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

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In a second modeling exercise, we translate reductions in growth of juvenile salmon from AChE<br />

inhibition <strong>and</strong> from reduced prey abundances to potential population impacts using individualbased<br />

growth <strong>and</strong> life history population models (Appendix 1). These two endpoints (AChE<br />

inhibition <strong>and</strong> reduced prey abundance) are combined in the model to evaluate population-level<br />

effects due to reductions in first year survival of juveniles (Appendix 1). Similar to the survival<br />

models, percent change in lambda is the output. We discuss the significance of population<br />

changes in the context of departures from normal variability of the unexposed population <strong>and</strong><br />

expected environmental concentrations. We conclude this section on population-level effects<br />

with a discussion of population-level responses to other affected salmonid endpoints that were<br />

not modeled. These include effects from other stressors of the proposed action, mixture effects,<br />

<strong>and</strong> effects to behaviors from impaired olfaction <strong>and</strong> AChE inhibition such as swimming<br />

behaviors.<br />

Salmonid Population Models<br />

We selected four generalized life history strategies to model (Appendix 1). We ran general life<br />

history matrix models for coho salmon (Oncorhynchus kisutch), sockeye salmon (O. nerka) <strong>and</strong><br />

ocean-type <strong>and</strong> stream-type Chinook salmon (O. tshawytscha). We did not construct a steelhead<br />

(O. mykiss) life history model due to the lack of demographic information. Chum salmon (O.<br />

keta) were omitted from the growth model exercise because they migrate to marine systems soon<br />

after emerging from the gravel <strong>and</strong> the model assesses early life stage growth effects over a<br />

minimum of 140 d in freshwater systems. The basic salmonid life history we modeled consisted<br />

of hatching <strong>and</strong> rearing in freshwater, smoltification in estuaries, migration to the ocean,<br />

maturation at sea, <strong>and</strong> returning to the natal freshwater stream for spawning followed shortly by<br />

death. For specific information on how we constructed the models see Appendix 1.<br />

Effects to salmonid populations from death of sub­yearling juveniles<br />

An acute toxicity model was constructed that estimated the population-level impacts of<br />

subyearling juvenile (referred to as juveniles within this section) mortality resulting from<br />

exposure to concentrations of carbaryl, carbofuran, <strong>and</strong> methomyl. These models excluded<br />

sublethal <strong>and</strong> indirect effects of the pesticide exposures <strong>and</strong> focused on the population-level<br />

outcomes resulting from an annual 4 d exposure of all juveniles in the population to carbaryl,<br />

carbofuran, <strong>and</strong> methomyl from single exposures. Death of juveniles was implemented as a<br />

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