PrepTest 26, Section 4, Question 17
Between June 1987 and May 1988, the bodies of at least 740 bottlenose dolphins out of a total coastal population of 3,000 to 5,000 washed ashore on the Atlantic coast of the United States. Since some of the dead animals never washed ashore, the overall disaster was presumably worse; perhaps 50 percent of the population died. A dolphin die-off of this character and magnitude had never before been observed; furthermore, the dolphins exhibited a startling range of symptoms. The research team that examined the die-off noted the presence of both skin lesions and internal lesions in the liver, lung, pancreas, and heart, which suggested a massive opportunistic bacterial infection of already weakened animals.
Tissues from the stricken dolphins were analyzed for a variety of toxins. Brevetoxin, a toxin produced by the blooming of the alga Ptychodiscus brevis, was present in eight out of seventeen dolphins tested. Tests for synthetic pollutants revealed that polychlorinated biphenyls (PCBs) were present in almost all animals tested.
The research team concluded that brevetoxin poisoning was the most likely cause of the illnesses that killed the dolphins. Although P. brevis is ordinarily not found along the Atlantic coast, an unusual bloom of this organism�such blooms are called "red tides" because of the reddish color imparted by the blooming algae�did occur in the middle of the affected coastline in October 1987. These researchers believe the toxin accumulated in the tissue of fish and then was ingested by dolphins that preyed on them. The emaciated appearance of many dolphins indicated that they were metabolizing their blubber reserves, thereby reducing their buoyancy and insulation (and adding to overall stress) as well as releasing stores of previously accumulated synthetic pollutants, such as PCBs, which further exacerbated their condition. The combined impact made the dolphins vulnerable to opportunistic bacterial infection, the ultimate cause of death.
For several reasons, however, this explanation is not entirely plausible. First, bottlenose dolphins and P. brevis red tides are both common in the Gulf of Mexico, yet no dolphin die-off of a similar magnitude has been noted there. Second, dolphins began dying in June, hundreds of miles north of and some months earlier than the October red tide bloom. Finally, the specific effects of brevetoxin on dolphins are unknown, whereas PCB poisoning is known to impair functioning of the immune system and liver and to cause skin lesions; all of these problems were observed in the diseased animals. An alternative hypothesis, which accounts for these facts, is that a sudden influx of pollutants, perhaps from offshore dumping, triggered a cascade of disorders in animals whose systems were already heavily laden with pollutants. Although brevetoxin may have been a contributing factor, the event that actually precipitated the die-off was a sharp increase in the dolphins' exposure to synthetic pollutants.
Between June 1987 and May 1988, the bodies of at least 740 bottlenose dolphins out of a total coastal population of 3,000 to 5,000 washed ashore on the Atlantic coast of the United States. Since some of the dead animals never washed ashore, the overall disaster was presumably worse; perhaps 50 percent of the population died. A dolphin die-off of this character and magnitude had never before been observed; furthermore, the dolphins exhibited a startling range of symptoms. The research team that examined the die-off noted the presence of both skin lesions and internal lesions in the liver, lung, pancreas, and heart, which suggested a massive opportunistic bacterial infection of already weakened animals.
Tissues from the stricken dolphins were analyzed for a variety of toxins. Brevetoxin, a toxin produced by the blooming of the alga Ptychodiscus brevis, was present in eight out of seventeen dolphins tested. Tests for synthetic pollutants revealed that polychlorinated biphenyls (PCBs) were present in almost all animals tested.
The research team concluded that brevetoxin poisoning was the most likely cause of the illnesses that killed the dolphins. Although P. brevis is ordinarily not found along the Atlantic coast, an unusual bloom of this organism�such blooms are called "red tides" because of the reddish color imparted by the blooming algae�did occur in the middle of the affected coastline in October 1987. These researchers believe the toxin accumulated in the tissue of fish and then was ingested by dolphins that preyed on them. The emaciated appearance of many dolphins indicated that they were metabolizing their blubber reserves, thereby reducing their buoyancy and insulation (and adding to overall stress) as well as releasing stores of previously accumulated synthetic pollutants, such as PCBs, which further exacerbated their condition. The combined impact made the dolphins vulnerable to opportunistic bacterial infection, the ultimate cause of death.
For several reasons, however, this explanation is not entirely plausible. First, bottlenose dolphins and P. brevis red tides are both common in the Gulf of Mexico, yet no dolphin die-off of a similar magnitude has been noted there. Second, dolphins began dying in June, hundreds of miles north of and some months earlier than the October red tide bloom. Finally, the specific effects of brevetoxin on dolphins are unknown, whereas PCB poisoning is known to impair functioning of the immune system and liver and to cause skin lesions; all of these problems were observed in the diseased animals. An alternative hypothesis, which accounts for these facts, is that a sudden influx of pollutants, perhaps from offshore dumping, triggered a cascade of disorders in animals whose systems were already heavily laden with pollutants. Although brevetoxin may have been a contributing factor, the event that actually precipitated the die-off was a sharp increase in the dolphins' exposure to synthetic pollutants.
Between June 1987 and May 1988, the bodies of at least 740 bottlenose dolphins out of a total coastal population of 3,000 to 5,000 washed ashore on the Atlantic coast of the United States. Since some of the dead animals never washed ashore, the overall disaster was presumably worse; perhaps 50 percent of the population died. A dolphin die-off of this character and magnitude had never before been observed; furthermore, the dolphins exhibited a startling range of symptoms. The research team that examined the die-off noted the presence of both skin lesions and internal lesions in the liver, lung, pancreas, and heart, which suggested a massive opportunistic bacterial infection of already weakened animals.
Tissues from the stricken dolphins were analyzed for a variety of toxins. Brevetoxin, a toxin produced by the blooming of the alga Ptychodiscus brevis, was present in eight out of seventeen dolphins tested. Tests for synthetic pollutants revealed that polychlorinated biphenyls (PCBs) were present in almost all animals tested.
The research team concluded that brevetoxin poisoning was the most likely cause of the illnesses that killed the dolphins. Although P. brevis is ordinarily not found along the Atlantic coast, an unusual bloom of this organism�such blooms are called "red tides" because of the reddish color imparted by the blooming algae�did occur in the middle of the affected coastline in October 1987. These researchers believe the toxin accumulated in the tissue of fish and then was ingested by dolphins that preyed on them. The emaciated appearance of many dolphins indicated that they were metabolizing their blubber reserves, thereby reducing their buoyancy and insulation (and adding to overall stress) as well as releasing stores of previously accumulated synthetic pollutants, such as PCBs, which further exacerbated their condition. The combined impact made the dolphins vulnerable to opportunistic bacterial infection, the ultimate cause of death.
For several reasons, however, this explanation is not entirely plausible. First, bottlenose dolphins and P. brevis red tides are both common in the Gulf of Mexico, yet no dolphin die-off of a similar magnitude has been noted there. Second, dolphins began dying in June, hundreds of miles north of and some months earlier than the October red tide bloom. Finally, the specific effects of brevetoxin on dolphins are unknown, whereas PCB poisoning is known to impair functioning of the immune system and liver and to cause skin lesions; all of these problems were observed in the diseased animals. An alternative hypothesis, which accounts for these facts, is that a sudden influx of pollutants, perhaps from offshore dumping, triggered a cascade of disorders in animals whose systems were already heavily laden with pollutants. Although brevetoxin may have been a contributing factor, the event that actually precipitated the die-off was a sharp increase in the dolphins' exposure to synthetic pollutants.
Between June 1987 and May 1988, the bodies of at least 740 bottlenose dolphins out of a total coastal population of 3,000 to 5,000 washed ashore on the Atlantic coast of the United States. Since some of the dead animals never washed ashore, the overall disaster was presumably worse; perhaps 50 percent of the population died. A dolphin die-off of this character and magnitude had never before been observed; furthermore, the dolphins exhibited a startling range of symptoms. The research team that examined the die-off noted the presence of both skin lesions and internal lesions in the liver, lung, pancreas, and heart, which suggested a massive opportunistic bacterial infection of already weakened animals.
Tissues from the stricken dolphins were analyzed for a variety of toxins. Brevetoxin, a toxin produced by the blooming of the alga Ptychodiscus brevis, was present in eight out of seventeen dolphins tested. Tests for synthetic pollutants revealed that polychlorinated biphenyls (PCBs) were present in almost all animals tested.
The research team concluded that brevetoxin poisoning was the most likely cause of the illnesses that killed the dolphins. Although P. brevis is ordinarily not found along the Atlantic coast, an unusual bloom of this organism�such blooms are called "red tides" because of the reddish color imparted by the blooming algae�did occur in the middle of the affected coastline in October 1987. These researchers believe the toxin accumulated in the tissue of fish and then was ingested by dolphins that preyed on them. The emaciated appearance of many dolphins indicated that they were metabolizing their blubber reserves, thereby reducing their buoyancy and insulation (and adding to overall stress) as well as releasing stores of previously accumulated synthetic pollutants, such as PCBs, which further exacerbated their condition. The combined impact made the dolphins vulnerable to opportunistic bacterial infection, the ultimate cause of death.
For several reasons, however, this explanation is not entirely plausible. First, bottlenose dolphins and P. brevis red tides are both common in the Gulf of Mexico, yet no dolphin die-off of a similar magnitude has been noted there. Second, dolphins began dying in June, hundreds of miles north of and some months earlier than the October red tide bloom. Finally, the specific effects of brevetoxin on dolphins are unknown, whereas PCB poisoning is known to impair functioning of the immune system and liver and to cause skin lesions; all of these problems were observed in the diseased animals. An alternative hypothesis, which accounts for these facts, is that a sudden influx of pollutants, perhaps from offshore dumping, triggered a cascade of disorders in animals whose systems were already heavily laden with pollutants. Although brevetoxin may have been a contributing factor, the event that actually precipitated the die-off was a sharp increase in the dolphins' exposure to synthetic pollutants.
Which one of the following most accurately describes the organization of the last paragraph?
One explanation is criticized and a different explanation is proposed.
An argument is advanced and then refuted by means of an opposing argument.
Objections against a hypothesis are advanced, the hypothesis is explained more fully, and then the objections are rejected.
New evidence in favor of a theory is described, and then the theory is reaffirmed.
Discrepancies between two explanations are noted, and a third explanation is proposed.
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