ammonia results from the production of 
manure on intensive livestock farms and its use as an agricultural 
fertilizer.  In all areas with intensive livestock farming, ammonia 
emission from animal manure production contributes 90 - 99% to the 
total NH3 emission.  The number of poultry and pigs used in 
livestock farms increased 3 - 5 times between 1950 and 1980, and it 
can be expected that the ammonia emission from animal manure 
production has increased similarly.  In only a few areas does most 
of the emitted ammonia result from industrial activities, such as 
the production of coke and fertilizers, and the combustion of 
fossil fuel. 

    In Denmark, Belgium, and some parts of the Federal Republic of 
Germany and France, animal manure production contributes 
significantly to atmospheric emissions of NH3 (Buysman et al., 

3.3.  Sources Discharging Ammonia into Water

    Ammonia is released into the aquatic environment from a variety 
of man-made point source discharges and from natural and man-made 
non-point sources. 

3.3.1.  Point sources of ammonia

    Major man-made point sources discharging ammonia into surface 
waters include sewage treatment plants, and plants producing 
fertilizers, steel, petroleum, leather, inorganic chemicals, 
non-ferrous metals, and ferroalloys, and meat processing plants.  
Amounts of ammonia discharged annually by these industries in the 
USA were estimated to be nearly 5.6 x 105 tonnes (API, 1981) 
(Table 5).  These estimates show that the industries examined 
contribute < 5% of the total ammonia discharged into surface 
waters while publicly owned sewage treatment plants (POTWs) 

contribute > 95% of the total.  It is important to note that the 
POTW figure is based on an estimated actual discharge, while 
several of the industrial figures are based on Best Practicable 
Control Technology (BPT) guidelines and other industrial data. 

    An estimate of ammonia discharge by sewage treatment plants was 
based on an average ammonia concentration of 15 mg/litre in 
secondary treatment waste waters (Metcalf & Eddy, Inc., 1972) and a 
total discharge of 104 billion litres per day.  However, some 
sewage treatment plants discharge waste waters containing much 
higher ammonia concentrations.  Using data from Mearns (1981), the 
US EPA (1981) estimated that the mean effluent concentration of 
ammonia from 5 major POTWs in southern California was 107 mg NH3-
N/litre (130 mg NH3/litre). 

    The iron and steel industries release ammonia, as a by-product 
of the conversion of coal to coke, and during blast furnace 
operations.  The source estimate in Table 5 is based on proposed 
BPT effluent control limits and steel production data. 

    The estimated ammonia contribution from the fertilizer industry 
was based on 1978 production figures for ammonia, ammonium nitrate, 
urea solutions, and urea solids, and on BPT guideline limits.  This 
contribution may be underestimated because relatively few of these 
producers meet BPT limits and because production is increasing (US 
EPA, 1981). 

    The estimated contribution of ammonia for all other industry 
groups in Table 5, except the meat processing and leather 
industries, was based on production figures and BPT guideline 
limits.  The effluents of the meat processing and leather 
industries were reported to contain about 40 and 100 mg NH3/litre, 
respectively (API, 1981). 

3.3.2.  Non-point sources of ammonia

    Non-point sources of ammonia for surface waters are not as easy 
to quantify as point sources.  Non-point sources include releases 
not discharged by a discrete conveyance.  They are variable, 
discontinuous, diffuse, and differ according to specific land use.  
They may be the result of runoff from urban, agricultural, 
silvicultural, or mined lands.  Urban runoff may sometimes be 
considered a point source, as it is frequently collected and 
discharged from drainage systems.  Several hydrological models are 
available to predict runoff and estimate pollutant loading, but 
there is still difficulty with this subject.  Major non-point 
sources of ammonia for surface waters include fertilizer runoff, 
animal feedlots, animal wastes spread on the soil, urban runoff, 
and precipitation. 

Table 5.  Estimates of aquatic emissions of ammoniaa from
point sources in the USA
Point source                       Estimated contribution
                                   (tonnes NH3-N/year)
Sewage treatment plants (POTWs)    535 922.3b

Steel industry                     12 951.0c

Fertilizer industry                5955.9c

Petroleum industry                 2826.1c or 2767.2b

Meat processing industry           1099.3b

Leather industry                   687.1b

Inorganic chemicals industry       99.8c

Non-ferrous metals manufacturing   0.9c

Ferroalloy manufacturing industry  0.3c

                     Total         559 542.7 tonnes/year
a Adapted from: API (1981).
b Estimated contribution based on reported or estimated 
  actual discharge concentrations.
c Estimated contribution based on production data and BPT 
  guidelines, not actual discharges.

    The ammonia content of urban runoff is variable, depending, in 
part, on specific land use.  In a study of urban runoff, the amount 
of ammonia present varied with the seasons of the year.  Ammonia 
concentrations ranged from 0.18 mg N/litre in the autumn to 1.4 mg 
N/litre in the early spring (Kluesener & Lee, 1974).  In another 
study, Struzewski (1971) reported that ammonia-nitrogen in urban 
storm water ranged from 0.1 to 2.5 mg/litre. 

    The ammonia content of rural runoff originates from natural 
and man-made sources, including wastes from wildlife and livestock, 
decaying vegetation, fertilizer applications, material originally 
present in the soil, and precipitation.  Estimating total rural 
runoff quantities and ammonia concentrations is extremely complex 
and no overall estimates are available.  Loehr (1974) reported 
that the ammonium-nitrogen concentrations in the drainage from 4 
forested watersheds ranged from 0.03 to 0.08 mg/litre.  The 
ammonium-nitrogen concentrations were 8 - 14% of the nitrate-
nitrogen concentrations. 

    Precipitation is also a significant non-point source of 
ammonia.  Concentrations may vary locally, reflecting local 
atmospheric sources.  The average concentration in rainfall at one 
rural location on Long Island, New York (0.18 mg NH3-N/litre) was 

less than half those at 2 other Long Island sites closer to the New 
York urban area (0.43 and 0.459 mg NH3-N/litre) (Frizzola & Baier, 
1975).  Among collection sites throughout Wisconsin, ammonia levels 
in urban rain samples differed little from those in rural samples 
not taken near barnyards (range, 0 - 3 mg NH3-N/litre); however, 
values for locations near barnyards were 4 - 5 times higher (range 
0 - 3 mg NH3-N/litre) indicating contamination from locally-
generated atmospheric ammonia (Hoeft et al., 1972). 

    Similar tendencies have been observed in the Netherlands, 
though the absolute data are much higher.  In agricultural areas 
with dense livestock farming, ammonia levels ranging from 2.9 mg 
NH4+-N/litre near slurry manured croplands to 5.4 mg NH4+-N/litre 
at a distance of 100 m from a poultry farm have been found.  In 
relatively unaffected areas along the northern coast, the average 
value was 1.2 mg NH4+-N/litre, because of the relatively high 
background levels of atmospheric ammonia.  The average 
concentration in wet deposition was 2.4 mg NH4+-N/litre (Schuurkes, 
in press). 

    Watershed studies from pristine forests (Fisher et al., 1968), 
rural wood and pasture lands (Taylor et al., 1971), and heavily 
fertilized crop lands (Schuman & Burwell, 1974) have all shown that 
rainfall nitrogen, including ammonia-nitrogen, accounts for a 
substantial proportion (50 - 100%) of nitrogen in surface runoff. 

3.3.3.  Comparison between point and non-point sources

    Little information is available for the accurate comparison of 
point and non-point sources of ammonia for surface waters.  In one 
study, Wilkin & Flemal (1980) examined 3 Illinois river basins to 
determine the relative sources of various pollution loadings (by 
mass balance accounting) and the possible extent of water quality 
improvement by controlling various types of sources.  The three 
river basins, showed differences in point sources, patterns of land 
use (which influences non-point sources), and ammonia-nitrogen 
concentrations.  The east DuPage basin (42% industrial and urban) 
contained 4.73 mg NH3-N/litre, the upper Sangamon basin (19% urban 
and industrial), 2.51 NH3-N/litre, and the west DuPage basin (2% 
urban and industrial), 0.22 mg NH3-N/litre.  The fraction of 
ammonia-nitrogen load from undefined (non-point) sources in the 
heavily-industrialized east branch DuPage was only 0.54 compared 
with 0.84 in the rural upper Sangamon.  The authors concluded that 
much of the pollution loading appeared to be related to undefined 
sources and that further restrictions on point-source contributions 
might not result in improved water quality. 

    These data indicate that, although point sources contribute a 
large fraction of ammonia loading to surface waters, the 
contribution of undefined non-point sources is also significant. 


    Ammonia in the environment is a part of the total biotic and 
abiotic nitrogen balance as represented by the nitrogen cycle.  The 
processes of the nitrogen cycle consist of nitrogen fixation, 
assimilation, ammonification, nitrification, and denitrification.  
Nitrogen fixation and ammonification are microbially-mediated 
processes that produce ammonium ions from nitrogen gas and organic 
nitrogen.  Assimilation is the uptake and incorporation of 
inorganic nitrogen into organic molecules by microbes and plants.  
Nitrification is the microbial oxidation of the ammonium ion to 
nitrite (NO2-) and nitrate (NO3-).  Denitrification converts 
nitrate to nitrogen gas or nitrous oxide. 

4.1.  Uptake and Transformation in Atmosphere

    Ammonia enters the atmosphere as a result of both natural and 
artificial processes on the Earth's surface; there is no known 
photochemical reaction by which ammonia could be produced in the 
atmosphere (NRC, 1979).  Atmospheric ammonia undergoes four main 
types of reaction, namely aqueous-phase reactions, thermal 
reactions, photochemical reactions, and heterogeneous reactions. 

    In the aqueous-phase reactions, oxidation of aqueous sulfur 
dioxide in the presence of ammonia results in the formation of 
atmospheric ammonium sulfate aerosols.  This process is favoured by 
high humidity, high ammonia concentrations, and low temperatures 
(NRC, 1979). 

    Thermal reactions involving anhydrous ammonia and sulfur 
dioxide may, via heteromolecular nucleation, also result in the 
formation of ammonium sulfate aerosols.  Thermal reactions of 
ammonia with ozone result in the formation of ammonium nitrate, but 
the importance of this mechanism in the production of atmospheric 
ammonium nitrate aerosols is not known (NRC, 1979). 

    Photolytic degradation and reaction with photolytically 
produced hydroxyl radicals (-OH) in the troposphere are major 
pathways for the removal of atmospheric ammonia.  While there is 
limited information on the relative importance of these different 
reactions, it has been suggested that one-half of the atmospheric 
ammonia may be destroyed by the reaction with hydroxyl radicals, 
with the balance being destroyed by reaction with soot particles or 
by deposition (wet and dry) as particulate ammonium (NRC, 1979). 

    In addition to the formation of ammonium sulfate and nitrate, 
various ammonium surface complexes may be formed by the 
heterogeneous reaction of atmospheric ammonia with nitric oxide-
soot surfaces in the atmosphere (NRC, 1979).  While these 
heterogeneous reactions are significant in combustion reactions, 
their importance in the atmosphere at much lower concentrations of 
both ammonia and soot particles, is not known (NRC, 1979). 

    Comparison of the findings of Robinson & Robbins (1971) and 
Sderlund & Svensson (1976) on global nitrogen balances for ammonia 
reveals differences and it is difficult to evaluate which is the 
more accurate. 

4.2.  Transport to the Earth's Surface

    Most of the ammonia entering the atmosphere will be transported 
back to the earth by both wet and dry deposition.  Wet deposition 
includes rainfall, snow, hail, fog, and dew, while dry deposition 
mainly concerns gaseous ammonia.  In the Netherlands, a comparison 
has been made between the total emission and total deposition of 
ammonia- and ammonium-nitrogen.  Almost 95% of the emitted ammonia 
(119 x 103 tonnes/year) is deposited back on the surface (van 
Aalst, 1984).  In this way, ammonia contributes 60 - 90% of the 
nitrogen loading of water and soil, with nitrogen oxides making up 
the other part. 

4.2.1.  Wet and dry deposition

    A part of the ammonia in the atmosphere is removed by washout 
and rainout.  Ammonium sulfate aerosols are produced by aqueous-
phase reactions.  Thus, wet deposition of ammonia can be estimated 
by measuring ammonium concentrations in precipitation.  Annual 
average concentrations in wet deposition at locations in 21 
European countries vary from 0.12 to 1.74 mg NH4+-N/litre (Fuhrer, 
1985).  In the Netherlands, the mean annual concentration for the 
period 1978 - 82 was 2.4 mg NH4+-N/litre, corresponding to a wet 
deposition of 12.2 kg/ha per year.  The wet deposition in Norway 
ranges from 1.3 kg/ha per year in the centre of the country to 
8.6 kg/ha per year in the south (calculated from Overrein et al., 
1980).  In the United Kingdom, it varies between 3.2 and 6.0 kg/ha 
per year (calculated from Warren Spring Laboratory, 1982). 

    A comparison has been made of the amounts of dry and wet 
deposition of ammonia and ammonium per area in the Netherlands.  
The data are summarized in Table 6. 

    Wet deposition plays only a minor part (1/3) in the total 
deposition of NH3 and NH4+.  On average, 28.4 kg NH3 + NH4+-N is 
deposited per ha per year.  However, in rural areas with dense 
livestock farming, values may reach up to 50 - 100 kg per year. 

Table 6.  Dry and wet deposition of NH3 + NH+4
per ha per year in the Netherlandsa
                mol/ha per year  kg/ha per year
dry deposition  1150             16.2

wet deposition  790              12.2

Total           1940             28.4
a From:  Van Aalst (1984).

4.2.2.  Contribution to acid rain

    Although ammonia is a base and thus increases the pH of rain 
water, it contributes to the acidifying action of deposition.  In 
particular, the conversion of ammonium to nitrate appears to be 
important in the acidification of soil and water in carbonate-poor 
environments (Roelofs, in press; Schuurkes, in press).  This 
potentially-acidifying action has been implicated in the acid rain 
problem in the Netherlands. On average, NH3 contributes about 32% 
of the total deposition of potentially-acidifying substances (Table 

Table 7.  Average deposition of acid 
and acidifying substances (acid eq.,/ha 
per year) in the Netherlandsa
                  SO2    NOx    NH3
Total deposition  2750   1310   1940
                  (46%)  (22%)  (32%)
a From:  The Netherlands Ministry of 
  Housing, Physical Planning, and 
  Environment (1984).

4.3.  Transformation in Surface Water

    Nitrification is important in preventing the persistence or 
accumulation of high ammonia levels in waters receiving sewage 
effluent or runoff.  The overall reaction is: 

    NH4+ + SO2 ---> 2H+ + NO3- + H2O

It occurs in two steps, involving primarily two bacterial genera, 
and forming nitrite as an intermediate. 

    NH4+ ------------>  NO2-

    NO2- ----------->  NO3-

The process depends on many factors, including the amount of 
dissolved oxygen, temperature, pH, the microbial population, and 
the nitrogen forms present.  Nitrification is an oxygen-consuming 
process, requiring 2 moles of O2 per mole of NH4+ consumed and 
yielding hydrogen ion (NRC, 1979).  Nitrification may thus lead to 
a depletion of dissolved oxygen and acidification, which may, in 
turn, inhibit microbiological nitrification (Knowles et al., 1965; 
Schuurkes et al., 1985). 

    Anthonisen et al. (1976) reported that, at high levels of 
total ammonia and a high pH, the resulting concentrations of free 
ammonia were toxic to both nitrifying forms, but especially to 
nitrobacters, occasionally leading to the accumulation of nitrite.  

Other authors (Kholdebarin & Oertli, 1977) have reported that high 
pH alone, in the absence of ammonia, can inhibit nitrite oxidation.  
At high nitrite levels, formation of free nitrous acid caused 
inhibition of nitrosomonad bacteria, resulting in the persistence 
of both ammonia and nitrite.  However, inhibitory conditions and 
persistence of reduced forms are usually transient (Anthonisen et 
al., 1976), and reports of high nitrite levels are rare (Ecological 
Analysts, Inc., 1981). 

    Other mechanisms also act to remove ammonia from natural 
waters.  Ammonia is assimilated by aquatic algae and macrophytes 
for use as a nitrogen source.  Ammonia in water may be transferred 
to sediments by adsorption on particulates, or to the atmosphere by 
volatilization at the air-water interface.  Both processes have 
been described as having measurable effects on ammonia levels in 
water; however, the relative significance of each will vary 
according to specific environmental conditions (API, 1981). 

4.4.  Uptake and Transformation in Soils

    Ammonia levels in soils are a function of the balance between 
natural and man-made activities.  As a result of aerobic 
degradation processes, ammonia is the first inorganic nitrogenous 
compound to be released from organic matter together with amines, 
which are rapidly converted to ammonia (Powers et al., 1977).  
Other important sources of ammonia in soil are fertilizers 
(primarily anhydrous ammonia, ammonium nitrate, and urea, which is 
rapidly converted to ammonia), wet and dry deposition, and animal 

    The ammonium cation is relatively immobile in soils, because 
it is adsorbed on the negatively-charged clay colloids present 
in all soils (Wallingford, 1977).  Ammonia may be lost from 
soils by volatilization, especially after the application of 
ammonia fertilizers (Walsh, 1977), sewage, or manures, and by 
uptake of ammonium ions into root systems.  However, the most 
likely fate of ammonium ions in soils is conversion to nitrate by 
nitrification.  Nitrate is, in turn, lost from soils by:  leaching, 
which occurs readily, since it is repulsed by the clay particles; 
denitrification, which occurs rapidly within a few days or weeks in 
warm, moist soils; and by uptake by the plant root system. 


5.1.  Environmental Levels

5.1.1.  Atmospheric levels

    Ammonia is present in the atmosphere in very low 
concentrations, which vary with underlying land use.  In most 
situations, urban atmospheres contain more than non-urban, but 
certain rural areas, for example, those characterized by intensive 
animal husbandry or use of organic manure, have atmospheric ammonia 
levels that exceed urban values.  Atmospheric ammonia levels also 
show a seasonal variation, the highest levels being attained during 
the winter and the lowest during the summer months.  In urban 
areas, the ammonia levels may increase substantially during 
pollution episodes.  However, they do not show any circadian 

    Urban and non-urban atmospheric levels of ammonia at some 
locations around the world are shown in Tables 8 and 9.  It can 
be seen that ammonia levels of 4 - 5 g/m3 and 20 g/m3 are 
typical of non-urban and urban sites, respectively.  Levels of 
particulate NH4+ ions in the atmosphere above the main oceans 
(Atlantic, Pacific, Indian, and Antartic) have been studied; in the 
southern hemisphere, remote from terrestrial sources, the NH4+ 
concentrations were found to be between 10 and 115 ng/m3.  The 
authors concluded that the oceans are a source of ammonia for the 
atmosphere (Servant & Delaporte, 1983). 

    Atmospheric levels of particulate ammonium at some non-urban 
and urban locations around the world are shown in Table 10.  It can 
be seen that concentrations of 1 g/m3 and 4 - 5 g/m3 are typical 
for non-urban and urban sites, respectively. 

5.1.2.  Levels in water

    The concentration of ammonia in surface waters varies 
regionally and seasonally.  Wolaver (1972) studied US Geological 
Survey data for total ammonia and reported average concentrations 
of < 0.18 mg/litre in most surface waters, and around 0.5 mg/litre 
in waters near large metropolitan areas.  Analysis of data from the 
Water Quality Control Information (STORET) System for the years 
1972 - 77 (US EPA, 1979a) showed that, although total ammonia-
nitrogen concentrations in surface waters in the USA tended to be 
slightly lower during summer months than during winter months, the 
percentage of areas in which non-ionized ammonia concentrations 
occasionally exceeded 0.02 mg/litre increased from 11% during 
winter to 23% during summer; these percentages were higher when 
waters had elevated pH values. 

Table 8.  Urban and industrial atmospheric levels of ammonia in a 
few global locationsa
Location              Year      Concentration        Reference
 Germany, Federal 
 Republic of
 Frankfurt-am-Main    pre-1963  8 - 20               Georgii (1963)

 Cagliari             -         37 - 280             Spinazzola et 
                                (highest conc.       al. (1966)
                                in the vicinity
                                of port)

 Tokyo                -         up to 210 (down-     TMRI (1971)
                                wind from two major
 Tokyo                1969      4.8 - 25.8           Okita & 
                                                     Kanamori (1971)
 Tsuruga              -         up to 6.8            FEPCC (1972)

 Bilthoven            1983      5                    Van Aalst 
 Delft                1979-81   4.4                  Van Aalst 

 Seattle, Washington  1975      0.8 - 77.0           Farber & 
                                                     Rossano (1975)
 St. Louis, Missouri  1972-73   up to 17.5           Breeding et al. 
 Five urban sites     -         3 - 60               Hidy (1974)
 in California                  (average 20.0)

 Chino-Corona area,   1975      up to 315            Pitts & 
 California                     (vicinity of         Grosjean (1976)
                                dairy farm)

 Environment of       1967      190                  Saifutdinov 
 metallurgical plant                                 (1966)

 West Berlin           -         up to 97             Hantzsch & 
                                (average 17.6)       Lahmann (1970)
a Adapted from: NRC (1979). Industrial activities include intensive
  farming activities.

Table 9.  Non-urban atmospheric levels of ammonia in a few global 
Location                  Year      Concentration   Reference
Harwell, England          1969      up to 5.1       Healy et al. (1970)
                                    (typical level
                                    0.85 - 1.7)

Maritime stations         pre-1963  2 - 5           Georgii (1963)
(North Sea, Italian
coast, and Hawaii)

Rural and mountain        pre-1963  5 - 8           Georgii (1963)
locations in Switzerland
and the Federal Republic
of Germany

Non-urban locations       -         4 - 5           Robinson & Robbins
                                                    (1968); McKay (1969)

Rural sites in USA        1971      1.4 - 4.2       Breeding et al. (1973)

Boulder, Colorado, USA    1975      2.0 - 3.1       Axelrod & Greenberg

American tropic           1967-68   3.5 - 21.7      Lodge et al. (1974)
                                    (average 10.5)

Non-urban sites in        1972      4.6 - 9.7       Hidy (1974)
California, USA
a Adapted from: NRC (1979).

    In the Netherlands, enhanced ammonium levels are also present 
in waters that are not influenced by surface run-off.  In 
particular, in hydrologically-isolated acidified small lakes, 
concentrations may reach up to 3 mg NH4+-N/litre.  In rural areas 
with high atmospheric ammonia levels, the loading of these small 
lakes with airborne ammonia substances appears to be responsible.  
The highest measured value near intensive pig and poultry farms was 
12 mg NH4+-N/litre (Leuven & Schuurkes, 1984). 

    There are few data on the concentrations of ammonia in 
drinking-water.  This is possibly because of the conversion of most 
of the available ammonia to N-chloramines (mono-, di-, and tri-
chloramines) during the chlorination of drinking-water (Morris, 
1978), which reduces ammonia concentrations to levels below 
analytical detectability.  The presence of these N-chloramines may 
contribute to the taste, odour, and also the potential health 
problems of drinking-water. 

Table 10.  Urban and non-urban atmospheric levels of particulate
ammonium in some global locationsa
Location              Year     Concentration  Reference

 Harwell              -        3 - 4          Healy (1974)
 (troposphere)        1971-73  1.3            Reiter et al. (1976)

 Germany, Federal
 Republic of
 Bavaria              -        1.0            Georgii & Muller
 (lower troposphere)                          (1974)

 28 non-urban sites   1968     0 - 1.2        US EPA (1972)
 Point Arguello,      -        0.36           Hidy (1974)
 Goldstone,           -        0.76           Hidy (1974)


 Ghent                1972     1.3 - 33.0     Demuynck et al. 
                               (severe        (1976)
 Nagoya               1973-74  2.7 - 4.2      Kadowaki (1976)

 Delft                1979-81  4.6            Van Aalst (1984)
 Terschelling         1982     2.7            Van Aalst (1984
 Houtakker            1983     19             Van Aalst (1984)

 Rao                  -        2.2 - 7.2      Brosset et al. (1975)
                               from England)
 United Kingdom
 Tees River Valley    1967     up to 33.0     Eggelton (1969)

Table 10.  (contd.)
Location              Year     Concentration  Reference
 Urban areas          1968     0 - 15.1       US EPA (1972)
 Five cities          1970-72  0 - 21         Lee & Goranson (1976)
 Tuscon, Arizona      1973-74  0 - 6.5        Keesee et al. (1975)
 Los Angeles,         1969-70  2.8 - 3.4      Gordon & Bryan (1973)
 15 urban sites in    -        average 5.3    Hidy (1974)
 Riverside,           1975     up to 30.1     Grosjean et al. 
 California                    (average 7.6)  (1976)
a Adapted from:  NRC (1979).

    Ground water is frequently used as drinking-water, without 
prior chlorination.  Ammonia levels in ground water are usually low 
because the adsorption of the ammonium ion on clay minerals, or its 
bacterial oxidation to nitrate, limit its mobility in soil (Feth, 
1966; Liebhardt et al., 1979).  However, nitrogen fertilizers, 
livestock wastes, or septic tanks may contribute significant 
amounts of ammonia to shallow ground waters, especially those 
underlying poorly-drained soils (Gilliam et al., 1974; Rajagopal, 
1978).  In domestic tap water from Michigan wells averaging 20 m in 
depth, mean levels of ammonia-nitrogen were between 0.04 and 0.18 
mg/litre; the highest reported single value was 0.57 mg/litre from 
a well 12.5 m in depth (Rajagopal, 1978). 

    In wells drilled for research purposes and not supplying 
drinking-water, levels of ammonia-nitrogen in shallow (3 m) wells 
beneath wood and crop land usually averaged less than 2 mg/litre 
(Gilliam et al., 1974).  Levels in shallow (3 - 6 m) ground water 
beneath plots spread with poultry manure varied typically between 1 
and 15 mg NH3-N/litre (Liebhardt et al., 1979); those in ground 
water beneath 29 feedlots averaged 4.5 mg NH3-N/litre and ranged up 
to 38 mg/litre (Stewart et al., 1967).  Levels in hot springs and 
other ground waters have been reported to reach > 1000 mg NH3-
N/litre (Feth, 1966). 

    The ammonia levels present in the runoff of receiving surface 
waters have been measured in various studies.  Kluesner & Lee 
(1974) found that levels ranged from approximately 0.23 mg 
ammonia/litre in the autumn to 1.8 mg ammonia/litre in the early 
spring in the urban runoff of Madison, Wisconsin.  Struzewski 
(1971) reported that ammonia levels in urban storm water ranged 
from 0.1 to 3.2 mg/litre. 

    Only limited data are available on nitrogen pools in the ocean.  
Sderlund & Svensson (1976) used values of 5 g NH3-N/litre for 
deep areas and 50 g NH3-N/litre for near-shore areas and estimated 
an ammonia inventory of approximately 9 x 103 g/litre in coastal 
upwelling systems. 

    Interstitial water in sediments rich in organic matter contain 
higher concentrations of ammonia.  Sholkovitz (1973) reported 
values of 1.4 - 23.8 g ammonia/litre in the interstitial waters 
of the Santa Barbara Basin.  The interstitial water of the Long 
Island Sound, 2 km off shore, contained concentrations ranging 
from 11.2 to 42 g ammonia/litre (Gold-haber & Kaplan, 1974). 

5.1.3.  Levels in soil

    The quantity of ammonia bound to clay in soil has not been 
estimated.  The ammonia present in soil is in dynamic equilibrium 
with nitrate and other substrates of the nitrogen cycle and is 
difficult to measure as its concentration is in constant flux (NRC, 

5.1.4.  Food

    There is very little ammonia in unprocessed food and in 
drinking-water derived from deep ground-water or chlorinated 
sources.  Various salts of ammonia are added to foods (Annex I). 

5.1.5.  Other products

    Ammonium chloride is a common ingredient in expectorant 
cough mixtures and is a component of tobacco smoke (about 
40 g/cigarette) (Sloan & Morie, 1974). 

5.2.  General Population Exposure

    Exposure via inhalation and ingestion must be compared to the 
endogenous production of ammonia in the intestinal tract, which is 
of the order of several grams per day (section 7.1.2).  The 
relative importance of the different sources is indicated in Table 

5.2.1.  Inhalation

    Assuming ammonia and ammonium concentrations in non-urban and 
urban air are 2 and 6 g/m3 and 24 and 25 g/m3, respectively, and 
that the amount of air breathed per day by an individual is 20 m3, 
the intake of total ammonia through inhalation can be calculated to 
be 0.1 - 0.5 mg/day; the amounts exhaled are considerably higher. 

    The average amount of ammonia inhaled from the smoking of one 
cigarette is approximately 42 g (Sloan & Morie, 1974).  Assuming 
an individual smokes 20 cigarettes per day, the inhalation of 
ammonia through cigarette smoking would be 0.8 mg/day. 

5.2.2.  Ingestion from water and food

    Most drinking-water in the USA is chlorinated, which 
effectively eliminates ammonia.  However, assuming the direct 
consumption of 2 litres per day of untreated surface water, at an 
average total ammonia concentration of 0.18 mg/litre (Wolaver, 
1972), the average human uptake from this source would be 0.36 mg 
per day. 

Table 11.  Intake of ammonia from 
different sources
Source                       mg/day
Endogenous                   4000


 Ingestion (food and drink)  ~18

 Inhalation                  < 1

 Cigarette smoking (20/day)  < 1

    Although ammonia is a negligible natural constitutent of food, 
it is formed in the intestine by deamination of the amino groups of 
food proteins.  In addition, ammonium compounds are added in small 
amounts (< 0.01 - 20 g/kg) to various foods as stabilizers, 
leavening agents, flavourings, and for other purposes (FASEB, 
1974).  Information concerning the usual concentrations of ammonium 
salt additives in foods and the estimated total quantities of these 
compounds used for this purpose in the USA in 1970 has been used to 
estimate the average daily intake of 6 ammonium salt additives 
(FASEB, 1974).  The estimates for ammonium bicarbonate, carbonate, 
hydroxide, monobasic phosphate, dibasic phosphate, and sulfate were 
42, 0.3, 7, < 0.1, 6, and 20 mg, respectively.  No estimate was 
available for ammonium chloride.  On this basis, the average daily 
ammonia intake from these compounds has been calculated to be 
18 mg. 

5.2.3.  Dermal exposure

    Very few data are available concerning levels of dermal 
exposure to ammonia or ammonium compounds.  Dermal exposure of 
human beings mainly occurs through the use of household cleaning 
products, accidental spillage, or under occupational conditions. 

5.3.  Occupational Exposure

    Exposure to ammonia or ammonium compounds can occur in certain 
occupations involving their production, transportation, and use in 
agricultural and farm settings, during fertilizer application, or 
as a result of animal waste decomposition. 

    It is estimated that about half a million workers in the USA, 
in a wide variety of occupations, have potential exposure to 
ammonia (NIOSH, 1974). 

    Ammonia is generated as a by-product in a wide variety of
industrial activities, and workplace atmospheric concentrations 
are given in Table 12.  Municipal waste incineration and gas-fired 
industrial incinerators generate concentrations of 20 and 0.4 
mg/m3, respectively (NRC, 1979) and shipboard and quayside levels 

for natural gas tankers may be about 30 mg/m3 (Avot et al., 1977).  
Levels in intensive livestock-rearing buildings are frequently 
reported to be up to 30 mg/m3 (Poliak, 1981) or more (Anderson et 
al., 1964b; Taiganides & White, 1969; Marschang & Petre, 1971).  
Ammonia levels in dairy farms and cattle-fattening facilities in 
Romania have been reported to range from 0.7 mg/m3 to 140 mg/m3 
(Marchang & Crainiceanu, 1971; Marschang & Petre, 1971). 

    Maximum daily intake from work-place concentrations such as 
these would normally be less than 300 mg/day and this may be 
compared with endogenous production (Table 11). 

    Occupational exposure limits for some countries in the world 
are shown in Table 13. 

5.4.  Exposure of Farm Animals

    Farm animals are exposed to ammonia through feed containing 
urea or various ammonium salts and to atmospheric ammonia due to 
bacterial decomposition and volatilization of ammonia from animal 

5.4.1.  Oral exposure

    (a)   Non-protein nitrogen additives

    Urea and various ammonium salts have been used for several 
years as non-protein nitrogen sources in ruminant nutrition.  It is 
used much more widely for this purpose than the ammonium compounds.  
Urea is hydrolysed to ammonia and carbon dioxide by the ruminal 
bacteria and, therefore, represents a source of ammonia exposure.  
The ammonia released is used by the ruminal microorganisms to 
synthesize microbial protein, which is then digested in the small 
intestine of the ruminant and used as a source of dietary amino 

    (b)   Refeeding of livestock wastes

    Results of studies on the refeeding of livestock wastes 
(Bhattacharya & Taylor, 1975; Arndt et al., 1979; Smith & Wheeler, 
1979) have indicated that manure could be of nutritive value, 
salvaging some nutrients ordinarily lost (Yeck et al., 1975).  The 
non-protein nitrogen (e.g., urea, uric acid) present in livestock 
wastes is available to ruminants because of microbial conversion in 
the rumen.  Wastes are of limited value for monogastrics such as 

Table 12.  Ammonia levels in some industrial processesa
Operation                             Level (mg/m3)
Machinery manufacturing (cleaning)    10.5

Diazo-reproducing machine             5.6

Mildew-proofing                       87.5

Electroplating                        38.5

Galvanizing, ammonium chloride flux   7 - 61.6

Blueprint machine                     7 - 31.5

Printing machine                      0.7 - 31.5

Etching                               25.2

Refrigeration equipment               6.3 - 25.9

Cementing insoles                     5.6 - 19.6

Chemical mixing                       42 - 308

Fabric impregnating                   ND
a From: NIOSH (1974).    
ND = Not detectable.

5.4.2.  Inhalation exposure

    (a)   Ruminants

    Marschang & Crainiceanu (1971) measured the ammonia 
concentrations in air (sampled at nose level of animals) in calf 
stables at 4 dairy farms in Romania.  The ammonia levels ranged 
from 0.7 to 140 mg/m3 (1 - 200 ppm).  Most of the observed values 
greatly exceeded the permissible upper limit of 18.2 mg/m3 (26 
ppm).  In a second study, Marschang & Petre (1971) measured the 
ammonia concentrations in the air of 3 cattle-fattening facilities 
in Romania in which the animals were being fed in total 
confinement; the capacities of the 3 operations were 3000, 3000, 
and 4900 animals.  The ammonia concentration ranged from 2 to 
1400 mg/m3 (3 to 200 ppm).  In general, the ammonia content was 
below the admissible upper limit during the summer months but 
exceeded it during the winter months, when extremely high 
concentrations were observed.  These high concentrations were 
primarily due to the blocking of the ventilation system, in order 
to maintain necessary stall temperatures.  The highest value 
(1400 mg/m3) was measured when the cleaning mechanism of the 
manure canals malfunctioned. 

Table 13.  Occupational exposure limits (mg/m3)a
Country                     Ammonia    Ammonium 
                   Ammonia  chloride   sulfamate
                   A   B    A   B      A   B
Australia          18       10         10

Belgium            18       10         10

Czechoslovakia     40  80

Finland            18

German Democratic      20       10

Germany, Federal   35       10         15
 Republic of

Hungary            20

Italy              20                  10

Japan              18

Netherlands        18       10         10

Poland             20

Romania            20  30   5   10     10  15

Sweden             18  36

Switzerland        18       6          10

USA (NIOSH/OSHA)   35                  15
 (ACGIH)           18  27   10  20     10  20

USSR               20                  10

Yugoslavia         35                  15

Council of Europe  18                  15
a From:  ILO (1970).
Column A represents average values.
Column B is higher quoted limits, which may 
 variously be ceiling values, short-term exposure 
 limits, etc.

Note: Occupational exposure levels and limits are derived in 
      different ways, possibly using different data, and expressed 
      and applied in accordance with national practices.  These 
      aspects should be taken into account when making comparisons. 

    (b)   Swine

    The increased use of confined housing for swine has caused 
concern about the purity of the air within the buildings and its 
effects on swine growth.  Bacterial decomposition of excreta 
collected and stored beneath slotted floors in enclosed buildings 
produces a number of gases, including ammonia, carbon dioxide, 
hydrogen sulfide, and methane (Curtis, 1972).  Miner & Hazen (1969) 
reported a range of ammonia concentrations of 4.2 - 24.5 mg/m3 
(6 - 35 ppm) determined 30 cm above the floor level in a swine-
rearing facility.  Levels in solid-floor confinement units were 
normally found to be < 35 mg/m3 (< 50 ppm), but they could be 
higher during cold months, when ventilation was at a minimum, 
particularly when the floor was heated (Taiganides & White, 1969).  
The normal ammonia concentration in the air above slotted floors 
was reported to be ~7 mg/m3 (~10 ppm), but this was increased by a 
factor of 5 - 10 by stirring the stored manure. 

    (c)   Poultry

    Poultry are usually exposed to ammonia, together with hydrogen 
sulfide, carbon dioxide, and methane, in the air of poultry houses.  
These compounds result from bacterial action on poultry wastes 
(Ringer, 1971).  In cold climates, proper ventilation rates cannot 
be maintained in many poultry houses, and gas production in the 
manure may build up to toxic levels.  Ammonia has been found at 
concentrations exceeding 35 mg/m3 (50 ppm) in modern poultry 
houses, and at up to 140 mg/m3 (200 ppm) in poorly-ventilated 
poultry houses (Anderson et al., 1964b; Valentine, 1964).  The 
toxic effects in poultry can be prevented through proper management 
practices (Lillie, 1970). 


6.1.  Microorganisms

    Many microorganisms are able to use ammonia as a nitrogen 
source for cellular nutrition.  Nitrifying organisms derive energy 
from the oxidation of ammonia to nitrate.  High levels of ammonia 
and high pH, which may occur, for example, in waste waters or 
fertilized fields, may inhibit nitrification and cause persistance 
or accumulation of ammonia and/or nitrite.  Improper maintenance of 
conditions in waste treatment processes may result in ammonia 
overloading and inhibition of the nitrification process, with 
consequent ammonia and/or nitrite pollution of receiving surface 
waters.  Other soil microorganisms may also be inhibited; fungi 
reportedly are more sensitive than bacteria.  However, these 
inhibitory effects are temporary.  Aqueous and gaseous ammonia have 
been used to control microbial growth in stored fruits, hay, and 
grains.  Ammonia treatment has proved more effective against fungal 
than against bacterial spoilage of food. 

    The bacterial species  Escherichia coli and  Bacillus subtilis 
were found to be sensitive to ammonium chloride (NH4Cl) (Deal et 
al. 1975); exposure to 1100 mg NH3/litre killed 90% of an  E. coli  
population in 78 min.   B. subtilis, an aerobic, spore-forming 
bacterium, was destroyed in less than 2 h in a solution of 620 mg 
NH3/litre.  Anthonisen et al. (1976) and Neufeld et al. (1980) 
studied NH3 inhibition of the bacterium  Nitrosomonas (which 
converts ammonium to nitrite) and the bacterium  Nitrobacter (which 
converts nitrite to nitrate).  The nitrification process was 
inhibited by NH3 at a concentration of 10 mg/litre (Neufeld et al., 
1980).  Concentrations that inhibited  Nitrosomonas (10 - 150 
mg/litre) were greater than those that inhibited  Nitrobacter 
(0.1 - 1.0 mg/litre), and NH3, not NH4+, was reported to be the 
inhibiting chemical species (Anthonisen et al. 1976). 
Acclimatization of the nitrifying bacteria to NH3, temperature, 
and the number of active nitrifying organisms are factors that may 
affect the inhibitory concentrations of NH3 in a nitrification 

    Langowska & Moskal (1974) investigated the inhibitory effects 
of NH3 on bacteria during 24-h exposure periods.  Ammonifying and 
denitrifying bacteria were most resistant to NH3; proteolytic and 
nitrifying bacteria were the most sensitive.  Concentrations of up 
to 170 mg NH3/litre did not adversely affect denitrifying and 
ammonifying bacteria; a concentration of 220 mg/litre caused a 
reduction in metabolic processes.  Proteolytic bacteria were 
unaffected at concentrations of 0.8 mg NH3/litre, but were affected 
at 13 - 25 mg/litre. 

    Jones & Hood (1980) conducted studies on 2 species of 
 Nitrosomonas isolated from 2 wetland environments, one estuarine 
and the other fresh water.  At 30 C and pH 8.0, the estuarine 
isolate showed peak ammonium oxidation activity at 18 mg NH3/litre; 
activity gradually declined to 30% of the peak at 80 mg NH3/litre.  
However, the fresh-water isolate was not inhibited by ammonia 
concentrations of up to 80 mg NH3/litre. 

    Application of anhydrous ammonia to soil may strongly affect 
soil microorganisms; however, the effect has been attributed more 
to alterations in pH than to ammonia toxicity  per se.  Henis & Chet 
(1967) found that ammonia reduced sclerotial germinability of the 
fungus  Sclerotium rolfsii only when the soil pH rose to 9.8 or 
higher.  According to Mller & Gruhn (1969), fungi were more 
sensitive than bacteria to ammonia application, the fungi 
disappearing at pH values above 8.  At pH 8.38, bacterial numbers 
initially decreased but then increased above control levels, 7 days 
after application, with an increased number of protein-decomposing 
and nitrifying forms. 

    Ammonia has been used to control microbial growth in food and 
cattle feed.  The growth of mould  (Penicillium digitatum) on fresh 
fruit was inhibited by 70 - 300 mg ammonia/m3 in the air, either 
applied directly or in the form of ammonia-releasing compounds 
(Eckert et al., 1963; Eckert, 1967).  Anhydrous ammonia has also 
been used to prevent spoilage in high-moisture hay (Lechtenberg et 
al., 1977; Wilkinson et al., 1978; Butterworth, 1979) and cattle 
feed derived from corn leaves and stalks (Johanning et al., 1978).  
Ammonium hydroxide and ammonium isobutyrate were shown to control 
the growth of mould in stored corn (Bothast et al., 1973, 1975a,b; 
Rempel, 1975; Peplinski et al., 1978).  Periodic addition of 
ammonia to stored corn, to a total of 30.4 g/kg, prevented the 
growth of mould, but was not fully effective as a bactericide 
(Peplinski et al., 1978). 

6.2.  Plants

    Ammonia may affect vegetation directly by acting on plant 
structure and function, and, indirectly, via its influence on soil 
condition after being deposited.  The effects of NH3 are shown in 
Fig. 1. 

6.2.1.  Terrestrial plants

    It is well recognized that nitrogen plays an important role in 
both plant metabolism and growth.  The principal nitrogen sources 
are ammonium and nitrate ions.  Ammonia is used primarily by the 
root system, but uptake of non-ionized ammonia or ammonium salts by 
the leaves also occurs.  Ammonia is a nitrogen source for the 
synthesis of proteins.  This use of ammonia in the synthesis of 
organic molecules can be regarded as a process for storing a 
valuable nutrient, but is also an important detoxifying mechanism.  
As ammonia is toxic, its uptake in large quantities can place a 
severe strain on the carbohydrate metabolism.  Since carbohydrates 
are used in the synthesis of amino acids and amides, carbohydrate 
availability is an important factor in ammonia metabolism. 


    Manifestations of ammonia toxicity can be traced to several 
metabolic disturbances.  Both photosynthetic and respiratory 
pathways are affected adversely by ammonia.  There is a direct 
relationship between ammonia concentration and respiratory 
metabolism, including oxygen uptake, glycolysis, and the 
tricarboxylic acid cycle (Matsumoto et al., 1976).  Ammonium ions 
may restrict photosynthesis through the uncoupling of noncyclic 
photophosphorylation in isolated chloroplasts (Gibbs & Calo, 1959; 
Losada & Arnon, 1963), though the mechanism of action is not known 
(Losada et al., 1973).  It is well documented that uncoupling leads 
to an increase in reducing power in the cell.  There is evidence 
that 1 - 3 mmol ammonium inhibits respiration in plants (Wedding & 
Vines, 1959; Vines & Wedding, 1960).  It is suspected that similar 
or identical inhibition occurs in ammonium toxicity in animals.  
The site of toxicity is thought to be in the electron-transport 
system; specifically, at the oxidation of NADH to NAD.  This may 
have a mechanism similar to the interference by ammonium ion with 
electron transfer in the photosynthetic reaction. 

    High atmospheric levels may have direct toxic effects.  Plant 
growth is inhibited by a decrease in the carbohydrate production as 
a consequence of inhibition of photosynthesis (Losada & Arnon, 
1963).  Ammonium increases the permeability of the cell membrane 
causing plasmolysis and necrosis.  Furthermore, the flexibility of 
cells may be decreased, which results in an increased sensitivity 
to frost.  Excess ammonia can be detoxified as long as amino acids 
are converted in the presence of carbohydrates (Fig. 1) (Van der 
Eerden, 1982). 

    Most data on the toxic exposure of plants to ammonia have been 
derived from controlled fumigation studies.  Such experiments have 
provided the following relative susceptibilities to ammonia: 
leaves > stems, fungi, and bacteria < seeds, sclerotia, and 
animals (McCallan & Setterstrom, 1940). 

    An exposure of 175 mg/m3 (250 ppm) for 4 min produced 50% 
foliar necrosis in tomatoes, whereas the same foliar injury was 
only produced in buckwheat and tobacco with exposure to 700 mg/m3 
(1000 ppm) for 5 and 8 min, respectively (Thornton & Setterstrom, 
1940).  Zimmerman (1949) reported that fumigation with ammonia at 
28 mg/m3 (40 ppm) for 60 min injured tomato, sunflower, and coleus 
completely, and a concentration of 2.1 mg/m3 (3 ppm) severely 
injured mustard (Benedict & Breen, 1955).  Other plant parts are 
more resistant to ammonia injury than the foliage.  Thornton & 
Setterstrom (1940) found 50% injury in tomato stems after exposure 
to 700 mg/m3 (1000 ppm) for 60 min.  Barton (1940) observed that 
moist spring rye seeds were killed in a 4-h exposure to 700 mg 
ammonia/m3 (100 ppm), whereas moist radish seeds were still viable 
after 16 h.  Exposure to a concentration of 175 mg/m3 (250 ppm) for 
16 h reduced germination of rye seeds by half, but had no effect on 
radish seeds. 

    Foliar injury is the most common toxic effect of anhydrous 
ammonia on vegetation (Linzon, 1971).  In broad-leaved woody plants 
exposed to high concentrations of ammonia, the injury begins as 

large, dark green water-soaked areas on leaves, which darken into 
black or brownish-gray bifacial necrotic lesions, widely 
distributed over the leaf surface.  In lightly injured leaves, 
these symptoms occur mainly on the upper surface.  Conifer foliage 
injured by ammonia exposure darkens to shades of gray-brown, 
purple, or black.  The entire needle is usually affected.  
Abscission of severely damaged leaves is often seen in broad-leaved 
and conifer species.  On trees or shrubs with crowded leaves, 
injury may be confined to particular sections of the leaf.  
Occasionally, the foliage of woody species turns a variety of 
colours, mimicking autumn colours.  Symptoms of injury in 
herbaceous plants are more variable, ranging from irregular, 
bleached, bifacial, necrotic lesions to dark upper-surface 
discolouration (Treshow, 1970).  Grasses and cereal grains develop 
tan to reddish-brown marginal or interveinal necrosis, and broad-
leaved weeds show red-brown to dark-brown upper surface 
discolouration on terminal or marginal portions of the leaf 
(Benedict & Breen, 1955).  Coleus leaves lose their brilliant 
colour after exposure to ammonia and appear green (Zimmerman, 
1949).  Injury to flowers by ammonia is rarely seen in the field, 
but the development of small necrotic spots on azalea flowers has 
been reported following ammonia exposure (Treshow, 1970). 

    Although parts of plants, other than the foliage, are less 
susceptible to the injurious effects of ammonia (McCallan & 
Setterstrom, 1940), injury to apples, peaches, and other fruits and 
vegetables, accidentally exposed during cold storage, has been 
reported (Ramsey, 1953).  Apparently, ammonia entered the fruit and 
turned red-pigmented tissues black, or brown, and yellow tissues, 
dark-brown.  Immediately on exposure to ammonia, the outer skins of 
red onions became greenish-black, and the skin of yellow and brown 
onions became dark brown.  These colour changes were usually 
permanent.  Fumigation of fruit with ammonia also caused overall 
darkening of the skin.  Peaches and apples showed such symptoms at 
140 mg/m3 (200 ppm) and 210 mg/m3 (300 ppm), respectively (Brennan 
et al., 1962).  These symptoms of injury were similar to those seen 
on fruits injured by the accidental release of ammonia. 

    In studies in the Netherlands, several vegetables and trees 
showed leaf damage by necrosis, growth reduction, and increased 
frost senstivity at concentrations of 75 g/m3 (annual average), 
600 g/m3 (during 24 h), and 10 000 g/m3 (during 1 h) (Van der 
Eerden, 1982).  The sensitivity of pine trees to exposure to 
ammonia differed between species (den Boer & Bastiaens, 1984).  A 
survey is given in Table 14.  Airborne ammonium sulfate deposits 
damaged the needles of pine trees.  Owing to the enhanced uptake of 
ammonium, the excretion of potassium, magnesium, and calcium 
increases, often resulting in potassium and/or magnesium 
deficiency, which may lead to premature shedding of needles 
(Roelofs et al., 1985). 

    Effects of ammonia on the root system have generally been 
studied by exposing the roots to different aqueous ammonium 

Table 14.  Relative sensitivity of some pine trees to NH3a
High sensitivity      Moderate sensitivity  Low sensitivity
 Picea abies          Picea omorika         Pinus sylvestris
 Picea sitchensis     Pinus nigra var.       Pinus nigra nigra
 Taxus                 maritima               Tsuga canadensis
 Cupressus leylandii  Taxus baccata         Taxus media
                      Pseutsuga menziesii   Pinus mugo var. mughus
a From:  den Boer & Bastiaens (1984).

    Exposure of tomato seedlings to ammonium solutions as the sole 
nitrogen source showed reduced growth.  The root system was 
sparsely branched and discoloured and the stem was easily bruised.  
There was considerable wilting of leaves, which developed marginal 
necrosis (Pierpont & Minotti, 1977).  Earlier, Maynard &  Barker 
(1969), using cucumber  (C. sativus), bean  (P. vulgaris), and pea 
 (Pisum sativum L.) in sand culture, demonstrated that ammonium 
toxicity was generally characterized by an immediate reduction in 
growth rate, wilting, marginal necrosis, interveinal chlorosis of 
terminal leaves and, finally, death of the entire plant.  However, 
these symptoms did not occur in the ammonium medium with added 
calcium carbonate (CaCO3) (Maynard & Barker, 1969; Pierpont & 
Minotti, 1977).  Several studies have shown that an increase in the 
ammonium concentration is more deleterious to root than to shoot 
growth (Bennett et al., 1964; Haynes & Goh, 1977).  Warncke & 
Barber (1973) observed that the ratio of root dry weight to shoot 
dry weight decreased significantly with increasing concentrations 
of nitrogen, but was not affected by the ammonium-to-nitrate ratio.  
The roots appeared darker and less branched.  The authors 
attributed the observed decrease in root production to greater 
acidity around the roots of ammonium-fed plants (Klemm, 1967; 
Warncke & Barber, 1973). 

    In the Netherlands, field observations and experiments have 
shown effects of ammonia and ammonium on pine forests, and 
heathland vegetation (Heil & Diemont, 1983; Van Breemen & Jordens, 
1983; den Boer & Bastiaens, 1984; Roelofs, in press; Schuurkes, in 
press).  In the United Kingdom, ombrotrophic mires (upland bogs 
deriving water only from rain) are affected by eutrophication (Lee, 
1985).  Forest ecosystems in the Federal Republic of Germany may 
also suffer from ammonia exposure (Hunger, 1978; Ulrich, 1983).  
Although only little information is available for other countries, 
it is expected that similar effects may occur in Belgium, Denmark, 
and the northwestern part of France, where high ammonia emissions 
occur as a consequence of the production of animal manure (Buysman 
et al., 1985). 

    The condition of forests may deteriorate as a consequence of 
direct exposure to ammonia.  Pine trees in areas near intensive 
livestock farms are particularly affected (Hunger, 1978; Janssen, 
1982).  In the Netherlands, there is a clear correlation between 
ammonia emission and forest condition (Van Aalst, 1984).  The 
damage observed is the result of both direct and indirect effects, 
and it is often difficult to distinguish between the two. 

    Field observations and experiments have shown deleterious 
effects on pine trees, namely: 

    -   decreased vitality (growth reduction and necrosis);

    -   higher susceptibility to fungal diseases and attack
        by insects; and

    -   increased sensitivity to meteorological stress
        factors, e.g., hard frost.

Most of these phenomena can be explained in terms of disturbed 
nutrient budgets in trees.  Enhanced ammonium sulfate uptake 
results in the excretion of essential nutrients, such as potassium 
and magnesium, by the needles, and the uptake of these ions by the 
root system is inhibited as a result of ammonium accumulation and 
cation leaching in soils (den Boer & Bastiaens, 1984; Roelofs, in 
press).  Increased ammonium uptake ultimately leads to enhanced 
nitrogen levels in the leaves of beech (Nihlgard, 1970) and pine 
tress (Roelofs et al., 1985). 

    More attention is being paid to the role of ammonium in the 
forest dieback in Europe (Nihlgard, 1985). 

    Heather communities on poorly-buffered, slightly-acidic, and 
nutrient-poor heathland soils are also disturbed as a result of the 
deposition of airborne ammonia compounds, the number of plant 
species declining in acidified and nitrogen-enriched heathland 
soils.  A succession from heather-dominated to grass-dominated 
heathlands has been observed (Heil & Diemont, 1983; Roelofs, in 
press).  The same effects can be expected in other western European 
countries where similar plant communities are present. 

6.2.2.  Aquatic plants

    In the aquatic environment, nitrogen plays an important role in 
determining the composition of phytoplankton and vascular plant 
communities; in some cases, it can act as a limiting factor in 
primary production.  Ammonia is important in nitrogen metabolism, 
because it functions as a nitrogen source in the synthesis of amino 

    Most species can use either ammonium or nitrate as the sole 
nitrogen source, though, when both forms are available, ammonium is 
used first.  Uptake takes place through both roots and leaves.  The 
relative importance of ammonium as a nutrient depends on the 
absolute concentration and the ratio of ammonium to nitrate.  
Assimilation of ammonium is less expensive in terms of energy than 
nitrate, because the first metabolic step in which nitrate is 
reduced is not needed.  Although ammonia is an important nutrient, 
it appears to be toxic at higher concentrations.  Its uptake in 
large quantities may put a severe strain on the carbohydrate 
metabolism of the species, because carbon skeletons are used for 
detoxification (Bidwell, 1974).  Increasing ammonia levels within 

the cell inhibit the utilization of nitrate.  Ammonia solutions 
seem to be more toxic at high than at low pH, indicating that 
toxicity is probably due primarily to NH3 rather than to NH4+. 

    Surface waters that are poorly buffered, nutrient poor, and 
hydrologically dependent on rainfall and/or snow melt are most 
sensitive to ammonia.  Deposition of ammonia and other nitrogen 
compounds may contribute significantly to the nitrogen enrichment 
of susceptible waters.  Ombrotrophic mire plant communities can be 
altered by this atmospheric pollutant (Lee, 1985).  In these 
 Sphagnum-dominated wetlands, seed plants become more dominant.  In 
small, poorly-buffered and nutrient-poor clear water lakes, both 
water composition and macrophyte composition are altered.  
Atmospheric ammonia deposition plays a major role in the 
acidification and nitrogen enrichment of surface waters in the 
Netherlands (Schuurkes, in press).  Typical plant species belonging 
to the Littorellion alliance disappear from acidified waters.  
These species may be supressed by the luxuriant growth of  Sphagnum 
species and  Juncus bulbosus.  Ammonium enrichment enables the last 
two species to form extremely high biomasses (Roelofs et al., 1984; 
Schuurkes, in press; Schuurkes et al., 1985).  It should be noted 
that these changes in the plant community also influence the 
structure of the animal population. 

6.2.3.  Fresh-water plants

    Experimental data concerning the toxicity of ammonia for fresh-
water phytoplankton are limited.  Przytocka-Jusiak (1976) reported 
the effects of ammonia on the growth of  Chlorella vulgaris.  A 50% 
inhibition was seen in 5 days of exposure to a concentration of 
2.4 mg NH3/litre; complete growth inhibition occurred in 5 days 
at 5.5 mg/litre.  The NH3 concentration resulting in 50% survival 
of  C. vulgaris after 5 days was found to be 9.8 mg/litre.  A  C. 
 vulgaris strain in which the tolerance to elevated ammonia 
concentrations was enhanced by prolonged incubation of the alga in 
ammonium carbonate solutions was isolated by Przytocka-Jusiak et 
al. (1977).   C. vulgaris was reported to grow well in solutions 
containing 4.4 mg NH3/litre, but growth was inhibited at 7.4 
mg/litre (Matusiak, 1976).  Tolerance to elevated concentrations of 
NH3 seemed to show a slight increase, when other forms of nitrogen 
were available to the alga, rather than when ammonia was the only 
form of nitrogen in the medium.  Bretthauer (1978) found that a 
concentration (assuming pH 6.5 and 30 C) of 0.6 mg NH3/litre 
killed  Ochromonas sociabilis, and that, at 0.3 mg/litre, 
development of the population was reduced.  Concentrations of 0.06 
to 0.15 mg NH3/litre had an insignificant effect on growth, and 
concentrations of 0.015 to 0.03 mg/litre enhanced growth. 

    Ammonia at concentrations exceeding 2.5 mg NH3/litre inhibited 
photosynthesis and growth in the algal species  Scenedesmus obliquus  
and inhibited photosynthesis in the algae  Chlorella pyrenoidosa, 
 Anacystis nidulans, and  Plectonema boryanum (Abelovich & Azov, 
1976).  Mosier (1978) reported that NH3 concentrations causing a 
50% reduction in oxygen production by the green alga  Chlorella 
 ellipsoidea and blue-green alga  Anabaena subcylindrica were 
16.0 x 10-8 and 251.0 x 10-8 g NH3-N/cell, respectively. 

    The rate of photosynthesis in the blue-green alga  P. boryanum  
was stimulated by NH4+, but inhibited by NH3 (Solomonson 1969); the 
magnitude of these effects was dependent on the sodium-potassium 
composition of the suspension media.  Inhibition of photosynthesis 
by NH3 was associated with a conversion of inorganic polyphosphate, 
stored in the cells, to orthophosphate. 

    Champ et al. (1973) treated a small natural water pond with 
ammonia to achieve a mean concentration of 25.6 mg NH3/litre.  A 
diverse population of dinoflagellates, diatoms, desmids, and blue-
green algae was present before ammonia treatment.  Twenty-four 
hours after treatment, the mean number of phytoplankton cells/litre 
was reduced by 84%.  By the end of 2 weeks (3.6 mg NH3/litre), the 
original concentration of cells had been reduced by 95%. 

    Some research has been carried out to investigate the possible 
use of ammonia as an aquatic herbicide.  Champ et al. (1973) 
reported virtually complete eradication of rooted aquatic 
vegetation (water shield,  Brasenia schreberi, and American lotus, 
 Nelumbo sp.).  The NH3 concentration was 25.6 mg/litre 24 h after 
ammonia addition, and 3.6 mg/litre, 2 weeks later.  The use of high 
concentrations of ammonia to eradicate aquatic vegetation has been 
described by Ramachandran & Ramaprabhu (1976) and Ramachandran et 
al. (1975). 

    In experiments with  Potamogeton lucens, Litav & Lehrer (1978) 
observed that ammonia caused appreciable injury to detached 
branches.  Ammonia inhibition of the growth of Eurasian 
watermilfoil  (Myriophyllum spicatum) affected both the length and 
weight of roots and shoots (Stanley, 1974). 

    Grube (1973) found that  Sium erectum was slightly injured at 
15 mg NH3-N/litre, and completely eradicated at 35 mg/litre after a 
10-week exposure.   Callitriche sp. showed slight injury at 5 mg 
NH3-N/litre, and the lethal dose was between 10 and 15 mg/litre.  
Injury was estimated from the amount of black colouring and the 
death of leaves.  Roelofs et al. (1984) reported that exposure of 
the isoebid  Littorella uniflora to 50 mol NH4+/litre for 10 weeks 
resulted in excretion of an equivalent amount of potassium, which 
may lead to discolouration and starvation. 

    Changes in the vegetation in 2 rivers subject to increased 
pollution from agricultural fertilizers, urban sewage, and 
industrial wastes, were studied by Litav & Agami (1976), who 
attributed the changes in the composition of the plant species 
primarily to a combination of ammonia and detergents.  Agami et al. 
(1976) transplanted 7 species of "clean water" macrophytes to 
various sections of a river, and found that ammonia affected only 
 Nymphaea caerulea. 

6.2.4.  Salt-water plants

    A concentration of 0.24 mg NH3/litre retarded the growth of 
most of 10 species of benthic diatoms cultured for 10 days by 
Admiraal (1977).  Pinter & Provasoli (1963) found that  Coccolithus 

 huxleyi was the most sensitive, and  Pavlova gyrans and  Hymenomonas  
sp. the most tolerant to ammonium sulfate with intermediate tolerance 
exhibited by  Syracosphaera sp. and  Ochrosphaera neapolitana. 

    Shilo & Shilo (1953, 1955) reported that the euryhaline alga 
 Prymnesium parvum was effectively controlled by applications of 
ammonium sulfate, which exerted a lytic effect that decreased with 
increasing pH, indicating that NH3 and not NH4+ is responsible for 
the lytic activity of ammonium sulfate on  P. parvum.  It was 
reported by Byerrum & Benson (1975) that added ammonium ion at 
concentrations found to stimulate the photosynthetic rate also 
caused the alga  Amphidinium carterae to release up to 60% of fixed 
14CO2 to the medium. 

    Natarajan (1970) found that the concentrations of fertilizer 
plant effluent that were toxic for natural phytoplankton 
(predominantly diatoms) ranged between 1.1 and 11 mg NH3/litre.  
Thomas et al. (1980) concluded that increased ammonium 
concentrations found near sewage outlets would not be inhibiting to 
phytoplankton in the vicinity.  Provasoli & McLaughlin (1963) 
reported that ammonium sulfate was toxic for some marine 
dinoflagellates, but only at concentrations far exceeding those in 
sea water. 

6.3.  Aquatic Invertebrates

    The toxicity of ammonia has been less extensively studied in 
invertebrates than in fish.  Most of the available invertebrate 
data consists of studies on arthropods, primarily crustaceans and 
insects.  Many of these studies are laboratory tests in which test 
animals were exposed to known concentrations of a toxic agent for 
specified periods of time.  Results may be expressed as a median 
lethal concentration (LC50) for a given time period (e.g., 48-h 
LC50) or, occasionally, as an effective concentration (EC), that 
is, the concentration at which the test animal is completely 
immobilized, though it might still be respiring (e.g., 48-h EC).  
Another method of reporting test results is as the estimated time 
required to kill 50% of a test population (LT50) at a given 
concentration of toxin (e.g., LT50 = 250 min). 

6.3.1.  Fresh-water invertebrates: acute toxicity

    The acute toxicity of ammonia for  Daphnia magna has been 
studied by Parkhurst et al. (1979, 1981) and Reinbold & Pescitelli 
(1982a) with reported 48-h LC50s values of 2.08 and 4.94 mg 
NH3/litre.  DeGraeve et al. (1980) reported a similar 48-h LC50 
value for  Daphnia pulicaria of 1.16 mg NH3/litre.  A threshold 
toxicity value for  D. magna of 2.4 - 3.6 mg NH3/litre lake water 
was reported by Anderson (1948).  Threshold concentration was taken 
as the highest concentration that would just fail to immobilize the 
test animals, under conditions of prolonged exposure (Anderson, 
1948).  A minimum lethal concentration of 0.55 mg NH3/litre was 
reported for  D. magna by Malacea (1966), and a 24-h LC50 value of 
1.50 mg NH3/litre was reported by Gyre & Olh (1980) for  Moina 

    Buikema et al. (1974) reported an EC50 for NH3 toxicity in the 
rotifer,  Philodina acuticornis, to be 2.9 - 9.1 mg NH3/litre 
(calculated using reported pH values of 7.4 - 7.9).  Tests of 
ammonia toxicity for the flatworm,  Dendrocoelum lacteum (Procotyla 
 fluviatilis), and a tubificid worm  (Tubifex tubifex) gave LC50 
values of 1.4 and 2.7 mg NH3/litre, respectively (Stammer, 1953). 

    Thurston et al. (1984a) conducted 25 flow-through toxicity 
tests with 3 mayfly, 2 stonefly, 1 caddisfly, and 1 isopod species; 
all tests were conducted with water of similar chemical 
composition.  The 96-h LC50 values ranged from 1.8 to 5.9 mg 
NH3/litre.  The results also indicated that a 96-h test is not long 
enough to determine the acutely lethal effects of ammonia on the 
species tested, because an asymptotic LC50 was not always obtained 
within 96 h.  Percentage survival data were reported for some 
mayfly, stonefly, and caddisfly tests in which LC50 values were not 
obtained; there was 60 - 100% survival at test concentrations 
ranging from 1.5 to 7.5 mg NH3/litre.  Gall (1980) tested NH4Cl 
with  Ephemerella sp. (near  excrucians).  Organisms were exposed 
to ammonia for 24 h, followed by 72 h in ammonia-free water; 
mortality observations were made at the end of the overall 96-h 
period. An EC50 value of 4.7 mg NH3/litre was obtained.  Hazel et 
al. (1979) reported a LC50 value of 8.0 mg NH3/litre for the beetle 
 Stenelmis sexlineata. 

    No deaths occurred in ammonia toxicity tests conducted on scud, 
 Gammarus lacustris, or  D. magna, using dilution water from a 
river, after a 96-h exposure to 0.08 mg NH3/litre.  In a second 
test, using river water buffered with sodium bicarbonate, 13% 
mortality occurred with scud at the several concentrations tested, 
including the highest and lowest of 0.77 and 0.12 mg NH3/litre, 
respectively; 7 and 13% mortality occurred with  D. magna at the 
same concentrations (Miller et al., 1981). 

    Five fresh-water mussel species,  Amblema p. plicata, Anodonta 
 imbecillis, Corbicula manilensis, Cyrtonaias tampicoensis, and 
 Toxolasma texasensis, were exposed for 165 h to a concentration of 
0.32 mg NH3/litre;  T. texasensis was most tolerant to ammonia, and 
 A. p. plicata was most sensitive (Horne & McIntosh, 1979).  During 
the tests, the more tolerant species generally had their shells 
tightly shut, whereas the least tolerant species continued 
siphoning or had their mantles exposed.  In 2 studies, acute 
exposure of the fresh-water crayfish,  Orconectes nais, to ammonium 
chloride gave LC50 values of 3.15 and 3.82 mg NH3/litre, 
respectively (Evans, 1979; Hazel et al., 1979). 

6.3.2.  Fresh-water invertebrates: chronic toxicity

    Few studies have been conducted on the long-term exposure of 
fresh-water invertebrates to ammonia.  In a long-term test 
conducted by Reinbold & Pescitelli (1982a), reproduction and growth 
of  D. magna were affected at a concentration of 1.6 mg NH3/litre. 

    Two tests lasting 42 days were conducted by Anderson et al. 
(1978) on the effects of ammonium chloride on the fingernail clam, 
 Musculium transversum.  Significant mortality (67 and 72%) occurred 
in both tests at a concentration of 0.7 mg NH3/litre.  In one of 
the studies, significant reduction in growth was observed after 14 
days of exposure to 0.41 mg NH3/litre.  Sparks & Sandusky (1981) 
reported that fingernail clams exposed to 0.23 and 0.63 mg 
NH3/litre showed 36 and 23% mortality, respectively, in 4 weeks; 
after 6 weeks, there was 47% mortality at 0.073 mg NH3/litre, and 
83% mortality at 0.23 and 0.63 mg NH3/litre.  After 6 weeks there 
was no growth in any test chamber (concentrations of 0.036 mg 
NH3/litre and higher), other than in the controls. 

    Two partial tests, lasting 24 and 30 days, respectively, were 
conducted by Thurston et al. (1984a) on the stonefly  Pteronarcella 
 badia.  Adult stonefly emergence was delayed with increasing 
ammonia concentration, and little or no emergence occurred at 
concentrations exceeding 3.4 mg NH3/litre.  There was no significant 
relationship between the food consumption rates of nymphs and 
concentrations up to 6.9 mg NH3/litre.  LC50 values for 24- and 
30-day exposures were 1.45 and 4.57 mg NH3/litre, respectively. 

    The effects of ammonia on the ciliary beating rate of clam 
gills were investigated by Anderson et al. (1978).  Concentrations 
of 0.036 - 0.11 mg NH3/litre caused a reduction in the ciliary 
beating rate of fingernail clams; the effects ranged from a 50% 
reduction in beating rate to complete inhibition.  Adult clams (> 5 
mm) were more sensitive than juveniles (< -5 mm); adults were also 
slightly more sensitive than the unionid mussel,  Elliptio 
 complanata, and the Asiatic clam,  C. manilensis.  Shaw (1960) 
investigated the effects of ammonium chloride on sodium influx in 
the fresh-water crayfish,  Astacus pallipes.  Ammonia produced an 
inhibition of sodium influx; a concentration of 18 mg NH4+/litre 
reduced the influx to about 20% of its normal value, and influx 
reduction was related to increasing ammonia concentration.  This 
effect was attributed to NH4+ ions and not to any toxic effect 
exerted on the transporting cells by non-ionized ammonia.  NH4+ did 
not affect chloride influx nor the rate of sodium loss. 

    Ammonia was added to a stream at a 24-h average concentration 
of 1.4 mg NH3/litre, and a 24-h drift net sampling was conducted 
(Liechti & Huggins, 1980).  No change in diel drift pattern was 
observed, but there was an increase in the magnitude of drift, a 
shift in the kinds of organisms present, and changes in benthic 
standing crop estimates; this ammonia concentration was non-lethal. 

6.3.3.  Salt-water invertebrates: acute and chronic toxicity

    Data on the acute toxicity of ammonia for salt-water 
invertebrate species are very limited.  A 96-h LC50 value of 1.5 mg 
NH3/litre has been reported for the copepod,  Nitocra spinipes  
(Linden et al., 1979).  Lethal effects of ammonium chloride on the 
quahog clam,  Mercenaria mercenaria, and eastern oyster, 
 Crassostrea virginica, were studied by Epifano & Srna (1975).  
There were no observed differences in susceptibility between 

juveniles and adults of the 2 species.  Armstrong et al. (1978) 
conducted acute toxicity tests (6 days) on ammonium chloride using 
prawn larvae,  Macrobrachium  rosenbergii.  LC50 values were highly 
pH-dependent.  The acute toxicity of ammonium chloride for penaeid 
shrimp was reported as a 48-h composite LC50 value of 1.6 mg 
NH3/litre for 7 species pooled, including the resident species 
 Penaeus setiferus (Wickins, 1976).  The acute toxicity of ammonium 
chloride for the caridean prawn,  M. rosenbergii, was reported 
(Wickins, 1976) as LT50 values of 1700 - 560 min at concentrations 
of 1.74 - 3.41 mg NH3/litre.  From the data of Hall et al. (1978), 
48-h LC50 values of 0.34 - 0.53 were estimated for grass shrimp, 
 Palaemonetes pugio.  Catedral et al. (1977a,b) investigated the 
effects of ammonium chloride on the survival and growth of  Penaeus 
 monodon; larvae had a lower tolerance to ammonia compared with 
post-larvae.  Brown (1974) reported a time to 50% mortality of 
106 min for the nemertine worm,  Cerebratulus fuscus, at a 
concentration of 2.3 mg NH3/litre. 

    Effects of ammonium chloride solutions on the American lobster, 
 Homarus americanus, were studied by Delistraty et al. (1977).  
Their studies were performed on fourth-stage larvae, which was 
considered to be the most sensitive life stage.  A 96-h LC50 value 
of 2.2 mg NH3/litre and an incipient LC50 value of 1.7 mg NH3/litre 
were reported.  A "safe" concentration of 0.17 mg NH3/litre was 
tentatively recommended. 

    The sublethal toxicity of ammonium chloride for the quahog clam 
and eastern oyster was studied by Epifano & Srna (1975) who 
measured the effect of a 20-h exposure to ammonia on the rate of 
removal of the alga,  Isochrysis galbana, from suspension (clearing 
rate) by the clams and oysters.  Concentrations of 0.06 - 0.2 mg 
NH3/litre affected removal; no differences were observed between 
juveniles and adults.  The effect of ammonia on the ciliary beating 
rate of the mussel,  Mytilus edulis, was studied by Anderson et al. 
(1978).  Concentrations of 0.097 - 0.12 mg NH3/litre resulted in a 
reduction in the ciliary beating rate ranging from 50% to complete 

    Exposure of unfertilized sea urchin,  Lytechinus pictus, eggs to 
ammonium chloride resulted in stimulation of the initial rate of 
protein synthesis, an event that normally follows fertilization 
(Winkler & Grainger, 1978).  Exposure of unfertilized eggs of 
 Strongylocentrotus purpurpatus, L.  pictus, and  Strongylocentrotus 
 drobachiensis to ammonium chloride (Johnson et al., 1976; Paul et 
al., 1976) caused "fertilization acid" to be released more rapidly 
and in greater amounts than after insemination.  Activation of 
unfertilized  L. pictus eggs by ammonium chloride exposure was 
also evidenced by an increase in intracellular pH (Steinhardt & 
Mazia, 1973; Shen & Steinhardt, 1978).  Ammonia treatment has also 
been reported to activate phosphorylation of thymidine and 
synthesis of histones in unfertilized eggs of the sea urchin, 
 S. purpuratus, (Nishioka, 1976).  Premature chromosome 
condensation was induced by ammonia treatment of eggs of  L. pictus  
and  S. purpuratus (Epel et al., 1974; Wilt & Mazia, 1974; Krystal 
& Poccia, 1979).  Treatment of  S. purpuratus and  S. drobachiensis  

fertilized eggs with ammonia resulted in an absence of the normal 
uptake of calcium following insemination.  However, calcium uptake 
was not inhibited when ammonia treatment preceded insemination 
(Paul & Johnston, 1978). 

    The polychetous annelid,  Nereis succinea, the channelled whelk, 
 Busycon canaliculatum, and the brackish-water clam,  Rangia 
 cuneata, were exposed to concentrations of 0.85, 0.37, and 0.27 mg 
NH3/litre and the ammonia excretion measured (Mangum et al., 1978).  
Excretion was inhibited by non-lethal concentrations of ammonia, 
and the authors concluded that ammonia crosses the excretory 
epithelium in the ionized form, and that the process is linked to 
the activity of the Na++K+ ATPases.  When blue crabs,  Callinectes 
 sapidus, were moved from water of 28 parts per thousand salinity 
to water of 5 parts per thousand, a doubling of the ammonia 
excretion rate occurred; addition of excess ammonium chloride to 
the low-salinity water inhibited ammonia excretion and decreased 
net acid output (Mangum et al., 1976).  The effect of gaseous NH3 
on haemoglobin from the blood of the common marine bloodworm, 
 Glycera dibrachiata, was examined by Sousa et al. (1977) in an 
attempt to determine whether there was competition between NH3 and 
oxygen in binding to haemoglobin; such an NH3/O2 relationship was 
not found. 

6.4.  Fish

    Ammonia is highly toxic for fish, and, because of its 
occurrence at high concentrations in some water systems, it can 
present a major pollution problem.  It enters aquatic environments 
from several sources, including sewage effluent, deposition of 
human wastes without treatment, industrial discharges, and runoff 
from animal culture and agricultural operations.  It is also a 
metabolic waste product of fish and, therefore, can be a problem in 
facilities involved with intensive fish culture. 

    Elevated ammonium ion (NH4+) concentrations within the bodies 
of fish, as with other vertebrates, cause convulsions and death.  
The concentration of non-ionized ammonia (NH3) in the environment 
of the fish is important, because ammonia is transferred between 
the water and fish largely in this form.  Thus, while NH3 is the 
more toxic chemical species in the water, within the fish, toxicity 
is related to the NH4 concentration. 

    Research by Chipman (1934), Wuhrman et al. (1947), Wuhrman & 
Woker (1948), and Tabata (1962) implicated NH3 as the ammonia 
species in water that is mainly toxic for fish, and reported that 
NH4+ was non-toxic or considerably less toxic.  More recent 
research by Robinson-Wilson & Seim (1975), Armstrong et al. (1978), 
and Thurston et al. (1981c) has demonstrated that the role of water 
pH in the toxicity of ammonia for fish is more than the regulation 
of the NH3/NH4+ equilibrium.  NH3 is considerably more toxic in 
water when pH values are lower than 7 - 9, and there is some 
evidence that the toxicity of NH3 is also increased above this 
range.  Temperature and dissolved oxygen and the ionic composition 
of the background water all play a role in the toxicity of NH3 for 
some fish. 

    In a comprehensive analysis of the data, it was concluded that 
a number of fish species that are phylogenetically similar are also 
similar in their sensitivity to the toxicity of ammonia, and that 
many of the factors that affect the toxicity of ammonia similarly 
affect all the species that have been studied (US EPA, 1985). 

    It was formerly considered that fish of the family Salmonidae 
were among the most sensitive to the effects of many pollutants, 
whereas other fish species, which have evolved in warm-water, low 
oxygen, or more turbid aquatic environments, may be less sensitive 
to many naturally-occuring pollutants, such as ammonia.  However, 
other fish species, including some that are frequently referred to 
as "warm water" fishes, are of comparable sensitivity (US EPA, 
1985).  In the "resident-species" approach for establishing water 
quality criteria for a toxic agent in a given water body, the 
tolerance of selected fish and invertebrate species, naturally 
resident in the water body, is used.  It must be borne in mind 
that, if these selected species are less sensitive than other 
species in different water bodies, the standards may be 
inappropriate for other water bodies. 

    Because of variation among different background test water 
conditions in different laboratories, as well as differences in the 
genetic pools of the same species, results of a single test on a 
given species may not be as meaningful as composite results from 
several tests conducted at different laboratories. 

    Much of the evidence on ammonia toxicity is empirical, so, for 
a more complete understanding of the biological actions of this 
chemical, the results of toxicity tests must be integrated with a 
knowledge of ammonia metabolism in fish. 

6.4.1.  Ammonia metabolism in fish  Ammonia production and utilization

    The major pathway for the production of ammonia in fish, as in 
other vertebrates, is through the transamination of various amino 
acids (Forster & Goldstein, 1969; Watts & Watts, 1974).  The 
primary site for ammonia production is probably the liver (Pequin & 
Serfaty, 1963), but the necessary enzymes have also been located in 
the kidneys, gills, and skeletal muscle tissue (Goldstein & 
Forster, 1961; McBean et al., 1966; Walton & Cowey, 1977).  Ammonia 
is also produced by the deamination of adenylates in fish muscle 
(Driedzic & Hochachka, 1976).  The quantitative importance of 
muscle ammoniogenesis in total ammonia excretion depends on the 
level of activity of the animal, and increases with increasing 
workload (Suyama et al., 1960; Fraser et al., 1966; Driedzic & 
Hochachka, 1976). 

    Ammonia toxicity can be ameliorated by the formation of less 
toxic compounds, namely glutamine and urea.  Levi et al. (1974) 
recorded high levels of glutamine in the brain of goldfish, 
 Carrasius auratus, and found that brain-glutamine levels increased 
with ambient ammonia concentrations.  Webb & Brown (1976) found 

high glutamine synthetase (EC activity in the brains of 
teleosts and elasmobranchs, and this may be important in protecting 
the brain from sudden surges in ammonia concentration.  Walton & 
Cowey (1977) were able to detect glutaminase activity in the gills 
of rainbow trout, but were unable to measure any  in vivo  
utilization of glutamine by the gills. 

    Ammonia can be converted, through carbamyl phosphate, to urea 
either via purines (uricolysis) or via the ornithine cycle.  The 
enzymes required for uricolysis have been found in most fish 
studied (Forster & Goldstein, 1969; Watts & Watts, 1974), but 
Florkin & Duchateau (1943) were unable to detect any activity of 
uricolytic enzymes in the cyclostome,  Lampetra.  The ratio of urea 
production via the ornithine cycle to production via uricolysis is 
about 100 to 1 in elasmobranchs and dipnoi, whereas in teleosts 
most of the urea is formed via uricolysis (Gregory, 1977).  Ammonia excretion

    The gills are the major site of ammonia excretion in fish, but 
smaller quantities of ammonia may also be eliminated by the kidneys 
(Edwards & Condorelli, 1928; Grollman, 1929; Fromm, 1963; Maetz, 
1972) and skin (Morii et al., 1978).  Although the majority of 
branchial ammonia excretion represents clearance from the blood, 
gill metabolism may contribute between 20% (Payan & Matty, 1975) 
and 5 - 8% (Cameron & Heisler, 1983) of the net ammonia excretion. 

    The excretion of ammonia by fish is variable, depending on the 
state of the animal, the environmental conditions, and the species.  
Ammonia excretion tripled in sockeye salmon,  Oncorhynchus nerka,  
following daily feeding (Brett & Zala, 1975) but remained low and 
unchanging during starvation (Brett & Zala, 1975; Guerin-Ancey, 
1976a).  In fresh-water fish, ammonia excretion increases in 
response to exercise (Sukumaran & Kutty, 1977; Holeton et al., 
1983), long-term acid exposure (McDonald & Wood, 1981; Ultsch et 
al., 1981), hypercapnia (Claiborne & Heisler, 1984), and NH4Cl 
infusion (Hillaby & Randall, 1979).  In contrast, increased levels 
of environmental ammonia (Guerin-Ancey, 1976b) and short-term 
exposure to acid or alkaline water (Wright & Wood, 1985) cause a 
decrease in ammonia excretion.  It is not known if these changes in 
excretion reflect change in the rate of ammonia production or in 
the ammonia content of the body.  The ammonia content of fish is 
likely to be the equivalent of the ammonia excreted in about 2 h, 
most of the ammonia being in the tissues with a lower pH, such as 
muscle.  Blood levels are around 0.2 to 0.3 mmol, but muscle at a 
lower pH may contain levels of up to 1 mmol; thus, a 1-kg fish may 
contain about 0.5 to 0.7 mmol of ammonia and have an excretion rate 
of about 0.3 mmol/h.  There is increased ammonia production in 
muscle during exercise (Driedzic & Hochachka, 1976).  Ammonia 
excretion by the spiny dogfish,  Squalus acanthias, in sea water is 
unaffected by temperature change, exercise, hyperoxia, hypercapnia, 
or the infusion of either HCl or NaHCO3 or anything that induces 
acid-base stress (Heisler, 1984).  This is surprising, because many 
of these changes affect pH and therefore would be expected to alter 
the ammonia content of body compartments and consequently ammonia 

    There is an elevation in blood-ammonia during starvation (Morii 
et al., 1978; Hillaby & Randall, 1979), even though ammonia 
excretion does not change (Brett & Zala, 1975).  Blood-ammonia 
concentrations also rise with increases in both temperature 
(Fauconneau & Luquet, 1979) and ammonia concentrations in the water 
(Fromm & Gillette, 1968; Thurston et al., 1984b).  Exposure of fish 
to either air (Gordon, 1970) or increased ammonia levels in water 
(Fromm, 1970; Guerin-Ancey, 1976b), raises blood-ammonia levels and 
reduces ammonia excretion; this is associated with a rise in urea 
production in many, but not all fish.  Unlike the authors of the 
above studies, Buckley et al. (1979) did not find any change in 
blood-total ammonia when coho salmon,  Oncorhynchus kisutch, were 
exposed to elevated ammonia levels in the environment.  However, a 
significant rise in plasma-sodium, indicating some coupling between 
sodium uptake and ammonia excretion, was observed. 

    The study of ammonia movement is complicated by the fact that, 
with present analytical techniques, it is impossible to distinguish 
between the transfer of a molecule of NH3 plus a H+ ion from the 
transfer of an NH4+ ion.  Thus, only indirect evidence can be 
obtained regarding the relative gas and ion movements across the 
gill epithelium. 

    Three possible mechanisms of ammonia excretion have received 
the most attention:  passive NH3 flux, ionic exchange of NH4+ for 
Na+, and passive NH4+ flux.  There seems to be little doubt that a 
significant pathway for branchial ammonia excretion is by the 
passive diffusion of NH3 down its partial pressure gradient.  
Changes in the NH3 partial pressure gradient are positively 
correlated with changes in net ammonia excretion in the channel 
catfish,  Ictalurus punctatus, (Kormanik & Cameron, 1981), and 
rainbow trout (Cameron & Heisler, 1983; Wright & Wood, 1985).  
Ammonia entry into the fish has also been shown to be dependent on 
the NH3 gradient (Wuhrmann et al., 1947; Wuhrmann & Woker, 1948; 
Fromm & Gillette, 1968). 

    The excretion of NH4+ is strongly coupled with the movement 
of other ions.  Many studies have attempted to link the 
transepithelial exchange of Na+ uptake to NH4+ efflux.  Although 
there is considerable indirect evidence for the presence of a 
coupled ionic exchange mechanism under certain conditions (Maetz & 
Garca-Romeu, 1964; Maetz, 1973; Payan & Maetz, 1973; Evans, 1977, 
1980; Payan, 1978; Girard & Payan, 1980; Wright & Wood, 1985), the 
ubiquity and stoichiometry of this exchange remain controversial.  
While Na+ influx can be monitored with isotopes, it is difficult to 
determine NH4+ efflux.  Investigators have attempted to quantify 
the relationship between Na+ uptake and NH4+ excretion by 
manipulating Na+ levels in the environmental water, by 
pharmaceutical inhibition of the Na+ influx mechanism, or by 
loading the fish with ammonia. 

    In goldfish (Maetz, 1973), and in irrigated rainbow trout gills 
(Kirschner et al., 1973), Na+ influx was best correlated with the 
sum of H+ and NH4+ ion efflux.  The possibility of a Na+ uptake 
carrier coupled to either NH4+ or H+ appears likely in other fish 

as well (Kerstetter et al., 1970; Payan & Maetz, 1973; Evans, 
1977).  In perfused heads of trout, Na+ uptake was tightly coupled 
with NH4+ efflux (Payan et al., 1975; Payan, 1978).  Wright & Wood 
(1985) demonstrated that, in intact trout, the rate of ion exchange 
was influenced by external water pH, increasing from no exchange at 
pH 4 to maximal rates at pH 8.  The relationship between Na+ and 
NH4+ was one-to-one at a pH of less than 8.  However, Payan et al. 
(1975) and Wright & Wood (1985) found that the majority of the 
ammonia was eliminated by gaseous diffusion, and only when NH3 was 
subtracted from total ammonia efflux was the NH4+/Na+ exchange 
evident.  In common carp,  Cyprinus carpio (de Vooys, 1968), and 
little skate,  Raja erinacea (Evans et al., 1979), ammonia 
excretion was unaffected by a reduction in environmental Na+ 
levels.  Cameron & Heisler (1983) found that, under resting 
conditions, diffusive movement of NH3 could account for ammonia 
excretion in trout, but when the ammonia gradient was reversed and 
directed inwards, an NH4+/Na+ exchange could counter-balance the 
diffusive uptake of NH3 from the water.  If this hypothesis is 
correct, then it would explain the unchanging blood-ammonia levels 
and increased Na+ levels in coho salmon exposed to elevated 
concentrations of ammonia in the water (Buckley et al., 1979). 

    The Na+/NH4+ (H+) exchange is probably located on the 
epithelial apical membrane.  Either acid conditions or amiloride in 
the water inhibits Na+ influx across the gills and both these 
conditions result in a reduction in ammonia excretion (Wright & 
Wood, 1985). 

    The ammonium ion can displace potassium in many membrane 
processes in, for example, the giant axon of squid,  Loligo pealei  
(Binstock & Lecar, 1969), and this is the probable reason that 
elevated ammonia causes convulsions in so many vertebrates.  In 
various aquatic animals, it is possible that NH4+ can substitute 
for potassium in oubain-sensitive sodium/potassium exchange (Payan 
et al., 1975; Towle & Taylor, 1976; Towle et al., 1976; Mallery, 
1979; Girard & Payan, 1980).  NH4+ ions will substitute for K+ ions 
across the epithelial basolateral border (Richards & Fromm, 1970; 
Shuttleworth & Freeman, 1974; Karnaky et al., 1976), but the 
importance to net ammonia transfer in fresh-water fish is unknown. 

    The passive movement of NH4+ down its electrochemical gradient 
may also contribute to net ammonia excretion (Claiborne et al., 
1982; Goldstein et al., 1982).  Lipid membranes are relatively 
impermeable to cations (Jacobs, 1940) and, because respiratory 
epithelial cells of fresh-water fishes are joined by tight 
junctions (Girard & Payan, 1980), it appears unlikely that NH4+ 
diffusion is of quantitative importance (Kormanik & Cameron, 1981).  
Indeed, Wright & Wood (1985) found a negative correlation between 
ammonia excretion and the NH4+ concentration gradient in rainbow 
trout exposed to 5 different water pH regimes.  Although it appears 
that NH4+ diffusion may be of minor importance, simultaneous 
measurements of the electrical and chemical gradient have not been 
made and are necessary before conclusions can be drawn. 

6.4.2.  Fish: acute toxicity

    The acute toxicity of ammonia for rainbow trout has been 
studied by many investigators, with reported 96-h LC50 values 
ranging from 0.16 to 1.1 mg NH3/litre.  Thurston & Russo (1983) 
conducted 71 toxicity tests on rainbow trout ranging in size from 
sac fry (< 0.1 g) to 4-year-old adults (2.6 kg), in water of 
uniform chemical composition.  LC50 values ranged from 0.16 to 
1.1 mg NH3/litre for 96-h exposures.  Fish susceptibility to NH3 
decreased with increasing weight over the range 0.06 - 2.0 g, but 
gradually increased above that weight range.  LC50 values for 12- 
and 35-day exposures did not differ greatly from 96-h values.  No 
statistically-significant differences in results were observed when 
different ammonium salts [NH4Cl, NH4HCO3, (NH4)2HPO4, (NH4)2SO4] 
were used.  Grindley (1946) also reported that there were no 
appreciable differences in toxicity between toxic solutions of 
NH4Cl and (NH4)2SO4 in rainbow trout tests.  However, Calamari et 
al. (1977, 1981) reported that embryos and fingerlings were less 
sensitive than the other life stages studied.  LC50 values (96-h) 
ranging from 0.16 to 1.02 mg NH3/litre for rainbow trout exposed to 
ammonia were reported by Calamari et al. (1977, 1981), Broderius & 
Smith (1979), Holt & Malcolm (1979), DeGraeve et al. (1980), and 
Reinbold & Pescitelli (1982b). 

    Although acute toxicity studies with salmonids have mainly been 
conducted on rainbow trout, some data are available for a few other 
salmonid species.  Thurston et al. (1978) investigated the 
toxicity of ammonia for cutthroat trout,  Salmo clarki, and 
reported 96-h LC50 values of 0.52 - 0.80 mg NH3/litre.  Thurston & 
Russo (1981) reported a 96-h LC50 value of 0.76 mg NH3/litre for 
golden trout,  Salmo aguabonita.  Brown trout,  Salmo trutta, were 
exposed to 0.15 mg NH3/litre for 18 h, resulting in a 36% 
mortality; when returned to ammonia-free water, the test fish 
recovered after 24 h (Taylor, 1973).  No mortality occurred during 
the 96-h exposure at 0.090 mg NH3/litre, although fish would not 
feed.  Exposure to 0.8 mg NH3/litre was not acutely toxic for brown 
trout according to Woker & Wuhrmann (1950).  However, Thurston & 
Meyn (1984) reported 96-h LC50 values of 0.60 - 0.70 mg NH3/litre, 
and Miller et al. (1981) reported a 96-h LC50 value of 0.47 mg 
NH3/litre for brown trout using test dilution river water.  Brook 
trout,  Salvelinus fontinalis, showed distress within 1.75 h at a 
concentration of 3.25 mg NH3/litre and within 2.5 h at 5.5 mg/litre 
(Phillips, 1950).  Thurston & Meyn (1984) reported 96-h LC50 values 
of 0.96 - 1.05 mg NH3/litre for brook trout, 0.40 - 0.48 mg 
NH3/litre for chinook salmon,  Oncorhynchus tshawytscha, and 0.14 - 
0.47 mg NH3/litre for mountain whitefish,  Prosopium williamsoni.  
Toxicity tests with (NH4)2SO4 on pink salmon,  Oncorhynchus 
 gorbuscha, at different early stages of development (Rice & Baily, 
1980) showed that late alevins near swim-up stage were the most 
sensitive (96-h LC50 = 0.083 mg NH3/litre), and eyed embryos were 
the most tolerant, surviving 96 h at > 1.5 mg NH3/litre.  Buckley 
(1978) reported a 96-h LC50 value of 0.55 mg NH3/litre for 
fingerling coho salmon,  Oncorhynchus kisutch, and Herbert & 
Shurben (1965) reported a 24-h LC50 value of 0.28 mg NH3/litre for 
Atlantic salmon,  Salmo salar. 

    There are acute toxicity data for ammonia in a variety of non-
salmonid fish species.  Thurston et al. (1983) studied the toxicity 
of ammonia for fathead minnows,  Pimephales promelas, ranging from 
0.1 to 2.3 g in weight and found that 96-h LC50 values in 29 tests 
ranged from 0.75 to 3.4 mg NH3/litre; toxicity was not dependent on 
the test fish size or source.  LC50 values ranging from 0.73 to 
2.35 mg NH3/litre for fathead minnows were also reported by Sparks 
(1975), DeGraeve et al. (1980), Reinbold & Pescitelli (1982b), 
Swigert & Spacie (1983).  LC50 values for white sucker,  Catostomus 
 commersoni, exposed to ammonium chloride solutions for 96 h 
(Reinbold & Pescitelli 1982c) were 1.40 and 1.35 mg/litre NH3, 
though a somewhat lower 96-h LC50 of 0.79 mg NH3/litre was 
determined by Swigbert & Spacie (1983).  Thurston & Meyn (1984) 
reported 96-h LC50 values of 0.67 - 0.82 mg NH3/litre for the 
mountain sucker,  Caststomus platyrhynchus. 

    Reported LC50 values for 96-h exposures of bluegill,  Lepomis 
 macrochirus, ranged from 0.26 to 4.60 mg NH3/litre (Emery & Welch, 
1969; Lubinski et al., 1974; Roseboom & Richey, 1977; Reinbold & 
Pescitelli, 1982b; Swigert & Spacie, 1983).  LC50 values (96-h) of 
0.7 - 1.8 mg NH3/litre for smallmouth bass,  Micropterus dolomieui,  
and 1.0 - 1.7 mg NH3/litre for largemouth bass,  Micropterus 
 salmoides, were reported by Broderius et al. (in press) and 
Roseboom & Richey (1977), respectively.  Sparks (1975) reported 
48-h LC50 values for bluegill of 2.30 mg NH3/litre, and for channel 
catfish of 2.92 mg NH3/litre.  For goldfish,  Carassius auratus,  
Dowden & Bennett (1965) reported a 24-h LC50 of 7.2 mg NH3/litre, 
and Chipman (1934) reported lethal threshold values of 0.97 - 
3.8 mg NH3/litre.  Turnbull et al. (1954) reported a 48-h LC50 for 
bluegill to be within the range 0.024 - 0.093 mg NH3/litre; during 
the exposure, they observed that the fish exhibited a lack of 
ability to avoid objects. 

    Reported 96-h LC50 values for channel catfish,  Ictalurus 
 punctatus, ranged from 1.5 to 4.2 mg NH3/litre (Colt & 
Tchobanoglous, 1976; Roseboom & Richey, 1977; Reinbold & 
Pescitelli, 1982d; Swigert & Spacie, 1983).  Vaughn & Simco (1977) 
reported a 48-h LC50 for channel catfish of 1.24 - 1.96 mg 
NH3/litre, and Knepp & Arkin (1973) reported 1-week LC50 values of 
0.97 - 2.0 mg NH3/litre.  The results of studies on bluegill, 
channel catfish, and largemouth bass (Roseboom & Richey, 1977) 
showed that bluegill susceptibility was dependent on fish weight, 
fish weighing 0.07 g being slightly more sensitive than those 
weighing either 0.22 or 0.65 g; size had little effect on the 
susceptibility of channel catfish or bass. 

    Hazel et al. (1979) reported 96-h LC50 values of 0.90 and 
1.07 mg NH3/litre for the orangethroat darter,  Etheostoma 
 spectabile, and red shiner,  Notropis lutrensis.  Largemouth bass, 
channel catfish, and bluegill were also exposed for 96 h to a 
concentration of 0.21 mg NH3/litre resulting in zero mortality for 
bluegill and channel catfish and one death (6%) among the 
largemouth bass tested.  A 96-h LC50 value for walleye, 
 Stizostedion vitreum, of 0.85 mg/litre NH3 was reported by 
Reinbold & Pescitelli (1982a). 

    LC50 values ranging from 2.4 to 3.2 mg NH3/litre for 
(NH4)2CO3, NH4Cl, NH4C2H3O2, and NH4OH, in 96-h exposures of 
mosquitofish,  Gambusia affinis, in waters with suspended solids 
ranging from < 25 to 1400 mg/litre were reported by Wallen et al. 
(1957).  Susceptibility of mosquito fish to ammonia was studied by 
Hemens (1966) who reported a 17-h LC50 of 1.3 mg NH3/litre; he also 
observed that male fish were more susceptible than females.  Rubin 
& Elmaraghy (1976, 1977) tested guppy,  Poecilia reticulata, fry 
and reported 96-h LC50 values averaging 1.50 mg NH3/litre; mature 
guppy males were more tolerant, with 100% survival for 96 h at 
concentrations of 0.17 - 1.58 mg NH3/litre.  LC50 values (96-h) of 
0.15 and 0.20 mg NH3/litre at pH 6.0, and of 0.52 and 2.13 mg 
NH3/litre at pH 8.0, were reported by Stevenson (1977) for white 
perch,  Morone americana.  LC50 values (96-h) of 1.20 and 1.62 mg 
NH3/litre for spotfin shiner,  Notropis spilopterus, were reported 
by Rosage et al. (1979), and of 1.20 mg NH3/litre for golden 
shiner,  Notemigonus crysoleucas, by Baird et al. (1979).  Swigert 
& Spacie (1983) reported 96-h LC50 values of 0.72 mg NH3/litre for 
golden shiner, 1.35 mg NH3/litre for spotfin shiner, 1.25 mg 
NH3/litre for steelcolour shiner,  Notropis whipplei, and 1.72 mg 
NH3/litre for stoneroller,  Campostoma anomalum. 

    Jude (1973), Reinbold & Pescitelli (1982a), and McCormick et 
al. (1984) reported 96-h LC50 values ranging from 0.6 to 2.1 mg 
NH3/litre for green sunfish,  Lepomis cyanellus.  In studies on the 
pumpkinseed sunfish,  Lepomis gibbosus, by Jude (1973) and Thurston 
(1981), 96-h LC50 values ranged from 0.14 to 0.86 mg NH3/litre.  
Mottled sculpin,  Cottus bairdi, were tested by Thurston & Russo 
(1981), yielding a 96-h LC50 value of 1.39 mg NH3/litre.  An 
asymptotic (6-day) LC50 of 0.44 mg NH3/litre was determined for 
rudd,  Scardinius erythropthalmus (Ball, 1967). 

    Rao et al. (1975) reported a 96-h LC50 value for the common 
carp,  Cyprinus carpio, of 1.1 mg NH3/litre.  Carp exposed to 
0.24 mg NH3/litre exhibited no adverse effects in 18 h (Vmos 
1963).  However, exposure to 0.67 mg NH3/litre caused gasping and 
equilibrium disturbance within 18 min, frenetic swimming activity 
at 25 min, then sinking to the tank bottom after 60 min; after 
75 min, the fish were placed in ammonia-free water and all revived.  
Kempinska (1968) reported a lethal concentration of 7.5 mg 
NH3/litre for carp.  Studies on the acute exposure of bitterling, 
 Rhodeus sericeus, and carp to ammonium sulfate revealed minimum 
lethal concentrations of 0.76 mg NH3/litre for bitterling and 
1.4 mg NH3/litre for carp (Malacea, 1966).  Nehring (1963) reported 
survival times for carp at concentrations of 9.7 and 2.1 mg 
NH3/litre of 2.4 and 6.0 h, respectively.  The survival time for 
tench,  Tinca tinca, was reported to be 20 - 24 h at 2.5 mg 
NH3/litre by Danecker (1964).  In a 24-h exposure of creek chub, 
 Semotilus atromaculatus, to ammonium hydroxide solution, the 
"critical range" below which all test fish lived and above which 
all died was reported to be 0.26 - 1.2 mg NH3/litre (Gillette et 
al., 1952). 

    In static exposures lasting 9 - 24 h, with a gradual increase 
in NH3 content, mortalities occurred in oscar,  Astronutus 
 ocellatus, at 0.50 mg NH3/litre (4%) to 1.8 mg/litre (100%) 
(Magalhaes Bastos, 1954).  Tests on oscar of two different sizes 
showed no difference in susceptibility, in relation to size.  A 
72-h LC50 value of 2.85 mg NH3/litre was reported by Redner & 
Stickney (1979) for blue tilapia,  Tilapia aurea.  Saltwater fish

    Very few acute toxicity data are available for salt-water fish 
species.  Holland et al. (1960) reported the critical level for 
chinook salmon,  Oncorhynchus tshawytscha, to be between 0.04 and 
0.11 mg NH3/litre and for coho salmon to be 0.134 mg NH3/litre.  A 
static test with coho salmon provided a 48-h LC50 value of 0.50 mg 
NH3/litre (Katz & Pierro, 1967).  Atlantic salmon smolts and 
yearling rainbow trout exposed for 24 h in 50 and 75% saltwater 
solutions exhibited similar sensitivities to ammonia (United 
Kingdom Ministry of Technology, 1963).  Holt & Arnold (1983) 
reported a 96-h LC50 value of 0.47 mg NH3/litre for red drum, 
 Sciaenops ocellatus.  LC50 values (96-h) of 1.2 - 2.4 mg NH3/litre 
were reported by Venkataramiak et al. (1981) for striped mullet, 
 Mugil caphalus, and 0.69 mg NH3/litre for planehead filefish, 
 Monacanthus hispidus. 

6.4.3.  Factors affecting acute toxicity

    A number of factors can affect the toxicity of ammonia for 
aquatic organisms.  These include the effects of pH, temperature, 
dissolved oxygen concentration, previous acclimatization to 
ammonia, fluctuating or intermittent exposures, carbon dioxide 
concentration, salinity, and the presence of other toxicants.  
Almost all studies of factors affecting ammonia toxicity have been 
carried out using only acute exposures.  pH

    The toxicity for fish of aqueous solutions of ammonia and 
ammonium compounds has been attributed to the non-ionized 
(undissociated) ammonia present in the solution.  The earliest 
reported thorough study of the pH dependence of ammonia toxicity 
was that of Chipman (1934), who concluded from studies on goldfish, 
amphipods, and cladocerans that ammonia toxicity was a function of 
pH and therefore of the concentration of undissociated ammonia in 
the solution.  Downing & Merkens (1955) tested rainbow trout at 
different concentrations of ammonia at both pH 7 and pH 8.  The 
results were consistent when ammonia concentration was expressed as 
NH3.  Tabata (1962) conducted 24-h tests on the toxicity of ammonia 
for  Daphnia (species not specified) and guppy at different pH 
values and calculated the relative toxicity of NH3/NH4+ to be 48 
for  Daphnia and 190 for guppy (i.e., NH3 is 190 times more toxic 
than NH4+). 

    More recently, Robinson-Wilson & Seim (1975) studied the 
toxicity of ammonium chloride for juvenile coho salmon in flow-
through bioassays within the pH range 7.0 - 8.5; the reported 
96-h LC50 for NH3 was approximately 60% less at pH 7.0 than at pH 
8.5.  The toxicity of ammonium chloride for larvae of prawn, 
 Macrobrachium rosenbergii, was studied by Armstrong et al. (1978) 
in 6-day tests within the pH range 6.8 - 8.3 with test solutions 
being renewed every 24 h.  The 96-h LC50 for NH3 at pH 6.83 was 
approximately 70% less than that at pH 8.34.  It was concluded that 
the toxicity of ammonia was not due solely to the NH3 molecule and 
that in solutions of different pH, but equal NH3 concentrations, 
survival was greatly reduced as NH4+ levels increased.  Tomasso et 
al. (1980) studied the toxicity of ammonia (NH3) for channel 
catfish at pH values of 7, 8, and 9 and reported that 24-h LC50 
values were significantly higher at pH 8 than at pH 7 or pH 9. 

    Thurston et al. (1981c) tested the toxicity of ammonia for 
rainbow trout and fathead minnows in 96-h flow-through tests at 
different pH levels within the range 6.5 - 9.0.  Results showed 
that the toxicity of ammonia, in terms of NH3, increased at lower 
pH values, and could also increase at higher pH values.  It was 
concluded that NH4+ exerts some measure of toxicity, and/or that 
increased H+ concentration increases the toxicity of NH3.  Acute 
(96-h) exposures of green sunfish and smallmouth bass at 4 
different pH levels over the range 6.5 - 8.7 showed that, for both 
species, NH3 toxicity increased markedly with a decrease in pH, 
with LC50 values at the lowest pH tested (6.6 for sunfish, 6.5 for 
bass) being 3.6 (sunfish) and 2.6 (bass) times smaller than those 
at the highest pH (8.7) tested (McCormick et al., 1984; Broderius 
et al., in press). 

    It is concluded that NH3 is more toxic for fish at lower pH 
values than within the pH range 7 - 9; the toxicity of NH3 may 
increase again above this range.  Temperature

    Information in the literature on the effects of temperature on 
ammonia toxicity is varied.  The concentration of NH3 increases 
with increasing temperature.  Several researchers have reported an 
effect of temperature on the toxicity of the non-ionized ammonia 
species, independent of the effect of temperature on the aqueous 
ammonia equilibrium. 

    McCay & Vars (1931) reported that it took three times as long 
for the brown bullhead,  Ictalurus nebulosus, to succumb to the 
toxicity of ammonia in water at 10 - 13 C than at 26 C.  The pH 
of the tested water was not reported but with the probable range 
tested (pH 7 - 8), the percent NH3 at the higher test temperature 
would have been approximately three times that at the mean lower 
temperature.  The toxicity of ammonium chloride for goldfish, 
bluntnose minnow,  Pimephales notatus, and the straw-coloured 
minnow or river shiner,  Notropis blennius, was reported (Powers, 
1920) to be greater at high temperatures than at low, but no 
consideration was given to the increase in the relative 

concentration of NH3 as the temperature increased.  Herbert (1962) 
suggested that the effects of temperature on the susceptibility of 
rainbow trout to NH3 toxicity was only slightly, if at all, 
affected by temperature change.  In studies on striped bass,  Morone 
 saxtilis, and stickleback,  Gasterosteus aculeatus, Hazel et al. 
(1971) found a slight difference in toxicity between 15 and 23 C 
in fresh water, with both fish species being slightly more 
resistant at the lower temperature. 

    However, there are other studies in which the toxicity of NH3 
decreased with increasing temperature over the ranges studied.  The 
toxicity of NH3 for rainbow trout has been reported to be much 
higher at 5 C than at 18 C (United Kingdom Ministry of 
Technology, 1968).  Brown (1968) reported that the 48-h LC50 for 
rainbow trout increased with increase in temperature over the range 
3 C - 18 C; the reported increase in tolerance between ~12 C - 
~18 C was considerably less than that between ~3 C - ~12 C.  A 
relationship between temperature and 96-h LC50 was reported for 
rainbow trout over the temperature range 12 C - 19 C with ammonia 
toxicity decreasing with increasing temperature (Thurston & Russo, 

    Thurston et al. (1983) reported that the acute toxicity of NH3 
for fathead minnows decreased with a rise in temperature over the 
range 12 C - 22 C.  Bluegill and fathead minnow were tested at 
low and high temperatures of 4.0 C - 4.6 C and 23.9 C - 25.2 C, 
respectively, and rainbow trout were tested at 3 C and 14 C 
(Reinbold & Pescitelli, 1982b).  All three species were more 
sensitive to NH3 at the low temperatures, with toxicity being 1.5 - 
5 times higher in the colder water.  Bluegill appeared to be the 
most sensitive of the three species to the effects of low 
temperature on ammonia toxicity.  Colt & Tchobanoglous (1976) 
reported that the toxicity of NH3 for channel catfish decreased 
with increasing temperature over the range 22 C - 30 C.  LC50 
values for bluegill, channel catfish, and largemouth bass at 28 C 
- 30 C were approximately twice those at 22 C (Roseboom & Richey, 
1977).  An effluent containing ammonia as the principal toxic 
component showed a marked decrease in toxicity for channel catfish 
over the temperature range 4.6 C - 21.3 C (Cary, 1976). 

    Lloyd & Orr (1969) investigated the effects of temperature 
(range 10 - 20 C) on urine flow rates in rainbow trout exposed to 
0.30 mg NH3/litre, and did not find any apparent temperature effect 
on the total diuretic response of the fish, though the relative 
increase in urine production was less at higher temperatures.  From 
a study of the behavioural response of bluegill to gradients of 
ammonium chloride, it was hypothesized that low temperatures 
increased the sensitivity of the bluegill and interfered with the 
ability, either to detect ammonia after a certain period of 
exposure, or, to compensate behaviourally for physiological stress 
caused by ammonia gradients (Lubinski, 1979; Lubinski et al., 

    The European Inland Fisheries Advisory Commission (1970)
has stated that, at temperatures below 5 C, the toxic effects of 
non-ionized ammonia may be greater than at above 5 C, though the 
basis for this is not clearly documented.  The evidence that 
temperature, independent of its role in the aqueous ammonia 
equilibrium, affects the toxicity of NH3 for fish argues for 
further consideration of the temperature/ammonia toxicity 
relationship.  Salinity

    Herbert & Shurben (1965) reported that the resistance of 
yearling rainbow trout to ammonium chloride increased with 
increasing salinity up to levels of 30 - 40% sea water; above this 
level, resistance appeared to decrease.  Fingerling coho salmon 
were tested at salinity levels of 20 - 30 parts per thousand (57 - 
86% salt water), and it was found that the toxicity of an ammonia-
ammonium waste increased as salinity increased (Katz & Pierro, 
1967).  These findings are in agreement, at the levels tested, with 
those of Herbert & Shurben (1965).  Atlantic salmon were exposed to 
ammonium chloride solutions for 24 h under both fresh-water and 30% 
salt-water conditions; LC50 values were 0.15 and 0.3 mg NH3/litre, 
respectively, in the 2 different waters (Alabaster et al., 1979).  
Harader & Allen (1983) reported that the resistance to ammonia of 
chinook salmon parr increased by about 500%, as salinity increased 
to almost 30% sea water, but declined as salinity increased beyond 

    There is a slight decrease in the NH3 fraction of total ammonia 
as ionic strength increases in dilute saline solutions, but the 
relative changes in NH3 toxicity, as salinity increases, are more 
directly attributable to changes in the rate of exchange of NH3 and 
NH4+ across the fish gill membranes.  Dissolved oxygen

    A decrease in dissolved oxygen concentration in the water can 
increase ammonia toxicity.  There is a reduction in fish blood 
oxygen-carrying capacity following ammonia exposure (Brockway, 
1950; Danecker, 1964; Reichenback-Klinke, 1967; Krting, 1969a,b; 
Waluga & Flis, 1971).  Hypoxia would further exacerbate problems of 
oxygen delivery and could lead to the early demise of the fish. 

    Vmos & Tasndi (1967) observed deaths of carp in ponds at 
ammonia concentrations lower than would normally be lethal, and 
attributed this to periodic low concentrations of oxygen.  On the 
basis of research in warm-water (20 C -  22 C) fish ponds, Selesi 
& Vmos (1976) projected a "lethal line", relating acute ammonia 
toxicity and dissolved oxygen, below which carp died.  The line ran 
between 0.2 mg NH3/litre at 5 mg dissolved oxygen/litre and 1.2 mg 
NH3/litre at 10 mg dissolved oxygen/litre.  Thurston et al. (1983) 
compared the acute toxicity of ammonia for fathead minnows at 
reduced and normal dissolved oxygen concentrations; seven 96-h 
tests were conducted within the range 2.6 - 4.9 mg dissolved 
oxygen/ litre, and 3 between 8.7 and 8.9 mg/litre.  There was a 

slight positive trend between 96-h LC50 values and dissolved 
oxygen, though it was not shown to be statistically significant. 
Atlantic salmon smolts were tested in both fresh water and 30% salt 
water at 9.6 - 9.5 and 3.5 - 3.1 mg dissolved oxygen/litre.  The 
reported 24-h LC50 values at the higher oxygen concentrations were 
about twice those at the lower (Alabaster et al., 1979). 

    Several studies have been reported on rainbow trout. Allan 
(1955) reported that below 0.12 mg NH3/litre and at about 30% 
oxygen saturation, the median survival time was greater than 24 h, 
but at the same concentration with oxygen saturation below 30%, the 
median survival time was less than 24 h.  In studies by Downing & 
Merkens (1955), fingerling rainbow trout were tested at 3 different 
concentrations of NH3 at 5 different levels of dissolved oxygen.  
In tests lasting up to 17 h, decreasing the oxygen level from 8.5 
to 1.5 mg/litre shortened the period of survival at all ammonia 
concentrations, and a decrease in survival time produced by a given
decrease in oxygen was greatest at the lowest concentration of NH3.  
Merkens & Downing (1957), in tests lasting up to 13 days, also 
reported that the effects of low concentrations of dissolved oxygen 
on the survival of rainbow trout were more pronounced at low 
concentrations of NH3.  Ammonia (NH3) was found to be up to 2.5 
times more toxic when the dissolved oxygen concentration was 
reduced from 100 to about 40% saturation (Lloyd, 1961).  It was 
reported by Danecker (1964) that the toxicity of ammonia increased 
rapidly when the oxygen concentration decreased below two-thirds of 
the saturation value.  Thurston et al. (1981b) conducted 15, 96-h 
acute toxicity tests on rainbow trout over the dissolved oxygen 
range 2.6 - 8.6 mg/litre.  A positive linear correlation between 
96-h LC50 and dissolved oxygen was reported over the entire range 

    When rainbow trout were treated in a channel receiving sewage 
discharge containing 0.05 - 0.06 mg NH3/litre, it was found that, 
at 25 - 35% dissolved oxygen saturation, more than 50% of the fish 
died within 24 h, compared with 50% mortality of test fish in the 
laboratory, at 15% dissolved oxygen saturation (Herbert, 1956).  
The difference was attributed to unfavourable water conditions 
below the sewage outflow, including ammonia, which increased the 
sensitivity of the fish to the lack of oxygen.  Carbon dioxide

    An increase in carbon dioxide (CO2) concentrations up to 
30 mg/litre decreased total ammonia toxicity (Alabaster & Herbert, 
1954; Allan et al., 1958).  Carbon dioxide causes a decrease in pH, 
thereby decreasing the proportion of non-ionized ammonia in 
solution.  However, Lloyd & Herbert (1960) found that, though total 
ammonia toxicity was reduced at elevated CO2 levels, the inverse 
was true when considering non-ionized ammonia alone; more NH3 was 
required in low CO2, high pH water to exert the toxic effect seen 
in fish in high CO2, low pH water.  The explanation presented by 
Lloyd & Herbert (1960) for the decreased toxicity of NH3 in low CO2 
water was that CO2 excretion across the gills would reduce the pH 
and, therefore, the NH3 concentration, in water flowing over the 

gills.  A basic flaw in this hypothesis has been discussed by 
Broderius et al. (1977).  Carbon dioxide will only form protons 
very slowly in water at the tested temperature.  The uncatalysed 
CO2 hydration reaction has a half-time of seconds or even min 
(e.g., at pH 8:  25 seconds at 25 C; 300 seconds at 0 C) (Kern 
1960), and water does not remain in the opercular cavity for more 
than a few seconds, and at the surface of a gill lamella for about 
0.5 - 1 second (Randall, 1970; Cameron, 1979).  Thus, the 
liberation of CO2 across the gills will have little, if any, effect 
on water pH or NH3 levels and the NH3 gradient across the gills 
between water and blood.  Prior acclimatization to ammonia

    The question of whether fishes can acquire an increased 
tolerance to ammonia by acclimatization to low ammonia 
concentrations is an important one.  If fish were able to develop 
such tolerance, they might be able to survive what would otherwise 
be lethal ammonia concentrations. 

    Observations by McCay & Vars (1931) indicated that brown 
bullheads subjected to several successive exposures to ammonia, 
alternating with recovery in fresh water, did not acquire 
tolerance.  However, a number of research workers have reported 
that previous exposure of fish to low concentrations of ammonia 
increases their resistance to lethal concentrations.  Vmos (1963) 
reported that carp exposed to 0.67 or 0.52 mg NH3/litre for 75 min, 
then transferred to fresh water for 12 h, followed by a solution 
containing 0.7 mg NH3/litre, exhibited symptoms of ammonia toxicity 
in 60 - 85 min, whereas control fish, exposed initially to 
0.7 mg/litre NH3, developed symptoms within 20 min.  Blue tilapia 
acclimatized for 35 days to 0.52 - 0.64 mg NH3/litre subsequently 
survived 48 h at 4.1 mg/litre, compared with the 48-h value for 
unacclimatized fish of 2.9 mg/litre (Redner & Stickney, 1979).  
Malacea (1968) studied the effects on bitterling of acclimatization 
to ammonium sulfate solutions.  A group of 10 fish was held in an 
acclimatization solution of 0.26 mg NH3/litre for 94 h, after which 
the fish were exposed to a 5.1 mg NH3/litre solution for 240 min.  
A control group of 10 bitterling received identical treatment, 
except that the acclimatization aquarium did not contain added 
(NH4)2SO4.  The ratio of the mean survival times of "adapted" to 
"unadapted" fish was 1:13, indicating a slightly higher ammonia 
tolerance for the adapted fish. 

    Schulze-Wiehenbrauck (1976) subjected 2 groups of rainbow trout 
(mean weights 56 g and 110 g) that had been held for at least 3 
weeks at sublethal ammonia concentrations, to lethal ammonia 
concentrations.  In the study on the 110-g fish, the 
acclimatization concentrations were 0.007, 0.131, and 0.167 mg 
NH3/litre.  The fish were then subjected for 8.5 h to 
concentrations of 0.45, 0.42 and 0.47 mg NH3/litre, respectively.  
Fish from the 2 higher sublethal concentrations showed 100% 
survival after 8.5 h in the 0.42 and 0.47 mg NH3/litre solutions, 
whereas fish from the 0.007 mg NH3/litre concentration showed only 
50% survival in 0.45 mg NH3/litre.  In the study on the 56-g fish, 

the acclimatization concentrations were 0.004 mg NH3/litre and 
0.159 mg NH3/litre; these fish were placed for 10.25 h in NH3 
concentrations of 0.515 and 0.523 mg/litre, respectively.  There 
was 100% survival in the acclimatized fish, and 85% survival in the 
fish acclimatized to 0.004 mg/litre.  The results of these studies 
showed an increase in resistance of trout to high ammonia levels 
after prior exposure to sublethal ammonia levels. 

    Alabaster et al. (1979) determined 24-h LC50 values of NH3 for 
Atlantic salmon smolts under reduced dissolved oxygen test 
conditions.  Fish acclimatized to ammonia before oxygen reduction 
had LC50 values 38% and 79% higher than fish without prior ammonia 

    In studies by Brown et al. (1969), rainbow trout were tested by 
moving back and forth between tanks in which the ammonia 
concentrations were 0.5 and 2.5 times a previously determined 48-h 
LC50 value.  If fish were transferred on an hourly basis, the 
median period of survival for the fluctuating exposure was reported 
to be the same as that for constant exposure (> 700 min).  When 
the fish were transferred at 2-h intervals, the median survival 
time for the fluctuating exposure was reported to be less (370 
min), indicating that the toxic effects from exposure to the 
fluctuating concentrations of ammonia were greater than those from 
exposure to the constant concentration.  Thurston et al. (1981a) 
conducted acute toxicity tests in which rainbow trout and cutthroat 
trout were exposed to short-term cyclical fluctuations of ammonia.  
Companion tests were conducted in which test fish were subjected to 
ammonia at constant concentrations.  The LC50 values for both 
average and peak concentrations of ammonia for the fluctuating 
concentration tests were compared with the LC50 values for the 
constant concentration tests.  Comparison of total exposures showed 
that fish were more tolerant to constant, than to fluctuating 
concentrations of ammonia.  Fish subjected to fluctuating 
concentrations of ammonia at levels below those acutely toxic were 
better able to withstand subsequent exposure to high fluctuating 
concentrations than unacclimatized fish.  There is reasonable 
evidence that fish with a history of prior exposure to sublethal 
concentrations of ammonia are better able to withstand an acutely 
lethal concentration for a period of hours and possibly days.  
Limited data on fluctuating exposures indicate that fish are more 
susceptible to fluctuating than to constant exposure with the same 
average NH3 concentrations. 

6.4.4.  Fish: chronic toxicity

    "Full-chronic" tests cover the entire life cycle of the test 
animal, beginning at a given stage of development of one generation 
(frequently as the fertilized egg) and continuing through to this 
same stage in the next generation.  Common end-points for measuring 
toxicity are survival, growth, and reproductive success, though 
recent research on ammonia toxicity for fish has demonstrated the 
desirability of also conducting histological examinations. 

    "Partial-chronic" tests on fish most frequently cover a period 
of 30 days or longer, from the egg incubation stage to the free-
swimming stage; for many toxins it has been demonstrated that 
these stages are the most sensitive.  However, in the case of 
ammonia it has been demonstrated that older, mature rainbow trout, 
 Salmo gairdneri, are potentially as susceptible to the effects of 
ammonia as newly-hatched larvae. 

    Long-term ammonia exposure of fishes, including complete life-
cycle tests on rainbow trout and fathead minnows with several end-
points, including effects on spawning and egg incubation, growth, 
survival and tissues, have been studied.  The effects of prolonged 
exposure to ammonia (up to 61 days) on the early life stages of of 
pink salmon were studied by Rice & Bailey (1980).  Three series of 
exposures were carried out, beginning at selected times after 
hatching.  These were for 21 days prior to completion of yolk 
absorption, for 40 days up to 21 days before yolk absorption, and 
for 61 days up to yolk absorption.  All test fish were sampled for 
size when the controls had completed yolk absorption.  Test 
concentrations ranged from zero up to 0.004 mg NH3/litre.  For fry 
at the highest concentration of 0.004 mg NH3/litre, significant 
decreases in weight were observed in all 3 exposed groups.  At a 
concentration of 0.0024 mg NH3/litre, the groups of fry exposed for 
40 and 61 days were significantly smaller, whereas a concentration 
of 0.0012 mg/litre had no significant effect on growth.  Effects 
were consistently more marked for the 61-day-exposed fish. 

    In a 3-generation, 5-year laboratory study, rainbow trout 
exposed for 5 months to concentrations of ammonia ranging from 0.01 
to 0.07 mg NH3/litre, spawned of their own volition.  There was no 
correlation between ammonia concentration and numbers of egg lots 
spawned, total numbers of eggs produced, or numbers of eggs 
subsequently hatched.  Parental fish were exposed for 11 months, 
the first filial generation (F1) for 4 years, and the second filial 
generation (F2) for 5 months.  Pathological lesions were observed in 
both parental and F1 fish, when ammonia concentrations reached and 
exceeded 0.04 mg NH3/litre.  Measurements of blood-ammonia 
concentrations in 4-year-old F1 fish showed an increase when test 
water concentrations reached or exceeded 0.04 mg NH3/litre.  The F1 
fish exposed for 52 months from day of hatching showed no 
relationship between growth and concentration at 10, 15, 21, and 52 
months (Thurston et al., 1984b). 

    Burkhalter & Kaya (1977) tested ammonia at concentrations 
ranging from 0.06 to 0.45 mg/litre on fertilized eggs and the 
resultant sac fry of rainbow trout.  Eggs were incubated at 12 C 
for 25 days in one test and at 10 C for 33 days in another; fry 
were maintained for 42 days.  No concentration response was seen in 
egg mortality or incubation time in either test.  Retardation in 
early growth and development occurred at 0.06 mg NH3/litre, the 
lowest concentration tested.  Fish exposed to 0.12 mg NH3/litre 
required 1 week longer than the controls to achieve a free-swimming 
state; fish at 0.34 and 0.45 mg NH3/litre did not achieve a free-
swimming state during a 42-day test period.  A 21-day LC50 value of 
0.30 mg NH3/litre was obtained.  For sac fry exposed for 42 days 

after hatching, hypertrophy of secondary gill lamellae epithelium 
occurred at 0.23 mg NH3/litre, and karyolysis and karyorrhexis in 
the secondary gill lamellae were observed after 28 days at 0.34 mg 
NH3/litre and higher. 

    Calamari et al. (1977, 1981) exposed rainbow trout to 
ammonium chloride solutions for 71 days, beginning 1 day after 
fertilization and ending when fry had been feeding for 30 days.  
A 72-day LC50 of 0.056 mg NH3/litre was calculated; 23% mortality 
occurred at a concentration of 0.025 mg/litre.  Examination of 986 
rainbow trout embryos at the hatching stage after exposure to 
concentrations of 0.010 - 0.193 mg NH3/litre for 24 days showed 
an increase in gross malformations with increasing ammonia 
concentration.  The deformities observed were various degrees 
of curvature from the median body axis, and various kinds of 
malformations in the head region with a number of cases of double 
heads.  At the highest concentration tested, 0.193 mg NH3/litre, 
60% of the observed fish were malformed.  Microscopic examination, 
at hatching, of 128 larvae from the same exposure showed 
abnormalities of the epidermis and pronephros, which were 
correlated with ammonia concentrations.  The epidermis was 
thickened with an irregular arrangement of the various layers of 
cells and an increase in the number and dimensions of mucous cells.  
The pronephros showed widespread vacuolization of the tubule cells, 
together with a thickening of the wall.  Increasing abnormalities 
were observed after exposure to concentrations exceeding 0.025 mg 
NH3/litre for the epidermis and 0.063 mg/litre for the pronephros. 

    Four 4-week-old rainbow trout fry were exposed for 30 days to 
concentrations  of ammonia (reported graphically) ranging from 
~0.06 to 0.31 mg NH3/litre.  Growth rate at ~0.06 mg NH3/litre was 
comparable with that of controls, but, above ~0.10 mg NH3/litre, 
growth rate decreased, in correlation with increased NH3 
concentration.  Survival at 0.32 mg NH3/litre was 70% of that of 
the controls (Broderius & Smith, 1979).  Schulze-Wiehenbrauck 
(1976) tested juvenile rainbow trout of different sizes, for 
periods of time ranging from 2 to 7 weeks, and at ammonia 
concentrations ranging from 0.012 to 0.17 mg/litre.  He concluded 
that a concentration of 0.05 mg NH3/litre caused a slight decrease 
in growth during the first 14-day interval in non-acclimatized 
fish, but that the decrease was completely compensated for in the 
next growth interval.  Exposure to 0.13 mg NH3/litre (apparently 
for 3 or 4 weeks) did not affect growth, food consumption, or food 

    Young rainbow trout were reared in 3 concentrations of ammonia 
(averaging 0.006, 0.012, and 0.017 mg/litre) for a period of 1 
year.  At 4 months, there was no significant difference in fish 
growth at the 3 concentrations.  At 11 months, there was a 
difference with the fish at 0.012 and 0.017 mg NH3/litre, which 
weighed 9% and 38% less, respectively, than the fish at 0.006 mg 
NH3/litre.  Microscopic examination of tissues from fish exposed to 
the highest concentration, examined at 6, 9, and 12 months, showed 
severe pathological changes in gill and liver tissues.  Gills 
showed extensive proliferation of the epithelium, which resulted in 

severe fusion of gill lamellae preventing normal respiration. 
Livers showed reduced glycogen storage and scattered areas of dead 
cells; these became more extensive with increase in exposure time 
(Smith, 1972; Smith & Piper, 1975). 

    Rainbow trout were exposed for 3 months to concentrations of 
0.069, 0.14, and 0.28 mg NH3/litre.  The cumulative mortality of a 
control group (0.005 mg NH3/litre) was ~2%; cumulative mortality at 
0.069 and 0.14 mg/litre was ~5%, and that at 0.28 mg/litre was ~15% 
(United Kingdom Ministry of Technology, 1968).  Reichenbach-Klinke 
(1967) performed a series of 1-week tests on 240 fish of 9 species 
(including rainbow trout, goldfish, northern pike,  Esox lucius, 
carp, and tench) at concentrations of 0.1 - 0.4 mg NH3/litre.  
Swelling of, and diminution of the number of, red blood cells, 
inflammation, and hyperplasia were observed.  Irreversible blood 
damage occurred in rainbow trout fry at concentrations above 
0.27 mg NH3/litre.  Low NH3 concentrations also inhibited the 
growth of young trout and lessened their resistance to disease. 

    In rainbow trout exposed to 0.30 to 0.36 mg NH3/litre, 81% 
mortality occurred over the 36-day duration of the test, with most 
deaths occurring between days 14 and 21.  Microscopic examination 
of the gills revealed some thickening of the lamellar epithelium 
and an increased mucous production.  The most characteristic 
feature was a large proportion of swollen, rounded secondary 
lamellae in which the pillar system was broken down and the 
epithelium enclosed a disorganized mass of pillar cells and 
erythrocytes.  Gill hyperplasia was not a characteristic 
observation (Smart, 1976). 

    In rainbow trout exposed to < 0.0005 or 0.005 mg NH3/litre for 
8 weeks, examination of the gill lamellae of fish from the lower 
concentration showed them to be long and slender with no 
significant pathology.  Fish exposed to 0.005 mg NH3/litre had 
shorter and thicker gill lamellae with bulbous ends, and some 
consolidation of lamellae was noticed.  Many filaments showed a 
definite hyperplasia of the epithelial layer, evidenced by an 
increase in the number of cell nuclei (Fromm, 1970). 

    Thurston et al. (1978) studied the toxicity of ammonia for 
cutthroat trout fry in tests that lasted up to 36 days.  Results of 
duplicate tests on 1-g fish showed 29- and 36-day LC50 values of 
0.56 mg NH3/litre.  Duplicate tests on 3-g fish provided 29-day 
LC50 values of 0.37 and 0.34 mg NH3/litre, slightly less than those 
of the 1-g fish.  The heart, gastrointestinal tract, and thymus of 
cutthroat trout fry exposed to 0.34 mg NH3/litre for 29 days were 
comparable with those of control fish, but the gills and kidneys 
showed degenerative changes.  The gills showed hypertrophy of 
epithelium, some necrosis of epithelial cells, and separation of 
epithelium due to oedema.  The kidneys had mild hydropic 
degeneration and accumulation of hyaline droplets in the renal 
tubular epithelium.  Reduced vacuolation was observed in livers. 

    Samylin (1969) studied the effects of ammonium carbonate on the 
early stages of development of Atlantic salmon.  The first set of 
studies, at  13 C, lasted 53 days and was conducted within the 
range 0.001 to > 6.6 mg NH3/litre beginning with the "formed 
embryo" stage.  Accelerated hatching was observed with increasing 
(NH4)2CO3 concentrations, but concentrations of > 0.16 mg 
NH3/litre were lethal for emerging larvae within 12 - 36 h.  
Because (NH4)2CO3 was used as the toxin, the pH in the test aquaria 
increased from 6.7 to 7.6 with increasing NH3 concentration.  Growth 
inhibition was observed at 0.07 mg NH3/litre.  Tissue changes were 
observed in eyes, brains, fins, and blood of Atlantic salmon 
embryos and larvae exposed to concentrations ranging from 0.16 
to > 6.6 mg NH3/litre, with more marked changes at higher ammonia 
concentrations.  The effects observed included erosion of membranes 
of the eyes and shedding of the crystalline lens, dilatation of 
blood vessels in the liver and brain, accumulation of blood in the 
occipital region and in the intestines.  Reaction to light and 
mechanical stimulation gradually disappeared with increased ammonia 
concentration, and the heart rate slowed.  Morphological 
differences in development between experimental and control larvae 
were observed from the tenth day of exposure, including a lag in 
yolk resorption, decrease in growth of the skin fold, and 
contraction of skin pigment cells causing the skin colour to become 
paler than it was after hatching.  At concentrations up to 0.07 mg 
NH3/litre, no significant morphological differences were observed. 

    A second series of studies, at 16.5 C, was carried out in 
the 0.001 - 0.32 mg NH3/litre concentration range, beginning 
with larval salmon (Samylin 1969).  Concentrations of > 0.21 
mg/litre were lethal and caused weight loss in fry; 0.001 - 
0.09 mg NH3/litre caused a decrease in weight gain, though there 
were no differences in feeding activity, behaviour, or development 
at these concentrations compared with controls.  Dissolved oxygen 
concentrations in this second series of studies dropped as low as 
3.5 mg/litre. 

    Burrows (1964) tested fingerling chinook salmon for 6 weeks in 
outdoor water channels into which ammonium hydroxide was 
introduced.  Two studies were conducted, one at 6.1 C and the 
other at 13.9 C, both at pH 7.8.  The fish were then maintained in 
fresh water for an additional 3 weeks.  A recalculation of the 
reported non-ionized ammonia concentrations, based on more recent 
aqueous ammonia equilibrium tables, shows that the concentrations 
at 6.1 C were 0.003 - 0.006 mg NH3/litre and, at 13.9 C, were 
0.005 - 0.011 mg NH3/litre.  At both temperatures, and at all 
ammonia concentrations, some fish showed excessive proliferation 
and clubbing of the gill filaments.  The proliferation was 
progressive for the first 4 weeks, after which no measurable 
increase was observed.  After 3 weeks in fresh water, examination 
of fish exposed at 6.1 C indicated that recovery from the 
extensive proliferation had not taken place. In the study on larger 
fish at 13.9 C, a marked recovery from hyperplasia was noted after 
the 3 weeks in fresh water.  In the first study, the proliferated 
areas had consolidated; in the second, they had not.  It was 
postulated that continuous ammonia exposure is a precursor of 
bacterial gill disease. 

    Duplicate groups (90 fish each) of hatchery-reared coho salmon 
were exposed for 91 days to "river-water" solutions of ammonium 
chloride at concentrations of 0.019 - 0.33 mg NH3/litre.  Control 
groups were reared at 0.002 mg/litre.  Haemoglobin content and 
haematocrit readings were slightly, but significantly, reduced in 
fish exposed to the highest concentration tested, and there was 
also a greater percentage of immature erythrocytes.  Blood-ammonia 
and -urea concentrations were not significantly different after 91 
days, regardless of the concentration of ammonia to which the fish 
were exposed (Buckley et al., 1979).  Rankin (1979) exposed embryos 
of sockeye salmon,  Oncorhynchus nerka, to ammonia from fertilization 
to hatching.  Total embryo lethality occurred at concentrations of 
0.49 - 4.9 mg NH3/litre.  The times required to achieve 50% 
mortality at these concentrations were 40 - 26 days.  Mortality of 
the embryos exposed to 0.12 mg NH3/litre was 30%, and time to 50% 
mortality was 66 days. 

    Two full life-cycle ammonia toxicity tests, each lasting 
approximately 1 year, were conducted on fathead minnows (Thurston 
et al., in press).  These tests began with newly hatched fry and 
were continued through their growth, maturation and spawning 
stages; progeny were exposed from hatching through growth to 60 
days of age.  While no statistically-significant differences were 
observed in survival, growth, egg production, and egg viability, at 
concentrations up to 0.4 mg NH3/litre, effects were seen at 0.4 mg 

    Tissues from fathead minnows subjected to prolonged (up to 304 
days) ammonia exposure were examined (Smith, 1984).  Growths, some 
massive, were observed on the heads of several fish exposed to 
concentrations of 1.25 or 2.17 mg NH3/litre, and swollen darkened 
areas were observed on the heads of several fish exposed to 0.639 - 
1.07 mg NH3/litre.  Thurston et al. (in press) also reported 
lesions at concentrations below those at which other effects were 
observed.  Brain lesions were common at concentrations of 0.21 mg 
NH3/litre and higher.  Grossly and histologically, the severity of 
the lesions, which varied from mild to severe, was positively 
correlated with ammonia concentration.  The lesions appeared to be 
of a cell type originating from the meninx primativa covering the 
brain.  The hyperplastic tissue often completely surrounded the 
brain but was not observed around the spinal cord. 

    An early life-stage test initiated at the blastula stage of 
embryogenesis and extending through 39 days post-hatching was 
conducted on green sunfish (McCormick et al., 1984).  Retardation 
of growth was found in green sunfish exposed from embryo through 
juvenile life stages to concentrations of 0.489 mg NH3/litre or 
more, but not at 0.219 mg NH3/litre.  In a long-term test on green 
sunfish, Jude (1973) reported that, at levels higher than 0.17 mg 
NH3/litre, mean fish weight increased less rapidly than that of the 
controls on the 4 days following the introduction of ammonia. 
Thereafter, fish exposed to 0.26 and 0.35 mg NH3/litre grew at an 
increasing rate, while fish exposed to 0.68 and 0.64 mg NH3/litre 
remained the same for 12 days before increases in growth occurred. 

    Four simultaneous early life-stage ammonia tests with 
smallmouth bass were carried out at 4 different pH levels, ranging 
from 6.6 to 8.7, in order to examine the effect of pH on chronic 
ammonia toxicity.  Exposure to ammonium chloride solutions began on 
2- to 3-day old embryos and lasted for 32 days.  The end-point 
observed was growth, and ammonia was found to have a greater effect 
on growth at lower pH levels than at high.  Concentrations found to 
retard growth ranged from 0.056 mg/litre at pH 6.60, to 0.865 
mg/litre at pH 8.68 (Broderius et al., in press). 

    In early life-stage tests (29 - 31 days' exposure) on channel 
catfish and white sucker, no significant effects on percent hatch 
or larval survival were observed for channel catfish exposed to 
ammonium chloride at concentrations as high as 0.583 mg NH3/litre 
and for white sucker at concentrations as high as 0.239 mg 
NH3/litre.  Significant retardation of growth, however, occurred in 
channel catfish at concentrations of 0.392 mg NH3/litre or more and 
in white sucker at 0.070 mg NH3/litre and higher.  A delay in time 
to swim-up stage was also observed for both species at elevated 
(0.06 - 0.07 mg/litre) ammonia concentrations (Reinbold & 
Pescitelli, 1982a). 

    In cultured channel catfish fingerlings, exposed for periods 
of approximately 1 month to concentrations of 0.01 - 0.16 mg 
NH3/litre, growth at 0.01 and 0.07 mg NH3/litre was not 
significantly different from that of control fish, but growth 
retardation at 0.15 and 0.16 mg NH3/litre was statistically 
significant (Robinette, 1976).  Colt (1978) and Colt & 
Tchobanoglous (1978) reported retardation of growth of juvenile 
channel catfish during a 31-day period of exposure to 
concentrations ranging from 0.058 to 1.2 mg NH3/litre.  Growth 
rate was reduced by 50% at 0.63 mg NH3/litre, and no growth 
occurred at 1.2 mg NH3/litre. 

6.5.  Wild and Domesticated Animals

6.5.1.  Wildlife

    Although ammonia has been known to be toxic for nearly a 
century (Hahn et al., 1983), studies describing the toxicological 
effects of ammonia on wildlife are very limited.  Normally, 
atmospheric ammonia does not appear to be a problem for wild 
animals, but concentrations of ammonia could reach harmful levels 
in accidents during transport near forests and remote areas.  NRC 
(1979) has reported 2 types of observations in relation to this 
topic:  (a) the use of anhydrous ammonia to exterminate wild birds 
and mice in farm buildings; and (b) the tolerance of bats to 
atmospheric ammonia. 

    The use of anhydrous ammonia has been recommended for 
exterminating wild birds and mice from farm buildings by Day et al. 
(1965).  The technique is simple, economical, and does not leave 
any harmful residue.  The farm buildings, after removal of the 
livestock, were sealed and treated with anhydrous ammonia at 1600 
mg/m3 (2285 ppm) for 7 min and then reopened.  Ammonia fumes were 
fatal for the wild inhabitants, particularly for wild birds.  

Within 0.5 h, dead starlings, sparrows, pigeons, and mice were 
removed from the barns.  Farm animals were allowed to enter the 
barns within 1 h of their reopening.  According to laboratory 
studies, the mouse appears to be more sensitive than other animal 
species such as the rat, rabbit, and guinea-pig.  When mice were 
exposed for 10 min to ammonia at 6140 - 9060 mg/m3 (8770 - 12 940 
ppm), death with convulsion began after 5 min of exposure, and over 
50% of the mice died before the study was completed.  The surviving 
animals appeared to recover rapidly, but another 4% died between 
the 6th and 10th days after exposure (Underwriters Laboratories, 

    Large colonies of Guano bats  (Tadarida brasiliensis) frequently 
inhabit caves or other areas, producing large amounts of guano, 
which, on bacterial decomposition, results in a very high 
concentration of ammonia in the atmosphere.  Although high ammonia 
concentrations, together with high relative humidity in caves, 
discoloured the pelage of bats (Eads et al., 1955; Constantine, 
1958; Mitchell, 1964), no other adverse physiological effects were 
observed in these mammals.  This apparent adaptation to inhaled 
ammonia prompted laboratory studies relating to the physiological 
mechanisms involved in ammonia tolerance in different species of 
bats (Mitchell, 1963; Studier, 1966; Studier et al., 1967). 

    California leaf-nosed bats  (Macrotus californicus) can 
tolerate exposure to 2100 mg/m3 (3000 ppm) for up to 9 h (Mitchell, 

    Ammonia toxicity at lethal doses was manifested by corrosion 
of the skin and mucous membranes, pulmonary oedema, and distinct 
visceral damage.  The blood-non-protein nitrogen in the exposed 
bats was significantly elevated without any increase in urinary-
urea or -ammonia. 

    Studier et al. (1967) studied the effects of increasing 
concentrations of atmospheric ammonia on ammonia tolerance and 
metabolic rates in rats, mice, and 3 species of bat.  Rats, mice, 
and 2 species of bat  (Myotis lucifugus and  Eptesicus fuscus)  
tended to show increased oxygen utilization, when exposed to 
increased ammonia levels.  However, the guano bat  (Tadarida 
 brasiliensis) exhibited a large decrease in oxygen utilization 
with increasing ammonia concentration (i.e., 74% depression) when 
exposed to air containing 4900 mg/m3 (7000 ppm) of gaseous ammonia.  
Earlier, Studier (1966) had shown that ~35% of gaseous ammonia 
filtered through the mucous linings in the respiratory passage in 
guano bats, when they were exposed to 2100 mg/m3 (3000 ppm) of 
ammonia.  There was no change in their normal blood pH during 
exposures to high ammonia concentrations.  The animals, however, 
exhaled measurable amounts of ammonia when transferred to normal 

6.5.2.  Domesticated animals  Oral exposure

    (a)   Ruminants

    The use of urea as a partial source of nitrogen in ruminant 
nutrition is limited by its toxicity, which results from its 
metabolism to ammonia. 

    The toxic effects of urea in ruminants are related to a high 
ammonia content in the blood.  Urea itself is not as toxic as the 
ammonia, which is rapidly released in the rumen by the action of 
bacterial urease (EC on ingested urea (Bloomfield et al., 
1960).  The absorption of this excess ammonia has been shown to 
depend on the pH of the ruminal contents. 

    Hogan (1961) examined the effects of pH on the absorption of 
ammonia from the rumen in sheep.  When an ammonia-containing buffer 
at pH 6.5 was placed in the rumen, absorption increased with the 
concentration gradient.  At a pH of 4.5, however, the concentration 
of ammonia in the rumen did not affect the absorption across the 
epithelium.  The net loss of ammonia-nitrogen from the rumen at pH 
6.5 was more than 3 times the loss at a pH of 4.5. 

    Additional support for the effect of pH on ammonia absorption 
across the ruminal epithelium in sheep has been presented by 
Bloomfield et al., (1962).  As the pH of the ruminal contents 
increased from 6.21 to 6.45, no ammonia was absorbed; however, as 
the pH increased to 7.59, the absorption rate was 16 mmol/litre per 
h.  One sheep with a ruminal pH of 7.7 died of ammonia toxicity 
within 30 min.  These data support the hypothesis that the non-
ionized ammonia, which increases at higher pH, penetrates the lipid 
layers of the ruminal epithelium more effectively than the charged 
ammonium ion (Coombe et al., 1960). 

    Toxic signs become apparent as the blood-ammonia-nitrogen 
increases to 10 mg/litre; tetanic spasms occur between 10 and 
20 mg/litre and are followed by death (Repp et al., 1955; McBarron 
& McInnes, 1968; Kirkpatrick et al., 1972, 1973; Webb et al., 
1972).  Wilson et al. (1968a) attributed the cause of death to the 
cardiotoxic effects of ammonia produced from the urea.  However, 
Singer & McCarty (1971) observed that only one sheep died of 
ventricular fibrillation and the remainder of respiratory failure.  
More recently, Edjtehadi et al. (1978) reported the arrest of 
respiration, and not cardiovascular collapse, as the cause of death 
in sheep. 

    Certain aspects of the blood chemistry have been described for 
sheep with urea poisoning (Kirkpatrick et al., 1973; Edjtehadi et 
al., 1978).  In general, during the initial stages of urea 
toxicosis, an alkalosis is induced, followed by systemic acidosis 
due to hyperventilation prior to death (Edjtehadi et al., 1978).  
In addition to increases in blood-ammonia and blood-urea levels, 
there is a marked increase in the blood-glucose level, with no 

change in ketone concentrations in the body (Singer & McCarty, 
1971).  The following changes have been recorded at death:  red-
cell count and haemoglobin concentration increased by 7.9%; white-
cell count decreased by 27.5%; and packed-cell volume increased by 
11.4%.  Mean corpuscular volume, mean corpuscular haemoglobin, and 
mean corpuscular haemoglobin concentration were not substantially 
changed (Kirkpatrick et al., 1973). 

    Pathological effects of ammonia toxicity in sheep have been 
described by Singer & McCarty (1971).  The changes were similar 
when sheep received intraruminal injections of ammonium chloride, 
ammonium sulfate, or a mixture of ammonium chloride, carbonate, 
phosphate, and sulfate.  General passive hyperaemia and numerous 
petechial and ecchymotic haemorrhages in the musculature, heart, 
thymus, and lungs were found.  The lungs were distended and 
severely congested.  On microscopic examination, the pulmonary 
lesions included severe hyperaemia, haemorrhage, alveolar oedema, 
and alveolar emphysema.  In the thymus, there was degeneration and 
necrosis of Hassall's corpuscles and centrilobular haemorrhages.  
Lesions in kidneys included severe generalized cloudy swellings and 
multiple foci of early coagulative necrosis of the proximal 
convoluted tubules, general hyperaemia of the glomerular tufts, and 
degeneration of the glomerular tuft cells. 

    In Marschang & Crainiceanu's (1971) study on the effects of 
ammonia in the air of calf stables, ammonia concentrations 
reportedly ranged from 0.7 to 140 mg/m3 (1 - 200 ppm).  During 
these periods of high ammonia concentration, high mortality rates 
were observed among the calves.  The authors suggested that the 
high ammonia content weakened the resistance of the animals and 
thus created conditions for the development of secondary 
infections.  Deaths were mainly caused by respiratory diseases.  
Autopsy indicated various types of change in the lungs, chiefly 

    Air-ammonia concentrations in 3 cattle-fattening facilities in 
Romania were measured by Marschang & Petre (1971), who found 
concentrations ranging from 2 to 1400 mg/m3 (3 - 2000 ppm).  
Morbidity (mainly from respiratory disease) and mortality rates 
increased with ammonia concentrations in the stalls and decreased 
as some of the toxic gas levels decreased to admissible 
concentrations.  The authors suggested that ammonia is the most 
important environmental factor in producing disease in cattle-
fattening stalls.  They did not refer to the growth rate of the 
cattle; however, in an additional report, Marschang (1972) observed 
a marked decrease in the growth rate of fattening cattle, when the 
ammonia content of the stable was high. 

    (b)   Monogastric animals

    Monogastric animals are considered relatively tolerant to 
dietary urea, since they lack the large amounts of bacterial urease 
present in the rumen of ruminants.  Horses may frequently consume 
cattle rations that contain urea or other non-protein-nitrogen 

    Hintz et al. (1970) found that the urease activity in the 
caecal fluid from ponies was 17 - 25% of that reported for bovine 
rumen fluid.  They subjected 8 ponies to oral doses of urea at 3.3 
- 3.6 g/kg body weight, to study the toxic effects of urea 
overdosage.  Seven of the ponies died of ammonia toxicity, 3 - 12 h 
after treatment.  Clinical signs of toxicosis were characteristic 
of severe central nervous system derangement.  These signs were 
similar to those previously reported for ruminants, with the 
exception of head pressing against a fixed object prior to loss of 
coordination.  No significant gross lesions were observed on 
necropsy.  Blood-ammonia increased linearly until death.  Blood-
alpha-keto-glutarate decreased initially, reached minimal values 
at about 30 min and then increased to 3 times the zero time value.  
Blood-glucose remained constant for the first 2.5 h and then 
increased to about 3 times the initial value.  Blood-pyruvate 
decreased during the first 3.5 h and then increased to 10 times 
the initial values.  Inhalation exposure

    (a)   Swine

    The acute inhalation effects of ammonia in swine are given in 
Table 15. 

    (b)   Poultry

    As discussed previously, poultry are exposed to ammonia in the 
atmosphere of poultry houses; this ammonia is released from the 
action of bacteria on poultry wastes.  The toxic effects of this 
exposure are primarily seen in the eyes and respiratory tract. 

    An idiopathic ocular disorder in young chicks, designated 
keratoconjunctivitis, was first described by Bullis et al. (1950), 
who attributed it to environmental factors in the rearing 

    Anderson et al. (1964a) reported that chickens exposed
continuously to ammonia at 14 mg/m3 (20 ppm) showed some signs
of discomfort, including rubbing of the eyes, slight lachrymation, 
anorexia, and, later, weight loss.  Chickens exposed to ammonia at 
14 mg/m3 for as little as 72 h were more susceptible to aerosol 
infection with Newcastle disease virus.  Gross and microscopic 
damage to the respiratory tract could be detected after 6 weeks of 
continuous exposure to ammonia at 14 mg/m3.  Valentine (1964) 
reported tracheitis in chicks exposed to ammonia at 42 - 49 mg/m3 
(60 - 70 ppm).  The breathing of the birds was audible as moist 
rales with bubbling sounds.  At post-mortem examination, some of 
the birds had slight congestion of the lungs with excess mucous in 
the respiratory tract.  The mucous membranes of the trachea were 
much thicker than in the control birds, and there was leukocytic 
infiltration of the tissue.  It was suggested that this tracheitis 
may predispose the affected birds to respiratory diseases with the 
added risks of secondary infections. 

    Charles & Payne (1966a) reported that exposure to atmospheric 
ammonia at 70 mg/m3 (100 ppm) caused a reduction in carbon dioxide 
production and depth of respiration and a 7 - 24% decrease in the 
respiration rate of laying hens.  The authors also observed that 
broilers reared to 28 days of age in atmospheres containing high 
concentrations of ammonia consumed less food and grew more slowly 
than unexposed chickens.  Pullets reared in high-ammonia 
atmospheres matured up to 2 weeks later than pullets reared in 
ammonia-free atmospheres. 

    Airsacculitis, one of many respiratory diseases in poultry, has 
been associated with high ammonia concentrations in poultry houses 
(Ernst, 1968).  High concentrations of dust were also noted during 
periods of winter confinement, when high ammonia concentrations 
were observed.  The incidence and severity of air-sac lesions in 
turkeys increased signficantly with high concentrations of dust 
(0.6 - 1.0 mg/m3 or 21 - 35 mg/m3) in the atmosphere.  Flocks with 
a high rate (47%) or a low rate (2%) of infection with  Mycoplasma 
 meleagridis were similarly affected.  No significant interaction 
between dust and ammonia concentrations (up to 21 mg/m3 or 30 ppm) 
with regard to effects on the development of air-sac lesions was 
found.  Mortality rate and feed conversion were not significantly 
affected by exposure to dust and ammonia.  There was considerable 
loss of cilia from the epithelium of the tracheal lumen and an 
increase in mucous-secreting goblet cells in turkeys exposed to 
high concentrations of dust and ammonia.  Areas of consolidation 
and inflammation were frequently observed in the lungs of these 
turkeys.  The air-sac lesions ranged from mild (lymphocytic 
infiltration) to severe (masses of gaseous material). 

    Airsacculitis has also been experimentally induced in chickens 
exposed to atmospheric ammonia and the stress of infectious 
bronchitis vaccination (Kling & Quarles, 1974).  Eighty Leghorn 
male chicks were maintained in 12 controlled-environment chambers.  
Ammonia at 0, 17.5, or 35 mg/m3 (0, 25, or 50 ppm) was introduced 
into the chambers from the 4th to 8th weeks of age.  An infectious 
bronchitis vaccination was administered to all chicks at 5 weeks of 
age.  Body weights and feed efficiencies were determined at 4, 6, 
and 8 weeks. At 4, 5, 6, and 8 weeks, lung and bursae of Fabricius 
weights, haematocrits, and air-sac scores were determined.  Body 
weights and feed efficiencies were significantly reduced in the 
ammonia chambers.  The bursae of Fabricius in the ammonia-stressed 
chickens were significantly larger than those of controls at 5 
weeks of age and significantly smaller at 8 weeks of age.  Chickens 
grown in ammoniated environments had significantly larger lungs at 
8 weeks.  Haematocrits were not significantly different among 
treatments.  Total air-sac scores were significantly higher in the 
ammonia-stressed chickens at 8 weeks.  The results indicated that 
chickens were stressed by the ammonia at 17.5 or 35 mg/m3, and by 
the infective bronchitis vaccination.  In a similar study (Quarles 
& Kling, 1974), exposure of broiler chicks to 17.5 or 35 mg/m3 (25 
or 50 ppm) from the 4th to the 6th week resulted in the observation 
of severe airsacculitis at 6 and 8 weeks of age.  During the test, 
airborne bacterial counts were significantly higher in chambers 
with ammonia than in control chambers. 

Table 15.  Acute inhalation effects of ammonia in swine
Ammonia concentration      Dose     Effects                                 Reference
196 mg/m3 (280 ppm)        single   frothing of the mouth and excessive     Stombaugh et al. (1969)
                                    secretion; after 36 h, convulsions
                                    occurred, and breathing was extremely 
                                    short and irregular; the effects 
                                    ceased after a few h

7, 35, 70, or 105 mg/mg3   5 weeks  high concentrations (70 and 105 mg/m3)  Stombaugh et al. (1969)
(10, 50, 100, or 150 ppm)           appeared to cause excessive nasal,
                                    lachrymal, and mouth secretion after 
                                    3 - 4 days of exposure at 35 mg/m3, 
                                    the secretory rate was only slightly
                                    higher than that in control animals; 
                                    after 1 - 2 weeks of exposure, the 
                                    signs noted appeared to lessen 
                                    gradually; examination of respiratory 
                                    tract did not reveal any significant 
                                    gross- or microscopic differences 
                                    related to ammonia exposure

0, 35, 70, or 105 mg/m3    4 weeks  decrease in pig growth was noted at     Drummond et al. (1980)
(0, 50, 100, or 105 ppm)            all concentrations; at 35 or 70 mg/m3, 
                                    pigs converted feed to body weight 
                                    gain more efficiently than either 
                                    controls or pigs exposed to 105 mg/m3; 
                                    an acute imflammatory reaction in the 
                                    tracheal epithelium and a mild-to-
                                    heavy exudate in the turbinate lumen 
                                    were observed at 70 and 105 mg/m3, 

0 and 70 mg/m3 (100 ppm)   2 - 6    conjunctival irritation after the       Doig & Willoughby (1971)
(1 - 7 weeks old)          weeks    first day which persisted for 1 week;
0 + dust                            dust alone had no effect; histopatho-
(100 ppm + dust)                    logical changes were limited to the
                                    nasal and tracheal epithelium; there 
                                    was no evidence of structural damage 
                                    in the bronchial epithelium or alveoli

    Charles & Payne (1966b) studied the effects of graded 
concentrations of atmospheric ammonia on the performance of laying 
hens.  At 18 C, ammonia at 73.5 mg/m3 (105 ppm) significantly 
reduced egg production, after 10 weeks of exposure.  No effects 
were observed on egg quality.  Food intake was reduced and weight 
gain was lower.  No recovery in egg production occurred when the 
treated groups were maintained for an additional 12 weeks in an 
ammonia-free atmosphere.  Similar results were observed at 28 C, 
under the same conditions.  Earlier work had indicated that egg 
quality could be affected by ammonia exposure (Cotterill & 
Nordskog, 1954).  Freshly-laid eggs were exposed to various 
concentrations of ammonia in a desiccator for 14 h at room 
temperature and then moved to normal atmosphere for another 32 h at 
50 C, before examination.  There was evidence of absorption of 
ammonia into the eggs and significant impairment of interior egg 
quality, as measured by Haugh units, pH, and transmission of light.  
The authors suggested that the quality of eggs left all day in hen 
houses containing high concentrations of ammonia might be adversely 


    Ammonia, a by-product of protein and nucleic acid metabolism 
and a minor component of the diet, is in a state of flux in the 
body, though it is present in low steady-state concentrations in 
body fluids.  In animals, metabolically-produced ammonia is 
conjugated and excreted.  Toxicity will only occur if these 
conjugation and excretion mechanisms are defective, or if they are 
overwhelmed by excessive exposure. 

7.1.  Absorption

7.1.1.  Respiratory tract

    Egle (1973) studied the retention, over a short period of time, 
of inhaled ammonia in air at concentrations in the range 150 - 
500 mg/m3 (214 - 714 ppm), in mongrel dogs of both sexes (7 - 37 
per study).  Retention was not materially affected by respiratory 
rate, tidal volume, or concentration.  Retention by the whole 
respiratory tract averaged 78%, but the complexity of the dynamics 
of this retention is illustrated by the fact that when respiration 
was via an endotracheal tube, limiting exposure to the lower 
respiratory tract, and when the upper respiratory tract (muzzle to 
tracheal bifurcation) was perfused tidally, the retention was 78% 
in each case.  However, unidirectional perfusion of the upper 
respiratory tract with ammonia in air produced a higher mean 
retention of 89%. 

    Schaerdel et al. (1983) exposed 4 groups of rats, 8 per group, 
to average ammonia concentrations of 11, 23, 220, or 826 mg/m3 
(15, 32, 310, or 1157 ppm) for 24 h.  Ammonia in blood was measured 
at 0, 8, 12, and 24 h.  At the 2 lowest concentrations, there was 
no increase in blood-ammonia.  However, after 8 h at 220 and 
826 mg/m3, significant increases of 0.192 and 0.244 mmol (3.26 and 
4.18 mg/litre) were noted.  After 12 and 24 h, the increases were 
not so marked, indicating an increase in ammonia metabolism. 

    In a study by Silverman et al. (1949), 7 male volunteers were 
exposed to 350 mg/m3 (500 ppm) for 30 min.  Initial ammonia 
retention was not reported for all subjects, but, in one instance, 
was around 75%.  Retention decreased progressively until at 
equilibrium it was 23% (range 4 - 30%); equilibrium was reached in 
10 - 27 min.  Some irritation was noted in the nose and throat, 
leading to the suggestion that ammonia at this concentration was 
primarily absorbed by the upper respiratory tract.  Levels of 
blood-urea-nitrogen (BUN), non-protein nitrogen, urinary-urea, and 
urinary-ammonia remained normal. 

    In another study (Kustov, 1967), exposure of human volunteers 
to ammonia for a longer duration (14 mg/m3 (20 ppm) for 8 h) was 
accompanied by a statistically-significant increase in BUN from 
23.9 to 30 mg%. 

    An early study was conducted by Landahl & Herrmann (1950) on 
the retention of gases by the human nose and lung.  At ammonia 
concentrations of between 40 and 350 mg/m3 (57 and 500 ppm) and a 
mean minute volume of 6 - 7 litre/min, for short durations (< 2 
min), they found that approximately 92%  2% was retained in the 
respiratory system (i.e., mouth, lungs, etc.) in 2 male volunteers, 
tested 4 times.  Differences in concentrations of ammonia did not 
affect retention values.  In a separate study, about 83% was 
retained in the nasopharnyx at a flow rate of 18 litre/min, but 
only 63 - 71% was retained when the flow rate was tripled.  These 
data are consistent with, though somewhat higher than, those 
reported by Egle (1973) for exposure in dogs. 

    It should be noted that experimental animals kept in cages may 
be exposed to relatively high concentrations of ammonia, even 
exceeding 100 mg/m3, due to the degradation of urea in urine and 
faeces (Flynn, 1968; Schaerdel et al., 1983). 

    Because ammonia is very water soluble, and thus absorbed by the 
mucous coating in the upper respiratory tract, the lungs are 
protected from the effects of exposure to low concentrations of 
ammonia (Haggard, 1924; Boyd et al., 1944).  At the levels of 
ammonia associated with ambient air (i.e., 1 - 200 g/m3), very 
little, if any, is absorbed through the lungs. 

    If a person breathes an ammonia concentration in air of 
18 mg/m3 (a common occupational exposure limit) at 1 m3/h and, 
if all the ammonia is retained, then 18/60 = 0.3 mg ammonia/min 
would require to be cleared by hepatic blood flow (say 1 
litre/min).  The rise in systemic blood-ammonia would be calculated 
at 0.3 mg/litre or 0.018 mmol.  If the more realistic assumption of 
30% retention were used, the corresponding increase in blood-
ammonia concentration would be 0.09 mg/litre, about mol.  An 
arterial fasting ammonia concentration of 1.05 mg/litre has been 
reported in healthy subjects (Conn, 1972), so the calculated rise 
is only 10% over fasting levels. 

7.1.2.  Gastrointestinal tract

    Ammonia is a trace compound in foods.  Ammonia that is absorbed 
from the intestinal tract arises primarily from the bacterial 
degradation in the intestine of amino and nucleic acids from 
ingested food, endogenous epithelial debris, and mucosal cell 
luminal secretions, or from the hydrolysis of urea diffusing from 
the systemic circulation into the intestinal tract.  The estimated 
ammonia production from various substrates in the human intestines 
ranges from 10 mg/day in the duodenum to 3080 mg/day in the colon 
and faecal contents.  Nearly all the ammonia formed is absorbed 
(about 99% or 4000 mg).  In healthy individuals, absorbed ammonia 
is mainly catabolized rapidly in the liver to urea; therefore, 
relatively small amounts reach the systemic circulation after 
absorption from the gastrointestinal tract as a consequence of this 
"first pass effect" (Summerskill & Wolpert, 1970). 

    Castell & Moore (1971) have shown that ammonia uptake from the 
human colon, the major site of ammonia production, increases with 
increased pH of the luminal contents.  A similar effect of pH has 
been shown for the absorption of ammonia from the rumen of sheep 
(Hogan, 1961; Bloomfield et al., 1962).  Since an increase in pH 
increases the proportion of non-ionized ammonia, the authors 
concluded that simple non-ionic diffusion was responsible for the 
majority of ammonia transport.  Evidence also exists for the active 
transport of the ammonium ion from the intestinal tract.  Castell & 
Moore (1971) showed that ammonia transport by the human colon, 
though greatly diminished, still occurred when the luminal pH was 
reduced to 5, at which value non-ionized ammonia would be virtually 
absent.  Mossberg & Ross (1967) and Mossberg (1967) studied the 
absorption of ammonia from isolated intestinal loops of the golden 
hamster and found that the ileal movement of ammonia against a 
concentration gradient was inhibited by cyanide, dinitrophenol, and 
anaerobiosis.  This suggested that an energy-dependent transport 
system was operable in the ileum, where ammonia was absorbed 
preferentially, but not in the jejunum. 

    Membrane transport of the ammonium ion by the human erythrocyte 
has been demonstrated (Post & Jolly, 1957). 

7.1.3.  Skin and eye

    Ammonia is highly mobile in all tissues and the ammonium ion 
readily penetrates the corneal epithelium.  Within 5 seconds, 
traces are present in the anterior chamber of the eye (Siegrist, 
1920).  However, systemic and intra-ocular absorption by these 
routes are not quantitatively important. 

7.2.  Distribution

    The ammonia normally present in all tissues in the body 
constitutes a dynamic pool throughout which absorbed ammonia is 
distributed.  The distribution of total ammonia between body 
compartments is strongly influenced by pH.  The non-ionized NH3 is 
freely diffusible, whereas NH4+ is less diffusible and relatively 
confined in compartments.  The lower the pH of a compartment, the 
greater its total ammonia content (NRC, 1979). 

    The fate of absorbed ammonia molecules has been studied in man, 
by measurement of blood constituents, and, in experimental animals, 
by following the distribution of 15N after the administration of 
15NH3 and compounds. 

7.2.1.  Human studies

    In human beings, inhalation of ammonia (350 mg/m3; 500 ppm) for 
30 min did not have any effect on blood-nitrogen levels (Silverman 
et al., 1949).  In another study, exposure of human subjects to 
14 mg ammonia/m3 (20 ppm), for a duration of 8 h, revealed a 
statistically-significant increase in BUN (from 23.9 to 30 mg%) 
(Kustov, 1967).  However, this is unlikely to have represented the 

metabolic conversion of absorbed ammonia, since the increase was 
far greater than could have been accounted for by the quantity of 
ammonia inhaled. 

    Administration of 9 mg NH4Cl/kg body weight, orally, to 20 
healthy adult male and female volunteers caused a transient 
increase in ammonia concentrations in arterial blood in 
approximately half of the subjects.  Concentrations peaked (mean, 
1.4 mg NH3/litre) at 15 min and returned to fasting levels (mean, 
1.05 mg NH3/litre) by 30 min.  However, in 50 male patients with 
cirrhosis of the liver, blood-ammonia levels increased from already 
elevated fasting levels (mean, 1.56 mg NH3/litre) to much higher 
peak concentrations (mean, 3.7 mg NH3/litre) at 15 min, followed by 
a slow decrease reflecting impaired hepatic urea synthesis.  Blood-
ammonia levels, before and after administration of ammonium 
chloride, were significantly higher among cirrhotic patients with 
portacaval anastomoses than among patients lacking such shunts 
(Conn, 1972). 

7.2.2.  Animal studies

    The distribution, as well as the metabolic fate of ammonia, 
depends on the route of administration.  After intestinal 
absorption, ammonium ions are primarily transformed by the liver 
to urea, and subsequently excreted in the urine.  In contrast, 
intravenously-administered ammonium salts are more available as 
non-essential nitrogen for protein synthesis (Furst et al., 1969).  
However, some orally-administered ammonia, has been found to be 
incorporated into tissue proteins.  Incorporation of 15N was higher 
in serum globulins than in albumin after intravenous dosing with 
15N-ammonium salts, but this order was reversed after oral 
administration (Furst et al., 1970).  The amount incorporated into 
protein by this route was greater, when protein intake was 
restricted (Richards et al., 1968). 

    Duda & Handler (1958) analysed the tissue of rats, 15 min after 
an intravenous injection of 15N-ammonium lactate, and found that 
its major metabolites, glutamine, and urea, were quickly 
distributed throughout the body.  The highest levels of labelled 
urea (in moles 15N/g tissue) were found in the kidney (0.0217) and 
liver (0.0159), while lesser amounts were found in the heart 
(0.0086), spleen (0.0067), brain (0.0029), testes (0.0027), and 
carcass (0.0070).  The highest levels of labelled glutamine (moles 
15N/g tissue) were found in the heart (0.086) and liver (0.055) and 
lesser amounts (0.005 to 0.032) in the brain, spleen, carcass, 
kidney, and testes. 

    Vitti et al. (1964) examined the distribution of 15N from 
ammonium citrate, administered by different routes, into the 
proteins of various tissues of hypophysectomized rats.  The liver, 
kidney, and spleen contained greater concentrations of 15N 
incorporated into proteins than heart or muscle fractions during 
72 h following intragastric, intraperitoneal, and subcutaneous 
administration of 15N-ammonium citrate.  After the first 6 h, 
during which the intragastric route gave higher values, the 

quantity of 15N incorporated into liver-protein was not 
substantially affected by the route of administration.  In most of 
the other tissues studied, however, 15N incorporation tended to be 
least by the intragastric route, followed, in increasing order, by 
the intraperitoneal and subcutaneous routes.  By the last route, 
more labelled ammonia was apparently made available to the widely 
distributed glutamine-synthetase (EC system (section 

7.3.  Metabolic Transformation 

    Most organisms have mechanisms for conjugating ammonia into 
non-toxic compounds for excretion.  Terrestrial mammals synthesize 
urea, which requires the concerted action of several enzymes of the 
Krebs-Henseleit (urea) cycle.  One of these enzymes, glutamine 
synthetase (EC, was present in the brains of all 
vertebrate species examined.  Glutamine synthetase was also present 
at significant levels in the liver in all organisms examined (Brown 
et al., 1957). 

    Exogenous ammonia, administered intravenously as an ammonium 
compound, is metabolized to glutamine as the major early product 
(Duda & Handler, 1958).  The ammonia fixed in glutamine may 
eventually end up in amino acids, purines, pyrimidines, or other 
nitrogen-containing compounds.  Ingested ammonium chloride or 
endogenous ammonia is absorbed into the portal vein and converted 
in the liver to urea (Furst et al., 1969; Goodman & Gilman, 1970; 
Pitts, 1971). 

    Results of studies on the metabolic fate of dietary ammonium 
citrate (Foster et al., 1939) and intravenously-administered 
ammonium lactate (Duda & Handler, 1958) in rats showed that urea 
synthesis represented a nearly constant fraction of the 
administered ammonia over a large concentration range.  Besides 
glutamine and urea, labelled nitrogen also appeared in creatine, 
glycine, alanine, proline, histidine, arginine, glutamic acid, and 
aspartic acid.  Vitti et al. (1964) examined the incorporation of 
15N from ammonium citrate into proteins of liver, heart, kidney, 
spleen, and muscle fractions of untreated and growth hormone-
treated, hypophysectomized rats, and found differences in the 
metabolic fate, depending on the route of administration.  
Subcutaneous injection facilitated the labelling of amide nitrogen, 
indicating extensive disposition via glutamine synthesis.  In 
contrast, intragastric or intraperitoneal administration resulted 
in the labelling of arginine, glutamic acid, and other alpha-amino 
acids of the liver.  Amide-nitrogen was labelled to a much lesser 
extent than by the subcutaneous route.  The tissue distribution of 
the label also differed according to the route of entry (section 

7.4.  Reaction with Body Components

    Ammonia-nitrogen is central in nitrogen metabolism and 
therefore becomes incorporated in all proteins and nitrogen-
containing components in the course of metabolic turnover.  Ammonia 
does not react with body components in the manner of alkylating 
agents or compounds that modify haemoglobin. 

7.5.  Elimination and Excretion

7.5.1.  Expired air

    Ammonia may be excreted through expired air.  Hunt (1977) 
reported human expired air levels of ammonia of between 105 and 
2219 g/m3; Larson (1977) reported values of between 196 and 
1162 g/m3, during mouth breathing.  These values are higher than 
those expected from equilibration with plasma- and lung-parenchyma-
ammonia levels (28 - 49 g/m3).  This is most likely due to the 
synthesis of ammonia from salivary urea by oral microflora (Biswas 
& Kleinberg, 1971).  Measurable amounts of free ammonia were also 
found in air expired by dogs given ammonium acetate intravenously 
(Robin et al., 1959), and normal dogs and human beings with 
hepatic-induced ammonia toxicity (Jacquez et al., 1957, 1959).  
Bloomfield et al. (1962) reported the presence of free ammonia in 
expired air from sheep during experimentally-induced urea toxicity. 
Normal levels of ammonia in the expired air of the rat have been 
reported to range from 7 to 247.1 g/m3, with a mean of 54.6 g/m3 
in nose-breathing animals and 23.8 - 520.8 g/m3, with a mean of 
200.2 g/m3 in tracheal-cannulated animals (Barrow & Steinhagen, 
1980).  The presence of ammonia in the expired air of human beings 
and experimental animals suggests that reaction products may be 
formed with a variety of airborne chemicals, thereby altering their 

7.5.2.  Urine and faeces

    Free ammonia is excreted by ammonotelic organisms (e.g., fish), 
uric acid by uricotelic animals (e.g., birds), and urea by 
ureotelic animals (e.g., mammals).  Mammals may also secrete 
ammonia directly into the urine.  Glutaminase (EC 
catalyses the release of ammonia in the kidney tubular epithelium, 
where it serves as an acceptor of H+ and regulates the acid-base 
balance (Van Slyke et al., 1943; White et al., 1973).  In acidosis, 
the renal concentration of glutaminase increases over several 
days, paralleling the increased excretion of ammonium ions (Davies 
& Yudkin, 1952; Muntwyler et al., 1956; Kamin & Handler, 1957); 
two-thirds of the urinary-ammonia is contributed by this pathway 
(Van Slyke et al., 1943), and approximately one-third by protein 
metabolism and ammonia clearance from the plasma by the kidney. 

    Oral and intravenous administration of ammonium lactate to 
healthy human volunteers produced different patterns of excretion, 
reflecting the effective barrier of the liver in preventing 
ingested ammonia from gaining access to peripheral circulation by 
converting most of the ammonia load to urea.  Urinary-ammonia 

excretion was increased 8-fold and urea excretion was reduced by 
one-half after intravenous injection, as opposed to oral 
administration (Gay et al., 1969), probably due to the anabolism 
involved in the "first pass" effect after oral administration. 

    Less than 1% of the 4 g total ammonia produced in the human 
intestinal tract, per day, is excreted in the faeces (Summerskill & 
Wolpert, 1970). 

7.6.  Retention and Turnover

    Some nitrogen derived from absorbed ammonia is incorporated in 
amino acids and proteins.  The rate of ammonia-derived nitrogen 
turnover is rapid, but depends on the nutritional state.  Thus, 
when 15NH4Cl had been administered orally to healthy male 
volunteers, for one week, 70% 15N was excreted by those on a 70-g 
protein/day diet, while only about 35% 15N was excreted by those on 
20 g protein/day (Richards et al., 1968, 1975). 

7.7.  Uptake and Metabolism in Plants

    Ammonia is used by many plants and preferentially by a few.  
However, ammonia is toxic, and its uptake in large quantities may 
put a severe strain on the carbohydrate metabolism of the plant in 
the provision of carbon skeletons for its detoxification.  The 
absorption of ammonium usually is coupled with the exchange of 
cations as H+.  Ammonia-nitrogen functions as a nitrogen source 
for the synthesis of amino acids, which are incorporated in 
proteins.  Plants that are able to absorb it in large amounts 
include many acid plants, such as Rumex, which are able to detoxify 
ammonia by forming ammonium salts of organic acids.  "Amide 
plants", such as beet, spinach, and squash, are able to form large 
amounts of the amides, glutamine, and asparagine and can withstand 
quite high concentrations of ammonium salts by detoxifying the 
ammonia.  Certain plants, such as rice, which live in water-logged 
anaerobic soils, require NH3 or reduced organic nitrogen 
fertilizer, alone. 


8.1.  Single Exposures

8.1.1.  Inhalation exposure

    LC50 studies and studies to determine the threshold for 
irritating effects on the respiratory system for the rat and mouse 
are summarized in Tables 16 and 17, respectively. 

Table 16.  Lethal concentrations (1-h exposure) of 
ammonia for rats and micea
Measured       Species  Mortality  Mean weight gain
concentration           ratiob     of survivors at
(mg/m3)                            14 days (g)
4347           rat      0/10       3.5
5474           rat      8/10       -c
6888           rat      9/10       -
controls       rat      -          21.4

2520           mouse    0/10       -0.2
3185           mouse    3/10       -0.7
4004           mouse    9/10       -
controls       mouse    -          1.6
a Adapted from:  MacEwen & Vernot (1972).
b Number dead/number exposed.
c Not enough survivors for comparison.

    The acute lethal dose of ammonia by inhalation has been 
determined for both the rat and the mouse (MacEwen & Vernot, 1972).  
The results are summarized in Table 16.  Male CFE rats ranging in 
weight from 200 to 300 g and male CF1 mice weighing from 20 to 30 g 
(ICR derived) were exposed for 1 h to several concentrations of 
ammonia.  Inhalation of ammonia gas produced immediate nasal and 
eye irritation followed by laboured breathing and gasping in all 
test groups.  In addition, convulsions were seen in mice.  
Surviving rats necropsied after 14 days showed moderate mottling of 
the liver, regarded as probable fatty infiltration, at the 5474 and 
6888 mg/m3 (7820 and 9840 ppm) dose levels.  Mice surviving the 2 
highest dose levels of 3185 and 4004 mg/m3 (4550 and 5720 ppm) 
showed mild congestion of the liver.  Pathological lesions were not 
seen in rats exposed to 4347 mg/m3 (6210 ppm) or mice exposed to 
2520 mg/m3 (3600 ppm).  The calculated 1-h LC50 values for the rat 
and the mouse were 5137 and 3386 mg/m3 (7338 and 4837 ppm), 

    In another inhalation study, an LC50 value for the rat, with a 
2-h exposure, was 7600 mg/m3 (10 860 ppm) (Alpatov, 1964).  In a 
further study, the threshold for acute effects (depression, then 
hyperactivity and convulsions) for a 2-h exposure was 85 mg/m3 (121 
ppm) (Alpatov & Mikhailov, 1963). 

Table 17.  Single-dose inhalation studies (LC50)
Species  Exposure time  LC50      Reference
         (min)          (mg/m3)
rat      120            7600      Alpatov (1964)

rat      60             5137      MacEwen & Vernot (1972)

rat      5              18 693    Prokop'eva et al. (1973)

rat      15             12 160    Prokop'eva et al. (1973)

rat      30             7035      Prokop'eva et al. (1973)

rat      60             7939      Prokop'eva et al. (1973)

rat      10             31 612    Appelman et al. (1982)

rat      60             11 620    Appelman et al. (1982)

mouse    10             7060      Silver & McGrath (1948)

mouse    60             3386      MacEwen & Vernot (1972)

mouse    60             2960      Kapeghian et al. (1982)

    Kapeghian et al. (1982) reported an acute inhalation toxicity 
study on male ICR mice, in which the 1-h LC50 with a 14-day 
observation period was calculated to be 2960 mg/m3 (4230 ppm).  
Lungs of mice that died during exposure were diffusely 
haemorrhagic.  Histology revealed acute vascular congestion and 
diffuse intra-alveolar haemorrhage.  A mild to moderate degree of 
chronic focal pneumonitis was also seen.  Focal atelectasis was 
evident in survivors sacrificed after the observation period.  
Liver damage was also seen in these mice.  There was evidence of 
swelling and increased cytoplasmic granularity of hepatocytes at 
2408 mg/m3 (3440 ppm) and scattered foci of frank cellular necrosis 
at 2954 mg/m3 (4220 ppm).  At 3402 mg/m3 (4860 ppm), necrosis was 
increased.  The liver lesions may have resulted from the 
compromised nutritional state of the mice.  Follicular hyperplasia 
in the spleen was also seen in surviving animals, but this was 
absent in animals that died during exposure. 

    The acute LC50 in male and female Wistar rats was 31 612 mg/m3 
(40 300 ppm) for a 10-min exposure, 20 017 mg/m3 (28 595 ppm) for a 
20-min exposure, 14 210 mg/m3 (20 300 ppm) for a 40-min exposure, 
and 11 620 mg/m3 (16 600 ppm) for a 60-min exposure (Appelman et 
al., 1982).  Survivors were observed for 14 days.  Clinical signs 
of restlessness, eye irritation, nasal discharge, mouth breathing, 
and laboured respiration were seen during exposure.  Gross necropsy 
revealed haemorrhagic lungs in animals that died during the study 
as well as in survivors.  No histopathology was performed. 

    Prokop'eva et al. (1973) reported that white rats exposed to 
high concentrations of ammonia (6000, 3000, 1000 mg/m3 or 6814, 
4307, 1436 ppm) for periods of 5, 15, 30, and 60 min exhibited 
dyspnoea, irritation of the respiratory tract and eyes, cyanosis of 
the extremities, and increased excitability.  The LC50 values for 
inhalation exposures of 5 and 15 min were 18 693 mg/m3 (26 704 ppm) 
and 12 160 mg/m3 (17 372 ppm), respectively, while for 30 and 60 
min, the values were 7035 mg/m3 (10 050 ppm) and 7939 mg/m3 (11 342 
ppm), respectively.  Inhalation of ammonia at concentrations of 
3000, 1000, or 300 mg/m3 (4307, 1436, 431 ppm) resulted in a drop 
in static muscular tension, leukocytosis, prolongation of the 
latent reflex time, increase in total protein and blood sugar, 
increased oxygen consumption, and a rise in the level of residual 
nitrogen.  No changes were observed in rats exposed to a 
concentration of ammonia of 100 mg/m3 (144 ppm), for 5, 15, 30, and 
60 min.  Animals exposed to high concentrations of ammonia (exact 
concentration not specified) developed pneumonia (Prokop'eva et 
al., 1973). 

    When exposed to toxic levels of ammonia, within 1 min, mice 
exhibited excitement, closing their eyes immediately and gasping 
(Silver & McGrath, 1948).  Groups of 20 mice were exposed to 
ammonia gas for 10 min at 9 concentrations ranging from 6100 to 
9000 mg/m3 (8758 to 12 921 ppm).  The median lethal concentration, 
calculated from the mortality at 10 days, was 7060  320 mg/m3 
(10 152  460 ppm).  Most (93%) deaths occurred rapidly, due to 
convulsions after 5 min of exposure.  Survivors usually recovered 
within 10 min. 

    The LC50 values for the rat and the mouse are summarized in 
Table 17. 

    Dose-dependent ultrastructural changes in the terminal airways 
of mice exposed for 3 - 60 min to ammonia (concentration 
unspecified) included oedema of the alveolar epithelium, 
development of intracapillary platelet thrombosis, increased 
secretions by the Clara cells, presumed to be phospholipids, and an 
increase in the number of empty lamellar bodies in the large 
alveolar cells (Niden, 1968). 

    Twenty cats were anaesthetized and exposed to 700 mg/m3 (1000 
ppm) for 10 min via endotracheal tube and then observed for up to 
35 days (Dodd & Gross, 1980).  All cats had severe dyspnoea, 
anorexia, and dehydration, 24 h after exposure.  Several measures 
of pulmonary function were impaired.  Gross pathology of the lungs 
showed various degrees of congestion, haemorrhage, oedema, 
interstitial emphysema, and collapse, all non-specific for any 
post-exposure day.  Bronchopneumonia was common, 7 days after 

    Barrow et al. (1978) exposed male Swiss-Webster mice to 
concentrations of ammonia ranging from 70 to 560 mg/m3 (100 -
1000 ppm) for 30 min.  The average respiratory rate depression in 
4 mice for each of 4 exposure levels was evaluated.  The maximum 
depression in respiratory rate at each exposure level occurred 

within the first 2 min.  The concentration expected to elicit a 50% 
decrease in respiratory rate (RD50) in mice, calculated by a 
regression equation for ammonia, was 212 mg/m3 (303 ppm) with 95% 
confidence limits of 132 - 343 mg/m3 (188 - 490 ppm).  Effects of 
ammonia exposure such as bradycardia and peripheral 
vasoconstriction accompanied respiratory rate depression at the 
RD50 and above. 

    A concentration of 350 mg/m3 (500 ppm) was reported by Wood 
(1979) to be the level at which unrestrained mice did not 
consistently adopt avoidance measures on inhalation of ammonia.  
Both this author and Barrow et al. (1978) claimed to offer more 
sensitive end-points for assessing ammonia irritation.  However, 
the no-observed-adverse-effect level reported by Wood (1979) was 
higher than the concentration determined by Barrow et al. (1978) to 
elicit 50% depression of respiratory rates in mice. 

    Dalhamn & Sjoholm (1963) tested  in vitro preparations of the 
tracheas of 8 rabbits.  Arrested ciliary activity was observed 
after 5 min of exposure to ammonia at 350 - 700 mg/m3 (500 - 
1000 ppm).  In  in vivo studies on rabbits, Dalhamn (1963) showed 
that the level of ammonia entering the nasal cavity, necessary to 
cause small changes in the rate of tracheal ciliary beating was 
1400 mg/m3 (2000 ppm).  This corresponds to a tracheal 
concentration of approximately 70 mg/m3 (100 ppm). 

    When anaesthetized male rabbits were exposed to 8 ammonia 
concentrations ranging from 700 to 14 000 mg/m3 (1000 - 20 000 ppm) 
(Richard et al., 1978b), bradycardia appeared at 1750 mg/m3 (2500 
ppm).  Hypertension, cardiac arrhythmia, macroscopic lung changes, 
and EEG abnormalities were also reported.  Signs appeared more 
rapidly at higher concentrations with the complete syndrome 
appearing at 3500 mg/m3 (5000 ppm). 

    Mayan & Merilan (1972) exposed 16 adult female New Zealand 
white rabbits to ammonia concentrations of 35 and 75 mg/m3 (50 and 
100 ppm) for 2.5 h.  The average decreases in respiratory rate, 
which were 34 and 32.7%, respectively, were significantly ( P < 
0.01) less than control values.  There were no histopathological 
changes in lung, liver, spleen, or kidneys. 

    Enzymatic alterations in rats following inhalation of low 
levels of ammonia have also been reported.  At concentrations of 
approximately 20 - 121 mg/m3 (29 - 173 ppm), there was a 
decrease in the activities of liver succinic dehydrogenase (EC, lactate dehydrogenase (EC, glucose-6-phosphate 
dehydrogenase (EC, and adenosine triphosphatase (EC  Liver acid phosphatase (EC activity was 
increased (Zlateva et al., 1974). 

    When 180 mice were exposed for 10 min to ammonia at 6139 -
9058 mg/m3 (8770 - 12 940 ppm), death with convulsions began to 
occur 5 min after exposure.  One hundred mice died during the 
exposure.  The surviving animals (80) recovered rapidly; however, 
7 died between the sixth and tenth days following exposure (NRC, 

8.1.2.  Oral exposure

    The effects of ammonia and its compounds are mainly of 2 types.  
The first is the effect of ammonia itself.  The second is the 
effect of the anion bound to the ammonium ion.  Ammonium chloride, 
especially, will mainly exert its effects in the mammalian body due 
to the formation of hydrogen chloride.  Most of the experimental 
work concerning the oral route of administration has centred on 
ammonium chloride, which has been used extensively in the study of 
metabolic acidosis.  There have been few studies in which attempts 
have been made to identify the role of the ammonium ion and ammonia 
in the effects (Table 18). 

    Median lethal doses (LD50s) of 4400 and 3100 mg/kg body weight 
have been reported for ammonium sulfamate in the rat and the mouse, 
respectively.  (Vinokurova & Mal'kova, 1963).  A similar figure for 
the oral LD50 in the rat of 4520 (4070 - 5020) mg/kg was reported 
by Bukhovskaya et al. (1966).  Frank (1948) reported a lethal dose 
for ammonium sulfate of between 3000 and 4000 mg/kg body weight in 
the rat.  Effects of metabolic acidosis induced by ammonium chloride

    The ingestion of ammonium chloride in doses of around 500 - 
1000 mg/kg body weight per day, for periods ranging from 1 to 8 
days, has induced metabolic acidosis in mice, guinea-pigs, rats, 
rabbits, and dogs.  However, Boyd & Seymour (1946) did not report 
any toxic effects at doses of up to 1 g/kg body weight in rats, 
rabbits, guinea-pigs, and cats (50 animals per group). 

    Clinical signs, depending on the severity of the acidosis, 
include:  a decrease in plasma- and urinary-pH; decreased appetite; 
decreased carbon dioxide-combining power; an increase in BUN and 
chlorides; an increase in plasma proteins; an increase in 
haematocrit (haemoconcentration); increased gluconeogenesis; 
increased phosphoenolpyruvate carboxykinase (EC activity; 
increased urinary ammonium; increased urea, sodium, chloride, 
calcium, and titratable acid excretion; an increase in malate and 
oxaloacetate concentrations in renal tissue; and decreased 
concentrations of glutamine, glutamate, and alpha-ketoglutarate in 
the kidney.  Pulmonary oedema, central nervous system dysfunction, 
and renal changes are reported to have occurred after ingestion of 
ammonium chloride. 

    Susceptibility to ammonium chloride differs among species.  For 
instance, pulmonary oedema is produced in cats, but not in rabbits; 
yet cats have been shown to be more resistant to oral poisoning by 
ammonium chloride than other animals studied. 

    Age is an important factor in the response of rats to oral 
doses of ammonium salts.  Benyajati & Goldstein (1975) found that 
the administration of a single dose of 5 mmol ammonium chloride/kg 
body weight (267.5 mg/kg) by gavage to 7- to 12-day-old rats (39 
animals) increased ammonia excretion by about 64%, within 4 h, 
compared to an increase of 155% in 20 adult rats after similar 

Table 18.  Selected studies on the acute oral effects of ammonia compounds in rats
Ammonium  Mode of     Sex, strain,    Num-  Dose             Effect                         Reference
compound  administ-   age, or weight  ber
Urea      drinking-   female, Holtz-  6     concentration    no renal hypertrophy           Lotspeich (1965)
          water       man, 200 -            of N equivalent                                        
                      250 g                 to that of 0.28
                                            mol/litre NH4Cl
                                            for 7 days  ad

Citrate   drinking-   female, Holtz-  6     0.28 mol/litre   no renal hypertrophy           Lotspeich (1965)
          water       man, 200 -            solution for                                        
                      250 g                 7 days  ad lib

Chloride  drinking-   female, Holtz-  9     0.28 mol/litre   metabolic acidosis; increase   Lotspeich (1965)
          water       man, 200 -            for 7 days,  ad   in kidney weight and total     
                      250 g                  lib (about 1000  N; increased capacity to
                                            mg/kg per day)   produce ammonia from 
                                                             glutamine in kidney; renal
                                                             hypertrophy; unilateral
                                                             nephrectomy plus acidosis
                                                             induced by NH4Cl caused a
                                                             greater hypertrophy than
                                                             either alone

Table 18.  (contd.)
Ammonium  Mode of     Sex, strain,    Num-  Dose             Effect                         Reference
compound  administ-   age, or weight  ber
Chloride  diet        female, 150 g   125   all on low-      consumption of food inversely  Motyl & Debski
                                            protein diet;    related to dosage of NH4Cl;    (1977)    
                                            Group I: no      dosage-related decrement in         
                                            NH4; Group II:   weight gain; increase in LD50
                                            1% NH4Cl (300    value for ip dose of 2.7% 
                                            mg/kg body       NH4Cl in Groups II and III, 
                                            weight per       indicating an increased 
                                            day); Group      adaptive capacity for ammonia 
                                            III: 2% NH4Cl    detoxification; LD50 value of 
                                            (380 mg/kg       Group IV same as Group III; 
                                            body weight per  LD50 value of Group V lower 
                                            day); Group IV:  than Group I; dose-dependent 
                                            4% NH4Cl (560    decrease in blood-glucose 
                                            mg/kg body       levels; decrease of muscle 
                                            weight per       and liver glycogen; dose-
                                            day); Group V:   dependent increase in delta-
                                            8% NH4Cl (540    ornithine transaminase and 
                                            mg/kg body       ornithine transcarbamylase; 
                                            weight per day,  increase in adenosine 
                                            for 7 days       triphosphate concentration in 
                                     Organ effects following oral administration

    (a)   Lung and central nervous system

    Toxic doses of ammonium salts induced acute pulmonary oedema in 
rats, guinea-pigs, and cats, but not in rabbits given ammonium 
chloride (6% aqueous solution) intraperitoneally or by gavage, 
though the doses were sufficient to cause death.  To induce similar 
effects in cats, a larger dose (unspecified) of ammonium chloride  
and a longer latency period (from 1 to 3 h) were required, 
indicating a greater resistance of this species to ammonium 
chloride (Koenig & Koenig, 1949). 

    In a limited study to assess the role of the ammonium ion in 
producing pulmonary oedema, Koenig & Koenig (1949) administered, by 
gavage, to 5 different guinea-pigs, 6 ml of 20% ammonium nitrate; 
7 ml of 6.4% ammonium acetate; 7 ml of 10% ammonium bromide; 7 ml 
of 6% ammonium chloride; or 7 ml of 7.4% ammonium sulfate, 
respectively.  The last 4 solutions contained approximately 
equivalent concentrations of ammonium.  All 5 animals died of acute 
pulmonary oedema; the lungs of a control animal that had received 
water by gavage remained normal.  The pulmonary oedema could not be 
attributed to the induced acidosis, since guinea-pigs and cats, 
made severely acidotic by gavage with sodium lactate or dilute 
hydrochloric acid, did not show lung oedema (Koenig & Koenig, 

    Progressive signs of ammonium poisoning caused by ammonium 
salts, given by gavage, indicative of both pulmonary and nervous 
system dysfunction, were reported in less than 30 min in guinea-
pigs and rats (Koenig & Koenig, 1949) including: 

    (i)  a rapid increase in the rate and depth of respiration;

   (ii)  weakness and difficulty in locomotion;

  (iii)  hyperexcitability for tactile, auditory, and painful
         stimuli; and

   (iv)  muscle fasciculations over most of the body followed
         by generalized tonic convulsions and then coma.

The respiratory rate was greatly reduced but the depth of 
respiration increased and was accompanied by gasping and stridor.  
Histological changes occurred in both the lung and brain, while 
oedema, congestion, and haemorrhage were found principally in the 
lung (Koenig & Koenig, 1949; Cameron & Shiekh, 1951). 

    The addition of ammonium chloride to rat feed resulted in 
reduced dietary consumption (Motyl & Debski, 1977).  The results of 
studies by Noda & Chikamori (1976) pointed to a direct effect of 
the ammonium ion on the brain area that regulates feeding.  Rats 
with bilateral lesions in the prepyriform cortical area of the 
brain consumed as much diet containing 3% ammonium chloride as 
basal diet.  A unilateral injection of 10 mg/litre of 2% NH4Cl/kg 

body weight into prepyriform cortical areas, in contrast to an 
injection into other areas of the brain, or an injection of sodium 
chloride, significantly reduced the food intake of 6 adult male 
Wistar rats.  The results of these studies suggest that ammonium 
ions directly influence appetite by their effects on prepyriform 
cortical areas. 

    (b)   Kidney

    Lotspeich (1965) reported that ingestion for 7 days of 
0.28 mol/litre (1.5%) ammonium chloride in water  (ad lib) produced 
renal hypertrophy with new cell formation and an enlargement of 
existing cells.  Some animals from each of the acidotic and control 
groups were subjected to unilateral nephrectomy.  Highly 
significant increases in kidney wet weight, dry weight, and total 
nitrogen were observed in the acidotic group.  Similar changes were 
produced by unilateral nephrectomy.  In unilaterally nephrectomized 
rats made acidotic by the ingestion of ammonium chloride, the 
remaining kidney was larger than that seen in animals with 
unilateral nephrectomy without induced acidosis, suggesting an 
additive effect of unilateral nephrectomy and ammonium chloride 

    The relationship between the renal hypertrophy and the ammonium 
ion, acidosis, non-specific intake of nitrogen, or increased solute 
load was examined (Lotspeich, 1965).  Isomolar (0.28 mol/litre) 
solutions of sodium chloride and ammonium chloride produced renal 
hypertrophy.  The increase due to sodium chloride was less marked 
(it was noted that the sodium chloride group drank 3 or 4 times as 
much solution each day as the ammonium chloride group).  Isomolar 
(0.2 mol/litre) solutions of sodium bicarbonate and ammonium 
citrate did not induce renal hypertrophy.  When 3 groups of 6 rats 
were given drinking-water containing 0.28 mol/litre sodium 
chloride, 0.28 ammonium chloride, or a urea solution containing 
nitrogen equivalent to that in the 0.28 mol/litre ammonium 
chloride, for 7 days, only the ammonium chloride solution induced 
acidosis.  The rats in both the sodium chloride and ammonium 
chloride groups had larger kidneys than the urea-drinking rats, 
though the kidneys of the sodium chloride-drinking rats were not as 
large as those of the ammonium chloride-drinking rats.  Since renal 
hypertrophy was produced by solutions containing the chloride ion, 
while ammonium citrate and urea did not cause any hypertrophy, the 
evidence does not support the hypothesis that renal hypertrophy is 
due to the ammonium ion. 

    Thompson & Halliburton (1966) also reported renal hypertrophy 
in rats that ingested 3% ammonium chloride in the diet for 6 days.  
The ingestion of ammonium citrate or sodium chloride in amounts 
that were equivalent to that of the ammonium chloride did not cause 
renal hypertrophy. 

    Janicki (1970) examined the kidneys of rabbits that had been 
administered 16.2 g ammonium chloride, by gavage, over a period of 
2 days and found the epithelium of the convoluted tubules swollen, 

vacuolated, and completely filling the lumen; nuclei exhibited 
karyolysis.  Findings were similar in 4 rabbits administered 5 - 
7 g ammonium chloride, by gavage, over a period of 3 - 7 days. 

    However, hyperaemia of the renal cortex of rabbits was noted 
after the administration, by gavage, of single doses of 0.8 and 1 g 
ammonium carbonate/kg body weight (Yoshida et al., 1957).  As the 
carbonate ion does not have an acidifying effect, this suggests 
that the ammonium ion produces some effects on the kidney.  Influence of diet on the effects of ammonia

    In 6 mongrel dogs, blood-urea levels were increased by a higher 
level of protein intake (6 g protein/kg per day) (Bressani & 
Braham, 1977).  Levels of ~30 mg BUN/litre were found 8 h after the 
daily feed.  When the protein intake was low (4 mg protein/kg per 
day), BUN levels of 14 mg/litre were reported 8 h after the daily 
feed.  The frequency of protein intake did not affect the maximum 
value of blood-urea levels when the protein intake was low (4 mg 
protein/kg per day).  This suggests that high levels of urea and 
ammonia in the blood might occur in animals that suffer from liver 
insufficiency and are fed high-protein diets. 

    Kulasek et al. (1975) studied the effects of nitrogen in the 
diet on ammonia detoxification, using 210 rats and 6 diets 
containing 50, 150, and 700 g casein/kg (low-, optimal-, or high-
protein diet, respectively), with or without the addition of 
ammonium chloride at 20 g/kg.  After 8 or 9 days of feeding, the 
LD50 from an intraperitoneal injection of a 2.7% solution of 
ammonium chloride was determined.  The LD50 increased in proportion 
to the amount of nitrogen in the diet.  The data suggest that 
higher doses of exogenous ammonia were tolerated by rats on 
protein-rich diets or diets containing an ammonium salt as an 
additive.  An adaptive capacity for ammonia detoxification was 
further demonstrated by Motyl & Debski (1977) in a study using rats 
fed low-protein diets with the addition of NH4Cl.  The LD50 values 
for the ip injection of 2.7% NH4Cl were higher in animals fed low-
protein diets supplemented with NH4Cl (Table 18).  Stevens et al. 
(1975) raised weanling rats for 3 - 6 weeks on a protein-deficient 
diet.  Subsequent challenge by a large, intraperitoneally-injected 
dose of ammonium chloride indicated that severe protein deprivation 
increased vulnerability to ammonia poisoning compared with that of 
control groups not prefed protein-deficient diets.  Thus, with the 
exception of animals suffering from liver dysfunction, animals on 
high-protein diets seem able to tolerate a higher oral intake of an 
ammonium salt. 

    A group of eight, 6- to 8-month-old cats, given a single meal 
of a complete amino acid diet without arginine, developed 
hyperammonaemia with elevated plasma levels of glucose and ammonia 
and showed clinical signs of ammonia toxicity within 2 h.  One cat 
died 4.5 h after ingesting only 8 g of the diet.  Five of the 
surviving cats given a single meal of complete amino acids, in 
which arginine was replaced with an equivalent amount of ornithine, 
did not show any unusual signs.  This finding indicates that the 

cat is unable to synthesize ornithine at the rate required by the 
urea cycle to dispose of ammonia from amino acid catabolism; 
however, the dietary requirements for cats may differ from those of 
other adult animals, including human beings, because the cat has a 
much higher protein requirement, i.e., it requires approximately 
20% of dietary calories as protein, as opposed to only 4 - 8% 
required by the rat, dog, sheep, and man (Morris & Rogers, 1978). 

    The lethal effects of ammonia poisoning have been prevented by 
the amino acids, ornithine and aspartic acid.  To test whether this 
was mediated by a sparing action of adenosine triphosphate (ATP) on 
ammonia metabolism, 20 dogs with chronic Eck's fistula were 
injected in the duodenum with ammonium acetate at 4.1 mmol/kg body 
weight (~219.4 mg/kg).  Half of the group was given 2 mg ATP/kg, 
1 h prior to administration of the ammonium acetate.  In 9 of the 
10 dogs, ATP prevented a rise in levels of ammonia in venous blood.  
Grossi et al. (1968) administered ATP (2 mg/kg) intravenously to 6 
dogs with chronic Eck's fistula and on high-protein diets.  Within 
1 h, high blood-ammonia levels returned to normal.  In chronic 
liver disease, there may be insufficient ATP available for ammonia 
detoxification, resulting in hyperammonaemia. 

8.1.3.  Dermal exposure

    No data are available regarding any systemic effects of dermal 
exposure to ammonia or ammonium compounds. 

8.1.4.  Effects due to parenteral routes of exposure

    The parenteral toxicity of ammonia and ammonium compounds has 
been studied extensively.  Toxicity is influenced by the route of 
administration, e.g., with oral administration, there is the 
capacity for detoxification of exogenous ammonia by the liver.  Lethality

    The intravenous (iv) and intraperitoneal (ip) LD50 values for a 
number of ammonium compounds in various species are summarized in 
Table 19.  The toxic syndrome was similar in all species studied.  
The signs, after iv injection, were characterized by immediate 
hyperventilation and clonic convulsions followed by either fatal 
tonic extensor convulsion or the onset of coma in 3 - 5 min.  The 
animals remained comatose for approximately 30 - 45 min.  At this 
stage, tonic convulsions and death can occur at any time, but 
animals that survive usually recover rapidly and completely 
(Warren, 1958; Warren & Schenker, 1964; Wilson et al., 1968a,b).  
After intraperitoneal injection, the signs did not appear until 
15 - 20 min after administration (Greenstein et al., 1956; Wilson 
et al., 1968b). 

Table 19.  Toxicity of several ammonium compounds in selected species
Ammonium     Species           Intravenous dose          Intraperitoneal dose
compound                       (mmol/kg of body weight)  (mmol/kg of body weight)
                               (LD50)                    (LD50)                    Reference
Acetate      rat               -                         8.20                      Greenstein et al. (1956)
             mouse             6.23                      -                         Warren (1958)
             mouse             5.64                      10.84                     Wilson et al. (1968a)
             chick             2.27                      10.44                     Wilson et al. (1968a)

Bicarbonate  mouse             5.05                      -                         Warren (1958)
             mouse             3.10                      -                         Wilson et al. (1968b)

Carbamate    mouse             0.99                      -                         Wilson et al. (1968b)

Carbonate    mouse             4.47                      -                         Warren (1958)
             mouse             1.02                      -                         Wilson et al. (1968b)

Chloride     mouse             6.75                      -                         Warren (1958)
             mouse (38.8 C)a  6.6                       -                         Warren & Schenker (1964)
             mouse (40.4 C)a  5.17                      -                         Warren & Schenker (1964)
             mouse (27.9 C)a  10.21                     -                         Warren & Schenker (1964)

Hydroxide    mouse             2.53                      -                         Warren (1958)
a  Body temperature.  Central nervous system effects

    Navazio et al. (1961) observed that characteristic toxic signs 
were not observed in rats until the ammonia concentration in the 
blood was double that of basal values (attained within 8 - 10 min 
of an ip injection of 601 mg ammonium acetate/kg body weight).  No 
substantial increase in brain-ammonia was observed.  However, when 
the blood-ammonia concentration reached more than 20 times the 
basal value, there was a sudden rise in the ammonia concentration 
in the brain, which reached a maximum of approximately 100 mg 
ammonia-nitrogen/kg (wet weight), between 10 and 26 min after 
injection.  Muscular contractions with occasional tetanic spasms, 
and then coma occurred, when the concentration of ammonia in the 
brain reached approximately 50 mg/kg.  Although the animals started 
to recover from the comatose state approximately 70 min after 
onset, blood- and brain-ammonia concentrations did not return to 
basal levels until 2 h after the injection of ammonium acetate. 

    However, other authors observed an immediate increase in brain-
ammonia after ip injection of ammonium acetate (Torda, 1953; du 
Ruisseau et al., 1957; Salvatore et al., 1963).  These authors 
found dramatic increases in the brain-ammonia content, 2 - 5 min 
after the injection of ammonium acetate.  Salvatore et al. (1963) 
suggested that there was no critical blood-ammonia concentration 
for diffusion through the blood-brain barrier. 

    Ammonia has been shown to be more highly toxic at elevated body 
temperature, whereas hypothermia affords marked protection 
(Schenker & Warren, 1962).  The LD50 values for ammonium chloride 
in the mouse, at various body temperatures, are shown in Table 19.  
The increased toxicity of ammonia at elevated body temperature was 
suggested to be due to a direct metabolic effect of hyperthermia on 
the brain, unrelated to dehydration or stress.  Effects on the heart

    Intravenous LD50 values for ammonium carbamate, ammonium 
carbonate, and ammonium bicarbonate have been determined in mice by 
Wilson et al. (1968a,b) (Table 19).  The physiological effects of 
the injected ammonium compounds in dogs and sheep were also 
investigated.  Electrocardiograms recorded during the toxic 
syndrome indicated that the animals died from ventricular 
fibrillation due to a direct effect of ammonia on the heart.  These 
findings were in agreement with the effects noted by Berl et al. 
(1962) during the iv infusion of ammonium chloride in cats when 
electrocardiograms were altered in a complex manner.  However, 
Warren & Nathan (1958) were unable to demonstrate any cardiotoxic 
effects of the ammonium compounds in mice and concluded that the 
toxicity syndrome was due primarily to a cerebral effect and not a 
direct effect on cardiac or skeletal muscle. 

8.2.  Short-Term Exposures

8.2.1.  Inhalation exposure

    When 48 rats were continuously exposed to 127 mg ammonia/m3 
(181 ppm) for 90 days, no abnormalities were found in organs or 
tissues.  Inhalation of 262 mg ammonia/m3 (374 ppm) for 90 days 
induced mild nasal irritation in about 25% of 49 rats and a mild 
leukocytosis in 4 of the rats.  Continuous exposure to 455 mg/m3 
(650 ppm) resulted in the death of 50 out of 51 rats by the 65th 
day of exposure.  All animals exhibited mild nasal discharge and 
laboured breathing.  In a second study, rats, guinea-pigs, rabbits, 
and dogs were continuously exposed to 470 mg/m3 (671 ppm) for 90 
days.  Thirteen out of 15 rats and 4 out of 15 guinea-pigs died. 
Marked eye irritation was noted in rabbits and dogs, with corneal 
opacities in about one-third of the rabbits.  At autopsy, all test 
animals examined had more extensive focal or diffuse interstitial 
inflammatory processes in the lungs than the controls (Coon et al., 

    White rats were exposed to ammonia, by inhalation, at 
concentrations of 100 and 30 mg/m3 (143 and 43 ppm) for 25 or 
60 min, every 48 h, for a period of 3 months.  Rats exposed to a 
concentration of 100 mg/m3 (143 ppm) showed only a mild 
leukocytosis, with no significant differences from the control 
group with regard to oxygen consumption, neuromuscular excitation 
threshold, heart rate, blood-sugar, blood-residual nitrogen, and 
total serum-protein (Prokop'eva & Yushkov, 1975).  In another study 
by Alpatov & Mikhailov (1963), the threshold level for toxic 
effects in a 2-month exposure was 40 mg/m3 (57 ppm).  Histological 
changes were seen in the lungs of the animals exposed to a 
concentration of 100 mg/m3 (143 ppm), including small areas of 
interstitial pneumonia with signs of peribronchitis and 
perivasculitis.  No changes were seen in other organs compared with 
those in the control group. 

    Broderson et al. (1976) exposed Sherman and Fisher rats to 
ammonia from natural sources, at an average concentration of 
105 mg/m3 (150 ppm) for 75 days, and to purified ammonia at 
175 mg/m3 (250 ppm) for 35 days.  Histological changes in the 
olfactory and respiratory epithelia of the nasal cavity were 
similar in all the exposed rats, showing increased thickness, 
pyknotic nuclei, and hyperplasia.  The submucosa was oedematous 
with marked dilation of small vessels.  Lesions decreased 

    Exposure to ammonia at concentrations of 17 - 175 mg/m3 (25 - 
250 ppm) increased the infectious effects of  Pasteurella multocida  
in mice and  Mycoplasma pulmonis in rats; this effect increased 
with the concentration of ammonia (Broderson et al., 1976; Richard 
et al., 1978a). 

    Richard et al. (1978a) selected a concentration of 350 mg/m3 
(500 ppm) for a study of effects of continuous exposure to ammonia 
after noting that general toxic effects, particularly on growth 
rate, were not found at 175 - 210 mg/m3 (250 - 300 ppm).  Young 
male specific-pathogen-free rats were age- and weight-matched with 
controls (27 per group) and exposed for up to 8 weeks.  Nasal 
irritation began on the fourth day.  After 3 weeks, exposed rats 
showed nasal irritation and inflammation of the upper respiratory 
tract, but no effects were observed on the bronchioles and alveoli. 
The number of pulmonary alveolar macrophages was similar to that in 
the controls.  After 8 weeks, none of these inflammatory lesions 
were present. 

    In a study by Coon et al. (1970), 15 rats, 15 guinea-pigs, 3 
rabbits, 2 dogs, and 3 monkeys were exposed to an ammonia 
concentration of 155 mg/m3 (221 ppm) for 8 h/day, 5 days a week, 
for 6 weeks.  Pathological effects were not observed in any of the 
species except for evidence of focal pneumonitis in the lungs of 
one of the monkeys.  Exposure to 770 mg/m3 (1100 ppm) for the same 
duration induced mild to moderate eye irritation and laboured 
breathing in the rabbits and dogs at the beginning of exposure, but 
these signs disappeared by the second week and no other signs of 
irritation or toxicity were noted.  Autopsy findings included non-
specific inflammatory changes in the lungs of the rats and guinea-

    Male Sprague Dawley rats were studied to determine whether 
ammonia was absorbed through the lungs into the blood, and the 
subsequent effects on the blood pH, blood gases, and hepatic drug-
metabolizing enzymes (Schaerdel et al., 1983).  Rats were exposed 
to ammonia at 7 - 840 mg/m3 (10 - 1200 ppm) for 1, 3, or 7 days.  
No significant changes were found in blood pH, pCO2, or in the 
histological appearance of the lungs or trachea.  Liver microsomal 
enzymes (ethyl-morphine- N-demethylase and cytochrome P-450) showed 
only minor changes.  Blood-ammonia levels increased in a linear 
fashion with increasing ammonia concentrations in air.  A 
concentration of 70 mg/m3 (100 ppm) or less produced only very 
small changes in blood-ammonia levels and had no measureable 
effects on any of the parameters studied. 

8.2.2.  Oral exposure  Histopathological effects

    Rats given ammonium salts, for periods ranging up to 90 days, 
did not appear to sustain renal damage (Freedman & Beeson, 1961; 
Gupta et al., 1979).  Twelve adult male Sprague Dawley rats were 
given ammonium chloride in the drinking-water at 16 g/litre, for up 
to 3 weeks.  Urinalysis did not reveal any evidence of renal 
injury, and no gross or histological "abnormalities" of the kidney 
were seen at autopsy (Freedman & Beeson, 1961).  Glutaminase 
activity per kg of kidney increased with duration of exposure; this 
is a physiological adaptation to acidosis.  Another group of 10 
rats, similarly treated and then given ammonium chloride in the 
drinking-water at 10 g/litre, for an additional 2.5 months also did 

not show any gross or microscopic renal abnormalities.  Assuming 
the rats weighed 250 g and consumed 25 ml of water per day, they 
could have ingested as much as 1.6 g/kg body weight per day while 
drinking the ammonium chloride at 16 g/litre and 1.0 g/kg body 
weight per day while drinking a level of 10 g/litre.  However, 
actual intake may have been lower, because ammonium chloride is 
known to affect the appetite and may render the water less 
palatable.  When ammonium chloride was given at 20 g/litre, food 
and water consumption were drastically reduced. 

    In Table 20, selected studies are presented on ammonium salts 
other than the chloride.  In general, at low doses, no detrimental 
effects were observed when rats and pigs were exposed to the NH4 
salts listed. 

    In a 90-day study by Gupta et al. (1979) on rats, there was not 
any evidence of renal damage.  Ammonium sulfamate (NH4SO3NH2) as a 
100 g/litre solution was given orally at rates of 100, 250, or 
5000 mg/kg body weight per day, 6 days a week for 30, 60, or 90 
days to adult female rats (ITRC colony-bred albino) and to weanling 
male and female rats (20/sex per age per dose level).  Under 
certain conditions, the sulfamate ion is hydrolysed to bisulfate 
ion and ammonia; however, it is unclear whether, and to what 
extent, hydrolysis occurs in the rat intestine.  Equivalent doses, 
listed in Table 20, were calculated on the assumption that no 
hydrolysis occurs.  The effects of the anion, sulfamate and/or 
sulfate, on the action of ammonium is a matter of conjecture.  
Ammonium sulfamate would be expected to produce metabolic acidosis 
on the basis of its structure, but this has not been verified 
experimentally.  The general health of both treated and control 
rats was good, and there were no significant differences in mean 
body weights throughout the study, except for a slight depression 
in the highest-dose adult females at 60 and 90 days.  Food and 
water consumption were unaffected, except in the highest dose 
weanlings of both sexes, which consumed less food and drank more 
water than control weanlings.  Interim sacrifice of 6 animals/sex 
per dosage group was performed for haematological and histological 
examination.  There were no significant differences in 
haematological values (packed cell volume, haemoglobin 
concentration, total red cell count, total and differential white 
cell count).  Relative organ weights in all treated groups did not 
differ significantly from those in the controls.  Histological 
examination of the kidney, liver, lung, stomach, heart, spleen, 
thyroid, adrenal, gonads, intestine, and lymph nodes did not reveal 
any abnormalities, except slight hepatic fatty degeneration in one 
adult female at 90 days. 

Table 20.  Dose-response data for short-term oral administration of ammonium compounds
Ammonium    Species,      Mode of                Duration     Daily Intakea       Response               Reference
salt        No/group,     administration                   (mg/kg   (mg NH3/kg
            sex                                            body     body 
                                                           weight)  weight)b
Sulfamate   rat, albino,  orally as 10%          30, 60,   100;     15.0;         no effects on body     Gupta et
            20 adult      solution; not          90 days   250      37.3          weight, food, and      al. (1979)
            female, 20    specified whether                                       water consumption,
            weanling      given by gavage                                         haematological values
            male, 20                                                              or organ weights; no
            weanling                                                              histological 
            female per                                                            abnormalities in 
            dose                                                                  organs (including

                                                           500      74.8          slight decrease in
                                                                                  body weight in adult
                                                                                  females; slightly
                                                                                  lower food and higher
                                                                                  water consumption in
                                                                                  weanlings of both
                                                                                  sexes; no effects on
                                                                                  haematological values  
                                                                                  or organ weights; no
                                                                                  abnormalities in 
                                                                                  organs (including 
-------------------------------------------------------------------------------------------------------------------                                                                                  kidneys)

Table 20.  (contd.)
Ammonium    Species,      Mode of                Duration     Daily Intakea       Response               Reference
salt        No/group,     administration                   (mg/kg   (mg NH3/kg
            sex                                            body     body 
                                                           weight)  weight)b
Diammonium  pig, male     3.75% diammonium       28 days   1820     274           body weight gain       Kagota et
citrate     22.5 kg,      citrate in diet                                         increased but % meat   al. (1979)
            3-4/group     containing 6.4% crude                                   and fat of carcass
                          protein                                                 unaffected; plasma- 
                                                                                  and urine-urea-
                                                                                  nitrogen increased 
                                                                                  but blood-ammonia-
                                                                                  nitrogen level 
                                                                                  unaffected; no effect 
                                                                                  on haematological 
                                                                                  values; no gross 
                                                                                  abnormalities or 

Diammonium  pig, 27.3 kg  basal diet contained   81 days   820      161 (10%      no effect on weight    Wehrbein
phosphate   3 males and   16% protein; 0,5,10,                      replacement)  gain, BUN, or food     et al.
and         3 females/    or 20% of dietary N                                     consumption (no        (1970)
diammonium  group         was replaced by N                                       effect on these 
citrate as                from equimolar                                          parameters at 5% 
equimolar                 mixture of designated  81 days   1600     322 (20%      either) slight  
mixture                   NH4+ salts                                replacement)  decrease in weight  
                                                                                  gain, BUN and food 
a Estimated for all studies except Gupta et al. (1979).
b Equivalent intake expressed as ammonia (NH3).
    Treatment of virgin female rabbits with ammonium carbonate, 
chloride, hydrophosphate, sulfate, or hydroxide at 0.1 - 0.2 g/kg 
body weight, orally, on alternate days, for periods of 3 weeks 
separated by 1-week intervals of no treatment, was associated with 
enlargement of the ovaries, follicle maturation, and formation of 
corpora lutea (Fazekas, 1949).  There was also enlargement of the 
uterus, hypertrophy of the teats, and secretion of milk. 

    Rabbits (10 - 80 per group) were given 0.1 - 0.2 g/kg body 
weight of an ammonium salt in 100 - 150 ml of drinking-water, twice 
daily.  One hundred and sixty rabbits (96 female, 64 male) 
received, twice daily, 50 - 80 ml of a 0.5% ammonium hydroxide 
solution (~135 - 210 mg/kg body weight), in gradually increasing 
doses.  The chemicals were given for periods of 3 weeks separated 
by 1-week intervals of no treatment.  In a related study, similar 
treatment of rabbits with ammonium chloride or ammonium sulfate 
resulted in fluctuations in serum-calcium and -phosphorus levels 
(Fazekas, 1954a).  Effects of ammonium as a dietary nitrogen supplement

    Ammonia from ammonium salts can stimulate the growth of animals 
on diets deficient in non-essential amino acids or restricted in 
protein content.  Weanling rats, given an artificial diet 
comprising essential amino acids, B vitamins, vitamin C, salts, and 
glucose for 21 days, grew poorly.  Rats given a similar diet in 
which some of the glucose was replaced with 8.6% ammonium acetate 
(equivalent to 15.7 g nitrogen/kg diet) showed a dramatically 
improved weight gain (Birnbaum et al., 1957).  The food 
consumption/weight gain ratio (feed/gain ratio) was also improved 
in animals receiving the ammonium salt. 

    Similar results were obtained with young male pigs given a more 
natural basal diet restricted in non-essential amino acids and 
containing the minimum requirement of essential amino acids (Kagota 
et al., 1979).  The crude protein level of this basal diet was 
6.4%.  Three pigs fed the basal diet supplemented with 3.75% 
diammonium citrate had a significantly greater weight gain and a 
slightly lower feed/gain ratio than 4 pigs fed the basal diet (the 
diets were made isocaloric by adjusting carbohydrate).  No 
significant differences in the packed cell volume or ammonia-
nitrogen level of the blood or in total protein concentration of 
plasma were found between the 2 groups.  Plasma- and urine-urea-
nitrogen were increased in the pigs fed the diet supplemented with 
diammonium citrate.  Autopsy of the pigs after 28 days on the basal 
or ammonium citrate diets did not reveal any lesions or 
abnormalities or any differences in the percentage of carcass meat 
and fat. The average daily food intake for pigs receiving 
diammonium citrate was 1.44 kg, which corresponds to 54 g 
diammonium citrate per day.  Using a body weight midway between the 
initial (22.5 kg) and final (36.7 kg) body weights, the mean intake 
of diammonium citrate can be estimated to be 1.82 g/kg body weight, 
per day, or 16.1 mEq NH4+/kg body weight, per day. 

    Addition of ammonium salts to diets with a higher protein 
content (10% crude protein) did not produce significant changes in 
weight gain in rats or pigs (Clawson & Armstrong, 1981).  
Similarly, no significant changes in weight gain occurred in pigs, 
when up to 10% of the nitrogen from crude protein (diet = 16% crude 
protein) was replaced with nitrogen from ammonium salts (Wehrbein 
et al., 1970).  Replacement of 20% of the dietary nitrogen with 
ammonium salts slightly decreased body weight gain in the pigs; 
food consumption and BUN also decreased.  The 20% replacement diet 
contained 1.54% diammonium phosphate and 2.07% diammonium citrate 
for a total of 3.61% ammonium salts and was fed for 81 days.  The 
estimated mean intake was 0.70 g diammonium phosphate and 0.94 g 
diammonium citrate/kg body weight per day, giving a total of 
18.9 mEq NH4+/kg body weight per day. 

8.2.3.  Dermal exposure

    There is no information regarding systemic toxicity from short-
term dermal exposure to ammonia or ammonium compounds. 

8.3.  Skin and Eye Irritation; Sensitization

    Ammonia in the form of a gas, an anhydrous liquid boiling at 
low temperatures, or an aqueous solution is a recognized skin and 
eye irritant.  Most of the information is human clinical data and 
is described in section 9. 

    Ammonia, partly because of its lipid solubility, penetrates 
the corneal membrane rapidly (NRC, 1979).  In rabbits, conjunctival 
oedema with ischaemia and segmentation of limbal vessels were noted 
within 30 min.  By 24 h, there was a reduction in the 
mucopolysaccharide contents of the corneal stroma, and extensive 
polymorphonuclear infiltration and anterior lens opacities were 
apparent.  Aqueous levels of glucose and ascorbate and intraocular 
pressure were depressed (NRC, 1979).  In rabbits with corneal 
burns, neovascularization occurred after 1 week, but it was delayed 
in animals with corneal and limbal burns.  Complications of severe 
burns included symblepharon, pannus, pseudopterygia, progressive or 
recurrent corneal ulcerations leading to perforations, permanent 
corneal opacity, corneal staphyloma, persistent iritis, phthisis 
bulbi, secondary glaucoma, and dry eye (NRC, 1979). 

    Ammonium persulfate is a recognized skin sensitizer for human 
beings.  There are no data on its sensitization potential in animal 

8.4.  Long-Term Exposures

8.4.1.  Inhalation exposure

    Weatherby (1952) exposed 12 guinea-pigs to an ammonia 
concentration of about 119 mg/m3 (170 ppm).  Chamber concentrations 
ranged from 98 to 140 mg/m3 (140 to 200 ppm) for 6 h/day, 5 days a 
week, for up to 18 weeks.  There were no significant findings at 
autopsy in animals sacrificed after 6 or 12 weeks of exposure.  In 

animals sacrificed after 18 weeks of exposure, there was congestion 
of the liver, spleen, and kidneys, with early degenerative changes 
in the adrenal glands.  Increased erythrocyte destruction was 
suggested by increased quantities of haemosiderin in the spleen.  
In the proximal tubules of the kidneys, there was cloudy swelling 
of the epithelium and precipitated albumin in the lumen with some 
casts.  The cells of the adrenal glands were swollen and the 
cytoplasm in some areas had lost its normal granular structure. 

    Coon et al. (1970) conducted studies in which rats, guinea-
pigs, rabbits, dogs, and monkeys were continuously exposed 
(24 h/day, 7 days per week) to ammonia.  No signs of toxicity were 
seen in any species following continuous exposure to ammonia at a 
concentration of 40 mg/m3 (57 ppm) for 114 days, and gross and 
microscopic examination did not reveal any lung abnormalities. 

8.4.2.  Oral exposure

    The administration of ammonium carbonate, chloride, sulfate, 
hydrophosphate, acetate, lactate, or hydroxide to a total of 296 
rabbits for 3 - 16 months resulted in enlargement of the 
parathyroids (Fazekas, 1954a).  Administration of sodium 
dihydrophosphate, sodium ammonium phosphate, calcium chloride, 
hydrochloric acid, acetate acid, or lactic acid gave similar 
results (Fazekas, 1954a). 

    Rabbits given 0.1 g ammonium hydroxide/kg body weight (as a 
0.5 - 1.0% solution) by gavage, initially, on alternate days and 
then daily for up to 17 months, had enlarged adrenal glands 
(Fazekas, 1939).  An initial fall in blood pressure of 2.67 - 
4.00 kPa (20 - 30 mmHg) was followed by a gradual rise to 1.33 - 
4.00 kPa (10 - 30 mmHg) above the baseline, after several months 
of treatment. 

    The results of studies on rats, rabbits, and dogs indicate that 
long-term administration of ammonium chloride can induce 
osteoporosis (Seegal, 1927; Bodansky et al., 1932; Jaffe et al., 
1932a,b; Barzel & Jowsey, 1969; Barzel, 1975).  During prolonged 
metabolic acidosis, the release of bone mineral by resorption is 
thought to provide additional buffering capacity, sparing 

8.5.  Reproduction, Embryotoxicity, and Teratogenicity

    Charles & Payne (1966b) studied the effects of graded 
concentrations of atmospheric ammonia on the performance of laying 
hens.  At 18 C, ammonia at 73.5 mg/m3 (105 ppm) significantly 
reduced egg production, after 10 weeks of exposure.  No effects 
were observed on egg quality.  Food intake was reduced and weight 
gain was lower.  No recovery in egg production occurred when the 
treated groups were maintained for an additional 12 weeks in an 
ammonia-free atmosphere.  Similar results were observed at 28 C, 
under the same conditions.  Earlier work had indicated that egg 
quality could be affected by ammonia exposure (Cotterill & 
Nordskog, 1954).  Freshly-laid eggs were exposed to various 

concentrations of ammonia in a desiccator for 14 h at room 
temperature and then moved to normal atmosphere for another 32 h at 
50 C, before examination.  There was evidence of absorption of 
ammonia into the eggs and significant impairment of interior egg 
quality, as measured by Haugh units, pH, and transmission of light. 

    The interaction of ammonium chloride with other teratogenic 
agents has been investigated in 2 studies.  Goldman & Yakovac 
(1964) used ammonium chloride to investigate the role of metabolic 
acidosis in salicylate-induced teratogenesis in Sprague Dawley 
rats.  Beginning on day 7 of gestation, rats received either 
0.17 mol/litre (0.9%) ammonium chloride in the drinking-water, a 
single subcutaneous injection of salicylate, or both.  Ammonium 
chloride alone inhibited fetal growth, but was not teratogenic.  
However, when administered with salicylate, ammonium chloride 
significantly increased maternal and fetal mortality and the fetal 
anomaly rate (dorsal midline, ventral midline, and eye defects) 
compared with that due to salicylate alone.  These effects were 
attributed to acidosis and not to ammonia.  However, it has been 
shown by Miller (1973) that the addition of 0.5% ammonium chloride 
to the 5%-glucose drinking-water of fasting, pregnant CFW mice 
significantly reduced the incidence of fast-induced cleft palate in 
the progeny. 

8.6.  Mutagenicity

    Ammonium sulfate was reported to be non-mutagenic in the 
 Salmonella and  Saccharomyces systems (Litton Bionetics, Inc., 
1975).  Demerec et al. (1951) tested ammonia for its ability to 
induce back-mutations from streptomycin dependence to non-
dependence in  Escherichia coli and found it to be mutagenic, but 
only in treatments that left less than 2% survivors.  Iwaoka et al. 
(1981a,b) showed that extraction of ingredients from fried 
hamburger and refrigerated biscuit products with ammonium hydroxide 
or ammonium sulfate increased the mutagenic activity in 
 S. typhimurium TA98 and TA1538, compared with sodium sulfate 
extraction.  This suggests that ammonium salts may, in some way, 
influence the mutagenic activity of some agents, or may themselves 
be responsible for false positive findings (Iwaoka et al., 1981a).  
However, it is also possible that ammonium salts extract mutagenic 
components from foods more efficiently. 

    Lobashov & Smirnov (1934) and Lobashov (1937) found ammonia to 
have a mutagenic effect on  Drosophila.  Ammonia showed slight 
mutagenic activity in studies in which survival of  Drosophila was 
lower than 2% after treatment.  In studies by Auerbach & Robson 
(1947), when  Drosophila was exposed to ammonia vapour in small 
glass containers, 0.5% sex-linked lethals were observed. 

    It was reported by Rosenfeld (1932) that ammonia induced 
clumping of chromosomes, arrest spindle formation, and induce 
polyploidy in chick fibroblasts  in vitro. 

    There are no data to show that ammonia is mutagenic in mammals. 

8.7.  Carcinogenicity

    There is no evidence indicating that ammonia is carcinogenic. 

    Gibson et al. (1971) observed that animals treated with ammonia 
developed inflammatory lesions of the colon.  It has been suggested 
that cell proliferation may increase errors in DNA replication 
(Zimber, 1970; Zimber & Visek, 1972), activate oncogenic agents 
present in sub-threshold doses (Anderson et al., 1964), and even 
unmask latent changes in the genetic material caused by mutagenic 
agents (Visek et al., 1978). 

    In a study on male Sprague Dawley rats (Topping & Visek, 1976), 
there was no evidence that ammonia increased the incidence of 
tumours with increased protein intake.  Development of lung 
tumours was observed in CFLP mice treated intra-gastrically with 
diethyl pyrocarbonate and ammonia, neither of which induces cancer 
independently in animals.  However, this may have resulted from a 
carcinogenic substance, possibly urethane, formed  in vivo from 
diethyl pyrocarbonate in the presence of ammonia (Uzvolgyi & Bojan, 

    Life-long ingestion of ammonium hydroxide in the drinking-water 
by Swiss and C3H mice did not produce any carcinogenic effects, and 
had no effect on the spontaneous development of adenocarcinoma of 
the breast in C3H females, a characteristic of this strain (Toth, 

    Ammonium chloride and ammonium tungstoantimonate and related 
compounds have been shown to have an inhibitory effect on malignant 
cells (Phillips, 1970; Anghileri, 1975; Flaks & Clayson, 1975; 
Flaks et al., 1973; Sof'ina et al., 1978). 

8.8.  Factors Modifying Effects

8.8.1.  Synergistic effects

    Stevens et al. (1975) raised weanling rats for 3 - 6 weeks on a 
protein-deficient diet.  Subsequent challenge by a large, 
intraperitoneally-injected dose of ammonium chloride indicated that 
severe protein deprivation increases vulnerability to ammonia 
poisoning in comparison with control groups not prefed protein-
deficient diets. 

    Dalhamn (1963) employed a technique in rabbits in which an air 
pollutant mixture was drawn into the nostrils and out through a 
tracheal cannula.  The effects of ammonia alone and ammonia mixed 
with (and presumably adsorbed on) carbon particles, on the beating 
rate of tracheal cilia was examined.  Ammonia alone had to be 
administered at a high concentration (1400 mg/m3 or 2000 ppm) to 
produce a tracheal concentration of 70 mg/m3 (100 ppm).  The 
reduction in beating rate was not substantially altered by the 
addition of carbon particles at 2 mg/m3. 

    Simultaneous injection of ammonium salts and a fatty acid into 
rats or cats produced coma at lower plasma levels of ammonia and 
free fatty acids than a single injection of either compound (Zieve 
et al., 1974). 

    Impaired handling of an ammonium load has been observed in 
animals with hepatic dysfunction.  Elevated levels of ammonia or 
urea have been reported in dogs with experimentally-bypassed livers 
(section 7.1.2).  The importance of the kidney in detoxification of 
an ammonium load is apparent in the studies of Lotspeich (1965) 
(section, where an additive hypertrophic effect of 
ammonium chloride and unilateral nephrectomy was observed on the 
remaining kidney.  Increased sensitivity to ammonia toxicity was 
found in young rats (Benyajati & Goldstein, 1975) and in rats that 
had been castrated, adrenalectomized, or thymectomized (Paik et 
al., 1975). 

8.8.2.  Antagonistic effects

    L-arginine and the related amino acids, ornithine and aspartic 
acid, substrates from urea synthesis, have been reported to exert a 
protective effect against acute ammonia poisoning in rats, dogs, 
and cats (Morris & Rogers, 1978; NRC, 1979). 

    High-protein diets exert an antagonistic effect on the toxicity 
of ammonium salts, unless liver dysfunction is present (section  In addition, an increase in toxic response has been 
observed with increase in age due to the adaptive response of 
glutaminase activity in rats to ammonia detoxication during 

8.9.  Mechanisms of Toxicity

    Hypotheses proposed for the mechanism of ammonia toxicity 
include impaired decarboxylation of pyruvic acid (McKhann & Tower, 
1961), NADH depletion slowing down the generation of ATP (Worcel & 
Erecinska, 1962), depletion of alpha-ketoglutarate resulting in 
impairment of the Krebs cycle (Bessman & Bessman, 1955; Fazekas et 
al., 1956; Warren & Schenker, 1964); depletion of ATP due to 
glutamine formation by the glutamine synthetase (EC system 
(Warren & Schenker, 1964; Nakazawa & Quastel, 1968), stimulation of 
membrane ATPase (EC producing increased nerve cell 
excitability and activity (Hawkins et al., 1973), and depletion of 
ATP causing a decrease in cerebral acetylcholine (Braganca et al., 
1953; Ulshafer, 1958). 


9.1.  Organoleptic Aspects

9.1.1.  Taste

    Campbell et al. (1958) determined the taste threshold 
concentration for ammonia in redistilled water with 21 - 22 
subjects in "difference tests of the triangle type".  At ammonia 
concentrations of 26, 52, and 105 mg/litre, the percentages of 
correct identifications were 61.9, 71.4, and 85.7, respectively. 

    Defining the threshold concentration as the level at which 
correct identification is 50% greater than that expected by 
chance, the taste threshold of ammonia was determined to be 
around 35 mg/litre.  However, this definition of the threshold 
concentration seems to be somewhat arbitrary and McBride & Laing 
(1979) have reported significant positional bias in using the 
triangle test to determine taste thresholds.  Furthermore, the 
triangle test is not intended to mimic environmental exposures 
in which the taste thresholds could be substantially higher.  It 
seems reasonable to conclude only that the palatability of water 
is not likely to be significantly affected by total ammonia levels 
of < 35 mg/litre (as NH3), but will be affected at higher levels. 

9.1.2.  Odour

    Odour thresholds reported in the literature may vary according 
to the definition of odour response, mode of presentation of the 
stimulus, chemical purity of the agent used, and the number of 
subjects and trials in the study.  The detection threshold for 
ammonia, defined as the concentration that produces the first 
detectable difference in odour over background, was reported to be 
37 mg/m3 (DallaValle & Dudley, 1939).  This reference, though often 
cited, gives no information on the study design from which this 
number was derived. 

    The considerable variability in threshold data prompted work by 
Leonardos et al. (1969), who used a standardized procedure to 
determine recognition thresholds rather than detection thresholds 
for 53 chemicals.  The odour threshold was defined as the first 
concentration at which all four panel members (trained odour 
analysts) were able to recognize the characteristic odour of the 
chemical.  The panel tested only one chemical per day.  
Concentrations examined were multiples by 10 of 0.7, 1.47, and 
3.3 mg/m3 (1, 2.1, and 4.6 ppm).  The recognition threshold for the 
odour of ammonia was 32.6 mg/m3 (46.8 ppm). 

    The results of several other studies suggest that human beings 
can detect ammonia at much lower levels.  Stephens (1971) reported 
2.7 mg/m3 (3.9 ppm) as the lowest concentration producing an odour 
response, when a contaminated air stream and a reference stream 
were compared by sniffing (number of subjects was not reported).  A 
report by Saifutdinov (1966), of an olfactory threshold of 0.55 - 
0.50 mg/m3 for the most sensitive of 22 subjects, did not include 

sufficient detail to evaluate this excessively low estimate.  
Carpenter et al. (1948) stated that "a group of 8 persons found 
that the least odour they could detect on entering a room 
containing various concentrations" was 0.7 mg/m3 (1 ppm) ammonia.  
Again, no other details were given. 

    The best estimates of the thresholds at which ammonia can be 
expected to be detected by taste and odour are 35 mg/litre (as NH3) 
and 35 mg/m3, respectively.  Sensitive individuals may detect 
concentrations an order of magnitude lower. 

9.2.  Clinical and Controlled Human Studies

9.2.1.  Inhalation exposure

    The severe effects resulting from acute exposure to ammonia 
have been described in case reports of accidents involving groups 
of people or individuals.  There are no data on actual levels of 
ammonia in air during such accidents, but estimates have been made 
(Yahagi et al., 1959; Takahashi et al., 1984; NRC, 1979). 

    Exposure to an ammonia concentration of 280 mg/m3 (400 ppm) has 
been reported to produce immediate throat irritation; 1200 mg/m3 
(1700 ppm) to produce cough; 1700 mg/m3 (2400 ppm) to be life-
threatening, and 3500 - 7000 mg/m3 (500 - 10 000 ppm) to cause a 
high mortality rate (Patty, 1963; Helmers et al., 1971). 

    A burning sensation in the eyes, nose, and throat, as well as 
respiratory distress accompanied by lachrymation, coughing, and an 
increase in respiratory rate are some of the irritant effects of 
ammonia (Caplin, 1941).  Chest X-rays are generally normal in such 
mild cases (Watson, 1973; Close et al., 1980).  More severe 
respiratory effects include laryngeal and pulmonary oedema and 
bronchopneumonia (Slot, 1938; Caplin, 1941; Levy et al., 1964; 
Taplin et al., 1976; Flury et al., 1983).  The signs and symptoms 
are generally reversible, but chronic bronchitis and bronchiectasis 
have been reported (Slot, 1938; Sugiyama et al., 1968; Taplin et 
al., 1976; Close et al., 1980). 

    In cases with a lethal outcome, the cause of death has been 
severe lung damage and secondary cardiovascular effects (Slot, 
1938; Mulder & van der Zalm, 1967). 

    There have also been some studies on volunteers exposed to 
ammonia under laboratory conditions.  Some of these studies are 
summarized in Table 21. 

    Silverman et al. (1949) reported on 7 human volunteers exposed 
to a concentration of 300 mg/m3 (500 ppm) ammonia for 30 min using 
an oral-nasal mask.  All 7 experienced upper respiratory 
irritation, which lasted up to 24 h in 2 of the volunteers.  Two 
subjects experienced marked lachrymation, in spite of the exposure 
being by oro-nasal mask.  The average respiratory minute volume 
increased markedly compared with control values, and in the 5 

subjects in which minute-by-minute expired volumes were measured, 
there was a marked cyclical variation in minute volume with a 
period of 4 - 7 min.  No coughing was noted. 

    After exposure, respiratory minute volumes fell to levels below 
the pre-exposure rate, but returned to pre-exposure values within 5 
min of exposure.  Ammonia retention decreased progressively until 
an equilibrium of 24% retention (ranging from 4 to 30%) was reached 
at approximately 19 min (range 10 - 27 min).  The indices of 
nitrogen metabolism (BUN, NPN, urine-urea, and urine-ammonia) 
remained normal.  The carbon dioxide combining power did not 

    Verbeck (1977) assessed respiratory function in 16 volunteers 
following exposure to 35, 56, 77, and 98 mg ammonia/m3 (50, 80, 
110, and 140 ppm) for 0.5, 1, and 2 h.  The respiratory variables of 
vital capacity (VC), forced expiratory volume (FEV), and forced 
inspiratory volume (FIV), measured before and after exposure, did 
not decrease by more than 10%.  Subjective variables, including 
smell, taste, irritation of the eyes, nose, or throat, urge to 
cough, headache, and general discomfort were monitored every 15 min 
and ranked by 8 experts and 8 non-experts (students) on a scale 
from 0 to 5.  Subjective responses were ranked higher by the non-
experts.  A concentration of 77 mg/m3 (110 ppm) was tolerated for 
2 h, but at 98 mg/m3 (140 ppm), all the subjects left the chamber 
because the exposure was intolerable. 

    Respiratory responses to ammonia during exercise were examined 
by Cole et al. (1977).  Eighteen males, aged 18 - 39 years, had 2 
periods of exercise in 3 consecutive half-day sessions.  Mean 
exposure levels were 71, 144, 106, and 235 mg/m3 (101, 206, 151, 
and 336 ppm).  Ventilation minute volume and total volume 
decreased, and mean respiratory frequency increased at exposure 
levels > 106 mg/m3 (151 ppm). 

    In a study by MacEwen et al. (1970), 6 volunteers were exposed 
to ammonia concentrations of 21 and 35 mg/m3 (30 and 50 ppm) for 10 
min.  The irritation was rated subjectively on a scale of 0 - 4.  
At 35 mg/m3 (50 ppm), irritation was rated as "moderate" by 4 of 
the volunteers, while 1 individual reported no detectable 
irritation.  None of the volunteers found the irritation at 
35 mg/m3 (50 ppm) to be "discomforting" or "painful". 

    The irritation threshold for ammonia was examined in 10 human 
volunteers by Industrial Bio-Test Laboratories, Inc. (1973).  The 
subjects were exposed to 4 different concentrations of 22, 35, 50, 
and 94 mg/m3 (32, 50, 72, and 134 ppm) for 5 min.  The frequency of 
positive findings for the 10 subjects was as follows:  at 22 mg/m3, 
1 subject complained of dryness of the nose; at 35 mg/m3, 2 
subjects experienced dryness of the nose; at 50 mg/m3, 3 subjects 
had eye irritation, 2 had nasal irritation, and 3 had throat 
irritation; at 94 mg/m3, 5 subjects demonstrated signs of 
lachrymation, 5 had eye irritation, 7 had nasal irritation, 8 had 
throat irritation, and 1 complained of chest irritation. 

Table 21.  Effects of inhaled ammonia in human volunteers
Number  Concentration  Duration   Effects and response              Reference
        (mg/m3)      (min)
7       300            30         irritation of upper respiratory   Silverman et al. (1949)
                                  tract (7/7); increase in minute
                                  volume; no change in blood

16      35 - 98        30 - 120   10% increase in VC, FEV, and      Verbeck (1977)
                                  FIV; 98 mg/m3 was not tolerated;
                                  77 mg/m3 was tolerated for 2 h
18      71 - 235       8 - 11     no effects noted during exercise  Cole et al. (1977)
                                  at 71 mg/m3 except slight
                                  irritation; decrease in
                                  ventilation minute volume and
                                  tidal volume and increase in
                                  respiratory frequency > 106 
6       35             10         "moderate irritation" (4/5)       MacEwen et al. (1970)

10      22             5          dryness of the nose (1/10)        Industrial Biotest
10      35                        dryness of the nose (2/10)        Laboratories (1973)
10      50                        eye irritation (3/10)
10      94                        throat irritation (8/10)
                                  eye irritation (5/10)

6       17.5, 35,      2 - 6 h,   increase in FEV1, with            Ferguson et al. (1977)
        or 70+         5 days/    increasing NH3; adaptation
                       week, for  to irritating effects
                       6 weeks
    A controlled study on human volunteers was conducted by 
Ferguson et al. (1977) to evaluate the responses to inhaled ammonia 
at concentrations of 17.5, 35, and 70 mg/m3 (25, 50, and 100 ppm).  
Six adults, not acclimatized to ammonia exposure, were divided into 
3 groups, which were exposed for 2 - 6 h each day, 5 days per week, 
for 6 weeks.  One pair of subjects was exposed only to 35 mg 
ammonia/m3 for 6-h periods throughout the test.  Subjects were 
examined daily for irritation of the eyes, nose, or throat, and 
periodically for pulse rate, respiration rate, pulmonary function 
(forced vital capacity (FVC) and forced expiratory volume in 1 
second (FEV1)), blood pressure, neurological responses, and 
interference in task-performance ability.  A statistical analysis 
of the results demonstrated that the only significant change among 
the vital functions measured was an increase in forced expiratory 
volume in 1 second (FEV1) with increasing ammonia concentration.  
In addition, the rate of mild eye, nose, or throat irritations over 
the last 3 weeks of the test was significantly less than during the 
first 2 weeks.  This indicated that an acclimatization process had 
occurred, with increased tolerance to the irritant effects of 
ammonia developing with increasing time of exposure.  Overall, the 
ammonia exposure produced 2 incidents of mild irritation (78 
observations made) at 17.5 mg/m3 (25 ppm), 22 incidents (198 
observations made) at 35 mg/m3 (50 ppm), and 11 incidents (84 
observations made) at 70 mg/m3 (100 ppm).  Among control subjects, 
4 irritation incidents were recorded during 45 observations.  When 
ammonia concentrations exceeded 105 mg/m3 (150 ppm), all subjects 
experienced lachrymation accompanied by dryness of the nose and 

    In an inhalation study, the threshold for effects on 
respiration, skin electric potential, and the electroencephalogram 
was found to be 22 mg/m3 (31 ppm) (Alpatov & Mikhailov, 1963; 
Alpatov, 1964). 

    Reports from industries with ammonia exposure indicate that 
irritative effects have appeared over a wide range of ammonia 
concentrations (Elkins, 1950; Vigliani & Zurlo, 1955; Mangold, 
1971).  A concentration of 88 mg/m3 was called "definitely 
irritating" (Elkins, 1950), and "barely noticeable" eye irritation 
was reported at 3 mg/m3 (Mangold, 1971). 

    Giguz (1968), in a study involving 140 subjects exposed to 
ammonia and nitrogen oxides, at concentrations not exceeding the 
"maximum permissible concentration" (20 mg/m3), 3 h per day during 
2 - 3 years of vocational training, demonstrated increased 
incidences of upper respiratory tract disease, compared with those 
in a control group of unexposed subjects. 

9.2.2.  Oral exposure  Effects of acute oral exposure

    Cases of the ingestion of large doses of ammonia have been 
reported.  When solutions of ammonia were ingested orally, a 
tissue-destructive caustic effect was noted for concentrated 

solutions, owing to their high pH.  A solution of ammonia at a 
concentration of 100 g/litre, for example, has a pH of 12.5. 

    Oesophageal burns were reported in 25 cases of accidental 
ammonia ingestion (Hawkins et al., 1980).  One child suffered a 
mild burn.  Four adults had mild burns limited to the mucosa and 
nine adults had oesophageal burns that were moderate or more severe 
in nature.  One adult female suffered from a complication of airway 
obstruction from supraglottic oedema.  Oesophageal stricture from 
the ingestion of ammonia (100 g/litre) was reported by Vancura et 
al. (1980) (Table 19). 

    A fatal outcome after ingestion of a solution containing 24 g 
ammonia/litre was reported by Klendshoj & Rejent (1966).  Autopsy 
showed haemorrhagic inflammatory changes in the oesophagus, 
stomach, and small intestine. 

    There are many reports on the effects of ammonium chloride, but 
since acidosis is caused by the chloride, such studies have little 
relevance for evaluating ammonia toxicity. 

    There are no data on acute effects of ingestion of ammonium 
compounds, other than the chloride. 

9.2.3.  Endogenous hyperammonaemia  Inborn errors of metabolism

    These affect the uptake of ammonia rather than its rate of 

    Congenital deficiency of carbamyl phosphate synthetase I (EC, and, to a lesser extent, of other enzymes of the 
ornithine cycle, and several other metabolic disorders may lead to 
hyperammonaemia and various abnormal urinary constitutents.  
Hyperammonaemia may be lethal in new-born infants, may cause severe 
symptoms in infancy, or may cause chronic remittent symptoms in 
older children or adults (Hsia, 1974). 

    Clinical features in neonates may resemble those of hepatic 
coma and may be precipitated by protein-rich milk feeds.  In older 
children, episodic vomiting, neurological disorders (including 
seizures) or coma are precipitated by high-protein foods.  Hepatic features

    Varied and complex functions of the liver may fail 
progressively in chronic liver disease or rapidly in acute 
disorders.  The syndromes differ in the extent to which portal 
blood from the intestine is shunted into the systemic venous 
circulation either by cirrhotic changes in hepatic vascular 
resistance or by surgical procedures to correct portal hypertension 
resulting from it. 

    In either case, a syndrome is recognised that comprises a 
spectrum of neurological features from irritability via 
inappropriate behaviour, tremors, hyperreflexia and generalised 
muscular rigidity, to delirium, stupor, convulsions and coma. 

    There is disagreement regarding the extent to which this 
syndrome is an expression of ammonia toxicity.  On the one hand, 
over 90% of persons with the disorder have elevated levels of 
ammonia in the blood or cerebrospinal fluid; the condition may be 
induced in those with marginal liver function by the administration 
of ammonium salts or an intestinal haemorrhage (which leads to 
intestinal ammonia production greater than that from an equivalent 
amount of meat) and the condition may be treated by reducing 
intestinal ammonia production, by the administration of antibiotics 
to eliminate ammonia-producing flora.  On the other hand, there is 
an imperfect correlation between the clinical state and the blood-
ammonia level and the condition may occur in the presence of normal 
blood-ammonia levels. 

    It is unlikely that the syndrome resulting from the failure of 
an organ as complicated as the liver should be explicable in terms 
of a single metabolic component, but the similarity between hepatic 
failure and certain expressions of congenital hyperammonaemias 
suggests an important role of ammonia toxicity in the pathogenesis 
of the syndrome. 


10.1.  Atmospheric Exposure and Effects

10.1.1.  General population exposure

    Background levels of ammonia in community air are low in 
comparison with levels that have been established as safe in 
occupational settings, but there is considerable variabilty 
according to the type of land use.  In general, levels in areas 
with intensive livestock husbandry or high rates of manure 
application are in the range of 100 - 200 g/m3, levels in urban 
areas range from approximately 5 to 40 g/m3, while those in rural 
areas, without intensive manure production or use, range up to 
10 g/m3.  This is in contrast to odour thresholds of the order 
10 000 g/m3, thresholds for irritation of the order 20 000 - 
50 000 g/m3, and the estimated LC for man of 5000 - 10 000 mg/m3.  
The LC50 estimation for the rat was 7 600 000 g/m3, for a 2-h
exposure.  In an occupational setting, workers did not voluntarily 
use respiratory protective devices at concentrations below about 
500 000 g/m3.  General ambient atmospheric levels are therefore 
of no concern in respect of discomfort or acute toxicity. 

    Ammonia is not mutagenic and long-term studies on both 
laboratory and farm animals have not shown any pathological effects 
at levels below 35 000 g/m3.  Long-term toxic effects are 
unlikely, even at levels much higher than ambient levels, both 
generally and in the neighbourhood of ammonia-emitting systems.  
There is a lack of evidence regarding recent trends in global 
atmospheric ammonia concentrations. 

10.1.2.  Occupational exposure

    Occupational problems are predominantly those of accidental 

    Though for certain groups in, for example, agriculture, the 
chemical industry, waste disposal and transport, occupational 
exposure levels may be very much higher than general, there is 
historical evidence that, even at levels significantly in excess of 
current occupational exposure limits, there was a low prevalence of 
adverse health effects. 

    The distribution kinetics of absorbed atmospheric ammonia 
suggest that the rise in blood-ammonia at a typical occupational 
exposure limit will be within the normal range of variation. 

    Thus, there is both historical and theoretical evidence that 
most recommended exposure limits are acceptable. 

10.2.  Exposure Through Water and Food

    Ammonia will have a toxic effect, only if intake exceeds the 
capacity of mammals to detoxify ammonia.  Unfortunately, there are 
no data permitting the evaluation of this capacity in healthy human 
beings or other terrestrial mammals.  In addition, there is some 
evidence that the mode of intake may be a factor in the capacity of 
individuals to detoxify ammonia.  Parenteral administration of 
ammonia results in patterns of metabolism and elimination that are 
markedly different from those seen in oral administration.  Thus, 
the considerable body of data on the parenteral toxicity of ammonia 
is not of direct relevance to criteria for oral exposure.  
Similarly, because of the different kinetic patterns between oral 
and inhalation exposure to ammonia, as well as the highly irritant 
effects of ammonia on the lung, the available inhalation data on 
ammonia are not applicable to the estimation of an acceptable daily 
intake (ADI) for ingestion.  However, it would be possible to 
define a clearly undesirable level of oral exposure to total 
ammonia (NH3 and NH4+) as well as a level that is clearly 
tolerable.  The range between these 2 levels would exceed the range 
within which an ADI could be established. 

    The amount of excess ammonia (i.e., over and above the amount 
normally produced in the body) that can be safely ingested and 
assimilated is difficult to define.  In short-term (28 - 90 days) 
studies carried out on rats and pigs, no adverse effects were 
reported at higher levels of ammonia intake (75 - 545 mg NH3/kg 
body weight per day) in the form of sulfamate, phosphate, citrate, 
or chloride. 

    The effects attributed directly to elevated ammonium ion levels 
are acute pulmonary oedema and central nervous system (CNS) 
toxicity, depression of appetite due to a direct effect of the 
ammonium ion on the brain, and promotion of growth via the use of 
ammonium salts as a source of non-essential nitrogen under certain 

    Some effects (such as renal growth and demineralization of 
bone) arising from the administration of ammonium chloride seem to 
be secondary effects of acidosis. 

    Surveys of total ammonia (NH3 + NH4+) concentrations in surface 
waters indicate an average of < 0.18 mg/litre in most areas, and 
0.5 mg/litre in waters near large metropolitan areas (Wolaver, 
1972; US EPA, 1979a).  Levels in ground water are usually low, 
since ammonia is generally immobile in soil.  Ammonia is practically 
absent when drinking-water is chlorinated. 

    Ammonia is a negligible natural constituent of food, but 
ammonium compounds are added in small amounts (< 0.001 - 3.2%) to 
various foods as stabilizers, leavening agents, flavourings, or for 
other purposes.  The daily human intake from these sources is 
estimated to be 18 mg as NH3. 

10.3.  Ocular and Dermal Exposure

    Ammonia in aqueous solution or in contact with body fluids is 
alkaline and causes burns or inflammation of eyes or skin.  The 
ocular irritation commonly experienced at atmospheric ammonia 
concentrations of > 20 mg/m3 (MacEwen et al., 1970; Keplinger et 
al., 1973; Verberk, 1977) is readily reversible when exposure 
ceases, and may also be reduced by acclimatization (Ferguson et 
al., 1977). 

    Serious ocular damage normally occurs, only with a direct blast 
or splash contact with anhydrous or aqueous ammonia (Grant, 1974).  
Skin damage is reported to occur at concentrations of ~7000 mg/m3 
(NRC, 1979). 

10.4.  Accidental Exposure

    High gaseous ammonia concentrations may be encountered locally, 
both in domestic and work-place environments, as a result of gaseous 
emissions and/or spillages of concentrated solutions, and 
respiratory (and skin and eye) injury may result.  On a larger 
scale, spillage from stock or transport tanks or refrigeration 
plant of concentrated ammonia liquor or anhydrous ammonia would 
constitute a severe environmental insult and would cause serious 
injury to the people, animals, and plants in the vicinity.  Because 
of its low density and short biopersistence, major spillages would 
be expected to disperse rapidly and not to persist in the 

10.5.  Evaluation of Risks for the Environment

    Environments that receive more ammonia than can be used may be 
acidified and nitrogen-enriched.  As a consequence of these 
physical-chemical changes, the structure and functioning of the 
ecosystem will be disturbed. 

    Ammonia plays an important role in the metabolism of all 
organisms as a nutrient at low concentrations, but becomes toxic at 
higher concentrations.  For example, microorganisms both assimilate 
and generate ammonia as a part of natural nutrient cycling 
processes.  High levels of ammonia may inhibit growth or survival 
of microbial organisms, including, at higher levels, nitrifying 

10.5.1.  The aquatic environment

    Ammonia concentrations in the aquatic environment are variable, 
reflecting the proximity and nature of sources (section 4). 

    Where there are large numbers of people and animals in relation 
to the volume of surface waters and drainage flow, the load of 
nitrogen added to surface waters from sewage and industrial 
effluent is the predominant source and may lead to ammonia 
concentrations that constitute a significant local and/or regional 
environmental problem. 

    Otherwise, ammonia deposition contributes a major input.  In 
surface waters that are poorly buffered, poor in nutrients, and 
hydrologically dependent on rainfall and/or snow melt, this may 
result in acidification and nitrogen enrichment resulting in marked 
changes in plant community structure with concommitant changes in 
the animal population structure. 

    The toxic effects on aquatic organisms are attributed to non-
ionized ammonia (NH3) rather than to ammonium ion levels.  This is 
because non-ionized ammonia easily penetrates biological membranes, 
whereas ammonium ions require specialized transport processes. 

    There are similarities between the modes of the acute toxic 
action of ammonia in mammals and in fish:  in the latter, however, 
environmental conditions (such as pH, ionic composition and 
concentration, temperature, and oxygen availability), which are 
more variable in water than in air, have a marked modulating 

    Aquatic animals have a limited ability to detoxify ammonia and, 
therefore, the body load is dependent on ammonia concentrations in 
the water.  Except in open oceans, exposure to environmental levels 
produces many chronic effects (including reduced growth, decreased 
survival, impaired reproduction) and may increase susceptibility to 
disease and also cause histopathological changes. 

    High levels of ammonia in aquatic systems are also toxic for 
plants.  The detoxification of excessive ammonia places a severe 
strain on the carbohydrate metabolism of the plant which 
subsequently results in foliar injury, and growth effects, and thus 
may modify plant community composition. 

    Where the dominant species, be it fish or plant, is also 
sensitive to ammonia the effects on the whole ecosystem will be 

10.5.2.  The terrestrial environment

    The most common effect of exposure of plants to atmospheric 
ammonia is foliar injury.  Prolonged exposure to high ambient 
concentrations of about 75 g/mg, such as occur in the vicinity of 
intensive livestock farms, adversely affects more susceptible 
species such as pine trees.  The observed damage is the result of 
both direct and indirect effects due to, changes in soil, and 
secondarily, to increased susceptibility to disease and 
meteorological stress. 

    The data on ammonia toxicity for wildlife are very limited.  
There is no evidence that wildlife populations, in general, are at 
risk from ammonia, but, there may be secondary effects associated 
with changes in plant communities.  Certain species of bats are 
able to withstand the very high ammonia levels found in caves where 
they live. 

10.6.  Conclusions

    The major groups of organisms at risk from elevated ammonia 
levels are aquatic animals and terrestrial plants.  There appears 
to be little danger for terrestrial animals, including man, except 
from acute accidental exposure. 

10.6.1.  General population

    There are no data suggesting that present environmental levels 
of ammonia are hazardous for the general population.  Only high-
level accidental exposures from domestic sources and transportation 
and storage accidents pose an occasional acute health hazard. 

10.6.2.  Sub-populations at special risk

    Groups likely to exhibit ammonia toxicity include those with 
hepatic or renal impairment, though, even in these cases, levels of 
exogenous ammonia are insignificant in comparison with endogeneous 
levels, so that, in the absence of any environmental exposure, such 
persons would still be affected.  The mechanism is different in the 
two cases.  Hepatic impairment limits the conversion of ammonia to 
urea, and renal failure, by increasing urea concentrations and its 
intestinal secretion, leads to increased endogeneous intestinal 
ammonia production. 

    There have been few studies on the chronic effects of ammonia 
inhalation.  It can be speculated that subpopulations that have 
been found to be hyperreactive to other respiratory irritants 
(e.g., sulfur dioxide, particulates, ozone) may also be 
hyperreactive to ammonia.  These subpopulations may include 
children, elderly persons with pre-existing cardiorespiratory 
symptoms, individuals with asthma or bronchitis, and those engaged 
in vigorous physical exercise (Calabrese, 1978).  However, there is 
also some indication that previous exposure to low levels of 
ammonia may cause inurement to its effects (Ferguson et al., 1977). 

10.6.3.  Occupational exposure

    Accidental exposures are the predominant problem (section  Otherwise, occupational exposure can be controlled by 
the application of most current occupational exposure limits and 
proper industrial hygiene. 

10.6.4.  Farm animals

    Farm animals may be at risk, because of continous exposure 
under confined housing conditions resulting in high atmospheric 
levels of ammonia within the confinement areas; this applies 
particularly to cattle, swine, and poultry.  Available reported 
data provide a range of measured exposure levels of from 2 to 
1400 mg/m3.  In winter months in colder climates, most of the 
measured concentrations exceeded the admissible upper limit of 
35 mg/m3 (50 ppm). 

10.6.5.  Environment

    Environments with a low buffer capacity and poor in nutrients 
are susceptible to acidification and nitrogen enrichment by 
elevated ammonia loading; prolonged high ammonia-loading results in 
changes in both the structure and function of plant and animal 
communities.  Levels of atmospheric ammonia necessary for the onset 
of these changes have not been established; however, changes in the 
structure of these communities have been observed where ammonia 
levels in the atmosphere were possibly up to 100 g/m3. 

    Plants use ammonia as a nutrient, but high levels can be toxic.  
Terrestrial plants show a susceptibility to reduced growth and 
reduced vitality, when exposed to levels as low as 75 g NH3/m3 in 
the atmosphere. 

    Aquatic animals have a low capacity to detoxify ammonia.  Acute 
effects on some fish have been demonstrated in laboratories at 
concentrations as low as 0.1 mg NH3/litre and chronic effects at 
concentrations as low as 0.02 mg NH3/litre.  Thus, as ammonia 
levels in some waters are often similar to those shown to cause 
chronic effects in some fish, it would appear that these animals 
are at risk.  Aquatic invertebrates are, in general, less sensitive 
to elevated ammonia levels in water. 

    Aquatic animals are at risk because of increases in ammonia 
concentrations in water systems, whereas some plant communities 
appear to be at risk from elevations in atmospheric ammonia 


11.1.  Research Needs

     1.  Long-term monitoring of ammonia and other pollutants in 
         water systems with different aquatic ecosystems. 

     2.  Studies of the long-term effects of ammonia on terrestrial 

     3.  Studies of the global nitrogen balance to identify long-
         term trends. 

     4.  Ecotoxicological studies to elucidate environmental 

     5.  Epidemiological studies in relation to ammonia exposure in 
         order to make better hygiene recommendations.

     6.  Long-term experimental animal studies to establish a no-
         observed-adverse-effect level of exposure. 

     7.  Studies on the role of ammonia in modifying physical and 
         chemical conditions of soil and water systems. 

     8.  More data are needed to assess accurately the relative 
         contributions of various point and non-point sources of 
         ammonia for surface waters. 

     9.  Research into methods and their application directed 
         towards reducing emissions from point sources. 

    10.  Additional acute toxicity tests with salt-water fish and 
         invertebrate species. 

    11.  Life-cycle and early-life-stage tests with representative 
         fresh-water and salt-water organisms from different 
         families, with investigation of pH effects on chronic 

    12.  Fluctuating or intermittent exposure tests under a variety 
         of exposure patterns on additional species. 

    13.  Both acute and long-term tests at cold-water temperatures.

    14.  Studies on the effects of dissolved and suspended solids 
         on acute and chronic toxicity. 

    15.  More histopathological and histochemical research with 
         fish, which would provide a rapid means of identifying and 
         quantifying sublethal ammonia effects. 

    16.  In fish, the relative concentration limits for both 
         acclimatization and subsequent acute response need better 
         definition and a more complete explanation. 


ABBAS, R. & TANNER, R.L.  (1981)  Continuous determination of 
gaseous ammonia in the ambient atmosphere using fluorescence 
derivatization.  Atmos. Environ., 15: 277-281.

ABELOVICH, A. & AZOV, Y.  (1976)  Toxicity of ammonia to algae 
in sewage oxidation ponds.  Appl. environ. Microbiol., 31(6): 

ADMIRAAL, W.  (1977)  Tolerance of estuarine benthic diatoms 
to high concentrations of ammonia, nitrite ion, nitrate ion 
and orthophosphate.  Mar. Biol., 43(4): 307-315.

AGAMI, M., LITAV, M., & WAISEL, Y.  (1976)  The effects of 
various components of water pollution on the behaviour of some 
aquatic macrophytes of the coastal rivers of Israel.  Aquat. 
 Bot., 2(3): 203-213.

ALABASTER, J.S. & HERBERT, D.W.M.  (1954)  Influence of carbon 
dioxide on the toxicity of ammonia.  Nature (Lond.), 174(4426): 

ALABASTER, J.S., SHURBEN, D.G., & KNOWLES, G.  (1979)  The 
effect of dissolved oxygen and salinity on the toxicity of 
ammonia to smolts of salmon,  Salmo salar L.  J. Fish Biol., 
15(6): 705-712.

ALLAN, I.R.H.  (1955)  Effects of pollution on fisheries. 
 Verh. Int. Ver. Theor. Agnew Limnol., 12: 804-810.

ALLAN, I.R.H., HERBERT, D.W.M., & ALABASTER, J.S.  (1958)  A 
field and laboratory investigation of fish in a sewage 
effluent.  Fish. Invest., 6(2): 1-76.

ALPATOV, I.M.  (1964)  [A study of gazeous ammonia toxicity.] 
 Gig. Tr. prof. Zabol., 2: 14-18 (in Russian).

ALPATOV, I.M. & MIKHAILOV, V.I.  (1963)  [Inquires into the 
gaseous ammonia toxicity. Communication 1.]  Gig. Tr. prof. 
 Zabol., 12: 51-53 (in Russian)

(1982)  Accuracy of determination of ammoniacal nitrogen in 
river waters: analytical quality control in the harmonised 
monitoring scheme.  Analyst, 107(June): 680-688.

ANDERSON, B.G.  (1948)  The apparent thresholds of toxicity to 
 Daphnia magna for chlorides of various metals when added to 
Lake Erie water.  Trans. Am. Fish Soc., 78: 96-113.

ANDERSON, D.P., BEARD, C.W., & HANSON, R.P.  (1964a)  The 
adverse effects of ammonia on chickens including resistance to 
infections with Newcastle disease virus.  Avian Dis., 8: 

ANDERSON, D.P., CHERMS, F.L., & HANSON, R.P.  (1964b)  Studies 
on measuring the environment of turkeys raised in confinement. 
 Poult. Sci., 43: 305-318.

ANDERSON, K.B., SPARKS, R.E., & PAPARO, A.A.  (1978)   Rapid 
 assessment of water quality, using the fingernail clam, 
Musculium transversum, Urbana, Illinois, Water Resources 
Center, University of Illinois, 115 pp (WRC Research Report 
No. 133).

ANGHILERI, L.G.  (1975)  Tumour growth inhibition by ammonium 
chloride-induced acidosis.  Int. J. clin. Pharmacol., 12: 320.

E.G.  (1976)  Inhibition of nitrification by ammonia and 
nitrous acid.  J. Water Poll. Control Fed., 48: 835-852.

APHA  (1976)   Standard methods for the examination of water 
 and wastewater, 14th ed., Washington DC, American Public 
Health Association, American Water Works Association, Water 
Pollution Control Federation, 1193 pp.

API  (1981)   The sources, chemistry, fate, and effects of 
 ammonia in aquatic environments, Washington DC, American 
Petroleum Institute, 145 pp.

APPELMAN, L.M., TEN BERGE, W.F., & REUZEL, P.G.J.  (1982)  
Acute inhalation toxicity study of ammonia in rats with 
variable exposure periods.  Am. Ind. Hyg. Assoc. J., 43(9): 

(1978)  Interaction of ionized and un-ionized ammonia on 
short-term survival and growth of prawn larvae,  Macrobrachium 
 rosenbergii. Biol. Bull., 154(1): 15-31.

ARNDT, F.L., DAY, D.L., & HATFIELD, E.  (1979)  Processing and 
Handling of animal excreta for refeeding.  J. anim. Sci., 48: 

ASTM  (1980)   Annual book of ASTM standards. Part 31. Water, 
Philadelphia, Pennsylvania, American Society for Testing and 

AUERBACH, C. & ROBSON, J.M.  (1947)  Tests of chemical 
substances for mutagenic action.   Proc. R. Soc. Edinburgh Sec. 
 Biol., 62B: 284-291.

(1977)   [Medical and sanitary aspects of sailors' work,] Riga, 
Zvaigzne, 132 pp (in Russian).

AXELROD, H.D. & GREENBERG, J.P.  (1976)  Determination of 
trace concentration of ammonia in the atmosphere using 
pyridine-pyrazolone reagent.  Atmos. Environ., 10: 495-496.

BAIRD, R., BOTTOMLEY, J., & TAITZ, H.  (1979)  Ammonia 
toxicity and pH control in fish toxicity bioassays of treated 
wastewaters.  Water Res., 13(2): 181-184.

BALL, I.R.  (1967)  The relative susceptibilities of some 
species of fresh-water fish to poisons. I. Ammonia.  Water 
 Res., 1(11/12): 767-775.

BARROW, C.S. & STEINHAGEN, W.H.  (1980)  NH3 concentrations in 
the expired air of the rat: Importance to inhalation 
toxicology.  Toxicol. appl. Pharmacol., 53: 116-121.

BARROW, C.S., ALARIE, Y., & STOCK, M.F.  (1978)  Sensory 
irritation and incapacitation evoked by thermal decomposition 
products of polymers and comparisons with known sensory 
irritants.  Arch. environ. Health, 33(2): 79-88.

BARTON, L.V.  (1940)  Toxicity of ammonia, chlorine, hydrogen 
cyanide, hydrogen sulphide and sulphur dioxide gases. IV. 
Seeds.  Contrib. Boyce Thompson Inst., 11: 357-363.

BARZEL, U.S.  (1975)  Effect of chronic ammonium chloride 
ingestion on parathyroid-hormone function.  Nephron, 14(15): 

BARZEL, U.S. & JOWSEY, J.  (1969)  Effects of chronic acid and 
alkali administration on bone turnover in adult rats.  Clin. 
 Sci., 36(3): 517-524.

BENEDICT, H.M. & BREEN, W.H.  (1955)  The use of weeds as a 
means of evaluating vegetation damage caused by air pollution. 
In:   Proceedings of the Third National Air Pollution 
 Symposium, Pasadena, California, April 1955, pp. 177-190.

BENNETT, W.F., PESEK, J., & HANWAY, J.J.  (1964)  Effects of 
nitrate and ammonium on growth of corn in nutrient solution 
sand culture.  Agric. J., 56: 342-345.

BENYAJATI, S. & GOLDSTEIN, L.  (1975)  Renal glutaminase 
adaptation and ammonia excretion in infant rats. 
 Am. J. Physiol., 228(3): 693-698.

Metabolic compartments  in vivo:  Ammonia and glutamic acid 
metabolism in brain and liver.  J. biol. Chem., 237: 2562-2569.

BESSMAN, S.P. & BESSMAN, A.N.  (1955)  The cerebral and 
peripheral uptake of ammonia in liver disease with an 
hypothesis for the mechanism of hepatic coma.  J. clin. 
 Invest., 34: 622-628.

BHATTACHARYA, A.N. & TAYLOR, J.C.  (1975)  Recycling animal 
waste as a feedstuff: A review.  J. anim. Sci., 44: 1438.

BIDWELL, R.G.B.  (1974)   Plant physiology, New York, 
MacMillan, 197 pp.

BINSTOCK, L. & LECAR, H.  (1969)  Ammonium ion currents in the 
squid giant axon.  J. gen. Physiol., 53: 342-361.

Quantitative nutritional studies with water-soluble, 
chemically defined diets. III. Individual amino acids as 
sources of "non-essential" nitrogen.  Arch. Biochem. Biophys., 
72(2): 428-436.

BISWAS, S.D. & KLEINBERG, I.  (1971)  Effect of urea 
concentration on its utilisation, on the pH and the formation 
of ammonia and carbon dioxide in a human salivary sediment 
system.  Arch. oral Biol., 16: 759-780.

BLOOMFIELD, R.A., GARNER, G.B., & MUHRER, M.E.  (1960)  
Kinetics of urea metabolism in sheep.  J. anim. Sci., 19: 1248.

(1962)  Ruminal pH and absorption of ammonia and VFA.  J. anim. 
 Sci., 22: 833 (Abstract).

BOCK, F., MICHELSON, I., BROSS, I.D., & PRIORE, R.L.  (1974)  
Carcinogenic activity of smoke condensate from cigarettes with 
ammonium sulfamate-treated paper.  Cancer, 33: 1010.

BODANSKY, A., JAFFE, M.L., & CHANDLER, J.P.  (1932)  Serum 
phosphatase changes in ammonium chloride osteoporosis.  Proc. 
 Soc. Exp. Biol. Med., 29: 871-875.

BOER, W.M.J., DEN & BASTIAENS H.  (1984)   [Effects of 
 acidification on vegetation,] Ministry of Agriculture and 
Fisheries, Ministry of Housing, Physical Planning and 
Environment, 82 pp (Report No. 84(2)) (in Dutch).

Ammonia kills spoilage moulds in corn.  J. Dairy Sci., 56: 241.

Effect of pH and substrate on growth.  Eur. J. appl. Microbiol, 
1: 55-56.

(1975b)  Preservation of high-moisture corn: a microbiological 
evaluation  J. Dairy Sci., 58: 386-391.

BOYD, E.M. & SEYMOUR, K.G.W.  (1946)  Ethylenediamine 
dihydrochloride or "chlorethamine". II. Untoward and toxic 
reactions.  Exp. Med. Surg.,  : 223-227.

BOYD, E.M., McLACHLAN, M.L., & PERRY, W.F.  (1944)  
Experimental ammonia gas poisoning in rabbits and cats. 
 J. ind. Hyg. Toxicol., 26: 29-34.

BRAGANGA, B.M., FAULKNER, P., & QUASTEL, J.M.  (1953)  Effects 
of inhibitors of glutamine synthesis in brain slices by 
ammonium ions.  Biochim. Biophys. Acta, 10: 83-88.

WARTBURG, A.F.  (1973)  Background trace concentrations in the 
central United States.  J. geophys. Res., 78: 7057-7064.

SHEESLEY, D.C., ENGLERT, T.R., & SEARS, D.R.  (1976)  
Measurements of atmospheric pollutants in the St. Louis area. 
 Atmos. Environ., 10: 181-184.

BRENNAN, E., LEONE, I.A., & DAINES, R.H.  (1962)  Ammonia 
injury to applies and peaches in storage.  Plant Dis. Rep., 46: 

BRESSANI, R. & BRAHAM, J.E.  (1977)  Effect of frequency of 
feeding on blood serum urea changes in dogs.  J. Nutr. Rep. 
 Int., 16(3): 305-316.

BRETT, J.R. & ZALA, C.A.  (1975)  Daily pattern of nitrogen 
excretion and oxygen consumption of sockeye salmon 
 (Oncorhyncus nerka) under controlled conditions.  J. Fish. Res. 
 Board Can., 32: 2479-2486.

BRETTHAUER, R.  (1978)  Some ecological limits of tolerance to 
 Ochromonas sociabilis. Verh. Internat. Verein. Limnol., 20(3): 

BROCKWAY, D.R.  (1950)  Metabolic products and their effects. 
 Prog. Fish-Cult., 12(3): 127-129.

BRODERIUS, S.J. & SMITH, L.L., Jr  (1979)  Lethal and 
sublethal effects of binary mixtures of cyanide and hexavalent 
chromium, zinc, or ammonia to the fathead minnow  Pimephales 
 promelas and rainbow trout  Salmo gairdneri. J. Fish. Res. 
 Board Can., 36(2): 164-172.

BRODERIUS, S.J., SMITH, L.L., Jr, & LIND, D.T.  (1977)  
Relative toxicity of free cyanide and dissolved sulfide forms 
to the fathead minnow.  Pimephales promelas. J. Fish. Res. 
 Board Can., 34(12): 2323-2332.

(in press)  Toxicity of ammonia to smallmouth bass, 
 Micropterus dolomieui, as related to pH.  Environ. Toxicol. 

BRODERSON, J.R., LINDSEY, J.R., & CRAWFORD, J.E.  (1976)  The 
role of environmental ammonia in respiratory mycoplasmosis of 
rats.  Am. J. Pathol., 85: 115-130.

BROSSET, C., ANDREASSON, K., & FERM, M.  (1975)  The nature 
and possible origin of acid particles observed at the Swedish 
west coast.  Atmos. Environ., 9: 631-642.

BROWN, A.C.  (1974)  Observation on the effect of ammonium 
nitrate solutions on some common marine animals from Table 
Bay.  Trans. R. Soc. S. Afr., 41(2): 217-223.

BROWN, V.M.  (1968)  The calculation of the acute toxicity of 
mixtures of poisons to rainbow trout.  Water Res., 2(10): 

BROWN, R.H., DUDA, G.D., KORKES, S., & HANDLER, P.  (1957)  A 
colorimetric micromethod for determination of ammonia: the 
ammonia content of rat tissues and human plasma.  Arch. 
 Biochem. Biophys., 66: 301-309.

BROWN, V.M., JORDAN, D.H.M., & TILLER, B.A.  (1969)  The acute 
toxicity to rainbow trout of fluctuating concentrations and 
mixtures of ammonia, phenol and zinc.  J. Fish Biol., 1(1): 1-9.

BUCKLEY, J.A.  (1978)  Acute toxicity of unionized ammonia to 
fingerling coho salmon.  Prog. Fish-Cult., 40(1): 30-32.

BUCKLEY, J.A., WHITMORE, C.M., & LIMING, B.D.  (1979)  Effects 
of prolonged exposure to ammonia on the blood and liver 
glycogen of coho salmon  (Oncorhynchus kisutch). Comp. Biochem. 
 Physiol., 63C(2): 297-303.

BUIKEMA, A.I., Jr, CAIRNS, J., Jr, & SULLIVAN, G.W.  (1974)  
Evaluation of  Philodina acuticornis (Rotifera) as a bioassay 
organism for heavy metals.  Water Res. Bull., 10(4): 648-661.

 [Methods for determination of harmful substances in air. A 
 practical guide,] 2nd ed., Moscow, Meditaina (in Russian).

keratoconjunctivitis in chickens.  Poult. Sci., 29: 386-389.

BURKHALTER, D.E. & KAYA, C.M.  (1977)  Effects of prolonged 
exposure to ammonia on fertilized eggs and sac fry of rainbow 
trout  (Salmo gairdneri). Trans. Am. Fish Soc., 106(5): 470-475.

BURROWS, R.E.  (1964)   Effects of acclimated excretory 
 products on hatchery-reared salmonids, Washington DC, Fish and 
Wildlife Service, US Department of the Interior, 12 pp 
(Research Report 66).

BUTTERWORTH, B.  (1979)  Nutritionally improved straw: the 
machines do the job.  Agric. Eng., 60(7): 41-42.

BUYSMAN, E.  (1984)   [Ammonia emissions in the Netherlands,] 
Ministry of Housing, Physical Planning, and Environment, 
Directorate Air (Report No. 22) (in Dutch).

BUYSMAN, E., MAAS, J.F.M., & ASMAN, W.A.M.  (1985)   Ammonia 
 emission in Europe, Utrecht, the Netherlands, Institute for 
Meteorology and Oceanography, State University Utrecht.

BYERRUM, R.U. & BENSON, A.A.  (1975)  Effect of ammonia on 
photosynthetic rate and photosynthate release by  Amphidinium 
 carterae (Dinophyceae).  J. Phycol., 11: 449-452.

CALABRESE, E.J.  (1978)   Pollutants and high risk groups, 
New York, Wiley-Interscience Publications.

CALAMARI, D., MARCHETTI, R., & VAILATI, G.  (1977)  [Effect of 
prolonged treatments with ammonia on stages of development of 
 Salmo gairdneri.] Nuovi Ann. Ig. Microbiol., 28(5): 333-345. 
(in Italian).

CALAMARI, D., MARCHETTI, R., & VAILATI, G.  (1981)  Effects of 
long-term exposure to ammonia on the developmental stages of 
rainbow trout ( Salmo gairdnerii Richardson).  Rapp. P.-V. Run. 
 Cons. Int. Explor. Mer, 178: 81-86.

CAMERON, J.N.  (1979)  Excretion of CO2 in water-breathing 
animals.  Marine Biol. Lett., 1: 3-13.

CAMERON, J.N. & HEISLER, N.  (1983)  Studies of ammonia in the 
rainbow trout physio-chemical parameter, acid-base behavior, 
and respiratory clearance.  J. exp. Biol., 105:: 107-125.

CAMERON, G.R. & SHEIKH, A.H.  (1951)  Experimental production 
of pulmonary edema with ammonium salts, together with 
classification of lung oedemas.  J. Pathol. Bacteriol., 63: 

(1958)  Effect of certain chemicals in water on the flavor of 
brewed coffee.  Food Res., 23: 575-579.

CAPLIN, M.  (1941)  Ammonia gas poisoning. Forty-seven cases 
in a London shelter.  Lancet, 2: 95-96.

CAPUCO, A.V.  (1977)   Ammonia, a modulator of 3T3 cell growth, 
Ithaca, New York, Cornell University (Ph.D Thesis).

CARPENTER, C.P., SMYTH, H.S., Jr, & SHAFFER, C.B.  (1948)  The 
acute toxicity of ethylene imine to small animals.  J. ind. 
 Hyg. Toxicol., 30: 2-6.

CARY, G.A.  (1976)   A report on the assessment of aquatic 
 environmental impact of Union Carbide's Uravan operations: 
 on-site toxicity bioassays, Tarrytown, New York, Aquatic 
Environmental Sciences, Union Carbide Corporation, 67 pp 
(Report prepared for Metals Division, Union Carbide 
Corporation, Uravan, Colorado).

CASTELL, D.O. & MOORE, E.W.  (1971)  Ammonia absorption from 
the human colon.  Gastroenterology, 60(1): 33-42.

QUIBUYEN, A.T.  (1977a)  Effect of some physico-chemical 
factors on the survival and growth of  Penaeus monodon 
postlarvae.  Q. Res. Rep. Aquacult. Dep. Southeast Asian Fish. 
 Dev. Cent., 1(3): 13-16.

C.M.  (1977b)  Effect of nitrite, ammonia, and temperature on 
 P. monodon larvae.  Q. Res. Rep. Aquacult. Dep. Southeast Asian 
 Fish. Dev. Cent., 1(3): 9-12.

MCCULLOUGH, J.D., Jr  (1973)  Effects of anhydrous ammonia on 
a central Texas pond and a review of previous research with 
ammonia in fisheries management.  Trans. Am. Fish. Soc., 
102(1): 73-82.

CHARLES, D.R. & PAYNE, C.G.  (1966a)  The influence of graded 
levels of atmospheric ammonia on chickens. I. Effects on 
respiration and on the performance of broilers and replacement 
growing stock.  Br. Poult. Sci., 7: 177-187.

CHARLES, D.R. & PAYNE, C.G.  (1966b)  The influence of graded 
levels of atmospheric ammonia on chickens. II. Effects on the 
performance of laying hens.  Br. Poult. Sci., 7: 189-198.

CHEMICAL AND ENGINEERING NEWS  (1980)  C and EN's top fifty 
chemical products.  Am. Chem. Soc., : 16.

CHIPMAN, W.A., Jr  (1934)   The role of pH in determining the 
 toxicity of ammonium compounds, Columbia, Missouri, University 
of Missouri, 153 pp (Ph.D. Thesis).

CLAIBORNE, J.B., EVANS, D.H., & GOLDSTEIN, L.  (1982)  Fish 
branchial Na+-K+-activated ATPase.  J. exp. Biol., 96: 431-434.

CLAIBORNE, J.B. & HEISLER, N.  (1984)  Acid-base regulation in 
the carp  (Cyprinus carpio) during and after exposure to 
environmental hypercapnia.  J. exp. Biol., 108: 25-43.

CLAWSON, A.J. & ARMSTRONG, W.D.  (1981)  Ammonium 
polyphosphate as a source of phosphorous and nonprotein 
nitrogen for monogastrics (in corn-soybean meal diets for 
growing rats and growing finishing [G-F] pigs).  J. anim. Sci., 
52(1): 1-7.

CLOSE, L.G., CATLIN, F.I., & COHN, A.M.  (1980)  Acute and 
chronic effects of ammonia burns of the respiratory tract. 
 Arch. Otolaryngol., 106: 151-158.

COLE, T.J., COTES, J.E., JOHNSON, G.R., & MARTIN, H.  (1977)  
Ventilation cardiac frequency and pattern of breathing during 
exercise in men exposed to  o-chlorobenzylidene malonitril and 
ammonia gas in low concentrations.  Q. J. exp. Physiol., 62: 

COLT, J.E.  (1978)   The effects of ammonia on the growth of 
 channel catfish, Ictalurus punctatus, Davis, California, 
University of California, 185 pp (Ph.D. Thesis).

COLT, J.E. & TCHOBANOGLOUS, G.  (1976)  Evaluation of the 
short-term toxicity of nitrogenous compounds to channel 
catfish,  Ictalurus punctatus. Aquaculture, 8(3): 209-224.

COLT, J.E. & TCHOBANOGLOUS, G.  (1978)  Chronic exposure of 
channel catfish,  Ictalurus punctatus to ammonia: effects on 
growth and survival.  Aquaculture, 15(4): 353-372.

CONN, H.O.  (1972)  Studies of the source and significance of 
blood ammonia. IV. Early ammonia peaks after ingestion of 
ammonium salts.  Yale J. Biol. Med., 45: 543-549.

CONSTANTINE, D.G.  (1958)  Bleaching of hair pigment in bats 
by the atmosphere in caves.  J. Mammal, 39: 513-520.

COOMBE, J.B., TRIBE, D.E., & MORRISON, J.W.  (1960)  Some 
experimental observations on the toxicity of urea to sheep. 
 Aust. J. agric. Res., 11: 247-256.

(1970)  Animal inhalation studies on ammonia, ethylene glycol, 
formaldehyde, dimethylamine, and ethanol.  Toxicol. appl. 
 Pharmacol., 16: 646-655.

COTTERILL, O.J. & NORDSKOG, A.W.  (1954)  Influence of ammonia 
on egg white quality.  Poult. Sci., 33: 432-434.

CRIBB, G.S.  (1964)  Nitrogen. In:  Mellor's comprehensive 
 treatise on inorganic and theoretical chemistry, London, 
Longmans, Vol. 8, Suppl. I, pp. 276-327.

CURTIS, S.E.  (1972)  Air environment and animal performance. 
 J. anim. Sci., 35: 628-634.

DALHAMN, T.  (1963)  Effect 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.  Int. J. Air Water Pollut., 7: 531-539.

DALHAMN, T. & SJOHOLM, J.  (1961)  Studies of SO2, NO2, and 
NH3: effect on ciliary activity in the rabbit trachea of 
single  in vitro exposure and resorption in rabbit nasal 
cavity.  Acta physiol. Scand., 58: 287-291.

DALLAVALLE, J.M. & DUDLEY, H.C.  (1939)  Evaluation of odor 
nuisance in the manufacture of kraft paper.  Public Health 
 Rep., 54(1): 35-43.

DANECKER, E.  (1964)  [The jauche poisoning of fish: an 
ammonia poisoning.]  Osterr. Fischerei., 3/4: 55-68. (in 

DAVIES, B.M.A. & YUDKIN, J.  (1952)  Studies in biochemical 
adaptation. The origin of urinary ammonia as indicated by the 
effect of chronic acidosis and alkalosis on some renal enzymes 
in the rat.  Biochem. J., 52: 407-412.

DAY, D.L., HANSEN, E.L., & ANDERSON, S.  (1965)  Gases and 
odors in confinement swine buildings.  Trans. Am. Soc. Agric. 
 Eng., 8: 118-121.

DEAL, P.H., SOUZA, K.A., & MACK, H.M.  (1975)  High pH, 
ammonia toxicity, and the search for life on the Jovian 
planets.  Origins Life, 6(4): 561-573.

DEAN, J.A., ed.  (1979)   Lange's handbook of chemistry, 12th 
ed., New York, McGraw-Hill Book Company.

Toxicity of underground coal gasification condenser water and 
selected constitutents to aquatic biota.  Arch. environ. 
 Contam. Toxicol., 9(5): 543-555.

R.F.  (1977)  Ammonia toxicity in cultured larvae of the 
American lobster  (Homarus americanus). In:  Proceedings of the 
 8th Annual Meeting of the World Mariculture Society, San Jose, 
 Costa Rica, pp. 647-673.

DEMEREC, M., BERTANI, G., & FLINT, J.  (1951)  A survey of 
chemicals for mutagenic action on  E. coli. Am. Nat., 85: 119.

DEMUYNCK, M., RAHN, K.A., JANSSENS, M., & DAMS, R.  (1976)  
Chemical analysis of airborne particulate matter during a 
period of unusually high pollution.  Atmos. Environ., 10: 21-26.

DE VOOYS, G.G.N.  (1968)  Formation and excretion of ammonia 
in Teleostei. I. Excretion of ammonia through the gills.  Arch. 
 int. Physiol. Biochimie., 76: 268-272.

DODD, K.T. & GROSS, D.R.  (1980)  Ammonia inhalation toxicity 
in cats.  Arch. environ. Health, 35: 6-14.

DOIG, P.A. & WILLOUGHBY, R.A.  (1971)  Response of swine to 
atmospheric ammonia and organic dust.  J. Am. Vet. Med. Assoc., 
159: 1353-1361.

DOWDEN, B.F. & BENNETT, H.J.  (1965)  Toxicity of selected 
chemicals to certain animals.  J. Water Pollut. Control. Fed., 
37(9): 1308-1316.

DOWNING, K.M. & MERKENS, J.C.  (1955)  The influence of 
dissolved-oxygen concentration on the toxicity of un-ionized 
ammonia to rainbow trout ( Salmo gairdneri Richardson). 
 Ann. appl. Biol., 43(2): 243-246.

DREWES, D.R. & HALES, J.M.  (1980)   Removal of pollutants from 
 power plant plumes by precipitation, Richland, Washington, 
Battelle-Northwest, US Electric Power Research Institute 
(Report to the EPRI).

DRIEDZIC, W.R. & HOCHACHKA, P.W.  (1976)  Control of energy 
metabolism in fish white muscle.  Am. J. Physiol., 230: 579-582.

(1980)  Effects of aerial ammonia on growth and health of 
young pigs.  J. anim. Sci., 50: 1085-1091.

DUDA, G.D. & HANDLER, P.  (1958)  Kinetics of ammonia 
metabolism  in vivo. J. biol. Chem., 232: 303-314.

S.M.  (1957)  Studies on the metabolism of amino acids and 
related compounds  in vivo.  VI. Free amino acid levels in the 
tissues of rats protected against ammonia toxicity.  Arch. 
 Biochem. Biophys., 68: 161-171.

(1955)  Wildlife rabies in Texas.  Public Health Rep., 70: 

ECKERT, J.W.  (1967)  Application and use of postharvest 
fungicides. In: Torgeson, D.C., ed.  Fungicides, New York, 
Academic Press, pp. 341.

ECKERT, J.W., KOLBEZEN, M.J., & GARBER, M.J.  (1963)  
Evaluation of ammonia-generating formations for control of 
citrus fruit decay.  Phytopathology, 53: 140-148.

ECOLOGICAL ANALYSTS, INC.  (1981)   The sources, chemistry, 
 fate, and effects of ammonia in aquatic environments, 
Washington DC, American Petroleum Institute.

(1967)  The renal response of children to acute ammonium 
chloride acidosis.  Pediat. Res., 1: 452-460.

urea toxicity in sheep.  Can. J. Comp. Med., 42: 63-68.

EDWARDS, J.G. & CONDORELLI, L.  (1928)  Studies on aglomerular 
and glomerular kidneys. II. Physiological.  Am.J. Physiol., 86: 

EGGELTON, A.E.J.  (1969)  The chemical composition of 
atmospheric aerosols on Tees-side and its relation to 
visibility.  Atmos. Environ., 3: 355-372.

EGLE, J.L., Jr  (1973)  Retention of inhaled acetone and 
ammonia in the dog.  Am. Ind. Hyg. Assoc. J., 34(12): 533-539.

ELKINS, H.B.  (1950)   The chemistry of industrial toxicology, 
New York, John Wiley and Sons, 84 pp.

ELKINS, H.B.  (1959)  Ammonia, NH3. In:  The chemistry of 
 industrial toxicology, 2nd ed., New York, John Wiley and Sons, 
86 pp.

(1975)  Aqueous ammonia equilibrium calculations: effect of pH 
and temperature.  J. Fish. Res. Board Can., 32: 2379-2383.

EMERY, R.M. & WELCH, E.B.  (1969)   The toxicity of alkaline 
 solutions of ammonia to juvenile bluegill sunfish (Lepomis 
 macrochirus Raf.), Chattanooga, Tennessee, Water Quality 
Branch, Division of Health and Safety, Tennessee Valley 
Authority, 31 pp (Mimeo).

An analysis of the partial metabolic derepression of sea 
urchin eggs by ammonia; the existence of independent pathways. 
 Dev. Biol., 40: 245-255.

EPIFANO, C.E. & SRNA, R.F.  (1975)  Toxicity of ammonia, 
nitrite ion, nitrate ion, and orthophosphate to  Mercenaria 
 mercenaria and  Crassostrea virginica. Mar. Biol., 33(3): 

ERNST, R.A.  (1968)  The effect of ammonia on poultry. 
 Feedstuffs, 40(32): 40.

 quality criteria for European freshwater fish. Report on 
 ammonia and inland fisheries, pp. 12 (EIFAC Technical Paper 
No. 11) (Also in:  Water Res., 7(7): 1011-1022 (1973)).

EVANS, D.H.  (1977)  Further evidence for Na/NH4 exchange in 
marine teleost fish.  J. exp. Biol., 70: 213-220.

EVANS, D.H.  (1980)  Osmotic and ionic regulation by 
freshwater and marine fishes. In: Ali, M.A. ed.  Environmental 
 Physiology of Fishes, New York, Plenum Publishing Co., 
pp. 93-122.

EVANS, D.H., KORMANIK, G.A., & KRASNY, E.J.  (1979)  
Mechanisms of ammonia and acid extrusion by the little skate, 
 Raja erinacea. J. exp. Zool., 208: 431-437.

EVANS, J.W.  (1979)   The construction and use of a 
 continuous-flow bioassay apparatus to determine a preliminary 
 un-ionized ammonia 96-h LC50  for the crayfish, Orconectes 
 nais, Lawrence, Kansas, University of Kansas, 76 pp (M.S. 

FARBER, R.J. & ROSSANO, A.T.  (1975)  A new approach for 
measuring atmospheric concentrations of ammonia.  Paper 
 presented at Annual Meeting of the Pacific Northwest 
 International Section of the Air Pollution Control 
 Association, Vancouver, British Columbia, November 19-21, 
36 pp.

FASEB  (1974)   Evaluation of the health aspects of certain 
 ammonium salts as food ingredients, Springfield, Virginia, 
Federation of American Societies for Experimental Biology, 
21 pp (Prepared for the US Food and Drug Administration under 
Contract No. FDA 72-85) (US NTIS PPB-254-532).

FAUCONNEAU, B. & LUQUET, P.  (1979)  Influence d'une lvation 
de temprature sur l'volution de l'aminoacidmie et de 
l'ammonimie aprs le repas chez la truite arc en ciel  (Salmo 
 gairdneri R.).  Ann. Biol. anim. Biochim. Biophys., 19(4A): 

FAZEKAS, I.G.  (1939)  Experimental suprarenal hypertrophy 
induced by ammonium hydroxide.  Endokrinologie, 21: 315-337.

FAZEKAS, I.G.  (1949)  [Experimental data on influencing 
ovarian functions by simple compounds.]  Orv. Hetil., 90: 
777-781 (in German).

FAZEKAS, I.G.  (1954a)  [Enlargement of the parathyroids by 
treatment with simple acidotic compounds.]  Kirchow's Arch. 
 Pathol. Anat. Physiol., 324: 531-542 (in German).

R.W.  (1956)  Cerebral metabolism in hepatic insufficiency. 
 Am. J. Med., 21: 843-849.

FEPCC  (1972)  [Investigation of air pollution in the city of 
Tsuruga.]  Annu. Rep. Fukui Environ. Pollut. Control Centre, 1: 
88-116 (in Japanese).

(1977)  Human physiological response and adaptation to 
ammonia.  J. occup. Med., 19: 319-326.

FETH, J.H.  (1966)  Nitrogen compounds in natural water. A 
review.  Water Resour. Res., 2: 41-58.

(1968)  Atmospheric contributions to water quality of streams 
in the Hubbard Brook Experimental Forest, New Hampshire.  Water 
 Resour. Res., 4: 1115-1126.

FLAKS, A. & CLAYSON, D.B.  (1975)  The influence of ammonium 
chloride on the induction of bladder tumors by 4-ethyl- 
sulfonylnaphthalene-1-sulfonamide.  Br. J. Cancer, 31: 585.

FLAKS, A., HAMILTON, J.M., & CLAYSON, D.B.  (1973)  Effect of 
ammonium chloride on incidence of bladder tumours induced by 
4-ethylsulfonylnapthalene-1-sulfonamide.  J. Natl Cancer Inst., 
51: 2007.

FLORKIN, M. & DUCHATEAU, G.  (1943)  Les formes du systme 
enzymatique de l'uricalyse et l'volution du catabolisme 
purique chez les animaux.  Arch. int. Physiol., 53: 267-307.

(1983)  Airway obstruction due to inhalation of ammonia.  Mayo 
 Clin. Proc., 58: 389-393.

FLYNN, R.J.  (1968)  A new cage cover as an aid to laboratory 
rodent disease control.  Proc. Soc. Exp. Biol. Med., 129: 

FORSTER, R.P. & GOLDSTEIN, L.  (1969)  Formation of excretory 
products. In: Hoar, W.S. & Randall, D.J. ed.  Fish Physiology, 
New York, Academic Press, Vol. 1, pp. 313-350.

Studies in protein metabolism. V. The utilization of ammonia 
for amino acid and creatine formation in animals.  J. biol. 
 Chem., 127: 319-327.

FRANK, J.F.  (1948)  The toxicity of sodium chlorate 
herbicides.  Can. J. comp. Med., 12: 216-218.

HINES, J.A.  (1966)  Glycolytic metabolites and their 
distribution at death in the white and red muscle of cod 
following various degrees of antemortem muscular activity. 
 Can. J. Biochem., 44: 1015-1033.

FREEDMAN, L.R. & BEESON, P.B.  (1961)  Experimental 
pyelonephritis. VIII. The effect of acidifying agents on 
susceptibility to infection.  Yale J. Biol. Med., 33: 318.

FRIZZOLA, J.A. & BAIER, J.H.  (1975)  Contaminants in 
rainwater and their relation to water quality.  Water Sewage 
 Works, 122: 94-95.

FROMM, P.O.  (1963)  Studies on renal and extra-renal 
excretion in a freshwater teleost,  Salmo gairdneri. Comp. 
 Biochem. Physiol., 10: 121-128.

FROMM, P.O.  (1970)  Effect of ammonia on trout and goldfish. 
In:  Toxic action of water soluble pollutants on freshwater 
 fish, Washington DC, US Environmental Protection Agency, 
pp. 9-22 (EPA Water Pollution Control Research Series No. 18050 
DST 12/70).

FROMM, P.O. & GILLETTE, J.R.  (1968)  Effect of ambient 
ammonia on blood ammonia and nitrogen excretion of rainbow 
trout  (Salmo gairdneri). Comp. Biochem. Physiol., 26: 887-896.

FUHRER, J.  (1985)  Formation of secondary airpollutants and 
their occurrence in Europe.  Experientia (Basel), 41: 286-301.

Nitrogen balance after intravenous and oral administration of 
ammonium salts to man.  J. appl. Physiol., 26(1): 13-22.

Distribution in muscle and liver vein protein of 15N 
administered as ammonium acidosis to man.  J. appl. Physiol., 
29(3): 307-312.

GALL, W.K.  (1980)   Effect of cow faeces on the ecology of 
 laboratory streams, Madison, Wisconsin, University of 
Wisconsin, pp. 73-83 (M.S. Thesis).

GAY, W.M.B., CRANE, C.W., & STONE, W.D.  (1969)  The 
metabolism of ammonia in liver disease: a comparison of 
urinary data following oral and intravenous loading of [15N] 
ammonium lactate.  Clin. Sci., 37: 815-823.

GEORGII, H.W.  (1963)  Oxides of nitrogen and ammonia in the 
atmosphere.  J. geophys. Res., 68: 963-970.

GEORGII, H.W. & MULLER, W.J.  (1974)  On the distribution of 
ammonia in the middle and lower trophosphere.  Tellus, 26: 

GIBBS, M. & CALO, N.  (1959)  Factors affecting light induced 
fixations of carbon dioxide by isolated spinach chloroplasts. 
 Plant Physiol., 34: 318-323.

GIBSON, G.E., ZIMBER, A., KROOK, L., & VISEK, W.J.  (1971)  
Nucleic acids and brain and intestinal lesions in ammonia 
intoxicated mice.  Fed. Proc., 30: 578.

GIGUZ, T.L.  (1968)  Effect of low concentrations of ammonia 
and nitrogen oxides on adolescents undergoing vocational 
training in the chemical industry.  Hyg. Sanit., 33(7-9): 

GILLETTE, L.A., MILLER, D.L., & REDMAN, H.E.  (1952)  
Appraisal of a chemical waste problem by fish toxicity tests. 
 Sewage ind. Wastes, 24(11): 1397-1401.

GILLIAM, J.W., DANIELS, R.B., & LUTZ, J.F.  (1974)  Nitrogen 
content of shallow ground water in North Carolina Coastal 
Plain.  J. environ. Qual., 3: 147-151.

GIRARD, J.O. & PAYAN, P.  (1980)  Ion exchanges through 
respiratory and chloride cells in freshwater and seawater 
adapted teleosteans.  Am. J. Physiol., 238: R260-R268 
(Regulatory Integrative Comp. Physiol. 7).

GOLDHABER, M.B. & KAPLAN, I.R.  (1974)  The sulfur cycle. In: 
Goldberg, D., ed.  The sea: ideas and observations on progress 
 in the study of the seas, New York, John Wiley and Sons, 
Vol. 5, pp. 569-655.

GOLDMAN, A.S. & YAKOVAC, W.C.  (1964)  Salicylate 
intoxication and congenital anomalies.  Arch. environ. 
 Health, 8: 648-656.

Ammonia excretion by the gills of two marine teleost fish: the 
importance of NH4+ permeance.  J. exp. Zool., 219: 395-397.
GOLDSTEIN, L. & FORSTER, R.P.  (1961)  Source of ammonia 
excreted by the gills of the marine teleost,  Myoxocephalus 
 scropius. Am. J. Physiol., 200(5): 1116-1118.

GOLYAKOVA, L.P.  (1971)  [Present-day state of industrial 
hygiene problems in hydrometallurgical production of tungsten 
and molybdenum salts and oxides.]  Gig. Tr. Prof. Zabol., 
15(2): 4-8 (in Russian with English summary).

GOODMAN, L.S. & GILMAN, A.  (1970)   The pharmacological basis 
 of therapeutics, 4th ed., New York, The Macmillan Company, 
1794 pp.

GORDON, R.J. & BRYAN, R.  (1973)  Ammonium nitrate in airborne 
particles in Los Angeles.  Environ. Sci. Technol., 7: 645-647.

GORDON, H.H., MCNAMARA, H., & BENJAMIN, H.R.  (1948)  Response 
of young infants to ingestion.  Pediatrics, 2: 290-302.

GRANT, W.M.  (1974)   Toxicology of the eye: drugs, chemicals, 
 plant venoms, 2nd ed., Springfield, Illinois, C.C. Thomas, 
pp. 96-101, 121-128.

OTEY, M.C.  (1956)  Studies on the metabolism of amino acids 
and related compounds  in vivo.  III. Prevention of ammonia 
toxicity by arginine and related compounds.  Arch. Biochem. 
 Biophys., 64: 342-354.

GREGORY, R.B.  (1977)  Synthesis and total excretion of waste 
nitrogen by fish of the  Periopthalmus (mudskipper) and 
 Scartelass families.  Comp. Biochem. Physiol., 51A: 33-36.

GRINDLEY, J.  (1946)  Toxicity to rainbow trout and minnows of 
some substances known to be present in waste water discharged 
to rivers.  Ann. appl. Biol., 33(1): 103-112.

GROLLMAN, A.  (1929)  The urine of the goosefish  (Lophius 
 piscatorius): its nitrogenous constituents with special 
reference to the presence in it of trimethylamine oxide. 
 J. Biol. Chem., 81: 267-278.

D.R., SMITH, J.P., & PITTS, J.N., Jr  (1976)  The 
concentration, size distribution, and modes of formation of 
particulate nitrate, sulfate, and ammonium compounds in the 
eastern part of the Los Angeles Basin. Presented at:  The 69th 
 Annual Meeting of the Air Pollution Control Association, 
 Portland, Oregon, June 27 - July 1 1976, 14 pp (Paper 76-20.3).

GROSSI, C.E., PRYTZ, B., & ROUSSELOT, L.M.  (1968)  Adenosine 
triphosphate in prevention of ammonia intoxication in dogs. 
 Surg. Forum, 19: 363-369.

GRUBE, H.J.  (1973)  [Load and loading capacity of submerged 
macrophytes in running water in southern Lower Saxony.] 
 Verh. Ges. Okol., Saarbrcken: 103-109 (in German with English 

GUERIN-ANCEY, O.  (1976a)  Etude experimentale de l'excretion 
azotee du bar  (Dicentrarchus labrax) en cours de croissance. 
II. Effets du jeune sur l'excretion d'ammoniac et d'uree. 
 Aquaculture, 9(2): 187-294.

GUERIN-ANCEY, O.  (1976b)  Etude experimentale de l'excretion 
azotee du bar  (Dicentrarchus labrax) en cours de croissance. 
III. Effets du volume et de la concentration initiale en 
ammoniac sur l'excretion d'ammoniac et d'uree.  Aquaculture, 
9(2): 253-258.

GUPTA, B.N., KHANNA, R.N., & DATTA, K.K.  (1979)  Toxicological 
studies of ammonium sulfamate in rat after repeated oral 
administration.  Toxicology, 13(1): 45-49.

GYORE, K. & OLAH, J.  (1980)  Ammonia tolerance of  Moina 
 rectirostris Leydig (Cladocera).  Aquaculture Hungarica 
 (Szarvas), 2: 50-54.

HAGGARD, H.W.  (1924)  Action of irritant gases upon the 
respiratory tract.  J. ind. Hyg., 5: 390-398.

HAHN, M., MASSEN, O., NENCKI, N., & PAWLOW, J.  (1983)  [The 
connection between the vena cava inferior and the portal vein 
and its consequences for the organism.]  Arch. Exp. Path. 
 Pharmakol., 32: 161-210 (in German).

HALL, L.W., Jr, BUIKEMA, A.L., Jr, & CAIRNS, J., Jr  (1978)  
The effects of a stimulated refinery effluent on the grass 
shrimp,  Palaemonetes pugio. Arch. environ. Contam. Toxicol., 
7(1) 23-35.

HANTZSCH, S. & LAHMANN, E.  (1970)  [Ammonia determinations in 
city air.]  Schriftner. Ver. Wasser- Boden- Lufthyg. (Berlin- 
 Dahlem), 33: 35-39 (in German).

HARADER, R.R. & ALLEN, G.H.  (1983)  Ammonia toxicity to 
chinook salmon parr: reduction in saline water.  Trans Am. 
 Fish. Soc., 112: 834-837.

HARDING, A.J.  (1959)   Ammonia manufacture and uses, London, 
Oxford University Press.

HAYNES, R.J. & GOH, K.M.  (1977)  Evaluation of potting media 
for commercial nursery production of container grown plants. 
II. Effects of media, fertilizer nitrogen and nitrification 
inhibitor on yield and nitrogen uptake of  Callistephus 
 chinensis (L.) nees "Pink Princess".  N.Z. J. Agric. Res., 20: 

(1973)  The acute action of ammonia on rat brain metabolism  in 
 vivo. Biochem. J., 134: 1001-1008.

HAWKINS, D.B., DEMETER, M.J., & BARNETT, T.E.  (1980)  Caustic 
ingestion: Controversies in management. A review of 14 cases. 
 Laryngoscope, 90: 98-109.

HAZEL, C.R., THOMSEN, W., & MEITH, S.J.  (1971)  Sensitivity 
of striped bass and stickleback to ammonia in relation to 
temperature and salinity.  Calif. Fish Game, 57(3): 138-153.

HAZEL, R.H., BURKHEAD, C.E., & HUGGINS, D.G.  (1979)   The 
 development of water quality criteria for ammonia and total 
 residual chlorine for the protection of aquatic life in two 
 Johnson County, Kansas streams, Washington DC, Office of Water 
Research and Technology, US Department of the Interior, 146 pp.

HEALY, T.V.  (1974)  Ammonia and related pollutants at 
Harwell.  Atmos. Environ., 8: 81-83.

(1970)  Ammonia and ammonium sulfate in the troposphere over 
the United Kingdom.  J. geophys. Res., 75: 2317-2321.

HEIL, G.W. & DIEMONT, W.M.  (1983)  Raised nutrient levels 
change heathland into grassland.  Vegetatio, 53: 113-120.

HEISLER, N.  (1984)  Acid-base regulation in fishes. In: Hoar, 
W. & Randall, D.J., ed.  Fish physiology,  New York, Academic 
Press, Vol. 10A.

HELMERS, S., TOP, F.H., & KNAPP, L.W., Jr  (1971)  Ammonia 
injuries in agriculture.  J. Iowa Med. Soc., 61: 271-280.

HEMENS, J.  (1966)  The toxicity of ammonia solutions to the 
mosquito fish ( Gambusia affinis Baird & Girard).  J. Proc. 
 Inst. Sewage Purif., 65: 265-271.

HENIS, Y. & CHET, I.  (1967)  Mode of action of ammonia on 
 Sclerotium rolfsii. Phytopathology, 57: 425-427.

HERBERT, D.W.M.  (1956)  La toxicit d'un effluent d'eau 
d'gout.  Bull. Cent. belge Etude Doc. Eaux, 32: 115-120.

HERBERT, D.W.M.  (1962)  The toxicity of rainbow trout of 
spent still liquors from the distillation of coal.  Ann. appl. 
 Biol., 50(4): 755-777.

HERBERT, D.W.M. & SHURBEN, D.S.  (1965)  The susceptibility of 
salmonid fish to poisons under estuarine conditions. II. 
Ammonium chloride.  Int. J. Air Water Pollut., 9: 89-91.

HIDY, G.M.  (1974)   Characterization of aerosols in California 
 (ACHEX), Thousand Oaks, California, Rockwell International, 
Vol. 1-4 (Final Report prepared for California Air Resources 

HILLABY, B.A. & RANDALL, D.J.  (1979)  Acute ammonia toxicity 
and ammonia excretion in rainbow trout  (Salmo gairdneri). J. 
 Fish. Res. Board Can., 36(6): 621-629.

HINTZ, H.F., LOWE, J.E., CLIFFORD, A.J. ET AL.  (1970)  
Ammonia intoxication resulting from urea ingestion by ponies. 
 J. Am. Vet. Med. Assoc., 157: 963-966.

HOEFT, R.G., KENNEY, D.R., & WALSH, L.M.  (1972)  Nitrogen and 
sulfur in precipitation and sulfur dioxide in the atmosphere 
in Wisconsin.  J. environ. Qual., 1: 203-208.

HOGAN, J.P.  (1961)  The absorption of ammonia through the 
rumen of sheep.  Aust. J. biol. Sci., 14: 448-460.

HOLETON, G.F., NEUMANN, P., & HEISLER, N.  (1983)  Branchial 
ion exchange and acid-base regulation after strenous exercise 
in rainbow trout.  Resp. Physiol., 51: 303-318.

(1960)   Experiments with inorganic pollutants - ammonia. Toxic 
 effects of organic and inorganic pollutants on young salmon 
 and trout, State of Washington, Department of Fisheries, 
pp. 183-187 (Research Bulletin No. 5).

HOLT, G.J. & ARNOLD, C.R.  (1983)  Effects of ammonia and 
nitrite on growth and survival of red drum eggs and larvae. 
 Trans. Am. Fish. Soc., 112: 314-318.

HOLT, J.D. & MALCOLM, S.A.  (1979)  Evaluation of fish loading 
rates in regulatory static bioassays.  Tech. Rep. -Fish. Mar. 
 Serv. (Can.)., 862: 146-160.

HORNE, F.R. & MCINTOSH, S.  (1979)  Factors influencing 
distribution of mussels in the Blanco River of central Texas. 
 Nautilus, 94(4): 119-133.

HSIA, Y.E.  (1974)  Inherited hyperammonemic syndromes. 
 Gastroenterology, 67: 347-374.

HUNGER, W.  (1978)  [Dying off of old spruce trees in the 
vicinity of a pig fattening station.]  Beitrage 
 Forstwirtschaft, 4: 188-189 (in German).

HUNT, R.D.  (1977)  Measurement of partial pressure of ammonia 
in breath and arterial blood. Evidence for secretion of 
ammonia into expired gas by metabolism of monoamines in the 
lung.  Diss. Abstr. Int. Ser. B, 37: 3279.

ILO  (1970)  Permissible levels of toxic substances in the 
working environment. In:  Proceedings of the 6th Session of the 
 Joint ILO/WHO Committee on Occupational Health, Geneva, 4-10 
 June 1968, Geneva, International Labour Office, 405 pp.

 threshold evaluation study with ammonia, Industrial Bio-Test 
Laboratories, Inc. (Report to International Institute of 
Ammonia Refrigeration, Publication No. 663-03161).

(1981a)  Effect of pH and ammonium ions on mutagenic activity 
in cooked beef.  Cancer Lett., 12: 335.

JOHNSON, C.A.  (1981b)  A source of error in mutagen testing 
of foods.  Cancer Lett., 11: 225.

JACOBS, M.H.  (1940)  Some aspects of cell permeability to 
weak electrolytes.  Cold Spring Harbour Sym. Quant. Biol., 8: 

K.E.  (1957)  Clinical significance of the partial pressure of 
ammonia (pNH3) in patients with ammonium toxicity.  Clin. Res. 
 Proc., 5: 20 (Abstract).

JACQUEZ, J.A., POPPELL, J.W., & JELTSCH, R.  (1959)  Partial 
pressure of ammonia in aveolar air.  Science, 129: 269-270.

JAFFE, H.L., BODANSKY, A., & BLAIR, J.E.  (1932a)  Effects of 
parathormone (parathyroid preparation) and ammonium chloride 
on bones of rabbits.  J. exp. Med., 55: 695-701.

JAFFE, H.L., BODANSKY, A., & CHANDLER, J.P.  (1932b)  Ammonium 
chloride decalcification, as modified by calcium intake: the 
relation between generalized osteoporosis and osteitis 
fibrosa.  J. exp. Med., 56: 823-834.

JANICKI, R.H.  (1970)  Renal adaptation during chronic NH4Cl 
acidosis in the rat: no role for hyperplasia. Am. J. Physiol., 
219(3): 613-618.

JANSSEN, Th. W.  (1982)   [Intensive animal husbandry in 
 relation to space and environment,] Utrecht, The Netherlands, 
Dutch State Forest Service (in Dutch).

JOHANNING, G.L., MUHRER, M.E., & GADDY, J.H.  (1978)  
Nutritional evaluation of chlorinated-ammoniated corn stover. 
Paper presented at:  The Joint Meeting of the American Dairy 
 Science Association and the American Society of Animal 
 Science, 11 July 1978.

JOHNSON, J.D., EPEL, D., & PAUL, M.  (1976)  Intracellular pH 
and activation of sea urchin eggs after fertilization.  Nature 
 (Lond.), 262(5570): 661-664.

JONES, K.  (1973)  Ammonia. In: Bailar, J.C., Jr, Emeleus, 
H.J., Nyholm, R., & Trotman-Dickenson, A.F., ed.  Comprehensive 
 inorganic chemistry, New York, Pergammon Press, Vol. 2, pp. 

JONES, R.D. & HOOD, M.A.  (1980)  Effects of temperature, pH, 
salinity and inorganic nitrogen on the rate of ammonium 
oxidation by nitrifiers isolated from wetland environments. 
 Microb. Ecol., 6: 339-347.

JUDE, D.J.  (1973)   Sublethal effects of ammonia and cadmium 
 on growth of green sunfish, East Lansing, Michigan, Michigan 
State University, 193 pp (Ph.D. Thesis).

KADOWAKI, S.  (1976)  Size distribution of atmospheric total 
aerosols, sulfate, ammonium and nitrate particulates in the 
Nagoya area.  Atmos. Environ., 10: 39-43.

(1979)  Diammonium citrate addition to a diet restricted 
non-essential amino acids for young pigs.  Jap. J. vet. Sci., 
41: 131-138.

KAMIN, H. & HANDLER, P.  (1957)  Amino acid and protein 
metabolism.  Annu. Rev. Biochem., 26: 419-490.

& WATERS, I.W.  (1982)  Acute inhalation toxicity of ammonia 
in mice.  Bull. environ. Contam. Toxicol., 29: 371-378.

C.E.  (1976)  Teleost chloride cell. II. Autoradiographic 
localization of gill Na, K-ATPase in killifish  Fundulus 
 heterclitus adapted to low and high salinity environments. 
 J. cell Biol., 70: 157-177.

KATZ, M. & PIERRO, R.A.  (1967)   Estimates of the acute 
 toxicity of ammonia-urea plant wastes to coho salmon, 
Oncorhynchus kisutch, Seattle, Washington, Fisheries Research 
Institute, College of Fisheries, University of Washington, 
15 pp (Final report).

KEESEE, R.G., HOPF, S.B., & MOYERS, J.L.  (1975)  The 
distribution and characteristics of particulate sulfates in 
the southwest desert atmosphere. Presented at: The 
 International Conference on Environmental Sensing and 
 Assessment, Las Vegas, Nevada, 14-19 September, 1975, Vol. 2, 
5 pp (Paper 23-6).

KEMPINSKA, H.  (1968)  [The effect of ammonia fertilizers on 
fish.]  Gospod. Rybn., 20: 3-5 (in Russian).

J.C.  (1973)  Irritation threshold evaluation study with 
ammonia. In:  Report to the Institute of Ammonia Refrigeration, 
Northbrook, Illinois, Industrial Bio-Test Laboratories, Inc.

KERN, D.M.  (1960)  The hydration of carbon dioxide.  J. Chem. 
 Ed., 37: 14-23.

the mechanisms of sodium ion transport by the irrigated gills 
of rainbow.  J. gen. Physiol., 56: 342-359.

KEYES, W.F.  (1975)  Nitrogen. In:  Mineral facts and problems, 
Washington DC, US Department of the Interior, pp. 749-760 
(Bureau of Mines Bulletin No. 667).

KHOLDEBARIN, B. & OERTLI, J.J.  (1977)  Effect of pH and 
ammonia on the rate of nitrification of surface water. 
 J. Water Pollut. Control Fed., 49: 1693-1697.

Serum- and tissue-ammonia nitrogen and tissue-water values in 
ammonia-intoxicated sheep.  Am. J. Vet. Res., 33: 1187-1190.

Hemogram of sheep acutely intoxicated with ammonia. 
 Am. J. Vet. Res., 34: 587-589.

Effect of amiloride on sodium transport across body surfaces 
of freshwater animals.  Am. J. Physiol., 224: 832-837.

KLEMM, K.  (1967)  The effect of N source on the yield of 
various crop plants.  Bodenkultur, 18: 210-218.

KLENDSHOJ, N.C. & REJENT, T.A.  (1966)  Tissue levels of some 
poisoning agents less frequently encountered.  J. Forensic 
 Sci., 11: 75-80.

KLING, H.F. & QUARLES, C.L.  (1974)  Effect of atmospheric 
ammonia and the stress of infectious bronchitis vaccination on 
Leghorn males.  Poult. Sci., 53: 1161-1167.

KLUESENER, J.W. & LEE, G.F.  (1974)  Nutrient loading from a 
separate storm sewer in Madison, Wisconsin.  J. Water Pollut. 
 Control Fed., 46(5): 920-936.

KNEPP, G.L. & ARKIN, G.F.  (1973)  Ammonia toxicity levels and 
nitrate tolerance of channel catfish.  Prog. Fish-Cult., 35(4): 

KNOWLES, G., DOWNING, A.L., & BARRETT, M.J.  (1965)  
Determination of kinetic constants for nitrifying bacteria in 
mixed culture, with the aid of an electronic computer. 
 J. gen. Microbiol., 38: 263.

KOENIG, H. & KOENIG, R.  (1949)  Production of acute pulmonary 
edema by ammonium salts.  Proc. Soc. Exp. Biol. Med., 70: 

KOPP, A., FELLER, U., & ERISMANN, K.H.  (1974)  [Studies on 
the regulation of nitrogen assimilation by  Lemna minor in 
transition from ammonium to nitrate feeding or from nitrate to 
ammonium feeding under conditions of photosynthesis.] 
 Z. Pflanzen physiol., 73: 456-460 (in German).

KORMANIK, G.A. & CAMERON, J.N.  (1981)  Ammonia excretion in 
the FW catfish: the role of diffusion.  Am. Soc. Zool., 21(4): 

KORTING, W.  (1969a)  [The harmful effect of ammonia on fish.] 
 Munch. Beitr. Abwasser-. Fisch.-Flussbiol., 16: 38-48 (in 

KORTING, W.  (1969b)  [Investigations on the effects of 
ammonia on the blood of fish.]  Wasser Abwasser Forsch., 4: 
154-159 (in German).

KRYSTAL, G.W. & POCCIA, D.  (1979)  Control of chromosome 
condensation in the sea urchin egg.  Exp. cell Res., 123(2): 

W.  (1975)  Effect of protein level and synthesize chloride 
addition to diet on ammonia detoxification in rats.  Zentralbl. 
 Veterinaermed., 22(3): 215-223.

MCLAREN, E.H.  (1970)   Non-photochemical aerosol formation 
 from the anhydrous reaction between ammonia and sulfur dioxide 
 gases. Mechanism for the formation of ammonium sulfate in the 
 atmosphere, Albany, New York, Department of Chemistry and 
Atmospheric Sciences Research Center, State University of New 
York (Report 165 of National Air Pollution Control 
Administration Research Grant 5RO1A).

KUSTOV, V.V.  (1967)  [Means of determining the maximum 
allowable concentration of toxic products of natural human 
metabolism.] In:  General questions of industrial toxicology, 
Moscow, pp. 63-65. (National Aeronautics and Space 
Administration Technical Translation NASA TT F-11,358) (in 

LANDAHL, H.D. & HERRMANN, R.G.  (1950)  Retention of vapors 
and gases in the human nose and lung.  Arch. ind. Hyg. occup. 
 Med., 1: 36-45.

LANGOWSKA, I. & MOSKAL, J.  (1974)  Effect of ammonia and urea 
on nitrobacteria in water environment.  Pol. Arch. Hydrobiol., 
21(1): 119-123.

(1977)  Ammonia in the human airways: neutralization of 
inspired acid sulfate aerosols.  Science, 197: 161-163.

PARSONS, S.D.  (1977)  Hay preservation by anhydrous ammonia 
treatment. In:  Grain and Forage Harvesting. Proceedings of the 
 First International Grain and Forage Conference, St. Joseph, 
American Society of Agricultural Engineers, pp. 327-328, 338.

LEE, J.A.,  (1985)  Effects of NO2 on aquatic ecosystems.  In: 
 Study on the need of NO2  long term limit value for the 
 protection of terrestrial and aquatic ecosystems (Final Report 
Feb. 1985).

LEE, R.E., Jr & GORANSON, S.  (1976)  National air 
surveillance cascade impact network. III. Variations in size 
of airborne particulate matter over a three-year period. 
 Environ. Sci. Technol., 10: 1022-1027.

LEITHE, W.  (1971)   The analysis of air pollutants, Ann Arbor, 
Michigan, Ann Arbor Science Publishers.

LEONARDOS, G., KENDALL, D., & BARNARD, N.  (1969)  Odour 
threshold determination of 52 odorant chemicals.  J. Air 
 Pollut. Control Assoc., 19: 91-95.

LEUVEN, R.S.E.W. & SCHUURKES, J.A.A.R.  (1984)   [Effects of 
 acid precipitation containing sulfur and nitrogen on weakly 
 buffered waters low in nutrients] The Netherlands, Laboratory 
of Aquatic Ecology, University of Nymegen, and Ministry of 
Housing, Physical Planning and Environment, 131 pp (in Dutch).

LEVI, G., MORISI, G., COLETTI, A., & CATANZARO, R.  (1974)  
Free amino acids in fish brain: normal levels and changes upon 
exposure to high ammonia concentrations  in vivo, and upon 
incubation of brain slices.  Comp. Biochem. Physiol., 49A: 

(1964)  Ammonia burns of the face and respiratory tract. 
 J. Am. Med. Assoc., 190: 873-876.

LIEBHARDT, W.C., GOLT, C., & TUPIN, J.  (1979)  Nitrate and 
ammonium concentrations of ground water resulting from poultry 
manure applications.  J. environ. Qual., 8: 211-215.

LIECHTI, P.M. & HUGGINS, D.G.  (1980)  Effects of a 24-h 
ammonia injection on stream drift and benthic standing crop. 
 Trans. Kansas Acad. Sci., 83(3): 140.

LIETZKE, M.H.  (1978)  A kinetic model for predicting the 
composition of chlorinated water discharged from power plant 
cooling systems. In:  Water chlorination environmental impact 
 and health effects, Ann Arbor, Michigan, Ann Arbor Science 
Publishers, Inc., Vol. 2, pp. 707-716.

LILLIE, R.J.  (1970)  Ammonia. In:  Air pollutants affecting 
 the performance of domestic animals. A literature review, 
Washington DC (Agriculture Handbook No 380).

(1979)  The acute toxicity of 78 chemicals and pesticide 
formulations against two brackish water organisms, the bleak 
 (Alburnus alburnus) and the harpacticoid  (Nitocra spinipes). 
 Chemosphere, 11(12): 843-851.

LINZON, S.N.  (1971)  Effects of air pollutants on vegetation. 
In: McCormac, B.M., ed.  Introduction to the scientific study 
 of atmospheric pollution, Dordrecht, Holland, D. Reidel 
Publishing Company, pp. 131-151.

LITAV, M. & AGAMI, M.  (1976)  Relationship between water 
pollution and the flora of two coastal rivers of Israel. 
 Aquat. Biol., 2(1): 23-41.

LITAV, M. & LEHRER, Y.  (1978)  The effects of ammonium in 
water on  Potamageton lucens. Aquat. Biol., 5(2): 127-138.

LITTON BIONETICS, INC.  (1975)   Mutagenic evaluation of 
 compound FDA 73-42 ammonium sulfate, granular, food grade, 
Washington DC, Litton Bionetics (Prepared for US Food and Drug 
Administration) (NTIS PB-245 506).

LLOYD, R.  (1961)  Effect of dissolved oxygen concentrations 
on the toxicity of several poisons to rainbow trout ( Salmo 
 gairdnerii Richardson).  J. exp. Biol., 38: 447-455.

LLOYD, R. & HERBERT, D.W.M.  (1960)  The influence of carbon 
dioxide on the toxicity of un-ionized ammonia to rainbow trout 
( Salmo gairdnerii Richardson).  Ann. appl. Biol., 48(2): 

LLOYD, R. & ORR, L.D.  (1969)  The diuretic response by 
rainbow trout to sub-lethal concentrations of ammonia.  Water 
 Res., 3(5): 335-344.

LOBASHOV, M.E.  (1937)  [Nature of the effects of chemical 
agents on the mutation process of  Drosphila melanogaster.] 
 Genetica, 19: 200-241 (in German).

LOBASHOV, M.E. & SMIRNOV, F.A.  (1934)  [Effect of acetic acid 
on nondisjunction and mutations in  Drosphila melanogaster.] 
 Dokl. Acad. Sci. USSR N.S., 2: 307 (in Russian with German 

WARTBURG, A.F.  (1974)  Atmospheric trace chemistry in the 
American humid tropics.  Tellus, 26: 250-253.

LOEHR, R.C.  (1974)  Characteristics and comparative magnitude 
of non-point sources.  J. Water Pollut. Control Fed., 46(8): 

LOSADA, M. & ARNON, D.I.  (1963)  Selective inhibitors of 
photosynthesis. In: Hochester, R. & Quastel, J.H., ed. 
 Metabolic inhibitors, New York, Academic Press, Vol. 2, p. 559.

(1973)  Mechanism of nitrate reductase reversible inactivation 
by ammonia in  Chlamydomonas. Plant Sci. Lett., 1: 31-37.

LOTSPEICH, W.D.  (1965)  Renal hypertrophy in metabolic 
acidosis and its relation to ammonia excretion. 
 Am. J. Physiol., 208(6): 1135-1142.

LUBINSKI, K.S.  (1979)   Monitoring bluegill swimming behaviour 
 and the effects of sublethal ammonium chloride gradients, 
Blacksburg, Virginia, Virginia Polytechnic Institute and State 
University, 99 pp (Ph.D. Thesis).

LUBINSKI, K.S., SPARKS, R.E., & JAHN, L.A.  (1974)   The 
 development of toxicity indices for assessing the quality of 
 the Illinois River, Urbana, Illinois, Water Resources Center, 
University of Illinois, 46 pp (Research Report No. 96).

LUBINSKI, K.S., DICKSON, K.L., & CAIRNS, J., Jr  (1980)  
Effects of abrupt sublethal gradients of ammonium chloride on 
the activity level, turning, and preference-avoidance 
behaviour of bluegills, In: Eaton, J.G., Parrish, P.R., & 
Hendricks, A.C. ed.  Aquatic toxicology, Philadelphia, 
Pennsylvania, American Society for Testing and Materials, 
pp. 328-340 (ASTM STP 707).

MACEWEN, J.D. & VERNOT, E.H.  (1972)   Toxic hazards research 
 unit annual technical report (NTIS AD 755-358).

MACEWEN, J.D., THEODORE, J., & VERNOT, E.H.  (1970)  Human 
exposure to EEL concentrations of monomethylhydrazine. In: 
 Proceedings of the 1st Annual Conference on Environmental 
 Toxicology, Ohio, Wright-Patterson Air Force Base, 
 9-11 September, 1970, Aerospace Medical Research Laboratory, 
pp. 355-363 (AMRL-TR-70-102, Paper No. 23).

MCBARRON, E.J. & MCINNES, P.  (1968)  Observations on urea 
toxicity in sheep.  Aust. Vet. J., 44: 90-96.

MCBEAN, R.L., NEPPEL, M.J., & GOLDSTEIN, L.  (1966)  
Glutaminate dehydrogenase and ammonia production in the eel 
 (Anguilla rostrata). Comp. Biochem. Physiol., 18: 909-920.

MCBRIDE, R.L. & LAING, D.G.  (1979)  Threshold determination 
by triangle testing: Effects of judgmental procedure, 
positional bias and incidental training.  Chem. Senses Flavor., 
4(4): 319-328.

MCCALLAN, S.E.A. & SETTERSTROM, C.  (1940)  Toxicity of 
ammonia, chlorine, hydrogen cyanide, hydrogen sulphide, and 
sulphur dioxide gases. I. General methods and correlations. 
 Contrib. Boyce Thompson Inst., 11: 325-330.

MCCAY, C.M. & VARS, H.M.  (1931)  Studies upon fish blood and 
its relation to water pollution. In:  A biological survey of 
 the St. Lawrence Watershed. Supplement to the 20th Annual 
 Report, 1930, Albany, New York, New York Conservation 
Department, pp. 230-233 (Biol. Survey (1930), No. V).

Toxicity of ammonia to early life stages of the green sunfish 
 Lepomis cyanellus. Environ. Pollut. Ser. A., 36: 147-163. 
 Erratum: Environ. Pollut. Ser. A. (in press).

MCDONALD, D.G. & WOOD, C.M.  (1981)  Branchial and renal acid 
and ion fluxes in the rainbow trout at low environmental pH. 
 J. exp. Biol., 93: 101-118.

MCKAY, H.A.C.  (1969)  Ammonia and air pollution.  Chem. Ind., 
34: 1162-1165.

MCKHANN, G.M. & TOWER, D.B.  (1961)  Ammonia toxicity in 
cerebral oxidative metabolism.  Am. J. Physiol., 200: 420-424.

MAETZ, J.  (1972)  Branchial sodium exchange and ammonia 
excretion in the goldfish  Carassius auratus. Effects of 
ammonia-loading and temperature changes.  J. exp. Biol., 56: 

MAETZ, J.  (1973)  Na+/NH4+, Na+/H+ exchanges and NH3 movement 
across the gill of  Carassius auratus. J. exp. Biol., 58: 

MAETZ, J. & GARCIA-ROMEU, F.  (1964)  The mechanism of sodium 
and chloride uptake by the gills of a freshwater fish, 
 Carassius auratus. II Evidence for NH4+/Na+ and HCO3-/Cl- 
exchanges.  J. gen. Physiol., 47: 1209-1227.

MAGALHAES BASTOS, J.A.  (1954)   [Importance of ammonia as an 
 ichthyotoxic substance,] Brazil, Serv. Piscicultura, Dept. 
nacl. obras contra secas, Ministerio viacao e obras publicas, 
pp. 115-132 (Publ. Ser. 1-C, No. 159) (in Portuguese).

MAI, K.L.  (1977)  Energy and petrochemical raw materials 
through 1990.  Chem. Eng., 84: 122-128.

MALACEA, I.  (1966)  [Contributions to knowledge of the 
cyanide, ammonia, mercury and arsenic toxic action on some 
species of fishes and on  Daphnia.] Stud. Prot. Epurarea Apelor 
 Inst. Stud. Cercet Hidrotehnice, 7(2: 751-792 (English 
summary)  Biol. Abstr., 50: 92715 (1969).

MALACEA, I.  (1968)  [Studies on the acclimatization of fish 
to high concentrations of toxic substances.]  Arch. Hydrobiol., 
65(1): 74-95 (in German with English summary).

MALLERY, C.H.  (1979)  Ammonium stimulated properties of a 
K+-dependent ATPase in  Opsanus beta, a marine teleost with an 
NH4+/Na+ exchange pump.  Am. Zool., 19: 944.

MANGOLD, C.A.  (1971)   Investigation of occupational exposure 
 to ammonia, Washington, Puget Sound Naval Shipyard, Industrial 
Hygiene Division of Investigation.

KRALL, A.R.  (1976)  The relationship between blood pH, 
ammonia excretion and adaptation to low salinity in the blue 
crab  Callinectes sapidus. J. exp. Zool., 195(1): 129-136.

(1978)  The excretion of NH4+ and its ouabain sensitivity in 
aquatic annelids and molluscs.  J. exp. Zool., 203: 151-157.

MARSCHANG, F.  (1972)  [The NH3 content of air in stables and 
the fattening capacity of cows.]  Dtsch. Tieraerztl. 
 Wochenschr., 79: 214-216 (in German).

MARSCHANG, F. & CRAINICEANU, E.  (1971)  [Investigations on 
the connections between cowshed climate and calf mortality.] 
 Berlin Mnchen Tieraerztl. Wochenschr., 84: 417-420 (in 

MARSCHANG, F. & PETRE, C.  (1971)  [The NH3 content of cowshed 
air and its influence on morbidity and animal lossess in 
cattle-fattening pens.]  Zentralbl. Veterinaermed., 18: 646-654 
(in German).

MATASA, C. & MATASA, E.  (1968)   L'industrie moderne des 
 produits azots, Paris, Dunod, pp. 63-208.

MATSUMOTO, H., OKAMURA, K., & TAKAHASHI, E.  (1976)  Changes 
in activity and isoenzymes of intervase in cucumber leaves due 
to nitrogen status.  Plant Cell Physiol., 17: 867-874.

MATUSIAK, K.  (1976)  Studies on the purification of 
wastewater from the nitrogen fertilizer industry by intensive 
algal cultures.  Acta microbiol. Pol., 25(3): 233-242.

MAYAN, M.H. & MERILAN, C.P.  (1972)  Effects of ammonia 
inhalation on respiratory rate of rabbits.  J. anim. Sci., 34: 

MAYNARD, D.N. & BARKER, A.V.  (1969)  Studies on the tolerance 
of the plants to ammonium nutrition.  J. Am. Soc. Hortic. Sci., 
94: 235-239.

MEARNS, A.J.  (1981)  Ecological effects on ocean sewage 
outfalls: observations and lessons.  Oceanus, 24: 45-54.

MERKENS, J.C. & DOWNING, K.M.  (1957)  The effect of tension 
of dissolved oxygen on the toxicity of un-ionized ammonia to 
several species of fish.  Ann. appl. Biol., 45(3): 521-527.

METCALF & EDDY, INC.  (1972)   Wastewater engineering, New 
York, McGraw-Hill.

MILES, F.D.  (1961)   Nitric acid manufacture and uses, London, 
Oxford University Press.

MILLER, T.J.  (1973)  Cleft palate formation: The effects of 
fasting and iodoacetic acid on mice.  Teratology, 7: 177-182.

E.S.  (1981)  Effect of domestic wastewater on trout in Dillon 
Reservoir, Colorado. Paper presented at:  The ASTM Symposium on 
 Aquatic Toxicology, St. Louis, Missouri, 13-14 October 1981, 
Philadelphia, Pennsylvania, American Society for Testing 

MINER, J.R. & HAZEN, T.E.  (1969)  Ammonia and amines: 
components of swine-building odour.  Trans. Am. Soc. Agric. 
 Eng., 12: 772-774.

MITCHELL, H.A.  (1963)  Ammonia tolerance of the California 
leaf-nosed bat.  J. Mammal, 44: 543-551.

MITCHELL, H.A.  (1964)  Investigations of the cave atmosphere 
of a Mexican bat colony.  J. Mammal, 45: 568-577.

MORII, H., NISHIKATA, K., & TAMURA, O.  (1978)  Nitrogen 
excretion of mudskipper fish  Periophthalmus cantonensis and 
 Boleophthalmus pectinirostris in water and on land.  Comp. 
 Biochem. Physiol., 60A(2): 189-193.

MORRIS, J.C.  (1967)  Kinetics of reactions between aqueous 
chlorine and nitrogenous compounds. In: Faust, S.D. & Hunter, 
J.V., ed.  Principles and applications of water chemistry,  
New York, John Wiley and Sons, pp. 23-53.

MORRIS, J.C.  (1978)  Chemistry of aqueous chlorine in 
relation to water chlorination. In: Jolley, R.L., ed.  Water 
 chlorination: Environmental impact and health effects,  
Ann Arbor, Michigan, Ann Arbor Science Publishers, Vol. 1, 
pp. 21-36.

MORRIS, J.C. & ROGERS, Q.R.  (1978)  Ammonia intoxication in 
near-adult cat as a result of a dietary deficiency of 
arginine.  Science, 199(4327): 431-432.

MOSIER, A.R.  (1978)  Inhibition of photosynthesis and 
nitrogen fixation in algae by volatile nitrogen bases. 
 J. environ. Qual., 7(2): 237-240.

MOSSBERG, S.M.  (1967)  Ammonia absorption in hamster iluem. 
Effect of pH and total CO2 on transport in everted sacs. 
 Am. J. Physiol., 213: 1327-1330.

MOSSBERG, S.M. & ROSS, G.  (1967)  Ammonia movement in the 
small intestine: Preferential transport by the ileum.  J. clin. 
 Invest., 46: 490-498.

MOTYL, T. & DEBSKI, B.  (1977)  The influence of increasing 
amounts of NH4Cl in the diet on ammonia detoxification in 
rats.  Zbl. Vet. Med., 24: 333-342.

MULDER, J.S. & VAN DER ZALM, H.O.  (1967)  [A fatal case of 
ammonia poisoning.]  Tijdschr. Soc. Geneeskd., 45: 458-460 (in 

MULLER, G. & GRUHN, M.  (1969)  [The effect of water-free 
ammonia fertilizer on soil microorganisms.]  Zentralbl. 
 Bakteriol. Parasitenkd. Infektionskr. Hyg. Abt. 2 Naturw., 
123: 667-676 (in German with English summary).

MUNTWYLER, E., IACOBELLIS, M., & GRIFFIN, G.E.  (1956)  Kidney 
glutaminase and carbonic anhydrase activities and renal 
electrolyte excretion in rats.  Am. J. Physiol., 184: 83-90.

NAKAZAWA, S. & QUASTEL, J.H.  (1968)  Inhibitory effects on 
ammonium ions and some amino acids on stimulated brain 
respiration and cerebral amino acid transport.  Can. J. 
 Biochem., 46: 543-548.

NATARAJAN, K.V.  (1970)  Toxicity of ammonia to marine 
diatoms.  J. Water Pollut. Control Fed., 42(5, part 2): 

NAVAZIO, F., GERRITSEN, T., & WRIGHT, G.J.  (1961)  
Relationship of ammonia intoxication to convulsions and coma 
in rats.  J. Neurochem., 8: 146-151.

NEHRING, D.  (1963)  [The toxic effect of urea solutions 
containing urease on various fish species.]  Z. Fischerei, 
11(7/8): 539-547 (in German).

NEUFELD, R.D., HILL, A.J., & ADEKOYA, D.O.  (1980)  Phenol and 
free ammonia inhibition to Nitrosomonas activity.  Water Res., 
14(12): 1695-1703.

NIDEN, A.H.  (1968)  Effects of ammonia inhalation of the 
terminal airways. In:  Proceedings of the 11th Aspen Emphysema 
 Conference,  Vol. 11, pp. 41-44.

NIHLGARD, B.  (1970)  Precipitation, its chemical composition 
and effects on soil water and beech and spruce forests in 
South-Sweden.  Oikos., 21: 208

NIHLGARD, B.  (1985)  The ammonium hypothesis: an additional 
explanation to the forest dieback in Europe.  Ambio, 14(1): 1-8.

NISHIOKA, D.J.  (1976)   The initiation of cell cycle events in 
 ammonia-treated eggs and merogons of the sea urchin, Berkeley, 
California, University of California, 107 pp (Ph.D. Thesis).

NODA, K. & CHIKAMORI, K.  (1976)  Effect of ammonia via 
prepyriform cortex on regulation of food intake in the rat. 
 Am. J. Physiol., 231: 1263-1266.

NRC  (1979)   Ammonia. Subcommittee on Ammonia. Committee on 
 Medical and Biologic Effects of Environmental Pollutants. 
 Division of Medical Sciences, Assembly of Life Sciences, 
 National Research Council, Baltimore, Maryland, University 
Park Press (NTIS No. PB 278-027).

OKITA, T. & KANAMORI, S.  (1971)  Determination of trace 
concentration of ammonia in the atmosphere using 
pyridine-pyrazolone reagent.  Atmos. Environ., 5: 621-627.

OVERREIN, L.N., SEIP, H.M., & TOLLAN, A., ed.  (1980)   Acid 
 precipitation: effects on forest and fish, Oslo (Final report 
SNSF Project 1972-80).

PAIK, W.K., LAWSON, D., & KIM, S.  (1975)  Effect of endocrine 
glands on the protection of rat from ammonia intoxication. 
 Life Sci., 15: 1189-1196.

(1979)  An evaluation of the acute toxicity to aquatic biota 
of a coal conversion effluent and its major components. 
 Bull. environ. Contam. Toxicol., 23: 349-356.

(1981)  A re-evaluation of the toxicity of coal conversion 
process waters.  Bull. environ. Contam. Toxicol., 26: 9-15.

PAUL, M., JOHNSON, J.D., & EPEL, D.  (1976)  Fertilization 
acid of sea urchin eggs is not a consequence of cortical 
granule exocytosis.  J. exp. Zool., 197(1): 127-133.

PAUL, M. & JOHNSTON, R.N.  (1978)  Absence of a Ca response 
following ammonia activation of sea urchin eggs.  Dev. Biol., 
67(2): 330-335.

PAYAN, P.  (1978)  A study of the Na+/NH4+ exchange across the 
gill of the perfused head of the trout  (Salmo gairdneri). J. 
 comp. Physiol., 124: 181-188.

PAYAN, P. & MAETZ, J.  (1973)  Branchial sodium transport 
mechanisms in  Scyliorhinis canicula:  evidence for Na+/NH4+ 
and Na+/H+ exchanges and for a role of carbonic anhydrase. 
 J. exp. Biol., 58: 487-502.

PAYAN, P. & MATTY, A.J.  (1975)  The characteristics of 
ammonia excretion by a perfused isolated head of trout 
 (Salmo gairdneri): effect of temperature and CO2-free ringer. 
 J. comp. Physiol., 96: 167-184.

PAYAN, P., MATTY, A.J., & MAETZ, J.  (1975)  A study of the 
sodium pump in the perfused head preparation of the trout, 
 Salmo gairdneri in freshwater.  J. comp. Physiol., 104: 33-48.

(1978)  High moisture corn: an extended preservation trial 
with ammonia.  Trans. Am. Soc. Agricul. Eng., 21: 773-776, 781.

PEQUIN, L. & SERFATY, A.  (1963)  L'excrtion ammoniacale chez 
un tlosten dulcicole  Cyprinus carpio. J. comp. Biochem. 
 Physiol., 10: 315-324.

PERRY, J.H., CHILTON, C.H., & KIRKPATRICK, S.D., ed.  (1963)  
 Chemical engineers' handbook, 4th ed., New York, McGraw-Hill, 
pp. 3-151.

PHILLIPS, A.M.  (1950)   The effect of metabolic products on 
 brook trout, Cortland, New York, New York State Conservation 
Department, pp. 14-16 (Fisheries Research Bulletin 14) 
(Cortland Hatcherry Report 19).

PHILLIPS, R.W.  (1970)  Further clinical studies of 
trimethylpuringyl ammonium chloride (NSA-51095) in malignant 
disease with special emphasis on cancer of urinary bladder. 
 Cancer Chemother. Rep., 54: 181.

PIERPONT, R.A. & MINOTTI, P.L.  (1977)  Effects of calcium 
carbonate on ammonium assimilation by tomato seedlings. 
 J. Am. Soc. Hortic. Sci., 102: 20-23.

PINTER, I.J. & PROVASOLI, L.  (1963)  Nutritional characteristics 
of some chrysomonads. In: Oppenheimer, C.M., ed.  Symposium on 
 Marine Microbiology,  Springfield, Massachusetts, Thomas 
Publishers, pp. 114-121.

PITTS, R.F.  (1971)  The role of ammonia production and 
excretion in regulation of acid-base balance.  New Engl. J. 
 Med., 284: 32-38.

PITTS, J.N., Jr & GROSJEAN, D.  (1976)   Detailed 
 characterization of gaseous and size-resolved particulate 
 pollutants at a south coast air basin smog receptor site: 
 levels and modes of formation of sulfate, nitrate and organic 
 particulates and their implications for control strategies, 
Riverside, California, Statewide Air Pollution Research 
Center, University of California (California Air Resources 
Board Contract 5-384, Six Month Progress Report, November 17, 
1975 to May 16, 1976).

POLIAK, V.E.  (1981)  [Air pollution by ammonia around swine- 
breeding complexes.]  Gig. i. Sanit., 6: 67 (in Russian).

POST, R.L. & JOLLY, P.C.  (1957)  The linkage of sodium, 
potassium and ammonium active transport across the human 
erythrocyte membrane.  Biochem. Biophys. Acta, 25: 118-128.

POWERS, E.B.  (1920)  Influence of temperature and concentration 
on the toxicity of salts to fishes.  Ecology, 1: 95-112.

POWERS, W.L., TERRY, R.V., & MURPHY, L.S.  (1977)  Fate of 
nitrogen from manure disposal. In:  Proceedings of the National 
 Conference on Disposal of Residues on Land, pp. 156-160.

PROPKOPIEVA, A.S. & YUSHKOV, G.G.  (1975)  [Toxicology of 
ammonia in animals repeatedly exposed for short lengths of 
time.]  Gig. Tr. Prof. Zabol., 9: 54-55 (in Russian).

[Materials for a toxicological characteristic of the one-term 
effect of ammonia on the organisms of animals after brief 
exposure.]  Gig. Tr. Prof. Zabol., 6: 56-57 (in Russian).

PROVASOLI, L. & MCLAUGHLIN, J.J.A.  (1963)  Limited 
heterotrophy of some photosynthetic dinoflagellates. In: 
Oppenheimer, C.M., ed.  Symposium on Marine Microbiology, 
Springfield, MA, Thomas Publishers, pp. 105-113.

PRZYTOCKA-JUSIAK, M.  (1976)  Growth and survival of  Chlorella 
 vulgaris in high concentrations of nitrogen.  Acta microbiol. 
 Pol., 25(3): 287-289.

MYCIELSKI, R.  (1977)  Properties of  Chlorella vulgaris strain 
adapted to high concentrations of ammonium nitrogen.  Acta 
 microbiol. Pol., 26(2): 185-197.

QUARLES, C.L. & KLING, H.F.  (1974)  Evaluation of ammonia and 
infectious bronchitis vaccination stress on broiler 
performance and carcass quality.   Poult. Sci., 53: 1592-1596.

RAJAGOPAL, R.  (1978)  Impact of land use on ground water 
quality in the Grand Traverse Bay region of Michigan. 
 J. environ. Qual., 7: 93-98.

RAMACHANDRAN, V. & RAMAPRABHU, T.  (1976)  Use of ammonia as 
herbicide: A Review. In: Varshney, C.K. & Rzoska, J., ed. 
Aquatic weeds in South East Asia, The Hague, B.V. Publishers, 
pp. 293-298.

Observations on the use of ammonia for the control of Pistia 
stratiotes Linn.  J. Int. Fish. Soc. India, 7: 124-130.

RAMSEY, G.B.  (1953)  Mechanical and chemical injuries. In: 
 The yearbook of agriculture 1953, Washington DC, US Department 
of Agriculture, Plant Diseases, pp. 835-837.

RANDALL, D.J.  (1970)  Gas exchange in fish. In: Hoar, W.S. & 
Randall, D.J., ed.  Fish physiology, New York, Academic Press, 
Vol. IV., pp. 253-292.

RANKIN, D.P.  (1979)  The influence of un-ionized ammonia on 
the long-term survival of sockeye salmon eggs.  Fish. Mar. 
 Serv. Tech. Rep., 912: 17.

RAO, T.S., RAO, M.S., & PRASAD, S.B.S.K.  (1975)  Median 
tolerance limits of some chemicals to the fresh water fish 
 "Cyprinus carpio". Indian J. environ. Health, 17(2): 140-146.

REDNER, B.D. & STICKNEY, R.R.  (1979)  Acclimatization to 
ammonia by  Tilapia aurea. Trans. Am. Fish Soc., 108(4): 

REICHENBACH-KLINKE, H.-H.  (1967)  [Investigations on the 
influence of the ammonia content on the fish organism.]  Arch. 
 Fischereiwiss., 17(2): 122-132. (in German).

REINBOLD, K.A. & PESCITELLI, S.M.  (1982a)   Effects of 
 exposure to ammonia on sensitive life stages of aquatic 
 organisms, Champaign, Illinois, Illinois Natural History 
Survey (Project Report: Contract No. 68-01-5832).

REINBOLD, K.A. & PESCITELLI, S.M.  (1982b)   Effects of cold 
 temperature on toxicity of ammonia to rainbow trout, blue 
 gills, and fathead minnows, Champaign, Illinois, Illinois 
Natural History Survey (Project Report: Contract No. 

REINBOLD, K.A. & PESCITELLI, S.M.  (1982c)   Acute toxicity of 
 ammonia to the white sucker, Champaign, Illinois, Illinois 
Natural History Survey, 11 pp (EPA Contract No. 2W-3946 NAEX).

REINBOLD, K.A. & PESCITELLI, S.M.  (1982d)   Acute toxicity of 
 ammonia to channel catfish, Champaign, Illinois, Illinois 
Natural History Survey, 11 pp (EPA Contract No. J 2482 NAEX).

REITER, R., SLADKOVIC, R., & POTZL, K.  (1976)  Chemical 
components of aerosol particles in the lower troposphere above 
central Europe measured under pure-air conditions.  Atmos. 
 Environ., 10: 841-853.

REMPEL, B.  (1975)  Use ammonia to stop corn deterioration. 
 Crops Soils, 27: 13-14.

REPP, W.W., HALE, W.H., CHENG, E.W., & BURROUGHS, W.  (1955)  
The influence of oral administration of non-protein nitrogen 
feeding compounds upon blood ammonia and urea levels in lambs. 
 J. anim. Sci., 14: 118-131.

RICE, S.D. & BAILEY, J.E.  (1980)  Survival, size, and 
emergence of pink salmon,  Oncorhynchus gorbuscha, alevins 
after short- and long-term exposures to ammonia.  Fish Bull., 
78(3): 641-648.

RICHARD, D., BOULEY, G., & BOUDENE, C.  (1978a)  Effets de 
l'inhalation continue d'ammoniac chez le rat et la souris. 
 Bull. eur. Physiopathol. resp., 14: 573-582.

RICHARD, D., JOUARY, J., & BOUDENE, C.  (1978b)  Toxicit 
aigu par voie arienne du gaz ammoniac chez le lapin. 
 C.R. Acad. X. Paris, 287(Srie D): 375-378.

RICHARDS, B.O. & FROMM, P.O.  (1970)  Sodium uptake by 
isolated perfused gills of rainbow trout  (Salmo gairdneri). 
 Comp. Biochem. Physiol., 33: 303-310.

& WRONG, O.  (1968)  Incorporation of orally administered 
ammonia into tissue proteins in man; the influence of diet and 
ureamia. In:  Nutrition and renal disease, Edinburgh, E. and S. 
Livingstone, pp. 93-98.

(1975)  The incorporation of ammonia nitrogen into albumin in 
man: The effects of diet, uremia and growth hormone. 
 Clin. Nephrol., 3(5): 172-179.

RINGER, R.K.  (1971)  Adaptation of poultry to confinement 
rearing systems.  J. anim. Sci., 3: 590-598.

& TYLER, J.M.  (1959)  Ammonia excretion by mammalian lung. 
 Science, 129: 270-271.

ROBINETTE, H.R.  (1976)  Effect of selected sublethal levels 
of ammonia on the growth of channel catfish  (Ictalurus 
 punctatus). Prog. Fish-Cult., 38(1): 26-29.

ROBINSON, E. & ROBBINS, R.C.  (1968)   Sources, abundance and 
 fate of gaseous atmospheric pollutants, Menlo Park, Stanford 
Research Institute, California, 123 pp (prepared for the 
American Petroleum Institute).

ROBINSON, E. & ROBBINS, R.C.  (1971)  Emissions, concentrations, 
and fate of gaseous atmospheric pollutants. In: Strauss, W., ed. 
 Air pollution control, New York, John Wiley and Sons, Part 2, 
pp. 1-93.

ROBINSON-WILSON, E.F. & SEIM, W.K.  (1975)  The lethal and 
sublethal effects of a zirconium process effluent on juvenile 
salmonids.  Water Resour. Bull., 11(5): 975-986.

ROELOFS, J.G.M., SCHUURKES, J.A.A.R., & SMITS, A.J.M.  (1984)  
Impact of acidification and eutrophication on macrophyte 
communities in soft waters in the Netherlands. II. Experimental 
studies.  Aquat. Bot., 18: 389-411.

ROELOFS, J.G.M.  (in press)  The effect of sulfur and nitrogen 
deposition on aquatic and terrestrial heathland vegetation. 
 Experientia (Basel).

J.  (1985)  The effect of airborne ammonium sulphate on  Pinus 
 nigra var maritima, in the Netherlands.  Plant Soil, 84: 45-56.

ROSAGE, T.F., SCHUTSKY, R.M., & RAPP, K.M.  (1979)  Toxicity 
of un-ionized ammonia to the spotfin shiner  (Notropis 
 spilopterus). Proc. Pa. Acad. Sci., 53: 39-42.

ROSEBOOM, D.P. & RICHEY, D.L.  (1977)   Acute toxicity of 
 residual chlorine and ammonia to some native Illinois fishes, 
Urbana, Illinois, Illinois State Water Survey, 42 pp (Report 
of Investigation 85).

ROSENFELD, M.  (1932)  Experimental modification of mitosis by 
ammonia.  Arch. exp. Zellforsch. Gewebezuecht., 14: 1.

RUBIN, A.J. & ELMARAGHY, M.A.  (1976)   Studies on the toxicity 
 of ammonia, nitrate, and their mixtures to the common guppy, 
Columbus, Ohio, Water Resources Center, Ohio State University, 
47 pp (Project No. A-033-OHIO).

RUBIN, A.J. & ELMARAGHY, G.A.  (1977)  Studies on the toxicity 
of ammonia, nitrate and their mixtures to guppy fry.  Water 
 Res., 11(10): 927-935.

SALVATORE, F., BOCCHINI, V., & CIMINO, F.  (1963)  Ammonia 
intoxication and its effects on brain and blood ammonia 
levels.  Biochem. Pharmacol., 12: 1-6.

SAIFUTDINOV, M.M.  (1966)  Maximum permissible concentration 
of ammonia in the atmosphere.  Hyg. Sanit., 176: 171-175.

SAMYLIN, A.F.  (1969)  [Effect of ammonium carbonate on early 
stages of development of salmon.]  Uchen. Zap. Leningr. Gos. 
 Pedagog. Inst. Im. A. I. Gertsena, 422: 47-62 (in Russian).

BOHNER, K.  (1983)  Localized and systemic effects of 
environmental ammonia in rats.  Lab. anim. Sci, 33(1): 40-45.

SCHENKER, S. & WARREN, K.S.  (1962)  Effect of temperature 
variation on toxicity and metabolism of ammonia in mice. 
 J. Lab. clin. Med., 60: 291-301.

SCHULZE-WIEHENBRAUCK, H.  (1976)  Effects of sublethal ammonia 
concentrations on metabolism in juvenile rainbow trout ( Salmo 
 gairdneri Richardson).  Ber. Dtsch. Wiss. Komm. Meeresforsch., 
24(4): 234-250.

SCHUMAN, G.E. & BURWELL, R.E.  (1974)  Precipitation nitrogen 
contribution relative to surface runoff discharges. 
 J. environ. Qual., 3: 366-369.

SCHUURKES, J.A.A.R.  (in press)  Ammonium sulfate deposition 
and its role in the acidification and nitrogen enrichment of 
poorly-buffered aquatic systems.  Experientia (Basel).

ROELOFS, J.G.M.  (1985)  Effects of acid and acidifying 
deposition on water composition and macrophyte composition of 
simulated poorly buffered aquatic systems. In:  Proceedings of 
 the Muskoka Conference, Toronto, Canada, September 1985.

SEEGAL, B.C.  (1927)  Chronic acidosis in rabbits and in dogs, 
with relation to kidney pathologic change.  Arch. intern. Med., 
39(4): 550-563.

SELESI, D. & VAMOS, R.  (1976)  [Factors affecting the lethal 
concentration of ammonia in fish ponds.]  Ichthyologia, 8(1): 
115-121 (in Serbocroation with English summary).

SERVANT, J. & DELAPART, M.  (1983)  Concentrations and origins 
of NO3- and NH4+ in oceanic air.  In:  CACGP Symposium on 
 Tropospheric Chemistry with Emphasis on Sulphur and Nitrogen 
 Cycles and the Chemistry of Clouds and Precipitation 
 (Abstracts), 28 August - 3 September 1983, Oxford, England, 
Oxford, New York, Sydney, Paris, Frankfurt, Pergamon Press, 
57 pp (Fifth International Congress of the Commission on 
Atmoshperic Chemistry and Global Pollution).

SHAW, J.  (1960)  The absorption of sodium ions by the cray- 
fish  Astacus pallipes Lereboullet. III. The effect of other 
cations in the external solution.  J. exp. Biol., 37(3): 

SHEN, S.S. & STEINHARDT, R.A.  (1978)  Direct measurement of 
intracellular pH during metabolic derepression of the sea 
urchin egg.  Nature (Lond.), 272(5650): 253-254.

SHERWOOD, T.K.  (1925)  Solubilities of sulfur dioxide and 
ammonia in water.  Ind. Eng. Chem., 17: 745-747.

SHILO, M. & SHILO, M.  (1953)  Conditions which determine the 
efficiency of ammonium sulphate in the control of  Prymnesium 
 parvum in fish breeding ponds.  Appl. Microbiol., 1: 330-333.

SHILO, M. & SHILO, M.  (1955)  Control of the phytoflagellate 
 Prymnesium parvum. Verh. Int. Ver. Limnol., 12: 233-240.

SHOLKOVITZ, E.  (1973)  Interstitial water chemistry of the 
Santa Barbara Basin sediments.  Geochim. Cosmochim. Acta, 37: 

SHUTTLEWORTH, T.J. & FREEMAN, R.F.  (1974)  Factors affecting 
the net fluxes of ions in the isolated perfused gills of 
freshwater  Anguilla dieffenbachii. J. comp. Physiol., 94: 

SIEGRIST, A.  (1920)  [Concentrated effect of alkali and acid 
on the eye.]  Z. Augenheilkd., 43: 176-194 (in German).

SILVER, S.D. & MCGRATH, F.P.  (1948)  A comparison of acute 
toxicities of ethylene amine and ammonia to mice.  J. ind. Hyg. 
 Toxicol., 30: 7-9.

Physiological response of man to ammonia in low 
concentrations.  J. ind. Hyg. Toxicol., 31: 74-78.

SINGER, R.H. & MCCARTY, R.T.  (1971)  Pathologic changes 
resulting from acute ammonium salt poisoning in sheep. 
 Am. J. Vet. Res., 32: 1239-1246.

SLOAN, C.H. & MORIE, G.P.  (1974)  Determination of ammonia in 
tobacco and tobacco smoke with the ammonia electrode.  Anal. 
 Chim. Acta, 69: 243-247.

SLOT, G.M.J.  (1938)  Ammonia gas burns: an account of six 
cases.  Lancet, 2: 1356-1357.

SMART, G.  (1976)  The effect of ammonia exposure on gill 
structure of the rainbow trout  (Salmo gairdneri). J. Fish 
 Biol., 8(6): 471-475.

SMITH, C.E.  (1972)  Effects of metabolic products on the 
quality of rainbow trout.  Am. Fishes US Trout News, 17(3): 
7-8, 21.

SMITH, C.E.  (1984)  Hyperplastic lesions of the primitive 
meninx of fathead minnows,  Pimephales promelas, induced by 
ammonia: species potential for carcinogen testing.  Natl Cancer 
 Inst. Monogr., 65: 119-125.

SMITH, C.E. & PIPER, R.G.  (1975)  Lesions associated with 
chronic exposure to ammonia. In: Ribelin, W.E. & Migaki, G., 
ed.  The pathology of fishes, Madison, Wisconsin, University of 
Wisconsin Press, pp. 497-514.

SMITH, L.W. & WHEELER, W.E.  (1979)  Nutritional and economic 
value of animal excreta.  J. anim. Sci., 48: 144.

SODERLUND, R. & SVENSSON, B.H.  (1976)  The global nitrogen 
cycle. In: Svensson, B.H. & Sderlund, R., ed.  Nitrogen, 
 phosphorus, and sulfur: global sources, Stockholm, pp. 23-76 
(SCOPE Report No. 7) (Ecology Bulletin No. 22).

SMETANKINA, O.Z.  (1978)  Tris (2-oxy-ethyl) ammonium salts of 
some synthetic phytohormones and their antitumor activity. 
 Khim Farm. 2h, 12: 74.

SOLOMONSON, L.P.  (1969)   Effects of ammonia and some of its 
 derivatives on photosynthesis in the blue-green alga, 
 Plectonema boryanum, Chicago, Illinois, University of Chicago, 
68 pp (Ph.D. Thesis).

SOUSA, R.J., MEADE, T.K., & FELBECK, G.T., Jr  (1977)  The 
exposure of ammonia to the photodissociated haemoglobin of the 
marine bloodworm,  Glycera dibranchiata. Comp. Biochem. 
 Physiol., 58A: 19-22.

SPARKS, R.E.  (1975)   The acute, lethal effects of ammonia on 
 channel catfish (Ictalurus punctatus), bluegills (Lepomis 
 macrochirus), and fathead minnows (Pimephales promelas), 
Chicago, Illinois, 15 pp (report to Illinois Institute for 
Environmental Quality, project No. 20.060).

SPARKS, R.E. & SANDUSKY, M.J.  (1981)   Identification of 
 factors responsible for decreased production of fish food 
 organisms in the Illinois and Mississippi Rivers, Havana, 
Illinois, River Research Laboratory, Illinois Natural History 
Survey, 63 pp (Project No. 3-291-R).

SPICER, C.W.  (1977)  The fate of nitrogen compounds in the 
atmosphere. In: Pitts, J.N., Jr, Metcalf, R.L., & Lloyd, A.C., 
ed.  Advances in environmental sciences and technology, New 
York, John Wiley and Sons, Vol. 7, pp. 163-261.

(1966)  [Study of the behaviour of some volatile toxic 
substances as an index of air pollution in the cith of 
Cagliari. Note III. Ammonia.]  Folia Med. (Naples), 49: 641-648 
(in Italian).

STAMMER, H.A.  (1953)  [The effect of hydrogen sulfide and 
ammonia on characteristic animal forms in the saprobiotic 
system.]  Vom Wasser, 20: 34-71 (in German).

STANLEY, R.A.  (1974)  Toxicity of heavy metals and salts to 
Eurasian watermilfoil  (Myriophylum spicatum). Arch. environ. 
 Contam. Toxicol., 2(4): 331-341.

STEINHARDT, R.A. & MAZIA, D.  (1973)  Development of 
K+-conductance and membrane potentials in unfertilized sea 
urchin eggs after exposure to NH4OH.  Nature (Lond.), 
241(5389): 400-401.

STEPHENS, E.R.  (1971)  Identification of odors from cattle 
feedlots.  Calif. Agric., 25: 10-11.

STEVENS, C., KENNAWAY, N.G., & FELLMAN, J.H.  (1975)  Ammonia 
intoxicaton: A hazard during rehabilitation of protein- 
deprived rats.  J. Nutr., i105: 1384-1390.

STEVENSON, T.J.  (1977)   The effects of ammonia, pH and 
 salinity on the white perch, Morone americana, Kingston, Rhode 
Island, University of Rhode Island, 154 pp (Ph.D. Thesis).

W.D.  (1967)  Nitrates and other water pollutants under fields 
and feedlots.  Environ. Sci. Technol., 1(9): 736-739.

STRUZEWSKI, E.J.  (1971)   Current status on control and 
 treatment of storm and combined sewer overflow, Edison Water 
Quality Laboratory (EPA Technology Transfer).

STUDIER, E.H.  (1966)  Studies on the mechanisms of ammonia 
tolerance of the guano bat.  J. exp. Zool., 163: 79-85.

STUDIER, E.H., BECK, L.R., & LINDBORG, R.G.  (1967)  Tolerance 
and initial metabolic response to ammonia intoxication in 
selected bats and rodents.  J. Mammal., 48: 564-572.

SUGIYAMA, K., YOSHIDA, M., & OYAMADA, M.  (1968)  [A case of 
chemical bronchiectasia induced by inhalation of ammonia gaz.] 
 Nippon Kyohbu Shikkan Gakkai Zasshi, 27: 797-803 (in Japanese).

SUKUMARAN, N. & KUTTY, M.N.  (1977)  Oxygen consumption and 
ammonia excretion in the catfish  Mystus armatus, with special 
reference to swimming speed and ambient oxygen.  Proc. Indian 
 Acad. Sci., 86B: 195-206.

SUMMERSKILL, W.H.J. & WOLPERT, E.  (1970)  Ammonia metabolism 
in the gut.  Am. J. clin. Nutr., 23: 633-639.

SUYAMA, M., KOIKE, J., & SUZUKI, K.  (1960)  Studies on the 
glycolysis and the formation of ammonia in the muscle and 
blood of elasmobranchs.  J. Tokyo Univ. Fish., 46: 51-60.

SWIGERT, J.P. & SPACIE, A.  (1983)   Survival and growth of 
 warmwater fishes exposed to ammonia under low flow conditions, 
Springfield, Virginia, National Technical Information Service 
(NTIS PB83-257535).

TABATA, K.  (1962)  [Toxicity of ammonia to aquatic animals 
with reference to the effect of pH and carbon dioxide.] 
 Hokoku, 34: 67-74 (in Japanese).

TAIGANIDES, E.P. & WHITE, R.K.  (1969)  The menace of noxious 
gases in animal units.  Trans. Am. Soc. Agric. Eng., 12: 

TAKAHASHI, H., WAKAI, K., & OHUCHI, K.  (1984)  [Experiences 
of chemical burns induced by ammonia gaz.]  Nippon Saigai 
 Igakkai Kaishi, 32: 741-749 (in Japanese).

TAPLIN, G.V., CHOPRA, S., YANDA, R., & ELAM, D.  (1976)  
Radionuclidic lung-imaging procedures in the assessment of 
injury due to ammonia inhalation.  Chest, 69: 5.

TAYLOR, A.W., EDWARDS, W.M., & SIMPSON, E.C.  (1971)  
Nutrients in streams draining woodland and farmland near 
Coshocton, Ohio.  Water Resour. Res., 7: 81-89.

TAYLOR, J.E.  (1973)  Water quality and bioassay study from 
Crawford National Fish Hatchery.  Trans. Nebr. Acad. Sci., 2: 

ENVIRONMENT  (1984)  Acidification in the Netherlands: effects 
and policies. In:  Proceedings of a Conference on Air Pollution 
 in Europe, Munich, 24-27 June, 1984, The Netherlands Ministry 
of Housing, Physical Planning and Environment, pp. 9.

THOMAS, W.H., HASTINGS, J., & FUJITA, M.  (1980)  Ammonium 
input to the sea via large sewage outfalls. Part 2. Effects of 
ammonium on growth and photosynthesis of southern California 
phytoplankton cultures.  Mar. environ. Res., 3(4): 291-296.

THOMPSON, R.Y. & HALLIBURTON, I.W.  (1966)  Effect of diet on 
the composition of the kidney.  Biochem. J., 99(3): 44.

THORNTON, N.C. & SETTERSTROM, C.  (1940)  Toxicity of ammonia, 
chlorine, hydrogen cyanide, hydrogen sulphide, and sulphur 
dioxide gases. III. Green plants.  Contrib. Boyce Thompson 
 Inst., 11: 343-356.

THURSTON, R.V.  (1981)   Acute toxicity of ammonia to the 
 pumpkinseed (Lepomis gibbosus), Duluth, Minnesota, US 
Environmental Protection Agency, Environmental Research 

THURSTON, R.V. & MEYN, E.L.  (1984)   Acute toxicity of ammonia 
 to five fish species from the northwest United States, 
Bozeman, Montana Fisheries Bioassay Laboratory, Montana State 
University, 13 pp (Technical Report Vol. 84, No. 4).

THURSTON, R.V. & RUSSO, R.C.  (1981)   Acute toxicity of 
 ammonia to golden trout (Salmo aguabonita) and mottled sculpin 
 (Cottus bairdi), Bozeman, Montana, Fisheries Bioassay 
Laboratory, Montana State University, 10 pp (Technical Report 
Vol. 81, No. 1).

THURSTON, R.V. & RUSSO, R.C.  (1983)  Acute toxicity of 
ammonia to rainbow trout.  Trans. Am. Fish. Soc., 112: 696-704.

THURSTON, R.V., RUSSO, R.C., & SMITH, C.E.  (1978)  Acute 
toxicity of ammonia and nitrite to cutthroat trout fry.  Trans. 
 Am. Fish. Soc., 107(2): 361-368.

Effect of fluctuating exposures on the acute toxicity of 
ammonia to rainbow trout  (Salmo gairdneri) and cutthroat trout 
 (S. clarki). Water Res., 15(7): 911-917.

(1981b)  Increased toxicity of ammonia to rainbow trout  (Salmo 
 gairdneri) resulting from reduced concentrations of dissolved 
oxygen.  Can. J. Fish. aquat. Sci., 38(8): 983-988.

THURSTON, R.V., RUSSO, R.C., & VINOGRADOV, G.A.  (1981c)  
Ammonia toxicity to fishes: Effect of pH on the toxicity of 
the un-ionized ammonia species.  Environ. Sci. Technol., 15(7): 

THURSTON, R.V., RUSSO, R.C., & PHILLIPS, G.R.  (1983)  Acute 
toxicity of ammonia to fathead minnows.  Trans. Am. Fish. Soc., 
112: 705-711.

THURSTON, R.V., LUEDTKE, R.J., & RUSSO, R.C.  (1984a)  
 Toxicity of ammonia to fresh-water insects of three families, 
Bozeman, Montana, Fisheries Bioassay Laboratory, Montana State 
University, 26 pp (Technical Report Vol. 84, No. 2).

E.L., CHAKOUMAKOS, C., WANG, K.C., & BROWN, C.J.D.  (1984b)  
Chronic toxicity of ammonia to rainbow trout.  Trans. Am. Fish. 
 Soc., 113(1): 56-73.

(submitted)  Chronic toxicity of ammonia to fathead minnows 
 (Pimephales promelas). Submitted to Trans. Am. Fish. Soc.

TMRI  (1971)  [Atmosphere division. On survey of air 
pollutants peculiar to factory-clustered area.]  Tokyo 
 Meteorol. Res. Inst. Environ. Prot., 2: 109-111 (Annual 
Report) (in Japanese).

(1980)  Effects of environmental pH and calcium on ammonia 
toxicity in channel catfish.  Trans. Am. Fish. Soc., 109(2): 

TOPPING, D.C. & VISEK, W.J.  (1976)  Nitrogen intake and 
tumourigenesis in rats injected with 1,2-dimethylhydrazine. 
 J. Nutr., 106: 1583.

TORDA, C.  (1953)  Ammonium ion content and electrical 
activity of the brain during the preconvulsive and convulsive 
phases induced by various convulsants.  J. Pharmacol. exp. 
 Ther., 107: 197-203.

TOTH, B.  (1972)  Hydrazine, methylhydrazine, and 
methylhydrazine sulfate carcinogenesis in Swiss mice. Failure 
of ammonium hydroxice to interfere in the development of 
tumors.  Int. J. Cancer, 9: 109.

TOWLE, D.W., PALMER, G.E., & HARRIS, J.L. III  (1976)  Role of 
gill Na+ + K+-dependent ATPase in acclimation of blue crabs 
 (Callinectes sapidus) to low salinity.  J. exp. Biol., 196: 

TOWLE, D.W. & TAYLOR, D.D.  (1976)  Effect of NH4+ and K+ on 
Na+-transport ATPase activity of blue crab gill  Am. Zool., 16: 

TRESHOW, M.  (1970)  Ammonia. In:  Environment and plant 
 response, New York, McGraw-Hill Book Company, pp. 362-363.

TURNBULL, H., DEMANN, J.G., & WESTON, R.F.  (1954)  Toxicity 
of various refinery materials to fresh water fish.  Ind. Eng. 
 Chem., 46(2): 324-333.

ULRICH, B.  (1983)  Soil acidity and its relation to acid 
deposition. In:  Effects of accumulation of air pollutants in 
 forest ecosystems, Ulrich and Pankrasth, The Netherlands, 
D. Reidel Publishing Company, pp. 127-146.

ULSHAFER, T.R.  (1958)  The measurement of changes in 
acetylcholine level (ACh) in rat brain following ammonium ion 
intoxication and its possible bearing on the problem of 
hepatic coma.  J. lab. clin. Med., 52: 718-723.

ULTSCH, G.R., JACKSON, D.C., & MOALLI, R.  (1981)  Metabolic 
oxygen conformity among lower vertebrates: the toadfish 
revisited.  J. comp. Physiol., 142: 439-443.

UNDERWRITERS LABORATORIES  (1933)   Report on the comparative 
 life, fire, and explosion hazards of common refrigerants. 
 Miscellaneous Hazard No. 2375, Chicago, Illinois, Underwriters 
Laboratories, pp. 26-28.

 pollution on fish; toxicity of mixutures of zinc, sulfate, and 
 ammonium chloride; toxicity of sewage effluents; the toxicity 
 of poisons under estuarine conditions, London, United Kingdom 
Ministry of Technology, pp. 76-83 (Water Pollution Research 

 pollution on fish, London, United Kingdom Ministry of 
Technology, pp. 56-65 (Water Pollution Research 1967).

US EPA  (1972)   Air quality data for 1968 from the National 
 Air Surveillance Networks and contributing state and local 
 networks, Research Triangle Park, North Carolina, US 
Environmental Protection Agency, Office of Air Programs, 231 
pp (Report No. APTD-0978).

US EPA  (1979a)   Ammonia study using STORET ambient monitoring 
 data, Washington DC, US Environmental Protection Agency, 
Monitoring and Data Support Division, Office of Water Planning 
and Standards.

US EPA  (1979b)   Methods for chemical analysis of water and 
 wastes, Cincinnati, Ohio, US Environmental Protection Agency, 
Environmental Monitoring and Support Laboratory (Report No. 
EPA 600/4-79-020).

US EPA  (1981)   Multimedia health assessment document on 
 ammonia, Cincinnati, Ohio, US Environmental Protection Agency, 
Environmental Criteria and Assessment Office (Report No. 

US EPA  (1985)   Ambient water quality criteria for ammonia - 
 1984, Duluth, Minnesota, US Environmental Protection Agency, 
Office of Research and Development.

US NIOSH  (1974)   Criteria for a recommended standard. 
 Occupational exposure to ammonia, Washington DC, National 
Institute for Occupational Safety and Health, pp. 74-136 (US 
DHEW Publication No. 246-699).

US NIOSH  (1977)   NIOSH manual of analytical methods. Part I. 
 NIOSH monitoring methods, Washington DC, National Institute 
for Occupational Safety and Health, Vol. 1, pp. 205.1-205.3 
(US DHEW Publication No. 77-157-A).

UZVOLGYI, E. & BOJAN, F.  (1980)  Possible  in vivo formation 
of a carcinogenic substance from diethyl pyrocarbonate and 
ammonia.  J. Cancer Res. clin. Oncol., 97: 205.

VALENTINE, H.  (1964)  A study of the effect of different 
ventilation rates on the ammonia concentrations in the 
atmosphere of broiler houses.  Br. Poult. Sci., 5: 149-159.

VAMOS, R.  (1963)  Ammonia poisoning in carp.  Acta. biol. 
 Szeged., 9(1-4): 291-297.

VAMOS, R. & TASNADI, R.  (1967)  Ammonia poisoning in carp. 3. 
The oxygen content as a factor influencing the toxic limit of 
ammonia.  Acta. biol. Szeged., 13(3-4): 99-105.

VAN AALST, R.M.  (1984)   [Atmospheric process and deposition,] 
Ministry of Agriculture and Fisheries, Ministry of Housing, 
Physical Planning and Environment, 76 pp (Report No. 84(2)) 
(in Dutch).

VAN BREEMEN, N. & JORDENS, E.R.  (1983)  Effects of 
atmospheric ammonium sulfate on calcareous and non-calcareous 
soils of woodlands in the Netherlands. In: Ulrich, B. & 
Panlerath, J., ed.  Effects of accumulation of air pollutants 
 in forest ecosystems, The Netherlands, Reidel Publishing 
Company, pp. 171-182.

(1980)  Toxicity of alkaline solutions.  Ann. emergency Med., 
9(3): 118-122.

VAN DER EERDEN, L.J.M.  (1982)  Toxicity of ammonia to plants. 
 Agric. Environ., 7: 223-235

R.M., FUTCHER, P.H., & MILLER, A.  (1943)  Glutamine as source 
material of urinary ammonia.   J. Biol. Chem., 150: 481-482.

VAUGHN, R.E. & SIMCO, B.A.  (1977)  Effects of ammonia on 
channel catfish,  Ictalurus punctatus. ASB Bull., 24(2): 92.

HARTWIG, E., & WILDE, P.  (1981)   Studies on toxicity of OTEC 
 plant components on marine animals from the Gulf of Mexico, 
Springfield, Virginia, National Technical Information Service 

VERBERK, M.M.  (1977)  Effects of ammonia in volunteers. 
 Int. Arch. occup. environ. Health, 39: 73 -81.

VIGLIANI, E.C. & ZURLO, N.  (1955)  [Experiences of the 
Clinica del Lavoro with their own maximal exposure limits for 
industrial chemicals.]  Arch. Gewerbepathol. Gewerbehyg., 13: 
528-534 (in German).

VINES, H.M. & WEDDING, R.T. (1960)  Some effects of ammonia on 
plant metabolism and a possible mechanism for ammonia 
toxicity.  Plant Physiol., 35: 820-825.

VINOKUROVA, M.K. & MAL'KOVA, V.B.  (1963)  [Toxicology of the 
selective herbicide ammonium sulfamate.]  Gig. Trud. Prof. 
 Zabol., 7(5): 56-57 (in Russian).

VISEK, W.J., KOLONDY, G.M., & GROSS, P.R.  (1972)  Ammonia 
effects in cultures of normal and transformed 3T3 cells. 
 J. cell Physiol., 80: 373.

VISEK, W.J., CLINTON, S.K., & TRUEX, C.R.  (1978)  Nutrition 
and experimental carcinogenesis.  Cornell Vet., 68: 3.

Utilization of ammonia nitrogen, administered by intragastric, 
intraperitoneal and subcutaneous roues: Effects of growth 
hormone.  Arch. Biochem. Biophys., 106: 475-482.

WALLEN, I.E., GREER, W.C., & LASATER, R.  (1957)  Toxicity to 
 Gambusia affinis of certain pure chemicals in turbid waters. 
 Sewage Ind. Wastes, 29(6): 695-711.

WALLINGFORD, G.W.  (1977)  Fate of nitrogen from fertilizer 
practices. In:  Disposal of residues on land,  Rockville, 
Maryland, Information Transfer, Inc., pp. 152-155.

WALSH, L.M.  (1977)  Updating the nitrogen cycle. In:  Disposal 
 of residues on land, Rockville, Maryland, Information 
Transfer, Inc., pp. 146-151.

WALTON, M.J. & COWEY, C.B.  (1977)  Aspects of ammoniogenesis 
in rainbow trout,  Salmo gairdneri. Comp. Biochem. Physiol., 
57B: 143-149.

WALUGA, D. & FLIS, J.  (1971)  [Changes in peripheral blood in 
carp ( Cyprinus carpio  L.) under the influence of ammonia 
solution.]  Rocz. Nauk Roln. Ser. H, 93(2): 87-94 (in Russian).

WARNCKE, D.D. & BARBER, S.A.  (1973)  Ammonium and nitrate 
uptake by corn ( Zea mays L.) as influenced by nitrogen 
concentration and NH4-/NO3-ratio.  Agric. J., 65: 950-953.

WARREN, K.S.  (1958)  The differential toxicity of ammonium 
salts.  J. clin. Invest., 37: 497-501.

WARREN, K.S. & NATHAN, D.G.  (1958)  The passage of ammonia 
across the blood, brain, barrier and its relation to blood pH. 
 J. clin. Invest., 37: 1724-1728.

WARREN, K.S. & SCHENKER, S.  (1964)  Effect of an inhibitor of 
glutamine synthesis (methionine sulfoximine) on ammonia 
toxicity and metabolism.  J. lab. clin. Med., 64: 442-449.

WARREN SPRING LABORATORY  (1982)   Acidity of rainfall in the 
 United Kingdom.

WATTS, R.L. & WATTS, D.C.  (1974)  Nitrogen metabolism in 
fishes. In:  Florkin, M. & Scheer, B.T. ed.  Chemical Zoology, 
New York, Academic Press, Vol. III, pp. 369-446.

WEAST, R.C., ed.  (1979)   CRC handbook on chemistry and 
 physics, 59th ed., Boca Raton, Florida, CRC Press Inc.

WEATHERBY, J.H.  (1952)  Chronic toxicity of ammonia fumes by 
inhalation.  Proc. Soc. Exp. Biol. Med., 81: 300-301.

WEBB, D.W., BARTLEY, E.E., & MEYER, R.M.  (1972)  A comparison 
of nitrogen metabolism and ammonia toxicity from ammonium 
acetate and urea in cattle.  J. anim. Sci., 35: 1263-1270.

WEBB, J.T. & BROWN, G.W., Jr  (1976)  Some properties and 
occurrence of glutamine synthetase in fish.  Comp. Biochem. 
 Physiol., 54B: 171-175.

WEDDING, R.T. & VINES, H.M.  (1959)  Inhibition of reduced 
diphosphopyridine nucleotide oxidation by ammonia.  Nature 
 (Lond.), 184: 1226-1227.

WEEKS, M.E.  (1968)   Discovery of the elements,  7th ed., 
Washington DC, Journal of Chemical Education, p. 197.

CUNNINGHAM, P.J.  (1970)  Diammonium citrate and diammonium 
phosphate as sources of dietary nitrogen for growing-finishing 
swine.  J. anim. Sci., 31: 327-332.

WHITE, A., HANDLER, P., & SMITH, E.L.  (1973)  Renal function 
and the composition of urine. In:  Principles of biochemistry, 
5th ed., New York, McGraw Hill Book Co., pp. 604-704 and 

WHO  (1966)   Specifications for the identity and purity of 
 food additives and their toxicological evaluation: some 
 antimicrobials, antioxidants, emulsifiers, stabilizers, flour- 
 treatment agents, acids, and bases. Ninth Report of the Expert 
 Committee, Geneva, World Health Organization (WHO Technical 
Report Series No. 339).

WHO  (1974a)   Toxicological evaluation of certain food 
 additives including anticaking agents, antimicrobials, 
 antioxidants, emulsifiers, and thickening agents, Geneva, 
World Health Organization (WHO Food Additives Series No. 5).

WHO  (1974b)   Toxicological evaluation of certain food 
 additives with a review of general principles and of 
 specification. 17th report of the Expert Committee, Geneva, 
World Health Organization (WHO Technical Report Series No. 

WHO  (1980)   Evaluation of certain food additives. 
 Twenty-third Report of the Expert Committee, Geneva, World 
Health Organization (WHO Technical Report Series No. 648).

WHO  (1982a)   Evaluation of certain food additives and 
 contaminants. Twenty-sixth Report of the Expert Committee, 
Geneva, World Health Organization (WHO Technical Report Series 
No. 683).

WHO  (1982b)   Toxicological evaluation of certain food 
 additives, Geneva, World Health Organization (WHO Food 
Additives Series No. 17).

WICKINS, J.F.  (1976)  The tolerance of warm-water prawns to 
recirculated water.  Aquaculture, 9(1): 19-37.

WILKIN, D.C. & FLEMAL, R.C.  (1980)  Feasibility of water 
quality improvement in three Illinois rivers.  J. Water Poll. 
Control Fed., 52(2): 293.

(1978)   Forage preservation by timed-slow release of NH3 (ASAE 
Paper No. 78-1523).

(1968a)  Toxicologic effects of ammonium carbamate and related 
compounds.  Am. J. vet. Res., 29: 987-906.

(1968b)  Comparative ammonia toxicity.  Comp. Biochem. 
 Physiol., 25: 295-301.

WILT, F.H. & MAZIA, D.  (1974)  The stimulation of cytoplasmic 
polyadenylyation in sea urchin eggs by ammonia.  Dev. Biol., 
37: 422-424.

ed.  (1976)   Merck Index, 9th ed., Rahway, New Jersey, Merck 
and Co. Inc., p. 69.

WINKLER, M.M. & GRAINGER, J.L.  (1978)  Mechanisms of action 
of NH4Cl and other weak bases in the activation of sea urchin 
eggs.  Nature (Lond.), 273(5663): 536-538.

WOKER, H. & WUHRMANN, K.  (1950)  [The sensitivity of 
different species of fish to ammonia, hydrocyanic acid and 
phenol.]  Rev. Suisse Zool., 57(3): 548-553 (in German).

WOLAVER, T.C.  (1972)   Distribution of natural and 
 anthropogenic elements and levels in precipitation across the 
 US: theory and quantitative models, Chapel Hill, North 
Carolina, University of North Carolina, 75 pp (Prepared for US 

WOOD, R.W.  (1979)  Behavioral evaluation of sensory 
irritation evoked by ammonia.  Toxicol. appl. Pharmacol., 50: 

WORCEL, A. & ERECINSKA, M.  (1962)  Mechanism of inhibitory 
action of ammonia on the respiration of rat liver 
mitochondria.  Biochim. Biophys. Acta, 65: 27-33.

WRIGHT, P.A. & WOOD, C.M.  (1985)  An analysis of branchial 
ammonia excretion in the freshwater rainbow trout: effects of 
environmental pH change and sodium uptake blockage. 
 J. exp. Biol., 114: 329-353.

WUHRMANN, K. & WOKER, H.  (1948)  [Contributions to the 
toxicology of fishes. II. Experimental investigations on 
ammonia and hydrocyanic acid poisoning.]  Schweiz. Z. Hydrol., 
11: 210-244 (in German).

WUHRMANN, K., ZEHENDER, F., & WOKER, H.  (1947)  [Biological 
significance for fisheries of ammonium-ion and ammonia content 
of flowing bodies of water.]  Vierteljahrsschr. Naturforsch. 
 Ges. Zurich, 92: 198-204 (in German).

YAHAGI, H., SUZUKI, K., & MATSUI, Y.  (1959)  [Fourteen cases 
of ammonia gas poisoning.]  Shuhkan Igaku Tsuhshin, 601: 26-30 
(in Japanese).

YECK, R.G., SMITH, L.W., & CALVERT, C.C.  (1975)  Recovery of 
nutrients from animal wastes. An overview of existing options 
and potentials for use in feed. In:  Managing livestock waste: 
 Proceedings of the Third International Symposium on Livestock 
 Wastes, St. Joseph, Michigan, American Society of Agricultural 
Engineers, pp. 192-196.

YOSHIDA, J., NAKAME, K., & NAKAMURA, R.  (1957)  Toxicity of 
urea and its control. II. Toxicity of ammonium salts and urea 
in rabbits and goats.  Nippon Chikusangaku Kaiho, 28: 185-191.

ZIEVE, L., DOIZAKI, W.M., & ZIEVC, F.J.  (1974)  Synergism 
between mercaptans and ammonia or fatty acids in the 
production of coma. A possible role for mercaptans in the 
pathogenesis of hepatic coma.  J. lab. clin. Med., 83: 16-28.

ZIMBER, A.  (1970)   Studies on the effect of ammonia on DNA 
 synthesis and on cellular proliferation and renewal in tissues 
 of the mouse and in Ehrlich ascites tumor cells, Ithaca, 
New York, Cornell University (Ph.D. Thesis).

ZIMBER, A. & VISEK, W.J.  (1972)  Effect of urease injection 
on DNA synthesis in mice.  Am. J. Physiol., 223: 1004.

ZIMMERMAN, P.W.  (1949)  Impurities in the air and their 
influence on plant life. In:  Proceedings of the First National 
 Air Pollution Symposium, Pasadena, California, 10-11 November, 
1949, pp. 135-141 (Sponsored by Stanford Research Institute).

ZLATEVA, M., VALCEVA, V., & ANTOV, G.  (1974)  Toxic organic 
changes in laboratory animals placed in an ammonia-rich 
working atmosphere.  Tr. Inst. Hig. Ohrana Tr. Prof. Zabol., 
22(1): 147-154.

Annex I.  Ammonium salts evaluations prepared by the Joint FAO/WHO 
Expert Committee on Food Additives (JECFA)a
Ammonium salt         Functional use                  Evaluation status                  Reference
                                                      (ADI, MTDI)b,c
acetate               pH-adjusting agent              not specifiedd (grouped with       WHO (1982a)
                                                      other ammonium salts and acetate)

alginate              thickening agent, stabilizer    0 - 50 (grouped with alginic acid  WHO (1974a,b)
                                                      and calcium, potassium, and
                                                      sodium alginate)

bicarbonate           leavening agent, buffer         not specified                      WHO (1982b)
(hydrogen carbonate)  neutralizing agent, alkali

chloride              dough conditioner, yeast, food  not specified (grouped with        WHO (1980)
                                                      hydrochloric acid and magnesium
                                                      and potassium chlorides)

hydrogen phosphate    buffering agent, dough          MTDI:, 70 expressed as phosphorus  WHO (1982a,b)
phosphate dibasic     conditioner, leavening agent,   (grouped with phosphates and
                      yeast                           polyphosphates, including 
                                                      phosphates occurring naturally in 

hydroxide (strong     alkali                          not specified                      WHO (1966)
ammonia solution)

lactate               buffer, dough conditioner       not specified                      WHO (1974a,b)

persulfate            flour-treatment agent           no ADI set                         WHO (1966)
a Queries concerning updated information should be addressed to: Joint WHO Secretary of the Joint 
  FAO/WHO Expert Committee on Food Additives, International Programme on Chemical Safety, World Health 
  Organization, Geneva, Switzerland.
b ADI = Acceptable daily intake for man expressed as mg/kg body weight.
c MTDI = Maximum tolerable daily intake for man, expressed as mg/kg body weight.
d ADI not specified = the total intake of the substance arising from its uses at the levels necessary 
  to achieve the desired effect does not represent a hazard to health.

WHO  (1966)   Specifications for the identity and purity of 
 food additives and their toxicological evaluation: some 
 antimicrobials, antioxidants, emulsifiers, stabilizers, flour- 
 treatment agents, acids, and bases. Ninth Report of the Expert 
 Committee, Geneva, World Health Organization (WHO Technical 
Report Series No. 339).

WHO  (1974a)   Toxicological evaluation of certain food 
 additives including anticaking agents, antimicrobials, 
 antioxidants, emulsifiers, and thickening agents, Geneva, 
World Health Organization (WHO Food Additives Series No. 5).

WHO  (1974b)   Toxicological evaluation of certain food 
 additives with a review of general principles and of 
 specification. 17th report of the Expert Committee, Geneva, 
World Health Organization (WHO Technical Report Series 
No. 539).

WHO  (1980)   Evaluation of certain food additives. 
 Twenty-third Report of the Expert Committee, Geneva, World 
Health Organization (WHO Technical Report Series No. 648).

WHO  (1982a)   Evaluation of certain food additives and 
 contaminants. Twenty-sixth Report of the Expert Committee, 
Geneva, World Health Organization (WHO Technical Report Series 
No. 683).

WHO  (1982b)   Toxicological evaluation of certain food 
 additives, Geneva, World Health Organization (WHO Food 
Additives Series No. 17).


    Ammonia (gas and liquid) is an extremely irritant chemical 
affecting the skin, eyes, and the respiratory tracts.  Ammonia gas 
can produce burning of the eyes, lachrymation, and severe eye 
damage.  When inhaled it can produce coughing, laryngitis, 
bronchitis, chest pains, and severe respiratory problems.  Contact 
with liquid ammonia can result in severe eye and skin burns due 
both to its irritant properties and chilling effect. 

    Those working with ammonia should be trained in its safe use 
including the dangers of improper handling, the use of protective 
equipment, and the avoidance of unnecessary inhalation of the gas 
and direct contact with liquid ammonia.  After handling liquid 
ammonia, the hands should be washed thoroughly before eating or 

    The provision of protective clothing and equipment is not an 
adequate substitute for safe working conditions.  However, where 
exposure cannot be adequately controlled, workers should be 
provided with suitable impervious clothing, boots and gloves, and, 
depending on the severity of the conditions, a face shield or 
safety goggles and a mask or self contained breathing apparatus.  
In places where very high gaseous ammonia concentrations are 
expected, complete gas suits should be used. 

    Emergency showers and eye wash or water sprays should be 
provided in all areas where ammonia is handled and where leaks, 
spills or splashes may occur.  Clothes contaminated with ammonia 
should be discarded immediately and not worn again until thoroughly 

    First aid

    If excessive exposure has occurred first aid treatment should 
be promptly initiated and medical advice obtained as soon as 

    Ammonia in the eye (gas, liquid, or liquor)

    Ammonia in the eye may cause severe injury and must be treated 
immediately by irrigation for at least 15 min with flowing water or 
sterile buffered eye irrigation solution. 

    Ammonia on the skin (liquid or liquor)

    Drench the affected area with water and remove contaminated 
clothing and footwear.  Wash the affected area continuously for 5 - 
10 min or until pain ceases. 

    Ingestion (liquid or liquor)

    If the patient is conscious large quantities of water may be 
given to dilute the chemical in the stomach.  No attempt should be 
made to induce vomiting. 

    Inhalation of gas/vapour

    1.  Remove from exposure, secure airway and place in semiprone 
        recovery position if unconscious.  Give artificial 
        respiration if not breathing. 

    2.  If heartbeat is absent give external cardiac massage.

    3.  If there is cyanosis (blueness of lips) or air-hunger 
        administer oxygen by facemask.

    4.  A conscious patient may be given water to drink.

     Further treatment

    Ammonia in the eyes

    Corneal damage is probable.  Use local anaesthetics and 
cycloplegics to enable thorough irrigation and examination.  If the 
cornea is damaged, administer topical antibiotics.  Refer to a 
specialist centre. 

    Ammonia on the skin

    Treat as a chemical burn.  Liquid ammonia may produce deep 
burns that may require grafting.  Refer deep or extensive burns to 
a specialist centre. 

    Inhalation of gas/vapour

    1.  Ammonia is irritant to the respiratory tract causing:

        (a) bronchial oedema, spasm, and hypersecretion 
            resulting in chest tightness, wheeze, and cough, 
            which may progress to severe dyspnoea; and

        (b) lower airway inflammation with exudative 
            pulmonary oedema and impaired gaseous 
            diffusion.  Symptoms may be delayed 24 h or 
            more.  Resolution may be by fibrosis producing a 
            restrictive defect.

    2.  Treat hypoxia with oxygen, ventilation, and bronchial 
        lavage, as appropriate. 

    3.  Consider administration of steroids by multiple metered 
        doses of topical aerosol, by inhalation, and/or by 
        injection.  Early prophylactic use may be indicated.

    4.  Administer bronchodilators by inhalation or injection, as 
        indicated.  Maintain with oral treatment.

    5.  Keep under medical surveillance for at least 48 h.  Treat 

   6.  Observe for secondary respiratory infection and treat as 

    See Also:
       Toxicological Abbreviations
       Ammonia (HSG 37, 1990)