Carbaryl, Carbofuran, and Methomyl - National Marine Fisheries ...

endpoints of salmonids remains a recognized data gap. Given the differences in olfactory
toxicity in salmonids for carbaryl (no observed toxicity) and carbofuran (inhibited olfaction at 10
μg/L) combined with no available information on methomyl’s affect on olfaction, no apparent
dose-response pattern of toxicity emerges for the three a.i.s.
Assessment endpoints: Toxic effects in salmonids from consuming contaminated prey
Assessment measures: Survival, swimming performance
A current uncertainty is the degree to which secondary poisoning of juvenile salmonids may
occur from feeding on contaminated dead and dying drifting insects. Secondary poisoning is a
frequent occurrence with OPs and carbamates in bird deaths (Mineau 1991), yet is much less
studied in fish. Uptake, metabolism, and accumulation of carbaryl by a salmonid prey item,
Chironomus riparius (midge), exposed for 24 h indicated significant uptake over the first 8 h,
significant metabolism (more than 85-99%) of parent carbaryl to metabolites and low
bioconcentration factors (5-10) (Lohner and Fisher 1990). These results suggest that
contaminated prey items, such as aquatic invertebrates, do not accumulate significant carbaryl,
and what they do accumulate is likely rapidly metabolized. That said, juvenile salmonids could
still get a dose of carbaryl from feeding on drifting, contaminated insects that have not had time
to metabolize carbaryl. Juvenile brook trout gorged on drifting insects following applications of
carbaryl and AChE activity was reduced (15-34%) in the trout (Haines 1981). However, it is not
possible to differentiate the contribution to AChE inhibition from the aqueous and dietary routes
because concentrations were not measured in the water, prey, or fish. In another study, resident
trout feeding on dying and dead drifting invertebrates (from the pyrethroid cypermethrin) caused
a range of physiological symptoms in brook trout: loss of self-righting ability and startle
response; lethargy; hardening and haemolysis of muscular tissue similar to muscle tetany; and
anemic appearance of blood and gills (Davies and Cook 1993). The possibility that the adverse
effects in the trout manifested from exposure to the water column instead of from feeding on
contaminated prey was ruled out by the authors as measured field concentrations of pesticides
did not produce known toxic responses. In a laboratory feeding study with the OP fenitrothion,
brook trout (S. fontinalis) were fed contaminated pellets (1 or 10 mg/g fenitrothion for four wks)
(Wildish and Lister 1973). Growth was reduced in both treatments. AChE inhibition was
measured at 2, 12, and 27 d following termination of contaminated diet treatments. Trout had
lower AChE activity than unexposed fish at both treatments, and by 27 d following termination,
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