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When fish or mammals ingest the chemical rotenone, enzymes in the digestive tract metabolize most of it, rendering it harmless, but if enough rotenone enters the bloodstream, it can kill them. Wildlife managers who use rotenone in rivers or lakes to reduce fish populations claim that the practice is harmless to aquatic mammals, but clearly if enough rotenone is used to kill fish, mammals must be at risk too.
Which of the following, if true, most seriously weakens the argument?
| Text from Passage | Analysis |
| When fish or mammals ingest the chemical rotenone, enzymes in the digestive tract metabolize most of it, rendering it harmless, but if enough rotenone enters the bloodstream, it can kill them. |
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| Wildlife managers who use rotenone in rivers or lakes to reduce fish populations claim that the practice is harmless to aquatic mammals |
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| but clearly if enough rotenone is used to kill fish, mammals must be at risk too. |
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The argument starts with scientific background about rotenone's effects, then presents wildlife managers' claims about safety, and finally argues against those claims using the initial scientific facts.
If rotenone is used in amounts sufficient to kill fish, mammals must also be at risk.
The author uses the premise that rotenone affects fish and mammals the same way (from the scientific background) to argue that wildlife managers' claims of mammal safety are wrong - if the dose kills fish, it should also threaten mammals.
Weaken - We need to find information that would make us less confident in the author's conclusion that mammals must be at risk if enough rotenone is used to kill fish.
The argument makes a direct comparison claim - if the same rotenone dose kills fish, it should also threaten mammals since both species process rotenone the same way (enzymes break it down, but high bloodstream levels are deadly).
Look for key differences between fish and mammals that could explain why the same rotenone concentration might kill fish but not harm mammals. Focus on biological differences in how they process rotenone, their exposure levels, or their sensitivity thresholds.
This identifies a critical biological difference between fish and mammals. If rotenone can enter fish bloodstreams directly through their gills, bypassing the protective digestive enzymes entirely, then fish would be much more vulnerable than mammals who only absorb rotenone through ingestion. This means the same rotenone concentration could kill fish (through direct gill absorption) while leaving mammals safe (protected by digestive enzymes). This directly weakens the argument's assumption that both species have equal vulnerability.
This discusses ecological effects of unchecked fish populations harming mammal populations, but this is irrelevant to the specific toxicity argument. The argument is about whether rotenone itself harms mammals, not about the ecological consequences of fish population management. This doesn't address the core issue of rotenone's direct effects.
The fact that rotenone travels downstream in fast-flowing rivers doesn't weaken the argument about mammal safety. If anything, this might suggest broader exposure risks. This choice doesn't address the fundamental question of whether mammals are at risk from rotenone concentrations that kill fish.
Knowing that fish constitute a substantial portion of aquatic mammals' diets doesn't help the argument either way. The passage already established that ingested rotenone is mostly broken down by digestive enzymes, so this information about dietary composition is irrelevant to the toxicity debate.
Comparing rotenone's toxicity to other chemicals used in the past doesn't weaken the current argument. Even if rotenone is less toxic than previous chemicals, this doesn't address whether rotenone concentrations that kill fish also threaten mammals. This is a relative comparison that doesn't resolve the specific safety question.