Environmental Engineering Reference
In-Depth Information
at concentrations less than half the 24-h LC
50
of 0.7
g L
−1
(Satapornvanit et al.
2009
). These effects persisted for at least 4 h after cessation of exposure to CPY,
but it is not known if these were truly behavioral responses or symptoms of sub-
lethal poisoning.
A number of studies of sublethal effects of CPY on fi sh have been conducted,
some of which have focused on olfactory perception and others on behavior. Much
of the research on effects of CPY and other pesticides on behavior has focused on
migratory species of salmon because of their societal importance and the need for
migratory species to be able to sense chemicals in water to successfully navigate to
breeding waters. Exposure of the olfactory epithelium of Coho salmon
(
Oncorhynchus kisutch
) to 0.7
μ
g CPY L
−1
caused a 20% loss of sensory function as
measured by neurophysiological response to salmonid bile salt and L -serine
(Sandahl et al.
2004
). Since these studies were conducted in the laboratory, the
changes in sensory function were not evaluated at the level of the whole-animal.
Several studies have linked effects of CPY on the sensory epithelium and behavior
to inhibition of AChE. Working with juvenile Coho salmon (
Oncorhynchus kisutch
)
exposed to CPY at concentrations between 0.6 and 2.5
μ
g L
−1
, Sandahl et al. (
2005
)
showed that spontaneous swimming rate and food strikes were correlated (r
2
0.58
and 0.53, respectively) with inhibition of AChE activity in the brain. Other studies
of effects of CPY in the same species showed that thresholds for different behaviors
were related to inhibition of AChE (Tierney et al.
2007
). Thresholds for effects of
CPY on swimming behavior ranged from 20 to 35% inhibition of AChE. Zebrafi sh
(
Danio rerio
) exposed to 220
μ
g CPY L
−1
for 24 h exhibited impaired swimming
behavior (p <0.01) and a concentration-response relationship was observed at con-
centrations greater than 35
μ
g L
−1
(Tilton et al.
2011
). Similarly, locomotory behav-
ior of mosquito fi sh,
Gambusia affi nis
, was affected by exposure to 60
μ
g CPY L
−1
for 20 d (Rao et al.
2005
). Although exposures to concentrations of CPY of 100 and
200
μ
60% of controls) in tadpoles
of
Rana sphenocephala
, there were no effects on swim-speed or vulnerability to
predation (Widder and Bidwell
2006
).
Most of the reported behavioral responses of fi sh to CPY were related to inhibi-
tion of AChE. These observations are consistent with current understanding of func-
tions of AChE in the nervous system. It is also not surprising that mixtures of
carbamate and organophosphorus pesticides have the same effect as single com-
pounds and that they act additively and sometimes synergistically (Laetz et al.
2009
). However, when assessed in the context of actual exposures in the environ-
ment, risks are small as the pesticides must co-occur temporally and spatially to
cause ecological effects. Even when total potencies of mixtures of insecticides are
considered, exposures that inhibit AChE at concentrations greater than the threshold
for effects on behavior rarely occur in key locations for valued species, such as
salmon in the Pacifi c NW (Moore and Teed
2012
).
Although effects on behavior due to inhibition of AChE can be observed in ver-
tebrates, these have not been experimentally related to effects on survival, develop-
ment, growth, and reproduction of individuals or ecosystem stability or function in a
quantitative manner. Therefore, they cannot be incorporated into an ERA at this time.
μ
g L
−1
caused depression of whole-body AChE (
≈
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