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

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habitats is then assessed. This portion of the analysis is conducted in the Integration <strong>and</strong><br />

Synthesis section.<br />

Below we discuss an example of one risk hypothesis to show the relationship between<br />

assessment endpoints <strong>and</strong> measures with species responses. In risk hypothesis 1 (d),<br />

aquatic exposure to carbaryl, carbofuran, <strong>and</strong> methomyl can impair a salmonid’s nervous<br />

system <strong>and</strong> consequently affect swimming ability of fish. Behavioral modifications, such<br />

as changes in swimming performance, are regularly considered in NMFS’ Opinions.<br />

Swimming performance therefore is an assessment endpoint. Measurable changes in<br />

swimming speed are the assessment measure used to evaluate this endpoint. Reductions<br />

in swimming performance could also affect other assessment endpoints such as migration<br />

<strong>and</strong> predator avoidance. We may or may not have empirical data that address these<br />

endpoints, resulting in a recognized data gap. This uncertainty would be identified<br />

during the problem formulation phase, <strong>and</strong> discussed in the risk characterization phase.<br />

In the problem formulation phase, we also identify the toxic mode <strong>and</strong> mechanism of<br />

action of chemical stressors, particularly for the pesticide a.i.s. This information helps us<br />

underst<strong>and</strong> what an organism’s physiological consequences may be following exposure.<br />

It also helps us evaluate whether mixture toxicity occurs because we identify other<br />

pesticides that share similar modes of action <strong>and</strong> the likelihood for co-occurrence in listed<br />

species habitats. A similar mode of action with other pesticides is a key determinant of<br />

the likelihood of mixture toxicity. With vertebrates (fish <strong>and</strong> mammals) <strong>and</strong><br />

invertebrates, the three a.i.s share a common mode <strong>and</strong> mechanism of action,<br />

acetylcholinesterase inhibition. Given this information, a range of potential adverse<br />

responses are possible (Figure 4). We then search, compile, <strong>and</strong> review the available<br />

toxicity information to ascertain which physiological systems are known to be affected<br />

<strong>and</strong> to what degree.<br />

49

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