PrepTest 103 · Section 4 · Passage 3

Competing explanations for an Atlantic bottlenose dolphin die-off

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Why are all these dolphins dying?

The 740 bodies that washed ashore already represent a substantial share of a population of 3,000 to 5,000. And that count may understate the disaster. A dead dolphin could sink or decompose without reaching shore. The suggestion that perhaps half the population died is an estimate, not a claim that researchers counted every dead animal.

The range of symptoms makes the cause harder to pin down. The dolphins had lesions on their skin and in several organs. Researchers thought this indicated an opportunistic infection: bacteria had attacked animals whose health was already compromised (paragraph 1). Opportunistic gives us the important relationship: the infection took advantage of animals whose defenses were already compromised. That leaves a question. What weakened them in the first place?

Paragraph 2 identifies two substances found in the dolphins: brevetoxin, produced by an alga, and synthetic pollutants called PCBs. We don't need to memorize the long chemical name. We do need to keep the two substances separate.

Finding a substance in a dead animal doesn't, by itself, show that the substance killed it. Was the amount unusual? Could it have been present before the animal got sick? Those are useful questions to bring to the next paragraph, which gives the research team's explanation.

The team chooses brevetoxin as the likely starting point. An unusual bloom of the toxin-producing alga occurred along the Atlantic coast in October 1987. Hold on: the deaths began in June. How does an October event explain dolphins that were already dying several months earlier? We should keep that timing concern in mind.

The researchers propose a route through the food chain. Fish accumulated the toxin, and dolphins then ate the fish. The dolphins wouldn't have to consume the algae directly to be exposed. That makes the proposed route understandable, but an understandable route isn't yet proof that it caused this disaster.

Next comes the loss of blubber. The dolphins' thin appearance suggested they were using up their fat reserves. Think of a body drawing on stored energy when it isn't getting enough from food. For these dolphins, losing blubber also meant losing buoyancy and insulation, adding stress. Why they were becoming so thin is still part of the explanation to investigate; thinness alone doesn't identify brevetoxin as the culprit.

There is a second problem with using up that fat: it releases synthetic pollutants already stored there. In the team's account, those released PCBs worsen the dolphins' condition. So the researchers aren't proposing that brevetoxin acted alone. They describe an initial illness followed by several additional stresses, including the release of pollutants, leaving the animals vulnerable to the bacterial infection that ultimately killed them.

The final paragraph finally gives us the writer's response: this explanation is “not entirely plausible.”

First, dolphins and the same algal blooms are both common in the Gulf of Mexico, but no comparable die-off has been observed there. If the algae explain the Atlantic disaster, why don't we see the same result in the Gulf? That challenges the explanation without proving that the toxin can never harm dolphins.

Second, the writer raises the timing problem we noticed. The deaths started before the October bloom—and hundreds of miles north of it. The proposed cause doesn't fit the beginning of the event.

Third, the effects of brevetoxin on dolphins are unknown, while PCB poisoning is known to impair the immune system and liver and cause skin lesions. Those problems were observed. Now the writer is doing more than questioning brevetoxin: the symptoms give a positive reason to consider synthetic pollutants.

The alternative is a sudden increase in pollution affecting dolphins already burdened with pollutants. Offshore dumping is suggested as a possible source. I'd still want evidence that such dumping actually occurred; “perhaps” doesn't turn that possibility into an established event.

The disagreement is about what started the chain. The writer allows brevetoxin to have contributed but puts increased exposure to synthetic pollutants first. Keep that distinction: a contributing factor isn't necessarily the trigger.

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