Allowable Ammonia for Fish Culture

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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,

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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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136

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-


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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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


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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


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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


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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.


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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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Documents

Allowable Ammonia for Fish Culture