| 2 | WATER QUALITY CRITERIA WORKSHOP |
| 2.1 | Review and Progress of Governments in the Control and Management of Persistent Toxic Substances: Development and Use of Water Quality Objectives |
In December 1997, the International Joint Commission directed the Great Lakes Water Quality Board, Great Lakes Science Advisory Board and the Council of Great Lakes Research Managers to assess governments' efforts to further determine the impact of persistent toxic substances on the Great Lakes, develop a control and prevention strategy, and advise on strategies of the governments in the implementation of the control and management programs for discharges of persistent toxic substances.
The Great Lakes Science Advisory Board held a workshop in Chicago at the Regional Headquarters of the U.S. Environmental Protection Agency, in March 1998. It discussed the adequacy of existing water quality objectives for protection of organisms, including humans, living in the Great Lakes basin exposed to persistent toxic substances from Great Lakes food chains. This section of the report is based on selected technical presentations, and interrelates the protection of human health with the restoration of extirpated Great Lakes wildlife populations, and the implementation of the Agreement. Parts of this report were published as a brief meeting report in the March 1999 issue of Environmental Health Perspectives.
Article IV of the Boundary Waters Treaty of 1909 that states in part "that the waters herein defined as boundary waters and waters flowing across the boundary shall not be polluted on either side to the injury of health or property on the other." One of the key ideas in the Agreement is that water quality can be maintained and restored by developing and adopting water quality objectives. This idea was incorporated into the first Agreement, signed in 1972. The rationale is that if scientists could recommend the concentration of a pollutant that could be tolerated by organisms in the Great Lakes, then engineers could build and operate waste treatment facilities to make sure that the pollutant stayed below that concentration. This rationale has been successfully used by governments to improve water quality in the Great Lakes basin for more than 40 years.
In 1978, with the renegotiation of the Agreement the Parties amended the policy regarding toxic substances by stating that the "discharge of any and all persistent toxic substances be virtually eliminated." Water quality objectives for both toxic substances and persistent toxic substances were incorporated into Annex 1. However, no specific definition of virtual elimination of discharge of persistent toxic substances has been developed for the Agreement.
To what extent has the policy been achieved and are additional actions needed? Persistent toxic substances continue to leach from chemical landfill sites and from contaminated sediments (U.S. EPA and NYSDEC,1997; Lakewide Management Plan for Lake Ontario 1998) and be deposited from the atmosphere (Cohen et al. 1995; Hoff et al. 1996), thereby maintaining concentrations high enough to continue to cause injury to fish, wildlife and human populations. Existing water quality objectives need to be reevaluated to determine whether they are sufficiently stringent to restore affected fish and wildlife populations, to protect human health and to fulfill the requirements of the Parties' policy of virtual elimination of discharge.
Injury to Human Health and to Fish and Wildlife Populations
The research on the reproduction of wildlife and on the developmental effects in infants exposed to persistent toxic substances pointed to the widespread presence of teratogenic substances that are causing irreversible transgenerational damage. These case studies were subsequently important in the formulation of the hypothesis on endocrine disruption that has become an explanatory principle in modern environmental toxicology (Cheek et al. 1998; U.S. Environmental Protection Agency 1997, 1998; Scientific Committee on Toxicity, Ecotoxicity and the Environment 1999). The various stages of the normal differentiation and development of the embryo, fetus and infant are under the control of specific chemical messengers that are programmed to be released from a certain tissue, transported in the blood, and produce specific effects at a certain concentration and particular time in another tissue or organ. The scientific community has recently become focused on the finding that some chemicals, including many persistent toxic substances that have been released to the environment, interfere with these chemical messengers and cause irreversible damage to the developing embryo and fetus. These effects occur at extremely low doses (Peterson et al. 1992; Welshons et al. 1999; Colborn et al. 1999) and include changes in the development and function of the reproductive system, deficits in neurological development affecting learning and deficits in the development of the immune system.
In the 1990s, the U.S. and Canadian governments have made significant progress in developing water quality objectives and criteria for persistent toxic substances. For example, in response to the Great Lakes Critical Programs Act of 1990, the U.S. Environmental Protection Agency developed water quality criteria for persistent toxic substances, under the Great Lakes Initiative (GLI), for protection of aquatic life, human health and wildlife. When regulatory officials in the Great Lakes states initially reviewed the toxicological and bioaccumulation data, they noted the extremely low water concentrations that would have to be achieved to restore wildlife populations and to protect humans from an unacceptable risk of cancer.
Three questions were posed by the Science Advisory Board to the workshop participants.
Water Quality Criteria for Protection of Human Health
At the workshop, independent presentations by senior scientists Dr. Milton Clark of the United States, and Dr. Deborah Rice of Canada showed a remarkable consistency in analyzing the available epidemiological and experimental studies concerning the neurological effects of PCBs. Neurological effects on humans are among the more sensitive endpoints for PCBs. The neurological findings in humans were supported by the results of the studies in monkeys, and the reference doses were similar. In addition, the water quality criteria derived from the cancer risk method, calculated as part of the Great Lakes Initiative, do seem to provide sufficient protection from neuro-behavioral and reproductive effects of PCBs and dioxins. The available environmental monitoring data indicate, however, that the present concentrations of PCBs in samples of Great Lakes water are about a hundred times higher than these criteria.
The board concludes that the water quality criteria for protecting humans from the carcinogenic effects of PCBs are adequate to protect developing infants from the neurological effects of prenatal exposures to PCBs.
The board concludes that, despite the significant improvements in water quality during the past two decades, there are still persistent toxic substances in fish and wildlife at concentrations that pose threats to human health and in some cases these concentrations are associated with actual effects on the more highly exposed individuals in critical subpopulations.
The board recommends the following.
The Bald Eagle as an Indicator of the Restoration and Protection of Water Quality and of Human Health
The monitoring of trends in the exposures to, and effects of, persistent toxic substances in human populations remain a challenge for scientists involved in Great Lakes research. Not only are basin human populations mobile and their various routes of exposures to chemicals uncertain, but also much of their food is imported and therefore does not represent the contamination of their local environment. Thus, there is a need for the selection of indicators as surrogates of human exposures and effects. An indicator has been defined (International Joint Commission 1996) as something that provides a clue to a matter of larger significance or makes perceptible a trend or phenomenon that is not immediately detectable.
In the 1950s and 1960s, many of the North American populations of bald eagles were extirpated through exposures to persistent toxic substances (Sprunt et al. 1973). The population of bald eagles that nested in the shoreline habitat around the Great Lakes was among the most severely contaminated on the continent and the most seriously affected. Prohibitions on the use of DDT in the early1970s resulted in restoration of many North American populations, but only partial reestablishment in the Great Lakes basin. Bald eagles need adequate nesting habitat, sufficient food for themselves and their young and no human disturbance. While much of the shoreline of the Great Lakes basin provides these minimal requirements, large areas remain so contaminated with persistent toxic substances that bald eagles have been unable to reestablish territories. For example, the bald eagle population that existed on Lake Ontario was extirpated by 1958 and no eagles have attempted to reestablish territories despite the availability of many suitable locales. However, a pair of bald eagles that nested on Wellesley Island in the Saint Lawrence River, downstream from Lake Ontario, produced one chick in 1999. The bald eagle has been demonstrated to be particularly sensitive to certain organochlorine contaminants in the environment and therefore the board suggests that it would make a good indicator of the restoration of water quality.
The development of water quality criteria to restore the Great Lakes populations of bald eagles nesting in habitat along the shorelines has taken two different approaches: one empirical and the other experimental. The empirical dose-response relationship between contaminant concentrations and reproductive success is well documented and there are field measurements of the biomagnification factors, for certain persistent toxic substances such as PCBs, between water and bald eagle eggs that range from 25 millionfold to 100 millionfold. In the development of the water quality criteria for the Great Lakes Initiative, scientists have used data derived from experimental dose-response relationships and biomagnification factors. Using the protection of humans from the carcinogenic effects of PCBs, the criteria based on empirical data is ten times more stringent. Whereas the criterion based on experimental data is ten times less stringent than the human carcinogenesis criterion.
The board concludes that the restoration and normal reproduction of a Great Lakes population of shoreline nesting bald eagles might provide a useful surrogate for the protection of human health. There are, however, differences in the criteria derived from experimental versus empirical evidence, and further discussion is needed of which data should take precedence.
The population status and reproductive success of bald eagles can serve as an indicator of the Parties' progress under the Agreement on achievement of the restoration of water quality and on the adequacy of the water quality criteria. Though the bald eagle has been used as an unofficial indicator for monitoring regional trends in concentrations and effects of persistent toxic substances in the Great Lakes basin for more than 30 years, this usage is in jeopardy because the species is being removed from the U.S. national list of endangered species and therefore funding for monitoring is being sharply curtailed.
The board recommends the following.
A Biochemical Indicator of Exposure
The final workshop discussion focused on the need to find a biological indicator of exposure to specific compounds or classes of compounds with specific modes of action that are relevant to potential or observed harmful effects. There have been several proposals to use the Ah receptor in fish and wildlife species as long-term monitors of the trends in exposure of Great Lakes organisms to certain persistent toxic substances, such as the planar PCBs, polychlorinated dibenzo-p-dioxins and furans. Other candidate physiological markers include porphyrin accumulation and retinoid depletion in the liver, and some measure of immune function. Some monitoring data on these physiological endpoints are already available from studies on various species of fish-eating birds collected at various periods and from various sites around the Great Lakes.
While monitoring Ah activity in a species of fish-eating bird might be a valuable measure of exposure to compounds with this mode of action, there are also other modes of action of toxicological importance that need to be monitored. For example, there are certain non-planar PCBs that cause neurological effects through interfering with dopamine metabolism. Theoretically, a biochemical measure could be devised for monitoring the trends in exposures to substances with this mode of action. Finally, there is evidence from herring gulls and salmonids of the presence in the Great Lakes of unidentified anthropogenic or natural substances with goitrogenic activity. There is, thus, a need for a biological indicator of exposures to these compounds since thyroid functioning is such an important process, not only in the normal functioning of adult organisms, but also in the normal differentiation and development of embryos, fetuses and juveniles of all vertebrates.
The Great Lakes Science Advisory Board recommends the following.
| 2.2 | Research and Regulatory Progress in Applying Toxic Equivalency Factors |
The Agreement, in Annex 2, section 6(a) (i), states that Lakewide Management Plans ". . . shall include a definition of the threat to human health or aquatic life posed by Critical Pollutants, singly or in synergistic or additive combinations with another substance, including their contribution to the impairment of beneficial uses." In preparing Lakewide Management Plans, the interpretation of analyses of organochlorine chemicals in environmental and biological samples has been complicated by the number of residues present. One of the most toxic substances in many of the samples from the Great Lakes is 2,3,7,8-tetrachloro dibenzo-p-dioxin. Some congeners of polychlorinated biphenyls (PCBs), some other congeners of polychlorinated dibenzo-p-dioxins (PCDDs) and some of the polychlorinated dibenzofurans (PCDFs) have the same mode of action by binding to the aryl hydrocarbon receptor (Ah). Though all these congeners have the same mode of action, they have different potencies. The relative potency of each congener is known as the toxic equivalency factor (TEF). The interpretation of analytical data has been made easier by converting the results of the concentrations of each of the congeners using the TEFs to calculate the toxic equivalent concentrations (TEQs) as though all the dioxin-like activity were due to 2,3,7,8-tetrachloro dibenzo-p-dioxin. It has been assumed that the dioxin-like activity in terms of TEQs of each of the congeners is additive.
Originally, TEFs were developed based on the relative toxicity in mammals or in mammalian cell cultures. Thus, there was a need to rationalize the TEFs from the different data sources. Later work on fish and birds showed that TEFs for these organisms were different from those for mammals. Thus, there was again a need to rationalize the TEFs. TEFs can be used not only to interpret analytical data and to make cause-effect cases, but also can be used for risk assessment and for permitting discharges into the environment.
In the late 1980s, the U.S. Environmental Protection Agency initiated the U.S. Great Lakes Water Quality Guidance, to develop water quality criteria for the protection of wildlife from exposures to persistent toxic substances. Because approval of the guidance had implications for species listed as threatened, rare and endangered, the agency entered into formal consultation with the U.S. Fish and Wildlife Service (FWS) to comply with Section 7(a)2 of the Endangered Species Act. In the final biological opinion issued by the FWS, the two agencies agreed to hold a workshop to develop a consensus on the use of TEFs for chlorinated dioxin-like compounds, that would be protective of wildlife. This proposed workshop was merged with one that was being organized by the World Health Organization (WHO) in Stockholm, Sweden for June 15-18, 1997. At that meeting, experts developed tables of TEFs, through consensus, for mammals, fish and birds. This work has recently been published, after peer review, in the primary scientific literature (Van den Berg et al. 1998); see Table ?X?below. The U.S. EPA and the U.S. FWS held a workshop in Chicago, January 20-22, 1998, to address the use of TEFs in ecological risk assessments. These TEFs were then presented by Tim Kubiak at the IJC Workshop on Water Quality Criteria held in Chicago on March 25-26, 1998 and at the Meeting to Assess Scientific Issues in Relation to Lakewide Management Plans, held in Windsor on February 25-26, 1999.
Risk estimates for regulatory purposes have traditionally been based on total PCBs, because these were the only data available. The implications of using TEFs for each of the PCB, PCDD and PCDF congeners to calculate toxic equivalent concentrations (TEQs), are that the estimated risks are generally larger than when they were based on total PCBs. The current Great Lakes Water Quality Guidance for human health assessment includes TEFs for PCDDs and PCDFs to calculate a TEQ that establishes the risk for these substances. But PCBs are still assessed separately as total PCBs, even though TEFs are available. Similarly, for wildlife, criteria are set for 2,3,7,8-tetrachlorodibenzo-p-dioxin, but not for other PCDDs and PCDFs; and criteria for PCBs are set on the basis of total PCBs and not on the basis of TEFs. Further, the current guidance does not address the subtle differences in the consensus WHO TEFs that were established for birds and mammals.
The Great Lakes Water Quality Guidance provides a process to derive water quality criteria for these compounds, but does not contain TEFs or total PCB criteria for fish, such as lake trout, and there is no guidance for integration of analytical data on PCBs, PCDDs and PCDFs across these families of chemicals. The current water quality criterion value of 14 ppt total PCB for protection of fish, is a carry-over from the EPA's 1986 Quality Criteria for Water or Gold Book, and seems to be a default value. This criterion relies on dated toxicological and bioaccumulative potential rather than a consideration of the effects of dioxin-like compounds on early life stage mortality, which is the basis for the WHO TEF scheme for fish. If the reproductive, developmental and congener-specific bioaccumulation factors were taken into consideration, the water criteria for some individual congeners would be at least two orders of magnitude lower. A similar scenario unfolds for birds and mammals.
The application of the TEF/TEQ approach has several other regulatory implications. For example, fish and wildlife consumption advisories have been developed for humans based on total PCBs. Human health would be better protected if advisory decisions considered resulting total TEQs using the WHO TEFs, which take into account the risk posed by the most significant chlorinated compounds present with dioxin-like activity. The resulting total TEQ risk could then be compared side by side with total PCB risk.
This scheme using the TEF/TEQ approach successfully addresses the risks posed by substances that exhibit dioxin-like activity. But there are other PCBs that are toxic through other modes of action. These kinds of toxicity are not addressed through the TEF/TEQ scheme. Data sets relating to total PCBs have been used for risk assessment for effects that are not mediated through the Ah receptor. The TEF/TEQ approach should therefore be viewed as a complementary approach to, and not a substitute for, total PCB assessments.
The TEF/TEQ approach is geographically neutral and has universal utility for estimating dioxin-like activity in fish, wildlife and human populations exposed in all ecosystems throughout the world. The variables that are subject to change in risk assessments in other locations will be: target organisms; the complexity of their supporting food chains; water bioaccumulation factors or biota to sediment accumulation factors; and toxicity data that are relevant to protection and restoration of fish and wildlife populations. Regardless of geographic location, the critical pathway can be identified by using the WHO TEF/TEQ approach as the unifying methodology for assessing different target species and food-chains in different ecosystems.
The WHO TEF/TEQ approach is applicable to a variety of regulatory circumstances. For example, it can be used in the preparation of Lakewide Management Plans for critical pollutants and of Natural Resource Damage Assessments. Similarly, in tributaries to the Great Lakes that have limited water quality, the WHO TEF/TEQ approach can be used by the states or U.S. EPA under the U.S. Clean Water Act's section 303(d), to derive Total Maximum Daily Loads (TMDLs). After additional collection of supporting data on TEQs in waste loads from point and nonpoint sources, a TMDL may be established taking into consideration an allocation for an adequate margin of safety. When based on food chain contamination, regardless of source, this could include contamination that arises directly from sediments or atmospheric deposition. To this end, U.S. EPA Region 5 is preparing a framework document, with the concurrence of the Agency's Science Advisory Board, on the application of the TEF/TEQ approach.
The Great Lakes Science Advisory Board concludes that the WHO TEF method would be a useful approach to determine additive effects of some critical pollutants related to Annex 2 of the Agreement.
The board recommends the following.
| Congener | Humans/Mammals | Fish a | Birds a | |||
| 2,3,7,8-TCDD | 1 | 1 | 1 | |||
| 1,2,3,7,8-PeCDD | 1 | 1 | 1 | b | ||
| 1,2,3,4,7,8-HxCDD | 0.1 | a | 0.5 | 0.05 | b | |
| 1,2,3,6,7,8-HxCDD | 0.1 | a | 0.01 | 0.01 | b | |
| 1,2,3,7,8,9-HxCDD | 0.1 | a | 0.01 | c | 0.1 | b |
| 1,2,3,4,6,7,8-HpCDD | 0.01 | 0.001 | <0.001 | f | ||
| OCDD | 0.0001 | a | <0.0001 | 0.0001 | ||
| 2,3,7,8-TCDF | 0.1 | 0.05 | 1 | b | ||
| 1,2,3,7,8-PeCDF | 0.05 | 0.05 | 0.1 | b | ||
| 2,3,4,7,8-PeCDF | 0.5 | 0.5 | 1 | b | ||
| 1,2,3,4,7,8-HxCDF | 0.1 | 0.1 | 0.1 | b,d | ||
| 1,2,3,6,7,8-HxCDF | 0.1 | 0.1 | d | 0.1 | b,d | |
| 1,2,3,7,8,9-HxCDF | 0.1 | a | 0.1 | c,d | 0.1 | d |
| 2,3,4,6,7,8-HxCDF | 0.1 | a | 0.1 | d,e | 0.1 | d |
| 1,2,3,4,6,7,8-HpCDF | 0.01 | a | 0.01 | e | 0.01 | e |
| 1,2,3,4,7,8,9-HpCDF | 0.01 | a | 0.01 | c,e | 0.01 | e |
| OCDF | 0.0001 | a | <0.0001 | c,e | 0.0001 | e |
| 3,4,4',5-TCB (81) | 0.0001 | a,c,d,e | 0.0005 | 0.1 | c | |
| 3,3',4,4'-TCB (77) | 0.0001 | 0.0001 | 0.05 | |||
| 3,3',4,4',5-PeCB (126) | 0.1 | 0.005 | 0.1 | |||
| 3,3',4,4',5,5'-HxCB (169) | 0.01 | 0.00005 | 0.001 | |||
| 2,3,3',4,4'-PeCB (105) | 0.0001 | <0.000005 | 0.0001 | |||
| 2,3,4,4',5-PeCB (114) | 0.0005 | a,d,e,f | <0.000005 | e | 0.0001 | g |
| 2,3',4,4',5-PeCB (118) | 0.0001 | <0.000005 | 0.00001 | |||
| 2',3,4,4',5-PeCB (123) | 0.0001 | a,d,f | <0.000005 | e | 0.00001 | g |
| 2,3,3',4,4',5-HxCB (156) | 0.0005 | d,e | <0.000005 | 0.0001 | ||
| 2,3,3',4,4',5'-HxCB (157) | 0.0005 | d,e,f | <0.000005 | d,e | 0.0001 | |
| 2,3',4,4',5,5'-HxCB (167) | 0.00001 | a,f | <0.000005 | e | 0.00001 | g |
| 2,3,3',4,4',5,5'-HpCB (189) | 0.0001 | a,d | <0.000005 | 0.00001 | g |
Abbreviations: CDD, chlorinated dibenzo-p-dioxins; CDF, chlorinated dibenzofurans, CB, chlorinated biphenyls; QSAR,