Environmental Factor

April 2011


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Pollution leads to rapid evolution in some fish species

By Robin Arnette
April 2011

Isaac Wirgin, Ph.D.

Wirgin explained that General Electric released approximately 1.3 million pounds of PCBs into the Hudson River from 1947 to 1976. Exposure to these pollutants and strong natural selection probably led to a rapid increase in the frequency of the standing AHR2 variant allele in the Hudson River population. (Photo courtesy of Gordon Cook)

Mark Hahn, Ph.D.

Hahn stressed that not all animal populations living under selective pressure from contaminants will evolve resistance like these fish. "Tomcod and killifish happen to have life-history characteristics, such as genetic variability, large population size, and short generation time, which allow them to adapt," he said. (Photo courtesy of Hahn's wife, Rachel Graber)

New research funded by the NIEHS Superfund Research Program (SRP) (http://www.niehs.nih.gov/research/supported/srp/index.cfm)demonstrates that a population of Atlantic tomcod (Microgadus tomcod) living in the Hudson River has rapidly evolved resistance to polychlorinated biphenyls (PCBs), man-made industrial chemicals known to cause cancer in animals. The published work appeared in the Feb. 17 online issue of Science magazine and represents the first study to identify the mechanism of resistance to toxicants in any vertebrate population, and the first to show that PCBs in the Hudson River have caused significant ecological change.

The study(http://www.ncbi.nlm.nih.gov/pubmed/21330491) Exit NIEHS was a collaborative effort by several researchers, including Isaac Wirgin, Ph.D., (http://www.med.nyu.edu/biosketch/wirgii01) Exit NIEHS and Mark Hahn, Ph.D., (http://www.whoi.edu/profile/mhahn/) Exit NIEHS two SRP scientists who have been studying animal adaptability to environmental stress for more than a decade. Their research team found that in Hudson River tomcod, the aryl hydrocarbon receptor 2 (AHR2) gene, responsible for mediating the toxicity of chemical contaminants, contained two variants.

One of these variants lacked two amino acids, which caused a structural change within the AHR2 receptor. The deletion made the fish 100-fold less sensitive to PCBs and 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), the most toxic of the polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs). Wirgin said that the research addressed the long-term debate over the number of genes required and the time needed to spur dramatic evolutionary change.

"In this case, resistance to toxicants can occur much more rapidly than previously thought and be due to a [small] change within a single gene," said Wirgin, an associate professor in the Department of Environmental Medicine at New York University School of Medicine, Tuxedo, N.Y., and lead author on the paper.

The consequences of resistance

Hahn, whose SRP sponsorship comes from Boston University, is a senior scientist in the Biology Department at the Woods Hole Oceanographic Institution, Woods Hole, Mass. He said that the AHR2 change and subsequent resistance to PCBs and TCDD isn't found in tomcod from cleaner waters. Hahn also pointed out that although the mutation allowed tomcod to continue to live in the Hudson River, it didn't come without biological consequences.

"One cost is that the fish can accumulate higher levels of PCBs and pass them up the food chain, possibly harming higher-level consumers," he noted. "Other potential costs might include altered sensitivity of these fish to additional stressors in their environment, such as other chemicals or severe depletion of oxygen in the water known as hypoxia."

In addition to his work with tomcod, Hahn studies another fish species known to experience similar evolutionary pressures - the Atlantic killifish (Fundulus heteroclitus). The much smaller killifish are like tomcod in that they live in various locations on the U.S. east coast in moderate-to-high levels of chemical contamination. Even though the same gene, AHR2, is experiencing evolutionary selection in these killifish, Hahn's work has identified 26 different AHR2 variants, as opposed to just two in tomcod.

SRP pushes environmental research forward

Richard Di Giulio, Ph.D. , (http://fds.duke.edu/db/Nicholas/esp/faculty/richd) Exit NIEHS although not an author on this paper, has also studied chemical resistance in the killifish, but in the Elizabeth River in North Carolina. Di Giulio is a professor of environmental toxicology and director of the SRP Center and Integrated Toxicology Program at Duke University in Durham, N.C. He said his work and the work of others "not only shows the remarkable ability of resident fish populations to adapt to toxicity, but could also be applied to other aquatic and estuarine systems that are chronically polluted."

Bill Suk, Ph.D., director of the Center for Risk and Integrated Sciences (CRIS), (http://www.niehs.nih.gov/research/supported/dert/cris/index.cfm) the center within the NIEHS Division of Extramural Research & Training (DERT) that manages the SRP, said he was happy that SRP played a role in this research because it is a great example of one of the goals of NIEHS.

"This work enforces the link between resistance and susceptibility and shows how important basic mechanistic research is in addressing a problem," Suk concluded.

Citation: Wirgin I, Roy NK, Loftus M, Chambers RC, Franks DG, Hahn ME.(http://www.ncbi.nlm.nih.gov/pubmed/21330491) Exit NIEHS 2011. Mechanistic basis of resistance to PCBs in Atlantic tomcod from the Hudson River. Science 331(6022):1322-1325. 

Atlantic tomcod resistance to toxins in the news

Since its publication, the results of the research have been mentioned in several news media outlets. A few are listed below.



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