In addition to the amounts discharged directly into the river, over 90,000 pounds of PCBs leaked into the fractured bedrock under the Hudson Falls plant and into a clay-lined area of sandy soil under the Fort Edward plant. The residue at the Fort Edward plant is well-contained; however, PCBs from the Hudson Falls site continue to leak into the river from the reservoir in the bedrock to this day. Both sites are actively being remediated by General Electric under a consent order with the NYS DEC. The remediation of these sites is referred to as “source control.”

Because PCBs are hydrophobic and do not easily dissolve in the water column, they preferentially adhere to particles of silt, sand or decaying organic debris moving downstream and quickly settle into the sediments at the bottom of the river. Records from water treatment facilities in the seven municipalities who take drinking water from the Hudson River consistently report “non-detect” for six representative congeners of PCBs, including at Waterford in the Upper Hudson. Drinking water is therefore not considered to be a significant route of exposure to humans. In 1986 U.S. Fish and Wildlife Service established a maximum allowable threshold level for affecting aquatic life at 14 parts per trillion.

PCBs are persistent organic compounds that move throughout the environment and bioaccumulate to very elevated concentrations in species higher up the food chain. Fish consumption is the major route of exposure to humans. However, PCBs also evaporate from exposed sediments and can become airborne. While inhalation is a less significant route of exposure, it is an involuntary one. PCBs are carried by atmospheric transport around the globe. PCBs matching the congener pattern of those from the GE plants in Fort Edward and Hudson Falls have been found as far away as the Canadian Arctic, where Inuit people have surprisingly elevated serum levels. Alternately, Richard Bopp has documented that as much as two-thirds of the PCBs deposited in NY/NJ harbor sediments in the mainstem of the Hudson originated from the Upper Hudson sites, washed downstream by river currents from 1970 to 1989. This amount has more recently been diluted from local contributions (Bopp et al. 1998). Richard Bopp also has shown that PCBs are generally found in the top 12 inches of sediment core samples, with a peak at 9 inches. The same layers that contain PCBs have also been shown to contain dioxins and furans, as well as heavy metals, which originated primarily from the Hercules pigment manufacturing facility currently owned by Ciba-Geigy upriver of the GE plant sites.

Because of the geomorphology of the river, a disproportionate amount of the approximately 500 lbs. per year of PCBs that are estimated to wash over the Federal Dam at Troy settle out between Kingston and Poughkeepsie, especially along Esopus Meadows. These sediments have the advantage of being diluted by large amounts of relatively-uncontaminated sediments from the Batten Kill, Mohawk River and other tributaries; however, despite low concentrations, the Mid-Hudson area of the river receives relatively high volumes of PCB-containing sediments (Bopp et al. 1998).

Historical Background

With the passage of the Clean Water Act in 1972, General Electric’s allowable discharge of PCBs was restricted to limits established in National Pollution Discharge Elimination System (NPDES) permits; however, GE frequently violated these limits and was fined for doing so.¹

In 1973, the Fort Edward Dam, located just south of the Fort Edward plant site, was removed by Niagara Mohawk Power Company at the recommendation of the Army Corps of Engineers and the NYS DEC. Prior to its removal, witnesses recall the sediment behind the dam was so deep that in a dry season that it was only a foot below the river water line – up to 18 feet deep. When the dam was removed a huge slug of PCB-containing sediment moved downstream, settling out primarily in the Thompson Island Pool and other “hot spots” along the upper Hudson, from Rogers Island to just north of Albany. In 1976, 1978 and 1982, NYS DEC surveyed these areas of relatively low flow where fine grained sediments contain high concentrations of PCBs, and defined hot spots to be in the range of 50 ppm or greater.

In 1974 and 1975, the New York State Department of Transportation (NYS DOT) dredged approximately 634,000 cubic yards of contaminated sediment and debris for navigational purposes and disposed of it in upland sites in Moreau. More contaminated sediments were removed in 1978 and 1979 by NYS DOT, but no further dredging has been done of the Upper Hudson River since that time.

Health advisories warning against fish consumption were issued by NYS DOH in 1975, and in 1976 fishing was banned in the Upper Hudson from Fort Edward to Troy, and the striped bass and other commercial fisheries were closed throughout the river.

1984 Record of Decision:

The 200 mile stretch of the Hudson River from Hudson Falls to the Battery in Manhattan was placed on the EPA’s Superfund National Priority List in 1983, making this one of the largest Superfund sites in the nation. In 1984 the EPA issued a Superfund Record of Decision (ROD) which called for an “interim action” of capping exposed contaminated sediments on the river’s shoreline, and recommended “no action” on contaminated river bottom sediments pending further review. This interim “no action” decision was based in part on findings that PCB levels in fish were declining towards the US Food and Drug Administration’s (US FDA’s) tolerance level of 5 parts per million (ppm) for PCBs in fish flesh, and that fishing restrictions would provide a measure of public health protection until PCBs in fish declined to “safe” levels. However, EPA used an outdated FDA tolerance level in this decision. The EPA ROD was signed on September 25, 1984. The new FDA tolerance level of 2 ppm went into effect August 20, 1984. While it is true that PCB levels have declined over the years, the average PCB concentrations for all species are still 644 ppm lipid-based PCBs (lpcb) in the Upper Hudson and 84 lpcb in the Lower Hudson, with levels as high as 3285 lpcb and 429 lpcb in Upper and Lower Hudson River fish respectively. In recent years contamination has generally stabilized at these levels.

In 1989, in response to a required five-year review, EPA announced its decision to reassess the interim No Action decision.

Allen Mill Event: In September 1991, routine sampling below the Remnant Deposits revealed increases in water column PCB concentrations. These increases are attributed to the failure of a wooden gate within the abandoned Allen Mill located on the banks of the Hudson River at the GE Hudson Falls plant site.

In 1992, EPA collected new data and commissioned modeling studies of human health and ecological risk. In 1998, EPA released a Feasibility Study Scope of Work and determined that, despite findings of statistically significant losses of PCBs from sediment to water column, there would be no interim remediation until the reassessment was complete.

On December 12, 2000, after a one year extension, EPA released its Proposed Remediation Plan for the Hudson River PCBs Superfund site – 23 years after PCBs were banned.

EPA’s proposed plan reevaluates four technologies, and selects a “preferred remedy” from five alternatives, in three sections of the Upper Hudson:

• Alternative 1: No Action without source control
• Alternative 2: Monitored Natural Attenuation (MNA) with current and future source control efforts at GE’s Hudson Falls and Fort Edward plant sites
• Alternative 3: Capping with source control, followed by MNA

  Removal with source control, followed by MNA:

• Alternative 4: REM 3/10/Select
• Alternative 5: REM 0/0/3

Because of persistent remobilization of toxic PCBs from the Upper Hudson sediments to the environment and the subsequent risk to human health, the December 2000 Proposed Plan of EPA’s Hudson River Reassessment Report now recommends removal.

REM 3/10/select refers to removing sediments containing 3 g/m² of PCBs or more in River Section 1; 10 g/m² of PCBs in River Section 2; and selected hot spots in River Section 3 containing 50 ppm or approximately 16.5 g/m². This is EPA’s preferred remedy and would reduce the amount of PCBs washed over the Federal Dam at Troy by at least 40%.

Likewise, REM 0/0/3 refers to full section removal in Sections 1 and 2 and removing sediments containing 10 g/m² of PCBs in River Section 3. Of the five proposed alternatives, this is the most rigorous, the most protective of human health, and would reduce PCBs remobilization by at least 53%.

Following a four month period of public comment and an additional four months to review the comments they receive, in August 2001 EPA is due to release its final Record of Decision (ROD). The ROD will initiate a three-year remedial design phase during which the details of the remediation will be spelled out, a request for proposals solicited and a contractor selected to do the remediation. Depending on which alternative is selected, the actual remediation is estimated to take five to seven years.

Legality of General Electric’s PCB Dumping

For over fifty years, General Electric Company (GE) has been discharging or leaking PCBs from below plant sites at Hudson Falls or Fort Edward into the Hudson River. While full retroactive liability for the PCB contamination in the Hudson River has already been established for GE under Federal Superfund Law, the question of the legality of these discharges often needs clarity.

There has not been a single day on which all of these discharges and leaks have complied fully with federal and state law concerning water quality. The only discharges or leaks that are legal are those that have reached the Hudson River in compliance with terms of a permit, and these comprise under 6% of the total amount of the PCBs released into the Hudson River over the past half century.

Federal Refuse Act

It can be argued that General Electric violated the Refuse Act (33 USC 407, which is section 13 of the Rivers and Harbors Act of 1899) from the time PCB discharges began into the Hudson River from the Hudson Falls facility in 1947 at least until 1973, when the General Electric Co. filed a valid application for a discharge permit.²

Several federal court cases established violations of the Refuse Act for discharges of fuel oil into navigable waters in the decades prior to 1966 when the US Supreme Court decisively found discharges of chemical pollutants constituted violations of the Refuse Act. While GE wasn’t prosecuted for their violations of this Act, these discharges were illegal.

State Law

GE’s PCB contamination of the Hudson River and its human and ecological inhabitants has violated state water quality standards from the time these standards were adopted in 1965 until the present day (NYS DEC, February 9, 1976). ³

While General Electric first submitted a valid permit to discharge PCBs into the river in 1973, the percentage of PCBs that have reached the Hudson pursuant to permits is a very small portion (at least under 6% and as low as 1.1%) of the total PCBs discharged to the Hudson River from 1947 to the present day (US EPA, 1975; NYS DEC, 1985; NYS DEC, 1993; NYS DEC, 1999).

Additionally, GE has caused at least 129 violations of its SPDES permit, not including unpermitted seeps to the river from fractured bedrock below the Hudson Falls plant (Butler and Lippes, 1984; Mezey, 1984; Huchro, 85; Herwig, 1993). ⁴

PCBs and Human Health

The primary goal of the Environmental Protection Agency’s Hudson River remediation project is to protect human health. EPA has presented compelling evidence that remediation of PCBs from the Hudson will have a positive impact on the health of residents of the Hudson Valley (EPA 2000c), and other studies have shown convincingly that PCBs represent a public health threat (for a recent review, see Carpenter, 1998).

In February 2001, Clearwater held a colloquium entitled “PCB Contamination in the Hudson Valley: A Victimless Crime?” at which several of the top researchers on PCBs described their work and recent advances in understanding of the mechanisms of PCB toxicity. The presenters were David Carpenter, M.D.; Larry Robertson, Ph.D., M.P.H.; John Vena, Ph.D.; Kathleen Arcaro, Ph.D.; Susan Schantz, Ph.D.; and Mary Wolff, Ph.D. The conference provided incontrovertible evidence that PCBs are highly toxic and carcinogenic. Abstracts of the presentations are attached as Appendix B, and a videotape of the entire conference is being submitted separately as Appendix E.

Acute and Chronic Effects

The International Agency for Research on Cancer and the Environmental Protection Agency classify PCBs as a probable human carcinogen. The National Toxicology Program has concluded that PCBs are reasonably likely to cause cancer in humans. The National Institute for Occupational Safety and Health has determined that PCBs are a potential occupational carcinogen.

It is important not to be misled by the apparent uncertainty of the term “probable.” One of the most studied carcinogens in tobacco smoke, benzo(a)pyrene, is also classified as a “probable” (B2) carcinogen (EPA 1992). Because people are exposed to such a large variety of chemicals in combination each day, and because cancer is so prevalent even without known carcinogenic exposure, it is simply not possible in most cases to definitively conclude that a specific chemical has caused a specific cancer. Scientifically rigorous double-blind designed studies on human subjects are not ethically feasible. Except for a very few chemicals with extremely well-known effects, most carcinogens are therefore classified as “probable” when there is conclusive proof of carcinogenicity in animal tests, and when there is substantial evidence from human studies that indicates the likelihood of human carcinogenicity.

Studies of PCBs in humans have found increased rates of melanomas, liver cancer, gall bladder cancer, biliary tract cancer, gastrointestinal tract cancer, and brain cancer (ATSDR 2000; Johnson et al. 1999). PCBs are known to cause a variety of types of cancer in rats, mice, and other study animals (Johnson et al. 1999).

2. Acute toxic effects

People exposed directly to high levels of PCBs, either via the skin, by food consumption, or in the air, have experienced irritation of the nose and lungs, skin irritations such as acne (chloracne) and rashes, and eye problems.

Clearwater believes that General Electric is sequestering the health records of 60-100 former capacitor workers who exhibited acute toxic effects. These workers are presumed to be candidates for long-term health monitoring. Clearwater urges EPA to acquire the unredacted health records of these people to augment the record on PCBs and human health effects (see Appendix F.)

3. PCBs cause developmental effects

Perhaps the most important health threat of PCBs is the potential for developmental effects in children exposed prenatally even at low levels. Women exposed to PCBs before or during pregnancy can give birth to children with significant neurological and motor control problems, including lowered IQ and poor short-term memory.

A group of children in Michigan whose mothers had been exposed to PCBs were found to have decreased birth weight and head size, lowered performance on standardized memory, psychomotor and behavioral tests, and lowered IQ. These effects lasted through at least 7 years (Jacobson and Jacobson 1996). Other studies have shown decreased head size and diminished performance on standardized behavioral tests (Rylander et al. 1998; Stewart et al. 2000). A group of women occupationally exposed to PCBs in upstate New York had shorter pregnancies and gave birth to children with lower birth weight (Johnson et al. 1999). Another study, of the children of women who ate contaminated Lake Ontario fish, found significant performance impairments on a standardized behavioral assessment test (Stewart et al. 2000).

Exposure of one (dioxin-like) form of PCB to rats resulted in retarded growth, delayed puberty, decreased sperm counts, and genital malformations (Gray et al. 1995). In other studies, exposure of PCBs to rats in utero led to behavioral and psychomotor effects that lasted into adulthood (Weinand-Harer et al. 1997).

4. PCBs disrupt hormone function

Lower-chlorinated PCBs can mimic the body’s natural hormones, especially estrogen. For example, women who consumed PCB-contaminated fish from Lake Ontario were found to have shortened menstrual cycles (Mendola et al. 1997). PCBs are also thought to play a role in reduced sperm counts, altered sex organs, premature puberty, and changed sex ratios of children (Vena in Clearwater 2001). More highly-chlorinated PCBs act like dioxins in altering the metabolism of sex steroids in the body, changing the normal levels of estrogens and testosterone (Arcaro et al. 1999). PCBs tend to change in the body and in the environment from more highly-chlorinated to lower-chlorinated forms, increasing their estrogenic effects.

5. Immune system and thyroid effects

In a study of adolescent Mohawk males in New York State, PCBs were shown to upset the balance of thyroid hormones, which may affect growth as well as intellectual and behavioral development (Schell et al. 2000).

Like dioxin, PCBs bind to receptors that control immune system function, disturbing the amounts of some immune system elements like lymphocytes and T cells (Summarized in Carpenter 1998). In a study of Dutch children, PCB levels were tied to an increased prevalence of ear infections and chickenpox and with lowered immune system function, and thus greater susceptibility to disease (Weisglas-Kuperus et al. 2000).

Bioaccumulation

Once PCBs enter a person’s (or animal’s) body, they tend to be absorbed into fatty tissue and remain there. Unlike water-soluble chemicals, they are not excreted, so the body accumulates PCBs over years. This means that PCBs also accumulate via the food chain: a small fish may absorb PCBs in water or by eating benthic organisms or plankton, and these PCBs are stored in its body fat. When a larger fish eats the small fish, it also eats and absorbs all the PCBs that have built up in the small fish. In this way, larger fish and animals can build up a highly concentrated store of PCBs; the top predators may have a concentration of toxins 25 million times that in sediment or water (Colborn et al. 1996). Some types of PCBs may partially degrade while stored in the body, but this process can take many years.

In the same way, PCBs accumulate in women and pass on to their infants through breast milk. This accumulation means that nursing infants ingest PCB levels as much as 50 times higher than the levels in fish and other foods consumed by their mothers (Korrick and Altshul 1998).

PCBs have been found all over the world, including significant amounts in the Arctic and Antarctic, far from any sources (Dewailly et al. 1993). It is thought that PCBs spread through the air, after evaporating from contaminated water and sediments, as well as through the water.

Routes of Exposure

The most common route of exposure to PCBs is from eating contaminated fish. The EPA estimates an increased cancer risk as high as 1 in 1000 for people eating fish from the Upper Hudson River—a thousand times higher than the EPA’s goal for protection (EPA 2000). Calculation of a non-cancer Hazard Index shows that fish consumers take in PCBs at rates ranging from 65 (for adult) to over 100 (for children) times safe levels. The EPA has concluded that consumption of contaminated fish is the only direct pathway that presents a current health threat for humans (for a comparison of risks, see Tables 1-9 and 1-10 in EPA 2000).

Municipalities that use the Hudson River as a drinking water source carefully monitor the water for PCBs, and there are no detectable levels in the water supplies (Poughkeepsie 2001). Potential resuspension of PCBs during dredging has been a concern for these communities. However, the maximum estimated amounts of resuspension are approximately 6 kg/year, which pales in comparison to the estimated 214 kg/year currently being transferred to the water column from contaminated sediment (EPA 2000). With proper precautions, resuspension should not be an issue for towns taking drinking water from the Hudson.

Although small amounts of PCBs can enter the body from swimming in highly contaminated water, this is unlikely to be significant except in the most extreme cases (EPA 2000).

Inhalation

Inhalation has been ruled out as an important PCB pathway in the EPA documents, due to insufficient research data and its apparently minor importance compared with fish consumption. Unfortunately, due to lack of available evidence, no standards have been established for the inhalation of PCBs. Although studies were made of the toxicity of PCB vapors as early as 1956 (Treon et al. 1956), this pathway has been generally ignored in favor of oral and, to a lesser extent, dermal routes of exposure.

Air near a contaminated site may be polluted by PCBs. By one estimate, residents of the Hudson Valley may inhale as many PCBs as they would get by eating one contaminated fish per year (Dr. David Carpenter, personal communication). Although inhalation is generally not currently thought to be a high level route, it is important as an involuntary route of exposure to which all Hudson Valley residents are subject. PCBs that enter the body through the lungs are not metabolized as ingested PCBs are. Instead, they mix with the bloodstream and become directly available to brain tissue.

The New York State Department of Health is currently conducting a study that examines airborne and fish consumption pathways of exposure in residential Fort Edward populations. The results of this study, called the Hudson River Communities Project, will not be available until at least 2002, but correlation of PCB body burden or health effects with airborne exposure could provide useful information about the current status of volatilization as a health risk.

In addition to volatilization from the river surface (see “Volatilization as an Input of PCBs into the Ecosystem,” below), contaminated sediment on the banks could be a significant source of airborne PCBs. Remnant deposits on the banks of the Hudson in Fort Edward, containing at least 46,000 pounds of PCBs, were capped in 1991 (EPA 1984). Continuous erosion of these deposits could lead to failure of the caps and volatilization of PCBs, although little data is currently available about the viability of the capped remnants or their potential as a source of airborne PCB exposure.

It is possible to calculate the importance of inhalation as a fraction of total PCB body burden, and this method has been used by at least one paper. Currado and Harrard (1998) calculated a daily intake from a combination of indoor and outdoor background levels of 23–590 ng of PCB per person. The mean exposure, 110 ng/day, amounts to about a third of the amount consumed in food (340 ng/person/day, a U.K. average), and about a tenth of the ATSDR’s chronic oral Minimal Risk Level for a 50 kg person (1000 ng/person/day). The highest level, 590 ng/person/day, is more than half the ATSDR chronic oral MRL. These numbers represent an upper bound, since 100% absorption in the lungs is assumed. It is sufficient to demonstrate, however, that even at background levels inhalation may be a significant contribution to PCB body burdens.

Currado and Harrard’s model assumes that PCB body burden derived from inhalation relates linearly with a combination of indoor and outdoor concentrations. Since indoor air generally has much higher levels of PCBs, the vast majority of the contribution is from home or workplace exposure. Two studies have found no general correlation of indoor and outdoor PCB air concentrations, indicating that indoor levels are primarily driven by indoor sources (for example, old fluorescent light ballasts).

We will discuss the potential for volatilization to increase during remediation below (see “Volatilization”); we would like to note here that, while inhalation can be a significant source of PCB body burden for non-fish-consumers, it generally falls far below dangerous levels. In addition, we can tentatively conclude that the greatest contribution to inhalation is indoor, rather than outdoor, sources of PCBs.

Fish Consumption

Fish consumption is the major route of exposure for humans and fish-eating wildlife. While GE’s PCBs have contaminated Hudson River fish since the Fort Edward plant went on-line in 1946, only since 1975 has there been public awareness of the problem with PCB contamination in Hudson River recreational and commercial fisheries. ⁵ Today, the recreational fisheries are limited to catch-and-release only or recommended consumption limits as determined by the New York State Department of Environmental Conservation (NYS DEC) and the New York State Department of Health (NYS DOH). Currently, the NYS DOH holds primary responsibility for communicating to the public the risks associated with consuming Hudson River fish (NYS DOH, 1999).

For the estuarine portion of the Hudson, the NYS DOH 2000-2001 Health Advisories for Chemicals in Game and Sportfish recommend that women of childbearing age and children under age 15 eat no fish from this entire section of the Hudson, and that males consume no more than one (1/2 lb.) fish meal per week (below Catskill) or month (Albany/Troy to Catskill), depending on fish species and location (NYS DOH, 2001).

Angler surveys conducted by Hudson River Sloop Clearwater, Inc. in 1991 (Barclay, 1993) and the New York State Department of Health in 1996 (NYS DOH, 1999) have found that many anglers are aware of the advisories for eating fish from the River. However, Clearwater’s angler survey found the same number of anglers unaware of the advisories as aware, and both surveys found that anglers eat and share their catch with others to eat, including women of childbearing age and children, whether they are aware of the advisories or not (Barclay, 1993; NYS DOH, 1999). These surveys also revealed that none of the survey respondents reported knowledge of the “eat none” advisory for women of childbearing age and children (Barclay, 1993) and that some of the fish caught in the river are illegally sold (NYS DOH, 1999).

Clearwater’s angler survey also found that fish consumption increases with age and that low-income, minority, and immigrant anglers whose diet is traditionally high in fish and who rely upon local fish as an inexpensive food source are most likely to eat their catch (Barclay, 1993; Belton, et al., 1986; Burger, 1998; Burger, et al., 1999; Pflugh, et al., 1999; May, et al., 1996). Knowledge of fish consumption habits among non-English speaking anglers that fish in the Lower Hudson River is very limited and anecdotal, though it is known that fish is an important source of inexpensive food among non-English speaking ethnic populations. Clearwater’s angler survey found higher fish consumption rates specifically among low income African-American and Latino populations (Barclay, 1993). The higher incidence of fish consumption among low-income anglers, and the greater likelihood that they are fishing primarily for food indicates that some part of the fish consumption on the Hudson River derives from subsistence rather than purely recreational fishing.

The National Academy of Sciences has found that individuals who engage in recreational or subsistence fishing face a higher risk of experiencing negative health effects than do members of the general public (NAS, 1991). More specifically, a study of PCB body burdens in Hudson River anglers conducted in 1999 observed that the body burdens of persistent environmental pollutants (including PCBs) generally are greater in Hudson River anglers who frequently consume locally caught fish and crabs than among similar individuals who rarely consume these foods (Golden et al., 1999). The same study also found positive exposure/response relationships between frequency of local fish and crab consumption and body burdens of persistent pollutants (including PCBs)(Golden et al., 1999). Still, there is very little available data on PCB body burdens for Hudson River anglers and others who eat Hudson River fish (Golden et al., 1999). This lack of data makes it difficult to accurately assess the range of human exposure to PCBs through fish consumption in the Lower Hudson and equally compromises our ability to examine the relative merits of various reductions in PCB levels in Lower Hudson River fish.

There is evidence of higher consumption and sharing rates for Hudson River fish meals and minimal awareness of the PCB contamination in fish from Hudson River waters among women, ethnic minorities, and low-income groups in the lower Hudson region (Barclay, 1993; NYS DOH, 1999); however, characterization of awareness and compliance with NYS DOH consumption advisories among women, ethnic minorities, and low-income groups for the Hudson River, particularly in metropolitan New York City, Westchester, Rockland and Putnam counties, has received limited treatment in angler surveys.

In the Lower Hudson River, anglers prefer to catch and eat species that rank among the highest in PCB levels, including striped bass, white catfish, white perch, American eel, and white suckers (NYS DOH, 1999). Many populations are not only unaware of proper techniques for reducing exposure to contaminants when cooking and preparing fish meals but also cook and eat the whole fish, maximizing exposure for their families, friends and selves (NYS DOH, 1999). On a “good” fishing day in the Lower Hudson, anglers will bring home a bucket of fish to feed the family or to freeze for later consumption.

Based on this information about fish consumption patterns and preferences, it is possible to conclude that PCBs in river sediments represent an important reservoir of aquatic, and thus ultimately, of human exposure (Golden et al., 1999). A significant environmental justice component is suggested as low-income, subsistence anglers face higher levels of exposure to chemical contamination through the consumption of Lower Hudson River fish. In the absence of thorough remediation of PCBs from identified sources in Upper Hudson River hot spots, human consumption of Hudson River fish will continue to expose anglers, their families and friends, and other people who consume fish, to PCBs.

Applicability of the Reasonable Maximum Exposure Scenario

One criticism of the EPA’s Proposed Remedy that has been raised by opponents of the cleanup is that the RME is unreasonable. It has been suggested that the amount of fish eaten in the RME scenario (one half-pound fish meal per week) is unrealistic, and that the maximum allowable levels of PCBs in fish are too low, particularly since the EPA target levels are well below the current standards set by the Food and Drug Administration. In this section we will try to determine whether the RME scenario outlined in the Proposed Remedy is reasonable. It is important to note that these numbers apply only to fish consumption, and that other pathways, notably inhalation, may exist (see “Volatilization as an Input of PCBs into the Ecosystem,” below).

The Food and Drug Administration has set a tolerance level for PCBs in commercially caught fish of 2 mg/kg (EPA 2000 FS 2-6). This is based on a “market basket” approach, in which consumers purchase a variety of fish from a variety of sources, only occasionally eating a contaminated fish (McCabe and Tomchuk, EPA, personal communication).

This approach, however, is not protective of subsistence or recreational anglers who frequently consume fish from a single source, and who are likely to consume fish targeted by health advisories (see “Fish Consumption,” above). The “market basket” approach is insufficient in these cases, as we can see by an estimate of PCB intake.

The Agency for Toxic Substances and Disease Registry has recently released an update for the Toxicological Profile for Polychlorinated Biphenyls (ATSDR 2000). The new Profile sets Minimal Risk Levels (MRL) for PCB consumption, but not for PCB inhalation (due to lack of research data). The MRLs are:

(ATSDR 2000)

These MRLs are based on lowest observed adverse effect levels showing non-cancerous effects (neurological and immune deficits) in tests on non-human primates.

The EPA calculates similar limits, referred to as the Reference Dose (RfD), for long-term exposure to Aroclor formulations. No RfD is obtained for total PCB. The current RfDs are:

(EPA 2000c)

These RfDs, based on developmental and immune deficits in nonhuman primates, are in close agreement with the ATSDR’s MRLs. Although most of the PCBs dumped in the Hudson were Aroclor 1242, natural dechlorination over time has altered the congener profile (EPA 2000c). EPA approximates the RfD for soil and sediment by using the Aroclor 1016 RfD, and approximates the RfD for PCBs in fish by using the Aroclor 1254 RfD, based on the similarity of the congener profiles in those two settings (EPA 2000c).

The FDA’s limit of 2 mg/kg in fish is well above EPA’s Remedial Action Objective. For subsistence angler with a body weight of 50 kg (110 lbs), eating one meal per week of fish contaminated at the FDA limit, we can roughly calculate PCB intake:

The Hazard Index, defined as the average dose divided by the reference dose (RfD), is intended to measure the risk of non-cancerous toxic effects due to consumption of xenobiotics. An HI above one indicates an increased risk. Although the EPA does not calculate an RfD for total PCB, we can use the ATSDR MRL and the RfD for Aroclor 1254 (which is most similar to the congener profile in fish) to calculate the HI for the RME:

based on Aroclor 1254:
HI = 0.0013 mg/kg-day / 0.00002 mg/kg-day = 65

based on ATSDR’s MRL for chronic exposure:
HI = 0.0013 mg/kg-day / 0.00002 mg/kg-day = 65

In this simple analysis, we are ignoring cooking loss (probably in the range of 10% to 40%, but assumed to be 0% in the RME scenario (EPA 2000c)), any in-body degradation of PCBs, and any additional sensitivity of children to PCB exposure.

We conclude that the FDA’s tolerance level for PCBs is greatly insufficient to protect the health of the RME individual. EPA’s Remedial Action Objective of 0.05 is an appropriate standard, and far more protective of human health than FDA’s tolerance level.

The Post-Remedial Situation

Dredging of PCBs from the Upper Hudson will dramatically reduce the risk to fish consumers, particularly those subsistence or recreational anglers who eat contaminated fish at or above the level of the Reasonable Maximum Exposure.

For example, the number of years required for safe fish consumption in the Upper Hudson varies greatly between different remedial scenarios:

Table 1. Years to Achieve Safe Consumption of Fish Meals:

	one per week	one per month	one every two months
No Action 6	>67 years	>67 years	>67 years
Monitored Natural Attenuation 6	>67 years	60 to >67 years	34 to >67 years
REM 3/10/Select	>67 years	35 years	20 years
REM 0/0/3	>67 years	26 years	11 years

(Adapted from EPA 2000b.)

Although no alternative provides complete coverage for the one-meal-per-week RME, the dredging alternatives provide dramatically reduced risk for fish consumers in the Upper Hudson. The more rigorous dredging alternative, REM 0/0/3, would permit Upper Hudson residents to safely consume fish on a regular basis several generations before the non-dredging alternatives.

Conclusions

Although much remains to be understood, the human health risks of PCBs have been well documented by recent research. The developmental and neurological effects, demonstrated in animal studies and reinforced by epidemiological studies in human populations, are of particular concern. For more than fifty years, the residents of the Hudson River Valley have been involuntarily subjected to an experiment in chronic exposure to PCBs. The EPA’s proposed remedy will dramatically reduce the health risks of PCB exposure to Hudson Valley residents, and particularly to subsistence and recreational anglers who are currently at great risk for PCB toxicity. Clearwater looks forward to a time when we can enjoy living and engaging in recreation in the Hudson River without compromising our, and our children’s, long-term health and well-being.

PCBs and Wildlife

The effects of PCBs on wildlife at environmentally realistic levels are actually quite well documented, and include various reproductive effects (Clark et al. 1998, Heaton et al. 1995, McCarty and Secord 1999), immunotoxicological effects (Ross et al. 1996, Sagerup et al. 2000), as well as endocrine disruption (Brouwer et al. 1999, Chiu et al. 2000). Despite the inherent difficulties in determining the specific effects of PCBs (as opposed to other organochlorine contaminants), the existing evidence of highly diverse and often quite adverse effects of PCBs on wildlife are serious enough to warrant high levels of precaution, both for wildlife and for humans.

One wildlife group that has been extensively studied in relation to the effects of PCBs is birds. Studies both in the lab and in the field have demonstrated that PCBs can have a number of adverse effects on birds, including endocrine disruption, immunotoxicity and teratogenesis, as well as reduced parental attentiveness and abnormal reproductive behavior.

One of the principal ways that PCBs can affect bird species is through embryotoxicity, since bird embryos are more sensitive than adults to PCBs' toxic effects (Barron et al. 1995). Field studies, such as Hoffman et al.'s study of black-crowned night herons, have shown PCBs to be associated with reduced embryo growth (1986). Another study found a link between delayed hatching in common terns and PCB contamination (Bosveld et al. 1995). Yet another study suggested a link between PCBs and embryo mortality in pheasants (Brunstrom and Halldin 2000).

In addition to embryotoxicological effects, a number of studies have implicated other reproductive and developmental effects of PCBs on birds, including effects on fertility, egg production, hatchling success and chick growth (Barron et al. 1995). These include one study conducted by Van den Berg et al. in 1994, which compared the breeding success of two cormorant colonies, one with high levels of PCB contamination, the other with low levels of PCB contamination. The study found that the number of hatchlings and fledglings in the highly contaminated colony was significantly reduced. Another study found that high PCB residues in bald eagle eggs collected from Lakes Michigan and Huron were associated with low reproductive rates when compared to less contaminated eggs from the same area. This study is supported by others, which have found consistently reduced nesting success in bald eagles at PCB levels above 12 µg/g (Clark 1998). Another study cites the threshold concentrations of PCBs causing reduced hatching success as ranging from 8-25 µg/g for terns, cormorants, doves, and eagles (Brunstrom and Halldin 2000). In addition, some studies have found reproduction to be affected by behavioral abnormalities presumably related to PCB contamination (Barron et al. 1995, McCarty and Secord 1999). This is probably due to the influence of PCBs on the endocrine system, which in turn regulates reproductive behavior (McCarty and Secord 1999). A recent example of this phenomenon is McCarty and Secord's 1999 study of tree swallow nesting behavior. The study assessed the quality of swallow nests built in three sites along the Hudson River, one of which was highly contaminated with PCBs, one of which was only slightly contaminated, and one of which was relatively uncontaminated. The researchers found that nest quality was significantly correlated with the level of PCB contamination (with the most contaminated site having the poorest quality nests, the moderately contaminated site having nests of intermediate quality, and the least contaminated site having nests of the highest quality), and that the nest building behavior of both sexes had been affected. Since concentrations of other contaminants such as polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and heavy metals were below levels associated with biological effects in birds, it can be deduced that PCBs are the most likely source of the behavioral abnormalities.

The other major effects that PCBs appear to have on bird species in the environment are immunotoxicological effects. As far back as 1970, one study found that mallards exposed to high levels of Aroclor 1254 (25 ppm) exhibited increased mortality following challenge with an infectious virus (Friend and Trainer 1970). More recently, it was found that American kestrels, when exposed to a mixture of Aroclors at the rate of 7 mg/kg kestrel/day, exhibited significantly altered antibody responses in comparison to controls, where females had a significantly raised antibody response and males showed significantly suppressed antibody production. Both suppression and stimulation of the antibody response are undesirable because they indicate that the immune system is not able to respond normally to challenges by infectious agents. In addition, these sex specific responses provide further evidence of the endocrine-disrupting behavior of PCBs (Smits and Bortolotti 2001). In one of the few field experiments on immunotoxicity of PCBs in birds, Sagerup et al. found, by examining the guts of 40 adult PCB-contaminated glaucous gulls, that although no single parasite species was significantly associated with concentrations of PCBs or chlorinated pesticides, the intensity of all nematodes grouped together was positively correlated with six different PCB congeners (Sagerup et al. 2000).

The other group of wildlife that has been studied rather extensively in terms of the effects of PCBs is mammals. This research is particularly relevant when looking at health, and in turn policy, implications for the exposure of humans to environmental PCBs. In mammals, the major types of effects of PCBs are similar to those found in birds, reproductive impacts and immunotoxicity, given the common mechanism of the Ah receptor (Van den Berg et al. 1998). In addition, PCBs have been implicated in behavioral alterations in mink and otters, perhaps causing behavioral abnormalities such as listlessness, nervousness, and disorientation (Heaton et al. 1995, Mason and O'Sullivan 1992), but these behavioral effects do not appear to ever have been studied directly or in a systematic way.

The reproductive impacts of PCBs on mammals are well documented. Lab studies conducted on ranch mink (Mustela vison) have shown adverse effects of PCBs on reproduction, even at environmentally realistic levels. One of the most frequently cited of these studies is the study conducted by Heaton et al. (1995), which showed that female mink fed a diet of 40% carp (taken from Saginaw Bay, Michigan and found to be naturally contaminated with 8.4 mg of PCBs/kg, or 8.4 ppm) whelped no kits that survived beyond 24 hours. Since concentrations of chlorinated hydrocarbons other than PCBs in the carp were minimal, PCBs can be deemed the most likely source of these reproductive effects. In addition, at least one study linked a decreased rate of reproduction in harbor seals to PCBs as well (Chiu et al. 2000).

The immunotoxicological effects of PCBs on mammals are also well documented. The most well known of these studies was conducted by Peter S. Ross and his colleagues on captive harbor seals (1996). The seals were fed herring from either relatively uncontaminated sites of the Atlantic Ocean or from the highly contaminated Baltic Sea. Seals fed the Baltic Sea herring showed significant levels of immunosuppression in comparison to the seals fed the relatively uncontaminated fish. Although the seals were not directly dosed with PCBs, the evidence implicates PCBs as the primary cause of the immunosuppression. In addition, Peter Bennett and Paul Jepson of the Institute of Zoology in London found that British harbour porpoises that died of infectious diseases had an average of 31.1 mg of PCBs/kg of blubber, as compared with only 13.6 mg PCBs/kg blubber in otherwise healthy animals that showed signs of having suffocated in fishing nets (Edwards 1999).

By looking at the studies mentioned above, one can see that there is a large (and growing) body of evidence that current environmental levels of PCBs can have potentially serious effects on wildlife in a number of ways. Although some of these studies were conducted on species that do not exist in the Hudson River Valley, it is clear that PCBs can have important effects at the ecosystem level, and these often extend far beyond the fish and the river itself, providing one more important reason for the safe disposal of the PCBs currently contaminating the Hudson River.

DEC Soil and Mammals Report

A preliminary report released on April 2, 2001 by NYS DEC showed markedly elevated levels of PCBs in flood plain soils and in piscivorous and ominivorous mammals such as mink (33 ppm) and river otters (172 ppm) that live within 10 km of the Upper Hudson River, according to DEC Commissioner Erin Crotty. These levels are comparable to those of a DEC mink survey conducted from 1982 to 1984. In current samples, soils in Saratoga and Washington County ranged from 0.018 ppm to as high as 360 ppm, with higher levels nearer the river and in close proximity to Fort Edward.

“The studies indicating high levels of PCB concentrations in soil and animals near the Hudson River raise concerns about the health of wildlife in these areas resulting from the river’s contamination,” said Commissioner Crotty, noting that the exposure extends beyond aquatic life as a result of exposure passed through the food chain, and that scientific research indicates that PCB levels in the upper Hudson may cause adverse health effects and reproductive disorders in these animals (NYSDEC News Release, 04/02/01).

The DEC studies were done in association with the National Oceanic and Atmospheric Administration (NOAA) and US Fish and Wildlife as part of the Natural Resource Damage Assessment (NRDA) for PCB contamination of the Hudson River. (NYSDEC News Release, 04/02/01).

Volatilization as a Pathway into Ecosystems

The volatilization of PCBs into the air, and their inhalation and inspiration by people and wildlife, is a route that has been little examined. PCBs have generally been considered insoluble and nonvolatile. However, it has been shown recently that volatilization of PCBs, and particularly of the lower-chlorinated congeners, can occur at substantial levels, and that inhalation may contribute significantly to the PCB body burdens of some people. Clearwater is concerned that these effects be examined carefully and taken into account during the design phase of EPA's remediation of the Hudson River.

Volatilization of PCBs from the water surface may be a significant input of PCBs to the ecosystem. While estimating the amount of PCBs volatilized from the Hudson River is fraught with unknowns, we may make an attempt. Achman et al. (1992) have calculated volatilization rates from Green Bay, Lake Michigan. The results varied widely, from 13 to 1300 ng/m²/day, and were strongly dependent on PCB concentration in water as well as wind speed; a factor of less than 10 for each of wind speed and water concentration result in a hundred-fold increase in volatilization. Converting units, multiplying by the area of the Upper Hudson, and adding a factor of 10 for the increased PCB concentration in the Hudson (approximately 60 ng/L, equivalent to 60 parts per trillion or ppt, compared with Lake Michigan’s “high” levels of approximately 6 ng/L), results in a range of approximately 6 (low wind) to 80 (high wind) kilograms of PCBs volatilized from the Upper Hudson each year. Water flow and turbulence will substantially increase this figure, which is based on the placid waters of Lake Michigan. Although this is at best a very rough estimate, it appears that volatilization of as much as hundreds of kilograms of PCBs is not unreasonable from the Upper Hudson alone. These PCBs can then be deposited into nearby areas; several studies have shown that atmospheric transport is a source of contamination of otherwise pristine bodies of water (e.g., Datta et al. 1998, Mackay 1989). In addition to contaminating the local ecosystem, PCBs have been shown to travel great distances after volatilization. Studies in the Arctic, far from any PCB sources, have found elevated levels in the breast milk of Inuit women (about 4 ppm) and in polar bear fat (3-8 ppm) (Dewailly et al. 1993).

Since volatilization depends at least linearly, and perhaps more strongly, on the water concentrations of PCBs, we conclude that dredging of the Hudson, and the resulting rapid reduction of PCBs in the water column, will substantially lower this massive release of PCBs to the ecosystem.

Current Levels of Volatilization also affect Human Health

Of the possible routes of exposure, fish consumption certainly carries the largest risk for Hudson Valley residents. In the Phase 3 Feasibility Study, EPA calculates the increased risk of cancer in the Upper Hudson due to inhalation at 2 x 10^-8 (central tendency) and 1 x 10^-6 (Reasonable Maximum Exposure), concluding that inhalation is not a pathway of concern for cancer in the Hudson River. Citing a lack of available research, EPA does not calculate a non-cancer Hazard Index for inhalation. Consequently, EPA has restricted itself to calculating Remedial Action Objectives for PCB levels in fish.

However, as we have seen (“Health Effects”, above), inhalation may represent a significant fraction of PCB body burden for Hudson Valley residents who are not fish consumers, while still falling below dangerous levels. By lowering PCB water levels and lowering volatilization, dredging will decrease the current export of PCBs to the local and global ecosystem as well as the inhalation levels for residents who do not eat fish. An active remediation program carries substantial ecological and public health benefits beyond lowering fish PCB levels.

We conclude that dredging of the Hudson River will dramatically lower volatilization, which is currently a large source of PCBs into the local and global ecosystem.

In addition, although inhalation is not currently a significant health threat in most cases, lowered volatilization rates following dredging will substantially reduce PCB exposure for Hudson Valley residents who do not eat fish.

Footnotes from Part 1

¹ NPDES permits changed to State Pollutant Discharge Elimination System (SPDES) permits in the 1980's. The legality of discharge violations pusuant to NPDES/SPDES permits is addressed later in this document.

² The Refuse ACt states: "Deposit of refuse in navigable waters generally... It shall not be lawful to throw, discharge, or deposit either from outside a ship, barge, or other floating craft of any kind, or from the shore, wharf, manufacturing establishment, or mill of any kind, any refuse matter of any kind or description whatever other than that flowing from streets and sewers and passing therefrom in a liquid state, into any navigable water from which the same shall float or be washed into such navigable water..."

³ In 1965 the affected reach of the Hudson River was classified as "D" according to its best uses. Fishing has been a protected use in Class D waters since 1974. Furthermore, fishing was a protected use in Class A and B waters long before then, and the waters into which HE's PCBs were discharged flows into Class A and B waters. In 1976, hearing officer Abraham Sofaer found GE liable for impairing that protected use (NYS DEC, February 9, 1976).

⁴ The 153 violations include 5 monthly average violations, each of which constitutes at least 30 violations of the permit, the Environmental Conservation Law, and the Clean Water Act, and nine other excedances, each of which is a violation of law.

⁵ In 1975 DEC Commissioner Ogden Reid informed the public of the problem of PCB contamination in Hudson River fish.

⁶ There is significant evidence that the recovery periods for these scenarios will be longer than that calculated from the HUDTOX model. For a more complete treatment, see Feasibility Study Modeling Considerations, below.