Effects of short-term ammonia exposure on fish
Environ. Toxicol. Chem. 19, 2000
2935
conclusion was reached by Thurston et al. [7] from the results
of a study on the effects of fluctuating exposures on the acute
toxicity of ammonia to rainbow trout. These authors found that
fish were able to withstand short-term excursions slightly
above acutely toxic (96-h LC50) concentrations of ammonia
without apparent long-term effects, provided that those ex-
cursions were accompanied by compensatory respite periods
below acutely toxic concentrations.
growth. This suggests that fish can withstand a certain degree
of gill damage without significant interference with the phys-
iological processes that affect growth. Thurston et al. [26] also
observed mild to moderate gill damage in fish exposed con-
tinuously to sublethal concentrations of ammonia without any
apparent effect on fish growth. Kirk and Lewis [35] found
some evidence of gill damage in rainbow trout exposed to 0.08
mg N/L for 2 h, a much less severe exposure regime than in
the present study. It appears, therefore, that gill condition is
a sensitive indicator of ammonia toxicity.
Other significant histopathological effects observed in the
repeated exposure experiment were reductions in liver weight.
One explanation is that the more frequently stressed fish were
placing greater demands on the energy stored in liver glycogen.
Reduced glycogen storage has also been reported by Smith
and Piper [30] for juvenile rainbow trout under conditions of
prolonged exposure to ammonia. Flis [36] has demonstrated
severe tissue damage to liver and kidneys in carp (Cyprinus
carpio) exposed continuously to ammonia, which appeared to
be associated with disruption of the blood vessels.
The results from the repeated exposure experiments here
show that, although fish may be able to withstand and recover
from short-term peaks in ammonia concentration, repeated ex-
posures have a significantly adverse effect on growth. In the
second test, growth was significantly affected at both of the
higher frequency exposures (vessels 4 and 5). Growth was also
significantly depressed at the once weekly exposure at the
lower exposure concentration (vessel 2) but not at the higher
concentration (vessel 3). This significant effect in the least
severe experimental treatment is difficult to explain, particu-
larly since, in the first test, the same regime did not affect
growth. The reason for this difference in effect between tests
is also unclear. Fish age-related effects are one possible factor,
though the coefficients of variation were higher in the first
test, particularly for the control (0.45 compared with 0.30 in
the second test), which reduces the power of the statistical test.
Considering the broader implications of the results, the
growth data suggest that, although fish can survive short-term
ammonia peaks, these pulses may result in a degree of inter-
ference with physiological processes that affect growth. Pro-
vided the exposure concentration exceeds the critical level at
which interference starts to occur, the overall effect on growth
appears to be related more to exposure frequency than to ex-
posure concentration.
A number of studies have been reported in which growth
of salmonids has been measured during prolonged exposure
to ammonia [26–30]. In all cases, fish were exposed contin-
uously. Concentrations that were reported to cause significant
growth retardation were considerably lower than those af-
fecting growth in the experimental regimes of the present
study. This suggests, again, that the interpulse recovery period
has a very important influence on the long-term sensitivity of
fish to ammonia exposure.
Although exposure to ammonia did not affect hemoglobin
concentrations or total blood cell counts in the fish, hematocrit
was significantly increased in some experimental groups in the
second test. Hematological effects in fish caused by ammonia
exposure have been reported elsewhere. Reicheuback-Klinke
CONCLUSIONS
The results of the present study indicate that both duration
and frequency of exposure have an important influence on the
toxicity of ammonia to fish. These findings have significant
implications for the derivation of environmental quality stan-
dards for intermittent pollution. First, duration of exposure to
ammonia has been demonstrated to be a critical factor affecting
fish survival and should therefore be incorporated into time-
dependent standards. Such an approach has been proposed by
Whitelaw and Solb e´ [20], who applied existing short-term tox-
icity data to produce a series of time-dependent LC50 stan-
dards. The results of the pulsed-exposure tests described in
this paper allow further development of this approach by al-
lowing a more accurate definition of what constitutes a safe
concentration for polluting episodes of different duration. Sec-
ond, the demonstrated influence of exposure frequency indi-
cates the need to take account of the return period of transient
pollution events in deriving appropriate standards since this
will fundamentally influence the degree of recovery following
exposure and, consequently, the long-term viability of fish
populations. Standards aimed at avoiding long-term effects
have been derived, and these are used as design criteria in the
upgrading of storm overflows from sewer systems.
The results of this study present important new information
on the sublethal effects of exposure duration and frequency.
However, there is a need for further validation of the findings,
in particular, assessment of the repeatability of the results, and
responses of different species would be valuable.
[
31] observed diminishing numbers of red blood cells in fish
exposed to 0.1 to 0.4 mg NH -N/L over one week. This author
3
also reported swelling of cells, which would be consistent with
the observations on blood from experimental fish from the
second test. However, unlike the results from the present study,
Buckley et al. [32] reported slightly, but significantly, reduced
hemoglobin concentrations and hematocrit in coho salmon ex-
Acknowledgement—This work was funded by the National Rivers
Authority. We thank the Urban Pollution Management Steering Group
and T. Owen.
REFERENCES
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3
The most marked histopathological effects on fish in both
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of exposure rather than ammonia concentration. Gill damage
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4
. Horner RR, Skupien JJ, Livingston EH, Shaver HE. 1994. Fun-
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