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Allowable Ammonia for Fish CultureJames W. Meade
a
aNational Fishery Research and Development Laboratory, U.S. Fish
and Wildlife Service, R.D.#4, Box 63, Wellsboro, Pennsylvania,
16901, USA
Available online: 09 Jan 2011
To cite this article:James W. Meade (1985): Allowable Ammonia for Fish Culture, The Progressive
Fish-Culturist, 47:3, 135-145
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THE
Progressiveish-Cultu
A Quarterly Journal for Aquaculturists
Volume 47 July 1985 Number 3
Allowable Ammonia for Fish Culture
JAMES W. MEADE
National Fishery Research and Development Laboratory
U,S. Fish and Wildlife Service
R.D,#4, Box 63
Wellsboro, Pennsylvania 16901
Abstract
A review of the published iterature on effectsof ammoniaon fish indicates hat un-ionized
ammonia alone is probably not the cause of gill hyperplasia, indicative of, or previously
attributed to, chronic ammonia poisoning. The maximum safe concentrationof un-ionized
ammonia is unknown, but in many cases t is not close to the 0.0125 mg/L value commonly
acceptedby fish culturists.
There is confusionconcerning the sublethal,
chroniceffectsof ammonia exposureon fish. In
this review I attempt to point out important
contributions, as well as contradictions, in the
literature. The safe or acceptable evels of am-
monia suggested or fish culture are at best
questionable, and at worst misleading, for
three reasons. First, the commonly accepted
maximum safe concentration of ammonia,
basedon gill histology (hyperplasia of epithe-
lium), has recently been directly and repeat-
edly contradictedby publishedempirical data.
There is great variation, diurnally and hourly,
in ammonia excretion rates due to differences
in diets and feeding regimes, and different
methodsof predicting ammonia levels, based
on diets and feeding, produce answers that
vary by several fold. Thus a predicted ammo-
nia production ate, calculated rom literature
examples for an unstudied rearing system,
may not be near the actual value. And third,
evidence based on studies of acute and chronic
ammonia effects indicates that the effects of
total metabolites cannot be predicted on the
basis of only the concentrationsof un-ionized
ammonia.
Researchers have used various methods in
reporting the form and unit of measurementof
ammonia. In this review un-ionized ammonia
is represented as NH3, the ionized form as
NH4 +, and that sum referred to as ammonia.
Concentrationsare reported n terms of nitro-
gen, and reviewed data not in this form were
converted by multiplying by the appropriate
factor (NH3-N = 0.8235 NH).
Allowable Concentration Guidelines
Colt and Armstrong (1981) reviewed effects
of nitrogen compounds n aquatic animals and
noted that sublethal effects were often re-
ported exclusively as the effects of un-ionized
Prog.Fish-Cult. 7(3), uly, 1985 135
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Meade
ammonia (NH3). Although the effects of am-
monia on growth are unknown for most cul-
tured animals, growth reduction may be the
most important sublethal effect. They sug-
gested that significant growth reduction oc-
curs in most aquatic animals at NH3-N con-
centrations of 0.05 to 0.2 mg/L (equals ppm).
However, many fish culturists regard this
level as inappropriatelyhigh and considergill
damage o be the indicator of chronicammonia
poisoning.
Westers (1981) used 0.0125 mg/L NH-N as
the maximum allowable concentration (taken
at the effluent) for fish culture. Burrows (1964)
reported extensivehyperplasia of gill epithe-
lium in chinook salmon, Oncorhynchus
tshawytscha, fter exposure o only 0.005 mg/L
NHs-N (reported as 0.006 mg/L NHs) for 6
weeks, and, recalculation of Burrows NH3-N
values based on Emerson et al. (1975) indi-
cates that the actual concentration was less
than 0.003 mg/L NHs-N. The European nland
Fisheries dvisoryCommitteeEIFAC) stated
that adverseeffectsof prolongedexposureare
lacking only at concentrations ower than
0.021 mg/L NH3-N (stated as 0.025 mg NHs/L)
(EIFAC 1970). Smith and Piper (1975) re-
ported mild pathological changes in gills
(hyperplasia of epithelium) of rainbow trout,
Salmo gairdneri, reared for 6 months or more
in serial reuse water containing 0.0125 mg/L
NHs-N, and growth reductionwith significant
gill and liver pathologyafter 6 monthsof rear-
ing in 0.0165 mg/L NHs-N (dissolved xygen
averaged less than 6 mg/L).
Criterion set by the EPA for protection of
aquatic ife was 0.016 mg/L NHs-N (statedas
0.02 mg/L NH3), basedon a safety factor of 0.1
applied to data available for 30-day-oldrain-
bow trout. Willingham et al. (1979) computed,
from the data used by the EPA, the acute
effect level on rainbow trout to be 0.27 mg/L
NH3-N, but noted hat the National Academy
of Sciences (1973) advocated an application
factor of 0.05. Ruffler et al. (1981), stated that
the 96-hour LCo is accepted s representative
of acute toxicity concentrations and summa-
rized ammonia trials on nine freshwater
fishes.The 96-hour LCo values ranged from
0.32 to 3.10 mg/L NHs-N, with rainbow trout
and channel catfish, Ictalurus punctatus, at
the respective extremes. A maximum of 0.01
mg/L NHs-N was recommended or salmonid
hatcheries by SECL (1983). The SECL report
includeda caution that more stringent criteria
may be necessary f pH is less than 6.5, dis-
solvedoxygen (DO) less than 5 mg/L, temper-
ature less than 5 C (41F) or sodium concentra-
tion less than that of ammonia. The 0.0125
mg/L NH-N level that Westers 1981) usedas
the maximum allowable concentration Harry
Westers, personal communication), and that
other fish culturists often refer to (Piper et al.
1982, Soderberget al. 1983), is based on the
study by Smith and Piper (1975).
Ammonia production in fish culture is
closely elated to feeding rate. Westers (1981)
indicated that, in salmonids, about 25 g (0.87
oz) of ammonia is producedper kilogram (kg)
of food.Thus it appears that a maximum safe
loading level could be determined simply by
computing, or predicting, from protein feeding
level and water pH and temperature, the
weight of fish that would producean NH-N
concentration of 0.0125 mg/L. Westers (1981)
proposed uch a computationand developeda
practical loading formula. However, use of the
NH-N concentration as a basis for the for-
mula is in question,primarily because ecent
evidence discounts much of the work that at-
tributes gill damage to NHs. Also, there is
significant variation in reported levels of am-
monia production. Moreover, other by-prod-
ucts of metabolism, ncluding fecal solids,bac-
terial solids, and yet undiscovered toxic me-
tabolites, cannot be ignored (Colt 1978) as fac-
tors that may contribute to tissue damage at-
tributed to ammonia.
Contradictions in Reported Effects
Smart (1981) reviewed the safe levels of
ammonia and noted some contradictions.
Smart compared the EPA criteria (Willing-
ham et al. 1979) with the finding of Schulze-
Wiehenbrauck (1976), that NH3-N concentra-
tions of up to 0.13 mg/L were harmless to
growth and food conversion of rainbow trout,
and 0.15 mg/L only temporarily affected
growth. Wickins (1981) suggested the maxi-
mum tolerable concentration for most fish and
shellfish s about 0.1 mg/L NH-N.
Mitchell and Cech (1983), using NHs-N ex-
Prog. Fish-Cult. 47(3), July, 1985
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Allowable Ammonia Review
posuresup to 0.18 mg/L for 83 days, found that
histology failed to confirm ammonia as a di-
rect cause of gill hyperplasia in channel cat-
fish. Their discussion contradicted conclusions
of Robinette (1976), who reported gill
hyperp]asia and weight loss n channel catfish
exposed o 0.12 mg/L NH3-N for 27 days. They
did show that moderate levels of ammonia in
conjunctionwith monochloramine,a chlorine
residual that passesactivated charcoal ilters,
causedseveregill hyperplasia.Robinetteused
activated charcoal to dechlorinate municipal
water and assumed the water to be chlorine
free. The Mitchell and Cech (1983) results de-
based proposals made by Smith and Piper
(1975) and Redner and Stickney (1979) that
gill hyperp]asia is a common sign of chronic
ammonia poisoning.Also, Mitchell and Cech
pointed out that Smart (1976) found macro-
scopic nd microscopic hanges n gills but no
hyperplastic gill damage in rainbow trout
exposed o 0.25-0.3 mg/L NH3-N for up to 36
days.
The most striking evidenceagainst the hy-
pothesis hat chronicexposure o NH3oN above
0.0125 mg/L causes ndicative gill damagewas
presentedby Daoust and Ferguson (1984), who
concluded hat ammonia per se doesnot cause
lesions n rainbow rout gills as viewedat light
microscopemagnification. Rainbow trout ex-
posed or 90 days to up to 0.348 mg/L NH3-N
(reportedas 0.423 mg/L NH3) , or 28 times the
maximum allowable level, displayedclinical
signs of neurological dysfunction,such as in-
termittent frantic side-swimming behavior,
but no lesion attributable to ammonia was
found on gills of any of the fish. In contrast to
this, Burkhalter and Kaya (1977) constantly
exposed ainbow trout eggs o 0.05-0.37 mg/L
NH3-N and observed in resulting sac fry
hypertrophiedgill lamellae epithelia, pale co-
loration and blue-sac diseaseat 0.19 mg/L and
higher, and inhibited developmentand growth
at 0.05 mg/L NH3oN.
Recently Thurston et al. (1984) described
the sublethal effectsof 0.01-0.07 mg/L NH3oN
on rainbow trout throughout their life cycle,
using three generations of fish over a 5-year
period. Histopathologicalchangesobserved n
parental and F 1 fish exposed o at least 0.04
mg/L NH3-N included hypertrophy of gill
lamellae with basal hyperplasia,separationof
epithelia from underlying membranes, ne-
Prog. Fish-Cult. 47(3), July, 1985
137
crosis,aneurysms,and fusion of gill lamellae.
Other effects noted in kidney tissues at 0.04
mg/L NHa-N and above included generalized
nephrosis,degenerationof renal tubule epithe-
lia, hyaline droplet degeneration,and some
partly occluded ubule lumens. Thurston et al.
(1984) reported a positive correlation between
the concentration of both total and un-ionized
ammonia in the blood and that in the water,
but no differences were found in hematocrit or
hemoglobin evels of fish reared at different
NHa concentrations for 7 months. After 11
months hematocrit and hemoglobin levels
were lower in fish held in 0.067 and 0.076
mg/L NH3-N than in fish held in 0.047 mg/L or
less.Notably, there wasno significant elation
between concentrationsof NHa-N and either
mortality or growth.
It appears, from these studies, that in some
culture systemsa reasonably safe maximum
concentration f NHa~N for rainbow trout pro-
duction raceways could be at least 0.04 mg/L,
as udged by the effectsof un-ionizedammonia
alone. However, that concentration would
probably not be applicable n many other fish
culture systemswhere water chemistry or var-
ious metabolite concentrations are different.
Toxicity: Mechanisms and Altering
Variables
Ruffler et al. (1981) summarized the pub-
lished hypotheses or mechanismsof ammonia
toxicity as: osmoregulatory mbalance, caus-
ing kidney failure; surpressed excretion of
endogenous mmonia, resulting in neurologi-
cal and cytological ailure; and gill epithelia
damage, leading to suffocation.A number of
extensive reviews and discussions are avail-
able on ammonia toxicity and mechanismsof
ammonia toxicity: Hampson (1976); Maetz et
al. (1976); Sousa and Meade (1977); Simco and
Davis (1978); Smart (1978); Thurston et al.
(1978, 1984); Shaffl (1980); Tomasso et al.
(1980); Arillo et al. (1981a,b); Colt and Arm-
strong (1981); and Thurston and Russo (1981,
1983). Most of these authors did not discuss
synergism, which must be considered n order
to establish safe levels of combinedtoxicants,
and in the words of Brockway (1950), Ammo-
nia, itself, may not be the culprit, but there is
reason to believe that the other metabolic
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138
Meade
productswill fluctuate proportionately.
Metabolic waste products identified by
Smith (1929) and later by Brockway (1950)
included urea, amine and amine oxide deriva-
tives, carbon dioxide (CO2) creatine, creatin-
ine, and uric acid. According to Forster and
Goldstein (1969) most of the undetermined
non-protein nitrogen in marine fish is trimeth-
ylamine oxide, the source of which has not
been determined. However, waste products
usually considered o be significantly toxic or
important in fish rearing include only ammo-
nia and, in water recirculation systems, ni-
trite. According to Colt and Armstrong (1981)
in the intensive culture of aquatic an-
imals... the toxicity of excreted nitrogen
compoundss the single most limiting param-
eter onceadequate DO levels are maintained.
Differencesor changes n water quality that
affect ammonia toxicity very likely account or
some, if not most, of the discrepancies n re-
ported evels of NH 3 that cause issue damage
or reduced growth in rainbow trout and other
fishes.The EIFAC (1970), Alabaster and Lloyd
(1980), and Thurston (1980) surveyed perti-
nent literature and outlined the action of var-
iables affecting ammonia toxicity, including
pH, CO2, DO, alkalinity, temperature, salin-
ity, and acclimation. Poxton and Allouse
(1982) summarizedNH 3 acute oxicity studies,
discussedwater quality, and identified a need
for more studies on marine water quality. The
SECL (1983) report contained a summary of
some important sublethal, as well as lethal,
toxicity data, and included a discussionof ef-
fects of ionic strength.
pH levels in both rainbow trout and fathead
minnows, Pimephales promelas. They con-
cluded hat NH4+ is toxic, or that increased
hydrogen on concentrationncreasesNH 3 tox-
icity. They recommended hat water quality
criteria include consideration of the pH de-
pendenceof ammonia toxicity. Below 20 mg/L
of total ammonia the effect of NH4 + toxicity
was negligible, and Thurston et al. (1981) spec-
ulated that NH 3 is 300-400 times as toxic as
NH +. However, Willingham et al. (1979)
noted hat even f NH + is one o two orders
ofmagnitude ess oxic han NH3,... NH + is
(usually) present at concentrationsone to two
orders of magnitude greater than NH3. Hil-
laby and Randall (1979) studied ammonia tox-
icity by intraarterial injection, and their re-
sults indicated that, while ammonia is ex-
creted as NH3, the NH 3 form is not acutely
toxic in fish, but either NH4 + or the total
ammonia load is toxic. Goldstein et al. (1982)
concluded that gill ammonia excretion was
related to the concentrationof NH4 + in the
medium, and not NH 3 concentration.
DO
Downing and Merkens (1955) demonstrated
an inverse relation between toxicity of NH 3
and DO concentration. Thurston et al. (1981)
described the relation of DO concentration to
ammonia toxicity for 2.6-8.6 mg/L DO, based
on 96-hour flow-through bioassays, and
showed that tolerance of rainbow trout at 5.0
mg/L DO is 30% less than at 8.5 mg/L DO.
NHz, NH4 +, and pH
Until 1962 only NH 3 was considered oxic
(Tabata 1962). Tomasso et al. (1980) investi-
gated effects of pH and calcium on ammonia
toxicity and found results inconsistent with
the generally accepted onclusionhat NH 3 is
the only toxic form. Thurston et al. (1981)
noted at least five recent studies ndicating the
role of pH in ammonia toxicity is more signif-
icant than simply that of controlling the equi-
librium betweenNH 3 and NH4 +. They found
that ammonia toxicity, if attributed to NH 3
alone, varied by more than 300% at different
CO2
Toxicity of NH 3 is related to free C02 in
solution (Lloyd and Herbert 1960), or to bicar-
bonate alkalinity (Lloyd 1961), which takes
into accountboth the effect of free C02 and pH.
Depressionof pH at the gill surface, rom C02
excretion, may result in the actual NH 3 expo-
sure concentration in high pH water being
much lower than the NH3 concentrationof the
bulk water (Alabaster and Lloyd 1980, SECL
1983). A computation or gill surfaceNH 3 con-
centration, applied to sets of toxicity data, in-
dicated that, while apparent toxicity was re-
lated to pH of the medium, actual NH 3 toxicity
Prog. Fish-Cult. 47(3), July, 1985
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Allowable Ammonia Review
139
was relatively independentof pH (Szumski et
al. 1982).
Temperature
Reduced emperature was shown o increase
NH3 toxicity, especially or values below the
growth optimum (Colt and Tochobanoglous
1976, Thurston and Russo 1983). However,
some studies have shown no effect or the re-
verse effect, indicating survival time may de-
crease as temperature increasesor decreases
from the growth optimum (Thurston 1980).
Ionic Gradients
Ammonia toxicity increases, in rainbow
trout, as salinity either increasesor decreases
from a concentration roughly isotonic with
blood EIFAC 1970). Lloyd and Orr (1969) sug-
gested hat any environmental actor that af-
fects water balance also affects ammonia tol-
erance. Tomasso et al. (1980) found that an
increase in environmental calcium increases
tolerance to ammonia.
In addition to passivediffusion of NH3, am-
monia excretion may be by active exchangeof
NH4 + for Na + (Maetz and Garcia-Romeu
1964). Bradley and Rourke (1985) hypothe-
sized that low environmental Na + concentra-
tions reduceNH4* excretionby the Na + ex-
change mechanism. They found that the addi-
tion of 20 mg/L Na +, 8 mg/L K +, and 30 mg/L
C1- to rearing water of low natural mineral
concentrations 1.2-1.6 mg/L Na +) reducedor
preventedgill swelling and high fish mortality
in juvenile steelhead trout (Salmo gairdneri).
Also, Bradley and Rourke found gill changes
resembling hosereportedly causedby NH 3 at
concentrationsof 0.004 mg/L NH3-N or less.
The importanceof Na + and other ion con-
centrations has been indicated in a variety of
recent studies. Hyperplasia of gill epithelia
has been noted in lake trout (Salvelinus na-
maycush) reared in NH3-N concentrations of
0.001 mg/L mean and 0.003 mg/L maximum,
in serial reuse water of low Na + concentration
(1.5-1.8 mg/L) at the National Fishery Re-
search and Development Laboratory (unpub-
lished). Low Na + and C1- concentrations were
implicated in periodic mortality increases n
coho salmon (Oncorhynchus kisutch) in the
Quilcene National Fish Hatchery even though
NH3-N was less than 0.001 mg/L maximum
concentration Glenn Gately, personal commu-
nication). High sodium concentration (230
mg/L) may have increased, by 2-4 fold, a
62-day LC5o for sockeyesalmon, Oncorhyn-
chus nerka (SECL 1983). Ruffler et al. (1981)
meteredNH4HCO3 into mixtures (with fresh
water) of 56-100% sewageeffluent for contin-
uous flow bioassays on bluegill, Lepomis
machrochirus.The NH 3 levels for estimated
96-hour LC5oequivalentvalues were similar
or high (toxicity was low) compared to other
reportedNH 3 96-hourLC5ovalues for bluegill
(0.90 mg/L NHz-N LC5o eportedby Ruffler et
al. 1981, versus a mean of 0.75 mg/L reported
by Roseboomand Richey 1977, as cited by
Ruffler et al.). However, the sewagewater in
the Ruffler et al. (1981) study had a high ion
concentration, ndicated by a conductivity of
1,820 mmhos/cm. Messer et al. (1984) showed
that previously published tabulations of per-
cent ammonia ionization often result in over-
estimation of NH 3 concentration n hard wa-
ters by 10-20%. Colt et al. (1979) stated that
there was no evidence that sublethal effects of
ammonia were due solely to the un-ionized
fraction, and speculated hat, on the contrary,
sublethaleffectsmay be related o NH4+ and
ambient Na + concentrations. More work is
required to clearly define the influences of
Na +, as well as temperature, pH, CO2, and
alkalinity on ammonia toxicity (SECL 1983).
Life Stage and Size
Before absorptionof the yolk, rainbow trout
withstood up to 50 times the NH 3 concentra-
tion found lethal in adults (Rice and Stokes
1975). However, Reichenbach-Klinke (1967)
found fry more sensitive to ammonia than
larger trout. The SECL (1983) report stated
that the start-of-feeding ife stage s the period
of highest ammonia sensitivity, and noted hat
Calamari et al. (1981) showed late alevins and
new fry are much more sensitive to ammonia
than eggs or developing alevins. In 96-hour
bioassayson eggs and alevins, pink salmon,
Oncorhynchusgorbuscha,were most sensitive
to ammonium sulfate solutionsat completion
of yolk absorption, which was before feeding
Prog. Fish-Cult. 47(3), July, 1985
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140
Meade
began and just prior to emergence, and some
concentrations, 0.025 mg/L NH3-N or more,
stimulated early emergenceof immature fry
(Rice and Bailey 1980). Large rainbow trout,
over 2 kg (4.4 lbs), are more vulnerable than
small trout, 20-300 g (0.04-0.67 lbs), to
acutely toxic ammonia levels (Thurston et al.
1981a).
Acclimation and Stress
Acclimation to low levels of NH3 increases
resistance o lethal levels (Lloyd and Orr 1969,
Redner and Stickney 1979, Thurston et al.
1981). Burrows (1964) reported that exposure
of chinook salmon to 0.08 mg/L NH3-N for
more than 12 hours per day had a greater
effect han exposure o 0.58 mg/L NHa-N for 1
hour per day. High swimming speedsor exer-
tion, as well as handling stress, may affect
resistance o NH3 toxicity (EIFAC 1970). But,
although many factors affect toxicity, the ef-
fect of ammonia depends argely on exposure,
which is a function of excretion or ammonia
production by the fish themselves (assuming
constantsourcewater quality and rearing sys-
tem exchange ates). Thus methodsof predict-
ing ammonia productionare important.
Ammonia Production Estimates
Waarde (1983) reported ammonia to be the
major componentof nitrogen excretion, and its
production rate directly related to protein ox-
idation. Kormanik and Cameron (1981) dis-
cussedbiochemicalpathways and mechanisms
of ammonia excretion. Production of ammonia
can be estimated as the product of the weight
(Wt) of fish in kg, the feeding rate as percent
bodyweight per day (R), the protein-nitrogen
percent of the diet (No) , the percent of protein
metabolized (NM), and the percent of excreted
nitrogen that is excretedas ammonia (NE) as
in the example from Meade (1974):
Wt x R x N o x NM x NE = kg(NH 3 +
NH4+)/day
Liao (1974) stated that ammonia production
can be estimated from oxygenconsumption y
0.053 x kg O 2 consumedper day.
There is much variation in reportedproduc-
tion rates. Fyock (1977) reported, for rainbow
trout in a reuse system, 60.4 to 78.5 g ammo-
nia produced/day/kg 27.4 to 35.6 g/lb) of diet.
Westers (1981) stated that under optimum
feedingammoniaproduction aries from 20 to
30 g/kg (9 to 14 g/lb) of diet/day. Gunther et al.
(1981), working with rainbow trout, reported
38 g ammonia production/kg 17 g/lb) of diet/
day and noted that Speece 1973) reported34
g/kg (15 g/lb) of diet/day. Piper et al. (1982)
used32 g/kg (14 g/lb) of diet for salmonids.The
range of ammonia production reported in the
five referencess 20 to 78.5 g/kg (9 to 35.6 g/lb)
of diet/day.Paulson 1980) developedmodelsof
ammonia excretion that showedgood agree-
ment betweenactual and predictedvalues.He
found that nitrogen consumptionwas by far
the most important factor influencing ammo-
nia excretion, ollowedby fish weight and tem-
perature. Thus not only diet compositionbut
also eedingregime is a key variable in calcu-
lation of ammonia production.
Becauseof its relationship to feeding, am-
monia excretion rate fluctuates drastically.
Brett and Zala (1975) showed that 4-4.5 hours
after feeding, ammonia excretion by sockeye
salmon ncreased o over 400% of pre-feeding
level, and the pre-feeding level was about
equivalent to the constant excretion level for
starved fish. Thus the pre-feeding evel pro-
vides a measure of the endogenous mmonia
production ate, or ammoniaproducedhrough
catabolism. Jobling (1981) discussed he use of
short-termnitrogenmonitoring or estimating
endogenous rates of excretion and mainte-
nance requirements and for a quick assess-
ment of food-growth elationship.
Culture Dynamics, nteractions, and Synergism
Although there is less han total agreement
on prediction of ammonia production levels,
and the meaningof those evels s unclear, t is
evident that daily feeding schedule,or distri-
bution of foodwith time, has a major effect on
peak concentrationsof ammonia. Conversely,
at a given daily diet amount, distribution
schedulehas little or no effect on total daily
ammonia production.Rearing unit designand
water exchangerate also affect ammonia level
fluctuations Harry Westers,personalcommu-
nication). Thurston et al. (1981) found that, for
rainbow trout and cutthroat trout, Salmo
Prog. Fish-Cult. 47(3), July, 1985
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Allowable Ammonia Review
141
clarki, in acute bioassays,exposures o fluctu-
ating concentrationsof NHs were more toxic
than exposureso constantconcentrations. ut
fish subjected to fluctuating concentrations
below the toxic level, like fish in nearly all
culture systems,were better able to withstand
exposure o higher fluctuating concentrations.
Ruffler et al. (1981) found that peak concen-
tration values are important determinants of
toxicity, but do not fully explain population
responses. he pattern of responses,hey con-
cluded, were due to a number of factors,
including degree of fluctuation, mean concen-
tration, and the acclimation ability of the fish.
The synergistic effect of more than one
potential toxicant must be consideredwhen
effects of ammonia, or any substance, s eval-
uated in a multifactor system.Considerationof
only a single metabolite, even if it is in some
way the overwhelming metabolite, as in
amount producedor in its acute toxicity, poses
several mportant questions.Are the effectsof
the aggregate metabolites limited to only the
effectsof NH s concentration? re the effectsof
all metabolites directly related, as additive or
proportional, o NH s concentration? nd con-
sequently, is the concentration of NH s an
adequate indicator of water quality for fish
culture planning and predicting purposes,as-
suming adequate sourcewater quality? If the
answer to any of the three questions s yes, one
could conclude that the only concern for a
productionmanager s that of identifying he
concentrationof NHs that is unacceptable,as
definedby growth, survival, disease isk, such
as correlation of NHs concentrationwith gill
disease t a particular facility, or other criteria.
However, the reviewed literature does not
support that conclusion. t has been demon-
strated that aggregate metabolite effects are
not due only to the NH s fraction. In responseo
the third question, regarding NHs as an
indicatorof water quality, he appa.rent reat
variation in effectsof NHs alone implies that
there would be great inaccuracy in estimating
true system imits, as well as oversight errors
caused y ignoringany metabolites hat might
produce ffectsunrelated o NH s. Also, f there
are effectsof other metabolites, any synergisms
would tcmd to increase the variation of effects,
further reducing accuracyof a single indicator.
The synergistic effect has been only indi-
rectly addressed. n a report on combinedef-
fects of toxicants in water (EIFAC 1980), re-
sults of bioassays n which ammonia was used
in eight combinationswere reviewed.None of
the assays were directly applicable to the
study of a fish productionsystem, however, a
pattern emerged that is described n an ex-
cerpt from the report:
The few (unpublished) ata available for the
long-term ethal joint effect on fish of toxicants
in mixtures, suggest hat they may be mark-
edly more than additive, a phenomenon that
needs confirmation and further investigation.
On the other hand, in the few studieson the
growth of fish, the joint effect of toxicantshas
beenconsistently ess-than-additivewhich sug-
gests that as concentrations of toxicants are
reduced towards the levels of no effect, their
potential for addition is also reduced. There
appear to be no marked and consistentdiffer-
ences between the responseof species o mix-
tures of toxicants.
Summary
In salmonids, evidence of gill damage, sim-
ilar to that described as characteristic of am-
monia poisoning, as well as reduced growth
and increasedmortality, have been associated
with ammonia at NH 3 concentrations ar be-
low that recommended as safe. Burrows
(1964) reportedhyperplasiaof gill epithelia in
rainbow trout exposed o less than 0.003 mg/L
NH3-N (reported as 0.006 mg/L NH3) for 42
days. However, other investigations have dem-
onstrated that exposure to high NH3 concen-
trations, up to 0.348 mg/L NH3-N for 90 days,
failed to result in characteristic gill damage
(Daoust and Ferguson 1984). Bioassay esults
indicate a neurological dysfunction nvolved in
NH3 toxicity, whereas the gill hyperplasia re-
ported in somechronic tests would indicate an
apparently unrelated respiratory impairment.
The reported chronic effects data may be con-
founded by differences n Na+ and other spe-
cific or total ion concentrations of the water
supplies,and the form of reagent ammonia in
some acute toxicity studies may have altered
the effects by changing ion concentrations in
rearing water. The accumulating evidence n-
dicates hat gill hyperplasia, reported as char-
acteristic of ammonia poisoning, s probably
not caused by un-ionized ammonia.
Prog. Fish-Cult. 47(3), July, 1985
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142 Meade
A truly safe, maximum acceptableconcen-
tration ofun-ionized, or total, ammonia for fish
culture systems s not known. Methods of pre-
dicting ammonia production yield a wide
range of results. All end products of metabo-
lism probably have not been identified, and
certainly their interactions in water of various
qualities and in various fish culture systems
have not been determined. The apparent tox-
icity of ammonia is extremely variable and
dependson more than the mean or maximum
concentration of NH 3.
In view of these negative assertions, one
might ask, rhetorically, what shoulda produc-
tion manager do? suggest that the use of a
calculated estimate of NH3 concentration o
determine maximum, or optimum, safe pro-
duction levels, is far better than the use of no
quantitative guidelines. However, it is also
certain that the production evel basedon that
estimate will nearly always be incorrect, nei-
ther maximum nor optimum, and therefore
inefficient. To remedy the situation, research-
ers must thoroughly identify metabolities and
determine the{r chronic effects on several
fishes. The effects of Na + and other ion con-
centrations need to be defined, both independ-
ently and in interaction with metabolities.
More work is needed on nitrogen balance, the
approachusedby Gunther et al. (1981). And,
to formulate production ndexes,holistic data
are needed,which could be generated by mon-
itoring a number of rearing systems.Armed
with more credible data, progressivehatchery
biologists can provide production managers
with more meaningful guidelines that will in-
crease efficiency and reduce costs.
Acknowledgments
Harry Westers, Cheryl Goudie, Glenn Gate-
ly, and an anonymous eviewer provided val-
uable suggestions.
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