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Hudson River PCBs Superfund Site

Frequently Asked Questions (FAQs)


General FAQs
FAQs About PCB Health Risk
  1. What are PCBs?
  2. Why are PCBs of concern to humans?
  3. Why are there fish consumption advisories on the Hudson River?
  4. What does "Bioaccumulation" mean?
  5. What is the history of the PCBs in the Hudson River?
  6. When did dredging begin?
  7. What happened to the sediment after it was dredged from the river?
  8. What were the engineering performance standards that were developed for the dredging project?
  9. Why were quality of life performance standards needed for the dredging project?
  10. What is a Natural Resource Damages Claim?
  11. Who are the Trustees of the Hudson River?
  1. What do other Agencies say about cancer and PCBs?
  2. How is the toxicity of PCBs determined?
  3. How does EPA evaluate toxicity information?
  4. Do PCBs cause cancer?
  5. How are non-cancer health effects evaluated?
  6. What is risk assessment?
  7. How is exposure to PCBs evaluated?
  8. How are risks calculated?
  9. How are hazards calculated?
  10. How is risk assessment used by risk managers?

General FAQs

  1. What are PCBs?
    PCBs or polychlorinated biphenyls are a class of chemicals consisting of 209 individual compounds. PCBs were widely used as a fire preventive and insulator in the manufacture of transformers and capacitors because of their ability to withstand exceptionally high temperatures.
  2. Why are PCBs of concern to humans?
    PCBs are classified by the U.S. EPA as probable human carcinogens. In addition, EPA recognizes neurological and developmental effects as additional toxic effects of PCBs. The agency considers all PCB mixtures to be toxic.
  3. Why are there fish consumption advisories on the Hudson River?
    PCBs bioaccumulate (see below) in fish.  In 1976, the New York State Department of Environmental Conservation (NYSDEC) banned all fishing in the upper Hudson River, from the Troy Dam north through Fort Edward, because PCB levels in Hudson River fish were in excess of Food and Drug Administration limitations. In August 1995, a catch and release fishing program was instituted by NYSDEC in the upper Hudson where the total ban had previously been in place. Although it is now legal to catch and release fish in the Hudson north of the Troy Dam, one can still not safely consume the fish caught. In addition, there are health advisories posted for various Hudson River species in the river south of Troy.  Women of childbearing age and children are at greatest risk.
  4. What does "Bioaccumulation" mean?
    Bioaccumulation refers to the process by which contaminants such as PCBs accumulate or become magnified as they move up the food chain.  PCBs concentrate in tissue and internal organs, and as big fish eat little fish, they accumulate all the PCBs that have been eaten by everyone below them in the food chain.  Another term for this is Biological Magnification.
  5. What is the history of the PCBs in the Hudson River?
    During a 30-year period ending in 1977, it is estimated that approximately 1.3 million pounds of PCBs were discharged into the Hudson River from two General Electric (GE) capacitor manufacturing plants located in Fort Edward and Hudson Falls, New York. Much of this PCB load adhered to fine sediments which accumulated behind the Fort Edward Dam. When the deteriorating dam was removed in 1973, the PCB-contaminated sediments were washed downstream. Studies conducted to evaluate the extent of the problem revealed that most of the contaminated sediments were in 40 hot spots situated in a 40-mile stretch of the river between Fort Edward and the Troy Dam.
  6. When did dredging begin?
    In February 2002, EPA issued a Record of Decision calling for the targeted environmental dredging and removal of approximately 2.65 million cubic yards of PCB-contaminated sediment from the Upper Hudson River from Fort Edward to Troy, NY. Dredging began in 2009 and ended in fall 2015. The project occurred in two phases. The first phase of the dredging project began in May 2009 and ended in November 2009. During this phase, General Electric removed approximately 283,000 cubic yards of PCB-contaminated sediment from a six-mile stretch of the Hudson River near Fort Edward, NY. The second, and final phase of dredging began in June 2011 and followed an evaluation by an independent group of scientific experts of data collected during the first phase of dredging. After the review, improvements were made to the project design to increase productivity and reduce the resuspension of dredged sediment. In December 2010, General Electric agreed to conduct and pay for the second phase of the cleanup. During the second phase, General Electric removed approximately 2.5 million cubic yards of sediment. In all, over six seasons of dredging, approximately 2.75 million cubic yards of contaminated sediment was removed from the river bottom.
  7. What happened to the sediment after it was dredged from the river?
    Sediment removed from the river was transported by a fleet of barges to a sediment dewatering facility located on the Champlain Canal in Fort Edward. At the facility, the water was squeezed from the sediment and treated on-site to a level that meets standards for drinking water before being returned to the Champlain Canal. The dewatered sediment was then loaded onto railcars for transport to a series of permitted out-of-state landfills.
  8. Now that the dredging has been completed, GE’s 100-acre processing facility will be taken apart and decontaminated in accordance with an EPA-approved facility demobilization and restoration plan. The demobilization process will continue in 2016.
  9. What were the engineering performance standards that were developed for the dredging project?
    The Engineering performance standards are technical requirements that were developed to help ensure that the dredging of the Upper Hudson was done safely, efficiently, and in keeping with the human health and environmental protection objectives that were set forth in the February 2002 Record of Decision (ROD) for the site. The engineering performance standards were an important part of EPA's cleanup plan for the Hudson River. The ROD required the development of performance standards for dredging-related resuspension of sediments from the river bottom, residual levels of PCBs after dredging occurs, and the productivity of the dredging work.
  10. Why were quality of life performance standards needed for the dredging project?
    In response to public concerns, quality of life performance standards for air quality, noise, odor, lighting, and navigation were developed by EPA to minimize the impacts of the Hudson River cleanup on local communities.
  11. What is a Natural Resource Damages Claim?
    A Natural Resource Damage Claim seeks financial compensation for damages done by a polluter to a natural resource (such as a river). It is completely separate from EPA's remedial action. Certain agencies are given the title of Natural Resource Trustee under the Superfund law and are empowered to pursue Natural Resource Damage Claims.
  12. Who are the Trustees of the Hudson River?
    The Trustees are the following agencies or entities: the State of New York, the U.S. Department of Commerce, represented by the National Oceanic and Atmospheric Administration (NOAA), and the U.S. Department of the Interior, represented by the U.S. Fish and Wildlife Service. The EPA is not a Trustee.


FAQs About PCB Health Risk

1. What do other Agencies say about cancer and PCBs?
EPA's concern regarding the carcinogenicity of PCBs (the ability of PCBs to cause cancer) is shared by other agencies.  The International Agency for Research on Cancer (IARC) Exit EPA disclaimerhas declared PCBs to be a probable carcinogen in humans based on sufficient evidence in animals and limited evidence in humans. IARC was established in 1965 by the World Health Organization to coordinate and conduct research on the causes of human cancer, and to develop scientific strategies for cancer control. In addition, the National Toxicology Program Exit EPA disclaimer, a part of the National Institutes of Environmental Health Science (NIEHS), has concluded that PCBs are reasonably anticipated to be carcinogenic in humans based on sufficient evidence in animals. The National Institute for Occupational Safety and Health (NIOSH) Exit EPA disclaimerhas determined that PCBs are a potential occupational carcinogen.

2.How is the toxicity of PCBs determined?
To evaluate the potential toxicity of chemicals and the levels associated with the toxicity, EPA uses data from human epidemiological studies, laboratory animal toxicity studies and supporting information that may include structure activity analysis or tests on cells.

  • Epidemiology is the study of the causes of disease. One type of human epidemiological study looks at people who have been exposed to the chemical over a long period of time.   These studies evaluate the occurrence of disease in the exposed population with the occurrence of disease in a non-exposed population. PCB epidemiology includes studies of workers exposed in factories that manufactured capacitors and people exposed by eating contaminated fish.
    The advantage of human epidemiological studies in determining human health risk assessment is obvious since we are concerned with risk to humans. The disadvantages include the difficulties in determining exposures that may have occurred over 30 years ago (based on known cancer lag times), finding individuals who may have moved over this long time period, the potential for populations to be exposed to other chemicals in addition to PCBs, and the fact that exposures may be limited to healthy workers while children, pregnant women and others in the general population may be of special concern to EPA. Epidemiological evidence provides important information that can be refined in laboratory experiments where animal exposures can be controlled.

    Animal toxicity studies are primarily conducted on mice, rats, and to a lesser extent in monkeys. These species share a similar evolutionary history to humans. The studies are conducted with appropriate animal safeguards including prior approval by institutional review boards on animal experimentation. Animal toxicity studies are designed to expose groups of laboratory-bred animals to:
        1. different levels of PCBs,
        2. for varying portions of the animal's lifetime, and
        3. through different routes of exposure (breathing, eating, etc.).

    These experiments provide information necessary to help determine short or longer term effects on the body, specific organ systems and biochemical processes (i.e., enzyme levels). The advantage of these studies is that the conditions of dose and exposure can be controlled and the specific effects of the PCBs evaluated. The disadvantage is that animals are not the primary species of concern for human toxicity. However, the value of animal studies has been well established.

    3.How does EPA evaluate PCB toxicity information?
    EPA scientists evaluate data from published human epidemiological and animal toxicity studies. The main questions are:

      1. Do PCBs have the potential to cause cancer in humans?
      2. And if so, at what level?
      3. What other effects can PCBs cause in the body?

    Through the Integrated Risk Information System (IRIS) process, EPA scientists evaluate the available scientific literature and develop a chemical file summarizing the available information and EPA's conclusions about the health effects of PCBs. The IRIS PCB files describe the non-cancer and potential cancer effects. These documents are reviewed by EPA scientists and scientists outside the Agency (external peer-reviewers).

    As new information becomes available, EPA may re-evaluate the toxicity data to determine if a reassessment of health effects may be necessary. 

    4.Do PCBs cause cancer?
    EPA evaluates the ability of a chemical to cause cancer based on the weight of evidence of human epidemiological and animal toxicity studies. EPA also develops risk factors that indicate the relative potency of the chemical (the ability of a given quantity or dose to cause cancer).

    Weight of Evidence: PCBs are classified as probable human carcinogens or likely to be carcinogenic in humans. As described in the IRIS file, the basis for this determination is a 1996 study in rats (sponsored by General Electric; reviewed by EPA and external peer reviewers) that found increased numbers of liver tumors in female rats exposed to Aroclors 1260, 1254, 1242 and 1016 and in male rats exposed to Aroclor 1260.  These mixtures contain overlapping groups of congeners that, together span the range of congeners most often found in environmental mixtures. The findings of the 1996 GE study strengthened earlier studies which also demonstrated carcinogenicity in rats. Several epidemiological studies on human populations are being updated.  EPA's evaluation of human epidemiological studies as summarized in IRIS identified limitations including the small number of individuals studied, short follow-up periods and confounding from exposures to other potential carcinogens. As a result, current human epidemiological evidence is inadequate to classify PCBs as known human carcinogens, but is suggestive that PCBs may cause cancer in humans.

    Risk Factors: To quantify the potential for PCBs to cause cancer, EPA developed three cancer slope factors based on the 1996 GE rat study. The different cancer slope factors deal with different routes of exposure. A cancer slope factor is an upperbound estimate of excess lifetime cancer risks per unit dose or exposure to a carcinogen. It is presented in risk per (mg/kg)/day. The highest slope factor is for ingestion (i.e., food chain) exposure. The Cancer Slope Factor Chart provides a list of the cancer slope factors for ingestion, inhalation and dermal exposure to PCBs in units of milligrams of material ingested/bodyweight in kilograms per day.

    5.How are non-cancer health effects evaluated?
    EPA evaluates all animal studies of non-cancer health effects to identify the study (critical study) that is most representative of human PCB exposure and that meets rigid scientific criteria. The analysis identified the level where there were no observed adverse effects. Based on the literature, the Agency identified the critical studies for Aroclor 1254 and Aroclor 1016, described below.

    Aroclor 1254: The critical study identified was a study of rhesus monkeys conducted by Dr. Arnold and others in 1994. The monkeys were exposed to varying doses of PCBs ingested in gelatin capsules for a period of five years. The critical effects identified were suppression of the immune system, inflammation of the Meibomian gland (a small gland in the inner portion of the eye), and distorted growth of fingernails and toenails. EPA developed a Reference Dose, the level below which adverse effects on the humans are not expected. EPA took the Lowest Observed Adverse Effect Level (LOAEL) found in the monkey study and divided it by a factor of 300 to protect sensitive humans. 
    The factor of 300 (reduction from animal to human exposure) was based on an evaluation of toxicity studies and the application of established factors for extrapolating from animals to humans. The Rhesus monkey has similar (to human) toxic responses and metabolism of PCBs in addition to sharing a general physiological similarity. Rhesus monkey studies predicted other changes noted in human studies such as chloracne, hepatic (liver) changes and effects on reproductive function. Where a No Observed Adverse Effect Level (NOAEL) cannot be identified or where a less than lifetime animal study was conducted, individual factors of 10 are applied in all studies in extrapolating from animals to humans to protect sensitive humans (including children). These factors of 10 may be reduced to 3 by EPA scientists, based on the available information. For example, with Arochlor 1254, a full factor of 10 was used to protect sensitive humans. The other factors were reduced to approximately 3 based on the availability of studies in Rhesus monkeys. The factors are then multiplied together and rounded to the nearest integer, resulting in the factor of 300 for Aroclor 1254.    
    Aroclor 1016: The critical studies identified were monkey reproductive studies conducted by Drs. Barsotti and VanMiller in 1994, Dr. Levin and others in 1988 and Dr. Schantz and others in 1989 and 1991. These are a series of reports that evaluated toxicity around birth and long-term neurobehavioral effects of Aroclor 1016 in the same groups of infant monkeys. In the studies, groups of eight female monkeys were exposed through diet seven months before delivery and four months immediately following delivery. The critical effect identified at the No Observed Adverse Effect Level (NOAEL) was reduced birth weights. In developing the Reference Dose, the NOAEL was divided by a factor of 100 to protect sensitive humans, including children. 

    A procedure similar to that described (above) for Aroclor 1254 was applied to extrapolate from Rhesus monkeys to humans. The uncertainty factor for Aroclor 1016 was 100. Based on the monkey reproductive studies, a full factor of 10 was not deemed appropriate since infants exposed through the placenta represent a sensitive subpopulation. An additional factor of 3 was applied since information on male reproductive effects and second generation studies were not available. The other factors for less than chronic exposure, and from animals to humans, was the same for both Aroclors 1254 and 1016. These factors were multiplied together and rounded, yielding a factor of 100.   

    6. What is risk assessment?
    Risk assessment is a process used by EPA to determine the potential health effects in humans (cancer and non-cancer) associated with exposure to chemicals. Risk assessment is used throughout EPA to evaluate chemical toxicity and potential health effects in humans.

    Under Superfund law (Comprehensive Environmental Response, Compensation and Liability Act -- CERCLA), EPA is required to conduct a baseline risk assessment that evaluates current and future risks at all Superfund sites.  Risk assessment was defined in 1983 by the U.S. National Academy of Sciences as involving one or more of the following four steps:

      1. Hazard identification - Do PCBs have the potential to cause cancer? What other health effects (such as changes in the immune system, reduced birth weight, etc.) are caused by PCBs? 
      2. Dose response - What amount of PCBs in the human body causes these effects?
      3. Exposure assessment - How people are exposed to PCBs (i.e., eating, drinking, breathing, skin contact) and at what levels.
      4. Risk characterization - The answers to the above three questions are used to calculate what risk an individual having significant exposure runs of developing cancer or experiencing a non-cancer effect. The uncertainties connected with answering the three questions are also described. The risk characterization is then used by risk managers in their decision making process.
    7 .How is exposure to PCBs evaluated?
    To evaluate exposure, the Agency looks at the concentration of PCBs in fish, water, soil, sediment and air; the frequency with which an individual may come into contact with the media; the length of time the individual may be exposed, and the bodyweight of the individual. For carcinogens, the exposure is averaged over a lifetime.  For non-carcinogenic effects, exposure is averaged over the portion of the lifetime during which the exposure occurs. Depending on the data available, separate analyses can be developed for children, adults and lifetime exposure.
    The data used in the assessment may be based on actual concentrations in the fish, soil, etc.  It may also be based on modeling that projects future concentrations. Information on exposure activities may be developed using national or local surveys of activities (i.e., fish consumption). The result of the exposure evaluation is a calculated level of dose for each route of exposure.

    8. How are risks calculated?
    Cancer risk calculates the increased probability of an individual developing cancer based on a number of assumptions concerning PCB exposure. The risks are calculated by multiplying the dose (from exposure) by the toxicity (cancer slope factor -- see above).  The individual risks for each pathway are added together to reflect the total cancer risk. The risk characterization presents the calculated risks along with discussion of uncertainties.

    9. How are hazards calculated?
    Non-cancer hazards are calculated by comparing the dose (from exposure) with the Reference Dose. Exceeding the Reference Dose results in an increased potential of adverse health effects. The individual hazards from each pathway are added together to reflect the total hazard.  The uncertainties associated with the exposure assumptions and Reference Doses are detailed in the risk characterization.

    10. How is risk assessment used by risk managers?
    During the Superfund process, risk assessments are performed as part of the Remedial Investigation of a site. The results from the risk assessment (cancer risk and non-cancer hazards) are used by Superfund risk managers to determine whether there is a need to take remedial action. The results of the risk assessment are documented in the Remedial Investigation Report and are made available to the community.

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