-------
-------
WATER QUALITY CRITERIA FOR THE PROTECTION OF AQUATIC LIFE AND ITS USES
AMMONIA
Final Draft
20 January 1983
Prepared By
U.S. Environmental Protection Agency
Office of Research and Development
Environmental Research Laboratory
Duluth, Minnesota
US Frv'r^r>?v^nt?! Protection Agency
-------
TABLE OF CONTENTS
Page
Introduction 1
Acute Toxicity to Animals 7
Chronic Toxicity to Animals 42
Toxicity to Plants 59
Bioaccumulat ion 64
Other Data 65
Unused Data 76
Summary 80
National Criteria 84
Examples of Site-Specific Criteria 87
Tables 91
1 . Acute values for ammonia 91
2. Chronic values for ammonia 110
3. Species and family mean acute values (corrected for pH)
for ammonia . . . . 114
4. Plant values for ammonia 117
5. Other data for ammonia 119
References 132
U.S. Envlronrnentc! Trctc^'cn Agenc
li
-------
INTRODUCTION*
In aqueous ammonia solutions, un-ionized ammonia exists in equilibrium
with the ammonium ion and the hydroxide ion. The equation expressing this
equilibrium can be written as:
^3(8) + nH2°U) * NH3'nH2°(aq) * m*+ + OH~ + (n-OH2°U)*
As indicated in this equation, the dissolved ammonia molecule exists in
hydrated form. The dissolved un-ionized ammonia is represented for
convenience simply as NHj. The ionized form is represented as NH^+.
The term total ammonia refers to the sum of these; i.e., NH3 + NH^ .
The toxicity of aqueous ammonia solutions to aquatic organisms is
primarily attributable to the NH-j Species, with the NH^"*" species being
relatively less toxic (Chipraan 1934; Wuhrmann et al. 1947; Wuhrmann and Woker
1948; Tabata 1962; Armstrong et al. 1978; Thurston et al. 1981c). It is,
therefore, important to know the concentration of NH-j in any aqueous
ammonia solution in order to determine what concentrations of total ammonia
are toxic to aquatic life.
The concentration of NH^ is dependent on a number of factors in
addition to total ammonia concentration (Emerson et al. 1975; Thurston et al.
1979). Most important among these are pH and temperature; the concentration
of NH-j increases with increasing pH and with increasing temperature. The
ionic strength is another important influence on this equilibrium. There
* The reader is referred to the Guidelines for Deriving Numerical National
Water Quality Criteria for the Protection of Aquatic Life and Its Uses (5
July 1983) (U.S. Environmental Protection Agency 1983 ) in order to
understand better the following text, tables, and calculations.
1
-------
is a decrease in tht; percentage of un-Ionized ammonia as the limit.: strength
increases in hard water or in dilute saline solution. In most natural
freshwater systems the reduction of percent NHg attributable to dissolved
solids is negligible. In saline or very hard waters there will be small but
measurable decreases in the percent NHo-
Current analytical methods do not permit measurement of NH3 and
NH^ separately. A number of analytical methods are available for direct
determination of total ammonia concentrations in aqueous solutions. Once
total ammonia is measured, and the pH and temperature of the solution
determined, the fraction of total ammonia present as NH3 can be calculated
based on the ammonia-water equilibrium. A review of analytical methods for
ammonia in aqueous solution has been prepared by Richards (1981).
Emerson et al. (1975) carried out a critical evaluation of the
literature data on the ammonia-water equilibrium system and published
calculations of values of pKa at different temperatures and of percent
NH-j in ammonia solutions of zero salinity as a function of pH and
temperature. The following table, reproduced from Emerson et al. (1975),
provides values for percent NHg at one-degree temperature intervals from 0
to 30 C, and pH intervals of 0.5 pH unit from pH 6.0 to 10.0. An expanded
version of this percent NH^ table is provided in Thurston et al. (1979),
which provides tabulated values of the NH-j fraction, expressed as
percentage of total ammonia, at temperature intervals of 0.2 degree from 0.0
to 40.0 C, and pH intervals of 0.01 pH unit from pH 5.00 to 12.00. For
salt water, reports by Whitfield (1974) and Skarheim (1973) provide
calculations of NHg as a function of pH, temperature, and salinity.
-------
Percent NH-j in aqueous ammonia solutions tor 0-30 C and pH b-10.
Temp.
(C)
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
6.0
.00827
.00899
.00977
.0106
.0115
.0125
.0136
.0147
.0159
.0172
.0186
.0201
.0218
.0235
.0254
.0274
.0295
.0318
.0343
.0369
.0397
.0427
.0459
.0493
.0530
.0569
.0610
.0654
.0701
.0752
.0805
6.5
.0261
.0284
.0309
.0336
.0364
.0395
.0429
.0464
.0503
.0544
.0589
.0637
.0688
.0743
.0802
.0865
.0933
.101
.108
.117
.125
.135
.145
.156
.167
.180
.193
.207
.221
.237
.254
7.0
.0826
.0898
.0977
.106
.115
.125
.135
.147
.159
.172
.186
.201
.217
.235
.253
.273
.294
.317
.342
.368
.396
.425
.457
.491
.527
.566
.607
.651
.697
.747
.799
7.5
.261
.284
.308
.335
.363
.394
.427
.462
.501
.542
.586
.633
.684
.738
.796
.859
.925
.996
1.07
1.15
1.24
1.33
1.43
1.54
1.65
1.77
1.89
2.03
2.17
2.32
2.48
pH
8.0
.820
.891
.968
1.05
1.14
1.23
1.34
1.45
1.57
1.69
1.83
1.97
2.13
2.30
2.48
2.67
2.87
3.08
3.31
3.56
3.82
4.10
4.39
4.70
5.03
5.38
5.75
6.15
6.56
7.00
7.46
8.5
2.55
2.77
3.00
3.25
3.52
3.80
4.11
4.44
4.79
5.16
5.56
5.99
6.44
6.92
7.43
7.97
8.54
9.14
9.78
10.5
11.2
11.9
12.7
13.5
14.4
15.3
16.2
17.2
18.2
19.2
20.3
9.0
7.64
8.25
8.90
9.60
10.3
11.1
11.9
12.8
13.7
14.7
15.7
16.8
17.9
19.0
20.2
21.5
22.8
24.1
25.5
27.0
28.4
29.9
31.5
33.0
34.6
36.3
37.9
39.6
41.2
42.9
44.6
9.5
20.7
22.1
23.6
25.1
26.7
28.3
30.0
31.7
33.5
35.3
37.1
38.9
40.8
42.6
44.5
46.4
48.3
50.2
52.0
53.9
55.7-
57.5
59.2
60.9
62.6
64.3
65.9
67.4
68.9
70.4
71.8
10.0
45.3
47.3
49.4
51.5
53.5
55.6
57.6
59.5
61.4
63.3
65.1
66.8
68.5
70.2
71.7
73.3
74.7
76.1
77.4
78.7
79.9
81.0
82.1
83.2
84.1
85.1
85.9
86.8
87.5
88.3
89.0
[From Emerson et al. 1975; reproduced with permission from the Journal of the
Fisheries Research Board of Canada.]
-------
Concentrations of ammonia have been reported in the .-U|u.-ic u~ toxu'ltv
literature as a variety of different forms, such as NH3» NH^, N^-N,
NH^Cl, and others. The use in a literature article of the terras
NHg, NH-j-N, or ammonia-nitrogen may not necessarily mean un-ionized
ammonia, but may be the author's way of expressing total ammonia. The use of
the term NH-j in this document always means un-ionized ammonia, and NH^N
means un-ionized ammonia-nitrogen.
Throughout the following, all quantitative ammonia data have been
expressed in terms of un-ionized ammonia, as mg/liter Nt^, for ease in
discussion and comparison. Authors' ammonia concentration values are given
as reported if authors provided data expressed as rag/liter NHg- If authors
reported only total ammonia values, or used concentration units other than
mg/liter, these were used with the reported pH and temperature values to
calculate mg/liter un-ionized NH3« For calculations of NH3 in fresh
water the table of Thurston et al. (1979) was used. For calculations in salt
water the table of Skarheira (1973) was used.
This Criterion Document was prepared in accordance with U.S.
Environmental Protection Agency guidelines for the derivation of national
water quality criteria (U.S. Environmental Protection Agency 1982a). The
literature cited herein was obtained from a search of the literature through
October 1982; data from primary references only were used.
Of the literature cited in this document, a significant number of papers
provided insufficient pH and temperature data to enable calculation of NH3
concentrations; such papers were relegated to the section on "Unused Data"
unless they provided useful qualitative or descriptive information. In some
instances information missing in published papers on experimental conditions
-------
,was obtained through correspondence with authors; data obtained in this
manner are so Indicated by footnotes.
Compounds used in the ammonia toxicity testing summarized here and their
formulas and Chemical Abstracts Services (CAS) Registry Numbers are given
below:
Compound Formula CAS No.
Ammonia NH3 7664417
Ammonium acetate ^^02^02 631618
Ammonium bicarbonate NH^Hct^ 1066337
Ammonium carbonate (NH^^COg 506876
Ammonium chloride NH^Cl 12125029
Ammonium hydrogen phosphate (NH^HPO^ 7783280
Ammonium hydroxide NH4OH (NH3'H20) 1336216
Ammonium sulfate (NHSQ 7783202
Papers stating use of other sources of ammonia were included if the source
(e.g., excreted NH^ from fish) was deemed satisfactory. Papers using
complex chemicals (e.g., ammonium ferricyanide, dec ylt rime thylammonium
bromide) were not used. Finally, papers on ammonium compounds (e.g., NH^F,
having anions that either might be themselves toxic or that
would preclude calculation of NH3 concentration from the aqueous ammonia
equilibrium relationship were not used.
A number of review articles or books dealing with ammonia as an aquatic
pollutant are available. Water quality criteria for ammonia have been
recommended in some of these. Liebmann (1960), McKee and Wolf (1963), Epler
(1971), Becker and Thatcher (1973), Tsai (1975), Hampson (1976), Steffens
(1976), Colt and Armstrong (1979), and Armstrong (1979) have published
summaries of ammonia toxicity. Literature reviews including factors
affecting ammonia toxicity and physiological effects of ammonia toxicity to
aquatic, organisms have been published by Lloyd (1961b), Lloyd and Herbert
5
-------
(1962), Warren (1962), Visek (1968), Lloyd and Swift (1976), and Kinne
(1976). Literature reviews of ammonia toxicity information relating to
criteria recommendations have been published by U.S. Federal Water Pollution
Control Administration (1968), European Inland Fisheries Advisory Commission
(1970), National Academy of Sciences and National Academy of Engineering
(1973), Willingham (1976), U.S. Environmental Protection Agency (1977, 1980),
National Research Council (1979), Willinghara et al. (1979), and Alabaster and
Lloyd (1980).
-------
ACUTE TOXICITY TO ANIMALS
1 i
Freshwater Invertebrates
Acute toxicity of ammonia to freshwater invertebrate species has been
much less studied than that to fishes. The preponderance of available
invertebrate data is comprised of studies with arthropods, primarily
crustaceans and insects. LC50 and EC50 data are summarized in Table 1 for 12
species representing nine families.
The acute toxicity of ammonia to Daphnia magna (Table 1) has been
studied by several investigators, with reported 48-hour LC50 values ranging
from 0.53 to 4.94 mg/liter NH3 (Parkhurst et al. 1979, 1981; Reinbold and
Pescitelli 1982a; Russo et al., in prep.).
Exposures (48 hours) of I), magna to NlfyCl in dilution water from two
different sources were conducted by Russo et al. (in prep.). LC50 values
(Table 1) ranged from 2.4 to 2.8 mg/liter NH3 in water of pH 7.95 to 8.15
and hardness 192 to 202 rag/liter CaC03, and from 0.53 to 0.90 mg/liter
NH3 in water of pH 7.4 to 7.5 and hardness 42 to 48 mg/liter CaC03- On
an acute (48-hour LC50) basis, in dilution water from the same source,
Ceriodaphnia acanthina, Simocephalus vetulus, and IK magna all exhibited
similar sensitivities (Table 1) to ammonia (Mount 1982; Russo et al., in
prep.). The 48-hour LC50 value (Table 1) of 1.16 mg/liter NH3 reported by
DeGraeve et al. (1980) for Daphnia pulicaria falls within the range of values
reported for IK magna. Anderson (1948) reported a threshold toxicity value
(Table 5) for £. magna of 2.4 to 3.6 mg/liter NH3 in Lake Erie water.
Threshold concentration was taken to mean the highest concentration that
would just fail to immobilize the test animals under prolonged exposure
(Anderson 1944). A minimum lethal concentration of 0.55 rag/liter NH3 was
reported for _D. magna by Malacca (1966), and a 24-hour I C50 value of 1.50
7
-------
rag/liter NH3 was reported by Gyore and Olah (1980) for Moina rectirostris
(Table 5).
Buikema et al. (1974) reported an EC50 (Table 5) for NH3 toxicity to a
bdelloid rotifer, Philodina acuticornis, to be 2.9-9.1 mg/liter NH3
(calculated using reported pH values of 7.4 to 7.9). Tests of ammonia
toxicity to a flatworm, Dendrocoelum lacteum (Procotyla fluviatilis), and
tubificid worm, Tubifex tubifex, yielded LC50 values (Table 1) of 1.4 and 2.7
mg/liter NH3, respectively (Stammer 1953).
Thurston et al. (in prep., a) conducted 26 flow-through toxicity tests
with three mayfly, two stonefly, one caddisfly, and one isopod species; all
tests were conducted with water of similar chemical composition.
Ninety-six-hour LC50 values ranged from 1.8 to 5.9 mg/liter NH3 (Table 1).
Results also indicated that a 96-hour test is not long enough to determine
the acutely lethal effects of ammonia to the species tested, inasmuch as an
asymptotic LC50 is not obtained within 96 hours. Percent survival data
(Table 5) were reported for some mayfly, stonefly, and caddisfly tests in
which LC50 values were not obtained; 60 to 100 percent survival occurred at
test concentrations ranging from 1.5 to 7.5 mg/liter NH3- Gall (1980)
tested NH^Ci with Ephemerella sp. near excrucians. Organisms were exposed
to ammonia for 24 hours, followed by 72 hours in ammonia-free water;
mortality observations were made at the end of the overall 96-hour period.
An EC50 value (Table 5) of 4.7 mg/liter NH3 was obtained.
Ammonia toxicity tests conducted using dilution water from the Blue
River in Colorado resulted in no mortalities of either scud (Gammarus
lac us tr is) or D^. majgjia after 96 hours' exposure to 0.08 ing/liter NH3« In a
second test using river water buffered with sodium bicarbonate, 13 percent
mortal icy occurred with scud at several concentrations tested, including the
8
-------
highest and lowest of 0.~"* And O.I? mg/Htov \'H^; *ov*n ami 1'» ;*«M .^ u
mortality occurrtvi with r>- '-c-a^'.ia at the s'ilie* ct =>l.
1981).
Five freshwater mussel species (Amblema _p. plicata, Anodonta imbecillis,
Corbicula manilensis, Cyrtonaias t amp i c o en si s, and Toxqlasma texasensis) were
exposed for 165 hours (Table 5) to a concentration of 0.32 rag/liter NH^J T_.
texasensis was most tolerant to ammonia, and A. j>. plicata was most sensitive
(Home and Mc.Tntosh 1979). During the ammonia tolerance tests, the more
tolerant species generally had their shells tightly shut, whereas the least
tolerant species continued siphoning or had their mantles exposed. Acute
exposures of the freshwater crayfish (Orconectes nais) to NH^Ci gave LC50
values (Table 1) of 3.15 and 3.82 mg/liter NH3 (Evans 1979; Hazel et al.
1979). An LC50 value (Table 1) of 8.00 mg/liter was reported for the beetle
(Stenelmis sexlineata) by Hazel et al. (1979).
Freshwater Fishes
Acute toxicity tests with freshwater fish species have been conducted
with 23 different species from nine families; 96-hour LC50 values are
summarized in Table 1.
The acute toxicity of ammonia to rainbow trout (Salmo gairdneri) has
been studied by many investigators, with reported 96-hour LC50 values ranging
from 0.16 to 1.1 mg/liter NH3 (Table 1).
Thurston and Russo (in press) conducted 71 toxicity tests with rainbow
tiout ranging in size from sac fry (<0.1 g) to 4-year-old adults (2.6 kg), in
wai er of uniform chemical composition. LC50 values (Table 1) ranged from
O.lo to 1.1 mg/liter NH-j for 96-hour exposures. Fish susceptibility to
NH-j 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
9
-------
exposures (Table 5) were not greatly different from 96-hour values. No
statistically significant differences in results were observed when different
ammonium salts [NH^Cl, NH^HCO-j, (NH^HPO^, (NH^SO^l were used as the
toxicants. Grindley (1946) also reported observing no appreciable difference
in toxicity between toxicant solutions of NH^Cl and (NH^)9So^ with
rainbow trout tests (Table 5).
LC50 values (Table 1) ranging from 0.16 to 1.0 mg/liter NH3 for
96-hour exposures of rainbow trout to ammonia were reported by Calamari et
al. (1977, 1981), Broderius and Smith (1979), Holt and Malcolm (1979),
DeGraeve et al. (1980), and Reinbold and Pescitelli (1982b). Ball (1967)
reported an asymptotic (five-day) LC50 value of 0.50 mg/liter NH3• Acute
exposures to ammonia of rainbow trout of life stages ranging from one to 345
days' post-fertilization (325 days post-hatch) were conducted by Calamari et
al. (1977, 1981). They reported a tenfold increase in the speed of
intoKication processes between the embryonic and free larval stages; embryos
and fingerlings (about one year old) were found to be less sensitive than the
other life stages studied.
LCSO values ranging from 0.49 to 0.70 mg/liter NH3 for 3-, 24-, and
48-hour exposures (Table 5) were reported by Herbert (1961, 1962), Herbert
and Shurben (1964, 1965), and Herbert and Vandyke (1964). Rainbow trout (826
days old) subjected to 29.6 mg/liter NH-j reacted rapidly and strongly,
overturned within two to three hours, and died within four hours (Corti 1951)
(Table 5). Rainbow trout embryos and alevins were reported (Rice and Stokes
1975) to tolerate 3.58 mg/liter NH3 during 24-hour exposures; suscep-
tibility increased during yolk absorption, with the 24-hour LCSO for
85-day-old fry being 0.068 mg/liter NH3 (Table 5). Nehring (1962-63)
reported survival times of 1.3 and 3.0 hours at concenttations of 4.1 and 0.7
10
-------
,mg/liter NH^, respectively (Table 5). Danecker (1964) reported survival
times of S to 60 minutes at 0.4 to 4.0 rag/liter NHy, respectively, with
<0.2 m,f*/l.1ter given as ,1 no-mortality concentration (Table 5). Allan et al.
(1958) reported a median survival time of 1000 minutes at 0.18 mg/liter NH3
(Table 5).
An acute value of 0.2 mg/liter NH3 attributed to Liebmann (1960) has
been widely cited, in the EPA "Red Book" (U.S. Environmental Protection
Agency 1977) and elsewhere, as being the lowest lethal concentration reported
for salmonids. It is worthwhile to mention here a clarification and
correction that was published in the American Fisheries Society's "Red Book
Review" (Willingham et al. 1979): The research reported by Liebmann (1960)
was that of Wuhrmann and Woker (1948); recomputation of the Wuhrmann and
Woker data, using more accurate aqueous ammonia equilibrium tables, indicates
an effect level of approximately 0.32 mg/liter NH3, not 0.2 mg/liter NH3
as cited by Liebmann.
A 96-hour LC50 value of 0.44 mg/liter NH3 was reported for rainbow
trout In a test conducted using dilution water from the Blue River in
Colorado (Miller et al. 1981). Pitts (1980) conducted toxicity tests using
ammonium chloride and river water. Tests were conducted with rainbow trout,
and LC50 values ranged from 0.2 to 0.9 mg/liter NH3 for 96-hour exposures
at temperatures of 10 and 15 C.
Although acute toxicity studies with salmonids have been conducted
preponderantly with rainbow trout, some data are also available for a few
other salmonid species. Thurston et al. (1978) investigated the toxicity of
a.timoriia to cutthroat trout (Salmo dark!), and reported 96-hour LC50 values
of 0.52 to 0.80 rag/liter NH3 (Table 1). Thurston and Russo (1981) reported
a 96-hoi,r LC50 value of 0.76 rag/liter NH3 for golden trout (Salmo
il
-------
aguabonlta) (Table 1). Taylor (1973) subjected brown trout (Salmo trutta) to
0.15 rag/liter NH3 for 18 hours, resulting in 36 percent mortality (Table
5); when returned to ammonia-free water, the test fish recovered after nearly
24 hours. No mortalities occurred during a 96-hour exposure at 0.090
mg/liter NH3, although fish would not feed. Woker and Wuhrmann (1950)
reported 0.8 mg/liter NH-J was not acutely toxic to brown trout (Table 5).
A 96-hour LC50 value of 0.47 mg/liter NII3 was reported for brown trout
tested using dilution water from the Blue River in Colorado (Miller et al.
1981). Phillips (1950) reported that brook trout (Salvelinus fontinalis)
evidenced distress within 1.75 hours at a concentration of 3.25 mg/liter
NH3 and within 2.5 hours at 5.5 mg/liter (Table 5).
Toxicity tests (Tables 1, 5) on (NH^^SO^ with pink salmon
(Oncorhynchus gorbuscha) at different stages of early life stage development
(Rice and Bailey 1980) showed that late alevins near swim-up stage were the
most sensitive (96-hour LC50 = 0.083 mg/liter NHg), and eyed embryos were
the most tolerant, surviving 96 hours at >1.5 mg/liter NH3. Buckley (1978)
reported a 96-hour LC50 value of 0.55 mg/liter NH3 for fingerling coho
salmon, Oncorhynchus kisutch (Table 1). Herbert and Shurben (1965) reported
a 24-hour LC50 value (Table 5) of 0.28 mg/liter NH3 for Atlantic salmon
(Salmo s_alar) . A comparison of relative susceptibilities of salmon smolts
and yearling rainbow trout to 24-hour exposures to NH^Cl showed that the
salmon were appreciably more susceptible than the trout in fresh water
(Ministry of Technology, U.K. 1963).
Data are available on the acute toxicity of ammonia to a variety of
non-salmonid fish species. Thurston et al. (in press, a) studied the
toxicity of ammonia to fathead minnows (Pimephales promelas) of sizes ranging
from 0.1 to 2.3 g; LC50 values from 29 tests ranged from 0.75 to 3.4 mg/liter
NH3 (Taoie 1). Toxictty was not dependent upon test tish size or source.
12
-------
'•LC50 values ranging from 0.73 to 1.7 rag/liter NH^ (Tables 1,5) for fathead
minnows were also reported by Sparks (1975), DeGraeve et al. (1980), and
Reinbold and Pescitelli (1982b). Toxicity tests with fathead minnows using
ammonium chloride and river water yielded 96-hour LC50 values ranging from
0.6 to 2.4 tng/liter Nt^J fathead minnows exposed to 0.12 mg/liter NH3 in
river water for 28 days incurred no mortalities (Pitts 1980).
LC50 values (Table 1) for white sucker (Catostomus commersoni) exposed
to ammonium chloride solutions for 96 hours (Reinbold and Pescitelli 1982c)
were 1.40 and 1.35 mg/liter NH3• Reported LC50 values (Table 1) for
96-hour exposures of bluegill (Lepomis macrochirus) ranged from 0.26 to 4.60
mg/liter NH3 (Emery and Welch 1969; Lubinski et al. 1974; Roseboom and
Richey 1977; Reinbold and Pescitelli 1982b; Smith and Roush, in prep.). LC50
values (Table 1) of 0.7 to 1.8 mg/liter NH3 for smallmouth bass
(Micropterus dolomieui) and 1.0 to 1.7 mg/liter NH-j for largemouth bass
(Micropterus saltnoides) were reported by Broderius et al. (in prep.) and
Roseboom and Richey (1977), respectively, for 96-hour exposures. Sparks
(1975) reported 48-hour LC50 values (in parentheses, as rag/liter ^3) for
bluegill (2.30) and channel catfish (2.92), Dowden and Bennett (1965)
reported a 24-hour LC50 value for goldfish (Carassius auratus) (7.2), and
Chipman (1934) reported lethal threshold values of 0.97 to 3.8 mg/liter NH3
for goldfish (Table 5). Turnbull et al. (1954) reported a 48-hour LC50 value
for bluegill to be within the range 0.024 to 0.093 mg/liter NH3 (Table 5);
during the exposure they observed that the fish exhibited a lack of
perception to avoid objects.
Reported 96-hour LC50 values (Table 1) for channel catfish (Ictalurus
pane, tat us) ranged from 1.8 to 4.2 mg/liter NH3 (Colt and Tchobanoglous
1976; Koseboora and Rirhey 1977; Reinbold and Pescitelli L982d). Vaughn and
13
-------
Simco (1977) reported a 48-hour LC50 for channel catfish of 1.24 to 1.96
mg/liter NH-j, and Knepp and Arkin (1973) reported one-week LC50 values of
0.97 to 2.0 mg/liter NH3 (Table 5). From studies with bluegill, channel
catfish, and largemouth bass, Roseboom and Richey (1977) reported that
bluegill susceptibility was dependent upon fish weight, with 0.07-g fish
being slightly more sensitive than either 0.22- or 0.65-g fish; size had
little effect upon channel catfish or bass susceptibility.
LC50 values (Table 1) were determined with two species of field-
collected fishes indigenous to Kansas streams, orangethroat darter
(Etheostoma spectabile ) and red shiner (Notrqpis lutrensis) (Hazel et al.
1979); 96-hour LC50 values were 0.90 and 1.07 mg/liter NH3 for darter and
2.83 for shiner. Commercially obtained largeraouth bass, channel catfish, and
bluegill (18 fish of each species) were also exposed for 96 hours to a
concentration of 0.21 mg/liter NH3, resulting in zero mortality for
bluegill and channel catfish and one mortality (6 percent) among the
largeraouth bass tested.
LC50 values (Table 1) ranging from 0.48 to 3.2 mg/liter NH3 for
NH4C2H3°2' (NH4)2C03, NH4Cl, NH4OH, and (NH4)2S04 in 96-hour
exposures of mosquitofish (Gambusia affinis) in waters with suspended solids
ranging from <25 to 1400 mg/liter were reported by Wallen et al. (1957).
Susceptibility of mosquitofish to ammonia was studied by Hemens (1966) who
reported a 17-hour LC50 value of 1.3 mg/liter NH3 (Table 5); he also
observed that male fish were more susceptible than females. Powers (1920)
reported the relative susceptibilities of three fish species to ammonium
chloride to be (most sensitive to least sensitive): straw-colored minnow
(Notropis b 1 ennius) > bluntnose minnow (Pimephale s no ta tusj > goldfish.
14
-------
Rubin and Elmaraghy (1976, 1977) tested guppy (Poecilla reticulata) fry
and reported 96-hour LC50 values (Table 1) averaging 1.50 mg/liter NH3;
mature guppy males were more tolerant, with 100 percent survival for 96 hours
at concentrations of 0.17 to 1.58 mg/liter NH3« LC50 values (Table 1) of
0.15 and 0.20 mg/liter NH3 at pH 6.0, and of 0.52 and 2.13 mg/liter NH3
at pTI 8.0, were reported by Stevenson (1977) for white perch (Morone
americana). LC50 values (96 hours) of 1.20 and 1.62 mg/liter NH3 for
spotfln shiner (Notr o pis sp1lopterus), and of 1.20 mg/liter NHj for golden
shiner (No t emi gonus cryso1eucas), were reported by Rosage et al. (1979) and
Baird et al. (1979), respectively (Table 1). Jude (1973), Reinbold and
Pescitelli (1982a), and McCormick et al. (in prep.) reported 96-hour LC50
values ranging from 0.6 to 2.1 mg/liter NH3 for green sunfish (Lepomis
cyanellus) (Table 1). Pumpkinseed sunfish (Lepomi8 gibbosus) were tested by
Jude (1973) and Thurston (1981), with reported 96-hour LC50 values ranging
from 0.14 to 0.86 mg/liter NH3 • Mottled sculpin (Cottus bairdi) were
tested by Thurston and Russo (1981), yielding a 96-hour LC50 of 1.39 mg/liter
NH3 (Table 1). Ball (1967) determined an asymptotic (six-day) LC50 value
(Table 5) of 0.44 mg/liter NH3 for rudd (Scardinius erythrophthalmus). He
compared the asymptotic LC50 values for this species against that obtained
within two days for rainbow trout. Although the trout had proven to be more
sensitive to ammonia than had rudd during the first day of the tests, the
asymptotic LC50 for both species showed little difference.
Rao et al. (1975) reported a 96-hour LC50 for carp (Cyprinus carpio) of
1.1 mg/liter NH3 (Table 1). Carp exposed to 0.24 mg/liter NH3 exhibited
no adverse effects in 18 hours (Vamos 1963). Exposure to 0.67 mg/liter NH3
caused gasping and equilibrium disturbance in 18 min, frenetic swimming
activity in 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. Similar
15
-------
effects were observed at a concentration of 0.52 rag/liter NHj (Table 5).
Pre-treating fish orally with 12.5 rag Suprastin (N-dimethyl-arainoethyl-N-p-
chlorobenzyl-o-aminopyridin hydrochlor) , a chemical which reduces cell
membrane permeability, somewhat reduced the toxic effect of ammonia.
A lethal concentration (Table 5) for carp was reported to be 7.5
rag/liter NHg (Kempinska 1968). Acute exposures (Table 5) to ammonium
sulfate of bitterling (Rhodeus sericeus) and carp were conducted by Malacca
(1966), who determined minimum lethal concentrations (i.e., after such
exposure, fish placed in ammonia-free water were unable to recover) of 0.76
mg/liter NH3 for bitterling and 1.4 mg/liter NH3 for carp. Nehring
(1962-63) reported survival times of carp to be 2.4 and 6.0 hours at NH3
concentrations of 9.7 and 2.1 mg/liter N^, respectively (Table 5).
Danecker (1964) reported survival time for tench (Tinea tinea) to be 20 to 24
hours at 2.5 mg/liter NH-} (Table 5). In a 24-hour exposure of creek chub
(Semotilus atromaculatus) to NlfyOH solution (Gillette et al. 1952), the
"critical range" below which all test fish lived and above which all died was
reported to be 0.26 to 1.2 mg/liter NH3 (Table 5).
In static exposures lasting 9 to 24 hours, with gradual increases in
NH-j Content, lethal concentrations (Table 5) were determined for oscar
(Astronutus ocellatus) (Magalhaes Bastos 1954); mortalities occurred at 0.50
rag/liter MH-j (4 percent) to 1.8 mg/liter (100 percent). Tests on oscar of
two different sizes (average weights 1.6 g for "small" fish and 22.5 g for
"medium" fish) showed no difference in susceptibility related to fish size.
A 72-hour LC50 value (Table 5) of 2.85 mg/liter NH^ was reported by Redner
and Stickney (1979) for blue tilapia (Tilapia aurea) .
Factors Affecting Acute Toxicity of Ammonia
There are a number of factors that can affect the toxicity of ammonia to
aquatic organisms. These factors include effects of dissolved oxygen
16
-------
.concentration, temperature, pH, previous acclimation to ammonia, fluctuating
or intermittent exposures, carbon dioxide concentration, salinity, and
presence of other toxicants. Almost all studies of factors affecting ammonia
toxicity have been carried out using only acute exposures.
(a) Dissolved Oxygen
A decrease in dissolved oxygen concentration in the water can increase
ammonia toxicity. Vamos and Tasnadi (1967) observed mortalities in carp
ponds at ammonia concentrations lower than would normally be lethal, and
attributed this to periodic low concentrations of oxygen. Based on research
in warmwater (20-22 C) fish ponds, Sel^si and Vamos (1976) projected a
"lethal line" relating acute ammonia toxicity and dissolved oxygen, below
which carp died. The line ran between 0.2 mg/liter Nltj at 5 mg/liter
dissolved oxygen and 1.2 mg/liter NH3 at 10 mg/liter dissolved oxygen.
Thurston et al. (in press, a) compared the acute toxicity of ammonia to
fathead minnows at reduced and normal dissolved oxygen concentrations; seven
96-hour tests were conducted within the range 2.6 to 4.9 mg/liter dissolved
oxygen, and three between 8.7 and 8.9 mg/liter. There was a slight positive
trend between 96-hour LC50 and dissolved oxygen, although it was not shown to
be statistically significant.
Alabaster et al. (1979) tested Atlantic salmon smolts in both fresh
water and 30 percent salt water at 9.6-9.5 and 3.5-3.1 mg/liter dissolved
oxygen. The reported 24-hour LC50 values at the higher oxygen concentrations
were about twice that at the lower.
Several studies have been reported on rainbow trout. Allan (1955)
reported that below 0.12 mg/liter NH3 and at about 30 percent oxygen
saturation, the median survival time was greater than 24 hours, but at the
same Concentration with oxygen saturation below 30 percent, the median
17
-------
survival time was less than 24 hours. Downing and Merkens (1955) tested
fingerling rainbow trout at three different concentrations of NH-j at five
different levels of dissolved oxygen. They reported, in tests lasting up to
17 hours, that decreasing the oxygen from 8.5 to 1.5 mg/liter shortened the
periods of survival at all ammonia concentrations, and that a decrease in
survival time produced by a given decrease in oxygen was greatest in the
lowest concentration of NH^. Merkens and Downing (1957), in tests which
lasted up to 13 days, also reported that the effect of low concentrations of
dissolved oxygen on the survival of rainbow trout was more pronounced at low
concentrations of NH3' Lloyd (1961a) found NHo to be up to 2.5 times
more toxic when dissolved oxygen concentration was reduced from 100 to about
40 percent saturation. Danecker (1964) reported 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-hour acute toxicity tests with
rainbow trout over the dissolved oxygen range 2.6 to 8.6 mg/liter. They
reported a positive linear correlation between 96-hour LC50 and dissolved
oxygen over the entire range tested.
Herbert (1956) reported on rainbow trout mortalities in a channel
receiving sewage discharge containing 0.05 to 0.06 mg/liter NH^. They
found that at 25-35 percent dissolved oxygen saturation more than 50 percent
of the fish died within 24 hours, compared with 50 percent mortality of test
fish in the laboratory at 15 percent dissolved oxygen saturation. The
difference was attributed to unfavorable water conditions below the sewage
outflow, including ammonia, which increased the sensitivity of the fish to
the lack of oxygen.
18
-------
There is a reduction in fish blood oxygen-carrying capacity following
ammonia exposure (Brockway 1950; Danecker 1964; Reichenbach-Klinke 1967;
Korting I969a,b; Waluga and Flis 1971). Hypoxia would further exacerbate
problems of oxygen delivery and could lead to the early demise of the fish.
(b) 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 un-ionized ammonia species, independent of the effect of
temperature on the aqueous ammonia equilibrium.
Hazel et al. (1971) tested ammonia with striped bass (Morone saxatilis)
and stickleback (Gas teros teus aculeatus) and found little difference in
toxicity between 15 and 23 C in fresh water, although both fish species were
slightly more resistant at the lower temperature; the influence of
temperature on toxicity was less for striped bass than for sticklebacks.
McCay and Vars (1931) reported that it took three times as long for brown
bullheads (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;
however, within the probable range tested (pH 7-8), the percent NH-j at the
higher test temperature is approximately three times that at the mean lower
temperature. Powers (1920) reported the toxicity of ammonium chloride to
goldfish, bluntnose minnow, and straw-colored minnow to be greater at high
temperatures than at low; however, in that study also no consideration was
given to the increase in relative concentration of NH-j as temperature
increased.
Thurston et al. (in press, a) reported that the acute toxicity of NH^
to fathead minnows decreased with a rise in temperature over the range 12 to
19
-------
22 C. Bluegill and fathead minnow were tested at low and high temperatures
of 4.0 to 4.6 C and 23.9 to 25.2 C, respectively; rainbow trout were tested
at 3.0 and 14.0 C (Reinbold and Pescitelli 1982b). All three species were
more sensitive to un-ionized ammonia at the low temperatures, with toxicity
being 1.5 to 5 times greater in the colder water; bluegill appeared to be the
most sensitive of the three species to the effect of low temperature on
ammonia toxicity.
Colt and Tchobanoglous (1976) reported that the toxicity of NH3 to
channel catfish decreased with increasing temperature over the range 22 to 30
C. LC50 values for bluegill, channel catfish, and largemouth bass at 28 to
30 C were approximately twice that at 22 C (Roseboom and Richey 1977). LC50
values for channel catfish tested in Iowa River water were 0.49 mg/liter
NH3 at 2.5 C and 0.56 mg/liter at 5.1 C (Miller and UNLV-EPA 1982). An
effluent containing ammonia as a principal toxic component showed a marked
decrease in toxicity to channel catfish over the temperature range 4.6 to
21.3 C (Gary 1976).
Herbert (1962) has reported that experiments with rainbow trout in his
laboratory suggest that the effect of temperature on their susceptibility to
NH-j toxicity is little if at all affected by temperature change; no details
were provided. The Ministry of Technology, U.K. (1968), however, has
reported that the toxicity of NH^ to rainbow trout was much greater at 5 C
than at 18 C. Brown (1968) reported that the 48-hour LC50 for rainbow trout
increased with an increase in temperature over the range 3 to 18 C; the
reported Increase in tolerance between -12 to ~18 C was considerably less
than that between ~3 to -12 C. Thurston and Russo (in press) reported a
relationship between temperature and 96-hour LC50 for rainbow trout over the
20
-------
temperature range 12 to 19 C; ammonia toxicity decreased with increasing
temperature.
Lloyd and Orr (1969) investigated the effect of temperature over the
range 10-20 C on urine flow rates of rainbow trout exposed to 0.30 mg/liter
NH^, and found no apparent temperature effect on the total diuretic
response of the fish, although the relative increase in urine production was
less at higher temperatures. From a study of the behavioral response of
bluegill to gradients of ammonia chloride it was hypothesized that low
temperatures increased the sensitivity of bluegill and interfered with their
ability either to detect ammonia after a certain period of exposure or to
compensate behaviorally for physiological stress caused by ammonia gradients
(Lubinski 1979; Lubinski et al. 1980).
The European Inland Fisheries Advisory Commission (1970) has cautioned
that at temperatures below 5 C the toxic effects of un-ionized ammonia may be
greater than above 5 C. The basis for such a statement is not clearly
documented in that report. Nevertheless, there is some merit to the argument
that a decrease in temperature may increase the susceptibility of fish to
un-ionized ammonia toxicity. It is important that this relationship be
further studied. The available evidence that temperature, independent of its
role in the aqueous ammonia equilibrium, affects the toxicity of NH3 to
fishes argues for further consideration of the temperature/ammonia toxicity
relationship.
(c) PH
Tha roxicity to fishes of aqueous solutions of ammonia and ammonium
compounds has been attributed to the un-ionized (undissociated) ammonia
present in the solution. Although there were observations in the early
literature that ammonia toxicity was greater in alkaline solutions, the
21
-------
earliest reported thorough study of the pH dependence of ammonia toxicity was
that of Chipman (1934). He concluded from experiments with goldfish,
amphipods, and cladocerans that the toxicity was a function of pll and
therefore of the concentration of undissociated ammonia in the solution.
Wuhrmann et al. (1947) discussed the importance of differentiating
between NH^ and NH^ when considering ammonia toxicity. They
summarized some unpublished experimental data indicating a correlation
between solution pH and ammonia toxicity to fish (indicated by persistent
loss of balance). Wuhrmann and Woker (1948) reported on the experiments
referred to in Wuhrmann et al. (1947); these were conducted using ammonium
sulfate solutions at different pH values on rainbow trout. Either four or
six fish were tested at each of nine ammonium sulfate concentrations. The
authors concluded from the experimental results that NH^ was much more
toxic than NH^+. Downing and Merkens (1955) tested rainbow trout at
different concentrations of ammonia at both pH 7 and 8. They reported a
consistency of results when ammonia concentration was measured as NH^-
Tabata (1962) conducted 24-hour tests (Table 5) on ammonia toxicity to
Daphnia (species not specified) and guppy at different pH values and
calculated the relative toxicity of N^/NH^"*" to be 190 for guppy (i.e.,
NH3 190 times more toxic than NH^+) and 48 for Daphnia. From tests of
the toxicity of ammonium chloride to juvenile coho salmon in flow-through
bioassays within the pH range 7.0 to 8.5, the reported 96-hour LC50 for NH3
was approximately 60 percent less at pH 7.0 than at 8.5 (Robinson-Wilson and
Seim 1975).
Armstrong et al. (1973) tested the toxicity of ammonium chloride to
larvae of prawn (Macrobrachium rosenbergii) in static six-day tests within
the pH range 6.8 to 8.3; test solutions were renewed every 24 hours. They
22
-------
'reported a 96-hour LC50 for NH3 at pH 6.83 which was approximately 70
percent less than that for pH 8.34. They concluded that the toxicity of
ammonia was not due solely to the NH3 "olecule, that in solutions of
different pH and equal NH3 concentrations survival was greatly reduced as
NH^+ levels increased. Tomasso et al. (1980) tested the toxicity of
ammonia at pH 7, 8, and 9 on channel catfish and reported that 24-hour NH-j
LC50 values were significantly higher at pH 8 than at pH 7 or 9.
Thurston et al. (1981c) tested the toxicity of ammonia to rainbow trout
and to fathead minnows in 96-hour flow-through tests at different pH levels
within the range 6.5 to 9.0. Results showed that the toxicity of ammonia, in
terras of NH3> increased at lower pH values. They concluded that NH^
exerts some measure of toxictty, and/or that increased H* concentration
increases the toxicity of NH3 •
Acute (96-hour) exposures of green sunfish and smallmouth bass were
conducted by McCorraick et al. (in prep.) and Broderius et al. (in prep.) at
four different pH levels over the range 6.5 to 8.7. 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 tested (8.7). LC50 values
found wltli rainbow trout for the ammoniacal portion (diammonium phosphate) of
a chemical fire retardant at two different pH levels indicated greater NH3
toxicity at lower pH; the LC50 at pH 7.0 was 0.15 mg/liter NH3 and at pH
R.O was 0.48 rag/liter NH3 (Blahra 1978).
(d) Acclimation and Fluctuating Exposures
The qviestion of whether fish can acquire an increased tolerance to
ammonia by acclimation to low ammonia concentrations is an important one. If
fish had an increased ammonia tolerance developed due to acclimation or
23
-------
conditioning to low ammonia levels, they would perhaps be able to survive
what otherwise might be acutely lethal ammonia concentrations.
Observations by McCay and Vars (1931) indicated that bullheads subjected
to several successive exposures to ammonia, alternated with recovery In fresh
water, acquired no immunity from the earlier exposures to the later ones. A
greater number of researchers have reported that previous exposure of fishes
to low concentrations of ammonia increases their resistance to lethal
concentrations. Vamos (1963) conducted a single experiment in which carp
which had been revived in fresh water for 12 hours after exposure to 0.67 or
0.52 mg/liter NHg for 75 min were placed in a solution containing 0.7
mg/liter NH3• The previously exposed fish exhibited symptoms of ammonia
toxicity in 60-85 min, whereas control fish developed symptoms within 20 min.
Redner and Stickney (1979) reported that blue tilapia acclimated for 35 days
to 0.52 to 0.64 mg/liter NH-j Subsequently survived 48 hours at 4.1
mg/liter; the 48-hour LC50 for unacclimated fish was 2.9 mg/liter.
Malacea (1968) studied the effect of acclimation of bitterling to
ammonium sulfate solutions. A group of ten fish was held in an acclimation
solution of 0.26 mg/liter NHg for 94 hours, after which the fish were
exposed to a 5.1 mg/liter NH3 solution for 240 min; a control group of ten
was treated identically, except their acclimation aquarium did not contain
added (MH^^SO^* The ratio of the mean survival times of "adapted" vs.
"unadapted" fish was 1.13; mean survival times for the adapted and unadapted
fish were 78 and 88 minutes, respectively, indicating somewhat higher ammonia
tolerance for adapted fish.
Fromm (1970) measured urea excretion rates of rainbow trout initially
acclimated to either 5 or 0.5 mg/liter NH3» then subjected to 3 mg/liter
24
-------
NH3' Fish previously exposed to 5 mg/liter NH3 excreted slightly less
urea than those exposed to the lower concentration. Lloyd and Orr (1969)
conducted acclimation experiments with rainbow trout and found that the rate
of urine excretion increased with a rise in the concentration of un-ionized
ammonia to which the fish were exposed. They presented some evidence for
acclimation of rainbow trout to sublethal levels of ammonia, although these
levels may be as low as 12 percent of the "lethal threshold concentration".
Acclimation was retained for 24 hours, but was not retained after three days.
They also suggested that environmental factors which affect the water balance
of fish may also influence susceptibility to ammonia toxicity. Fromm (1970)
acclimated goldfish to low (0.5 mg/liter) or high (5.0 or 25.0 rag/liter)
ambient NH^ for periods of 20 to 56 days and found that urea excretion rate
in subsequent 24-hour exposures to concentrations ranging from 0.08 to 2.37
rag/1iter was independent of the previous acclimation concentration or
duration.
Schulze-Wiehenbrauck (1976) subjected to lethal ammonia concentrations
two groups of rainbow trout (56 g and 110 g) which had been held for at least
three weeks at sublethal ammonia concentrations. In the experiment with
110-g fish, the sublethal acclimation concentrations were 0.007 (control),
0.131, and 0.167 mg/liter NH-jJ the fish from these three tanks were then
subjected to concentrations of 0.45, 0.42, and 0.47 mg/liter NHg,
respectively, for 8.5 hours. Fish from the two higher sublethal concentra-
tions had 100 percent survival after 8.5 hours in the 0.42 and 0.47 mg/liter
NH3 solutions, whereas fish ,from the 0.007 mg/liter NHj concentration had
only 50 percent survival in 0.45 mg/liter NH^• In the experiment with 56-g
fish, the acclimation concentrations were 0.004 mg/liter NH3 (control) and
0.159 nirf/liter NH35 these fish were placed in NH3 concentrations of 0.515
25
-------
and 0.523 mg/llter, respectively, for 10.25 hours. There was 100 percent
survival of the acclimated fish, and 85 percent survival of the control fish.
The results of these experiments thus showed an increase in resistance of
trout to high ammonia levels after prior exposure to sublethal ammonia
levels.
Alabaster et al. (1979) determined 24-hour LC50 values of NH3 for
Atlantic salmon smolts under reduced dissolved oxygen test conditions. Fish
acclimated to ammonia before oxygen reduction evidenced LC50 values 38 and 79
percent higher than fish without prior ammonia acclimation.
Brown et al. (1969) tested rainbow trout in static tests in which fish
were moved back and forth between tanks in which the ammonia concentrations
were 0.5 and 1.5 times a previously determined 48-hour LC50. 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 rain). If the fish were transferred at two-hour 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 was greater than those from exposure to the
constant concentration.
Thurston et al. (1981a) conducted acute toxicity tests on rainbow trout
and cutthroat trout in which fish were exposed to short-term cyclic
fluctuations of ammonia. Companion tests were also conducted in which test
fish were subjected to ammonia at constant concentrations. Median lethal
concentration (LC50) values in terms of both average and peak concentrations
of ammonia for the fluctuating concentration tests were compared with LC50
values for the constant concentration tests. Based on comparisons of total
dose exposure, results showed that fish were more tolerant of constant
concentrations of ammonia than of fluctuating concentrations. Fish subjected
26
-------
to fluctuating concentrations of ammonia at levels below those iicuteiy toxic
were subsequently better able to withstand exposure to higher fluctuating
concentrations than fish not previously so acclimated.
In static renewal exposures to ammonium chloride using river water as
the dilution water, fathead minnows were reported (Pitts 1980) to survive for
28 days exposures fluctuating from 0.1 mg/liter NH3 for four days to 0.2 or
0.3 mg/liter Nil-} for three days. Four-day excursions above 0.1 mg/liter to
concentrations of 0.42, 0.48, and 0.52 rag/liter resulted in 80 to 100 percent
mortality in 28 days, as did four-day excursions to 0.73 mg/liter. No
constant exposure tests were conducted simultaneously for comparative
purposes; however, constant exposure tests conducted approximately a year
earlier yielded LC50 values ranging from 0.6 to 2.4 mg/liter NHg •
In summary, there is reasonable evidence that fishes with a history of
prior exposure to some sublethal concentration of ammonia are better able to
withstand an acutely lethal concentration, at least for some period of hours
and possibly days. The relative concentration limits for both acclimation
and subsequent acute response need better definition and a more complete
explanation. Limited data on fluctuating exposures indicate that fish are
more susceptible to fluctuating than to constant exposure to equivalent NH^
dose concentrations. Much more research is needed to examine further the
effects of fluctuating and intermittent exposures under exposure regimes
simulating actual field situations.
(e) Carbon Dioxide
An increase in carbon dioxide concentrations up to 30 rag/liter decreases
total ammonia toKicity (Alabaster and Herbert 1954; Allan et al. 1958).
C02 causes a decrease in pH, thereby decreasing the proportion of
un-ionized ammonia in solution. Lloyd and Herbert (i960) found, however,
27
-------
that although total ammonia toxicity was reduced at elevated CC>2 levels,
the inverse was true when considering un-ionized ammonia alone; more NH-j is
required in low C(>2» high pH water to exert the same toxic effect as seen
in fish in high C02> low pH water. The explanation presented by Lloyd and
Herbert (1960) for the decreased toxicity of NH3 in low CC>2 water was
that Cr>2 excretion across the gills would reduce pH, and therefore NH3
concentration, in water flowing over the gills.
The basic flaw in Lloyd and Herbert's (1960) hypothesis has been
discussed in Broderius et al. (1977). C02 will only form protons very
slowly in water at the tested temperature. The uncatalyzed CC>2 hydration
reaction has a half-time of seconds or even minutes (e.g., at pH 8: 25
seconds at 25 C, 300 seconds at 0 C (Kern I960)), 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 to 1 second (Randall 1970; Cameron 1979). Thus
the liberation of C02 will have little, if any, effect on water pH or,
therefore, NH^ levels while the water body is in contact with the gills.
Hence the liberation of C02 across the gills can have little, if any,
effect on the NH3 gradient across the gills between water and blood.
Szumski et al. (1982) hypothesized that in the course of its excretion C02
is converted in the gill epithelium to H+ and HCO^" which then pass
directly Into the gill chamber where they cause an instantaneous pH
reduction. Their interpretation of the published literature on fish
respiratory physiology is questionable, and experimental evidence in support
of their evaluation is required before it can be given serious
consideration.
28
-------
. (f) Salinity
Herbert and Shurben (1965) reported that the resistance of yearling
rainbow trout to ammonium chloride increases with salinity up to levels of
30-40 percent seawater; above that level, resistance appears to decrease.
Katz and Pierro (1967) tested fingerling coho salmon at salinity levels of 20
to 30 parts per thousand (57 to 86 percent saltwater) and found that toxicity
of an ammonia-ammonium waste increased as salinity increased. These findings
are in agreement at the levels tested with those of Herbert and Shurben
(1965). Atlantic salmon were exposed to ammonium chloride solutions for 24
hours under both freshwater and 30 percent saltwater conditions; LC50 values
(Table 5) were 0.15 and 0.3 rag/liter NH3, respectively, in the two
different waters (Alabaster et al. 1979).
As was discussed in Willingham et al. (1979), decreased NH3 toxicity
with increased salinity may be partially explained, at least for low salinity
levels, by the fact that there is a slight decrease in the NH^ fraction of
total ammonia as ionic strength increases in dilute saline solutions
(Thurston et al. 1979). At higher salinity levels, however, the toxicity to
fishes of ammonia solutions must be attributable to some mechanism or
mechanisms other than the changes in the NH^+/NH3 ratio. Further work
is needed to confirm results already reported and to clarify the observed
mitigating effect of total dissolved solids.
(g) Presence of Other Chemicals
The presence of other chemicals may have an effect on ammonia toxicity,
and some experimental work has investigated this topic. Herbert and Vandyke
(1964), testing rainbow trout, determined the 48-hour LC50 value for a
solution of ammonium chloride and that for a solution of copper sulfate.
They reported that a solution containing a mixture of one half of each of
29
-------
these LC50 concentrations was also the 48-hour LC50 for the two toxicants
combined; i.e., the toxic response was simply additive. This information was
also reported by the Ministry of Technology, U.K. (1964); it is not clear
whether this was a separate study or the same study.
Shemchuk (1971) measured copper uptake in two-year old carp from
solutions of Cu(NH-j)^^ ; copper uptake in various fish tissues was
reported, but no information was provided about toxicity. Vamos and Tasnadi
(1967) applied cupric sulfate to a "carp pond" to reduce the concentration of
free ammonia and reported that this measure proved successful to reduce the
toxic effect of ammonia; few details were provided.
Ministry of Technology, U.K. (1962, 1963) reported on the results of
tests on rainbow trout in which 48-hour LC50 concentrations were determined
for solutions of ammonium chloride, zinc sulfate and mixtures of these two
salts. A fraction of each of those 48-hour LC50 concentrations, when
combined in such a way that those fractions equalled unity, provided a
mixture with a 48-hour LC50 concentration equal to that of either of the two
toxicants alone. Results were similar for tests conducted in waters with
alkalinities of 240 and 50 mg/liter CaC03.
Herbert (1962) studied the toxicity to rainbow trout of ammonia-phenol
mixtures. The mixtures contained fractions of the 48-hour LC50
concentrations of phenol and of ammonia; the combined fractions equaled
unity. The toxicity of the combined fractions approximated the toxicity of
either phenol or ammonia when tested separately but under test conditions of
similar water chemical characteristics. The same information was reported by
Ministry of Technology, U.K. (1961); it is not clear whether this was a
separate study or the same study.
30
-------
Brown et al. (1969) conducted 48-hour tests on rainbow trout in mixtures
of anraonia, sine, and phenol; the mixture coi\tain»d equal portions, by
48-hour LC50 concentration, of the three toxicants. They reported that each
chemical nominally contributed equally to the toxicity. In a second series
of three tests in which the mixture was adjusted to include approximately 75
percent of a 48-hour LC50 concentration of one toxicant and the balance split
equally between the other two, they reported that the principal toxicant
contributed about three-fourths of the toxicity.
Broderius and Smith (1979), in 96-hour flow-through tests with rainbow
trout, reported a synergistic effect for NH3 and HCN except at extremely
low concentrations. Rubin and Elmaraghy (1976, 1977) estimated the
individual and joint toxicities of ammonia and nitrate to guppy fry; the
toxicities of the two in mixture were additive, except at very low
ammonia-to-nitrate ratios. Tomasso et al. (1980) reported that elevated
calcium levels increased the tolerance to ammonia of channel catfish.
Derivation of Maximum Criterion for Fresh Water
(a) pH Dependence of Acute Ammonia Toxicity
The acute toxicity of total ammonia to aquatic organisms has been found
to increase markedly with pH, with LC50s declining by as much as an order of
magnitude per unit pll increase. Much of this variation can be accounted for
by expressing toxicity on the basis of un-ionized ammonia concentration
rather than total ammonia concentration, un-ionized ammonia being considered
the principal source of toxicity. Although such a mode of expression
substantially reduces the variation with pH, available data indicate that a
residual dependence exists, with NH^ LCSOs increasing with increasing pH
and the rate of increase declining as pH increases, apparently leveling off
at high pH.
31
-------
The task at hand was to select a suitable mathematical expression to
describe the pH dependence of LC50s, on an un-ionized ammonia basis, in the
pH 6.S-9.0 range (this range being dictated by the water quality criterion
for pH (U.S. Environmental Protection Agency 1977)) and to determine whether
the available data support the use of a common (i.e., for all species)
expression that has only a single species-dependent parameter. The data used
(Figure 1) were for Daphnia sp., rainbow trout, fathead minnow, and coho
salmon (Tabata 1962; Robinson-Wilson and Seim 1975; Thurston et al. 1981c).
This includes all available sets for which, for a given species, the same
investigators determined LC50s at a minimum of four pHs distributed over at
least 1.5 pH units in the pH 6.5-9.0 range. Furthermore, a minimum of six
data points (either by testing at more distinct pHs or by replication at some
pHs) was required so that meaningful regression analysis was possible.
Inspection of the data suggested that, for all data sets and for the pH
range of concern, log(LCSO) versus pH has a slope that decreases with
Increasing pH, nearing zero at the upper part of the range and perhaps
approaching a limiting value at the lower part of the range. A suitable
mathematical expression for such behavior is:
XI
L.C50 = v, / v~ H7 (1)
I + 10X3(X2-pH) v '
where XI is the limiting LC50 at high pH as the slope approaches zero,
X3 is the limiting slope of log(LCSO) vs. pH at low pH,
X2 allows the intermediate portion between the limits to occur at a
variable pH.
This equation is not only consistent with the form of the data, but also with
suggestions that the p!l dependence of ammonia toxicity is due to both
32
-------
5.0
I
i.o
a
0.5
7.0
OAPHNIA
8.0
PH
9.0
0.5
I
IO
0.2
o
10
So.,
0-05L_i—^
RAINBOW
TROUT
7.0 8.0 9.0
pH
I.Or
^ 0.5
10
^0.2
O.I
O
0.05
2.0r
7.0
COHO
SALMON
8.0
9.0
PH
i.o
10
O>
O
in
o
0.2
O.I
FATHEAD
MINNOW
7.0
8.0
9.O
PH
Figure 1.
Acute NH3 toAicity at different pH values (data from Taoata 1962,
Robinson-Wilson and Seim 1975, Thurston et al. 1981c). Dotted
lines « regression based on individual data set; solid lines =
regression based on pooled data sets.
33
-------
un-ionized and cationic ammonia being toxic, but with different potencies
(Armstrong et al. 1978; Thurston et al. 1981c).
Estimates for XI, X2, and X3 were obtained (Erickson 1982) for each of
*
the available data sets by least-squares, nonlinear regression, using
log(LC50) as the dependent variable and pH as the independent variable. A
logarithm transform was employed because the errors in LC50 estimates are
largely proportional to LC50.
The results of these analyses indicated X2 and X3 did not differ
significantly (at the 0.10 confidence level) between data sets and were in
fact quite similar (X2 » 7.3-7.7, X3 = 0.7-1.2). The data sets were
therefore pooled for further regression analysis in which X2 and X3 were
assumed to be the same for all sets. Deviations of this pooled analysis from
the individual regressions (Figure 1) were not statistically significant and
were, in fact, quite minor, the maximum deviation being less than 0.08 log
units and the average being less than 0.03 log units. The individual
regressions accounted for 89%, 96%, 99%, and 96% of the variance of log(LCSO)
in the Daphnia, rainbow trout, coho salmon, and fathead minnow data sets,
respectively. Respective percentages for the pooled analysis were 87%, 92%,
99%, and 92%.
It was therefore concluded that the common values for X2 (7.32) and X3
(1.03) from the pooled analysis could be justifiably applied to these data
sets. Equation 1 can then be interpreted as having a data set-dependent
numerator, the limiting LC50 at high pH (XI), and a set-independent
denominator, a multiplicative, pH correction factor (1 + 101>^3(7.32-pH)^.
Four other d.-ita sets were available for which acute ammonia toxicity to
a species was tested by the same investigators at three or more distinct pHs
distributed over at Least 1.5 pH units in the pH 6.5-9.0 range. These sets
34
-------
• .were for Macrobrachium rosenbergii (a saltwater prawn), channel catfish,
green sunfish, and sraallmouth bass (Armstrong et al. 1978; Tomasso et al.
1980; McCormick et al., in prep.; Broderius et al., in prep.). These data
sets were not used in the previously-discussed analysis due to inadequate
size, but rather were used to evaluate the applicability of the relationship
derived above (Erickson 1982) . A line was fit to each set by taking the
above common estimates for X2 and X3 and calculating XI as the geometric
average of LC50 x (1 -I- 101 -03(7 -32-pH)) for the individual data (this
minimizes the variance of the residuals between the observed log (LC50)s and
the fitted line). Two of the sets (prawn, green sunfish) showed a marked pH
dependence qualitatively identical with the previous discussion and had good
P
quantitative agreement with the lines so estimated (r = 99% and 83%,
respectively).
Of the other two sets, one (smallmouth bass) showed a marked increase of
LCSOs with pH, but with a noticeably different shape in the pH range of
Interest; the other set (channel catfish) showed no apparent pH trend at all.
2
Neither of the lines fitted to these two sets produced a significant r ,
but they also did not deviate enough from the data to reject statistically
either the general mathematical model or the common estimates for X2 and X3.
Furthermore, the residuals between the data of these two sets and the fitted
lines were at most 0.3 log units (a factor of 2) and had standard deviations
of only 0.13 log units (a factor of 1.5). Additionally, if the common
estimates of X2 and X3 are used to correct an LC50 in these sets from the pH
it was measured at to a pH of another datum in the set, the discrepancy
between the two LC50s are lar^e (>0.2 log units) only if the pH difference is
large (>1 unit) and one of the pHs is <7.5.
-------
Available acute toxiclty data therefore suggest that the proposed
relationship will perform well in most circumstances and will produce large
errors only under restricted circumstances. Although the proposed
relationship cannot be considered universally applicable, especially if
residuals between fitted lines and data are not to exceed measurement error,
the alternatives of using no pH relationship or of basing criteria only on
species tested over a range of pHs are clearly less desirable.
Deviations of some data sets from the proposed relationship are probably
due to a combination of experimental error, species effects, and temperature
effects. The relative contributions of each source are uncertain. It may be
possible in the future to develop parameter estimates that better account for
variations due to temperature and species, but the current data base will not
support such an exercise. Of course, in site-specific applications, if
evidence exists for significantly different pH relationships for species of
importance to setting criteria, appropriate modifications should be
considered.
(b) Temperature Dependence of Acute Ammonia Toxicity
Investigations of the temperature dependence of LCSOs on an un-ionized
ammonia basis have produced conflicting results, varying from constancy with
temperature to major increases with temperature (see earlier discussion).
The relative contributions to this variability of species differences,
experimental error, and the relationship of test temperatures to species
temperature tolerance are uncertain and not definable from available data.
Lacking a broadly-applicable description of the temperature dependence
of ammonia toxicity, it will be assumed that, above 10 C, LC50s on an
un-ionized ammonia basis are constant with temperature. Where LC50s do
36
-------
increase with temperature, this assumption will result in overprotection at
temperatures above that at which data most important to the criterion were
gathered and underprotection at lower temperatures. Because data for
criteria were mostly collected in the 10-25 C range, large errors probably
will not accumulate over this range, due to limited extrapolation from tested
temperatures. Extension of such an assumption to low temperatures is
questionable, however, because the paucity of the data in this range makes
such a move a substantial extrapolation and because the temperature effects
data presented earlier, unlike at higher temperature, consistently indicated
increased sensitivity associated with low temperatures. At temperatures less
than 10 C, it will be assumed that LC50s on a total ammonia basis are
constant. Due to the effect of temperature on
the pK of ammonia, from 10 C to 0 C this is equivalent to approximately a
two-fold lowering of the LC50s on an un-ionized ammonia basis. Such a
lowering is not inconsistent with temperature effects discussed earlier and
constitutes a very simple algorithm.
Of course, as for pll, where data for a species of importance to the
setting of a criterion value contradicts the above assumptions regarding
temperature, appropriate modifications should be made.
(c) Application of pH and Temperature Relationships of Acute Ammonia Toxicity
to Determination of Final Acute Values
A Species Mean Acute Value (SMAV) Is the geometric average of the acute
values (AVs), usually LC50s, available for a given species. A Family Mean
Acute Value (FMAV) is the geometric average of the SMAVs available for a
given family. A Final Acute Value (FAV) for a material is an estimate of the
-------
FMAV at the 0.05 cumulative proportion in the cumulative distribution of
FHAVs for all families tested for that material. These computations (see
Guidelines) are not a subject of this discussion, but their application to pH
and temperature dependent data is.
The existence of pH and temperature dependence in AVs requires that they
be corrected to a common pH and temperature basis before computing a FAV.
After a FAV at this common pH and temperature is computed, it can be applied
to other pHs and temperatures using the same equations used to correct the
AVs.
Since AVs on an un-ionized ammonia basis are assumed constant with
temperature above 10 C, the "common" temperature can be the whole temperature
range XIO C. Only AVs measured at <10 C must be temperature corrected, to 10 C,
based on the assumption that AVs on a total ammonia basis are constant
with temperature below 10 C. The temperature correction equation for AVs
from <10 C is therefore:
(1 + ioPKT-pH)
10 (1 + 10PK10-PH) T
where AV-p is an AV measured at a temperature T <10 C, AV^Q is the
estimated AV at temperatures >10 C, pH is the pH at which the AV was
measured, pK-p is the pK of ammonia at the measurement temperature (=0.902 +
) , and pK^Q is the pK at 10 C (=9.73) (pK/temperature relationship
,- • ?7'-- _y
from Emerson et al. 1975).
After any necessary temperature corrections are made, Equation 1, with
the common estimates for X2 and X3, can be applied for correction to a common
pH. Equation 1 has a single species-dependent parameter, XI, the limiting AV
at high pH, hereafter called LIMAV. This limiting value will be considered
38
-------
the common pH value. All available AV^gS will therefore be converted to
LIMAVs by the relationship:
LIMAV - AV1Q x (1 + io1.03(7.32-pH))
The limiting SMAV (LIMSMAV) for a species then can be computed as the
geometric average of the LIMAVs for that species, and the limiting FMAV
(1IMFMAV) can be computed as the geometric average of the LIMSMAVs for that
family. The limiting FAV (LIMFAV) for un-ionized ammonia then can be
computed from the LIMFMAVs available, by the same procedures used for
computing FAVs from FMAVs for any material. A FAV on an un-ionized ammonia
basis at a particular pH for temperatures XLO C can be computed as:
_ LIMFAV _
FAV10 = l + 101.03(7.32-PH) <4>
A FAV on an un-ionized ammonia basis at a temperature T < 10 C can be
computed from the >10 C FAV at the same pH as follows:
(I + l09.73-pH)
(5)
Application of these techniques to the data proceeded as follows. AVs
from Table 1 were corrected for temperature (where necessary) and pH and
averaged to obtain the LIMSMAVs and LIMFMAVs reported in Table 3. The fifth
percentile was estimated, by the Guidelines method, to be 0.74 mg/liter
NH3 • This number, however, exceeds the LIMSMAVs of important species
(walleye and rainbow trout) and thus, by Guidelines procedures, should be
decreased to the lower of these two LIMSMAVs. Additionally, the rainbow
trout data in Table 1 indicate that sexually mature fish (M kg) are
significantly more sensitive than the average of the tested fish. Since a
species is not protected if such an important life stage is not protected,
the LIMFAV was lowered to 0.30, the geometric average of the LIMAVs of
rainbow trout in this size range. Thus, for temperatures >10 C:
39
-------
0.30
3 (1 + 101.03(7.32-pII))
For temperatures <10 C:
0.30 (1 + 109-73-pH)
FAVl " (1 + K)l-03(7.32-pH)) x (1 4
Available Information indicates that the acute response to ammonia is
rapid. Therefore, a criterion based on the FAV cannot be treated as an
average over any appreciable span of time, since such averaging implicitly
allows significant excursions over the criterion value for an appreciable
fraction of the averaging period and thus allows the occurrence of a time
sequence of concentrations which would violate the intent of the criterion.
Consequently, the criterion based on the FAV is a concentration that at no
time should be exceeded.
Saltwater Invertebrates
Data on acute toxicity of ammonia to saltwater invertebrate species are
very limited. LC50 values are summarized in Table 1 for five species
representing five families. A 96-hour LC50 value (Table 1) of 1.5 mg/liter
NH3 was reported (Linden et al. 1979) for the copepod, Nitocra spinipes.
Lethal effects of NH^Ci on the quahog clam (Mercenaria mercenaria) and
eastern oyster (Crassostrea virginica) were studied by Epifanio and Srna
(1975) (Table 1). There was no observed difference in susceptibilities
between juveniles and adults of the two species. Armstrong et al. (1978)
conducted acute toxicity tests (6 days) on ammonium chloride using prawn
larvae (Macrobrachium rosenbergii). LC50 results (Tables 1, 5) were highly
pH-dependent. Acute toxicity of NH^Cl to penaeid shrimp was reported as a
48-hour composite LC50 value of 1.6 mg/liter NH^ for seven species pooled,
including the resident species Penaeus setiferus (Wickins 1976). The acute
40
-------
' toxicity of NH^Cl to the carldean prawn, >1. rosenbergii, was reported
(Wicklns 1976) as LT50 values of 1700-560 minutes at concentrations of 1.74
to 3.41 mg/liter NH3 (Table 5). Hall et al. (1978) measured the acute
toxicity of NH^Cl to grass shrimp (Palaemonetes pugio) (Table 5). Catedral
and coworkers (1977a,b) investigated the effect of NH^Cl on survival and
growth of Penaeus monodon; larvae had lower tolerance to ammonia compared
with postlarvae. Brown (1974) reported a time to 50 percent mortality of 106
min for neraertine worm (Cerebratulus fuscus) at 2.3 mg/liter NH3 (Table 5).
Effects of NH^Cl solutions on American lobster (Homarus americanus)
were studied by Delistraty et al. (1977). Their tests were performed on
fourth stage larvae which they believed to be the most sensitive life stage,
or nearly so. They reported a 96-hour LC50 value (Table 1) of 2.2 mg/liter
NH3 and an incipient LC50 (Table 5) of 1.7 mg/liter NH3. A "safe"
concentration of 0.17 mg/liter NH3 was tentatively recommended.
Saltwater Fishes
Very few acute toxictty data are available for saltwater fish species.
Holland et al. (1960) reported the critical level for chinook salmon
(Oncorhynchus tshawytscha) to be between 0.04 and 0.11 mg/liter NH3 and for
coho salmon to be 0.134 rag/liter NH3« A static test with coho salmon
provided a 48-hour LC50 value (Table 5) of 0.50 mg/liter NH3 (Katz and
Pierro 1967). Atlantic salmon smolts and yearling rainbow trout tested for
24 hours in 50 and 75 percent saltwater solutions exhibited similar
sensitivities to ammonia (Ministry of Technology, U.K. 1963).
41
-------
CHRONIC TOXICITY TO ANIMALS
The following discussion of chronic and partial chronic ammonia toxicity
includes both data used in the derivation of the numerical 30-day average
criterion (Table 2 data) and data that were not included in the criterion
derivation, but that are important for an understanding of long-terra lethal
and sublethal effects of ammonia on aquatic organisms (Table 5 data).
Freshwater Invertebrates
Few studies have been conducted on long-term exposure of freshwater
invertebrates to ammonia, and life-cycle tests were conducted only for
cladocerans.
The lowest concentrations affecting reproduction in two life-cycle tests
(Table 2) with ID. magna were 0.74 and 0.76 mg/liter NH-j (Russo et al., in
prep.); a 28-day LC50 of 1.53 mg/liter NH^ was reported. In a chronic test
(Table 2) conducted by Reinbold and Pescitelli (1982a), reproduction and
growth of I), magna were affected at a concentration of 1.6 mg/liter NH^- A
life-cycle test (Table 2) with £. acanthina (Mount 1982) showed effects on
reproduction at a concentration of 0.463 mg/liter NH3•
Two tests lasting 42 days were conducted by Anderson et al. (1978) on
Nl^Cl with the fingernail clam, Musculium transversum (Table 5).
Significant mortalities (67 and 72 percent) occurred in both tests at a
concentration of 0.7 mg/liter NH^. In one of the experiments, significant
reduction in growth was observed after 14 days of exposure to 0.41 mg/liter
NH3• Sparks and Sandusky (1981) reported that fingernail clams exposed to
0.23 and 0.63 mg/liter NH3 incurred 36 and 23 percent mortality,
respectively, In four weeks; after six weeks, 47 percent mortality occurred
at 0.073 rig/liter NH^, and 83 percent mortality occurred at 0.23 and 0.63
42
-------
mg/liter NH-^- No growth at All occurred In all test chambers (conoontra-
tions of 0.036 mg/liter NH3 and higher) other than the control after six
weeks (Table 5).
Two partial chronic tests, of 24- and 30-days' duration, were conducted
by Thurston et al. (in prep., a) with the stonefly Pteronarcella badia (Table
5). Adult stonefly emergence was delayed with increasing ammonia concentra-
tion, and little or no emergence occurred at concentrations exceeding 3.4
mg/liter NH-j. There was no significant relationship between food
consumption rates of nymphs and concentrations up to 6.9 mg/liter NH-j •
LC50 values for 24- and 30-day exposures were 1.45 and 4.57 mg/liter NH3,
respectively.
Freshwater Fishes
A number of researchers have conducted long-term ammonia exposures to
fishes, including complete life-cycle tests on rainbow trout and fathead
minnows. Several '<1nds of endpoints have been studied, including effects on
spawning and egg incubation, growth, survival, and tissues.
The effects of prolonged exposure (up to 61 days) to ammonia of pink
salmon early life stages was studied by Rice and Bailey (1930). Three series
of exposures were carried out, beginning at selected times after hatching:
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. NHg
concentrations ranged from 0 (control) up to 0.004 mg/liter. For fry at the
highest concentration of 0.004 mg/liter NH3 (Table 2), significant
decreases in weight were observed for all three exposure groups. At a
concentration of 0.0024 mg/liter NH3 (Table 2) the group of fry exposed for
40 and 61 dayu were significantly smaller, whereas a concentration of 0.0012
43
-------
mg/liter had no significant effect on growth. Effects were consistently more
adverse for the 61-day-exposed fish.
Thurston et al. (In press, b) tested rainbow trout in a laboratory study
In which adult fish exposed for five months to concentrations of ammonia from
0.01 to 0.07 mg/llter NH^ Spawned of their own volition; baskets containing
crushed rock served as the spawning substrate. 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 (F^) for four
years, and the second filial generation (F2) for five months. Pathologic
lesions were observed in both parental and F^ fish when ammonia concentra-
tions reached and exceeded 0.04 mg/liter NH^ (Table 2). Measurements of
blood ammonia concentrations in four-year-old F^ fish showed an increase
when test water conditions reached or exceeded 0.04 mg/liter NH-j • Trout
exposed for 52 months from day of hatching showed no dose/growth relationship
,it 10, 15, 21, and 5?. months.
Burkhalter and Kaya (1977) tested ammonia at concentrations from 0.06 to
0.45 mg/liter NH-j On fertilised eggs
-------
. after hatching, hypertrophy of secondary gill lamellae epithelium occurred at
0.23 rag/liter NH3, and karyolysis and karyorrhexis in the secondary gill
lamellae were observed after 28 days at 0.34 mg/liter NH3 and higher.
CalaraarL et al. (1977, 1981) exposed rainbow trout to ammonium chloride
solutions for 72 days, beginning one day after fertilization and ending when
fry were fed for 30 days. A 72-day LC50 of 0.056 mg/liter NH3 was
calculated (Table 5); 23 percent mortality occurred at a concentration of
0.025 rag/liter NH3 (Table 2). Examination of 986 rainbow trout embryos at
hatching stage after exposure to NH3 Concentrations of 0.010 to 0.193
mg/liter for 24 days showed an increase in macroscopic malformations with
increasing ammonia concentration. Kinds of deformities observed were varying
degree of curvature from median body axis, which in extreme cases produced a
complete spiral shape, 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/liter NH-j > 60 percent of the observed fish were malformed.
Microscopic examination at hatching of 128 larvae from the same exposure
showed abnormalities on the epidermis and pronephros that 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
abnormalitLes were observed after exposure to concentrations over 0.025
mg/liter NH3 for epidermis and 0.063 mg/liter NH3 for pronephros.
Broderius and Smith (1979) tested four-week-old rainbow trout fry for 30
days at concentrations of ammonia (reported grahically) ranging from -0.06 to
0.32 rag/liter NH3 (Table 5). Growth rate at -0.06 mg/liter NH3 was
45
-------
comparable to that of controls; above -0.10 mg/liter NH-j growth rate
decreased, correlated with Increased NH3 concentration. The survival at
0.32 mg/liter NHg was reduced to 70 percent that of the controls. Schulze-
Wiehenbrauck (1976) tested juvenile rainbow trout, approximately
one-half-year-old but of different sizes, for periods of time from two to
seven weeks, and at ammonia concentrations from 0.012 to 0.17 mg/liter NH3 •
He concluded that 0.05 mg/liter NHj caused a slight decrease in growth
during the first 14-day interval on nonacclimatized fish, but that decrease
was completely compensated in the next growth interval; exposure to 0.13
mg/liter NH-j (apparently for 3 or A weeks) did not affect growth, food
consumption, or food conversion.
Smith (1972) and Smith and Piper (1975) reared young rainbow trout at
three concentrations of ammonia (averaging 0.006, 0.012, and 0.017 mg/liter
NH^) for a period of one year. There was no significant difference in fish
growth reported among the three concentrations at four months. There was,
however, a difference reported at 11 months; the fish at 0.012 and 0.017
mg/liter NH3 weighed 9 and 38 percent less than the fish at 0.006 mg/liter.
Microscopic examination of tissues from fish exposed to the highest
concentration, examined at 6, 9, and 12 months, showed severe pathologic
changes in gill and liver tissues. Gills showed extensive proliferation of
epithelium which resulted in severe fusion of gill lamellae which prevented
normal respiration. Livers showed reduced glycogen storage and scattered
areas of dead cells; these were more extensive as exposure titae increased.
Ministry of Technology, U.K. (1968) reported on tests in which rainbow
trout wore exposed for three months to concentrations of 0.069, 0.14, and
0.23 mg/liter NH3• The cumulative mortality of a control group (0.005
46
-------
tog/liter NTH^) was -2 percent. Cumulative .nortallty «t 0.069 and O.lt
mg/liter NH-j was ~5 percent, and that at 0.28 mg/llter was -15 percent.
Reichenbach-Klinke (1967) performed a series of one-week ammonia tests on 240
fishes of nine species (including rainbow trout, goldfish, northern pike
(Esox lucius), carp, and tench) at concentrations of 0.1 to 0.4 mg/liter
NH3• He observed swelling of and diminishing of the number of red blood
cells, inflammations, and hyperplasia. Irreversible blood damage occurred in
rainbow trout fry in ammonia concentrations above 0.27 mg/liter NH3 - He
also noted that low NH^ concentrations inhibited the growth of young trout
and lessened their resistance to disease.
Smart (1976) exposed rainbow trout to 0.30 to 0.36 mg/liter NH3 (Table
5); 81 percent mortality occurred over the 36-day duration of the test, with
most deaths occurring between days 14 and 21. Microscopic examination of the
gills of exposed rainbow trout 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
these 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.
Fronrn (1970) exposed rainbow trout to <0.0005 and 0.005 mg/liter NH3
for eight weeks. Subsequent examination of the gill lamellae of fish from
the trace concentrations showed them to be long and slender with no
significant pathology. Fish exposed to 0.005 mg/liter NH-j had shorter and
thicker gill lamellae with bulbous ends; some consolidation of lamellae was
noticed. Photomicrographs revealed that many filaments showed limited
hyperplasia accompanied by the appearance of cells containing large vacuoles
whose contents stained positive for protein. Other lamellae showed a
47
-------
definite hyperpLasi-i ot the epithelial layer, evidenced by an Increase Li Uie '
number of cell nuclei.
Thurston et al. (1978) studied the toxicity of ammonia to cutthroat
trout fry in flow-through tests which lasted up to 36 days (Table 5).
Results of duplicate tests on 1.0-g fish both showed 29- and 36-day LC50
values of 0.56 mg/liter NT!-} • Duplicate tests on 3.3-g fish provided 29-day
LC50 values of 0.37 and 0.34 mg/liter, slightly less than those of the 1.0-g
fish. Tissues from heart, gastrointestinal tract, and thymus of cutthroat
trout fry exposed to 0.34 mg/liter NH^ for 29 days were comparable to those
of control fish. However, gills and kidneys of exposed fish showed
degenerative changes. Gills showed hypertrophy of epithelium, some necrosis
of epithelial cells, and separation of epithelium due to edema; kidneys
showed mild hydropic degeneration and accumulation of hyaline droplets in
renal tubule 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 o£ experiments
(temperature = 13 C) was conducted within the range 0.001 to >6.6 mg/liter
NH-j beginning with the "formed embryo" stage; the experiment lasted 53
days. Accelerated hatching was observed with increasing (NH^^^G^
concentrations, but concentrations X).16 rag/liter NH^ were lethal in 12-36
hours to emerging larvae. Because (NH^^CO-j was used as the toxicant,
the pll in the test aquaria Increased from 6.7 to 7.6 with increasing NH|j
concentration. Growth inhibition was observed at 0.07 mg/liter NH-j (Table
?). Tissue disorders wore observed in eyes, brains, fins, and blood of
MlanM^* salmon embryos and larvae exposed to concentrations from 0.16 to
>6.6 mg/liter NH^, with increased degree of symptom at increased ammonia
concentrations. Effects observed included erosion of membranes of the eyes
48
-------
and shedding of the crystalline lens, dilation of blood vessels in liver and
brain, accumulation of blood in the occipital region and in intestines.
Reaction to light and mechanical stimulation gradually disappeared with
increased ammonia concentration, and the pulseheat 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 color to become paler than it was after hatching. At
concentrations up to 0.07 rag/liter NHj no significant morphological
differences were observed.
A second series of experiments (temperature = 16.5 C) was carried out
in the 0.001 to 0.32 rag/liter NHj concentration range, and began with
larval salmon (Samylin 1969). Concentrations of 0.21 rag/liter NH3 and
higher were lethal and caused weight loss in fry; 0.001 to 0.09 rag/liter
NH^ caused a decrease in weight gain, although no differences in feeding
activity, behavior, or development were observed in these concentrations
compared to controls. Dissolved oxygen concentrations in this second series
of experiments dropped as low as 3.5 mg/liter.
Burrows (1964) tested fingerling chinook salmon for six weeks in outdoor
raceways into which ammonium hydroxide was Introduced. Two experiments were
conducted, one at 6.1 C and the other at 13.9 C, both at pH 7.8. In both
cases fish were subsequently maintained in fresh water for an additional
three weeks. A recalculation of Burrows' reported un-ionized ammonia
concentrations, based on more recent aqueous ammonia equilibrium tables,
indicates that the concentrations at 6.1 C were 0.003 to 0.006 mg/liter
NH3> and at 13.9 C were 0.005 to 0.011 mg/liter 1^3. At both
temperatures some fish at all ammonia concentrations showed excessive
proliferation and clubbing of the gill filaments; the degree of proliferation
49
-------
was progressive for the first four weeks, after which no measurable increase
was discernible. Examination of a sample of the fish tested at 6.1 C after
three weeks in fresh water indicated no recovery had taken place from the
extensive proliferation. In the experiment with larger fish at 13.9 C a
marked recovery from hyperplasia was noted after the three-week fresh water
exposure period. In the first experiment the proliferated areas had
consolidated; in the second they had not. Burrows postulated that continuous
ammonia exposure is a precursor of bacterial gill disease.
Buckley et al. (1979) exposed duplicate groups (90 fish each) of
hatchery-reared coho salmon for 91 days to "river-water" solutions of NH^Cl
at concentrations of 0.019 to 0.33 mg/liter Nl^; these were compared with
control groups reared at 0.002 mg/liter NI^- Hemoglobin content and
hematocrit readings were reduced slightly, but significantly, at the highest
concentration tested, and there was also a greater percentage of immature
erythrocytes at the highest concentration. Blood ammonia and urea
concentrations were not significantly different after 91 days, regardless of
concentration of ammonia to which the fish were exposed. Rankin (1979)
conducted ammonia tests with embryos of sockeye salmon (Oncorhynchus nerka)
from fertilization to hatching. Total embryo mortality occurred at
concentrations of 0.49 to 4.9 mg/liter NH-j; times to 50 percent mortality
at these concentrations were 40 to 26 days. Mortality of the embryos exposed
to 0.12 mg/liter NTl^ was 30 percent, and time to 50 percent mortality was
66 days.
Two full life-cycle ammonia toxicity tests (291 and 337 days) were
conducted with fathead minnows (Thurston et al., in prep., b). 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. No statistically significant difference was
observed based on spawning data (number of egg lots, egg lot size, egg lots
per female, eggs per female per day) for any of the concentrations tested, up
to 0.96 mg/liter NH3• However, there was a significant effect of ammonia
on hatching success (Table 2), with the number of fry hatching decreasing as
NH-j concentration increased to 0.187 mg/liter NH^ and higher; no effect
on hatching success was observed at concentrations of 0.088 mg/liter and
lower. Also, there was some indication that length of time for incubation
from spawning to hatching increased with increasing NH3 Concentrations. No
effect on fish growth was observed for either parental fish or progeny after
60 days' exposure and at exposure termination. Significant mortalities
occurred among the parental generation at concentrations of 0.9 to 1.0
mg/liter NH3 after 30 and 60 days' exposure, and there were significant
mortalities among progeny at concentrations of 0.2 to 0.4 mg/liter NH-j
after 30 and 60 days' post-hatch exposure.
Tissues from fathead minnows subjected to prolonged (up to 337 days)
ammonia exposure were examined, including brain, heart, gills, kidneys,
liver, and gastrointestinal tract (Smith 1981; Thurston et al., in prep., b).
Growths, some massive, were observed on heads of several fish
exposed to concentrations of 0.425 and 0.955 mg/liter NHg, and swollen
darkened areas were observed on heads of several fish held at 0.216 and 0.228
mg/liter. Grossly and histologically the severity of the lesions, which
varied from mild to severe, was positively correlated with ammonia
concentration. Lesions appeared to be a connective tissue type that
51
-------
originated from the raeninx primativa covering the brain. At the higher
ammonia concentrations proliferated tissue often completely surrounded the
brain but was not observed around the spinal cord. Pathological changes were
not observed in other tissues.
An early-Hfe-stage test initiated at the blastula stage of embryo-
genesis and extending through 39 days post-hatching was conducted with green
sunfish by McCormick et al. (in prep.). Retardation of growth of green
sunfish exposed from embryo through juvenile life stages was found at NHg
concentrations of 0.489 mg/liter and higher, but not at 0.219 rag/liter and
less (Table 2). In a long-term test on green sunfish, Jude (1973) reported
that for treatments greater than 0.17 mg/liter NHg, mean fish weight
increased less rapidly than controls after introduction of toxicant over the
next four days. Thereafter, fish exposed to 0.26 and 0.35 mg/liter NHj
grew at an increasing rate while fish exposed to 0.68 and 0.64 mg/liter NH^
remained the same for 12 days before greater increases in growth occurred.
An early-life-stage test with bluegill from embryo through 30 days
post-hatch was conducted on ammonia by Smith and Roush (in prep.).
Significant retardation of growth due to ammonia exposure was observed at
0.136 mg/liter NH^; the no-observed-effect concentration was reported to be
0.063 ing/liter NH3 (Table 2).
Broderius et al. (In prep.) conducted four simultaneous early-life-stage
ammonia tests with smallmouth bass. These were carried out at four different
pH levels, ranging from 6.6 to 8.7, to examine the effect of pH on partial
chronic ammonia toxicity. Exposure to ammonium chloride solutions began with
two- to three-day-old embryos and lasted for 32 days. The effect endpoint
observed was growth, and ammonia was found to have a greater effect on growth
at lower pH levels than at high. NH3 concentrations Cound to retard growth
-------
(table 2) ranged from 0.05S8 mg/liter at pH 6.60 to 0.865 mg/Liter at pH
8.68.
Early-life-stage tests (29-31 days' exposure) on ammonium chloride with
channel catfish and white sucker were conducted by Reinbold and Pescitelli
(1982a). No significant effect on percent hatch or larval survival was
observed for channel catfish at concentrations as high as 0.583 rag/liter
NH3 and for white sucker as high as 0.239 mg/liter NH3• Significant
retardation of growth, however, occurred for channel catfish at
concentrations of 0.392 mg/liter NHg and higher and for white sucker at
0.070 mg/liter NH3 and higher (Table 2). A delay in time to swim-up stage
was also observed for both species at elevated (0.06 to 0.07 mg/liter Nl^)
ammonia concentrations.
Robinette (1976) cultured channel catfish fingerlings for periods of
approximately one month at concentrations of 0.01 to 0.16 mg/liter NH3«
Growth at 0.01 and 0.07 mg/liter NH3 was not significantly different from
that of control fish; growth retardation at 0.15 and 0.16 mg/liter NH3 was
statistically significant. Colt (1978) and Colt and Tchobanglous (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/liter
NH3« Growth rate was reduced by 50 percent at 0.63 mg/liter NH3, and no
growth occurred at 1.2 mg/liter NH3» The authors hypothesized that growth
may be inhibited by high concentrations of NH^"*" and low concentrations of
Na+ in solution, and/or the NH^/Na4" ratio.
Ammonia exposure for 30 to 40 days of goldfish and tench resulted in
lesions .and diffuse necrosis of the caudal fin, causing it to degenerate
progressively to the point of breaking off by degrees, ultimately leaving
only a necrotized stump (Marchetti I960).
53
-------
Ver> li'-cle work has .n'eii ..uvu" to tiwost i «!:••; »• >vr ; >•» i • >•» .'. t ', v.- • .• .1.
factors on chronic ammonia to
-------
(1) At pH 7.7 and near 10 C, the threshold concentration for chronic
toxicity of ammonia to rainbow trout has been estimated to be 0.031
mg/liter NH-j • Given the importance of this species, the FCV must
be. at or below this number. The FCV at pH 7.7 and 10 C is
therefore set to 0.031 mg/liter NH3•
(2) Both the acute data and the chronic data of Broderius et al. (in
prep.) indicate little or no increase of effect concentrations with
pH above 7.7. The FCV is therefore set to 0.031 mg/liter for all
pH >7.7 at 10 C.
(3) At pH <7.7, the pooled salmonid chronic toxicity data (Table 2)
show trends consistent with smallmouth bass chronic toxicity data
(Broderius et al., in prep.) and the acute data. Thus, the pink
salmon datum at pH 6.4 is not only important in its own right, but
also likely lies close to where other trout and salmon would be at
pH 6.4. The FCV will therefore be set to 0.0021 (the geometric
average of the pink salmon data) at pH 6.4 and 4 C. Between pH 6.4
and pH 7.7, the log(FCV) will be assumed to vary linearly with pH,
a trend which causes it to pass close to other salmonid data and
which is similar to the trend in the acute toxicity pH relationship.
(4) Temperature effects will be assumed to be the same as for acute
toxicity. Based on this assumption, the pink salmon data point was
corrected upward, to 0.0034 at 10 C, before computing the pH
relationship between pH 6.4 and 7.7.
(5) Therefore, for temperatures _>1G C and pH>7.7,
FCV10 = 0.031
For temperatures MO C and pH <7.7,
0.031
100.74(7.7-pH)
55
-------
For temperatures <10 C,
(1 + 109.73-PH)
FCVT - FCVin x A. _ ~x
i 1 -^ 1 OP^T P" i
The criterion based on the FCV will be considered as a 30-day average.
Provisions to limit excursions above this criterion for time intervals
shorter than 30 days are believed to be unnecessary, given currently
available data.
(c) Acute/Chronic Ratios
Although the ratios of acute effect concentrations to chronic effect
concentrations were not used in the derivation of FCV above, they will be
used in site-specific applications and therefore merit some consideration
here. Acute/chronic ratios are available for ten species (Table 2). Because
these ratios vary so widely (2.8-44), their dependence on species and
physico-chemical factors should be evaluated so that they are properly
applied.
A clear trend exists in the species-dependence of the ratios. Of the
ten species, the five most acutely sensitive have ratios >11 and the five
least acutely sensitive have ratios <6. This has considerable significance
because ratios are applied to FAVs which reflect species with high acute
sensitivities. To produce an appropriate FCV therefore requires using a
ratio appropriate to such species. The question thus arises as to the range
of acute sensitivity from which ratios can be justifiably used. The five
highest ratios here cover the LIMSMAV range <1.8. This range includes a
large number of diverse families and the FAV is unlikely ever to exceed this
value; thus there is little reason ever to consider the five lowest ratios.
Within the LIMSMAV range <1.8, there is no clear trend of ratio with
56
-------
sensitivity; thus there is also no good reason to try to limit further this
set of ratios based on proximity to the FAV.
The sraallmouth bass data in Table 2 indicate that acute/chronic ratios
may increase with decreasing pH. This is consistent with the comment earlier
that the effect of pH on chronic toxicity in the 6.5-7.5 pH range is greater
than the effect of pH on acute toxicity. The large ratio for pink salmon
also suggests such a pH dependence of the ratio, if it is assumed all
salmonids have similar chronic and acute sensitivities. The paucity of data
makes firm conclusions impossible, but it is probably inappropriate to apply
the pink salmon ratio (measured at pH 6.4) to the pH range (>7.5) at which
other ratios were measured.
Eliminating the pink salmon ratio from the five highest ratios leaves
four ratios for diverse fish species (white sucker, fathead minnow, bluegill,
rainbow trout) that were measured at similar pHs (7.7-8.3). These four
ratios have a geometric average of 16 and have no apparent trends with pH,
temperature, or species sensitivity. This average is therefore as
appropriate as can be derived from the available data for application to FAVs
derived in the pH >7.5 range (this range being based on the range in which
the ratios were measured (7.7-8.3), with extrapolation to lower pH being
modest because of the indications of effects on ratios of pHs <7.5, and
extrapolation to higher pH being liberal because of the lack of significant
effects of pH in this range). No recommendation is made here about
appropriate ratios for lower pHs, except that they should probably be higher
than 16 and will require further testing.
Use of a constant ratio, of course, implicitly makes the assumption that
the pH dependency of chronic toxicity is the same, on a relative scale, as
for acute toxicity. Although this assumption was rejected earlier, the
57
-------
rejection was based on a broad pH range that extends below pH 7.5. For a
limited pH range and/or one restricted to pHs above 7.5, this assumption
should cause only minor errors as long as the ratios are, as advised above,
derived from data within the range in question.
An acute/chronic ratio should also be based on acute data consistent
with the FAV it is applied to. Specifically, if sensitivity varies with
organism size, the ratio should be modified based on this variation so that
it reflects acute data from the same size range as the acute data on which
the FAV Is based, or the original ratio should be applied to the value the
FAV would have had if a sensitive size range had not been used.
Saltwater Animals
Little information is available on long-term effects of sublethal
ammonia exposures on saltwater species, and no chronic data are available for
any saltwater fish species.
Three-week exposure (Wickins 1976) of P_. setiferus to NH^Cl yielded an
EC50 value (Table 5), based on growth reduction, of 0.72 mg/liter ^3. A
six-week test (Table 5) with M. rosenbergii resulted in reduction in growth
to 60-70 percent that of controls for prawn exposed to concentrations above
0.12 mg/Hter NH3 • A "maximum acceptable level" was estimated to be 0.12
mg/liter NH3• Armstrong et al. (1978) conducted growth tests (Table 5) on
NH^Cl using prawn larvae (M. rosenbergii). Retardation in growth was
observed at sublethal concentrations (0.11 mg/liter NH-j at oH 6.83 and 0.63
mg/liter NH-j at pH 7.60), and this effect was greater at low pH.
58
-------
TOXICITY TO PLANTS
Bacteria and Freshwater Plants
Ammonia is known to play an important part in the nitrogen metabolism of
aquatic plants. In the aquatic environment, nitrogen plays an important role
in determining the composition of phytoplankton and vascular plant communi-
ties and in some cases can act as a limiting nutrient in primary production.
Ammonia can also be toxic at certain concentrations. Data concerning the
toxicity of ammonia to freshwater vascular plants and phytoplankton are
contained in Table 4. Few of the papers examined contained sufficient
information to enable calculation of un-ionized ammonia concentrations,
altough total ammonia solutions were more toxic at high than at low pH, indi-
cating that toxicity was likely due primarily to NHj rather than NH^ .
Some information on ammonia effects on bacteria is also included here.
The bacterial species Escherichia coll and Bacillus subtills were found
to be sensitive to NH^Cl (Deal et al. 1975); 1100 mg/liter NH3 killed 90
percent of an ]5. coli population in 78 minutes. _B. sub tills, an aerobic,
spore-forming bacterium, was destroyed in less than two hours in 620 mg/liter
NH-j • NH-} inhibition of the bacteria Nltrosomonas (that convert ammonium
to nitrite) and the bacteria Nltrobacter (that convert nitrite to nitrate)
was studied by Anthonisen et al. (1976) and Neufeld et al. (1980). NH3
inhibited the nitrification process at a concentration of 10 mg/liter
(Neufeld et al. 1980). The NH-j concentrations that inhibited nitrosomonads
(10 to 150 rag/liter) were greater than those that inhibited nitrobacters (0.1
to 1.0 mg/liter), and NH^, not NH^"1", was reported to be the inhibiting
species (Anthonisen et al. 1976). Acclimation of the nitrifiers to NH3>
temperature, and the number of active nitrifying organisms are factors that
may aftect the inhibitors' concentrations of NH-j in a notification system.
59
-------
Langowska and Moskal (1974) investigated the inhibitory effects of
24-hour exposures to NH-j on pure cultures of ammonifying and denitrifying
bacteria. Effects examined were based on ability of the bacteria to produce
some specific metabolic processes, such as proteolysis, aramonification,
denitrification, and nitrification. Ammonifying and denitrifying bacteria
were most resistant to MR-}', proteolytic and nitrifying bacteria were the
most sensitive. Concentrations ranging from 0.8 to 170 mg/liter NH-j did
not adversely affect denitrifying and ammonifying bacteria; 220 mg/liter
caused reduction of the examined metabolic processes. Proteolytic bacteria
were unaffected at 0.8 nig/liter NH^, but were reduced to zero at 4.2
mg/liter; nitrifying bacteria were unaffected at 2.6 to 5.1 rag/liter and
reduced to zero at 13 to 25 mg/liter.
Experimental data concerning the toxicity of ammonia to freshwater
phytoplankton are limited. Przytocka-Jusiak (1976) reported ammonia effects
(Table 4) on growth of Chlorella vulgaris with 50 percent inhibition in five
days at 2.4 mg/liter NH-j, and complete growth inhibition in five days at
5.5 rag/liter. The MR-} Concentration resulting in 50 percent survival of C_.
vulgaris after five days was found to be 9.8 mg/liter NH^• In a separate
study, Przytocka-Jusiak et al. (1977) were able to isolate a C. vulgaris
strain with enhanced tolerance to elevated ammonia concentrations, by
prolonged incubation of the alga in ammonium carbonate solutions. C_.
vulgaris was reported to grow well in solutions containing 4.4 mg/liter
NH-}, but growth was inhibited at 7.4 mg/liter (Matusiak 1976). Tolerance
to elevated concentrations of NH-j Seemed to show a slight increase when
other forms of nitrogen were available to the alga than when ammonia was the
only form of nitrogen In the medium. The effects of ammonia on growth of the
algal species Ochromonas sqciabii is was studied by Brettliauer (1978). He
60
-------
fpund that concentrations (assuming pH 6.5 and 30 C) of 0.6 mg/liter NH3
killed the organisms, and at 0.3 mg/liter development of the population was
reduced. Concentrations of 0.06 to 0.15 mg/liter NHg had insignificant
effect on growth, and 0.015 to 0.03 mg/liter enhanced growth.
Effects of ammonia on four algal species (Table 4) were studied by
Abeliovich and Azov (1976). Ammonia at concentrations over 2.5 mg/liter
NH3 inhibited photosynthesis and growth of the algal species Scenedesmus
obliquus and inhibited photosynthesis of the algae Chlorella pyrenoidosa,
Anacystis nidulans, and Plectonema boryanum. Hosier (1978) reported that
NH^ concentrations causing 50 percent reduction in oxygen production by the
green alga Chlorella ellipsoidea and blue-green alga Anabaena sub cy1indrica
were 16.0 x 10~8 and 251.0 x 10~8 Vig NH3-N/cell, respectively.
The rate of photosynthesis in the blue-green alga _P. boryanum was
observed to be stimulated by NH^+, but inhibited by NH3 (Solomonson
1969); the magnitude of these effects was dependent on the sodium-potassium
composition of the suspending media. NH3 inhibition of photosynthesis was
associated with a conversion of inorganic polyphosphate stored in the cells
to orthophosphate.
Champ et al. (1973) treated a central Texas pond with ammonia to a mean
concentration of 25.6 mg/liter Nl^. A diverse population of dinoflagel-
lates, diatoms, desmids, and blue-green algae were present before ammonia
treatment. Twenty-four hours after treatment the mean number of
phytoplankton cells/liter was reduced by 84 percent. By the end of two weeks
(NH-j = 3.6 mg/liter) the original concentration of cells had been reduced
by 95 percent.
Much of the work concerning the response of freshwater vegetation to
high ammonia concentrations is only descriptive or is a result of research
exploring the possible use of ammonia as an aquatic herbicide.
61
-------
Champ et al. (1973) reported virtually complete eradication of rooted
aquatic vegetation (water shield, Brasenia schreberi, and American lotus,
Nelumbo sp.) in a central Texas pond within two weeks after treatment with
anhydrous ammonia; NHg concentration was 25.6 rag/liter 24 hours after
ammonia addition, and 3.6 rag/liter two weeks later. In experiments with
Potamogeton lucens, Litav and Lehrer (1978) observed that ammonia, which
forms a readily available nitrogen source for the plant, can be toxic when
present at high concentrations, with ammonia causing appreciable injury to
detached branches. Ammonia inhibition of growth of Eurasian watermilfoil
(Myriophyllum spicatum) affected length and weight similarly and affected
roots and shoots similarly (Stanley 1974).
Litav and Agami (1976) studied changes in vegetation in two rivers
subject to increased pollution from agricultural fertilizers, urban sewage,
and industrial wastes, and attributed the changes in plant species
composition primarily to ammonia and detergents. Agami et al. (1976)
transplanted seven species of "clean water" macrophytes to various sections
of river, and found that ammonia affected only Nymphaea caerulea. Use of
high concentrations of ammonia to eradicate aquatic vegetation was described
by Ramachandran (1960), Ramachandran et al. (1975), and Ramachandran and
Ramaprnbhu (1976).
Saltwater Plants
Data concerning the toxicity of ammonia to saltwater phytoplankton are
presented in Table 4. Ten species of estuarine benthic diatoms were cultured
for ten days in synthetic media at a range of NH3 Concentrations from 0.024
to 1.2 mg/liter NH3 (Admlraal 1977). A concentration of 0.24 mg/liter
NH-j retarded the growth of most of the tested species (Table 4) . Relative
tolerance to ammonium sulfate of five species of chrysomunads was studied by
62
-------
Pinter and Provasoli (1963). Coccolithus huxleyi was most sensitive, and
Pavlova gyrans and Hymenomonas sp. were most tolerant, with intermediate
tolerance exhibited by Syracosphaera sp. and Ochrosphaera neapolitana.
Shilo and Shilo (1953, 1955) reported that the euryhaline algae
Prynmesium parvum was effectively controlled with applications of ammonium
sulfate, which exerted a lytic effect. Laboratory and field tests showed
that the concentration of ammonium sulfate necessary for cell lysis decreased
with increasing pH, indicating that un-ionized ammonia and not the ammonium
ion is responsible for the lytic activity of ammonium sulfate on P^. parvum.
Effect of ammonia on the dinoflagellate Amphidinium carterae was studied by
Byerrura and Benson (1975), who reported that added ammonium ion at
concentrations found to stimulate the photosynthetic rate also caused the
algae to release up to 60 percent of fixed CC>2 to the medium.
Natarajan (1970) found that the concentrations of fertilizer plant
effluent toxic to natural phytoplankton (predominantly diatoms) in Cook
Inlet, Alaska, were between 0.1 percent (1.1 mg/liter NH^) and 1.0 percent
(11 mg/liter NH-j). At 0.1 percent effluent concentration * C uptake
was reduced only 10 percent, whereas at 1.0 percent effluent concentration a
24-33 percent reduction in the relative C uptake was observed. Effects
of ammonium sulfate on growth and photosynthesis of three diatom and two
dinoflagellate species were reported by Thomas et al. (1980), who concluded
that increased ammonium concentrations found near southern California sewage
outfalls would not be inhibiting to phytoplankton in the vicinity. Provasoli
and McLaughlin (1963) reported that ammonium sulfate was toxic to some marine
dinoflagellates only at concentrations far exceeding those in seawater.
No data were found concerning the toxicity of ammonia to saltwater
vegetal ion.
63
-------
BIOACCUMULATION
No data are available concerning the accumulation of ammonia by aquatic
organisms.
64
-------
OTHER DATA
A number of investigators have studied effects of ammonia on behavior
and various metabolic processes of exposed animals, or have conducted field
studies. This research has dealt predominantly with freshwater fishes.
Freshwater Invertebrates
The effect of ammonia (Table 5) on the ciliary beating rate of clam
gills was investigated by Anderson et al. (1978). Concentrations of 0.036 to
0.11 ing/liter NHj caused a reduction in ciliary beating rate of fingernail
clams; the effect of these concentrations ranged from 50 percent reduction in
beating rate to complete inhibition of cilia. Adult clams (>5 mm) were more
sensitive than juveniles (<5 mm); adults were also slightly more
sensitive than the unionid mussel (Elliptic complanata) and the Asiatic clam
(C. manilensis). Shaw (1960) investigated effects of ammonium chloride on
sodium influx in the freshwater crayfish, Astacus pallipes. Ammonia produced
an inhibition of sodium influx; a concentration of 18 rag/liter NH^+
reduced the influx to about 20 percent of its normal value, and influx
reduction was related to greater ammonia concentration. This effect was
attributed to NH^ ions and not to any toxic effect exerted on the
transporting cells by un-ionized ammonia. NH^"1" did not affect chloride
influx nor the rate of sodium loss.
Ammonia was added to a Kansas stream at a 24-hour average concentration
of 1.4 mg/liter NH3, and a 24-hour drift net sampling was conducted
(Liechti and Muggins 1980). No change in diel drift pattern was observed,
but there was an increase in magnitude of drift, a shift in kinds of
organisns present, and changes in benthic standing crop estimates; the
ammonia concentration was concluded to be nonlethal.
-------
Fre shwa te r Fi she s
Herbert and Shurben (1963) Investigated the effect on susceptibility to
ammonium chloride solutions of rainbow trout forced to swim continuously
against water currents of different velocities prior to ammonia exposure.
Forcing rainbow trout to swim for one to two days at 85 percent of the
maximum velocity they could sustain increased their susceptibility only
slightly, corresponding to a 20 to 30 percent reduction in the 24- or 48-hour
LC50.
The behavioral response of blacknose dace (Rhinichthys atratulus) to
ammonium chloride solutions has been studied (Tsai and Fava 1975; Fava and
Tsai 1976); the test fish did not avoid concentrations of 0.56 or 4.9
mg/liter NH^, nor did these concentrations cause significant changes in
activity. Avoidance studies were conducted by Westlake and Lubinski (1976)
with bluegill using ammonium chloride solutions. Bluegill detected
concentrations of approximately 0.01 to 0.1 mg/liter NH3» and evidenced a
decrease in general locomotor activity. No apparent avoidance of ammonia was
observed, and there was some indication of an attraction. Behavioral
responses of bluegill to a five-hour exposure to 0.040 mg/liter XH-j>
although variable, were related to at least a small amount of physiological
stress either at the gill or olfactory surfaces. At a concentration of 0.004
mg/liter NH^, bluegill evidenced slight temporary increases in both
activity and turning behavior; no preference or avoidance was demonstrated,
with responses seemingly exploratory (Lubinski et al. 1978, 1980). Wells
(1915) investigated the avoidance behavior of bluegill to ammonium hydroxide
solutions and reported that fishes did not avoid ammonia prior to being
killed by it. In a study of the repelling ability of chemicals to green
sunfish, Summerfelt and Lewis (1967) concluded that concentrations of ammcaia
66
-------
'high enough to repel fish would ho rapidly tcit» .-»v>>tJtn, ,-i <-«.»>..-i f.-u->u i
with threespine stickleback, solutions of ammonia concentration O.J/ mg/liter
NH-j elicited a positive (attraction) response from the test fish (Jones
1948).
Weltering et al. (1978), in tests with largemouth bass and mosquitofish,
demonstrated that predator-prey interactions were sensitive to sublethal
concentrations of NHj- Ammonia concentrations of 0.63 and 0.86 mg/liter
NH3 decreased prey consumption and bass growth; bass were reported to be
more sensitive than mosquitofish to NH3« The effect of ammonium chloride
on consumption of juvenile chinook salmon by brook trout was studied by
Hedtke and Norris (1980). At the lowest test concentration of 0.29 mg/liter
NH3> trout consumption rates decreased as much as 65 percent. As ammonia
concentration increased, however, consumption of prey increased and was
double that of controls at the highest tested concentration of 0.76 mg/liter
NH-j- Increased consumption rate was related to both increased NH-j
concentration and increased prey density. The magnitude of the effect of
ammonia was not the same at all prey densities, having a greater effect on
consumption rate at high than at low prey densities. Mortalities were
observed among prey salmon at the highest NH3 levels, and these were
attributed to the combined effect of NH^ and stress from presence of the
predator. Brook trout exhibited toxic effects due to NH-j •
NH/^Cl and NH^HcOg Solutions were injected intraarterially into
rainbow trout (Hillaby and Randall 1979). The same dose of each compound was
required to kill fish, but there was a more rapid excretion of NH3 after
NH4HC03 infusions, resulting in higher NH3 Concentrations in blood,
than after NH^Cl infusions. Ammonium acetate solutions of different
concern rations were injected intraperltoneally into three species of fishes
67
-------
(Wilson 1968; Wilson et al. 1969). LD50 values (mmoles/kg body weight) for
channel catfish for one to four hours was 26.7 to 18.7, for goldfish for one
hour were 29.3 and 29.6 in two separate tests, and for rainbow trout for one
hour was 17.7. Goldfish was the most resistant species tested and rainbow
trout the least resistant. Nehring (1964) compared toxicity of ammonia in
the water to toxicity of ammonia administered orally and concluded that the
threshold and lethal concentration values were considerably lower for ammonia
in water than for ammonia administered orally.
Acute symptoms of NH-j toxicity to brown trout sac fry and 12-day-old
fry were described by Penaz (1965), who exposed fry to concentrations ranging
from 0.08 to 50.0 mg/liter NH^- Symptoms caused by Ntt-^ exposures were:
rapid spasm-like movements at concentrations of 2.0 mg/liter NH-j and higher
within 16-17 minutes of exposure; after 40 minutes these symptoms were also
observed at 0.4 mg/liter NH-j > After 2.5 hours these abnormal movements
ceased, and at 10 hours heart activity was decreased and fish lost movement
ability at the higher (>2.0 mg/liter N^) concentrations. Other symptoms
included Inability to react to mechanical stimulation and disorders in rhythm
of mouth movements culminating in the mouth's staying rigidly open. Thumann
(1950), working with rainbow trout and brook (=brown?) trout, described
observed symptoms of ammonia poisoning to fishes to be convulsions and
frequent equilibrium and positional anomalies.
Smart (1978) reported that exposure of rainbow trout lo an acutely
lethal concentration of 0.73 mg/liter NH^ resulted in an increase in oxygen
consumption, increase in ventilation volume, decrease in percent oxygen
utilization, increase in respiratory frequency and amplitude (buccal
pressure), decrease in dorsal aortic blood PQ? » increase in dorsal aortic
blood pressure, and increase in mean heart rate. Physiological parameters
68
-------
not significantly affected by NH_-j exposure were "cough" race, dorsal aort li-
blood pH, blood P50, erythrocyte count, heraatocrit, and hemoglobin
concentration. Coho salmon exposed to concentrations ranging from 0.094 to
0.162 rag/liter Nll-$ (Souea and Meade 1977) exhibited hyperexcitability,
hyperventilation, ataxia, and progressive acidemia; metheraoglobin
concentrations in blood of exposed fish did not differ significantly from
those of controls. Effects on trout (species not specified) blood with
exposure to accumulated excreted NHg were investigated by Phillips et al.
(1949) and were reported to include an increase in blood carbon dioxide
content and a decrease in oxygen content.
Arillo et al. (1979d) measured gill sialic acid content in rainbow trout
exposed to NH^Ofl or NH^Cl solutions ranging from 0.05 to 0.5 mg/liter
NH-j, and reported that increasing NH^ concentrations produced increasing
gill sialic acid content. Elevated gill sialic acid levels were also
produced by higher ammonium ion (NH^ ) concentrations at identical NH^
concentrations, and the authors concluded that NH^ was a stressor
causing elevated sialic acid levels. Exposure of rainbow trout (14-cm
length) for four hours to NH^Cl and NH^On solutions of concentrations
ranging from 0.094 to 0.50 mg/ltter NH^ resulted in increased proteolytic
activity and free amino acid levels in the fish livers, but no statistically
significant change in fructose 1,6-biphosphatase enzyme activity (Arillo et
al. 1978, 1979a). Renal renin activity was reported (Arillo et al. 1931b) to
increase in rainbow trout exposed to concentrations of 0.048 to 0.61 rag/liter
NH-j • A significant decrease in liver glycogen and increase in free glucose
were observed in rainbow trout exposed to NH^Cl solutions for four hours at
a concentration of 0.048 mg/liter NH3, and a decrease in total carbo-
hydrates was observed at 0.12 mg/liter NH3 (Arillo et al. 1979b). For
69
-------
trout similarly treated with .umnonlum hydroxide, .-slgivif ti-aui. Uei-redsiea ii>
glycogen and carbohydrates, and increase in glucose occurred at 0.097
mg/liter N!^.
A statistically significant increase in rainbow trout liver
concentrations of cyclic-31,5'-adenosine-raonophosphate (cAMP) was reported by
Arillo et al. (1979c) to be induced by a four-hour exposure to elevated
ammonia concentrations of 0.011 to 0.124 mg/liter NH3« Decreases in liver
glycogen levels were also measured and were significantly different from
controls only in the trout exposed to 0.048 mg/liter NHj, the highest
exposure used for glycogen measurements. The authors concluded that cAMP
measurements provided a very sensitive means of discerning fish stress even
at very low toxicant concentrations, although quantitative measurement of
stress intensity was not possible. Lysosoraal lability was also investigated
as an indicator of stress in rainbow trout due to ammonia exposure (Arillo et
al. 1980) , and was reported to increase significantly for fish subjected to
concentrations of 0.048 to 0.61 mg/liter NHj. Exposure of rainbow trout
for four to 48 hours to 0.024 to 0.61 mg/liter NH3 resulted in changes in
various brain and liver metabolites; the magnitude of the changes was depen-
dent on both exposure time and NH-j concentration (Arillo et al- 1981a) .
Exposure of walking catfish (Clarias batrachus) to ammonia caused
inhibition of fish brain cholinesterase and kidney peroxidase activity
(Mukherjee and Bhattacharya 1974, 1975a). Plasma corticosteroid
concentrations were measured (Tomasso et al. 1981) in channel catfish exposed
to 1.1 mg/liter NH^ for 24 hours; corticosteroid levels increased
initially, peaked after eight hours, then decreased. The overall increase
was approximately tenfold over normal levels.
Korting (I969b) reported that carp exposed to 1 mg/liter NH-j exhibited
an increase in number of blood erythrocytes, reaching an initial maximum
70
-------
after several hours followed by a gradual decrease; after 50 hours the number
was less than the average for non-exposed fish. Other blood changes from the
ammonia exposure were: thickening of individual erythrocytes, reduction of
osmotic resistance of erythrocytes, increase in concentrations of urea and
lactic acid, and decrease in ATP concentration. Levi et al. (1974) reported
that goldfish exposed for 24 hours to NH^Cl solutions exhibited increases
in cerebral and blood concentrations of glutamine and in other amino acids,
with changes most pronounced in the brain. Concentrations of free amino
acids in livers showed only slight increases of a few amino acids, including
glutamine, and the concentration of lysine decreased. No change in
concentrations of free amino acids was observed in kidneys. Rainbow trout
exposed to 0.33 mg/liter NH^ had significantly higher packed cell volumes;
exposures to concentrations of 0.24 rag/liter NH^ and higher resulted in
significantly raised blood glucose and plasma cortisol concentrations (Swift
1981).
Diuretic response of rainbow trout exposed to concentrations of 0.09 to
0.45 mg/liter NH3 was studied by Lloyd and Orr (1969). After an initial
lag period, urine production increased rapidly during exposure then returned
to normal within a few hours after discontinuation of NH3 exposure. A
no-obs^rved-effect concentration was reported to be 0.046 mg/liter NHo -
Goldfish were exposed to solutions containing 1.0 to 1.9 mg/liter NH^
(Fromm 1970; Olson and Fromm 1971); onset of death was characterized by a
gradual cessation of swimming movements and settling to the bottora of the
tank. Some goldfish near death were returned to ammonia-free water in which
they recovered to at least some degree. In similar experiments (Fromm 1970;
Olson and Fromm 1971) rainbow trout were exposed to ambient total ammonia
concentrations of 0.04 to 0.2 mg/litei NH3• There wad a decrease in total
71
-------
nitrogen excreted with increase in ambient NH-p and a concomitant decrease
in the. NH^ portion of total nitrogen excreted; urea and protein nitrogen
excretion rates showed no changes as ambient NH-j increased. Onset of death
for trout was characterized by violent thrashing movements.
Exposure of rainbow trout to solutions of NH^Ci for 24 hours (Froram
and Gillette 1968; Fromm 1970) showed that an increase in ambient water NH3
concentration resulted in a corresponding increase in blood NH-j
concentrations, and a decrease in total nitrogen and NH-j excretion. The
decrease in NH^ excretion accounted for half or less of the total nitrogen
excretion, depending on the water NH^ concentration, indicating that the
reduction in NH3 excretion was to some extent compensated for by increased
excretion of some other nitrogenous compound(s).
Young fry (2-20 days old) of loach (Misgurunus anguilicaudatus) and carp
were exposed for five to 70 hours to N-labeled ammonium chloride
solutions at six concentrations from 0.002 to 0.064 mg/liter NH-j (ito
1976), and the proportion of ^N relative to total N in the fishes
determined. Ammonia was shown to be directly absorbed by the fry; nitrogen
conversion rate increased with increasing ammonia concentration and exposure
time. Nitrogen conversion rates for carp fry decreased as fry age increased
from 3 to 20 days. After 48 hours of exposure to 0.064 mg/liter NH-j
followed by transfer to ammonia-free water, rapid excretion (15-20 percent)
of the absorbed N occurred during the first hour in ammonia-free water.
Excretion rate then slowed, with about 50 percent of the absorbed N
being retained after 48 hours in ammonia-free water. Comparison of N
absorption rates between live and sacrificed three-day-old carp fry showed
one-third to one-half the uptake of N by dead fry compared with live,
12
-------
indicating that the uptake of ammonia from water by live fish occurs not only
by simple membrane permeation but also by metabolic action.
Flagg and Hinck (1978) reported that exposure to NH3 lowered the
resistance of channel catfish to the pathogen Aeromonas hydrophila. In 17-
and 28-day tests, increasing exposure concentrations from 0.02 to 0.04
rag/liter NH^ resulted in increasing numbers of bacteria in host livers.
Schreckenbach et al. (1975) reported that ammonia in pond water leads to
outbreaks of gill necrosis in carp, accompanied by an increase in ammonia
concentration in serum of the fish. This is aggravated at elevated pH levels
due to increasing inhibition of ammonia excretion at increasing pH levels,
with ammonia excretion being almost totally blocked at pH values above 10.5.
After investigating the possible role of parasites, bacteria, viruses, and
other ultramicroscopic agents in causing gill necrosis, the authors concluded
that pH-dependent intoxication or autointoxication with ammonia was the sole
cause of the gill damage. Studies of the treatment and prophylaxis of gill
necrosis using 28 different therapeutical preparations led to the conclusion
that only those preparations that lowered the water pH level and/or ammonia
concentrations resulted in an improvement in clinical symptoms.
Increase in frequency of opercular rhythm in fishes was monitored as a
means to measure fish response to sublethal concentrations of ammonia (Morgan
1976, 1977). Ammonia threshold detection concentration (Table 5) for
largemouth bass was approximately 30 percent of the lethal concentration
(LC50) for that species. Increases in largemouth bass opercular rhythms and
activity were electronically monitored (Morgan 1978, 1979) to determine
threshold effect ammonia concentrations (Table 5); for a 24-hour exposure the
effect concentration for opercular rhythms was 0.028 mg/liter NH-j and for
activity was 0.0055 mg/liter. Lubinski et al. (1974) observed that ammonia
stress apparently caused bluegill to consume more oxygen.
73
-------
In field experiments in an Arizona mountain lake, mortalities of oa
rainbow trout were attributed to high un-ionized ammonia concentrations and
high pH levels; 20 to 100 percent of test fish died in 24 hours at NH^
concentrations of 0.109 to 0.225 mg/liter (Fisher and Ziebell 1980). Ammonia
added to a Kansas stream at 24-hour average concentrations of 1.4 mg/liter
NH3 resulted in fry of slender madtora (Notorus exllis), Notropis sp., and
orangethroat darter being collected in large numbers in a 24-hour drift net
sampling; these fishes are not normally found in drift net samples, and their
presence was attributed to toxic effects of the ammonia (Liechti and Huggins
1980).
Saltwater Invertebrates
Sublethal toxicity of NH^Cl to the quahog clam and eastern oyster was
studied by Epifanio and Srna (1975) who measured the effect of ammonia over
20 hours on the rate of removal of algae (Isochrysis galbana) from suspension
(clearing rate) by the clams and oysters. Concentrations of 0.06 to 0.2
mg/liter MH3 affected clearing; no difference was 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 to 0.12 mg/liter NH3 resulted in a reduction in
ciliary beating rate from 50 percent to complete inhibition (Table 5).
Exposure of unfertilized sea urchin (Lytechinus pictus) eggs to NH^Cl
resulted in stimulation of the initial rate of protein synthesis, an event
that normally follows fertilization (Winkler and Grainger 1978). NH^l
exposure of unfertilized eggs of St rongylocent rot us purpuratus, L^. pictus,
and Strongylocentrotus drobachiensis was reported (Paul et al. 1976; Johnson
et al. 1976) to cause release of "fertilization acid", more rapidly and in
greater amounts than after insemination. Activation of unfertilized L_.
pictus eggs by NH/jCl exposure was also evidenced by an increase in
74
-------
Intracellular pH (Shen ami Stelnhardt 1978; Steinhardt and Mazia 1973).
Ammonia treatment was also reported to activate phosphorylation of thymidirce
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 and Mazia 1974; Krystal and Poccia 1979). Ammonia treatment of S^.
purpuratus and S. drobachiensis fertilized eggs resulted in absence of the
normal uptake of calcium following insemination, but did not inhibit calcium
uptake if ammonia treatment preceded insemination (Paul and Johnston 1978).
The polychetous annelid (Nereis succinea), the channeled whelk (Busycon
canalieulaturn), and the brackish water clam (Rangia cuneata) were subjected
to ammonia concentrations of 0.85, 0.37, and 2.7 mg/liter NH3 and ammonia
excretion measured (Mangura et al. 1978). The excretion of ammonia in these
species was inhibited by non-lethal concentrations of ammonia; 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 crab (Callinectes sapidus) were moved from water of 28 ppt salinity
to water of 5 ppt, a doubling of ammonia excretion rate occurred; addition of
excess NH^Ci to the low salinity water inhibited ammonia excretion and
decreased net acid output (Mangura et al. 1976). The effect of gaseous NH3
on hemoglobin from blood of the common marine bloodworm (Glyeera dibrachiata)
was examined (Sousa et al. 1977) in an attempt to determine whether there was
competition between NH^ and oxygen in binding to hemoglobin; such an
NH-j/02 relationship was not found.
Saltwater Fishes
Mo other data were found for saltwater fish species.
-------
UNUSED DATA
Many references cited In the References section were not used in the
text or tables, for a variety of reasons. Listed below are unused
references, with a brief explanation for their being relegated to this
category. For those several cases where more than one reason applies to a
given paper, it is listed only under the principal reason for its not being
used.
The following references were not used because the research they
reported was conducted using aquatic organisms not resident in North America:
Alderson (1979), Arizzi and Nicotra (1980), Brown and Currie (1973), Brownell
(1980), Chin (1976), Currie et al. (1974) Dockal and Varecha (1967), D'Silva
and Verlencar (1976), Giussani et al. (1976), Greenwood and Brown (1974),
Grygierek et al. (1978), Inamura (1951), Nicotra and Arizzi (1980),
Orzechowski (1974), Reddy and Menon (1979), Sadler (1981), Saha et al.
(1956), Shaffi (1980b), Singh et al. (1967), Stroganov and Pozhitkov (1941),
Thomas et al. (1976), Turoboyski (1960), Vailati (1979), Woker (1949),
Wuhrmann (1952), Wuhrmann and Woker (1953), Wuhrmann and Woker (1955),
Wuhrmann and Woker (1958), Yamagata and Niwa (1982).
The following references were not used because insufficient water
chemical composition data were provided to permit calculation of NH-j:
Belding (1927), Binstock and Lecar (1969), Chu (1943), Danielewski (1979),
Das (1980), Ellis (1937), Hepher (1959), Joy and Sathyanesan (1977), Kawamoto
(1961), Mukherjee and Bhattacharya (1978), Oshima (1931), Oya et al. (1939),
Patrick et al. (1968), Rao and Ragothaman (1978), Roberts (1975), Rushton
(1921), Scidmore (1957), Shelford (1917), Shevtsova et al. (1979), Sigel et
al. (1972), Southgate (1950), Wolf (1957a), Wolf (1957b), Zgurovskaya and
Kustenko (1968).
76
-------
The following references were not used because they report or)
published elsewhere which was cited in this Jiviuarut ! row t h«» .»thoi
publicatlon(s): Burkhalter (1975), Colt (1974), Dept. of Environment, U.K.
(1972), Herbert (1955), Hillaby (1978), Larmoyeux and Piper (1973), Ministry
of Technology, U.K. (I960), Ministry of Technology, U.K. (1966), Rice (1971),
Smart (1975), Wilson (1974).
The following references were not used because they were foreign-
language papers for which no translation was available, and no useful
information could be obtained from the abstract: Desavelle and Hubault
(1951), Fedorov and Smirnova (1978), Frahm (1975), Garcia-Romeu and Motais
(1966), Guerra and Comodo (1972), Guseva (1937), Hubault (1955), Jocque and
Persoone (1970), Kawamoto (1958), Korting (1976), Krauss (1937), Kuhn and
Koecke (1956), Leclerc and Devlaminck (1950), Maraontova (1962), Oya et al.
(1939), Pequignot and Moga (1975), Pora and Precup (1971), Revina (1964),
Saeki (1965), Schaperclaus (1952), Scheuring and Leopoldseder (1934),
Schreckenbach and Spangenberg (1978), Steinmann and Surbeck (1922a),
Steinmann and Surbeck (1922b), Svobodova (1970), Svobodova and Groch (1971),
Teulon and Simeon (1966), Truelle (1956), Varaos and Tasnadi (1962a), Vamos
and Tasnadi (1962b), Vamos et al. (1974), Yasunaga (1976), Yoshihara and Abe
(1955).
The following references were not used because they relate more to
ammonia metabolism in fishes, than to ammonia toxicity: Bartberger and
Pierce (1976), Becker and Schmale (1978), Brett and 7,ala (1975), Cowey and
Sargent (1979), Creach et al. (1969), Cvancara (1969a), Cvancara (1969b), De
and Bhattacharya (1976), De Vooys (1968), De Vooys (1969), Driedzic and
Hochachka (1978), Fauconneau and Luquet (1979), Fechter (1973), Fellows and
Hird (1979a), Fellows and Hird (1979b), Flis (1968a), Flis (1963b), Florkin
and Duchateau (1943), Forster and Goldstein (1966), Forster and Goldstein
77
-------
(I960), Fromm (1963), Cirard and Payan (1980), Goldstein and Forster (1961),
Goldstein and Forster (1965), Goldstein et al. (1964), Gordon (1970),
Gregory (1977), Grollman (1929), Guerin-Ancey (1976a), Guerin-Ancey (1976b),
Guerin-Ancey (1976c), Guerin-Ancey (1976d), Hays et al. (1977), Hoar (1958),
Muggins et al. (1969), Janicki and Lingis (1970), Katz (1979), Kaushik and
Luquet (1977), Kloppick et al. (1967), Kutty (1978), Lawrence et al. (1957),
/»
Lum and Hatnraen (1964), Maetz (1973), Maetz and Garcia-Roraeu (1964),
Makarewicz and Zydowo (1962), Mason (1979a), Mason (1979b), Matter (1966),
McBean et al. (1966), McKhann and Tower (1961), Moore et al. (1963), Morii et
al. (1978), Morii (1979), Morii et al. (1979), Mukherjee and Bhattacharya
(1977), Nelson et al. (1977), Payan (1978), Payan and Maetz (1973), Payan
and Matty (1975), Payan and Pic (1977), Pequin and Serfaty (1963), Pequin and
Serfaty (1966), Pequin and Serfaty (1968), Pequin et al. (I969a), Pequin et
al. (1969b), Raguse-Degener et al. (1980), Ray and Medda (1976), Read (1971),
Rice and Stokes (1974), Rychley and Marina (1977), Savitz (1969), Savitz
(1971), Savitz (1973), Savitz et al. (1977), Schooler et al. (1966), Smith
(1929), Smith (1946), Smith and Thorpe (1976), Smith and Thorpe (1977),
Storozhuk (1970), Sukumaran and Kutty (1977), Tandon and Chandra (1977),
Thornburn and Matty (1963), Vellas and Serfaty (1974), Walton and Cowey
(1977), Watts and Watts (1974), Webb and Brown (1976), Wood (1958), Wood and
Caldwell (1978).
The following references were not used because the material the authors
used was a complex compound or had an anion that might in itself be toxic:
Curtis et al. (1979), Johnson and Sanders (1977), Simonin and Pierron
(1937), Vallejo-Freire et al. (1954).
The following references were not used because they dealt with complex
effluents or waste waters, of which ammonia was a primary component: Brown
78
-------
•'et al. (1970), Calamari and Marchetti (I1)?1*). <7upM et al. (t, Twan ami
Cella (1979), Janicke and Liidemann (1967), Lloyd and Jordan (196J), Lloyd and
Jordan (1964), Martens and Servizi (1976), Matthews and Myers (1976), Mihnea
(1978), Nedwell (1973), Okaichi and Nishio (1976), Perna (1971), Rosenberg et
al. (1967), Ruffier et al. (1981), Sahai and Singh (1977), Shaffi (1980a),
Vamos (1962), Vamos and Tasnadi (1972), Ward et al. (1982).
Three references consisted only of an abstract, providing insufficient
information to warrant their use: Liebmann and Reichenbach-Klinke (1969),
Mukherjee and Bhattacharya (1975b), and Redner et al. (1980).
79
-------
SUMMARY
All concentrations used herein are expressed as un-ionized ammonia
(Nil-}), because NH^, not the ammonium ion (NH^ ) has been demonstrated
to be the principal toxic form of ammonia. The data used in deriving the
criteria are predominantly from flow-through tests in which ammonia
concentrations were measured. Ammonia was reported to be acutely toxic to
freshwater organisms at concentrations (uncorrected for pH) ranging from 0.53
to 8.00 rag/liter NH-j for 12 Invertebrate species representing nine families
and from 0.083 to 4.60 mg/liter NH3 for 23 fish species from nine families.
Among fish species, reported 96-hour LC50 values ranged from 0.083 to 1.09
mg/liter for salmonids and from 0.14 to 4.60 mg/liter NH-j for non-salmonids.
Reported data from chronic or partial chronic tests on ammonia with two
freshwater invertebrate species, both daphnids, showed effects at concentra-
tions (uncorrected for pH) ranging from 0.304 to 1.2 mg/liter Nt^i and with
nine freshwater fish species, from five families, ranging from 0.0017 to
0.612 mg/liter NH3-
Concentrations of ammonia acutely toxic to fishes may cause loss of
equilibrium, hyperexcitability, increased breathing, cardiac output and
oxygen uptake, and, in extreme cases, convulsions, coma and death. At lower
concentrations ammonia has many effects on fishes including a reduction in
hatching success, reduction in growth rate and morphological development, and
pathologic changes in tissues of gills, livers, and kidneys.
Several factors have been shown to modify acute NH3 toxicity in fresh
water. Some factors alter the concentration of un-ionized ammonia in the
water by affecting the aqueous ammonia equilibrium, and some factors affect
the toxicity of un-ionized ammonia itself, either ameliorating or exacer-
bating the effects of ammonia. Factors that have been shown to affect
80
-------
ammonia toxicity include dissolved oxygen concentration, temperature, pH,
previous acclimation to ammonia, fluctuating or intermittent exposures,
carbon dioxide concentration, salinity, and the presence of other toxicants.
The most well-studied of these is pH; the acute toxicity of NH-j has
been shown to increase as pH decreases. Sufficient data exist from toxicity
tests conducted at different pH values to formulate a mathematical expression
to describe pH-dependent acute NH^ toxicity. The very limited amount of
data regarding effects of pH on chronic NH^ toxicity also indicate
increasing NH-j toxicity with decreasing pH, but the data are insufficient
to derive a broadly applicable toxicity/pH relationship. Data on temperature
effects on acute NH^ toxicity are limited, and somewhat variable, but
indications are that NH3 toxicity is greater at low (<10 C) temperatures.
There is no information available regarding temperature effects on chronic
NH3 toxicity.
Examination of pH-corrected acute NH-j toxicity values among families
of freshwater organisms tested showed that the most sensitive families are
Percidae and Salraonidae, with walleye and rainbow trout being the most
sensitive tested species in each of these families; invertebrates are
generally more tolerant than fishes. Available chronic toxicity data for
freshwater organisms show that the most sensitive families among those tested
are Salmonidae and Catostomldae (suckers), with pink salmon and white sucker
being the most sensitive tested species in these families. Limited data for
invertebrates, mostly cladocerans and one insect species, indicate they are
generally more tolerant than fishes; however, the fingernail clam appears to
be as sensitive as salmonids. The range of acute/chronic ratios for ten
species from six families was 2.8 to 44, and acute/chronic ratios were higher
for the species found to be the most sensitive on -in acute (pH-corrected)
81
-------
basis. Available data indicate that differences in sensitivities between
warm and cold water families of aquatic organisms are inadequate to warrant
discrimination in the national ammonia criterion between bodies of water with
"warm" and "cold" water fishes; rather, effects of organism sensitivities on
the criterion are most appropriately handled by site-specific criteria
derivation procedures.
Data for concentrations of NH3 toxic to freshwater phytoplankton and
vascular plants, although limited, indicate that freshwater plant species are
appreciably more tolerant to NH^ than are invertebrates or fishes. The
ammonia criterion appropriate for the protection of aquatic animals will
therefore in all likelihood be sufficiently protective of plant life.
Available acute and chronic data for ammonia with saltwater organisms
are very limited, and insufficient to derive a saltwater criterion. A few
saltwater invertebrate species have been tested, and the prawn Macrobrachium
rosenbergii was the most sensitive. Acute toxicity of NH^ appears to be
greater at low pH values, similar to findings in freshwater. Data for
saltwater plant species are limited to diatoms, which appear to be more
sensitive than the saltwater invertebrates for which data are available.
Although a great deal of information has been published about ammonia
toxicity to aquatic life, much of it provides little, if any, quantitative
data. There are some key research needs that need to be addressed in order
to provide a more complete assessment of ammonia toxicity. These are:
(1) acute tests with saltwater fish species, and additional saltwater
invertebrate species; (2) life-cycle and early-life-stage tests with
representative freshwater and saltwater organisms from different families,
with investigation of pH effects on chronic toxicity; (3) fluctuating or
intermittent exposure tests for a variety of species anJ exposure patterns;
82
-------
(4) tests at cold water temperatures, both acute and chronic; (5) more
hlstopathological and histochemical research with fishes, which would provide
a rapid means of identifying and quantifying sublethal ammonia effects; (6)
studies on effects of dissolved and suspended solids on acute and chronic
toxicity.
83
-------
NATIONAL CRITERIA
To protect freshwater aquatic life, the criteria for ammonia (in
rag/liter un-ionized NH-j) are:
(1) the concentration at all times should be less than or equal to the
numerical value given by 0.15 x f(T)/f(pH), where
f(pH) - 1 + 10l-03(7.32-pH)
f(T) - I, T _> 10 C
* 1 4- 109-73-pH
pKT-pH
' T < 10 C
(2) The average concentration over any 30 consecutive days should be less
than or equal to 0.031 x f(T)/f(pH), where
f(pH) = 1, pH _> 7.7
» 100.74(7.7-pH)> pH < 7.7
f(T) « 1, T >_ 10 C
! + iQ9.73-pH
* 1 + iOPKT~pH • T < 10 C
Criteria values for the pH range 6.5 to 9.0 and the temperature range 0 C to
30 C are provided in the following tables. Total ammonia concentrations
equivalent to each NH-j criterion are also provided in these tables.
Data available for saltwater species are insufficient to derive a
criterion for saltwater.
84
-------
(1) Maximum allowed concentrations for ammonia.*
pH
0 C
5 C
10 C
15 C
20 C
25 C
30 C
Un-ionized Ammonia (rag/liter NHj)
6.50
6.75
7.00
7.25
7.50
7.75
8.00
8.25
8.50
8.75
9.00
6.50
6.75
7.00
7.25
7.50
7.75
8.00
8.25
8.50
8.75
9.00
0.008
0.014
0.021
0.030
0.040
0.049
0.056
0.061
0.065
0.068
0.071
31.9
29.5
25.7
20.8
15.5
10.6
6.84
4.22
2.54
1.53
0.94
0.013
0.021
0.032
0.046
0.061
0.074
0.084
0.091
0.096
0.100
0.104
31.9
29.5
25.7
20.8
15.5
10.6
6.84
4.22
2.54
1.53
0.94
0.019
0.031
0.048
0.069
0.091
0.110
0.125
0.135
0.141
0.145
0.147
Total Ammonia
31.9
29.5
25.7
20.8
15.5
10.6
6.84
4.22
2.54
1.53
0.94
0.019
0.031
0.048
0.069
0.091
0.110
0.125
0.135
0.141
0.145
0.147
(mg/liter
21.8
20.1
17.6
14.2
10.6
7.29
4.71
2.92
1.78
1.09
0.69
0.019
0.031
0.048
0.069
0.091
0.110
0.125
0.135
0.141
0.145
0.147
NH3)
15.0
13.9
12.1
9.84
7.34
5.06
3.28
2.05
1.27
0.80
0.52
0.019
0.031
0.048
0.069
0.091
0.110
0.125
0.135
0.141
0.145
0.147
10.5
9.69
8.48
6.89
5.15
3.56
2.33
1.47
0.93
0.60
0.41
0.019
0.031
0.048
0.069
0.091
0.110
0.125
0.135
0.141
0.145
0.147
7.41
6.86
6.00
4.88
3.66
2.55
1.68
1.08
0.70
0.47
0.33
* To convert these values to mg/liter N, multiply by 0.822.
85
-------
(2) 30-day average allowed concentrations for ammonia.*
pH
0 C
5 C
10 C
15 C
Un- ionized Ammonia (mg/liter
6.50
6.75
7.00
7.25
7.50
7.75
8.00
8.25
8.50
8.75
9.00
6.50
6.75
7.00
7.25
7.50
7.75
8.00
8.25
8.50
S.75
9.00
0.0018
0.0027
0.0042
0.0064
0.0098
0.0138
0.0139
0.0140
0.0142
0.0145
0.0150
6.82
5.87
5.06
4.36
3.77
2.99
1.70
0.97
0.56
0.33
0.20
0.0027
0.0041
0.0063
0.0096
0.0148
0.0208
0.0209
0.0210
0.0211
0.0214
0.0219
Total
6.82
5.87
5.06
4.36
3.77
2.99
1.70
0.97
0.56
0.33
0.20
0.0040
0.0061
0.0094
0.0144
0.0220
0.0310
0.0310
0.0310
0.0310
0.0310
0.0310
Ammonia
6.83
5.89
5.07
4.37
3.78
3.00
1.70
0.97
0.56
0.33
0.20
0.0040
0.0061
0.0094
0.0144
0.0220
0.0310
0.0310
0.0310
0.0310
0.0310
0.0310
(mg/liter NH3
4.65
4.01
3.45
2.98
2.58
2.05
1.17
0.67
0.39
0.23
0.14
20 C
NH3)
0.0040
0.0061
0.0094
0.0144
0.0220
0.0310
0.0310
0.0310
0.0310
0.0310
0.0310
)
3.21
2.76
2.38
2.06
1.78
1.42
0.81
0.47
0.28
0.17
0.11
25 C
0.0040
0.0061
0.0094
0.0144
0.0220
0.0310
0.0310
0.0310
0.0310
0.0310
0.0310
2.24
1.93
1.67
1.44
1.25
1.00
0.58
0.34
0.20
0.13
0.09
30 C
0.0040
0.0061
0.0094
0.0144
0.0220
0.0310
0.0310
0.0310
0.0310
0.0310
0.0310
1.58
1.37
1.18
1.02
0.89
0.72
0.42
0.25
0.15
0.10
0.07
* To convert these values to rag/liter N, multiply by 0.822.
86
-------
KXAMP1.KS OF SITR-SrKOU'lO CR
National criteria are subject to modification, if appropriate, to
reflect local conditions. One method provided in the Site-Specific Criteria
Guidelines (U.S. Environmental Protection Agency 1982b) for such modification
is to base certain calculations only on those species that occur in the body
of water of interest. As an example of how site-specific criteria for
ammonia may differ from the national criteria, calculations were performed
for several sites.
The sites were chosen on the basis of readily available information on
the presence of fish and invertebrate species and on a reasonable diversity
between sites. The sites were:
(1) St. Louis Bay - mouth of the St. Louis River on Lake Superior at
Duluth, Minnesota/Superior, Wisconsin (A. R. Carlson, pers. comra.
1982)
(2) Straight River at Owatonna, Minnesota (A. R. Carlson, pers. comm.
1982)
(3) Piceance Creek, Colorado (Goettl and Edde 1978; Gray and Ward 1978)
(4) Poudre River at Fort Collins, Colorado (W. T. Willingham, pers.
comm. 1982)
(5) Colorado River at Utah/Colorado border (W. T. Willingham, pers.
comm. 1983)
The calculations here are limited to temperatures of 15 C and to a single pH
typical of the site (see following table). Therefore, the criteria here
should not be considered as final criteria for the sites because variation
with pH and temperature was not explored.
For each site, available surveys of species occurrence were used to
identify which of the families tested for acute toxicity (Table 3) were
-------
present. Minimum data set requirements for the diversity of families were
met except where inappropriate to a site (U.S. Environmental Protection
Agency 1982b). The national LIMFMAV (Table 3) was used for each family, even
if it is based in part or whole on species not occurring at the site, unless
LIMSMAVs were available for all species in the family at the site, in which
case a site-specific LIMFMAV was computed that was based only on site
species. The LIMFMAVs so developed for each site are listed in the following
table.
The Guidelines method for estimating the FAV as the fifth percentile of
FMAVs was applied to the set of LIMFMAVs selected for each site. If the
LIMFAVs so computed exceeded the LIMSMAV of an important species at a site,
or of an important size class of an important species, the LIMFAV was lowered
to the lowest such LIMSMAV. The FAVs at each site were then computed by
adjusting the LIMFAVs to the site pHs, using the acute pH relationship
already discussed. The maximum criterion at each site was set to one-half of
the site FAV.
In all cases, the site pH was >7,5, so an acute/chronic ratio of 16 was
used. At sites 2, 4, and 5, this ratio was applied directly to the FAV to
obtain an FCV. At sites 1 and 3, where the LIMFAV was lowered to reflect an
age/size class, the ratio was applied to the value the FAV would have had if
the LIMFAV was only lowered to LIMAVs averaged over all data for a species,
not just an age/size class. If the resultant PCV at a site exceeded the
average chronic value (measured at pH >7.5) of an important species present
at the site, the FCV was lowered to this species' chronic value. The 30-day
average concentration was set to the FCV.
If rainbow trout are present at a site, the maximum allowable
concentration is the s^uie as the national value. If raiubow trout are
88
-------
ab,sent, but percids or other salmonids are present, the maximum allowable
concentration Is about twofold higher than the national number. This is not
due to differences in general species sensitivities, but rather reflects
unavailability of information on the sensitivity of different age/size
classes for species other than rainbow trout; these higher numbers should
therefore be treated with caution as perhaps being relatively underprotective
compared to the national criterion. Only where both Percidae and Salmonidae
are absent (site 5) is the maximum allowable concentration greatly higher,
about fourfold, than the national number. Again, however, a large part of
this difference may be due to the dearth of toxicity information on sensitive
age/size classes.
The 30-day average criterion shows even less variation among sites than
the maximum criterion, due to the size class issue not affecting sites
differently. If rainbow trout are present, the average criterion is near the
national value. If rainbow trout are absent, but percids or other salmonids
are present, the average criterion is only slightly (<20%) higher than the
national value. Only if both Percidae and Salmonidae are absent from the
site is the number substantially higher than the national value and the
difference is little more than twofold.
89
-------
Site-specific aramoni.* criteria examples for t lv
Site Number
LIMFAVs:
Elmidae
Ephemerellidae
Asellidae
Actacidae
Tubificidae
Tctaluridae
Perlodidae
Poeciliidae
Baetidae
Percichthyidae
Cyprinidae
Daphnidae
Cottidae
Dendrocoelidae
Catostomidae
Centrarchidae
Salraonidae
Percidae
pH
Temperature (C)
1
a
6.22
3.86
3.46
3.03
2.87
2.70
a
a
a
1.92
1.84
1.65
a
1.57
1.49
0.90
0.82
7.6
15
2
8.30
6.22
a
3.46
3.03
2.87
a
a
2.36
a
1.92
a
a
a
1.57
1.49
a
0.82
7.5
15
3
a
6.22
3.86
a
3.03
a
2.70
a
2.36
a
1.92
a
1.65
a
1.57
a
0.90
a
8.1
15
4
a
a
3.86
3.46
3.03
2.87
a
a
2.36
a
1.92
1.84
a
a
a
1.30b
a
0.82
7.9
15
5
8.30
6.22
3.86
3.46
3.03
2.37
2.70
a
2.36
a
1.92
1.84
a
a
1.57
1.49
a
a
8.1
15
Maximum allowed concentration
(ing/liter NH3):
as un- ionized ammonia
(as total ammonia)
30-day average concentrat
(mg/liter NH3) :
as un-ionized ammonia
(as total ammonia)
0.10C
(9.3)
ion
0.028
(2.6)
0.21
(25)
0.026
(3.0)
0.13C
(3.9)
0.03ld
(0.9)
0.27
(13)
0.034
(1.6)
0.5S
(18)
0.073
(2.2)
(a) Family not present at site.
(b) LIMFAV adjusted to reflect only site species.
(c) LIMFAV lowered to L1MAV of adult rainbow trout.
(d) FCV lowered to CV of rainbow trout.
90
-------
jO
«
8
li
*.
*
ox
• tf
°5
4-
18
t~
irlratlon
L NH»I
in
o
jO
4»
^
*••
^»
Ul
«
J
i
5
I
o
|s
- X
— 3 E0>
1 *" 23
— 10 3
- — h-
CM
oo
•"
c
3
*
K-,
in
i
00
CM
8
^
•o
o
o
o
in
^
i
£s
t
o
5
G -o
I —
CM O
V
1C
c
•t-
c
10
U
ID
10
C C
10 £i
Cladocer
Cer i odap
r-
2
*
ID
d>
o
in
3
„.
4
f^
1O
2;
o
CO
ON
*
CM
O
in
O
»-J
y
tn
CJ
X
_,-
4--
(M O
V
ID
C
c" in
10 e
Cladocer
Daphn la
g-
fal
c
—
-
10
4.
03
O
in
3
or
co
*
*o
o
o
CM
O\
O
CO
CM
O
in
o
,£
to
"„.
5
x:
4 —
CM O
V
10
c
•> o
c ro
10 c
Cladocer
Daphn la
g-
h.
c
~
-~»
10
4.
a>
8
Ul
3
ce
(
O
*
in
CO
r—
i-
CM
0
in
0
s:
to
o
X
^
i -o
CM O
V
£
» a
10 E
Cladocer
Daphn la ,
g-
h.
c
3
^
10
.
*
8
U)
3
K
1
co
CM
CM
O
03
CM
O
in
O
„(
s
•I
to
0
vr
X
_,_
I -o
CM O
V
10
c
- a
lo E
Cladocer
Daphn la
§-
h.
c
Z
j
a
4-
e
o
t/)
DC
O
c
r-
•
in
^
in
o
o
in
O
_,_f
2
to
vr
X
_c
4- —
CM O
V
<0
c
c
Q c?
Cladocer
Daphn la i
8-
5s.
c
^
_?
nj
*
s>
IA
y
K
O
co
8
in
^
8
o
o
in
O
s
to
o
$
J-
4 2
CM O
V
10
c
c ID
ID e
Cladocer
Daphn i a ,
Q.
ID
CS
C
^
10
4.
o
0
VI
or
0
cd
vO
C3
CM
^.
"^
tr\
CD
O
in
O
J
£
to
O
5
J-
I -o
CM O
V
ID
C
» o;
c 10
10 E
Cladocer
Daphn i a i
g-
JL
c
^
_!
ID
4_
-------
0*^1 !£>
D-5I ID
& Pescitel 1 i
Tl
"o
— CO
CC r-
XJ
4-
W* ID
in L.
ON 3
O
CO
ID
ON
;> r—
o
ID +-
0 1
JQ
LLJ j
1
CO CM
• » 1
f- CO
£ h.
c c
« •
ID ID
b a>
cr c
O O
4- 4-
1/1 l/l
1- U
3 3
»- t-
r— (/>
ON CO
a.
ID
Si
c
ID
4-
Q)
C
O
4-
Ul
3
I—
CO
00
a.
ID
c
"in
c
O
4-
(/)
I.
3
1-
*ff
CO
Q.
C
"S
4-
f\ u
Tl* ^O *" " *^ ^* C^f O \O 00 \C
C?^ *~" ^O ^^ ^~" CO CO C^ CO CO
*t*~O OsitOfO •— sfiAro
ooo ooo oooo
ir»irsu> mmm ur\iriir\io
OOO OOO OOOO
i_j i i j i i_j i
2 -z ^ x y ^ ^ s ^ z
u.CTu_ C LI_ u. tZ C IZ uT
VO — 1
r^ co r~- KI in
a a « » •
O K1
vO O O CO
OOOO
fl • » *
CM (N CO O
OOOO
id in in in
OOOO
__J 1 1 J
S 2 5.
• • - - S
tZ U- u^ C/)
O*
"CM
OOO 1 3 O O O O O O O O O ^
^" •tf' **!r ^ *i" ^ ^y~ **f "*t" ^-f "^ "^ *^ n
~XX I X X IXIXZXXZ
z ^ z zzz z2z2z22^
O>0>
a N
l/V V>
**• o
•—
-*}
§c ^
e £
TT — i *r —
CNO CNOfMCO 1 O — •— O
v v •— r^- ^~^-^-^-
fsi
in i_
3 ID I/,
— .- ID — —
"0 3 ID C -O -O
— +- N C C
U0)4- t/lt/1. (DID
— — — a. s. i_
ffiO > IDIt)l/> CTCT
C — U) O — C c '
- a »— « 3 o(0 <" > ra !D
CIOC3C— (ON 1/1 l/> — U) — —
•OE.UO.IDIO ut- -o «a> 4-n — —
I- L L.C •— -C4--C4- fflC ffl C
«
a.
(BID $10 i/lU U1O *(D|D «t. • U
o- y~ yO) -D3O —ID — ja-(- ->-o >-S >
Oc oc OU o— O t- c -»-c _._c — E — E —
TD x: -a .c "° Q d-— ID >-O >-o •< Q ~*-5 -«-$ •*-
t3d {nci •— c >* J^ >*x; >
— ID — ID — — Wio Uf- t_l_ (PID (Dd IDCt K
(on OQ oco — . >^ t/> C 3
— ,. l-l O .C
— -« «(B i/l EO
ffl >.+. ->-4- — — C
»l_ — o — Q. «E ID>-
^fl> ^*-O -^O O"~ ^/1-C
6 (DC OC — C t.
O c •>• c> 4-c J^O
-£ OO OO OO CO
a f-i_ +-i_ O+- — c
uj) vo < o < co "> a. o
-------
1
8
*
**-
.-
• CR
o e
s
^M
ID o>
Co
t-
||
.C
5 — J
I-
JO
4-
»*-
LJ
1
5
|
V
o
0) 0
n N
to in
« L.
•*- 0
Zi
Species
U"\ lT\
r~- r*^
2 2
F F
O *
O
CO *<5 *<"*
— C C
O O
>* in in
cp — —
~ 3E 5
ID 1 1
CQ c c
00
*<3 U1 !/.
C C
d> .-.. ,—
CJ ,Q jO
z & &
1 ! 1
1
!-- OO
ft ft
K"\ *y in in
I
K1 in O O
CNJ O
r-~ 00
— CM CM
COO
O O O
in in m
0 0 CJ
z •<•
co L d
ex)
•a- O CJ
5 5 5
0) 0?
— — -
.— .—•
c c
CD CO
L. D 3
ID
U JZ JC
in u u
34-4-
-O 3 3
L en w
cr v v
- tn "in •• in
w 3 C 3 C 3
O .c ox: 0 -^
e. o e o e o
._ c — c — c
ID >- ft) >- (0 >•
UT £ (/i £ in -C
.* b o b o b
CO -CO -C O
— c o c 0 c
Q- O o o O O
in
r-
c*
£
C
1/5
•a
c
s
—
3t
1
C
SI
c
JO
c?
1
m
in
0
in
in
0
0
in
O
s
t—
o
i
(1)
. —
• —
c
CD
D
—>
£
O
4-
.!?
V
- in
c ^
O -c
& o
— c
(T3 ^>-
0) JT
ob
£. O
O C
o o
in
r--
2
C
J?
*^
C
s
—
3C
1
C
O
in
c
o
C?
1
in
in
r-
CO
CM
in
o
o
in
o
,_
u-
o
i
(D
-. —
• —
c
(B
5
.c
O
V
3
V)
^
•» in
C 3
c: t
e o
— c
Coho sa
Oncorhy
m
f^.
CTi
F
V
•O
c
st
—
i
i
c
O
c
-O
£
1
in
o
00
—
• —
C
fl)
§
"
_£;
O
4-
3
m
V
« Ul
C 3
0 x:
E 0
•*- c
ob
.c o
5 c
C5 o
in
^^
Ox
r
S'
«o
c
s
—
3:
1
c
O
in
c
jQ
£
in
m
00
o
OD
00
c>
o
in
O
s;
t
CJ
I
CO
_
—
C
fl)
5
—3
_,;;
O
b-
in
_^;
•. in
c 3
O -<~
e u
— c
ob
.c o
0 C
0 0
co
ON
—
cT
_~
o
3
00
oro
A 3
4-
ro
CO
i
I «
*r o\
i
CM O
— —
0
in
in
o
o
8
s
t
o
1
Ol
>£>
j:
o
4-
3
in
V"
« in
C 3
O ^
6 0
— c
SI
ob
.c o
O C
o o
k A'
— OA
a ".
tn —
3 (0
or
- •£
c c
O O
in t/)
L. l_
3 3
1- t—
0 ^>
• «
00 CO
CM —
« «
IO t^\
\o —
O 00
00 i~
lA
in o
r~ co
CO O
o o
in in
q o
-j _j
s: z
t— t—
u. u
0 0
i i
CT
D)
O 0
O -^
a •
4- 4-
— 3
« C 0
4- O L —
3 J3 f JC
on) L.
1_ 3 4- 1C
•F CT 10 —
K] O C,
So i g
•o_e 4- i
o~a a Tc
O c/> CJ en
P- r-
C^ O^
^— r-*
^ m
10 (0
4— 4—
0 CD
C C
O O
4- 4-
in in
3 D
£-C
H-
*
oo oo
co <»
CM CM
o o
00 00
,•
f> CM
vO vO
C3 O
O O
m in
O CJ
^ '5
U. L-
0 CJ
i i
Ol CT)
O fl
•— ro
4-" 4-"
3 3
0 0
+~ ^ 4— ^
^_ ^_
I- (D 4-10
ro — to —
o o o o
CO ,c O
4-6 4-6
4 4
3 ID 3 ID
O «
— t.
O *~
10
Rainbow
Sal mo g
93
-------
1
c
o
z
8
i
4-
Si
«•*
• _l
O 6
w
a
? ^
n o
r
&
ft
151
^- ~J
c ^v
O IS
c **
M
W
**-
**-
LU
"»
1
8
1
5
«
O)
ID e
(/)
e
3
8
"^
V
a.
CO
o
.,
£
.
—
T3
4-
0)
,.„
§
__
»
CD
Vi4-
0 ID
^3
4-
ID
to
in
*
t
*
yD
CO
**fr
»
o
A
O
in
O
_J
^
*
(— •
U-
o
$*
T? >•
— L.
O •*-
t
+.*k
3 C
0 0
ID
2CT
5 0
c E
'TJ ID
££ ^n
03
O>
„
~
.
ft}
•t~
Q)
I
(C
0
"8
>A 4-
O ID
4-
ID
tn
^
.
*f
*
in
CN
Kl
O
o
in
O
_i
^
t
O
r
T-)
O
1
•a
i
3 C
o -o
(0
* CT
li
ff* (0
OD
O
•<
^
s
_—
(0
0)
._
L.
(0
™
8
"8
^^ 4-
O 1C
CO l-
4-
10
(0
in
*
•t
*
O
I—
K>
O
o
vn
o
_j
s
m
k—
LL.
O
5*
in
O
1
T3
1
4^ 0)
3 C
O TJ
(0
* CT
c e
10 (O
a: to
CO
o^
fc
r;
^
»
iD
4-
O -0 O T)
(O ID (0
BO » o * a
5 O O
5 O O O 5 O
- e cr s c i
D 10 ID ID ID (0
i to or to x. to
1/5
3)
Ss.
C
5>
^
3
cc
•^
c
01
3
i:
*c
9
03
^
tf
KV
g.
vO
«?f
"f
9
O
o
in
B
•s.
ft
t
o
5
0)
\o
o
•
o
3 C
O T)
ID
B o
e 6
ID ID
a: to
S
CD
k-
r_
Co
3
a'
•a
c
O
in
r:
H-
^"0
co
o
e
K1
5.
CO
f-
*
0
o
m
5;
%
t
0
I
01
vO
o
*
0
3 C
C T>
ID
got
^i
^ (D
or to
o
h.
C"
oi
lA
3
•£
C
1—
in
CO
_
*
s.
1~—
o
(N
O
O
in
"
z
•,
tz
o
^
01
00
0
fl
o
3 C
o-o
ID
lg
ID ID
a to
ul
1/1
(D
s,
o
Cn
v)
3
a'
•o
c
3
I-
CN
01
co
CN
00
CO
CN
CN
O
O
in
S
ilk
t
o
f
CT
CM
*~~
O
4- O
3 C
L l-
4
10
* CT
c S
ID ID
a: co
t/i
01
c
K.
>i
*/>
3
a'
~3
C
O
Ul
3
jC
h-
00
CO
CT>
,
CN
co
co
^O
fO
K>
O
O
in.
O
S
tz
o
*
ai
^j-
f—
o
- i.
4- 0)
3 C
O ^D
ID
lo
c 6
ID ID
cc to
(/I
I/)
a
H
>i
vi
3
a
^}
c
in
^
a
CO
co
0>
t
CN
oo
*
r-
fO
o
o
in
y
£
M
t
O
*
Ol
in
^
•
o
'l) C
ID
* a
So
c e
(0 ID
a: co
-------
^^
1
A
Jo
u
fe
«*-
S
.-
ox
c
+- ~
wo
r
si
i*
C X
r
JU
4"
o
H-
UJ
W
1
i
1
i
*
o
£8
(/)
6
•••» o
_)
IS
«
i
to
"in
i/i
n
k
c
O
i/i
3
cr
«5
C
0
f-
•3
1—
0
0
in
,
CM
in
o
r'
^
r-
O
O
O
S
t
c;
I
CD
IT-
. —
•
o
3 C
0 0
-t k"
10
s cr
O '
JO O
c E
ID ID
CC CO
1?
l/^
O
L.
CX
c
S
l/J
^3
rr
•s
c
0
t-
L.
f-
o
*
CO
o
"1
CD
0
•*
O
o
in
0
•5
t
o
X
z>~>
CO
• —
o
1* [__
-1- 0)
3 C
O -0
1C
ID 10
D: en
"Ti
u)
h.
cr
O
u)
^
cr
=a
c
O
•H
10
L,
3
^
CO
C7v
a
CM
r-
CO
r-
CM
K>
o
o
in
O
S
t
o
if
•7)
CO
«-*
0
3 c
O T3
10
JD O
C E
It! It)
a: eo
in
in
at
k
c
0
V
a
or
.«
c
O
11'
^
(^
CO
-u-
0
rO
CO
CO
r-
\o
CM
O
o
§
X
t
c?
:L
en
K1.
cv
*
o
3 C
O "d
(O
* a
So
c E
ID ia
cr co
"^
lO
ffl
k
c
S
I/)
3
or
•xl
C-
O
u
3
(S
CM
00
,
«
"~\
r-
00
^
o
o
0
o
in
0
S
t
c3
^
(.Tl
f*~(
cv
o
» L.
•i-
*
O
3 C
O T3
10
Ii
m its
cc to
10
I/I
ID
fe.
C
0
U)
3
•3
C
^
U
.C
t-
v
0
co
CM
co
o
CO
CO
in
P-
o
o
o
S
k
C.)
5
cn
S?
(M
o
3 C
ro
Ra
li
(9 (D
cr co
i/i
in
o
k
c
0
in
i/i
3
a:
-<3
C
O
L*
1—
O
C,
r-
e
CM
CO
^
CM
in
o
o
in
IT
t
O
•£.
Z
cn
r^
T3-
o
3 C
O -a
«i
ig ID
& to
^n
U)
a>
k
c
S
m
3
a:
•0
c
^
in
u
3
^
O
O
in
CM
in
co
r-
o
r~
m
o
o
in
S
E,
H-
h.
O
X
m
i-^
•ct
o
3 C
O T3
ID
c 6
10 (0
a: to
'in
in
k
c
S
in
3
•4
C
$.
W
1-
3
C
K
r-
CO
j _-
4
r^i
in
CO
r-^
el
i^
vO
O
O
in
O
sr
t
O
5
OT
^_
ID
o
3 C
O TJ
10
* a
C E
m 10
CC CO
"tfi
in
k
c
0
in
3
a:
•e
c
£
3
CO
CO
CN
""\
S
CO
o
o
in
0
£
t
O
X
ra
,
o
r^.
r> c
O -o
ra
* a
c e
(D ID
o: co
U)
m
k
c
8
in
3
•0
C
I.
3
fr-
CD
M
*
CM
in
CO
r-
r_
\o
0
o
in
O
S
r-
CJ
5
cn
(M
O
^_
3 C
O T3
Ja
o
c 6
ID 10
cr to
10
in
a>
a.
c
O
m
in
d
°e
c
in
i_
3
)—
co
^
9
C-l
^
^
>o
CD
o
in
o
£
^
CJ
X
2
cn
r^-
^.
§1
>s
li
(O (^
a: trt
to
<5
k
c
o
10
U)
3
ce
.3
c
O
L.
h-
co
CO
^_
•
CO
r^
CM
r-
CD
o
m
O
z
H-
O
i*
0)
1—
,
3 C
O "0
ID
n O
c E
ID IO
ce co
95
-------
1
o
10
0
c
L.
£
2
>3
O V.
• Q
Q5
e
Ss^
loo
kt.
*l
It
S *5i
c •**
.0
tj
V
*•
*»
Ul
«
in
S
I
a
0
J~
o
a>
1C 3)
4- N
CO —
» "*
_l
*
8
1
"in
L'j
o
fa
C
O
if)
13
o:
«3
C
1/1
01
fa.
c
o
1/1
3
o:
•o
c
0
Ul
3
"
CM
«
0N
.—
«
CM
1—
00
r»
00
vO
O
o
in
CJ
_J
z
•*
1 —
u.
o
X
CD
o
(N
•t i
4~ w
3 C
O T5
«3
* a
o
c E
10 10
in
m
in
ID
fa.
-
8
U!
3
cc
•3
C
O
ui
x:
H-
*
9
oo
03
CM
•s-
•*
*""
O
in
CM
o
o
in
o
f.
A
t
0
*
01
rO
vO
* l-
4- 0)
3 C
O -0
<0
r cj
So
c E
IO (D
(£ CO
"in
in
5.
-
o
m
m
3
a:
•6
C
O
VI
3
»
co
CM
v
CM
3
^
c?>
«g-
•
0
o
f_>
_J
s;
t
o
X
rji
r--
•
'£»
** i.
•f~ w
3 C
*" «
* 01
So
c E
10 IO
a: co
in
3>
i
=
0
Ul
>n
3
cc
•a
c
Ul
!-5
P
Oi
9
^*.
CM
0
CM
O
^
CM
t^\
O
O
in
o
.j
5-
t
o
if
en
C'
; -
._
* ^_
4* 0}
3 C
0 -0
n
RQ
2 0
c e
(0 ID
in
C!
L
n.
c
O
Ul
1/1
^
or
^s
c
o
Ul
3
JT
1-
CM
03
C7N
M
—
O
o.
^
^
«f
0
0
o
m
o
i
2
1—
U.
0
X
^
C.D
O"i
r-
* L.
4~ Q)
3 C
0 -0
(0
s cr
So
c 6
(D (0
-------
«
8
w
V
"S
K
~
°!>
0 If
CO
fa.
c:
'~
O
CO
3
o:
-3
c
O
en
3
xr
K
0.
vO
LO
CD
fa.
c
s
in
3
a:
-3
c
O
-*-
m
3
c:
>—
ON
^
I/I
CD
fa.
c
O
in
CO
^
a
«fl
c
O
CO
3
x:
t-
vO
VO
in
in
(D
fa.
c
O
in
en
3
0)
fa.
C
O
CO
CO
3
££
«3
C
O
-t-
(fi
3
f^
''"
co
*
I/I
k
c
0
in
3
^,
C
0
in
3
f
^
10
^;
oo
r
i
JB
«
K> C7\ O
CM CM lO
in ^- o
r-. co O-.
• « •
| r- r~ r^
O K1 K*
•— CM rO
in 10 co
o o o
o o O
in IA in
O O 0
S S Z»
t t t
C 3 O O
i* £ i*
en CD en
— O K^
CO Os O^
^ t •. L_ ^ i
0 C 3 C 3 C
O T) O "0 O T3
fD (O *D
* a 3; cr * a
O O ' 5
jQ O JS O jO O
c e c e c e
TO 10 (D fO (0 (D
ttT CO CC (/) Cti C/)
ON ^^ O
£ £ £
o o r-
l^~ C7N CO
• • •
r^ r- r-*
CM VO •»
«t r- r-
O C3 C5
o cp o
in ir\ in
O O 0
t t t
O O 0
•»«»•«*
X g X
CD
co en
m r~ •
O\ ON —
3 C 3 C DC
o -o o -o o -o
ID ID ID
* cr * cr * cr
0 O 0
-Ci O ^ O -O O
c e eg c E
ID ID (D ID ID ID
a: to cr co a: co
CTi
o
CO
•
f-
1O
(M
CD
o
ITl
o
t
o
en
CN
•
3 C
0 13
ID
sc
li
ID ID
a: to
1*1 o "* «—
•a- •«••<»• to
in r-- CM "cr
vO lO lO VO
• • • •
r*- r^ r~- r^-
•a- ON in <•
O 00 f^~ *^
•a~ to ro to
o o o o
o o o o
in in in in
O O CJ O
z: s s s
t t t t
o cJ tl tJ
i* i* i" f
en co en o>
tO CO *~ ON
CN •f in co
3C 3C 3C 3C
OT3 OT3 OT3 OXJ
ID ID ID ID
*CT *CT *O *O
O 0 O Q
^)Q ^JO ^jQ xlO
cE c6 cE cE
IDID 'O.fl? IDIO lOID
CttO Qfto Q?co OTco
VC (M < Ox
w^ tO l*"l (M
\O in CTN o
IO vO lO VO
• • • •
r- r- r~- t^
CN r~ CN *—
OO vO CJ^ CO
to to to CM
O O O O
O O O O
in in in in
CJ 0 0 0
s . z; s:
t L t t
O O O O
CD en cr> en
\o oo *o 10
• • • •
fNJ (Nl J^i *f
CM CSJ CM CM
oc nc ac 3c
O"O O"O O"O O T3
(0 ro ro to
*o| *cr( *<^j sea
eg ce CE ci
(0(0 (0(0 (0(0 (0 o:(/) crco ctto
07
-------
8
3
9
*
«ij
• s
°5
«
•£,-,
«o
k*
H
li
T™ '
11
r
XI
w
+-
LLI
in
^j
£
i
8
§
V
5
0>
£ 8
W) —
to
^™ i
Zj
1
3
e
+•
I
: «
~Z K
o i
K w)
tn
m
(D
k
c
O
m
3
CE
•a
c
O
in
3
j~
t~
f*.
co
«
—
iA
(•-
•
vO
IA
O
O
lA
O
S
t-
u
c)
f
CO
CD
o
iTA
CN
3 C
o r>
1: ^
(0
So
c e
a 10
cr co
U)
L.1
o>
k
—
8
ji
3
a:
•a
c
O
4-
in
3
XL
t—
CN
f~
CO
•
CSI
vO
NO
(N
O
0
lA
O
J
2
t—
u_
O
*
0)
o
IO
CN
•t- (B
3 C
O -0
V- l_
10
S cr
n o
c E
10 IO
cr to
in
en
Q>
k
c
s
in
3
or
•o
c
o
in
3
c:
(-
K1
r-
O
ft
fO
O
1 —
CO
CN
O
o
in
o
s
t
CJ
*
en
o
CO
CN
o -o
U 1_
ID
t a
10 (0
cr to
w
o
k
c
0
l/>
Z3
cr
•a
c
O
in
3
rr
I-
CN
^
OA
^
-------
1
I
tfi (/)
in i/» (/>(/>
(D 3) 3
orcrcrororororc
.c £ x:
in in in
c c c c cincmcu)
O o O O o CD o ® O w
4- +- 4- 4- 4. i 4. < 4. • .
in *n in in m Q. m o. m o.
£Z- a jC C. C "~ jC *"~ £T •—• .
i~ H ^_ |- j-^-* 1— ^ H- v- h
or^'Or-'CO'—rs*'
i^* r~* •ii r*- co o* ^> c
r~^ o\ vO co u
« CD CO O • • »
O « • •f*"\f^O^C
o\'^rmrMOrN«^a
s£)v01£>*J!3*"*-"^C
r^r-r^f^cooDr^f"
*tQr\(\jK>p-'i>J^Q''
po ^f ^ \O r**- ^ r^ c
(Sj c^i r~ ^~ yD \O vO ^
OOOC3CDCDOC
oooooooc
inininLnmintnt/
oooooooc
S'SSirXEJ
U. IT [Z Lu CT IZ U- U.
c? c
ro K^ X 3
O O CN
o-o 5 V V % -
f f f i 55% I
CO O") CT CT*
•J) D) O) C
O \Ct CO vD
*^ ch o^ C7N r^- co r~~ *-
— T \o in • • •
( ._ ._
3C 3C 3C 3C 3C 3C 3C r
On O-o, O t3 0 tJ OX) O T3 O -a C
10 ID 10 10 10 10 10
*cr >o; *CT »a *cr *CT BCT J
O OO 0 0 OO(
cE CE cE CE eg CE eg c
a. m B. on v) m in in
§£ be be b b b b b
"CNOxOfO*— CN^
NONONvOvor^-^OND
~i ^ in — r- o — CN
*JCS4CNVQ\QCT»CTi Ol
soNjrmcp — — 10
-p-r^-r~-r^r~~r*- r^
ft — vo-— r-iM —
^yOCNinoc7N<P^O>COCOCOO CJv
3OC5CDC?OOO
3OOOOOOO
•\inininininmin
30000000
^ ^ s: s y -s s s:
: t t t t t" t t
5 •«• •«
o <~.
* CO
M CN Cvi
•«• "V t o o o o o
:xx ^•••J-^-TJ-^
' S 5 I i I I i
O> CO O)
T) 05 cn cn en
O> ' — \O
- oo *— *r 9 f— • *
« • • »v— «oco
j •— CN CT* -— r^* *—
rfe +-"fe ^"fe ^k 4."^ +ri5 ^"fe ^rk
3C 3C 3C 3C 3C 3C 3C 3C
)T3 OT3 O"O OTJ OT3 O-O O"D O"O
(Dfl3(O(0(O(C(D(0
•CT XCT SO" JCT XO1 JCT 3ECT XCT
' ooo o o o o
:6 ce cE cE eg c£ cE cE
3 CO m (0 (Q crc/> crto (Ten OT(/> (roo a:i/> txc/5
99
-------
JQ
n
8
c
fe
I
>2
^5 *^'
o't
*•*
5^
"So
*-
-r
*
!•;
ID §
i
T™ mj
C ^^
1?
C •"••
Ti
«*.
•*-
LU
in
H
1
8
1
V
6
$,
£ 8
o
±b
1
"5
w
o
:
•7
CO
c
o
in
b
.c
t—
o\
^
*
u~\
_
NO'
u
CO
in
f~
O
o
o
s
t
o
5*
O)
NO
o
+" «
3 C
O -0
ID
SCT
§g
2£
0
CC
IT
0)
c
O
in
l_
3
.c
ON
f
r*
^
§
NO
O
co
o
o
in
o
3:
t
o
^
en
o
ON
t* is
3 C
O T3
t i
10
8a
13 0
c E
c
p
l/>
jE
00
e
""•
^
R
CO
0
ON
ON
O
8
o
_J
X
t
o
i
CT)
O
ON
» L.
V fl>
3 C
o -o
gs
li
e?3
o
OD
*S
4>
C
0
in
I-
9
CO
ON
CSI
CO
00
O
•U
CO
NO
c?
0
in
O
s
t
o
5
O)
o
o
v"c5
3 C
O ~O
•t i
5 CT
O
(0 ID
CC CO
—'
.
c
Q
CJ
_J
E
t
o
*
O)
I-*
in
v"iB
3 C
O -a
ti
*s
c £
ID 10
a to
^-'
;
u
to
c
O
•t-
tfl
l_
|5
r-
m
tt
NO
in
CM
NO
r-
r-
o
\Q
0
0
in
O
E
t
O
i
O)
o
in
+-*!5
3 C
O "G
•ti
gS
n o
c e
ID 10
oc. co
• •>
\
C
a>
c
O
4-
10
jC
H-
NO
NO
in
CM
m
r-
r~
^
ON
0
O
_J
•s.
t
0
g
O)
NO
4
+-*i
3 C
O T3
t i
10
li
ID 03
Ct t/1
n
t
-,1
'cs
c
o
in
3
jC
^
g
ir.
o
UA
r^
K>
^.
•£>
A
O
o
in
O
i
•s.
t
o
5*
t7)
CN
M
+-* c5
3 c
o -o
i. l_
oS
li
10 ID
Ot l/V
-
*'
AN
0.
•0
•o
Is
c?2
^^
00 10
in ^
O
•
in
i
CO CO
o
NO
m
o
o
o
_J
•£.
U.
0
X
z
C7)
^«
co
+-*k
3 C
O 0
ti
10
la
c E
ID 10
CL' CO
•''
i1
a
<*3
•o
O
-D -Q
£2
~2
in ID
CO V.
1 3
9,
CM
1
CM in
o in
CO CO
o
ON
P-^
100
-------
t
'
' ~
CO
1 ._
(J
m
(D
Q_
-3
8
s
1
-a
1.0
C CM
.- 00
(D (^
H "S
« _ll VI 4-
Q it T 3
w>' r£"io
1/5
5^
a o
L •
1"
1
cs
^>
t—
I
OfM
o| co oo
c
151
4* «J
C *N
Q g
r
1
HI
*
in
1
I
(N
O
•
in
O
S
t
_i
8
1
o
&
+• 2.
in
3 5
o
5
CD
08
O
^^
1
c
1: « ™
O 4- IP
o 3 c
— o -o
L k-
• 10
n a
1- 01
Ra tnbow
Sa Imo g
._
^_ ^_
o o
4- 4-
o o in
in in r**
® o o^
CL CL —
i i
in vo CM ON
oo oo oo co r-
t^ r^ "o
h- CJ^ •—
O O —
O O O
in in in
CJ O O
s: 5; ^
t t «r*
cJ c3 o
/ f 5
CD CD £
\o r^-
r- ^r in
• « i
o — -q-
— —
4-" l5 4^ CO
J C 3 C *
0 "O O T} a.
4- — -F — io
10 (0 U
s a * cr
0 0 ' c
.Q O JJ O O
c e c e E
1C 10 «3 10 8
CC to CC 10 O
r- p-
C7* C?v
• •
10 ro
a> o>
r -5
— N
& s
1O c
„ ^ [ QJ
a L o u.
l_ £ 4-
Sc in - 3
— 3 L —
*: c ®
1/1 in o c in
3 a — —
C C — .CO.
— (BE in O
I. -o a) u
V O O dP O
o) c5 ^ or z
Ov
r--
cr»
•
**,
a>
en
1C
1
%*2
^ ID
CO L.
1 3
— 4-
CO 10
to
in
0
IO
CM
r~ CM
r~ oo
o
Q
CM
—-
O
in
o
s:
•s
t
o
£
in
00
1
IO
in
3
L
» a
b —
— a
c. in
in
m
Spotfin
Notropi
O^
Cft
•
—~
10
^_
o
8
s
Lu
Cj
*
CD
S
0
m
10
» E
O L.
C Q.
18
Fathead
Plmepha
in
in
E
0 L,
C Q.
18
Fathead
Pi mepha
m
in
CO
cl
c
*
(0
4-
6
0 t.
c a
c
— in
e m
Fathead
P imepha
m
Q>
cl
c
ff
IO
4-
urston
f
DO
oo
in
9
fO
w
vO
"^
00
^
ON
%
O
o
u^
o
y
f;
o
^
O)
CTi
O
in
a
• E
Si!
C Q
C
— in
E
h.
c
•
IO
4-
urston
^r
h-
iO
r?
A
CM
OJ
O
00
fO
r-
CM
O
O
y
tz"
o
I
CD
CM
(M
O
in
10
» E
O 1-
C Q
C
Fathead
P I mepha
i/i
m
0)
b.
c
•
m
4-
¥
urston
jr
10
t—
o
CM
vO
O
oo
Q^
in
CM
o
in
O
3E
h-*
U
o
X
2:
CD
CM
CM
O
in
10
(D
O l-
c a
Is
Fathead
Pi mepha
101
-------
S
c
k
o
cc
~
OX
O'g
1C
^
m
in
n>
k
c
.
(0
4-
c
o
in
b
£T
t—
in
t
CO
(0
fc
01
I/I
k
c-
.
1C
4-
c
O
tn
b
c
0
1C
*
in
in
(C
u
Q.
C
.
10
4-
co
1C
%
in
«
0)
k
c
.
1C
4-
c
O
3
r:
i—
CO
(0
^
i/j
m
0)
k
c
.
10
^_
®
c
$.
in
b
r;
CN
CO
ro
*
m
t/i
ID
k
c
0
1C
4-
C
O
^.
U.
3
H
CO
CO
10
*
in
ift
C5
k
c
.
10
4-
CD
C
0
I/I
f
\-
*
co
10
•i
in
V)
CD
k
c
.
10
^,
0
c
d
U)
f
!-•
ID
«*
in
tn
0)
k
c
.
1C
^_
CO
c
o
b
^
*
r^
(D
»
(/)
(A
o
k
c
.
(0
^.
CD
C
o
U1
b
_£-
K
\o
«
CO
(D
^
y)
i/l
o
k
c
e
«
4-
O
c
0
in
|
f
CO
(0
%
c/1
(/I
©
^
C
*
(0
,
to
c
o
in
b
.t
V-
p-
01
10
^
in
in
C
o
^_
3
t-
co
(0
«.
(/)
^A
CO
k
C
**"
.
10
^_
CD
C
1
in
b
t-
K1
O
CO
in
0
CO
o
CN
a
O
co
co
0
§
0
o
L
e ^
ft "**
^
^
<«••
UJ
CN
co
o
o
in
o
""
• !
M
1J
*
8
J_
1
c «
4- N
l/) —
to
A
_l
Z
f
o
TJ-
i
O)
VC
CN
0
m
10
"m
j O
0 u
c a
c
'i co
U)
CD
in
10
§~
O u
C Q
C
18
^2
G) Ci
r- av
4~ t
10 —
u- a
•—
o
in
O
Z
f
o
•
4- e
li- Q.
in
r'-
I**-
o
o
in
O
. j
I
t
CJ
w
i
(7)
CN
^J"
O
in
10
S
^t o
0 L.
c a
— in
6 CO
X) (0
SJ=
a
f: CD
4- E
ID —
in
o
in
O
•z
t
o
TT
i
Oi
r*-
T
O
in
10
a
^ o
O 1_
c a
c
- in
E o
X) (0
9 -c
CD a
jC O
10 —
IX O-t ii- 0_
in K
co r-
1 CN »"
CN !'
• »
*l —
o o o o o
in in in in in
O C
z a
) 0 C
: z 3
t tz t t
3 O
: s
: t
O CJ O O O
••t
en r
r~ c
'J- u
:* ^
~n
0) r
5
^ co c
•a- •«•
I 5
-o n
j «•
f^-
S
O
i
Z
f
o
^»
C7)
^f
c?e><3-^ — •-'•-•~
in
(0
ID
* 0
0 L. <
C 0.
c
is -
•0 (0 T
ID £
CD a
.C CD J
4-1 4
10 —
Vi- CL u
in in
1C 10
(JJ flj
CO jt O '
D t O U <
r S. c a i
: ^ c ^ i
- tn •— tn
= CD E CO
3 10 "on 1
gjc ro ^r o
a CD a. (
~ ffl J CD -I
- E 4- E 4
0 — (0 — <
i_ CL U- CL U
in i/i (A
U O !_
: a era
re
- ui — in
= (B E CD
3 (O -o «a
0 .C (Of
) a CD a
- © .c so
- E 4- E
o — ro —
L CL U- Q
(0
"5
^ o
O U
c a
c
— in
E CD
-o to
10 .C
CD a
.e CD
4- E
10 —
U- CL
01
10
li>
j O
O U
c a
c ~
IS
T3 (0
(0 £
co a
4- e
10 ~
i_L Q^
10
(0
-------
1
0
a
'
8
1
c5<
%)
9
£ **
jj o
l~
(-
i^
Concentr
\
t
LJ
1
1
8
J"
o
f S
tn
*
_j
f
V)
(f>
1/1
CO
h.
c
.
"3
£)
r~
O
O
o
^-
t
CJ
5
en
f
Ul
(0
* §
O L.
c a
c
18
io sz
•H E
ID —
U- Q-
l/l
m
CD
h.
c
—
.
10
0)
Thurston
r~
^3
CM
CM
(M
in
O
r--
°i
a
s
t
o
i
en
m
in
10
.f
gcj
c
18
® a
•*- E
10 —
u- a.
tn
to
h.
C
—
.
(0
•f-
1
00
00
0V
CM
VO
f-
I--
^
o
in
s
t
O
5
ai
in
in
10
'1
O I.
c a
c
18
•0 10
li
10 —
la- O.
l/)
(/I
01
h.
c
—
.
10
t
Thurston
CM
•o
r-
, —
(M
<^-
CO
t"
O
CM
0
IA
0
x
t
CJ
1
CD
r-
i/t
10
.1
O L.
c a
c
18
a> a
f 1
10 —
U- Q.
1/1
IA
,
t
m
"
\o
r^-
r-
S
o
in
j.
t
o
i
0)
-~
CM
10
.1
C d
C
— in
E CD
n 5
8 a
f 1
ID —
ll- CL
Ifl
r-
^
o
o
in
a
s
t
o
5
01
CM
(N
in
10
.i
O L.
c a
c
18
It
ID —
a. CL
in
if)
ID
h.
c
—
.
10
0>
Thurston
o
CO
ON
t
in
•
v.—
a\
r—
"^
o
in
O
X
t
o
i
Ol
HI
CM
in
10
.1
O U
c o
c
18
X? <0
tn .c
Is
4- E
10 —
u. a.
o
CO
.
10
4*
Thurston
HI
c£
0
H"\
"
•_
in
\o
u
O
CM
O
O
in
o
•x
t
o
I
01
CO
10
«I
OU
c a
c 1
18
•0 10
S.C
a
£!
10 —
U. 0-
u
00
.
10
0
Thurston
vO
OA
00
H-\
»—
»—
O
^
o
CM
m
o
o
s
s
t
o
i
O)
o
CM
W
10
* e
f O
O L.
c B.
c
if
10 ~
u- a.
o
CO
.
10
*
Thurston
0>
0?
0
CM
CM
00
^
O
oo
o
#
o
in
a
£
t
o
5
01
o
CM
in
10
-I
z o
O 1-
c a
c
18
If
u. a.
u
CO
.
10
1i>
Thurston
vO
ON
00
r—
ff\
00
^
o
r-
o
o
a
E
t
O
i
Ol
CO
in
10
* 1
0 t.
c a
c
1 0
"O (0
JO C.
f i
ID —
U. CL
O
00
.
10
1s
Thurston
CO
c£
in
HI
r-t
in
oo
0
00
o
in
a
X
t
o
I
01
o
CM
in
10
•1
X O
O t_
c a.
c
18
•0 10
S€
£1
(0 —
U- 0-
o
CO
ON
.
ID
S
Thurston
in
ON
CM
HI
HI
O
c*
u
f-
o
in
s
t
O
5
O)
CO
I/I
IO
•§
i k
c
18
~O 10
S£
Q
ID —
U. Q.
—
n
o
o
tf)
0-
*3
Reinbold
19826
X)
o
in
a
^
U-
o
I
Ol
o
HI
O
o
U)
10
ID
0 \-
c a
c
1$
II
(0 —
li- Q.
103
-------
8
R*faren
*^«i
• .,jj
O V
Qfl
1-
oo
1-
— .
*
ll
^ «J
§^
I
r
"t
w
LU
\
I
i
V
O
O
W 9
4"* M
—
•
«
—
n
C
Q
10
10 C.
^ ®
4- e
tJ- CL
—
01
4.
U
o>
f.
0^7
^-,
Reinbol
1982b
"O
(D
* a
-C 01
4- E
IO —
Li- Q-
<••
"5
4-
O
01
a
^_
•^
T)
Reinbol
1982c
•M
V
4-
«3
ai
o
i?
1
0 (N
CO CO
t)
o
«t
,
o
in
o
X
if
o
i
cn
S
c
O
U)
fe
p
• B
$
-^ 01
0 3
u) 0
4-
a) m
4- O
— 4-
-C ID
^ O
__
"5
4-
O
a.
•a
X)
Reinbol
1982c
T~l
V
4-
10
M. L
§5
10
in
O CO
O CM
co co
o
in
IO
,_
o
in
O
S
1—
a.
ei
i
Dl
IO
c
O
in
1
C
i* g
m
X 01
O 3
3 e
01 O
4-
0) 01
4- O
— 4-
f O
>£)
cn
*—
01
0
cf
c
"o
jr
o
t-
•c
4-
cS
C
o
4-
U ID
ID l_
a
VO CO
co co
^
CM
O
O
cn
o
5
g
o
r-
a
i/)
3
+-
- (D
^: -»-
01 O
* §
4- a
0 01
3
0 3
C —
cr ID
ID 4-
£: O
o -
*0
r>
•— •
01
O
C
j5
O
o
h-
4-
8
c
o
4-
t. O
(0 I-
8
S
i
VO 00
CO 03
u\
CM
O
in
O
co-
CJ
5
fe
O
I^M
8
in
3
4-
xt
01 O
— C
•4- 3
4- a
801
3
IB 3
C —
10 4"*
j^ O
O —
IO
o\
••—
tfl
1
r*
O
1-
"o
o
c
O
4-
l. (0
(0 l-
ffl 3
Z 4-
10
0)
O
IO
1
co oo
CO
to
o
in
C3
"
o
i
g
VO
r—
8
01
3
« 10
x: 4-
01 O
~ §
4- a.
0 o>
3
0 3
C —
C 10
10 4-
C O
O —
r--
r-
ON
>v
11
a.
•e
g
a>
in
r?
-Q
(D
%•%. 4*~
O (0
m u
09 in
H
p- —
r^ oo
3£
r—
CM
O
in
O
s:
tf
o
5
O)
,
CM
T
*
f--
01
3
• 10
.C 4-
01 O
— C
•»- 3
4- a
8 in
3
Q> 3
C —
C 10
(0 4-
.C (J
O —
r~--
f~f\
*~
O
i^
•<3
g
d>
in
T3
O
VI 4"-
O (0
Ol i-
00 ID
OO
CM
£8
r-- co
j^
CM
^
O
in
0
t
o
5
01
IO
03
1
in
01
3
4-
• (0
£ 4-
l/l O
~ §
4- a
So,
3
C —
c 10
10 4-
sz o
o —
_
"5
1
•0
-D
"o
X) T3
C CM
52
T3
3
C —
C 10
10 4-
J= 0
O —
__
lj
1
^
•o
T>
Reinbol
1982d
o
o
4-
10
fe^. l_
S3
4-
(0
CO
00
fe
CM
1
r- IN
r- co
O
in
F~-
_?
O
in
O
t—
0
i
CD
05
•
in
3
4-
« 10
n 4-
01 U
•*- 3
4- a
801
3
03-
C —
c 10
ID 4-
c. o
' J —
T--.
*
...
10
ti
C
O
i
tn tA
N (SJ
,U
\O CO
•o
r-.
in
o
O
in
o
n
CM
Q
X
i™
$
01
o
•*- —
— 13
3 g
TJ 55
01
c
J_*~
0> -4-
— ID
O ID
— 01
3 3
crxi
01 6
O ID
s: iO
r-
f*
™
1i>
(D
i
r-- CM
'- CM
1
vO «t
r— oo
•o
CM
O
in
O
CO
(0
s
CM
"~W
H
4~ — •
— 10
-o S
<. «4-
01
c
^T"
01 *-
— 10
*»-
O ID
V —
— 01
3 3
CTX)
01 E
O ID
S- CD
t-
t'1*
_.
(0
4--
0
S
i
1
r- —
— CM
I
r- oo
•o
CM
rO
O
in
a
CO
0
i*
i/>
ij)
4^ _
— in
55
M-
01
C
j-."Z
01 •*-
— ID
O 10
— 01
3 3
o-xi
(/) g
5~
104
-------
£
i
!
• -j
# o
QI
a
•? *-.
«3 U
L •
h-
•"£
1
ll
T" -J
5 ^i
e *-*
JO
1
UJ
1
JJJ
i
8
i
w
5
CD
£8
e
$
1
r- r
Ift L
2 ^
— .
10
+-
0)
c
0)
I :
i
i* c
-
O)
10
~ 10
TI e
UJ
t>
£ c
_ r~
J3 r~
D 3 0t
1
CO CSI
tO CO
U m
S CM CSI
I
I in o
^ >^ Cr\ in
j r*- to p**
O
O f-
3 —
? 0
i in
J C)
J i
3 5"
H «l
O CO
1
•>
(SI
^f O
' I
_ 8
- ID
3 E 0
8 I CO'!
ID
10
in —
— 3
C O
: •*- -t-
n ^*- 0)
-ID 1-
3 ID ID
-in •» —
3 3 >- —
7 jo a. u
n s ex «
3 10 30
: (5 C5 CL
to"
o\
"
>-
O)
I.
10
E
LU
C
ja r-
K —
1
tO CM
tO CO
(N
I
3Z
o
in
o
in
O
zr
M
CO
o
i
CSI
ID
ID
O
L
(0
C9 Q.
tO*
&
*~
>*
cn
ID
1C
e
UJ
•a
c
— r-
i
— CSI
r~ co
in
(SI
(
°R
o
^
0
in
0
jr
u~t
O
5
p-
co i
10
(0
3
O
(E
L.
10
„
G O
0 0.
r^ r^ r
r^ p- r
CJt I3t i
c c
O V
> >
ID IT
•(- +- 4
CO LO I
1 |
v£) SO \
O O C
O O
i in m
J O O
_l __J __J
s
^" ^
« t-
o
^»~ «~ U) C
& i g CO
' 10 $ ID 3
x a. in in
|| || ||
—
"3
-t-
0
Q-
•o
5.
II ;
?
S*
3 C
S
Csi «
•
CM C
(
%$ :
CO CO ti
o *
CO C
O u
— c
o c
£ c
n
t t
o c
i i
2 ,
o
13
1 f
oS «
in
3
jc O J
in c i
•- 10
c; O i
01 in c
C E I
<$ — 1 C
h h.
c c
_* ^,
^ _
10 10
•t-
0 in
^ o
j i
^ *
L. U
3 O
r $
? i1
_ ,_
3 2
in in
3 3
: ^5 ^ »
n c in c
-10 — (0
> H- >
. U CO
3 3
n in in in
5 _j CD —i
K
c
^
10
+-
®
^
o
McCorm
—
CO
M-
CM
CM
CSI
P-
^
tO
«
O
in
a
B
t
O
i*
i1
,—
S
in
3
j="5
in c
— ID
H- >.
C 0
3
in in
§ O
05 Q.
K
c
.
_r
10
4-
0
jt
O
McCorm
—
CO
^.
CM
CM
CJt
tO
CO
•—
•—
*
(N
o
in
o
[ J
3:
t*
o
£
i1
V—
ro
tO
w
3
J="®
lA C
— ID
t- >•
C O
3
in in
||
105
-------
1
1
o
n
10 O
1"
1
*
ll
Concentr
(ma/L
.O
I
tu
I/I
1
I
8
i
V
S
A
S1*
4- N
(A
o o ^ ^
i^J v£) v£) \O >*.
O> 0\ ON Ch (P
r— • — ^— «— • j^
(j
*•— *— »— /7 _£; c* _£ „
oococoooooor
> — ^— ^— Q) fl) (I) ffl «fl
ro i I 3E 3t
CT^ O O O »<9 *<3 «6 *fl Q
r- +-+-•*- O
ui ->->->.jQ
H~ j— ^— ij3 LU L3 u] fy
p*- ^o vO
^ K> K^ *— < — ' — v— *— ^^
• »»«»««»m
CO CO CO f"** O^ O^ O^ ^ C^
OIAO^ LT\tr\ir>iA
• • ••*••»
CN'* •^•inoococooorsi
'-- — -----CNJ
1 1 1 1 1
r"~- r*^ r^- »~~ vO vo m ^ ^ cr* O C? T*~
r- r- r- f- oi o^ Ot OE u*\E fnE t^-
in • • * • • O
.r--ocorsi — (Ntn •
«3- . « — CM^-^mo
^O OD
U> V) IA IA
3333
1- 1_ L. U
in v) m ui — • — __
3333-C^rJZ^r
j\(riu>tfiOuoo
OOOOoOOO
-.O *jQ ->i *^ L. l_ U L.
f-QTJ.OiO.O^.0 O O O U
CT (DO! 1DD! ®O" "E *£ •*£ •*£ ••
tf) */> ID W — — — — —
ct/> c(/» ct/> cin — —
r\ Q Q. O Q, O Q. O (DO flPO wO (DO w
§a 6a Ea Ea 3Q- ^a 3£ 3Q 3
ID 3 Cu 3 ID 3 ID — ~ CD — ID -~ ID •"• ID ~~
Q 1 Q__J CL — 1 OL — 1 O3_l O3~l 03 .-J OC| — 1 OD
(D ID CD
>->>>> 4. V 4-
jC £: i: O O U
o u o in in in
__ _ ._ <5 (B a)
OL a: 01 a_ a. CL
o& «^ *<3 ed o£ «d
£ £ E T3 T3 TJ
O O O ~0 ~Q ~O
O ID II) Cl-MCCMCCSI
in i/i in ~ co — co — co
Q)
4- 4- 4- 4. o 4- VI •»->%•)-
ic ^^ ic ^^ ic %*^- ic o ic m ic i*^ 10
L mu rou. — i. -- i. cot. ou
3 O>3 O>3 O>3 |3 13 13
4- 4- 4- +-!<•> 4- t 4- r- 4-
ic ip io (or^ic1 cocoic
Ln CO C/> to i-T> U^ CO
O 0 if
CM CM CO *J in ^
CM CM CM i-\i
t 1 1 1 1 1
m (7* CM o^ [™^ CM co cs r^~ co in vo vo
— CO— OOO\ — CM IO * CTvCM OCM
co r^co r^r*- coco cooo r^-ao coco
x. u o o
SJC H O CO vO
•— co in c*v c^j
• • • • t •
O — — O — 0
O O O O O 0
in in in in in in
O O O O O O
3C S £ X S S
t t t t t t
O O O O O O
i i i 5 I 5
O) CD C7) CO Cfl U)
r*- '-O CN CXJ •— O
CN O Kv, O — *M
• *•*«•*
o o o o c o
in in in in in in in
3333333
C I- L. L. I- l_ l_
f /r _£; f _£; f^ f
8888888
L l_ L L U L 1-
O O O U O O U
i -I .i .g -I «g .1
in — in — in — in — in — in — in
s ys yi y g
-------
jQ
D
a
k
•
^^
• _j
°^
a I
^
L
ON
or —
^
5
CT1
E
in
VO
CN
-
3
0)
^ O
Ul —
in o
S3 "O
Ul
1 k
0 4-
= £
Ix
CL
0)
K
C
*„
.
~.
ft
4-
Ul
D
1
L.
cn
r^
C7^
p*
t
(SJ
CN
•
•
10
IB
a>
N
t
\Q ^~
r- oo
.-—
CN
^.
co
o
Q
ON
O
0
in
s
£•
t
O
i
cn
oo
r-
C5
U>
fcs
4- 10
L 4-
10 U
' S
4- in
O 10
angethr
heostom
O LU
r--
v—
•
ID
IB
N
|
in •—
P~ CD
CN
CN
r> in
t— CO
u
f-
o
o
in
O
S
t
CJ
5
0)
p:
•
« _
® O
tl 4^
ID O
-O 0)
OL
4- 0)
O (D
angethr
heostom
O LU
3)
».
0
in
0)
Q_
•O
13
Ifl
— oo
T3
0)
4-
vi us
O L.
O 3
— 4-
ID
•
00
1
— VO
00 OO
O
vO
O
o
in
o
z
t
o
X
z:
"O XJ
4^ "5
E
3
(B
4-
C
0
•o
•> 0)
ID 4-
>- 01
CD O
— N
f 1/1
j>
t"
O
Ul
0>
CL
"fl
•o
C CN
— co
c?2
T3
O
4-
VI. 10
r» L
ON 3
A3
CN
*
co
l
CO HI
r~ co
o
m
CO
d
o
in
o
|
5T
t
O
5*
•o xi
t —
vO O
C
|
L.
4-
C
O
E - 0)
5 ai 4-
0) >- in
L (DO
Y- — N
> ID 4-
f 01
:<
f>
in
1/1
3
o;
«3
C
O
4-
01
b
^
ON
CO
«
fN
"
CN
O
oo
ON
O
in
i
X
!r
o
^
cn
00
•
^
c
Q. —
— T3
13 k.
O —
£ J3
3 -0
o d) 01
- 4-4-
— 4-4-
> O Oi
sol
107
-------
o
Q
c
9
fe
1
O^^ !
7N|
°5
e
4- ««
IDO
L •
1
^
^^
+- ±
O Z
T" — J
S^^
J^M*
ja
1j
O
4-
Ul
%>
•o
2
i
^B,
8
1
o
U>
•P *
to —
* W
_j
1
.»
^f
e
3
e
»~ tf>
• -
CO 00
p^- r^
Ov O*
• •
— —
ID ID
4- 4-
CD CD
C71 O)
o o
l_ L
4- 4-
ui in
E £
k k
fO K1
r- r~
CO CO
CM CM
«f O
^ VD
co r—
**-
co -4- in
Lu ^ O*
— • •
0 — 0
UJ
a.
i/)
a:
LU
i -
f
_J O O
< in in
en 0 0
X Z
r? a£
o o
X I
in in
10 ID
"O "O T3 "O
co O co O
lA A
CT a
co <5
_2 n
c c
O CD
in «
O O
E E
jr .c
0 0
ID 10
L. U
•* o « n
CO CO
no ID o
L. 10 1_ ID
as CL s:
CO
r--
B
_
ID
^_
CD
O)
C
O
4-
E
fi
r^
CO
CM
CO
vD
l^_
00
4
o
o
o
5;
°'
o
5
I/I
ID
CO O
pl>
a
senber
0
E
-C
O
ID
L.
Prawn,
Macrob
in
c*
•
ID
C
Wi
•0
o
c
ID
**-
CL
LU
1
O CM
l~- 00
0
CM
l
r- CM
r~ co
O
•o
i —
ff\
i
IN
O
in
O
—i
•5
oo
o
X
CM
f i
$
ID
O
C
a
• i.
d> >
>. 8
O i_
fi
C l/>
Faster
Crasso
in
r-
•~
ID
C
u
CO
•a
O
c
ID
•4-
Q.
UJ
1
O CM
r- co
0
CM
° fQ
r~ co
CD
•o
(—
1
9
CO
o
in
O
_J
;j
00
CJ
I
Jf-fc
T i
2
10
o
c
CT
« |L
4-
in (0
>~ CD
0 l_
c ui
Easter
Crasso
in
c*
•—
(D
C
CO
•3
0
c
ID
Q.
UJ
(
O CM
r-- co
o
CM
(
O rO
r- co
CD
0
in
I
CM
c
f*"*
O
in
y
^
CO
o
i*
CM
T i
8
ID
U
ID
C.
CD
O
L_
» I
ID 10
— — ~—
0 L.
10
Qua hog
Mercen
in
r-
•^
(0
c
1/1
«5
O
C
(0
o.
UJ
1
OCN
r- co
o
CM
1
r- co
(D
<^J
f
p«K
1
c
^>
O
in
O
jr
CO
O
i*
CM
in
r- 1
^
ID
L.
ID
C
CD
O
L.
- 1
ID IU
__ *^
O I-
10
Qua hog
Mercen
r^
en
cn ~~
&, —
~- ID
. 4-
— CD
(0
^
•»- "f7
(D 10
i
c f
VCD in
? Z
_- a
CTi
ui . •
A 1 >O
o\
t
CM CM
CO •-
1- CO
•O T3
in CM
0 t
— CM
0 0
in in
y y
-, ^
CO CO
CJ
i" /
Jt
2 TD 1**\
~ \p 01
vo O 16
1 IN
tf\ CM
• 3
in L c
CD CO (0
a 4- o
— m —
a. — E
I/) ID
• c
•O ID (0 l/>
O 1- O 3
CD 8 u (5
CX 4- g £
8^ < x
j;
VO
0\
in
(D
s:
in
<- c
O
O ~t~
*- ID
O
qj . —
U C
3 3
01 E
o e
ex 0
CD °
$ •*- ra
L. O C
3 0
in c i/i
no u
64- ex
§ g
II T5 UI
r> •
J= O
T? \£> "
CD IB .a
JD O
or CD -f. -
4- r H. C
« L, K. 4- O
0 ® X C —
•> Z 4- 4-
4- c 10
ID — - —
4- in 1/1 3
in i_ L L. o
o 5 6 —
II •*-£;£ ID
4- 4- CJ
CO CD 3 3
^_ ID 'D K^
jc in £ E Z
O> C O 0
3 a. L 1_ C
o x •*-•»- —
L. CD
£ X3 T3 T3
4- -4- CD CD CO
1 O 4- 4- in
> ID ID 3
O - — -
— O 3 ^ ID
•*- - O U 4-
••_ — — IT
ii 'f 10 in *o
l_ O U
h- 3 CD U O 0)
108
-------
1
c
£
I
•
a
.0
e
1
1
1
1
!
l
1
i
-C
CL
(0
L.
O
_
irt
U
o
-C
V
^
m
1
C.
•«-
-o
0)
+-
.f
-t-
ip
c
o
4-
£
1/1
(D
F
c
«J
•t-
l/>
1)
-f-
*+-
o
v<
o
u^l
o
tr\
F >
lij
•
C
O
+-
(D
(J
C
Z!
£
O
_
10
c
o
to
i_
•
*
£X
C
O
-f-
tf
L.
3
(E
.,
c
Q
L
-p
5)
c
It)
4-
-D
Q
ID
-»-
!TJ
-o
C
CD
CT
>-
X
0
-o
0>
>
o
in
ui
._-
Q
mmun leaf ion.
o
o
_
(0
c
o
I/I
i_
S
a.
•k
•
>•
cr
C
o
4-
i/l
i_
3
jC
H
L.
«*-
Tp
0
C
(D
4-
n
O
(D
4-
(0
T3
0>
N
U)
_c:
U1
•4-
-o
c
-.
X
o
TJ
0)
>
o
IA
in
O
•
1
+-
ro
o
c
•3
P
Q
10
C
0
1/1
i,
i.
^
CD
•,
4-
O1
U
D
JT
JK:
c.
ra
fL
*•
£
25
c.
^
c
It)
-)-
«
U1
c
o
.—I
4-
~o
C
O
O
4-
0)
4-
c
O
c
o
. —
4
t"
K>
$
•-
in
e
5
4-
n
in
e
o
L
*+-
-a
ai
-f-
(M
-
Z3
( )
—
(D
-------
9
U
s
fc
>•-
s.
CM
CO
(^
^~
+-
C
3
5
S.
c
»
ID
4-
®
8
in
3
a.
£
C
^f
•
in
•»-
0)
8
i/l
ct
escltel 1 i
o_
«3
•o
"o
"c rS
— 00
a> 01
or —
o
co
>*
a>
ID
CO
•<5
0)
U
CC
O
00
CTi
>-
u>
ID
CO
•a
-
ID
<0
CD
•9
(t>
O
r-
CTl
IO
(D
• —
u
ID
10 —
— 00
ID
• ID
ro — *•
.a .y!
15 . .
I/I 5>
CM 4-
O Q) —
•1- U 10
in a. jr
t, -* r~
S c cf-
t- ^ m —
10
•3
fc
n
i_ f^
ca£
o*
CTi
c
>-
$
•
ID — .
J3
* .
•
C O.
o ®
•f- u
t/> Q.
3 C
1— •>— f
*
(0
2
.
o
I
5
y
g
?
Q
•
CM
•
S
V
3 —.
— !•
5i
U-l
*"* Xk
SI
r
^*
$4
^<
j?
•w*
o5
QS
e
^
a o
v *^
K
*r*
5,
•
1
r
5
*t r^
O (N
H^ IT\
• »
O O
en
KI in
\O ro
^r r^
• •
? ?
a\ co
CT\ r^
— f>
CD CD
CO
LU
O
LU 1
n p* ^j" O
S> . .
m vo \o
(£.
UJ
1-
I
UJ
or
io -
« • •
•» m csi
CM CM CM
iCT*
in o
r^ r~ oo
O O
_J _J
— r»
•o CM 8 8
• • • •
o — o o
*t CM
§ 8
r— vo o o
• >ll
O — •* CM
1 1 CM —
»^l \O O O
in o o o
O O O CD
^
r^ •— (0
• ON L. 1 1
'"' 4i 3
ao 10
CO
1
CM CO OO
• • •
o r- o ^r •*
CM — CM
1
vo 10 r~- K> in ro m
h^ r~- 00 ^ \O ^o vO
CO CO
O O -l -J
_J — I UJ LU
n
8
•
0
CM
o
O
Q
CM
i
c5
i
•*
m in
vO vo
CO
-J
LU
"^0 —
O O
• •
0 0
j^
in •<»
CM O
o •
• o
O 1
O CM
— CM
O O
0 C5
^
O 10 K1 >O
•4-
in ro
• •
•^t a>
i
cr* CM
^ vo r^*
r^ r» r-
co
_i o
LU _1
c
O JC
10 m
O 00 —
• O o
o • •
v o o
+-
i
_ _
O)
t. r-
ffl CM O
Q. — •
a. • o
3 O 1
Y CM
VO ^ O
o o o
0 CD 0
CO CO O
A A *~
O CM O r*- \O r-
(/) C/) CO
_J _J _J
UJ LU LU
12
O
GO
00
»
?
CO
oo
o
CD
VD
O
•
CM
O
00
o
_J
ID
C
£1
C
IO
o
CD
IT}
C C
ID -C
t_ a.
(D 10
T3 —
- *
0 0
ID
C
• CT
C ID
ID E
10
*O -C
ID d
oS
ID
C
» a
c ID
ID 6
|1
10 Q
(D
C
- CT
C ID
*D E
0) ID
O —
O c.
•c jc
10 c^
— (0
0 Q
10
-C
u
I/I
j3
^
rr
K (/i
C 3
O .C
f O
sl
d O
a. o
10
-C
o
in
O
CT
• 10
C 3
O JC
E U
— C
C U
— c
Q_ O
10
u
I/I
5
h
CT
« I/I
81
E O
sl
c o
a. o
_
» L_
4- ®
3 C
O XI
4~ *-~
10
j§ O
c e
a 10
or co
* L.
4- ffl
3 C
O T?
•r~ "••
c E
10 10
a: co
._
* u
+- $
3 C
0 -0
^ .—
10
* CTi
la
L§ "
.—
** L.
4- »
3 C
O TJ
4— •—
ID
* CT
la
<0 10
a: co
c
o
6
SL-
ID
— —
+-
10 M
t(S
tft
(D
-1
* O
O L.
C O.
C
— in
e o
© o
10 ~
u- CL
110
-------
i
I
— "3
U -J
"c'cj
r
„
jE_i
^*
aj
r r h.
CD CD
4-4- C
• O O — ^-
— l/> to ID
ID " 0> - CD 3
a> . •« «3 .* ~; (g
SCX TJ T3 U a.
CD — — — 0> -5
•t- L O O EL
1/1 Ci. <*t (Q O u) t f\ r~
t- C CM C CSI 0 4-
DC — CO — CO O C —
x* •— ij) o^ fl) c^ o *~ E
I- ~ or — ft— S— co
VO
co KI r- CM
m in co CM os
— o CM r CX ^d. OCX
Oc Oc Oc Oc
05 ^-^ ^5 ^-* 00 *^^ CD ^^
i —
fO CO O^ CM
o -— tn vo
O 0 O O
CO
m
m csi o m
O CO *O *O
< O CM A
10 CM r~ rA
O — * »»
C3 O C3 O
OS CO (N CO
vo \o r^ r^
r~ r- r— r»
m CM pi CM
CM CM CSI CM
Csl CM CM CM
O in ro CO
UD CN CO vO
\D r~- r^ co
CO CO CO CO
-I _J _) _l
LU LU LJJ Ul
_o
4-
C?
o
•
•*
o
I
3
X
6~
®_
re x
> z
® _1
3?
< —
o
*
o
r-
CM
in
VO
•
O
CO
in
ID
C
•> a
c -
ID
w ID V ID
OO
•a .
ID
— ID
o a
10 a
— ID
o a
1
5 ID
c —
••» CD
v - i
J* o
0 L.
c a.
^f C
— in
K 05
C^W M
e
i i
—
"O (0
(5 -c
a> a.
r: a>
15 1
"- Q.
O
in
i_
CD
C
0
V
-* tfl
O 3
i/) 0
-t-
CD (/>
ji ro
3C 0
in
+~
- UJ
^ 4-
in o
<4- 3
4- a
in
3
— t.
CD 3
C ID
ID 4-
•C U
O —
in
3
in
3
__
£ 0)
in c
— ID
•*- >-
c o
3
m m
.~-
H
CD J
u
£
8
u
ID
. e
— in
._ «•
0) 6
IB 0
3 a.
— CD
ffi _J
3
CD
c
* O
1/1 —
in O
in
,C 3
4- L
3 $
O +-
E a
— o
0 U
J
in —
in O
5! •o
X3
in
JC 3
4- i.
3 0)
E4-
0
— O
g 0
CO iE
5
ID
l/l -••
m o
1/1
j± 3
4- t
3 3
fc a
- 0
— L.
ID O
CP
in —
u> o
in
i •
3 (D
O 4*
6 a
- 0
a b
co -E
111
-------
o\
CM
in
csi
vO
•
in
o
O
o
o
o
•
o
03
in
o
oo
(N
CM
HI
o
o
o
•
o
o
•
o
CD
1*1
ID
in
r—
CM
oo
Tf
O
ID
.C
in
XI
b
a
(O
c
* C7
adoceran
phnia ma;
— 10
O o
• in
C 3
nk salmo
corhynch
*~" C
CL 0
ID
U
tfl
jQ
a
* in
C -3
nk salmo
corhynch
— c
CL O
ID
-C
o
m
b
a
« in
C 3
n k sa 1 mo
corhynch
— c
CL O
' C
ID
" t
+- $
3 C
O t3
ID ID
ce to
D
* I
> 0
o u
c a
c
thead mi
mep hales
ID —
li- 0-
in
•1
k o
O L,
C 0.
c
thead mi
mep hales
ID —
U. CL
O
in
IB O
ID
I te suck
tostomus
-C. ID
3
in
•t-
in u
— e
t- 3
+- a
annel ca
talurus
C. 0
o —
in
a
in
3
« w
£ tt)
in c
— ID
•*- >•
in in
<£> a
L. «
c5 -i
2
Q
Q
j_
O
ID
— in
'oil
* O
3 a
~~ 4)
CD -1
0
.§
Ifl —
ifl O
j5
1/1
al Imouth
cr opter u
£ *~"
tn S
3
.1
in —
in O
STJ
in
at Imouth
cropteru
P HW
CO 2t
I
N
9
112
-------
0
— (SJ 1^
4- •
JD (SI CNI
$4
"I
U — 1 ON (N
— X 0\ -
§ J "2 ^
o J? *"
— o
^v
z
w O^ ^0
t • -J 04 r-
4 w 8
^ "^ '
,_ ,
3 3
m o
™ _
» o * o
tf _- 4/1 —
tno in O
(D "O to "O
& J5
01 tfl
JC D -C 3
t k ^b
»O 4- O 4-
E a E a
— — 0 — O
0 — L — U
• ID (J 10 O
6 g ~ E —
oj| y? Z to z
m
QO GO ir\
(N " II
f II
II t 01
i in
ID M 0 10
C C JO
01 c c
ID O ~ -C
6 E E 4-
— 3
(0 ID "O O
-C Jt x: —
a. c 4- m
ID — ID £
o O- •*— in
• Lit.
•*- £• *~ 2.
8
—
4-
10
O
C
0
i_
JC-
o
i)
4-
3
U
ID
O
c;
ID
ID
e
o
t.
o
o
^
1
c
£
C
5
«^
•
•
A
a
h-
.
ir\
O
o
V
Q
JE.
4-
i
0
i_
O)
•p
$
J^
~ r •—
5- -Z
i_ in ft
10-4-
0) v. in
0 (D
II C. 4-
4-
l^ 3 C
-J ID O
UI .-
6 4-
• O <0
03 t_ I—
— •*- 4-
O c
>- 73
d)
4~
3
(0
o
c
10
i
O
(D
§
5)
e
"i
*
^_
3
U
®
.
4—
in
n>
4-
O
C
O
O
Q
M»
'S
s
3
m
10
!p
4-
$
(D
9!
c
*~" '
ul
U)
--_
c
0
3
• — >
/
t"
3K
yl
c
"5
T)
3
O
(D
ID
m
o
in
^
4-
4-
m
Q)
4-
IP
O
O
0)
>*-
~
§
u
0)
10
.V
ID
0
(D
te
\Ti
•t"
"5
Q)
^)
tf
TO
_Q
1/1
O
£
«3
O
o
8
ID
k
4-
•_
b
c
(D
in
3
4-
O
c:
ffl
ID
£
ID
3
^
^
O
C
O
•g
O
1C
Q-
4?
"T3
-2
o
*
^
a>
3
ID
—
113
-------
O
r^i
•
ao
CN
tM
•
vO
VO
co
•
fi
CM
•
IN
O
•
CM
O
t
I/I
10
10
c
1
m
8
I
oT—
+- c
Id
0
UJ
O-
• KM-
0$ g
y^.8
< 5>9
a
UJ
i-
I
UJ
a:
U-
0 0)
en to
o
m
•a
c
t_
CT
10
"5
s4- §
fo^
UJ
UI
10
N
+-
>
0
o
~ o
10 10 o
L 6^
(T5
c *•
0 —
* J3
3
0 X
E3
3 3
1— >-
*5
«1 O
— c
*- 3
+• a
3
C —
C 10
o —
_—
10
!s
a
X
>
i
5^-t-
— a
*• O
2Z
i/> <
s
L 3
10
+-
10
c
£. t-
Ul H-
— 10
£ 10
~ I/I
CT.O
in 6
o (o
S 0
3
o
£
Q)
L
ID
CL O
a$
r o
O CL
S«
—
C 0
1?
a. to
in o
•» •—
in si L
_. . o $
•i- uif L e
« V-
fc°
C Wl
— D
^8
® i
•o $
iS
O 0*4 \O vO K"\ r**- O t"*- *O C^ CM
• •• ••••• • *•
CO vD N"\ (*"> f~\ C^J CM O*( CM CN •-"
i
J3
a
a.
UJ
®
10
•a
ui
<
0)
CL
01
10
•o
h.
>-
i
114
-------
00
•
CM
in
IN
vo
•
in
in
•
in
in
vO
(M
CO
O
CSI
F"-
K1
in
r-
o
CM
in
vO
O
in
in
3
in
in
c
O
L-
4-
. 3
Species
Red shiner
Notr op i s 1
U
$
« a
to
—
c —
~ a
Spotf i n sh
Notrop i s s
2
in
n
ip
* c
* 0
c Q
c ~
Fathead ml
PImephales
m
3
ID
^_
ID
CO
« 5
Cladoceran
Daphnia ma
o
_
•v _
Cladoceran
Daphnia pu
_
3
^.
o
in
» 3
Cladoceran
Simocepha 1
^
4-
C
10
ID
Cladoceran
Cer iodaphn
in
g
a>
« u
c (0
a.—
— -o
3 l_
Monied sc
Cottus bal
E
3
Flatworm,
Dendrocoe 1
^ .
4-
n
^
3
^
ID
1.
S
in
$
c
e
* O
L O
-------
I
c
.0
IB
o
ii
at i_
£ O
•it
11"
co <
1 III II 1 1 1 1 1
Tt —
| ^
Q *+O
S ** ''*'"
"5 *• u
• 3 _J U
o. ox 5
— o *— vo CM •— •—
CM
—
C*l
ID U
in .C Q) (0(0 CD
CO O JC .— E U — -0
-O in O L. — 3 — C. C
— 34- ffl-OO) ClOinl CO
HO 3 I-IOL. — C « 3 in
t- in (0 » 1-4-4- CTlCDUCcnO
in— O — 4-4- — 10 O •- -1- OCDIO CO i-
inio en a — 3 »I_~OCD > i~ — L_ 4- o o.
(Din * C O 4- CD Q. CD > CD in •— — E
-O • in • in +- O i_ •— a c +- in c 4- » 6 .0 L. c 3
inc3C3bjQ+-jCO-00 O U) "0 £ OO — —
.c3O.cp.cO(0 i_ u i- O 10 — >- CD ID ID — E Q. .c
4-1- 6 O SO l_ 3 4- ID -F ™ L, 6 -0 O L. — — ID in O
1
o
CO
3<»£ 4-OL.c « 10
O4- IO>^IO>- ID OO >CF>4~4- CD4-3 cm 10 IDintDID i-
Po.m_cinj:c L. O CDi/i^inco i_ooico3Oi- +•&
So u i- coo jro -ao cno CDOU coin OCD —i- o-o co
OIL. -*O OO T>E 4-g CE CCO — N H- 4-in -CO 1-10 COO >L.
l_O CO .CU -* — — 10-C — ,— — into IOU ®E CL4- IOO
ID— — C OC OIO 310 1010 1-4- (04-> 101- 3CO EO O— *-(0
-JE Q-O OO cjco CJirt 0:1/1 OLD *co co ixio OS • ^ V
E 3_l U
B OV. 0
c ^^ i
1 5
CO
cr
UJ
(—
<
o CM X o in co oo
o^ co I — CT^ o in CT^ *=J-
o o «**. — \O JC 4- TO
— L. 4- C O c —
10 CD ut CO ID *C tT
co a. o > z o a.
M
y
C
§.
CM •— in *r f^ CM •—
in
(1)
+-
c
CO
CD
c
ID
L
10
in
10
c
CD
O)
(fi
10
X
0.
in CD
CD l-
3 CD
— £1
ID *
•o
t; 1
o
< CD
3
c —
ID ID
CD >
E
>.£
._ CO
E CT)
ID c:
U- (0
O -o
.—
XJ S^
0
in
-D c
o
4-
— o
4- CD
— t.
(/) I—
c O
CD O
in
in
p **-
O c
CD in ex
> in
— 3 T3
•t- O c
•— in ID
U1 —
C "O ^~
CD
O CD
4- H
in -D
SO 10
t 1-
— 1
§ ^ £
i_ in <+-
**- CD
01 in
•0 10 4-
CD O- —
J^ 3
c cp in
ID CD CD
a: co t-
10 -^
lib
-------
e
CL
.o
a
o
o
g
k
*-
0>
!„
•P 1
n x
e _i
j!
s
^
UJ
0
*
«~
w •
ID
r~
>
O
NJ
<
0*1
j-
o
o
"»
.G
_£3
V
r—
C
(D
co en
UJ >.
O O
LU
CL «
to o
a: o
UJ LU
H~
<
3C
i
LU
or
LL-
o
to
c
0
4-
—
jD
jr
c
c
•f-
o
"o
>
O
N
<
~3
.c
u
>
0
—
1
<
10
•
in
c
O
~
(0
c —
E
O 10
+- (0
0 O
3 +-
"O O
$ rr
*" a>
28 £
o
to
ID
r-
cn
.„
O
INi
<
•o
£.
O
O
"o
.f
10
00
to
c
o
(0
F
C —
O m
— in
tjS
3 +-
-g O
« x:
l_ Q.
VI 0*-
00 Q 10
o5O L,
o
tO
IO
J^.
CM
>
o
N
<
«3
£
O
>
O
•—
®
"*
10
co
•
o
c
o
•~
ro
c —
F
c —
O "i
.- in
ti8
3 •(-
L a.
O
N
<
10
CO
to
c
O
~
10
c —
E
C —
O m
— in
+- 5
u 0
3 +-
?l
to
W. CVH
r- o ro
r-O L
o
?^
\o
p*.
2
>
o
N
<;
•d
JC
O
o
"~
s
<
10
00
•
o
c
0
•—
10
r. —
e
c —
o in
ti
3 +-
"O O
(5 jc
1- Q-
IB
•« CMI-
\D O ID
— O \.
o
to
\Q
r-
2
>
o
N
<
«3
_c
o
O
•—
£>
<
10
c
O
~
10
c —
6
c —
O in
— i/)
•(- (0
o o
72 O
1. a.
v«. CM£
CM Q (0
O
KS
10 y3
r~ r-
., >
O O
N N
< <
«3 «a
£ jr
o u
s 'i
—~ *~-
5 jS
< <
10
00
• 10
O Op
c c
O 0
7- •—
io n
c: — r —
F E
5 in cm
— in .-in
•f- IU t- <0
(JO u O
1? J? 1> £
L. Q. (_ °-
ID 0
Vt CM*- »«. CMf-
»— O (0 O> O *0
•— O u r~ O L
0 0
to to
vO
r-
*~
£Z
10
.—
in
i
S
o
o
•!-
>^
N
C
Q-
10
00
•
c^
o
y
v£)
(N
^^
r*
••"
j^
(O
«~
3
I
5
8
+-
N
L.
CL
10
— 0
! I/)
-(-I +-
in in
X} U| (0 O
CT 10 I C71 10
i <| < <
p
5
c
10
>
i_
o
£l
P
C
o
•»+-
10 y
OT
U
5
c
c
O
»*-
ro o
0)
« V.
10 O
01 —
— c
< o
10
1
0
ij.
o.
10
_
a>
• u
10 O
01 —
in
i-
10
a
3
>
10
,_ -
(D
» 1_
(O O
cn —
t o| < o
in
t_
10
CT
•5
>
(0
„ »
CD
* W
(D O
< O
117
-------
1
9
k
•4-
5
M ^F
i*
J|
£
o
ID
10
E
5
10
(SI
o
i—
i—
2
10
(0
1.
E
2
(D
0^
O
t1*- r*- r-
(** ^ r-
O\ (7* ^
10 ID «J
ID 10 10
L U t-
E E E
10 ID
CSI (SJ (N
O — O
t— r-
10 (0
IO ID
U L.
'i E
3 5
10 10
(SI (N
O O
r- P»
2! 2
10 10
ID ID
E E
3 3
10 10
(SI (S|
0 0
r-
2
"a
(0
u
"e
10
(SI
O
$
"+-
UJ
i
W f*
r
X
8
1
o
••^
1
e
I
*
: «
— w
-Q $
ID a
h-
§°
H
CO O >-
LU 3 .C
— TJ Q.
o £ o
LU l_ L
D. 5
CO VI —
IA JT
g (S, 0
•g
$
(SI
o
CO*
0
X
z
ID
ro
i
10
ID
6* "a
-f- —
ID >
- 10
Q Z
c ID c (0| c
o o c
H 4- — +•
0 >- 0 >- t
3 £ D x: :
•D a. -o o- ^
So o) o <
l_ W u C L
^% — ^4 -« V
(si jc. rr\ c r-
>O o r-- u f-
(SJ (SJ 0-
o o c
oo oo oc
O O C
TJ- ^r
ID
+-
10
a
— Ul
i/< E
5 1
* «—
*- JD
. 3
0 -0
10 10
•— • »_
«£: »jr
6- O >- > O>- O>- O >- O>-
I.C 3£ 3X: 3£ 3£ 3.C 3^:
3CL "OCL ^QQ- "2O- "OQ- "y^- TD^L
'O WO wO ®O ®O OO 3)O
O O O O r O O O
i— *»~ M.— *«.— V*.— Wl— M.—
'^ ^O-'- K^X! V-C 00^ lOJ^ \D -C
U ^O fOO »-*O •— O VOU IOO
J (M C*J (S) (SI *N (SJ
> o o o o o o
' oo oo oo co oo eo
o cT o 0 o o
-r- T^ *f" -** "T- -T-
i 5 5 i i i
10
in
O ro
t3 ID —
§3 4- 10
- 0 J=
— ID — a g —
u a> u O 3 i,
ID 4- y i_ 8
4- • in O IO O Q
m *• c 4- c c £
O • O tl — 0) CT
— o o >> — a —
o i- 10 in m
10 U. — 10 lO
— o 01 (o 10 e —
• j= «i_ »c: » — «— «a «j:
-M 4-£ 4-5 4 4 4-O 4-N
J4- 1D<1 'dlO I0> I0> IOI_ ID4-
j z o* coo oz 02; ocojaz
in
(D
_
§
ID
1
S
ID
O J=
4- a.
n
in en
5 !•)
4™ U.
3 3
JO C
•v-
§3
f\J
jr c
a
m t-
10 ~o
— Q)
3 4-
O (0
"io
0 4-
0) in
o: LU
«3 -^
118
-------
f
ID
1
b
«••
ID
0
T?
fc
o
m
in
e
3
(0
i-
9
|
fe
1
c
t— *"^
4- *
L Z
£
§>
J1
*
•4-
•4.
UJ
8
(0
a
*
£~
(00
r
*~
^
a
o
J"~
oo
r-~ ON
ON —
r—
t
1 __
— 1C
(0
4- O
c
jo o
JC $
3 C
CO <
ID
• -O
I r-
ON O
CM O
4-
O) C
I — O CO
t> _ ._ 4-
1- 4- >- 10
p
o
in
fc
•o
JD
O
c
O vl)
ti^C
3 10
1 .— ._
O 4-
VI 1C
0 C $
ON — J3
r-
_
V 1
co
in
fv^
0
%
00
^.
ON
c
_
10
^
i
k
X3
JD
CM
—
Q
)
O
,
c *-
~ o
O c
4- 5
— 4- (0
§f^ —
_ ^ "<3
,c
^_
v 1
00
in
r--
O
$
ON
r*.
ON
«c
in
O
c
U
•6
C
*
JO
CM
K1
O
£•
10
^A l_
Rl
JC
in
NO
I
CM CM
1
CO CM
r~ CO
O
J^
%
ON
f^.
Q\
•—
JC
in
O
c
o
X
0)
*
n
CM
K1
C3
£•
ID
VI L.
IRS
r:
m
NO
i
CM CM
CO CM
r- co
O
¥
X
ON
ON
i— •
C.
in
O
c
U
3E
C
*
JO
CM
0
4-
(0
4-
^^ L.
?l
t~
in
NO
•^ vO
CM CM
1
CO CM
r~ oo
o
x5
5*
ON
r-
C7N
«—
f~
I/I
O
4-
C
"o
X
-3
C
£
/*>
CM
CD
4-
10
4-
Vt L
Si
f~
m
NO
i
CM CM
1
CO CM
r- co
p
g
aa
r—
ON
fff
^
-
ID
"15
§
in
£
_Q
^~
NO
0
CD
O ID
ifee
~o •— o>
t .— *—
O 4-
VX IO
-C
.
V |
co
in
r-
' ^
5
co
r-
ON
M
«-
(0
15
c
O
in
!E
<
X)
0
o
c
o ®
4- >~ (0
O U l-
3 (0
( *«* ,—
O 4-
VI ID
O C $
ON — X)
.c
_
V I
CO
in
r-
(J
X
00
r-
ON
0
*_.
10
®
8
^
13
C
XI
CM
•—
Q
J
0
1
C M-
— o
CO —
— 4-10
J,Q ~~
2o
jC
v!
CO
in
f^
O
X
ON
r—
ON
V—
e~
in
O
c
U
^
0
1
XI
CM
O
4-
(0
4-
VI L.
x:
in
NO
CM CM1
CO CM
r-^oo
o
x5
X
10
»—
c
L_
o
o
~m.
4-
3
U
10
(0
« c
L. ••"
*+- O
If
in
c
(0
4-
10
C
10
I
o
o
% — •*
— 4-
a> a
in —
in —
s: Hi
(0
4--
10
C
10
_-
1
O
* *--
ID a
in —
3 —
10
4-
10
C
10
-~.
i
o
o
•I '-•
QJ CL
to —
S LU
10
4-
IO
O
a
«.
—
•_
0
5
E
a|
* Q
a
— c
a> o
in 4-
in u
3 >•
X O
in
in
0
in
10
1
n
g
M W
— 10
(P —
in o
in x
i.2
tn
1/1
1
»
ji
0 io
O 3
— o
10 JO
in
in
c
(9
„.
• C
0 10
O 3
— o
4- —
10 XI
in 5
< 0
in
in
1
t^.
• c
E 10
io E
O (0
-_
O 3
— U
in o
< 0
in
in
c
«.
_«
E§
10 E
U 10
—
U 3
4~ ~~
10 X)
in o
< O
119
-------
8
|
k
i
8
•K J
10 X
C -1
p
S
*»
*-
Ul
§
%
=•
a
e
*-
oo
L»
v *•*
1-
"T"
%
8
o
CO CO
r- r-
CTN ON
• •
<3 IT
4- 4-
CD 03
c c
O 0
in in
CD 5)
5 *
< <•
-O O
(M K*l
O O
O 0
ID ID
**• W ** K
r~ 0
• •
ro rsi
CM CM
! 1
ON O CO CO
O CM O —
co co an oo
o o
•^ *?
5 ?
00
t—
2
•
r
•*-
a>
c
O
i
c
*_
o'
c .c
O 4-
4- O
0 U
3 CTI
^.
*"~
ON
*
CN
CM
1
CO CO
o —
co co
o
*
00
r^
o*
•
ID
4-
to
C
O
J5
•D
C
n
8
o
o
c
O 01
4- >• 10
O L L
^o£
Q c S
in — j3
f_
vl
co
in
r-
O
t
in
ID
o
1
in
A
«4-
o
CO
p^
ON
•
10
•»-
IS
c
8
-IO 0
"5»i
^O^Vl
NM 15 '
cp c tt) *-
in •- ja o
,
vl
CO
in
r-
t3
•«•
9
CO
i—
ON
•
ID
CO
c
8
IE
|
\
o
o
in
o B
+- >- 10 O
= fe ^|
L _ _ in
o +- A
NM ID
x:
*-" ' i
v|
CO
in
o
X
z
CO
r-
•
ID
•t-
(D
C
O
in
1
c
ON
O
O
S CO (D
4- >- ID U
0 u 1.
3 ID g
•o — en E
CO — c
^o^l
Vi. (D '
O C (D **"
^,
vl
CO
in
r~
O
•3-
5
OO
r*-
cr»
•
A1
t
C
8
fe
T3
<
I-O
\o r-
O o
CD O
1
c ••- in
- O A
(B c "t-
4- O O
ID ._
^±^i
E JO — 10
(8 J= O O
¥».
Vl
CO
in
I--
o
5*
00 en
CO ON ON
ON "~~ ""
> ^'
• U' t/N
•V V.1 C'
c c
4- (OH)
CD t/> co
C «3
£°~ "P -°K>
O — O CM
• • • •
O O O 0
1
c •<- in.
- 0 V|
<6 C *- 4- 4-
4- O O — —
0) — _ —
— 4- (D in ID (0
E 4- 4-
jQ — 10 NS«. 1- **. W
— •— — r~ O NO O
c. o u «* S ro S
^ J£
JT * *
— . NO M-
Vl
1 1
r- ON r~ ON
co — — — —
— CM CM CM CM
1 1
in in in in
in r*- co r*- oo
r- r- p~ r^ r-
o o o
if / ?
••** E
T5 3
9 in
3 L
C (D
+- em
C ID C
6 — ID
O « L.
•^ 4-
, p
•
IA (A
t> —
* 1
t— V)
ID 3
C —
is 3
cno
C I/I
i^ s:
E
3
I/I
a>
E in
ID C
oC
4-
~ E
ID 3
cj ^
o> o
c in
"™~ 3
IA- SI
I/I
is
E in
10 C
— ID
— 6
10 3
fe ~3
0)O
£3
u- s:
E
i/t
cB
E in
10 c
— 10
•— E
10 3
C —
b ^
O) (J
u- s:
E
3
I/I
b
• >
E m
ID C
4-
~ E
10 3
C —
k 3
0) O
c in
— 3
in
(5
E in
ID C
— e
ID 3
c —
<5 3
O) O
Li- 2!
i/l
»
G i/l
(0 C
u£
§~
IB ^
O) O
C I/I
— 3
i] y
l/»
P
E u)
4-
•— 6
ID 5
cr —
ffl "a
010
C U)
— 3
U- Z
E
ri
IT,
u
a.
E in
85 c
oE
— e
«J 3
b "5
O)O
u- Z
E
3
•Jl
fe
e m
^1
.
c —
<£ ^
cno
C I/I
il z
t/l
J
- >
E (/>
— (0
0 u
— S
-------
CO
*—
>,
_*r
3
"D
C
fO
O)
o
u
s
SB
•*•
&
r*«
J2
i.
10
a.
CO
8
+• j
1*
v ^s
O *^"
o
K^
v£>
t
O
.
M
**•
H-
LU
(N
g
a
b
o
i.
3
4- ^
10 O
jit.
Q.
1
S
rr
1
f~~
CN
1
tn
p-
oJ f^~
w
8
i
o
>-
4-
~
4-
£
c*\
*—
CN
in
CO
r~-
co
—
>~
in
^3
-£3
(0
CO
«9
J2
u
a
CO
JO
vO
KV.
O
O
[
_
JO
£Z
C
0) —
CO .C
Htc
6 O 0
CJ CT>4-
j«:
X
VD
1
. — .—
CN CN
1
in in
r— co
• •
r- r-
CO
o>
c
S
TJ
5
vO
•
HI
I
•
CN
-a
1
in ID
CO 3
i_ —
i- >
z:
VO
in
(N
1
-3
o a>
in u
in to
ce O
HI O
m m
• •
o o
in in
y y
-o x:
co ^t
CN CN
^~
•
CN in
CN CN
o^
0 K>
• •
CO CO
•
15 -»
10
CN CN CN t
^h O\ O^ •
^- — — CO.
10 p 10 +- L
+- 4- +- in a.
ro to ID L
10 10 ID jc —
t- 1- H t- —
O
• O O
(0 « »
r~ io 10 o
— t — CN
• • • •
o — in vo
_
10
o o o >
in in in vt i_
O O O O 3
—1 _J _J 10 to
a c. c c.
t t «* iO
CN CN CN Cj!
o
in in in CN
CN CN CN —
in
O O O CO
• • « »
\o r-- co r^
«
„ _
10 ~
10
IB .
^
c a.
1/1 a.
be
.c —
I—
>
O 3
co to
jc:
S
vO
•
K1
•"
,_
O^
• *
_ — .
(0 — fO ^
(t) (0
(D * >
»* > >
03 03
• — CO C7V tO
£ -C
£ £
r^ o
• •
O —
rO •""
CO 0>
• •
r- r^
CO
CN
o
T)
X
r •>
~Tf
f )
XT
X
z
X
CJ>
X
^
o
X
O o o o
5" j" i* 5*
O
5*
0 0
$" 5*
<-> £
X> 3
o in
3 i_
C CD
•4- Em
c a
S i
35 10
o c
10 a
— 10
O Q
O
u
10 O
as *
O (D
(0 —
o s
TO T> T> —
CD O CD in
.— — _ -o
*4- »*-»*- "O
._ ._ ._ o
U (J u TJ
Q. Q. Q. ID
in m in —
10
c
a
IO
Q
O IO
C —
c
a. a
in 10
-' Q
O ID
C —
C
a. a
in a
•^ Q
4- ID
» c
Q. >.JC
in (0 £3.
.«
in
-o
-o
0
TJ
10
ID
>- CD
">-jC
10 a
s: ui
,—
t/1
-^
o
XJ
10
CD
>- cE
^_§
10 Q
Z LU
._
l/l
TJ
Q
TJ
(0
O
_ e
M- O
to a
3: uj
121
-------
w
L.
0
"e
ce
ti ^^
10
0) .
t
C Q.
0 ®
I/I CL
3 c
.C —
H- —
^ ^
ID
0
C Q.
O N!)
in Q.
L
3 c
JZ —
1— •—
IO '-*
10
+-
CD .
t
O -f-
— O L-
> in O
Sb ^5
JC
jr i:
ON ^f CM
CM r~
L in
iB O
•t- a. —
-t- x >
1 O L. IA
NO ^" CO 3 CJ
ON CM — CO _J
>-
3S jr -o
O NO O
g ON ^
l-
C
O
•(-
JD
5
"D
R
— o
±5
-O O)
— i
TJ
t
CM
,„.
10
vt >
0 l_
O 3
— CO
t*~
*
«.
ID
VI I-
CO CO
JfT
NO
ON
_
ID
VI l_
ON CO
jr
NO
ON
_
ID
VI L
O 3
NO CO
e~
NO
ON
in
C5
o
(M
CM
HI
05
CM
NO
o
CO
r-
S ON
o
CO
o
00
OP
t-.
s
in
ON
ao
£C
o
o
M-
X
O
'j-
I
w
5
O
I
•z.
o
tr
CJ
O
i-
X
~
5
o
•*
X
-
ID
JD en
c ^
— c
•f- ID
5 CT
Q
N^< (0
• ~y>
& (a >~£
a a 10 a
t— in s: LU
in
-^
c
ID
V.
a
ID
O
•» c
*~ S
>~J=
ID Q
S LU
cfl
•Q
c
ID
a
ID
0)
* W
>• gj
H~ 5
>»J=
ID a
Z LU
*
•Q
e
(0
ID
CO
^
•4- Q
>-c
ID a
2^ M i
ia ra
ffl ._
C TJ
5
CL
in
ID
-J=
ID Cl
S LU
I/I
C
- 1.
Stonef 1
Pterona
10
x>
§
(D
~~
CD
• O
>~ l-
Stonef 1
Pterona
»
T3
5
ID
0
(D
- U
>~ 1-
Stonef 1
Pterona
10
"^3
5
(0
«
• o
>» L.
Stonof !
Pterona
ra
•^
5
S3
— »
- O
>- 1-
Stonef !
Pterona
*
t)
c.
a>
Q
X
i.
>-+-
Stonef 1
Arcynop
ID
1
10
ID
a
X
3-
.fc
>-•»-•
Stonef t
Arcynop
10
ID
— -
ID
ID
a
X
« ®
^ 4~
— a
*- 0
O C
c >•
o o
CO <
(0
£
ID
V.
ID
a
X
• is
•>-•(-
Stonef 1
Arcynop
122
-------
1
ITS
e
8
S
fe
»-
§
£ r
I5
6 -J
f>
O *"*
+-
y
•
t
UJ
|
£
a
55
o
o
4s
w "^
h-
_
8
J~
81
«
a
!
ID
O o r-
00 CJ* Gl •—
• • < — •
— — • f —
10 '"•' TJ ^~* ^-° "-* ~~ 10
10 10 o? 10 10
4- +- — CT> O\ 4-
Q>*o)fc — 4- r- r- 4- G>
• • 10 * 01 o CD
ccxco.cn _ ,— c
O CD O CD "O T3 O
4- 1. 4- L «<3 C C C C 4-
inciuio. 10 — — 10 - >•
10 ioE"5?mio *~ —ID
> >l_CPOO — — O
— — I0>^>-— — 10 (U *~ — O
> >-CQ)u4-CD 4- **. 4- 4- tt> in
**.i. vii_ ^i — > OO.L. OL — > o
03 03 ^pE i**D OO CD 0 V-® -^
C^CO OOoO 2+-CD O — fOS ' — -* O —
-c jr -o T^ jc x>
JC jT
ID CM (M CM CM VO
vo ^o cj^ r*- \D *o r^- ^
0 0
ro ao r- oo CN ro •—
• • • • • • •
K*\ r^"\ K^^J" ^f O O IA K^
SCN 1 CM U"\ •—
O^ K^ LO O ^" ^ vO 00
• • •• • • • • *
r- i-- uDvo co co cO r*- p*-
•o-
o
to
fM
O O TT OOOOO
i i 5 5IIii
10
10 O
x: ui
0 -C 4-
m in in o >
— 3 4- ro (0 *
•O T3 JO 3 .* .* IO
CCL I/I 1. t- JC «
fO 10 O — "CD "CD »l/>4~
L. I. C7 JCCCCCC4-3
CT a o o o o
"i/i "*/) Ein E»/> Em L —
-o >-o e—>•— C — C C C CIO —
•*-m **-in io> iri> a>> ©> J^> oo
inci I/IQ injc tAj^ >*jd >-jr O-C t_
— o — O t. u coi_ CDi. ot^cQ
T74- a4- JtO OO J^O •* O CO 4-E
rat_ ITL — c oc Oc Oc: jcc 3(0
c_i < o •? a o c- o en o co o o o o to
OO CO CO
r~ r*- t^-
O* CT* O^
•- — — CO
t "^
• • • (y C7^
(0 10 10 O
-f •
CD V CO •$ .— IO
m
c c c c ov 4-
O o O c ^— ®
4-4-4-10
i/) ui in 6 — c
b b b iS? t 5
jc jC jC 3 ON o —
1- 1- H •*— O <
lO f- *f CM 10 -O
in K"! K^ K*t ^JO OO
• •••••—
O O O O Cfr •
CN O
CD
E
j^.
>• —
O 4- 10
4- — TJ C >
XT > CD H) —
O O O ® 4- — l/l — >
in in in E o 4- g ~o L.
O O CJ — CO O CD CO 3
_j _i —i 4--oiooE O if1 O
K1 CM CM \O « O
(•-! fO —
co TJ- CM in CM
• • • • •
CM (N CM t tO in
O o oo in CM
oo oo r~ in •* M
• •••••
r^ i^- r- r-- o> r^
*t
fM
O O 0 -WOO
5 5 5 5 i i
+-* +T +T
3 3 3 «L »1_ -L.
O O O 4-C04-0)4-CO
,._ ,_ ,_ 3C 3C 3C
•P-Si -P-x: f ^ O -0 OXI OT3
1- l_ l-l_ULl-Ll.
4-10 4-(0 4-10 f — f — -F —
(0 — 3 — 10 — IO CO 10
oo oo oo *o *a *a
L. I. t. O O O
JCO JCO -CO -OO -DO jOO
4-6 4-E 4-E eg CE cE
3(0 310 3(0 1010 10(0 IUIO
Oco oco Ocn Ten rrcn cttn
123
-------
s
s
fe
4-
£
I
loi
£
c — i
5 v
0
Effect
g
c
jj
a
o
i
CO
X
I
c
o
fO rO
vQ MD
i i
•- CM CM CM
*O vO vO VO
ON ON ON ON
— — — —
4- 4- en o)
1_ L C t
fl) $ — —
t_ L_ £ £
* * 1 5
It) o
O C7^
• • • *
o o t o
o o
f -^
O O ® 4- 4- T3
.c x:
.c co in
^: CM o
CO • •
00 CO
in in — —
• •II
r~~ r~- vO vO
o m
co i in —
r-^ oo oo
O O ID ID
TT *)- ID fl>
«T rr
vO vD
O ON
C 0)
~
b I
x: «3
to >.
•a *4
4- 4-
1_ L.
$> 5
U L.
10 <0
VO V0
v «
O O
O O
in in
B y
sz s:
CO CO
in o
^ «
r-- r-
co ao
0 O
/ i
vO vo
0> Ov
,_ ,_
J? ^
& ^
C C
(0 10
O O
o
^
1 CM
. 0
O V
*
L
O O
4- in 4-
^ ^3 0
(35 +•> O 3)
—
J3
i.
3
£
to
•0
•j"
J
^_
*
10
o
r--
o
0
in
B
JC
Tf
CM
VO
«
K\
CO
r-
(3
i
vO VO
2 2
VO >~ >-
CTv ID G)
•a -o
— C C
(DUO
-O (D «J
O — in
in r~ 03
• • •
0 CM 0
0) 0)
c c
c c
O l_ O t-
4-3 *• 3
_ 4- 4-
O O L. $ L
in t vD 60;
B v§ ^§
c c
1 'E
-o to o
in r- o
A
i
in vo
o •— co oo
vO CS
co (M ON r^-
r- co vo t—
O 0 0
* <* v
i i i
VO
Ov
^
0
•g
*-~
A
(0
4
*
en
c
c
time to
overtur
c
1
00
ON
CO
-•
o
to
CM
i
ON
2
L-
o
•*
"SI
o
.^
co
o
o
in
Diuresi
-Q
^-
t
in
^
0
CO
o
to
CM
X
-z.
3 C
O'XJ
JB
ID
-S
ID ID
a:
(O
r
ID ia
or co
O -O
b o
c S
ID ID
ct in
O -a
ID ID
ce oo
3 C
O X)
ID ID
cc to
O -o
ID ID
or to
O •§
r
3 C
O -o
10 10
or co
3 C
O -O
ID
or
4- IB
3 C
O -D
Ȥ^
5
n
o*
^ C
O X)
1C ID
co
or
3 C
O -a
i*
10 10
or to
ID_,
* a
4- 0)
3 c
0 -a
«.
i CT
ID ID
K to
124
-------
in
r-
k
d.
8
e
«
0
ce
0.
°6
_c
•*•
c;
CO
in
f-
in
0)
^
O
uO
~3
IJ
or
'-O
r-.
<3\
•t-
l_
10
-t-
*
„
u
L
— 5
o — •
»
r-
r-
•
is
+-
s>
._
L
10 —
_ co
10 Ov
o —
r^
10
>-
10
•>3
L,
$
+-
.
10
.C
_*
3
CD
£
•t-
1
•«
in
3
0
k
i
CO
in
in
k
c
Si
in
3
ce
«d
C
O
in
L.
.C
1-
m
in
c
O
in
in
3
ce
"3
C
O
+-
3
.C
t—
U)
I/)
0
h.
c
O
m
in
3
ce
•6
c
O
4-
in
3
f~
t~
tn
$
fa.
c
s
m
3
ce
•a
c
Q
in
^*
h-
l/l
in
CD
c
s
in
3
ce
•a
c
O
+-
in
3
£
h-
in
in
CD
h.
c
O
m
in
3
ce
«3
C
O
+-
in
i.
3
.C
1-
m
in
CD
b.
c
O
in
in
3
ce
^3
C
O
4-
in
b
.c
(_
in
r-
k
o.
.—
8
«
k
•4-
o
ce
s ,
— *^
!*
C -J
il
«
Q-
x:
•t-
c.
<*
m
LT\
^»-
o
*
0
JC
& ~
£ * m
+- CD
•4-
^
»*-
»»-
U)
1
A*>
T^
ID
k
o
»
+• ^»
10 U
fU — m —
0. (0 ¥• —
o o y c
^ CD CD
tn ™^- >
— 8-4-3
X — CD — )
g
S
CN
"~
O
in
r-
in
0)
^
O
uO
~3
a>
o
a:
CO
vO
o
•
o
o
in
y
-C
«t
CM
o
LT\
O
*
0
i
£
+-
(0
a.
O
tn
X
JC
-4-
^ in
CD
rt) T~ *~*
^^s
g-t I
— CD — )
CO
vO
O
O
O
in
O
_j
i \O
CO
• #
0 5?
>.
+-
,
ID
+• 0
** is "^
5 s — i
IO ^
in o
O ro
• •
O O
o o
ir\ in
SO
_i
O
•
^
n
T3 O
a ai
o
^r
•
o
o
in
O
_j
^
vO
^
•
O
o
in
o
_i
« CN
CO lO
vO (M
• •
0 0
c? o
in in
_J -J
CN
?i
O
0
in
O
_j
Kl
CD
*J
•
O
O
in
o
-j
oo
o>
in
•
o
o
in
O
_j
s
•o
o
•a
CM
co
*
o\
o
•
o
-o
in
in
r-
in
— 3
3 2
-. o
JT T3 Kl
O ex
UJ ^*
i
c
A- •— '
T^
J« l_
+- ffl
3 C
«-« or>
• 10
in M * CT
v 0
jjj X ._ «_
O Q (H fl3
1- V>| (T c^
I in
lO \O tt ^t "(J- ^O O*
• • • • • • *
co r- r^ r** i**- r*» r^-
^j-
o
{SI — _ _ _
"• O O 0 O
*r I ^r ^r •v ^r
1 5 5 x 5
"o
>~
i
i__
4-" k +-"c5 4^fe +-"!B +-"c5 +-"k
3C 3C 3C 3C 3C 3C
O -0 O X) O -0 O T) O T> O TJ
10 10 ID ID o y
• • •
r^ r- r- r
O f • i : c
«T -=t *d-
X X 'J, D
z ^ ?• *
^cj ^"L ^-^ +
3 C 3 C 3 C
O ^5 O 'O O ^C3
•F — f — +^ — H
SID ID
X C7J * O1
-Q O ^5 O -DO J
c E c E c 6 i
10 10 ID 10 ID ID (
ce co ce co ce co Q
3 *T r*-
3 «3 CO
• • •
r~ r-
> O 0
TC »f •*
-xx
"is +-"fe +TCS
3 C 3 C 3 C
5 T) O TJ O -0
10 ID 10
t cq > oj * a
5 o ^> o -a Q
: E c E eg
0 (0 ID (0 (0 10
t co ce co ce co
o>
co
•
r-
Hr
X
+- «>
3 C
O "O
»8
5o
c E
10 ID
ce co
125
-------
in in
in in
0>
3 3
o: or
8
§
b
oc
U
*
_j
V,
1
c c
o o
4- 4-
in i/i
L I.
3 U
H- H
\O CM
CM CM
•* K1
0 0
fc
£
H-
UJ
1
a
o
O O
in in
o o
_i ±i
TO T)
in in
in
in
»
k
c
*-*
0
in
in
tr
c
o
4-
L
3
-C
1—
Oi
ITi
VO
C?
o
in
0
T3
in
m
vO
a-
c
3
3
r
1/5
«5
I.
l_
X
ID
00
CM
O
O
in
•C
,j.
CM
C?i
r—
*—
•
10
4-
CD
fe
4-
in
5
10
*
in
—
d
4?
C CO
o m
in Q)
O i_
— i **-
c
^j-
CM
O
g;
-~
•
10
4-
(D
c5
4-
in
£
10
<
to
o
*«.
o
ro
tr
O
m
0
-C
^
CM
<0
in
o
in
i
3
00
o
in
£> U
O $
in
CM
in
(D
in
-o
9,
m
•
in
4-
o
c
c
(D
CD
0
I
(0
CM
O
in
a
x:
CM
T3
O
C
a
a.
10
T
r-
o
6
10
co
ID
CM
3
•o
in
•o
O O o
— c — £: — .C 4-
10 in to m 10 in
e~ Q) f" (J) f~ Q) Q) -
4-l_ 4- 1_ 4- u E
CD -C Q .C CC XT —
CM
CM
O
*
CM
O
*
CM
CM
CM
I
i o o co
co in co in co m —
CO O 00 O CO O vO
— CM <— fM — CM —
s
O
*
r-
O
r—
O
*
CO
in
co
X
z
o
X
2
ID d
u in
o —
O
X
o
to
CM
8
CN
X
»~ in
I
C C
4. .—
o •*-
O 3 c
ii o -D
ji i_
•
o
o —
— «
ja a
a a
I-
10
•» CT
0
a G
r2
-------
K1
^ OO
CN \o \o o** \o
U3 \O O^ •*"" tO ^3
C1"1 ^ «— • rO tO K"* f*- ^
Q
b
•*-
$
§
3P T!
IJ
gisJ
o a
O "**
-—< — ratOioiOOt' — r^
C7)(o cp in t— »— — 10 ot
c CO * c in CO .-
— O o — to in «n Jt y
L>IO $a.OOOu>io —
•2— cEEEes— —
CD >IQ 1C CO tio \(0 VlO O- *ffl 10
srz crt«;>.>.>i/>s oa
10 il
(0 m-O ^•r^csiaoto <•
<— *t •incsiiomtOf^- ^f
• • »—•••••• •
csi— vr-ooo — o o
c c
O O
~ -o e E —
4- CO — 3 3 4- O
(0 > (0 — — 10 —
*
2
§
£
10
b
0
0
j>~
100
L«
0 v^
H-
1 1 f~ 1 1 1 ^.
•I- 3 — c in v ffl O •— O — 5 — c +-
jreiocD^ox: — — — e 10 co a.
m +- ~ jrooco-*- in — in ~ o — -c O E o
Era c-t-c »*- to -f- in3 i/>3in c4-c >-m
._Q — OO O-*- * b OCr OCTO — 4> O iflO
+--0 s—o 20 -o 2 _ico _i» _< s: — o io_i
Co c: c
^r — £ x: F g ^: T3 -o
-o E
o — c/> to
CSI CO ro (N fN CN C^J
§«!• 3(J TTWWO J 'J
I crroixxx •» j: •«•
l-Z TO* ZZZIZ I
m
3
E
10
JZ
** 4—
J ^ ^ ^ _ ^ Ul a
3 -a TP -o ip t» — - L
— ._.-._.__ (1) 0, .C
4- OO <_^-vi_H-x-«63 +-
c — - _-._.__._ j 5 $ ;>.
o ex CL yy^vyo^-^ ^~
'— • ro ro CLQ.Q.CXQ.C ^^L.
u u in i/i in m t/i — wow in
6 CO c in 3
• into 4~-f--»--*-4~ — — —
in yi
iu>- rain tow! roin njw 101/1 (0~ — .c 30
oo cjo O-— o^. o-' ci^ o--- u_a. cnct orco
ISI
in
a* to t^>
— r- r-
at at
_ .
10 TT C C
»o _
•*- at jc Jt
"" <: <
j: 5 •» •*
CO y a. a.
— w a. CL
i 1 1 1
CN
*
— (0
1 «t 10
>£> r~ r-
CN in ot CN
• • • •
O CN O —
«_
(D
2-_ 4?
•H (D -C
— CO CO +~ O O
i_ c E 10 in in
O 10 — T O O
r L. +- TI — i -J
£:
„
x: CN -x: j^
1 * *
-sf O
(N (M •— —
csi — r-
i » •
in co — —
*- *~ CN CN
to r^ oo
• I . •
co r~ r-
-j -a
3 CO
0) £- Q) x:
0 i «n L. i/l
-1- :. - O —
© (D X ^ X **~
o 30 e e
^9" C (O f<~IO tOO
i f * li: ii
in
3
(0
— 1/1 U)
3 33
U 4-4-
§•> (O * 10
£ -1- .C 4-
in o ui o
-H •+- 3 **- 3
• 10 IB 4- a 4- CL
^2 O (0 ^ (0
3 in c o m O i/i
f— ^ __ ^ ^j
0 — 4- — I- — L.
— • CD 3 CO 3
J^4- -C(O c — c —
COO OU CIO CIO
COE CC 104- 104-
UCO CO— -CO -C O
OtO 1— H- O— O —
127
-------
fl>
O
1
§
+- *?
^
s<
u d
c J
4-
*
>f-
•4-
UJ
8
+•
«J
*
Q
ft
fc
•f- — •
B O
L*
D »^
K
51
Jt
S
$
"5
Q.
U)
C C
.* -*
L. U
4- 4-
CO .C 0 .C
l_ ul ,_ tr,
o — o —
e e
5i it
in in
3 3
4- V
* (D « ID
.C 4- .C +-
i/> u in o
•— c •— c
•»-3 "4-3
4- Q. 4-a
ID ID
o m o m
3 3
i C — C —
c (0 c 10
•O 4- ID 4-
.c o .co
1 0- 0-
in
f«».
CT<
T—
U
CO
CN
a*
•
CN
O
m
0
_i
.c
°P
•9
CO O
• •
ON O
— CN
PS
• «
r- co
o
£
in
3
4-
• 10
C. 4-
in u
— c
4- a
8m
3
"5 3-
C —
C 10
10 4-
-c o
O —
\O O c: • • • •
r- 05 — — — —
ON E -O (D ID ID ID
— — O l£
11 £ 4- 4- 4- 4- i£
® O QJ CO ID CO 0
4- «3 1— —
4- O O Q O
O C«<3 Ifl I/I 1/1 10 U
r ^ in in in in c
CT)4-COIOIDIDIO!
x> 3 — r- E g e g i
0 lOOONOOOOi
tr S-CJ^-Ht-H-h-I
K^ | <}• J3 Zl JD J3
O -^sOCN ON r^. ^- »-
— CNON*— lO-— CMCOK
• ••• • • • •
O — — O — CN CM — •-
JT SL
"8 •- in 1? •— in
£. t (D .n * co
in — u> —
C 4- C C 4- C
— X CO O — * fl> O O O O C
EO>m Eo>tn in in in u-
— 1-30 —1-30 0 0 O C
O.O1 — )_J Q CO -* i — J —1 -J — J —
* JTTI £j=Ci:j:
^t co*— «f-^>-^-^tr-
•* K^ fN CM r-~t--eoaNi-
o t> o o c3 o c
i i i i i I i
in m in in
— c — c — c — c — c — = — =
**-3 H-3 -4-3 ^-3 ^-3 H-3 ^-3 £.
4-aJ 4-a. 4-a 4-Q 4-0. 4-a +- a i
ID IDID IDIClDIv"
Oin um om Oin Om Oin O ir. *
3 33 3 3 3 J
CL
> CM !N
) NO lO "<3
N ON ON
— — TO
) 10 10 O
: 4- 4- -a m
i <0 ID C CN
: ^ .£) — 00
ID ID co cy>
t- H cr —
(0 (D O
N. CO ^T CO
• • • •
o •— o
>-
4-
ID ID
> O O > 4-
N in in i- L.
; CJ tJ q 0
J _) _l _3 E
: .c i: is
(M CM K1
1
> ^ f!
• • •
in in N"N. r-
* CM CM CM CM
1
CM NO
3 O O CO in
9 • • • •
r- i) r- co
•i o o o
• i i i
«j .
CO
D (0 ID ID 3
. _ — .— If! ul
13 >* ~- > C E
T^5 O.O CXO COO
nE Q.6 O.CD CO O.
DID 3o 3O Leo
"CD OO. OQ_ CD— J
128
-------
r~
ON
9
ce
ID X
I. Z
o
ID
a
t_
MU
*
CN CN
CM O
r- o
in
lO
ON
•4-
co
c
c
0)
CD
•a
c
T3
^
•4-
10
—
00
o
m
CJ
J_
^D
C?N
(Nl
ON
r-
*j
in
^
_•
10
4-
-
ID O IB
— c in
3 e o to
O .C 3 *• Q} U
O-.C L C
a 1. 1- —
£
^j.
(N
CM
CM
O
r-^
C^
ON
co
r—
ON
c
10
0)
1
ID
in
in
o
o
o
c
-D -
O (04-
c (D —
in a) i- >
0) 3 O —
I- — C 4-
-C (D — U
1— > *— ID
u
in
CM
O
r—
C*N
ON
cxT
^*.
ON
C
ID
O)
f.
ID
00
CM
O
O
c:
-o a> u
— in 10
2 §3?
.
.c ID — fi-r:
t- > ~ O l-
in
CM
CM
o
r^
in
ON
in
O
in
ID
CD
(/)
\m
sz.
~~-
ID
en
5
oro
in oo
o —
^
4~
•w.~
O (D
O 4-
7 Q
«» E
^y
CN
1
ON
in
in
CM
t
00
in
ON
f~
in
O
in
&
in
.0)
\IO
£L
__
ID
O)
ID
ID
•*
--
^
4-
ID
4-
W. U
rO
»—
m
in
CM
in
co
ON
ON
-^
5
o
00
•a
L_
D
C
"8
ce
in
oo
CM
O
in
3
CM
in
(N
i
t-?
en
ON
c
8
CO
ID
•
CM
01
liJ
O
LU
CL
to
o:
UJ
o
in
_
ID
•o
C
O
•
O
O
8
in
3
4-
O
* C
t- O
10 1_
O 4-
in in
0<
in
3
ID
__
O
10
r>
•f"
o
* C
U O
IO L.
O 4-
in in
O <
• 10
ID -
s s:
129
-------
CO CO
r- r--
8
§
*
1
•— ^
i?
!~
-»-
H-
Ul
Duration
i
CO
u.
SI
8
u
10 "0
>o
•f- +- r—
c cr
O o m
ifi in c
k i ^
•o -o o
555
o
JD 1^1 n
— — CM CM
O OO O
C
O 0) 1
— •(- C ><-
•1- >~ 10 — O
0 t. i-
3 !0 0°*
H3 (0 tO
f-w r*» f** [•»- (BOO
c^ o^ o\ &\
•— — —••— O) en CT
c c c
in v) tf ui O O O
c c c c u i. L
u o o o E e e
5 *3t TT *i £ k k
& ^ & (M lO vO O
f-* r~» ^f r~- vp (M *~
— CM fl O O O CM
c
0
o -i- o
O O O ^r 3= 3 O O O
in in m i O ~o m in in
(- 1- K O L, $ O O O
_l _J _l hnC9L-J _l -J
o . . . -v: jz -c
o r o c o c 3t -c
f-^ — O — 1.0 •— ^J" V
— 6 t E in E vO •* "t CM
— CM —
IN CM CM
O <7^ ON CO 00 CO CO
CM CM CM fM CM CM CM
O O O 1 CO CO VO
• • • • • •
r^ i — r-~ vo ^o r^
O O O O O O O
5* i* 5* f i' i' ^
CO CO
r~ i»-
CT* CTv
Armstrong et al .
Armstrong et al .
O CO
co m
O fO
0 0
in m
0 0
JZ jC
«t CM
CO CO
CM CM
O ^t
» •
r~ CO
0 0
•o- M-
i 5
CO
ON
10
o
in
I
in
—
0
5
CO
CM
Kl
•
CO
o
^J-
3:
CO
1 —
(0
•f-
« — 1 a —
— ul ..o —
.0 »| m +-
,
r- -
s: S
^
a>
in
m
• 3
c: 0)
* 10
ID C
Q- 0
in
O
L
U
ID
c O
* L
ro o
l_ 10
CL S
cr
c
IB
in
O
L
.C
O
10
1
c O
10 O
CL 2?
CJ
c
0)
in
O
L
E
3
£
U
10
^
c 0
* t-
(0 O
Q- 2
cr
c
(D
in
O
E
3
O
10
L
c O
v u
<7 O
X 2E
cr
xi
c
in
0
c
E
3
'JJ]
O
10
».h
!-. O
IO O
C_ E
a
T
c
0)
8
i-
E
3
'^
U
10
•>.b
E^ °
10 O
(- (0
a. s
CT
fe
c
e
in
O
u
£
^J
^
8
^i
c O
* L-
(0 O
CL -S.
130
-------
f—
co r-
r*- cj*
-— r--
• 00 — O>
_ |~- (0 —
(O C7\
— 4- O
4- CD L
CD . U
— •>. CD
8 g 10 a.
k4- in
in — — N
*. e — — 4-
• 1_ 10 d> 10
OC -2 -n a ^
§
£i
4- 1 <->
C -J K^i -tf- K°\ £) O
a N^ vo ro in r~ tn
y g . ...
c B o o o — o
3~
c
+- c: ro
O O L.
•*• 4- .C
UJ 3 * O O O
-o O in m in
i? L S B S
s
— SZ -0 -C
.
s
£
in
c
L)
in
4-
3
in
1
•j-
CL
0
c
O
m
^
a.
B ^ oo 00 ao j E
*
0
1, 1
g o\ in
0 O oo o — in f>
L • CM (N CN •— ~-
9-
X
*-
4?
3
-o
—
4?
a.
3
^
•°
SI -o
O CN ~— •/ O
TI .... i j in
oJ r^ co co co j . 153
in 9
* i_
1 3 0
— C
§
en
10 • •"
._ in
8
§a> T>
3 —
E — 3
— — — — — 610 O
SO 0 U 0
*r ^f xj- •**•
n > .0
.c
£XXXX — ^ t"1
O^ Z z ^ ic I . * H)
4- m in o 3
0 X -C I. —
—
CT
-D jC
C O
CO O U5 4-
4- z a. o> ID
10 >
- - k. C
m in O) — z
L L. I
O O - c 10
c JT in O x
+- 4- L. — 2
3304-
4- 3 CD
SE 3 TJ 4-
O IO 35 10
in~33 l_L- l_ —
O CT C. U) j *• •*- S 3
a o -*
E » ^ —
3 a. m L -in
»— 60) w C 3
jr — 4- I o -c
O u 0) 10 E U
10 £ c « — c
8L. (/) O L I/I 10 >-
•» jD £ Cp 3 in ^r
— CO i/) O 4- k. L.
U *u 1/110 inio OO
0 IOO 10— ^16 -CO
a i_ig LID oo oc
i/i in
334-5-
o o a -Q u
10 ID — O -C
o u 4- m 4-
a> o 3
o: cr uJ uj <
ID -O U TD CD
K%
in
•—
c
0
t
s
*•
10
4-
10
CD
3
4-
HJ
k
t
4?
^
C
10
X
a.
•*-
^
c
O
4-
(D
O
C
3
g
__
10
C
O
I/I
o.
•
<«
c
o
As
s
<4^
v
K1
X
2
in
5
•£
(O
§
^_
**-
_
•^
10
3
O
tr
^z
131
-------
REFERENCES
Abeliovich, A. and Y. Azov. 1976. Toxicity of ammonia to algae in sewage
oxidation ponds. Appl. Environ. Microbiol. 31(6): 801-806.
Admiraal, W. 1977. Tolerance of estuarine benthic diatoms to high concentra-
tions of ammonia, nitrite ion, nitrate ion and orthophosphate. Mar.
Biol. 43(4): 307-315.
Agami, M., M. Litav, and Y. Waisel. 1976. The effects of various components
of water pollution on the behavior of some aquatic macrophytes of the
coastal rivers of Israel. Aquat. Bot. 2: 203-213.
Alabaster, J.S. and D.W.M. Herbert. 1954. Influence of carbon dioxide on the
toxicity of ammonia. Nature 174(4426): 404.
Alabaster, J.S., D.G. Shurben, and G. Knowles. 1979. The effect of dissolved
oxygen and salinity on the toxicity of ammonia to smolts ot salmon, Salmo
salar L. J. Fish Biol. 15(6): 705-712.
Alabaster, J.S. and R. Lloyd. 1980. Ammonia. Pages 85-102 in: Water quality
criteria for freshwater fish. Butterworth and Co. Ltd., London.
Alderson, R. 1979. The effect of" ammonia on the growth of juvenile Dover
sole, Solea solea (L.) and turbot, Scophthalmus maximus (L.). Aquaculture
17(4): 291-309.
Allan, I.R.H. 1955. Effects of pollution on fisheries. Verh. Int. Ver.
Theor. Angew. Limnol. 12: 804-810.
Allan, I.R.H., D.W.M. Herbert, and J.S. Alabaster. 1958. A {r.eld and labora-
tory investigation of fish in a sewage effluent Fish. Invest. 6(2):
1-76.
Anderson, B.C. 1944. The toxicity thresholds of varjous substances found in
industrial wastes as determined by the use of Daphnia magjia. J. Water
Pol Int. Control }•>.]. 16(6): 1156-1165.
132
-------
Anderson, B.C. 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, K.B., R.E. Sparks, arid A.A. Paparo. 1978. Rapid assessment of
water quality, using the fingernail clam, Musculium transversum. WRC
Res. Rep. No. 133, Water Resources Center, University of Illinois, Urbana,
IL: 115 p.
Anthonisen, A.C., R.C. Loehr, T.B.S. Prakasam, and E.G. Srinath. 1976.
Inhibition on nitrification by ammonia and nitrous acid. J. Water Pollut.
Control Fed. 48(5): 835-852.
Arillo, A., L.L. Doria, C. Margiocco, F. Melodia, and P. Mensi. 1978. Attivita
della fruttosio 1-6 difosfatasi epatica in eseraplari di Salmo gairdneri
sottopasti a diverse concentrazioni di ammoniaca indissociata. (Liver
fructose - 1,6-diphosphatase activity in Salmo gairdneri exposed to
various concentrations of undissociated ammonia.) Mera. 1st. Ital.
Idrobiol. Dott. Marco de Marchi Pallanza Italy 36: 163-170. (In Italian).
Arillo, A., N. Maniscalco, C. Margiocco, F. Melod^'a, and P, f- ~i 1979a
Fructose 1,6-bisphosphatase and total proteolytic activity i" the liver
of Salmo gAi1^!1?!^ •' effects of pH and amn,,,,j \..., Comp. Biocnem. Physiol.
63C(2): 325-331.
Arillo, A., R. Mantovani, C. Margiocco, F. Melodia, and P. Mensi. 1979b. Ef-
fects of exposure to high environmental pH and to sublethal ammonia con-
centrations on liver carbohydrates in Salmo gairdneri. Mem. 1st. Ital.
Idrobiol. 37:51-61.
Arillo, A., C. Margiocco, and F. Melodia. 1979c. Influence of various ambient
un-Lonized ammonia levels on the liver cyclic -3',5'-adenosine-monophos-
133
-------
phate concentrations in Salmo gairdrieri. Boll. Mus. 1st. Biol. Univ.
Genova 47:83-91.
Arillo, A., C. Margiocco, and F. Melodia. 1979d. The gill sialic acid content
as an index of environmental stress in rainbow trout, Salmo gairdneri,
Richardson. J. Fish Biol. 15(4): 405-410.
Arillo, A., C. Margiocco, F. Melodia, and P. Merisi. 1980. Lysosomal lability
in ammonia-treated rainbow trout (Salroo gairdneri Rich.). Pages 12-13 in:
Proc. 2nd Conf. on Control Processes, European Society for Comparative
Physiology and Biochemistry, 23-25 April 1980, Southampton, England.
Arillo, A., C. Margiocco, F. Melodia, P. Mensi, and G. Schenone. 1981a. Ammo-
nia toxicity mechanism in fish: studies on rainbow trout (Salmo gairdneri
Rich.). Ecotoxicol. Environ. Saf. 5:316-328.
Arillo, A., B. Uva, and M. Vallarino. 198lb. Renin activity iii rainbow trout
(Salmo gairdneri Rich.) and effects of environmental ammonia. Comp.
Biochem. Physiol. 68A(3): 307-311.
Arizzi, M. and A. Nicotra. 1980. Effects of ammonia activation in sea urchin
eggs. Ultrastructural observations. Ultraraicroscopy 5(3): 401.
Armstrong, D.A., D. Chippendale, A.W. Knight,and J.E. Colt. 1978. Interac-
tion of ionized and un-ionized ammonia on short-term survival and growth
of prawn larvae, Macrobrachium rosenbergii. Biol. Bull. 154(1): 15-31.
Armstrong, D.A. 1979. Nitrogen toxicity to Crustacea and aspects of its
dynamics in culture systems. Pages 329-360 in: Proc 2nd Biennial
Crustacean Health Workshop. D. Lewis and J. Li^ag (Eds.),, Texas A & M
Sea Grant, TAMM-SE-79-114.
Baird, R., J. Bottomley, and H. Taitz. 1979. Ammonia tcxicity and pH control
in fish toxicity hioassays of" treated wastewaters. Water Res. 13(2):
181-184.
134
-------
Ball, I.R. 1967. The relative susceptibilities of some species of Ire&h-water
fish to poisons. I. Ammonia. Water Res. 1(11/12): 767-775.
Bartberger, C.A. and S.K. Pierce, Jr. 1976. Relationship between ammonia
excretion rates and hemolymph nitrogenous compounds of a euryhaline
bivalve during low salinity acclimation. Biol. Bull. 150(1): 1-14.
Becker, C.D. and T.O. Thatcher. 1973. Ammonia, amines and related compounds.
Pages D.1-D.28 in: Toxicity of power plant chemicals to aquatic life.
United States Atomic Energy Commission, Battelle Pacific Northwest Labo-
ratories, Richland, WA.
Becker, W. arid H. Schmale. 1978. The ammonia and urea excretion of
Biomphalaria glabrata under different physiological con^i^ions: starva-
tion, infection with Schistosoma mansoni, dry keeping. Comp. Biochem.
Physio 1. 59B(1): 75-79-
fielding, D.L. 1927. Toxicity experiments with fish in reference to trade
waste pollution. Trans. Am. Fish. Soc. 57: 100-119.
Binstock, L. and H. Lecar. 1969. Ammonium ion currents in the squid giant
axon. J. Gen. Physiol. 53(3): 342-361.
Blahm, T.H. 1978. Toxicity of chemical fire retardanl , to juven?]- coho sal-
mon and rainbow Lrout. Ph.D. Thesis, Un: . Idaho, Moscow, ID: 40 p.
Brett, J.R. and C.A. Zala. 1975. Daily pattern of nitrogen excretion and
oxygen consumption of sockeye salmon (Oncorhynchug nerka) under con-
trolled conditions. J. Fish. Res. Board Can. 32(12): 2479-2486.
Bretthauer, R. 1978. Some ecological limits of tolerance to Ochromonas
sociabilis. Verh. Internat. Verein. Limnol. 20(3):1850-1854.
Brockway, D.R. 1950. Metabolic products and their effects. Prog. Fish Cult.
12(3): 127-129.
-------
Broderius, S.J., L.L. Smith, Jr., and D.T. Lind. 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.
Broderius, S.J. and L.L. Smith, Jr. 1979. Lethal and sublethal effects of
binary mixtures of cyanide and hexavalent chromium, zinc, or a0imonia to
the fathead minnow (Pimephales promelas) and rainbow trout (Salmo
gairdneri). J. Fish. Res. Board Can. 36(2): 164-172.
Broderius, S.J., R.A. Drummond, J.T. Fiandt, and C.L, Russoci. (In preparation).
Toxicity of ammonia to smallmouth bass, Micropterus dolomieui, as related
to pH. Environmental Research Laboratory, U.S. Environmental Protection
Agency, Duluth, MM.
Brown, A.C. and A.B. Currie. 1973. Tolerance of Bullia digital is (Prosobran-
chiata) to solutions of ammonium nitrate in natural sea water. S. Afr.
J. Sci. 69(7): 219-220.
Brown, A.C. 1974. Observations 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): 723-733.
Brown, V.M., D.H.M. Jordan, and B.A. Tiller. 1969. The acute toxicity to
rainbow trout of fluctuating concentrations and mixtures of ammonia,
pheno] and zinc. J. Fish Biol. 1(1): 1-9.
Brown, V.M. , D.G. Shurben, and D. Shaw. 1970. Studies on wr CPJ: quality and
the absence of fish from some polluted English rivers. Water Res. 4(5):
363-382.
136
-------
Brownell, C.L. 1980. Water quality requirements for first-feeding in marine
fish larvae. I. Ammonia, nitrite, and nitrate. J. Exp. Mar. Biol.
Ecol. 44: 269-283.
Buckley, J.A. 1978. Acute toxicity of unionized ammonia to fingerling coho
salmon. Prog. Fish-Cult. 40(1): 30-32.
Buckley, J.A., C.M. Whitmore, and B.D. Liming. 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.L., Jr., J. Cairns, Jr., and G.W. Sullivan. 1974. Evaluation of
Philodina acuticornis (Rotifera) as a bioassay organism for heavy metals.
Water Resour. Bull. 10(4): 648-661.
Burkhalter, D.E. 1975. Effects of prolonged exposure to ammonia on rainbow
trout (Salmo gairdneri) eggs and sac fry. M.S. Thesis, Montana State
University, Bozeman, MT: 67 p.
Burkhalter, D.E. and C.M. Kaya. 1977. Effects of prolonged exposure to am-
monia on fertilized eggs and sac fry of rainbow trout (Salmo gairdneri j.
Trans. Am. Fish. Soc. 106(5): 470-475.
Burrows, R.E. 1964. Effects of accumulated excretory t j d=,cts -. '>atchery-
reared salmonids. Research Report 66. i ,-.i and Wildlife- Service, U.S.
Dept. interior, Washington, D.C.: 12 p.
Byerrum, R.U. and A.A. Benson. 1975. Effect of ammonia on photosynthetic
rate and photosynthate release by Amphidinium carterae (Dinophyceae). J.
Phycol. 11: 449-452.
Calamari, U. and R. Marchetti. 1975. Predicted and observed acute toxicity of
copper and ammonia in rainbow trout (Salmo gairdneri Rich.). Prog. Water
Technol. 7(3/4): 569-577.
137
-------
Calamari, D., R. Marchetti, and G. Vailati. 1977. Effetti di trattamenti
prolungati con amraoniaca su stadi di sviluppo del Salmo gairdneri.
(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., R. Marchetti, and G. Vailati. 1981. Effects of long-term ex-
posure to ammonia on the developmental stages of rainbow trout (Salmo
gairdneri Richardson.). Rapp. P.-v. Reun. Cons. int. Explor. Mer 178:81-
86.
Cameron, J.N. 1979. Excretion of CO. in water-breathing animals. Marine
Biol. Lett. 1:3-13.
Gary, G.A. 1976. A report on the assessment of aquatic environmental impact
of Union Carbide's Uravan operations: on-site toxicity bioassays. Re-
port prepared for Metals Division, Union Carbide Corporation, Uravan, CO.
Aquatic Environmental Sciences, Union Carbide Corp., Tarrytown, NY: 67 p.
Catedral, F.F., R. Coloso, N. Valera, C.M. Casalmir, and A.T. Quibuyen. 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.
Catedral, F.F., D.D. Gerochi, A.T. Quibuyen, and C.M. Casalmir. 1977b. Effect
of nitrite, ammonia, arid temperature on P. monodon Larvae. Q. Res. Rep.
Aquacult. Dep. Southeast Asian Fish. Dev. Cent. 1(3): 9-12.
Champ, M.A., J.T. Lock, C.D. Bjork, W.G. Klussmann, and J D McCullough, Jr.
1973. Effects of anhydrous ammonia on a central IVxas pond and a review
of previous research with ammonia in fisheries Management. Trans. Am.
Fish. Soc. 102(1): 73-82.
Chin, P. 1976. Nitrogen and phosphorus excretion in Neomysis awatschensis.
1. Effects of temperature and salinity. Pusan Sus^n Taehak Haeyang
138
-------
Kwahak Vonguso Yongu Pogo 9: 1-6. (In Korean). (Chew. Absti $1: l U'J'i
(1977)]
Chipman, W.A., Jr. 1934. The role of pH in determining the toxicity of ammo-
nium compounds. Ph.D. Thesis, University of Missouri, Columbia, MO: 153
P-
Chu, S.P. 1943. The influence of the mineral composition of the medium on the
growth of planktonic algae. II. The influence of the concentration of
inorganic nitrogen and phosphate phosphorus. J. Ecol. 31(2): 109-148.
Colt, J.E. 1974. Evaluation of the short-term toxicity of nitrogenous com-
pounds to channel catfish. M.S. Thesis, University of California, Davis,
CA: 94 p.
Colt, J. and G. Tchobanoglous. 1976. Evaluation of the short-term toxicity of
nitrogenous compounds to channel catfish, Ictalurus P_uJi£t£tuj;. Aqua-
culture 8(3): 209-224.
Colt, J.E. 1978. The effects of ammonia on the growth of channel catfish,
Ictalurus punctatus. Ph.D. Thesis, University of California, Davis, CA:
185 p.
Colt, J. and G. Tchobanoglous. 1978. Chronic exposur3 of ch/wth and survival. Aqua-
culture 15(4): 353-372.
Colt, J.E. and D.A. Armstrong. 1979. Nitrogen toxicity to fish, crustaceans
and molluscs. Paper presented at Bio-Engineering Symposium, 15-19 Octo-
ber, Traverse City, MI, Fish Culture Section, American Fisheries Society:
30 p.
Corti, U.A. 1951. Poissons et combinaisons azotees. La "matrix" des poissons.
XI. (Fish and nitrogen compounds. The "matrix" of fish. XI.) Verh.
Int. Ver. Theor. Angew. Limnol. 11: 84-87. (In English translation).
139
-------
Cowey, C.B. and J,R. Sargent. I^.TV>
ogy, Vol. VIII, W.S. Hoar, D.J. Randall and J.R. Brett, (Kds.), Academic
Press, New York, N.Y.
Creach, Y., L. Nopoly and A. Serfaty. 1969. Variations de 1'activite
proteolytique des tissus de la carpe conunune (Cyprinus carpio L.) pendant
un jeune prolonge. (Variations in the proteolytic activity of tissues of
the common carp (Cyprinus carpio) during a prolonged fast.) Arch. Sci.
Physiol. 23(3): 351-364.
Currie, A.B., A.C. Brown, and G.R, Bennett. 1974. The effect, of ammonium
nitrate solutions on some aspects of the biology of the black mussel,
Choromytilus meridionalis. Trans. R. Soc. S. Afr 41(2): 209-215.
Curtis, M.W., T.L. Copeland, and C.H. Ward. 1979. Acute toxicity of 12
industrial chemicals to freshwater and saltwater organisms. Water Res.
13(2): 137-141.
Cvancara, V.A. 1969a. Distribution of liver allantoinase and allantoicase
activity in fresh-water teleosts. Comp. Biochem. Physioi. 29:631-638.
Cvancara, V.A. 1969b. Studies on tissue arginase and ureogenesis in fresh-
water teleosts. Comp. Biochem. Physiol. 30:489-496.
Danecker, E. 1964. Die Jauchevergiftung von Fischen—eine Ammoniakvergiftung.
(The jauche poisoning of fish~-an ammonia poisoning.) Gsterr. Fischerei.
3/4: 55-68. (In English translation.)
Danielewski, S. 1979. An attempt to disinfect fisb ponds with ammonia water.
Rocz. Nauk Roln. Ser. H Rybactwo 99(1): 69-80. [Bid. Abstr. 70: 29446
(1980)]
Das, A.B. 1980. Physiological and biochemical effects of sublethal ambient
ammonia on Channa punctatus (Bloch). Indian J. Biorhem. Biophys. 18(4):5.
140
-------
De, S.N. and S. Bhat tacharya. l*)?t\. Kffect ot .torn*" ituius trial t>oHut ant * >>u
fish thyroid peroxidase activity and role of cytochrome c thereon. Tnd
J. Exp. Biol. 14(5): 561-563.
Deal, P.H., K.A. Souza, and H.M. Mack. 1975. High pH, ammonia toxicity, and
the search for life on the Jovian planets. Origins Life 6(4): 561-573.
DeGraeve, G.M., R.L. Overcast, and H.L. Bergman. 1980. Toxicity of under-
ground coal gasification condenser water and selected constituents to
aquatic biota. Arch. Environ. Contam. Toxicol. 9(5): 543-555.
Delistraty, D.A., J.M. Carlberg, J.C. Van Olst, and R.F. Ford. 1977. Ammonia
toxicity in cultured larvae of the american lobster (Horoarus americanus).
Pages 647-672 in: Proc. World Mariculture Society,, 8th Anna, Meet., San
Jose, Costa Rica.
Department of the Environment, U.K. 1972. Effects of pollution on fish.
Page 37 in: Water Pollution Research 1971, H.M. Stationery Office, London,
U.K.
Desavelle, H. and E. Hubault. 1951. La pollution des eaux par les effluents
industriels. (Pollution of water by industrial wastes), "'ill Cent
Beige Fitude Doc. Eaux 14: 197-207.
De Vooys, G.G.N. 1968. Formation and excretic .- -'"«.onia in Teleostei. I
Excretion of ammonia through the gills. Arch Int. Physio], Biochim.
76(2): 268-272.
De Vooys, C.G.N. 1969. Formation and excretion of ammonia in Teleostei. II.
Occurrence and transport of ammonia in the blood. Arch. Int. Physiol.
Biochim. 77(1): 112-118.
Dockal, P. and A. Varecha. 1967. Havarijni znecistenf reky Becvy cpavkem.
(Destructive ammonia pollution of the Becva River). Vod. Hospod. 17(9):
388-391. (In English translation).
141
-------
Dowden, B.F. and H.J. Bennett. 1965. Toxicity of selected chemicals to cer-
tain animals. J. Water Pollut. Control Fed. 37(9): 1308-1316.
Downing, K.M. and J.C. Merkens. 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,
Driedzic, W.R. and P.W. Hochachka. 1978. Metabolism in fish during exercise.
Pages 503-543 in: Fish Physiology, Vol. VII, W.S. Hoar at;d P.J. Randall,
(Eds.), Academic Press, New York, N.Y.
D'Silva, C. and X.N. Verlencar. 1976. Relative toxicity of two ammoiiiuni
compounds found in the waste of fertilizer plants. Mahasagar 9(1-2);
41-44.
Ellis, M.M. 1937. Detection and measurement of stream pollution. Bull. U.S.
Bur. Fish 48(22): 364-437.
Emerson, K., R.C. Russo, R.E. Lund, and R.V. Thurston. 1975. Aqueous ammonia
equilibrium calculations: effect of pH and temperature. J. Fish. Res.
Board Can. 32(12):2379-2383.
Emery, R.M. and E.B. Welch. 1969. The toxicity of alkaline solutions of
ammonia to juvenile bluegill sunfish (Lepomis macrochirus Raf.). Water
Quality Branch, Division of Health and Safety, Tennessee Valley Authority,
Chattanooga, TN: 31 p. (Mimeo).
Epel, D., R. Steinhardt, T. Humphreys, and D. Mazia. 1974. An analysis of
the partial metabolic derepression of sea urchin eggs by ammonia; the
existence of independent pathways. Dev. Biol. **0: 245-255
Epifanio, C.E. and R.F. Srna. 1975. Toxicity of ammonia, nitrite ion, nitrate
ion, and orthophosphate to Mercenaria mercenaria and Crat.sosti.-ea virginica.
Mar. Biol. 33(3): 241-246.
142
-------
Epler, P. ]971. Oddzialywanie zanieczysczenia wod na ich ichtiofaune, Czesc
II. Toksycznosc araoniaku, fenoli i cyjankow. (Effect of water pollution
on ichthyof auxia. II. Toxicity of ammonia, phenols, and cyanides.)
Postepy Nauk Ro n. (4): 67-90. (In English translation).
Erickson, R.J. 1982. Mathematical description of pK-dependent ammonia toxic-
ity. Internal Report, Environmental Research Laboratory, U.S. Environ-
mental Protection Agency, Duluth, MN: 20 p.
European Inland Fisheries Advisory Commission. 1970. Water quality criteria
for European freshwater fish. Report on ammonia and inland fisheries.
EIFAC Tech. Paper No. 11: 12 p. (also in Water Res. 7(7): 1011-1022
(1973).)
Evans, J.W. 1979. The construction and use of a continuous-flow bioassay
apparatus to determine a preliminary un-ionized ammonia 96-hour LC50 for
the crayfish, Orcojiectes nais. M.S. Thesis, Univ. of Kansas, Lawrence,
KS: 76 p.
Fauconneau, B. and P. Luquet. 1979. Influence d'une elevation de temperature
sur 1'evolution de 1'aminoacidemie et de 1'ammoniemie apres le repas chez
la truite arc en ciel (SaJLmo gairdneri R.). (Effect of temperature rise
on blood aminoacids arid ammonia in rainbow tr>ut (Salmo gairdneri R.)
after feeding.) Ann. Bioi. Anim. Biochim. Biophys. 19(4A): 1063-1079.
Fava, J.A. and C. Tsai. 1976. Immediate behavioral reactions of blacknose
dace, Rhinichthys atratalus, to domestic sewage and its toxic constituents.
Trans. Am. Fish. Soc. 105(3): 430-441.
Fechter, H. 1973. Die stickstoffhaltigen Stoffwechselendprodukte und ihre
Exkretion bei Pa ra cervtrp t.us lividus . (Nitrogenous metabolic end products
and their excretion in Pa_r3^en_trotjJis lividus.) Mar. Biol. 19(4): 285-289.
(In English translation).
143
-------
Fedorov, K. Ye. and Zh. V. Srairnova. 1978. Dynamics of ammonia accumulation
and its effect on the development of the pink salmon, Oncorhynchus
gorbuscha, in closed circuit incubation systems. Vopr. Ikhtiol. 19(2):
320-328.
Fellows, F.C.I, and F.J.R. Hird. 1979a. From whence comes ammonia in crusta-
ceans? Proc. Aust. Biochem. Soc. 12: 37.
Fellows, F.C.I, and F.J.R. Hird. 1979b. Nitrogen metabolism and excretion in
the freshwater crayfish Cherax destructor. Comp. Biochem. Physiol,
64B(2): 235-238.
Fisher, C.J. and C.D. Ziebell. 1980. Effects of watershed use on water
quality and fisheries in an Arizona mountain lake. Eisenhower Consortium
Bull. 7: 11 pp.
Flagg, R.M. and L.W. Hinck. 1978. Influence of ammonia on aeromonad suscepti-
bility in channel catfish. Proc. Ann. Conf. S.E. Assoc. Fish & Wildl.
Agencies 32: 415-419.
Flis, J. 1968a. Anatomicohistopathological changes induced in carp (Cyprinus
carpio L.) by ammonia water. Part I. Effects of toxic concentrations.
Acta Hydrobiol. 10(1-2): 205-224.
Flis, J. 1968b. Anatomicohistopathological changes induced in carp (Cyprinus
carpio L.) by ammonia water. Part II. Effects of subtoxic concentra-
tions. Acta Hydrobiol. 10(1-2): 225-238.
Florkin, M. and G. Duchateau. 1943. Les formes du systeme enzymatique de
1'uricolyse et 1'evolution du catabolisme purique chez les animaux.
(Forms of uricolytic enzyme systems and the evolution of purine metabolism
in the animal kingdom). Arch. Int. Physiol. 53: 267-307.
144
-------
'Forster, R.P. and L. Goldstein. 1966. Urea synthesis in the lungtish:
relative importance of purine and ornithine cycle pathways. Science
153(3744): 1650-1652.
Forster, R.P. and L. Goldstein. 1969. Formation of excretory products.
pages 313-350 in: Fish physiology, Vol. I, W.S. Hoar and D.J. Randall,
(Eds.). Academic Press, New York, N.Y.
Frahm, J.-P. 1975. Toxitoleranzversuche an Wassermoosen. (Toxicity toler-
ance studies utilizing periphyton). Gewasser and Abwasser 57/58: 59-66.
Freeman, L. 1953. A standardized method for determining toxicity of pure
compounds to fish. Sew. Ind. Wastes 25(7):845-848.
Fromm, P.O. 1963. Studies on renal and extra-renal excretion in a freshwater
teleost, Salroo gairdneri. Corap. Biochem. Physiol. 10(2): 121-128.
Fromm, P.O. and J.R. Gillette. 1968. Effect of ambient ammonia on blood
ammonia and nitrogen excretion of rainbow trout (Salmo gairdneri). Comp.
Biochem. Physiol. 26(3): 887-896.
Fromm, P.O. 1970. Toxic action of water soluble pollutants on freshwater
fish. Pages 9-22 in: EPA Water Pollut. Control Res. Ser. 18050 DST
12/70: 56 p.
GalJ, W.K. 1980. Effect of cow feces on the ecology of laboratory streams.
M.S. Thesis, Univ. of Wisconsin, Madison, WI: 73-83.
Garcia-Romeu, F. and R. Motais. 1966. Mise en evidence d'echanges Na /NH,
chez 1'anguille d'eau douce. (Study of the Na+/NH, exchange in the
fresh water eel.) Comp. Biochem. Physiol. 17(4): 1201-1204.
Gillette, L.A., D.L. Miller, and H.E. Redman. 1952. Appraisal of a chemical
waste problem by fish toxicity tests. Sewage Ind. Wastes 24(11): 1397-
1401.
-------
Girard, J.P. and P. Payan. 1980. Ion exchanges through respiratory and
chloride cells in fresh water- and seawater-adapted teleosteans. Am. J.
Physiol. 238(7): R260-R268.
Giussani, G., I. Borroni, and E. Grimaldi. 1976. Role of un-ionized ammonia
in predisposing gill apparatus of Alburnus alburnus alborella to fungal
and bacterial diseases. Mem. 1st. Ital. Idrobiol. 33: 161-175.
Goettl, J.P. and J.W. Edde. 1978. Environmental effects of oil shale mining
and processing. Part I - Fishes of Piceance Creek, Colorado, prior to
oil shale processing. EPA Ecol. Res. Ser. EPA-600/3-78-096. Environ-
mental Research Laboratory, U.S. Environmental Protection Agency, Duluth,
MN: 18 p.
Goldstein, L. and R.P. Forster. 1961. Source of ammonia excreted by the
gills of the marine teleost, Myoxocephalus scorpius. Am. J. Physiol.
200(5): 1116-1118.
Goldstein, L,, R.P. Forster, and G.M. Fanelli, Jr. 1964. Gill blood flow and
ammonia excretion in the marine teleost, Myoxocephalus scorpius. Comp.
Biochem. Physioi. 12(4): 489-499.
Goldstein, L. and R.P. Forster. 1965. The role of uricolysis in the produc-
tion of urea by fishes and other aquatic vertebrates. Comp. Biochem.
Physioi. 14(4): 567-576.
Gordon, M.S. 1970. Patterns of nitrogen excretion in amphibious fishes.
Int. Congr. Ser. - Excerpta Med. 195: 238-242.
Gray, L.J. and J.V. Ward. 1978. Environmental effects of oil shale mining
and processing. Part II - The aquatic macroinvertebrates of the Piceance
Basin, Colorado, prior to oil shale processing. EPA Ecol. Res. Ser.
EPA-600/3-78-097. Environmental Research Laboratory, U.S. Environmental
Protection Agency, Duluth, MN: 39 p.
146
-------
Greenwood, P.J. and A.C. Brown. 1974. Effect of ammonium nitrate solutions
on fertilization and development of the sea urchin, Parechinus angulosus.
Zool. Afr. 9(2): 205-209.
Gregory, R.B. 1977. Synthesis and total excretion of waste nitrogen by fish
of the Periophthalmus (mudskipper) and Scartelaos families. Corap. Bio-
chero. Physiol. 57A(1): 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
trimethylaraine oxide. J. Biol. Chem. 81(2): 267-278.
Grygierek, E., M. Januszko, D. Kru'ger, and B.E. Wasilewska. 1978. Wplyw wody
amoniakalnej na bakterie, plankton i faune denna stawow. (The influence
of ammonia water on bacteria, plankton, and bottom fauna of ponds.)
Rocz. Nauk Roln. Ser. H 99(1): 121-140. (In English translation).
Guerin-Ancey, 0. 1976a. Etude experimentale de 1'excretion azotee du bar
(Dicentrarchus labrax) en cours de croissance. I. Effets de la temper-
ature et du poids du corps sur 1'excretion d1ammoniac et d'uree. (Exper-
imental study of the nitrogen excretion of bass (Picentrar.ch.us labrax)
during growth. I. Effects of temperature and weight on the excretion of
ammonia and urea.) Aquaculture 9: 71-80.
Guerin-Ancey, 0. 1976b. Etude experimentale de 1'excretion azotee du bar
(Dicentrarchus labrax) en cours de croissance. II. Effets du jeune sur
J'excretion d1ammoniac et d'uree. (Experimental study of the nitrogen
excretion of bass (DicJLI?tr_Jr_cJiH5 labrax) during growth. II. Effects of
starvation on the excretion of ammonia and urea.) Aquaculture 9: 187-194.
147
-------
Guerin-Ancey, 0. 1976c. Etude experimentale de 1'excretion azotee du bar
(Dicentrarchus labrax) en cours de croissance. III. Effets du volume et
de la concentration initiale en ammoniac sur 1'excretion d1ammoniac et
d'uree. (Experimental study of the nitrogen excretion of bass
(Dicentrarchus labrax) during growth. III. Effects of water volume and
initial ammonia concentration on the excretion of ammonia and urea.)
Aquaculture 9: 253-258. (In English translation.)
Guerin-Ancey, 0. 1976d. Etude experimentale de 1'excretion azotee du bar
(Dicentrarchus labrax) en cours de croissance. IV. Effets de la
manipulation et du MS-222 Sandoz sur 1'excretion d'ammoniac et d'uree.
(Experimental study of the nitrogen excretion of bass (Dicentrarchus
labrax) during growth. IV. Effects of handling and MS-222 Sandoz on the
excretion of ammonia and urea.) Aquaculture 9: 367-372.
Guerra, M. and N. Comodo. 1972. Possibilita di utilizzazione del test di
ittiotossicita per una valutazione dei limiti di accettabilita negli
eftluenti industrial! di alcune sostanze tossiche. (Ichthyotoxicity as a
means of determining the acceptability limits of toxic substance in
industrial effluents.) Boll. Soc. Ital. Biol. Sper. 48(22): 898-901.
Gupta, S.K., A.V.S. Prabhakar Rao, and S.D. Bokil. 1979. Treatment of nitro-
genous fertiliser waste by floculating algal-bacterial system. Indian J.
Environ. Health 21(2):105-112.
Guseva, K.A. 1937. K gidrobiologii i raikrobiologii uchinskogo vodokhranilishcha
kanala Moskva-Volga. (The hydrobiology and microbiology of the Ucha-
reservoir of the Moscow-Volga canal. II. Observations on the develop-
ment of Anabaena letnmermanni Richter, Aphanizomenon flos-aquae Breb, and
Asterionella fqrmosa Hassall in the reservoJr during the first summer of
its existence.) Microbiologiia 6(4): 449-464.
148
-------
•Gyore, K. and J. Olah. 1980. Ammonia tolerance of Moina rectirqstris Leydig
(Cladocera). Aquacultura Hungarica (Szarvas) 2: 50-54.
Hall, L. W. , Jr., A. L. Buikema, Jr., and J. Cairns, Jr. 1978. The effects
of a simulated >efinery effluent on the grass shrimp, Palaemonetes pugio.
Arch. Environ. Contain. Toxicol. 7(1): 23-35.
Hampson, B.L. 1976. Ammonia concentration in relation to ammonia toxicity
during a rainbow trout rearing experiment in a closed freshwater--sea-
water system. Aquaculture 9(1): 61-70.
Hays, R.M., S.D. Levine, J.D. Myers, H.O. Heinemann, M.A. Kaplan, N. Franki,
and H. Berliner. 1977. Urea transport in the dogfish kidney. J. Exp.
Zool. 199(3): 309-315.
Hazel, C.R., W. Thomsen, and S.J. Meith. 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., C.E. Burkhead, and D.G. Muggins. 1979. The development of water
quality criteria for ammonia and total residua] chlorine for the protec-
tion of aquatic life in two Johnson County, Kansas streams. Office of
Water Research and Technology, U.S. Dept. of the Interior, Washington,
D.C.: 146 p.
Hedtke, J.L. and L.A. Morns. 1980. Effect of ammonium chloride on predatory
consumption rates of brook trout (Salvelinus fontinalis) on juvenile
chinook salmon (Oncorhynchus tshawytscha) in laboratory streams. Bull.
Environ. Contam. Toxicol. 24(1): 81-89.
Hemens, J. 1966. The toxicity of ammonia solutions to the mosquito fish
(Gambusia affinis Baird & Girard). J. Proc. Inst. Sewage Purif. 65:
265-271.
-------
Hepher, B. 1959. Use of aqueous ammonia in fertilizing fish ponds. Bamidgeh
11(4): 71-80.
Herbert, D.W.M. 1955. Measurement of toxicity to fish. Anal. Chem. 27(1):
160.
Herbert, D.W.M. 1956. La toxicite d'un effluent d'eau d'egout. (Toxicity of
a sewage effluent.) Bull. Cent. Beige fitude Doc. Eaux 32: 115-120.
Herbert, D.W.M. 1961. Freshwater fisheries and pollution control. Proc.
Soc. Water Treat. Exam. 10(2): 135-161.
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. and D.S. Shurben. 1963. A preliminary study of the effect of
physical activity on the resistance of rainbow trout (Salmo gairdnerii
Richardson) to two poisons. Ann. Appl. Biol. 52(2): 321-326.
Herbert, D.W.M. and D.S. Shurben. 1964. The toxicity to fish of mixtures of
poisons. I. Salts of ammonia and zinc. Ann. App. Biol. 53(1): 33-41.
Herbert, D.W.M. and J.M. Vandyke. 1964. The toxicity to fish of mixtures of
poisons. II. Copper-ammonia and zinc-phenol mixtures. Ann. Appl. Biol.
53(3): 415-421.
Herbert, D.W.M. and D.S. Shurben. 1965. The susceptibility of salmonid fish
to poisons under estuarine conditions -- IT. ammonium chloride. Int. J.
Air Water Pollut. 9: 89-91.
Hillaby, B.A. 1978. Ammonia toxicity to rainbow trout (Sjilmo gairdneri).
M.S. Thesis, The University of British Columbia, Vancouver, B.C., Canada:
73 p.
Hillaby, B.A. and D.J. Randall. 1979. Acute ammonia toxicity and ammonia
excretion in rainbow trout (Salmo gairdneri). J. Fish. Res. Board Can.
36(6): 621-629.
150
-------
Hoar, W.S. 1958. Effects of synthetic thyroxine and gonadal steroids on the
metabolism of goldfish. Can. J. Zool. 36: 113-121.
Holland, G.A., J.E. Lasater, E.D. Neumann, and W.E. Eldridge. 1960. Experi-
ments with inorganic pollutants - ammonia. Pages 183-187 in: Toxic
effects of organic and inorganic pollutants on young salmon and trout.
Res. Bull. No. 5, Dept.. of Fisheries, State of Washington.
Holt, J.D. and S.A. Malcolm. 1979. Evaluation of fish loading rates in reg-
ulatory static bioassays. Tech. Rep.-Fish. Mar. Serv. (Can.) 862: 146-160.
Home, F.R. and S. Mclntosh. 1979. Factors influencing distribution of
mussels in the Blanco River of central Texas. Nautilus 94(4): 119-133.
Hubault, E. 1955. The noxiousness of different chemical substances for the
fish. Compt. Rend. 27th Congr. Intern. Chim. Ind. (Brussels) 1954, 1;
Ind. Chim. Beige 20: 352-356. [Chem. Abstr. 50: 5194b (1956)]
Huggins, A.K., G. Skutsch, and E. Baldwin. 1969. Ornithine-urea cycle enzymes
in teleostean fish. Comp. Biochem. Physiol. 28(2): 587-602.
Iriamura, S. 1951. Effect of various sorts of ion on the sensoria of the
labyrinth of eel (Anguilla japonica). The Tohoku J. Exp. Med. 54(2):
145-150.
Ito, T. 1976. Absorption of dissolved ammonium • .td nitrate ions from sur-
rounding water by the fry of common carp, crucian carp, and loach.
Tansuiku Suisan Kenkyusho Kenkyu Hokoku 26(1): 27-33. (In English trans-
lation) .
Iwan, G.R. and G.E. Cella. 1979. On-site critical life stage bioassay with
the fathead minnow, Pimephales promelas, on the city of Austin, Minnesota
wastewater treatment facilities effluent. 4th ASTM Symposium on Aquatic
Toxicology, October 16-17, Chicago, IL: 18 p.
151
-------
Janicke, W. and D. Liidemann. 1967. Uber die fischtoxikologischen Eigenschaften
des Ablaufs einer Schlammbelebungsanlage. (On the toxicity to fish of
the effluent from an activated sludge plant.) Wasserwirtschaft 57(8):
291-293. (In German with English summary.)
Janicki, R. and J. Lingis. 1970. Mechanism of ammonia production from aspar-
tate in teleost liver. Comp. Biochem. Physiol. 37(1): 101-105.
Jocque, R. and G. Persoone. 1970. Eutrofie'ring en vissterfte in twee
parkvijvers te Oostende. (Eutrophicatian and fish mortality in two ponds
at Osten). Natuurwet. Tijdschr. (Ghent) 52: 168-198.
Johnson, J.D., D. Epel, and M. Paul. 1976. Intracellular pH and activation
of sea urchin eggs after fertilization. Nature 262(5570): 661-664.
Johnson, W.W. and H.O. Sanders. 1977. Chemical forest fire retardants:
acute toxicity to five freshwater fishes and a scud. Technical Papers of
the U.S. Fish and Wildlife Service No. 91., U.S. Dept. Interior, Washing-
ton, D.C. 7 p.
Jones, J.R.E. 1948. A further study of the reactions of fish to toxic sol-
utions. J. Exp. Biol. 25(1): 22-34.
Joy, K.P. and A.G. Sathyanesan. 1977. Ammonium sulphate as a thyroid inhib-
itor in the freshwater teleost Clarias batradius (L.). Curr. Sci. 46(19):
671-673.
Jude, D.J. 1973. Sublethal effects of ammonia and cadmium on growth of green
sunfish. Ph.D. Thesis, Michigan State University, East Lansing, MI: 193
P-
Katz, B. 1979. Relationship of the physiology of aquatic organisms to the
lethality of toxicants: a broad overview with emphasis on membrance
permeability. Pages 62-76 in: Aquatic Toxicology, ASTM STP667, L.L.
152
-------
Marking and R.A. Kimerle, (Eds.), American Society for Testing and Mater-
ials, Philadelphia, PA.
Katz, M. and R.A. Pierro. 1967. Estimates of the acute toxicity of ammonia-
urea plant wast« s to coho salmon, Oncorhynchus kisutch. Final report,
Fisheries Research Institute, College of Fisheries, University of
Washington, Seattle, WA: 15 p.
Kaushik, S. and P. Luquet. 1977. Endogenous nitrogen loss from the muscle of
rainbow trout starved in fresh water and sea water. Ann. Hydrobiol.
8(2); 129-134.
Kawamoto, N.Y. 1958. Fresh water fish culture from the physiological point
of view--I. Influences of ammonia nitrogen excreted by fishes on their
growth in the culture ponds. Rep. Fac. Fish., Prefect Univ. of Mie 3(1):
104-121. (In Japanese.)
Kawamoto, N.Y. 1961. The influence of excretory substances of fishes on
their own growth. Prog. Fish-Cult. 23(2): 70-75.
Kempinska, H. 1968. Wplyw nawozow amonowych na ryby. (The effect of ammonia
fertilizers on fish.) Gospod. Rybna 20: 3-5. (In English translation.)
Kern, D.M., I960. The hydration of carbon dioxide. J. Chem. £d. 37:14-23.
Kinne, 0. 1976. End products of nitrogen metabolism. Pages 80-100 In:
Marine Ecology. A Comprehensive, Integrated Treatise on Life in Oceans
and Coastal Waters, Vol. 3, Part 1: Cultivation, 0. Kinne (Ed.), John
Wiley and Sons, London.
Kloppick, E., G. Jacobasch, and S. Rapoport. 1967. Steigerung der Glykolyse
durch den Einfluss von Ammoniumionen auf die Phosphofruktokinaseaktivitat.
(Enhancement of the glycolytic rate by action of ammonium ions on phos-
phofructokinase activity). Acta. Biol, Med. German. 18: 37-42.
153
-------
Knepp, G.L. and G.F. Arkin. 1973. Ammonia toxicity levels and nitrate toler-
ance of channel catfish. Prog. Fish Cult. 35(4): 221-224.
Korting, W. 1969a. Die schadigende Wirkung des Ammoniaks auf Fische. (The
harmful effect of ammonia on fish.) Miinch. Beitr. Abwasser-, Fisch.-
Flussbiol. 16: 38-48. (In English translation.)
Korting, W. 1969b. Untersuchungen zur Einwirkung des A0n>oniaks auf das Blut
der Fische. (Investigations on the effects of ammonia on the blood of
fish.) Wasser Abwasser Forsch. 4: 154-159. (In English translation.)
Korting, W. 1976. Der Ammoniakgehalt im Wasser und sein Einflup auf den
Fisch. (Ammonia in water and the influence upon the fish.) Fisch Umwelt
2: 111-114.
Krauss, D. 1937. Uber die Wirkung verschiedener geloster Dungemittel und von
K-, Na- und Ca-Salzen auf Haut und Kiemen von Fischen. (The action of
different fertilizers and o:T K, Na, and Ca salts on the skin and gills of
fish.) Z. Fisch. 34(5): 787-817.
Krystal, G.W. and D. Poccia. 1979. Control of chromosome condensation in the
sea urchin egg. Exp. Cell Res. 123(2): 207-219.
Kuhn, 0. and H.U. Koecke. 1956. Histologische und cytologische Veranderungen
der Fischkieme nach Einwirkung ira Wasser enthaltener schadigender
Substanzen. (Histological and cytological changes in gills of fish due
to the action of harmful substances contained in water.) Z. Zellforsch.
43(6): 611-643.
Kutty, M.N. 1978. Ammonia quotient in sockeye salmon (Qncorhynchus nerka).
J. Fish. Res. Board Can. 35(7): 1003-1005.
Langowska, I. and J. Moskal. 1974. Effect of ammonia and urea on nitrobac-
teria in water environment. Pol. Arch. Hydrobiol. 21(1): 119-123.
-------
Larmoyeux, J.D. and R.G. Piper. 1973. Effects of water reuse on rainbow
trout in hatcheries. Prog. Fish Cult. 35(1): 2-8.
Lawrence, W., Jr., J.A. Jacquez, S.G. Dienst, J.W. Poppell, H.T. Randall, and
K.E. Roberts. 1957. The effect of changes in blood pH on the plasma
total ammonia level. Surgery 42(1): 50-60.
Leclerc, E. and F. Devlaminck. 1950. Etude toxicologique de quelques sub-
stances generalement presentes dans les effluents d'usines a gaz. (Toxi-
cological studies of some substances generally present in effluents from
gas works.) Bull. Cent. Beige Etude Doc. Eaux 8: 486-493.
Levi, G., G. Morisi, A. Coletti, and R. Catanzaro. 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: 623-636.
Liebmann, H. 1960. Toxikologie des Abwassers. Sauerstoffmangel und anor-
ganische Gifte. Gasformige Gifte. Ammoniak und Ammonium (NH , NH,).
(Toxicology of waste waters. Lack of oxygen and inorganic poisons.
Gaseous poisons. Ammonia and ammonium (NH0, NH,.) Pages 720-724 in:
J H ' —
Handbuch der Frischwasser und Abwasser Biologic. Vol. II. R. Oldenbourg
(Publishers), Miinchen. (In English translation.)
Liebmann, H. and H.H. Reichenbach-Klinke. 1969. Effect of ammonia on the
blood of carp. FAO Fish Cult. Bull. 1(3): 17.
Liechti, P.M. and D.G. Huggins. 1980. Effects of a 24 hour ammonia injection
on stream drift and benthic standing crop. Trans. Kansas Acad. Sci.
83(3): 140.
Linden, E., B.-E. Bengtsson, 0. Svanberg, and G. Sundstrom. 1979. The acute
toxicity of 78 chemicals and pesticide formulations against two brackish
-------
water organisms, the bleak (Alburnus alburmis) and the harpacticoid
Nitocra spinipes. Chemosphere 11/12: 843-851.
Litav, M. and M. Agarai. 1976. Relationship between water pollution and the
flora of two coastal rivers of Israel. Aquat. Bot. 2(l):23-4l.
Litav, M. and Y. Lehrer. 1978. The effects of ammonium in water on
Potamogeton lucens. Aquat. Bot. 5(2): 127-138.
Lloyd, R. and D.W.M. Herbert. 1960. The influence of carbon dioxide on the
toxicity of un~ionized ammonia to rainbow trout (Salmo gairdnerii
Richardson). Ann. Appl. Biol. 48(2): 399-404.
Lloyd, R. 196la. Effect of dissolved oxygen concentrations on the toxicity
of several poisons to rainbow trout (Sjilmo gairdnerii Richardson). J.
Exp. Biol. 38(2): 447-455.
Lloyd, R. 196lb. The toxicity of ammonia to rainbow trout (Salmo gairdnerii
Richardson.) Water Waste Treat. 8: 278-279.
Lloyd, R. and D.W.M. Herbert. 1962. The effect of the environment on the
toxicity of poisons to fish. Inst. Public Health Eng. J. 61: 132-143.
Lloyd, R. and D.H.M. Jordan. 1963. Predicted and observed toxicities of
several sewage effluents to rainbow trout. J. Proc. Inst. Sewage Purif.
1963(2): 167-173-
Lloyd, R. and D.H.M. Jordan. 1964. Predicted and observed toxicities of
several sewage effluents to rainbow trout: a further study. J. Proc.
Inst. Sewage Purif. 1964(2): 183-186.
Lloyd, R. and L.D. Orr. 1969. The diuretic response by rainbow trout to
sub-lethal concentrations of ammonia. Water Res. 3(5): 335-344.
Lloyd, R. and D.J. Swift. 1976. Some physiological responses by freshwater
fish to low dissolved oxygen, high carbon dioxide, ammonia and phenol
witti particular reference to water balance. Pages 4/-6y _i_n: Society for
156
-------
experimental biology seminar series. Vol. 2. Effects of pollutants on
aquatic organisms, A.P.M Lockwood, (Eds.). Cambridge University Press,
Cambridge, MA.
Lubinski, K.S., R.E. Sparks, and L.A. Jahn. 1974. The development of toxicity
indices for assessing the quality of the Illinois River. Res. Rep. No.
96, Water Resources Center, University of Illinois, Urbana, IL: 46 p.
Lubinski, K.S., J. Cairns, Jr., and K.L. Dickson. 1978. Quantifying the
effects of ammonia on the swimming behavior of bluegills. Pages 508-514
in: Trace substances in environmental health - XII, A symposium, D.D.
Hemphil], (Ed.), University of Missouri, Columbia, MO.
Lubinski, K.S. 1979. Monitoring bluegill swimming behavior and the effects
of sublethal ammonium chloride gradients. Ph.D. Thesis, Virginia Poly-
technic Institute and State University, Blacksburg, VA:99 p.
Lubinski, K.S., K.L. Dickson, and J. Cairns, Jr. 1980. Effects of abrupt
sublethal gradients of ammonium chloride on the activity level, turning,
and preference-avoidance behavior of bluegills. Pages 328-340 in Aquatic
Toxicology. ASTM//STP 707, J.G. Eaton, P.R. Parrish, A.C. Hendricks,
(Eds.). American Society for Testing and Materials, Phiiau< Iphia , PA.
Lum, S.C. and C.S. Hammen. 1964. Ammonia excretioi1 of Lingula. Comp. Bio-
chem. Physiol. 12(2): 185-190.
Maetz, J. and F. Garcia-Romeu. 1964. The mechanism of sodium and chloride
uptake by the gills of a fresh-water fish, Carassius auratus. II. Evi-
dence for NH*/Na+ and HCO~/C1~ exchanges. J. Gen. Physiol. 47(6): 1209-
1227.
,laetz, J. 1973. Na /NH , Na /H exchanges and NH., movement across the gill
•3 J
of Carassius auratus. J. Exp. Biol. 58(1): 255-275.
157
-------
Magalhaes Bastos, J.A. 1954. Importancia da amonia cooto subs I anna ictiolox-
ica. (Importance of ammonia as an ichthyotoxic substance.) Pages 115-
132 in: Publ. Ser. 1-C, No. 159, Serv. Picicultura, Dept. nacl. obras
contra secas, Ministerio viacao e obras piiblicas, Brazil. (In English
translation.)
Makarewicz, W. and M. Zydowo. 1962. Comparative studies on some ammonia-pro-
ducing enzymes in the excretory organs of vertebrates. Comp. Biochem.
Physiol. 6: 269-275.
Malacca, I. 1966. Contributii la cunoasterea actinuii toxice a cianurilor,
amoniacului, mercurului si arsenului asupra unor specii de pesti si a
Dafniei. (Contributions to knowledge of the cyanide, ammonia, mercury
and arsenic toxic action on some species of fishes and on the Daphnia.)
Stud. Protect Epurarea Apelor Inst. Stud. Cercet Hidrotehnice ?(2):
751-792. (English summary). [Biol. Abstr. 50: 92715 (1969)]
Malacea, I. 1968. Untersuchungen fiber die Gewohnung der Fische an hone
Konzentrationen toxischer Substanzen. (Studies on the acclimation of
fish to high concentrations of toxic substances). Arch. Hydrobiol.
65(1): 74-95. (In English translation.)
Mamontova, L.N. 1962. Udobrenie prudov sul'fatom ammoniaya. (Fertilization
of ponds with ammonium sulfate.) Dokl. Mosk. Skh. Akad. Im. K. A.
Timiryazeva 78: 359-362.
Maagum, C.P., S.U. Silverthorn, J.L. Harris, D.W. Towle, and A.R. Krall.
1976. The relationship between blood pH, ammonia excretion and adapta-
tion to low salinity in the blue crab, Callinectes sapidus. J. Exp.
Zool. 195(1): 129-136.
158
-------
Mangum, C.P., J.A. Dykens, R.P. Henry, and G. Polites. 1978. The excretion
of NH, and its ouabain sensitivity in aquatic annelids and molluscs. J.
Exp. Zool. 203:151-157.
Marchetti, R. 1960. Nouvelles etudes sur la toxicologie des poissons, au
point de vue du controle des eaux usees. (New studies on the toxicology
of fish, with respect to control of waste waters.) Ann. Stn. Cent.
Hydrobiol. Appl. 8: 107-124. (In English translation).
Martens, D.W. and J.A. Servizi. 1976. Acute toxicity at three primary sewage
treatment plants. International Pacific Salmon Fisheries Commission,
Progress Report 33: 20 p.
Mason, P.R. I979a. Ammonia excretion by Bulinid snails. S. Afr. J. Sci.
75(9): 420-421.
Mason, P.R. 1979b. Ammonia excretion by planorbid snails - a possible mech-
anism for host selection by schistosome miracidia. J. Parasitol. 65(5):
819-820.
Matter, R.M. 1966. Studies on the nitrogen metabolism of Amia calva with
special reference to ammonia and urea production and elimination. Ph. D.
Thesis, University of Missouri, Columbia, MO: 112 p.
Matthews, J.E. and L.H. Myers. 1976. Acute toxic e/fects of petroleum refin-
ery wastewaters on redear sunfish. EPA Environ. Protn. Technol. Ser.
EPA-600/2-76-241. Robert S. Kerr Environmental Research Laboratory.
U.S. Environmental Protection Agency, Ada, OK: 62 p.
Matusiak, K. 1976. Studies on the purification of wastewater from the nitro-
gen fertilizer industry by intensive algal cultures. Acta Microbiol.
Pol. 25(3):233-242.
159
-------
McBean, R.L., M.J. Neppel, and L. Goldstein. 1966. Glutamate dehydrogenase
and ammonia production in the eel (Anguilla rostrata). Comp. Biochem.
Physiol. 18(4): 909-920.
McCay, C.M. and H.M. Vars. 1931. Studies upon fish blood and its relation to
water pollution. Pages 230-233 in: A biological survey of the St.
Lawrence Watershed. Suppl. to Twentieth Annual Report, 1930 (Biol.
Survey (1930), No. V), New York Conservation Dept., Albany, NY.
McCormick, J.H., S.J, Broderius, and J.T. Fiandt. (In preparation). Toxicity
of ammonia to early life stages of the green sunfish, Lj?£pou:s cyane] lus.
Environmental Research Laboratory, U.S. Environmental Protection Agency,
Duluth, MN.
McKee, J.E. and H.W. Wolf. (Eds.). 1963. Pages 132-137 in: Water quality
criteria. 2nd ed., Publ. No. 3-A, State Water Quality Control Board,
Sacramento, CA.
McKhann, G.M. and D.B. Tower. 1961. Ammonia toxicity and cerebral oxidative
metabolism. Am. J. Physioi. 200(3): 420-424.
Merkens, J.C. and K.M. Downing. 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-
Mihnea, P.-E. 1978. Influence de certaines eaux residuelles a tenuer en
ammoniaque, uree et methanol, sur les algues unicellulaires marines.
(Influence of certain waste waters containing ammonia, urea and methanol
on unicellular marine algae). Pages 465-469 in: Workshop on Pollution of
the Mediterranean. Antalya, Nov. 24-27, 1978. International Commission
for the Scientific Exploration of the Mediterranean Sea, Monaco: United
Nations Environment Programme, Nairobi (Kenya). Pybl^_by I.C.S.E.M.;
Monaco (Monaco). [Aqua. Sc i . and Fish. Abstr. 10(tb): 7692-1Q10 (1980JJ.
160
-------
Miller, G.R., G.F. Shimp, H.O. Andrews, D.W. Nimmo, and E.S. Iley. 1981. Ef-
fect of domestic wastewater on trout in Dillon Reservoir, Colorado. Pa-
per presented at the ASTM Symposium on Aquatic Toxicology, 13-14 October
1981, St. Louis MO.
Miller, T.G. and UNLV-EPA Cooperative Research Laboratory (T.W. La Point, Dir-
ector). 1982. Iowa ammonia toxicity study, Iowa River. Progress Rep.
prepared for Criteria and Standards Division, U.S. Environmental Protec-
tion Agency, Washington, D.C. and Iowa Dept. of Environmental Quality,
Des Moines, IA:11 p. (Mimeo.)
Ministry of Technology, U.K. 1960. Toxicity of un-ionized ammonia. Toxicity
of gas liquors. Pages 74-80 in: Water Pollution Research 1959, H.M.
Stationery Office, London, U.K.
Ministry of Technology, U.K. 1961. Effects of pollution on fish. Toxicity
of gas liquors. Pages 76-81 in: Water Pollution Research 1960, H.M.
Stationery Office, London, U.K.
Ministry of Technology, U.K. 1962. Effects of pollution on fish. Toxicity
of mixtures of zinc sulphate and ammonium chloride. Pages 90-93 in:
Water Pollution Research 1961, H.M. Stationery Office, London, U.K.
Ministry of Technology, U.K. 1963. Effects of pollution on fish: Toxicity
of mixtures of zinc sulphate and ammonium chloride; Toxicity of sewage
effluents; The toxicity of poisons under estuarine conditions. Pages
76-83 in: Water Pollution Research 1962, H.M. Stationery Office, London,
U.K.
Ministry of Technology, U.K. 1964. Effects of pollution on fish. Toxicity
of mixtures of poisons. Copper and ammonia. Pages 80-81 in: Water
Pollution Research 1963, H.M. Stationery Office, London, U.K.
161
-------
Ministry of Technology, U.K. 1966. Effects of pollution on fish; Laboratory
studies with mixtures of poisons. Pages 149-150 in: Water Pollution
Research 1965, H.M. Stationery Office, London, U.K.
Ministry of Technology, U.K. 1968. Effects of pollution on fish. Pages
56-65 in: Water Pollution Research 1967, H.M. Stationery Office, London,
U.K.
Moore, E.W., G.W. Strohmeyer, and T.C. Chalmers. 1963. Distribution of ammo-
nia across the blood-cerebrospinal fluid barriers in patients with hepatic
failure. Amer. J. Med. 35: 350-362.
Morgan, W.S.G. 1976. Fishing for toxicity: Biological automonitor for con-
tinuous water quality control. Effluent Water Treat. J. 16(9): 471-472,
474-475.
Morgan, W.S.G. 1977. Biomonitoring with fish: An aid to industrial effluent
and surface water quality control. Prog. Water Technol. 9(3): 703-711.
Morgan, W.S.G, 1978. The use of fish as a biological sensor for toxic com-
pounds in potable water. Prog. Water Technol. 10(1/2): 395-398.
Morgan, W.S.G. 1979. Fish locomotor behavior patterns as a monitoring tool.
J. Water Pollut. Control Fed. 51(3): 580-589.
Morii, H., K. Nishikata, and 0. Tamura. 1978. Nitrogen excretion of mud-
skipper fish Periophthalnms cantonensis and Bolepphthalinus pectinirostris
in water and on land, Comp. Biochem. Physiol. 60A(2): 189-193.
Morii, H. 1979. Changes with time of ammonia and urea concentrations in the
blood and tissue of mudskipppr fish, Peripphth aImus cantonensis and
Boleophthalnius pectinirostris kept in water and on land. Comp. Biochem.
Physiol. 64A(2): 235-243.
Morii, H., K. Nishikata, and 0. Tamura. 1979. Ammonia and urea excretion
from mudskipper fishes Periophthalmus cantonensis and Boleophthalnius
162
-------
transferred from land to water. Corop. Biochem. Physiol.
63A(1): 23-28.
Hosier, A.R. 1978. luhibition of photosynthesis and nitrogen fixation in
algae by volatile nitrogen bases. J. Environ. Qual. 7(2):237-240.
Mount, D.I. 1982. Memorandum to R.C. Russo, 6 August 1982.
Mukherjee, D.K. and S. Bhattacharya. 1978. Response of a fish Channa
punctatus to the chronic sublethal exposure of ammonia with special
reference to brain cholinesterase. Indian Biol. 10(2): 57-63.
Mukherjee, S. and S. Bhattacharya. 1974. Effect of some industrial pollut-
ants on fish brain cholinesterase activity. Environ. Physiol. Biochem.
4(5): 226-231.
Mukherjee, S. and S. Bhattacharya. 1975a. Changes in the kidney peroxidase
activity in fish exposed to some industrial pollutants. Environ. Physiol.
Biochem. 5(5): 300-307.
Mukherjee, S. and S. Bhattacharya. 1975b. Histopathological lesions and
variations in a-amylase activity in the hepatopancreas of a teleost,
9£lli5££!}^LlH£ punctatus, exposed to some industrial pollutants. Proc.
62nd. Tnd. Sci. Congr., Part III (Abstracts): 176.
Mukherjee, S. and S. Bhattacharya. 1977. Variations in the hepatopancreatic
or-amylase activity in fishes exposed to some industrial pollutants.
Water Res. 11(1): 71-74.
Natarajan, K.V. 1970. Toxicity of ammonia to marine diatoms. J. Water
Pollut. Control Fed. 42(5, Part 2): R184-R190.
National Academy of Sciences, National Academy of Engineering. 1973. Ammon-
ia; Nitrate-Nitrite. Water quality criteria 1972. EPA Ecol. Res. Ser.
EPA-R3-73-033, U.S. Environmental Protection Agency, Washington, D.C.:
55, 73.
163
-------
National Research Council. 1979. Ammonia. Subcommittee on Ammonia, Commit-
tee on Medical and Biologic Effects of Environmental Pollutants, National
Research Council. University Park Press, Baltimore, MD: 384 p.
Nedwell, D.B. 1973. Abattoir pollution in the Wainibuku Creek. Fiji Agric.
J. 35(2): 99-100. [Chem. Abstr. 83: 120384p (1975)]
Nehring, D. 1962-1963. Die Giftwirkung ureasehaltiger Harnstofflosungen auf
verschiedene Fischarten. (The toxic effect of urea solutions containing
urease on various fish species.) Z. Fischerei. N.F. 11(7/8): 539-547.
(In English translation.)
Nehring, D. 1964. Die Schadwirkung von Kupfersulfat, Zinksulfat, Kaliiimzyanid,
Ammoniak und Phenol gegeniiber Karpfen (Cyprinus carpio) vom Wasser her
und nach peroraler Applikation. (The toxicity of copper sulfate, zinc
sulfate, potassium cyanide, ammonia and phenol against carp (Cyprinus carpio)
from water and by oral application.) Z. Fischerei, N.F. 12(8-10): 717-724.
Nelson, S.G., A.W. Knight, and H.W. Li. 1977. The metabolic cost of food
utilization and ammonia production by juvenile Macrobrachiiua rosenbergii
(Crustacea: Palamonidae). Comp. Biochem. Physiol. 57A(1): 67-72.
Neufeld, R.D., A.J. Hill, and D.O. Adekoya. 1980. Phenol and free ammonia
inhibition to Nitrosomonas activity. Water Res. 14(12): 1695-1703.
Nicotra, A. and M. Arizzi. 1980. Studio ultrastrutturale degli effetti di
NH.OH sulla fecondazione di uova di riccio di mare. (An ultrastructural
study on the effects of NH.OH on the fertilization of sea urchin eggs.)
Riv. Biol. 73(2): 221-234. (In Italian with English translation).
Nish.oka, D.J. 1976. The initiation of cell cycle events in ammonia-treated
eggs and raerogons of the sea urchin. Ph.D. Thesis, University of Cali-
"ornia. Berkeley, CA: 107 p.
164
-------
Okaichi, T. and S. Nishio. 1976. Identification of ammonia as the toxic
principle of red tide of Noctiluca miliaris. Bull. Plankton Soc. Jpn.
23(2): 25-30. (in Japanese.)
Olson, K.R. and P.O. Fromm. 1971. Excretion of urea by two teleosts exposed
to different concentrations of ambient ammonia. Comp. Biochem. Physiol.
40A(4): 999-1007.
Orzechowski, B. 1974. The correlation between the respiration metabolism of
Gammarus fossarum (Koch) and the presence of some ammonium salts in
water. Acta Univ. Nicolai Copernici Pr. Limnol. 34(8): 3-16.
Oshima, S. 1931. On the toxic action of dissolved salts and electrolytes
upon young eels (Anguilla japonica). J. Imp. Fish. Exp. Station (Tokyo)
2: 139-193. (In Japanese).
Oya, T., Y. Usui, M. Kimata, and K. Isikawa. 1939. Effects of chemical
substances dissolved in water on pisces and mollusca. Nippon Suisan
Gakkaishi 7(5): 281-187. (In Japanese).
Parkhurst, B.R., A.S. Bradshaw, J.L. Forte, and G.P. Wright. 1979. An eval-
uation of the acute toxicity to aquatic biota of a coal conversion ef-
fluent and its major components. Bull. Environ. Contam. Toxicol. 23:349-
356.
Parkhurst, B.R., J.S. Meyer, G.M. DeGraeve, and H.L. Bergman. 1981. A re-
evaluation of the toxicity of coal conversion process waters. Bull. En-
viron. Contam. Toxicol. 26:9-15.
Patrick, R., J. Cairns, Jr., arid A. Scheier. 1968. The relative sensitivity
of diatoms, snails, and fish to twenty common constitutents of industrial
wastes. Prog. Fish Cult. 30(3): 137-140.
165
-------
Paul, M. , J.D. Johnson, and D. Epel. 1976. Fertilization acid of sr.-i uivhiu
eggs is not a consequence of cortical granule exocytosis. J. Exp. Zool.
I97(l): 127-133.
Paul, M. and R.N. Johnston. 1978. Absence of a Ca response following ammonia
activation of sea urchin eggs. Dev. Biol. 67(2): 330-335.
Payan, P. and J. Maetz. 1973- Branchial sodium transport mechanisms in
Scyliorhinus canicula: evidence for Na /NH, and Na /H exchanges and
for a role of carbonic anhydrase. J. Exp. Biol. 58: 487-502.
Payan, P. and A.J. Matty. 1975. The characteristics of ammonia excretion by
a perfused isolated head of trout (Salmo gairdneri): effect of tempera-
ture and C02~free Ringer. J. Comp. Physiol. 96(2): 167-184.
Payan, P. and P. Pic. 1977. Origine de 1'ammoniuin excrete par les branchies
chez la truite (Salmo gairdneri). (Origin of the ammonia excreted by the
gills in the trout (Salmo gairdneri).) Acad. Sci., Paris, C. R., Ser. D
284: 2519-2522. (In English translation).
Payan, P. 1978. A study of the Na /NH, exchange across the gill of the
perfused head of the trout (Salmo gairdneri). J. Comp. Physiol. 124:
181-188.
Pen3z, M. 1965. Vliv amoniaku na jikry a pludek pstruha obecneho, Salmo
Lrutta m. fjnrio. (The influence of ammonia on the eggs and young of the
common trout, Salmo trutta var. farip.) Zool. Listy 14(1): 47-54. (In
English translation.)
Pequignot, J. and A. Moga. 1975. Effet de differents toxiques (Pb, Cu,
formol, NH,) chez la carpe: alterations histologiques des organes
excreteurs et hematopoietiques. (Action of several toxic substances (Pb,
Cu, formol, NH,) on carp: histological impairments observed on excretory
Ib6
-------
and hematopoietic organs.) Eur. J. Toxicol. 8(6): 361-369. (In English
translation).
Pequin, L. and A. Serfaty. 1963. L'excretion ammoniacale chez un teleosteen
dulcicole: Cypr oius carpio L. (Anunonia excretion by a freshwater teleost:
Cyprinus carpio L.) Comp. Biochem. Physiol. 10(4): 315-324. (In English
translation.)
Pequin, L. and A. Serfaty. 1966. Acide glutamique et excretion azotee chez
la carpe commune, Cyprinus cajrpjto L. Comp. Biochem. Physiol. 18(1):
141-149.
Pequin, L. and F. Serfaty. 1968. La regulation hepatique et intestinale de
I'ammoniemie chez la carpe. (Hepatic and intestinal regulation of blood
ammonia in the carp.) Arch. Sci. Physiol. 22(3): 449-459.
Pequin, L., F. Vellas, and G. Bouche. 1969a. La glutamine synthetase chez la
carp (Cyprinus carpio). Observations sur les repartitions tissulaire et
intracellulaire. (Glutamine synthetase in the carp (Cyprinus cargio).
Tissue and intracellular distribution). Arch. Sci. Physiol. 23: 469-480.
Pequin, L. , F. Vellas, and A. Serfaty. 1969b. Les precurseui ilLJLlY0. ^e ^a
glutamine dans differents tissus de la Carpe commune. .J Physiol. Paris.
61: 367-368.
Perna, A. 1971. I fertilizzanti agricoli a base di urea quali cause di
inquinamento delle acque superficial! e di gravi episodi di mortalita nei
pesci. (Agricultural fertilizers with a urea base as the cause of water
pollution and mortality among fish.) Soc. Ital. Sci. Veterinarie 25:
408-410.
Phillips, A.M., Jr., D.R. Broadway, M. Bryant, E.G. Rodgers, and J. Maxwell.
1949. Metabolic product accumulation and its effect. Pages 19-20 in:
16/
-------
Cortland Hatchery Report 18, Fisheries Research Bulletin 13, New York
State Conservation Dept., Cortland, NY.
Phillips, A.M. 1950. The effect of metabolic products on brook trout. Pages
14-16 in: Cortland Hatchery Report 19, Fisheries Research Bulletin 14,
New York State Conservation Dept., Cortland, NY.
Pinter, I.J. and L. Provasoli. 1963. Nutritional characteristics of some
chrysomonads. Pages 114-121 in: Symposium on marine microbiology. C.M.
Oppenheimer (Ed.), Thomas Publishers, Springfield, MA.
Pitts, T. 1980. Presentation of evidence concerning water quality classifi-
cations and standards for the Cache la Poudre River, Big Thompson River
and South Platte River. Colorado Water Quality Control Cojcmission
Hearing - South Platte River, July 14-30, Fort. Collins et al. Exhibit
Number 1: 159 pp.
Pora, E.A. and 0. Precup. 1971. Nitrogen excretion of Black Sea Gobius
melanostomus during several (4-7) days' adaptation to variations in
salinity. Stud, Cercet. Biol., Ser. Zool. 23(1): 35-46. (Chera. Abstr.
75: 31964v (1971)]
Powers, E.B. 1920. Influence of temperature and concentration on the toxic-
ity of salts to fishes. Ecology 1: 95-112.
Provasoli, L. and J.J.A. McLaughlin. 1963. Limited heterotrophy of some
photosynthetic dinoflagellates. Pages 105-113 In: Symposium on Marine
Microbiology. C.H. Oppenheimer (Ed.), Thomas Publishers, Springfield,
MA.
Przytocka-Jusiak, M. 1976. Growth and survival of ChJ^orejQa vulgaris in high
concentrations of nitrogen. Acta Microbiol. Pol. 25(3): 287-289.
168
-------
Przytocka-Jusiak, M., A. Mlynarczyk, M. Kulesza, and R. Mycielski. 1977.
Properties of Chlorella vulgaris strain adapted to high concentration of
ammonium nitrogen. Acta Microbiol. Pol. 26(2): 185-197.
Raguse-Degener, G., li. Pietschroann, F. Walvig, and H. Stolte. 1980. Excretory
systems in the hagfish Myxine glutinosa. Contrib. Nephrol. 19: 1-8.
Ramachandran, V. 1960. Use of ammonia for the eradication of aquatic vegeta-
tion. J. Sci. Ind. Res. 19C: 284-285. [Chem. Abstr. 55: 9765f (1961)]
Ramachandran, V., T. Ramaprabhu, and P.V.G.K. Reddy. 1975. Observations on
the use of ammonia for the control of Pistia stratiotes Linn. J. Inl.
Fish. Soc. India 7: 124-130.
Ramachandran, V. and T. Ramaprabhu. 1976. Use of ammonia as herbicide - A
Review. Pages 293-298 In: C.K. Varshney and J. Rzoska (Eds.), Aquatic
Weeds in South East Asia, B.V. Publishers, The Hague, The Netherlands.
Randall, D.J. 1970. Gas exchange in fish. Pages 253-292 In: Fish physiology.
W.S. Hoar and D.J. Randall (Eds.), Vol. IV, Academic Press, New York, NY.
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 p.
Rao, T.S., M.S. Rao, and S.B.S.K. Prasad. 1975. Median tolerance limits of
some chemicals to the fresh water fish "Cyprt.jus carpio". Indian J.
Environ. Health 17(2): 140-146.
Rao, V.N.R. and G. Ragothaman. 1978. Studies on Amphora coffeaeformis. II.
Inorganic and organic nitrogen and phosphorus sources for growth. Acta
Botanica Indica 6 (Suppl.):146-154.
Ray, A.K. and A.K. Medda. 1976. Effect of thyroid hormones and analogues on
ammonia and urea excretion in Lata fish (Ophicephalus punctatus). Gen
Comp. Endocrinol. 29(2): 190-197.
169
-------
Read, L.J. 1971. The presence of high ornithiiie-urea cycle enzyme activity
in the teleost Opsanus tau. Comp. Biochem. Physiol. 39B(2): 409-413.
Reddy, N.A. and N.R. Menon. 1979. Effects of ammonia and ammonium on toler-
ance and byssogenesis in Perna viridis. Mar. Ecol. Prog. Ser. 1(4):
315-321.
Redner, B.D. and R.R. Stickney. 1979. Acclimation to ammonia by Tilapia
aurea. Trans. Am. Fish. Soc. 108(4): 383-388.
Redner, B.D., J.R. Tomasso, and B.A. Simco. 1980. Short term alleviation of
ammonia toxicity by environmental sodium chloride in channel catfish
(Ictalurus punctatus). J. Tenn. Acad. Sci. 55(2): 54.
Reichenbach-Klinke, H.-H. 1967. Untersuchungen iiber die Einwirkung des
Ammoniakgehalts auf den Fischorganismus. (Investigations on the influence
of the ammonia content on the fish organism.) Arch. Fischereiwiss.
17(2): 122-132. (In English translation.)
Reinbold, K.A. and S.M. Pescitelli. 1982a. Effects of exposure to ammonia on
sensitive life stages of aquatic organisms. Project Report, Contract No.
68-01-5832, Illinois Natural History Survey, Champaign, IL. (Draft)
Reinbold, K.A. and S.M. Pescitelli. 1982b. Effects of cold temperature on
toxicity of ammonia to rainbow trout, bluegills and fathead minnows.
Project Report, Contract No. 68-01-5832, Illinois Natural History Survey,
Champaign, IL. (Draft)
Reinbold, K.A. and S.M. Pescitelli. 1982c, Acute toxicity of ammonia to the
white sucker. Final Report, EPA Contract No. 2W-3946 NAEX. Illinois
Natural History Survey, Champaign, IL:11 pp.
Reinbold, K.A. and S.M. Pescitelli. 1982d. Acute toxicity of ammonia to
channel catfish. Final Report, EPA Contract No. J 2482 NAEX. Illinois
Natural History Survey, Champaign, IL:11 pp.
170
-------
•Revina, N.I. 1964. Nekotorye elementy azotistogo obmena u segoletkov stavridy.
(Some aspects of the nitrogen metabolism in fingerling horse-mackerel).
Tr. Azovo-Chernomorsk. Nauchno-issled. Inst. Morsk. Rybn. Khoz. Okeanogr.
22: 133-136.
Rice, S.D. 1971. A study of nitrogen waste product metabolism in the eggs
and fry of rainbow trout, Salmo gairdneri. Ph.D. Thesis, Kent State
University, Kent, OH: 77p.
Rice, S.D. and R.M. Stokes. 1974. Metabolism of nitrogen wastes in the eggs
and alevins of rainbow trout, Salmo gairdneri Richardson. Pages 325-337
in: The Early Life History of Fish, J.H.S. Blaxter, (Ed.), Springer-Verlag
Berlin.
Rice, S.D. and R.M. Stokes. 1975. Acute toxicity of ammonia to several
developmental stages of rainbow trout, Salmo gairdneri. Fish. Bull.
73(1): 207-211.
Rice, S.D, and J.E. Bailey. 1980. Survival, size, and emergence of pink
salmon, Qncorhynchus gorbuscha, alevins after short- and long-term ex-
posures Lo ammoaia. Fish. Bull. 78(3): 641-648,
Richards, F.A. 1981. The determination of ammonia in aqueous solution.
Fisheries Bioassay Laboratory, Montana State University, Bozeman, MT.
(Mimeo.)
Roberts, F.W. 1975. Ammonia as a toxic chemical. Effluent Water Treat. J.
15(9): 489.
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.
171
-------
Robinson-Wilson, E.F. and W.K. Seiro. 1975. The lethal and sublethal effects
of a zirconium process effluent on juvenile salmonids. Water Resour.
Bull. 11(5): 975-986.
Rosage, T.F., R.M. Schutsky, and K.M. Rapp. 1979. Toxicity of un-ionized
ammonia to the spotfin shiner (Notropis spilopterus). Proc. Pa. Acad.
Sci. 53: 39-42.
Roseboom, D.P. and D.L. Richey. 1977. Acute toxicity of residual chlorine
and ammonia to some native Illinois fishes. Illinois State Water Survey,
Report of Investigation 85, Urbana, IL: 42 p.
Rosenberg, D.H., D.C. Burrell, K.V. Natarajan, and D.W. Hood. 1967. Oceanog-
raphy of Cook Inlet with special reference to the effluent from the
Collier Carbon and Chemical Plant. Pages 60-75 in: IMS - 67-3, Institute
of Marine Science, University of Alaska, Colleges AK.
Rubin, A.J. and M.A. Elmaraghy. 1976. Studies on the toxicity of ammonia,
nitrate and their mixtures to the common guppy. Project No, A-033-OHIO,
Water Resources Center, Ohio State University, Columbus, OH: 47 p.
Rubin, A.J. and G.A. Elmaraghy. 1977. Studies on the toxicity of ammonia,
nitrate and their mixtures to guppy fry. Water Res. 11(10): 927-935.
Ruffier, P.J., W.C. Boyle, and J. Kleinschmidt. 1981. Short-term acute
bioassays to evaluate ammonia toxicity and effluent standards. J. Water
Pollut. Control Fed. 53(3): 367-377.
Rushton, W. 1921. Biological notes. Salmon Trout Mag. 25: 101-117.
Russo, R.C., A. Pilli, and E.L. Meyn. (In preparation). Acute and chronic
toxicity of ammonia to Dajjhnaa magna. Fisheries Bioassay Laboratory,
Montana State Univ., Bozeman, MT.
Rychly, J. and B.A. Marina. 1977. The ammonia excretion of trout during a
24-hour period. Aquaculture 11: 173-178.
172
-------
Sadler, L. 1981. The toxicity of ammonia to the European eel (Anguillu
anguilla L.). Aquaculture 26(1; 2): 173-181.
Saeki, A. 1965- Studies on fish culture in filtered closed-circulating
aquaria. II. Oi the carp culture experiments in the systems. Nippon
Suisan Cakkaishi 31(11): 916-923. (In English translation.)
Sana, K.C., D.P. Sen, and P. Mazumdar. 1956. Studies on the mortality of
spawn and fry of Indian major carps during transport. III. Effect of
inimical substances from decomposition of metabolic products in the
medium on spawn life and their control. Indian J. Fish. 3(1): 135-140.
Sahai, R. and S.P. Singh. 1977. Effect of domestic waste on the growth
performance of CeratophyHum demersum Linn. Indian J. Eco]. 4(1): 118-
120.
Samylin, A.F. 1969. Effect of ammonium carbonate on the early stages of
development of salmon. 3Jch. Zap. Leningr. Gos. Pedagog. Inst. Im. A. I.
Gertsena 422: 47-62. (In English translation.)
Savitz, J. 1969. Effects of temperature and body weight on endogenous nitro-
gen excretion in the blnegill sunfish (Lfjpomis macrochi rus) . J. Fish.
Res. Board Can. 26(7): 1813-3821.
Savitz, J. 1971. Nitrogen excretion and protein consumption of the bluegill
sunfish (Lejaomis macrochirus). J. Fish. Res. Board Can. 28(3): 449-451.
Savitz, J. 1973- Influence of low level handling stress on nitrogen excretion
of bluegill sunfish (Leporais macrocfairus Rafinesque). Trans. Am. Fish.
Soc. 102(3): 629-630.
Savitz, J., E. Albanese, M.J. Evinger, and P. Kolasinski. 1977. Effect of
ration level on nitrogen excretion, nitrogen retention and efficiency of
nitrogen utilization for growth in Ijrgemouth bass (Micropterus salmoides).
,1. Fish RioL. 11(2): 185-192.
173
-------
Schaperclaus, W. 1952. Fischerkrankungen und Fischsterben durch
Massenentwicklung von Phytoplankton bei Anwesenheit von Aramoniumverbin-
dungen. (Disease and death of fish by mass development of phytoplankton
in the presence of ammonium compounds.) Z. Fischerei, N.F. 1(1/2): 29-44.
Scheuring, L. and F. Leopoldseder. 1934. Die Wirkung der wichtigsten
Diingersalze auf Fische. (The action of the most important fertilizer
salts on fish.) Arch. Hydrobiol. 27(2): 203-220.
Schooler, J.M., L. Goldstein, S.C. Hartman, and R.P. Forster, 1966. Pathways
of urea synthesis in the elasmobranch, S
-------
'Shaffi, S.A. 1980a. The acute industrial effluent toxicity to fresh water
fish. Toxicol. Lett. 5(3-4): 183-190.
Shaffi, S.A. 1980b. Ammonia toxicity: metabolic disorder in nine freshwater
teleosts. Toxicol. Lett. 6(6): 349-356.
Shaw, J. 1960. The absorption of sodium ions by the crayfish, Astacus pallipes
Lereboullet. III. The effect of other cations in the external solution.
J. Exp. Biol. 37(3): 548-556.
Shelford, V.E. 1917. An experimental study of the effects of gas waste upon
fishes, with especial reference to stream pollution. Bull. Illinois
State Lab. Natural History 11(6): 381-412.
Shemchuk, V.R. 1971. Anuniakat medi (AM) i ego vliyaaie na organizm ryb.
(Copper ammoniate (AM) and its effect on the bodies of fish.) Rybn.
Khoz. Resp. Mezhved. Temat. Nauchn. Sb. 12: 92-98. (In English trans-
lation . )
Shen, S.S. and R.A. Steinhardt. 1978. Direct measurement of intracellular pH
during metabolic derepression of the sea urchin egg. Nature 272(5650):
253-254.
Shevtsova, L.V., T.A. Kharchenko, and V.A. Movchan. 1979. Toxic effect of
ammonium nitrate on Dreissena polymorpha. fi^ d:;obiol. Zh. 15(3): 74-79.
Shilo, M. and M. Shilo. 1953. Conditions which determine the efficiency of
ammonium sulphate in the control of Pryrnnesium parvum in fish breeding
ponds. Appl. Microbiol. 1: 330-333.
Shilo, M. and M. Shilo. 1955. Control of the phytoflagellate Prymnesium
parvum. Verh. Int. Ver. Theor. Angew. Limnol. 12: 233-240.
Sigel, M.M., G. Ortiz-Muni?:, and R.B. Shouger. 1972. Toxic effect of ammonia
dissolved in sea water. Comp. Biochem. Physiol. 42A(1): 261-262.
17b
-------
Simonin, P., and A. Pierron. 1937. Toxicite brute des derives fluores.
(Acute toxicity of fluorine compounds.) Compt. Rend. Soc. Biol. 124:
133-134.
Singh, S.B., S.C. Banerjee, and P.C. Chakrabarti. 1967. Preliminary observa-
tions on response of young ones of Chinese carps to various physico-chemi-
cal factors of water. Proc. Nat. Acad. Sci. India Sect. B: 37(3): 320-324.
Skarheim, H.P. 1973. Tables of the fraction of amraonia in the undissociated
form for pH 6 to 9, temperature 0-30°C, IDS 0-3000 rag/1, and salinity
5-35 g/kg. SERL Report No. 73-5, Sanitary Engineering Research Labora-
tory, University of California, Berkeley, CA: 33 p.
Smart, G.R. 1975. The acute toxic mechanisms of ammonia tc rainbow trout
(Salmo gairdneri). Ph.D. Thesis. University of Bristol, U.K.
Smart, G. 1976. The effect cf ammonia exposure on gill structure of the
rainbow trout (Salmo gairdneri). J. Fish Biol. 8(6): 471-475.
Smart, G.R. 1978. Investigations of the toxic mechanisms of ammonia to
fish--gas exchange in rainbow trout (Salmo gairdneri) exposed to acutely
lethal concentrations. J. Fish Biol. 12(1): 93-104.
Smith, C.E. 1972. Effects of metabolic products on the quality of rainbow
trout. Am. Fishes U.S. Trout News 17(3): 7-8, 21,
Smith, C.E. and R.G. Piper. 1975. Lesions associated with chronic exposure
to ammonia. Pages 497-514 in: The pathology of fishes, W.E. Ribelin and
G. Migaki (Eds.), University of Wisconsin Press, Madison, WI.
Smith, C.E. 1981. Potential usefulness of the fathead minnow, Pimepbales
promelas, in carcinogenicity testing: proliferative lesions in the brain
induced by ammonia exposure. Proc. Symposium on the Use of Small Fish
Species iJi Carcinogenicity Testing, National Cancer Institute, Bethesda,
MD, 8-10 December 1981.
176
-------
Smith, H.W. 1929. The excretion of ammonia and urea by the gills of fish.
J. Biol. Chem. 81: 727-742.
Smith, M.A.K. and A. Thorpe. 1976. Nitrogen metabolism and trophic input in
relation to grot th in freshwater and saltwater Salmo gairdneri. Biol.
Bull. 150(1): 139-151-
Smith, M.A.K. and A. Thorpe. 1977. Endocrine effects on nitrogen excretion
in the euryhaline teleost, Salmo gairdnerii. Gen. Comp. Endocrinol.
32(4): 400-406.
Smith, S. 1946. Studies in the development of the rainbow trout (Salmo
ir ideas) . I. The heat production and nitrogenous excretion. J. Exp.
Biol. 23(3&4): 357-378.
Smith, W.E. and T.H. Roush. (In preparation). Toxicity of ammonia to early
life stages of the bluegill (Lepomis macrochirus) . Environmental Research
Laboratory, U.S. Environmental Protection Agency, Duluth, MN.
Solomonson, L.P. 1969. Effects of ammonia and some of its derivatives on
photosynthesis in the blue-green alga, Plectonema boryanum. Ph.D. Thesis,
Univ. of Chicago, Chicago, IL; 68 p.
Sousa, R.J. and T.L. Meade. 1977. The influence of ammonia on the oxygen
delivery system of coho salmon hemoglobin. Comp. Biochem. Physiol. 58A:
23-28.
Sousa, R.J., T.L. Meade, and G.T. Felbeck, Jr. 1977. The exposure of ammonia
to the photodi ssocia ted hemoglobin of the marine bloodworm, Glycera
Comp. Biochem. Physiol. 58A: 19-22.
Southgate, B.A. 1950. Pollution of streams: some notes on recent research.
Inst. of Civil Eng . (British), Pub. Health Eng. Div. , Oct. [Sewage Ind.
Wastes 24(8): 1045 (1952)]
177
-------
Sparks, R.E. 1975. The acute, lethal effects of ammonia on channel catfish
(Ictalurus punctatus), bluegills (Lepomis macrochirus), and fathead
minnows (Pimephales Pjromelas). Project No. 20.060. Report to the
Illinois Institute for Environmental Quality, Chicago, IL. 15 p.
Sparks, R.E. and M.J. Sandusky. 1981. Identification of factors responsible
for decreased production of fish food organisms in the Illinois and
Mississippi Rivers. Final Report, Project No. 3-291-R, River Research
Laboratory, Illinois Natural History Survey, Havana, IL: 63 pp.
Stammer, H.A. 1953. Der EinflufJ von Schwefelwasserstof£ und Amraoniak auf
tierische Leitformen des Saprobiensystems. (The effect of hydrogen
sulfide and ammonia on characteristic animal forms in the saprobiotic
system.) Vom Wasser 20: 34-71. (In English translation.)
Stanley, R.A. 1974. Toxicity of heavy metals and salts to Eurasian watermil-
foil (Myriophylum sjgicatum). Arch. Environ. Contain. Toxicol. 2(4):331-
341.
Steffens, W. 1976. Zur NH -Empfindlichkeit der Regenbogenforelle (Salmo
j
gairdneri). (On the sensitivity of rainbow trout (Salmo gj*i_r_djiej£i) to
NH3>) Z. Binnenfisch. DDR, 23(10): 315-319. (In English translation.)
Steinhardt, R.A. and D. Mazia. 1973. Development of K -conductance and mem-
brane potentials in unfertilized sea urchin eggs after exposure to NH/OH.
Nature 241(5389): 400-401.
Steinmann, P. and G. Surbeck. I922a. Fischvergiftungsversuche mit frischem
und fauligem Harn, mit Ammoniak und Ammoniumverbindungen. (Experiments
on the poisoning of fish with fresh and putrid urine, with ammonia and
ammonium compounds.) Schweiz. Fisch. Zeit. 30: 123-129.
178
-------
Steinmann, P. and G. Surbeck. 1922b. Fischvergiftungsversuche mit frischera
und fauligem Harri, mit Ammoniak und Ammoniuraverbindugen. Schlup. (Ex-
periments on the poisoning of fish with fresh and putrid urine, with
ammonia and amrm nium compounds. Conclusion.) Schweiz. Fisch. Zeit.
30(6): 145-152.
Stevenson, T.J. 1977. The effects of ammonia, pH and salinity on the white
perch, Morone americana. Ph.D. Thesis, University of Rhode Island,
Kingston, R.I.: ISA p.
Storozhuk, A.Y. 1970. Osobennosti azotistogo obmena ikry, lichinok i rannei
molodi kazpiiskogo osetra. (The distinctive characteristics of nitrogen
metabolism in eggs, larvae and fry of Caspian sturgeon.) Tr. Vses.
Nauchno-Issled. Inst. Morsk. Rybn. Khoz. Okeanogr. 4: 82-87. (In English
translation.)
Stroganov, N.S. and A.T. Pozhitkov. 1941. Experimental study to establish
the physiological boundaries for the toxic effect of copper and ammonia
ions on fish and certain invertebrates. Uch. Zap. Mosk. Cos. Univ. No.
60: 25-88. (In English translation from Russian.)
Sukumaran, N. and M.N. Kutty. 1977. Oxygen consumption and ammonia excretion
in the catfish My_st_us armatjjs, with special reference to swimming speed
and ambient oxygen. Proc. Indian Acad. Sci. 86B:(3): 195-206.
Summerfelt, R.C. and W.M. Lewis. 1967. Repulsion of green sunfish by certain
chemicals. J. Water Pollut. Control Fed. 39(12): 2030-2038.
Svobodova, Z. 1970. Hladina N-amoniaku a N-raocoviny v Krevnim seru a v mozku
kaprfl (Cyprinus carpio L.) zdravych a intoxikovanych amoniakem. (The
level of N-ammonia and N-urea in the blood serum and brain of healthy and
amonia-intoxicated carps (Cyprinus carpio L.).) Bull. Vyzk. Ustavu
Ryba'r. Vodnany 6(1): 11-19.
179
-------
Svobodova, Z. and L. Groch. 1971. Moznosti diagnostiky intoxikace ryb amouia-
kem. (Possibilities of the diagnosis of ammonia-intoxication of fish.)
Bull. Vyzk. Ustavu Rybar. Vodnany 7(1): 9-18.
Swift, D.J. 1981. Changes in selected blood component concentrations of
rainbow trout, Saltno gairdneri Richardson, exposed to hypoxia or sublethal
concentrations of phenol or ammonia. J. Fish Biol. 19:45-61.
Szumski, D.S., D.A. Barton, H.D. Putman, and R.C. Polta. 1982. Evaluation of
EPA un-ionized ammonia toxicity criteria. J. Water Pollut. Control Fed.
54(3): 281-291.
Tabata, K. 1962. Suisan dobutsu ni oyobosu amonia no dokusei to pH, tansan
to no kankei. (Toxicity of ammonia to aquatic animals with reference to
the effect of pH and carbon dioxide.) Tokai-ku Suisan Kenkyusho Kenkyu
Hokoku 34: 67-74. (In English translation.)
Tandon, R.S. and S. Chandra. 1977. Cyclic changes in blood urea levels of
fresh water cat fish Clarias batrachus. Z. Tierphysiol. Tierernahr.
Futtermittelkd. 38(4): 211-214.
Taylor, J.E. 1973. Water quality and bioassay study from Crawford National
Fish Hatchery. Trans. Nebr. Acad. Sci. 2: 176-181.
Teulon, F. and C. Simeon. 1966. Essais toxicologiques de produits chimiques
sur des poissons d'eau douce. (Toxicological tests of chemical products
on freshwater fish.) Rep. No. CEA-R-2938, Centre de Pierrelatte, Com-
missariat a 1'Energie Atomique, Pierrelatte, France: 42 p.
Thomas, J.D., M. Powles, and R. Lodge. 1976. The chemical ecology of
Biomphalaria glabrata: the effects of ammonia oil the growth rate of
juvenile snails. Biol. Bull. 151(2): 386-397.
Thomas, W.H., J. Hastings, and M. Fujita. 1980. Ammonium input to the sea
via large sewage outfalls - Part 2: etfects of amn-ouiiun on growth and
180
-------
photosynthesis of Southern California phytoplankton cultures. Mar. En-
viron. Res., 3(4):291-296,
Thornburn, C.C. and A.J. Matty. 1963. The effect of thyroxine on some as-
pects of nitrogen metabolism in the goldfish (Carassius auratus) and the
trout (Salrao trutta). Comp. Biochem. Physiol. 8(1): 1-12.
Thumann, M.-E. 1950. Uber die Wirkung von Ammoniumsalzlosungen auf Regenbogen-
und Bachforellen und einige Fischnahrtiere. (The effect of ammonium salt
solutions on rainbow and brook (=brown?) trout and on some fish nutrient
animals.) Abh. Fischerei. 2: 327-348. (In English translation).
Thurston, R.V., R.C. Russo, and K. Emerson. 1979. Aqueous ammonia equilibrium
tabulation of percent un-ionized ammonia. EPA Ecol. Res. Ser. EPA-600/3-
79-091. Environmental Research Laboratory, U.S. Environmental Protection
Agency, Duluth, MN:427 p.
Thurston, R.V., R.C. Russo, and C.E. Smith. 1978. Acute toxicity of ammonia
arid nitrite to cutthroat trout fry. Trans. Am. Fish. Soc. 107(2): 361-
368.
Thurston, R.V. 1981. Memorandum to R.C. Russo, 16 November 1981.
Thurston, R.V., C. Chakoumakos, and R.C. Russo. 198la. Effect <>i fluctuating
exposures on the acute toxicity of ammonia to rainbow trout (Salmo
gairdneri) and cutthroat trout (S. clarki). Water Res. 15(7):911-917 .
Thurston, R.V., G.R. Phillips, R.C. Russo, and S.M. Hinkins. 1981b. Increased
toxicity of ammonia to rainbow trout (Salmo gairdneri) resulting from
reduced concentrations of dissolved oxygen. Can. J. Fash. Aquat. Sci.
38(8):983-988.
Thurston, R.V. and R.C. Russo, 1981. Acute toxicity of ammonia to golden
trout (Salmo agjia_b_onij.a) and mottled sculpin (Cottus bairdi) . Internal
181
-------
Report. Fisheries Bioassay Laboratory, Montana State University, Bozeman,
MT.
Thurston, R.V., R.C. Russo, and G.A. Vinogradov. 1981c. Ammonia toxicity to
fishes: effect of pH on the toxicity of the un-ionized ammonia species.
Environ. Sci . Technol. 15(7) -.837-840.
Thurston, R.V. and R.C. Russo. (In press). Acute toxicity of ammonia to
rainbow trout (Saltno gairdneri). Trans. Ara. Fish. Soc.
Thurston, R.V., R.C. Russo, R.J. Luedtkes and G.R. Phillips. (In press, a).
Acute toxicity of ammonia to fathead minnows (Pimephales promelas).
Trans. Am. Fish. Soc.
Thurston, R.V., R.C. Russo, R.J. Luedtke, C.E. Smith, E L. Meyri, C. Chakoumakos,
K.C. Wang, and C.J.D. Brown. (In press, b). Chronic toxicity of ammonia
to rainbow trout (Salmo gairdneri). Trans. Am. Fish. Soc.
Thurston, R.V., R.J. Luedtke, and R.C. Russo. (In preparation, a). Acute toxi-
city of ammonia to selected freshwater arthropods. Fisheries Bioassay
Laboratory, Montana State Univ., Bozeman, MT.
Thurston, R.V., E.L. Meyn, R.K. Zajdel, and R.C. Russo. (In preparation, b).
Chronic toxicity of ammonia to fathead minnows (Pirnephales promelas).
Fisheries Bioassay Laboratory, Montana State Univ., Bozeman, MT.
Tomasso, J.R., C.A. Goudie, B.A. Simco, and K.B, Davis, 1980. Effects of
environmental pH and calcium on ammonia toxicity in channel catfish.
Trans. Am. Fish. Soc. 109(2): 229-234.
Tomasso, J.R., K.B. Davis, and B.A. Simco. 1981. Plasma cortxcosteroid dy-
namics in channel catfish (Ictalurus punctatus) exposed to ammonia and
nitrite. Can. J. Fish. Aquat. Sci. 38(9): 1106-1112.
Truelle, M.A. 1956. 0 skodlivosti amoniaku pro ryby. (On the harmfulness of
ammonia to fish.) Cesk. Rybarstvi 10: 150.
182
-------
Tsai , C. 1975. Ammonia. Pages 63-104 in: Effects of sewage treatment plant
effluents on fish: a review of literature. Contribution No. 637, Center
for Environmental and Estuarine Studies, University of Maryland; CRC
Publ. No, 36, Chesapeake Research Consortium, Inc.: 229 p.
Tsai, C. and J.A. Fava Jr. 1975. Chlorinated sewage effluents and avoidance
reaction of stream fish. Tech. Rep. No. 35, Water Resources Research
Center, University of Maryland, College Park, MD: 59 p.
Turnbull, H., J.G. DeMann, and R.F. Weston. 1954. Toxicity of various re-
finery materials to fresh water fish. Ind. Eng. Chem. 46(2): 324-333.
Turoboyski, L. 1960. Proba okreslenia wplywu wysokich dawek niekotorych
zwiazkow chemicznych na narybek karpia. (Attempt to determine the in-
fluence of high doses of some chemical compounds upon carp fry.) Rocz.
Nauk Roln. Ser. B. 75B: 401-445.
U.S. Environmental Protection Agency. 1977. Ammonia. Pages 10-13 in: Qual-
ity criteria for water. Office of Water and Hazardous Materials, U.S.
Environmental Protection Agency, Washington, D.C.
U.S. Environmental Protection Agency. 1980. Toxic pollutant l'?t; proposal
to add ammonia. Fed. Regis. 45(2): 803-806.
n*3.
U.S. Environmental Protection Agency. lQQ2u. (XuH ines for deriving numerical
national water quality criteria for the protection of aquatic life and
its uses. Office of Research and Development, U.S. Environmental Protec-
tion Agency, Washington, D.C. (24 September 1982, Draft).
U.S. Environmental Protection Agency. 1982b. Guidelines for deriving numerical
aquatic site-specific water quality criteria by modifying national cri-
teria. Office of Research and Development, U.S. Environmental Protection
Agency, Washington, D.C. (December 1982, Draft).
183
-------
U.S. Federal Water Pollution Control Administration. 1968. Water quality
criteria. Report of the National Technical Advisory Committee, U.S.
Department of the Interior, Washington, D.C. 234p.
Vailati, G. 1979. Effetli teratogeni di acque variaraente inquinate. (Tera-
togenic effects of differently polluted waters.) Riv. Biol. 72(3-4):
229-256. (In Italian and English).
Vallejo-Freire, A., 0. Fonseca Ribeiro, and I. Fonseca Ribeiro. 1954.
Quaternary ammonium compounds as molluscacides. Science 119: 470-472.
Vamos, R. 1962. Ammonia okozta halpusztulas rizsfb'idon, (Poisoning of fish
with ammonia in a rice field.) Halaszat 8(4): 104. (In English trans-
lation. )
Vamos, R. and R. Tasnadi. 1962a. Ammonias halpusztulas tunetei es tenyezoi.
(Symptoms and factors in the death of fish caused by ammonia.)
Allattenyesztes 11(4): 367-371.
Vamos, R. and R, Tasnadi. 1962b. Az ammonia hatas es toxikus hatarerteke a
pontynal. (Effect of ammonia and the limiting level for its toxic action
on carp.) Halaszat 8(5): 116-117. (In English translation.)
Vamos, R. 1963. Ammonia poisoning in carp. Acta Biol. Szeged 9(1-4): 291-
297.
Vamos, R. and R. Tasnadi. 1967. Ammonia poisoning in carp. 3. The oxygen
content as a factor influencing the toxir limit, of ammonia. Acta Biol.
Szeged 13(3-4): 99-105.
Vamos, R. and R. Tasnadi. 1972. Die okologischen Faktoren des durch H S und
Ammoniak bedingteri Fischsterbens. (Ecological factors of the fish kill
caused by H-S and ammonia.) Tiscia (Szeged) 7: 5-12. (In English trans-
lation. )
184
-------
Vamos, R., R. Tasnadi, and Gy. Szollosy. 1974. Az ammonia letalitasanak
tenyezol a halastavakban. (The factors of ammonia lethality in fish
ponds.) Allatten yesztes 23(5): 67-71. (In Hungarian.)
Vaughn, R.E. and B.A. Simco. 1977. Effects of ammonia on channel catfish,
i?.t£iH£ii?. pmictatus. ASB Bull. 24(2): 92.
Vellas, F. and A. Serfaty. 1974. L'ammoniaque et 1'uree chez un Teleosteen
d'eau douce: la carpe (Cypriuus carpio L.). J. Physiol. (Paris) 68:
591-614. (In French with English summary.)
Visek, W.J. 1968. Some aspects of ammonia toxicity in animal cells. J.
Dairy Sci. 51(2): 286-295.
Wallen, I.E., W.C. Greer, and R. Lasater. 1957. Toxicity to Gambusja affinis
of certain pure chemicals in turbid waters. Sewage Ind. Wastes 29(6):
695-711.
Walton, M.J. and C.B. Cowey. 1977. Aspects of ammoniogenesis in rainbow
trout, Salmo gairdneri. Comp. Biochem. Physiol. 57B(2): 143-149.
Waluga, D. and J. Flis. 1971. Zmiany we krwi obwodowej karpia (Cyprinus
caj-£.Lo L.) pod wplywem wody amoniakalnej . (Changes in peripheral blood
in carp (Cjjnririus £££P__io !••) under the influence of ammonia solution.)
Rocz. Nauk Roln. Ser. H 93(2): 87-94. (In English translation.)
Ward, G.S., G.C. Cramni, P.R. Parrish, and S.R. Petrocelli. 1982. Effect of
ammonium jarosite on early life stages of a saltwater fish, Cyprindon
varijegatus. Marine Po]lut. Bull. 13(6): 191-195.
Warren, K.S. 1962. Ammonia toxicity and pH. Nature 195(4836): 47-49.
Watts, R.L. and D.C. Watts. 1974. Nitrogen metabolism in fishes. Pages
369-446 in: Chemical Zoology, Vol. VIII, M. Florkin and B.T. Scheer
(Eds.), Academic Press, New York, NY.
185
-------
Webb, J.T. and G.W. Brown, Jr. 1976. Some properties and occurrence of
glutamine synthetase in fish. Comp. Biochem. Physiol. 54B(1): 171-175.
Wells, M. M. 1915. Reactions and resistance of fishes in their natural
environment to acidity, alkalinity and neutrality. Biol. Bull. 29(4):221-
257.
Westlake, G.F. and K.S. Lubinski. 1976. A chamber to monitor the locomotor
behavior of free swimming aquatic organisms exposed to simulated spills.
Pages 64-69 in: Control of Hazardous Material Spills. Proceedings of
1976 N-itional Conference on Control of Hazardous Material Spills. April
2.5-28, 1976. New Orleans, LA.
Whitfielr<, M. 1974. The hydrolysis of ammonium iors in sea W3ter -- z theor-
etical study. J. Mar. Biol. Assoc. IKK. 54:565-580.
Wickins, J.F. 1976. The tolerance of warm-water prawns to recirculated
water. Aquaculture 9(1): 19-37.
Willingham, W.T. 1976. Ammonia toxicity. EPA-90R/.V76-001, Control Tech-
nology Branch, Water Division, U.S. Environmental Protection Agency,
Region VIII, Denver, CO: 103 p.
Willingham, W.T., J.E. Colt, J.A. Fava, B.A. Hillaby, C.L. Ho, M. Katz, R.C.
Russo, n.L. Swanson, and R.V. Thurston. 1979. Arosnonia. Page? 6-18 In:
A review of th?? EPA R
-------
Wilson, R.P. ]968. Comparative ammonia toxicity and metabolism. Ph.D.
Thesis, University of Missouri, Columbia, MO. [Diss. Abstr. 29: 879-B
(1968/1969)]
Wilson, R.P., R.O. Anderson, and R.A. Bloomfieid. 1969. Ammonia toxicity in
selected fishes. Comp. Biochem. Physiol. 28(1): 107-118.
Wilt, F.H. and D. Mazia. 1974. The stimulation of cytoplasmic polyadenylya-
tion in sea urchin eggs by ammonia. Dev. Biol. 37: 422-424.
Winkler, M.M. and J.L. Grainger. 1978. Mechanisms of action of NH.C1 and
other weak bases in the activation of sea urchin eggs. Nature 273(5663):
536-538.
Woker, H. 1949. Die Temperaturabhangigkeit der Giftwirkung von Amnioriiak auf
Fische. (The temperature dependence of the toxic effect of ammonia on
fish.) Verh. Int. Ver. Theor. Angew. Limriol. 10: 575-579. (In English
translation.)
Woker, H. and K. Wuhrmann. 1950. Die Empfindlichkeit verschiedener Fischarten
gegemiber Ammoniak, Blausaure und Phenol. (The sensitivity of different
species of fish to ammonia, hydrocyanic acid and phenol.) Rev. Suisse
Zool. 57(3): 548-553. (In English translation.)
Wolf, K. 1957a. Blue-sac disease investigations: microbiology and laboratory
induction. Prog, Fish-Cult. 19(l):l4-18.
Wolf, K. 1957b. Experimental induction of blue-sac disease. Trans. Am.
Fish. Soc. 86: 61-70.
Weltering, D.M., J.L. Hedtke, and L.J. Weber. 1978. Predator-prey interac-
tions of fishes under the influence of ammonia. Trans. Am. Fish. Soc.
107(3): 500-504.
Wood, C.M. and F.H. Caldwell. 1978. Renal regulation of acid-base balance in
a freshwater fish. J. Exp. Zool. 205: 301-308.
187
-------
Wood, J.D. 1958. Nitrogen excretion in some marine teleosts. Can. J. Biochem.
Physiol. 36(12): 1237-1242.
Wuhrmann, K., F. Zehender, and H. Woker. 1947. Uber die fischereibiologische
Bedeutung des Ammonium- und Ammoniakgehaltes fliessender Gewasser.
(Biological significance for fisheries of ammonium-ion and ammonia content
of flowing bodies of water.) Vierteljahrsschr. Naturforsch. Ges. Zurich
92: 198-204. (In English translation.)
Wuhrmann, K. and H. Woker. 1948. Beitrage zur Toxikologie der Fische. II.
Experimentalle Untersuchungen fiber die Ammoniak- und Blausaurevergiftung,
(Contributions to the toxicology of fishes. II. Experimental investiga-
tions on ammonia and hydrocyanic acid poisoning.) Schweiz. Z. Hydrol.
11: 210-244. (In English translation.)
Wuhrmann, K. 1952. Sur quelques principes da la toxicologie du poisson.
(Concerning some principles of the toxicology of fish.) Bull. Cent.
Beige. Etude Doc. Eaux 15: 49-60. (In English translation.)
Wuhrmann, K. and H. Woker. 1953. Beitrage 2ur Toxikologie der Fische. VIII.
Uber die Giftwirkungen von Ammoniak- und Zyanidlosungen mit verschiedener
Sauerstoffspannung und Temperatur auf Fische. (Contributions to the
toxicology of fishes. VIII. On the toxic effects of ammonia and cyanide
solutions on fish at different oxygen tensions and temperatures.) Schweiz.
Z. Hydrol. 15: 235-260. (In English translation.)
Wuhrmann, K. and H. Woker. 1955. Influence of temperature and oxygen tension
on the toxicity of poisons to fish. Verb. Int. Ver. Theor. Angew. Limnol.
12: 795-801.
Wuhrmann, K. and H. Woker. 1958. Vergiftungen der aqu-atischen Fauna durch
Gewasserverunreinigungen. (Poisoning of aquatic fauna by polluted waters.)
\\n c .,,;*-nmcnt->! Protection Agency
/ 188
.1 '; ,1 G.';'3Ct
(• , . ), iiiificjis 60604
-------
Verb. Int. Ver. Theor. Angew. Limnol. 13: 557-583. (In English transla-
tion) .
Yamagata, Y. and M. Niwa. 1982. Acute and chronic toxicity of ammonia to eel
Anguilla japonics. Nippon Suisan Gakkaishi 48(2): 171-176.
Yasunaga, Y. 1976. The influence of some pollutants on the survival of eggs
and larvae of two species of flatfish, Limanda yokohamae and Paralichthys
olivaceus. Bull. Tokai Reg. Fish. Res. Lab. 86: 81-111.
Yoshihara, T. and H. Abe. 1955. The toxicity of chemicals to fish. I. Death
of young carp, Cyprinus carpio, by chemicals. Nippon Suisan Gakkaishi
21:950-953. [Chem. Abstr. 50:13333f (1956)]
Zgurovskaya, L.N. and N.G. Kustenko. 1968. The effect of ammonia nitrogen on
cell division, photosynthesis and pigment accumulation in Sceletonema
costatum (Grev.) Cl., Chaetoceros sp. and Prorocentriun micans Ehr.
.Okeanologiya 8(1):116-125.
189
------- |