October 4, 1999
Pursuant to the Great Lakes Water Quality Agreement (Agreement), Lakewide Management Plans (LaMPs) for open lake waters are to be developed and implemented by the Canadian and United States Governments (Parties) in cooperation with State and Provincial Governments. The GLWQA states such plans shall be designed to reduce loadings of Critical Pollutants in order to restore beneficial uses. The LaMPs are to be submitted to the International Joint Commission (Commission) for review and comment at four stages and shall include:
The Stage 1 LaMP for the open waters of Lake Ontario has been submitted to and reviewed by the Commission. The criteria for its evaluation are based on the relevant portions of the 1987 Protocol to the Agreement.
As defined in 6(c)(i) and 6(a)(i-iii), respectively, of Annex 2, Stage 1 LaMPs are to contain the requirements outlined above.
In addition to the required Stage 1 elements, Annex 2 of the Agreement states general principles for LaMPs including:
Accordingly, the Commission's evaluation of a LaMP at any stage incorporates consideration of an ecosystem approach to the restoration and protection of beneficial uses in open lake waters and assesses the adequacy of public consultation, as well as considering the specific Annex 2 requirements for that particular stage. Thus, the Commission's review and comment regarding the Stage 1 Lake Ontario LaMP, received by the Commission on June 1, 1998, reflects an assessment of the document submitted in relation to the three specific Stage 1 LaMP requirements and consideration of an ecosystem approach to the restoration and protection of beneficial uses in open lake waters and of the adequacy of public consultation.
Has the threat to human health or aquatic life that is posed by Critical Pollutants been defined?
The threat to human health or aquatic life posed by Critical Pollutants is not well-defined in the Stage 1 LaMP. Annex 2 of the Agreement states, in part, that LaMPs "shall include a definition of the threat to human health or aquatic life posed by Critical Pollutants . . . including their contribution to the impairment of beneficial uses . . ." Human health effects observed from exposure to persistent toxic substances (PTSs) were reported by Humphrey (1983). Since that time, there have been a number of epidemiological studies conducted in the Great Lakes Basin (Basin) that are relevant to the Lake Ontario LaMP. Their findings support earlier reports of an association between the consumption of contaminated Great Lakes fish and body burdens of PTSs (Johnson et al. 1998). The body burdens of some consumers are two- to four-fold higher than those in the U.S. general population (Johnson et al. 1998). Some findings include:
The LaMP states that "except in cases where individuals are exposed to relatively high levels of contaminants that can cause clearly recognizable health effects, it may not be possible to separate out any adverse effects due to environmental contaminants . . ." This statement may be true for the general population. But, as outlined above, several high-risk sub-populations exist in the Basin and more specifically in the Lake Ontario Basin and adverse effects have been identified.
With respect to the Lake Ontario LaMP, the limited human health information provided is contained in the "Introduction" rather than the "Problem Identification" section. This information does not adequately address the specific cohorts which have been studied to better document potential health consequences associated with certain Critical Pollutants. In particular, no information is provided concerning findings related to the Oswego cohort. Information on this and other Lake Ontario-related studies as well as other human population exposure studies undertaken in the Basin is provided in Appendix A of these comments.
Due to this research, the case regarding human health impacts is much clearer for certain highly-exposed [at-risk] sub-populations in the Lake Ontario Basin than for the general population in the Basin. The LaMP's Introduction correctly states "consumption of contaminated sport fish and wildlife can significantly increase human exposure to Lake Ontario critical pollutants." This is an important first step in defining the threat to human health.
Epidemiologic investigations have been conducted in relation to exposures of individuals to certain Critical Pollutants through the consumption of Great Lakes fish. The LaMP states "These studies have demonstrated increased tissue levels of toxic substances in these populations that may be associated with or potentially result in reproduction, developmental, behavioral, neurologic, endocrinologic, and immunologic effects." Despite this acknowledgment, the LaMP has not directly addressed findings derived from the Oswego cohort. In this research, Lonky et al. (1996) examined and documented neurobehavioral effects on infants from maternal consumption of environmentally contaminated Lake Ontario salmon or trout. Five hundred and fifty-nine newborns of women who had high exposure, low exposure, or no Lake Ontario fish exposure were examined using the Neonatal Behavioral Assessment Scale (NBAS) 12 to 24 hours after birth and again at 25 to 48 hours after birth. The results indicate that newborns of mothers who consumed 2.3 Lake Ontario salmon or trout meals per month scored more poorly on the NBAS than those newborns from the low exposure or control group. In particular, newborns of high-fish-consuming mothers exhibited these deficits:
The LaMP documents the evaluation of population status and reproduction impairments in mink, otter, bald eagles, colonial water birds, and a variety of fish species. It also notes the loss of several fish species and reductions in native fish populations between the early 1800s and the 1960s and attributes the effects primarily to overfishing, loss of habitat, and the impact of exotic species, although no citations were provided. The document also states "The contribution of persistent toxic substances to the loss of certain fisheries is unclear because fish populations were already severely degraded by the time that significant levels of contaminants began to be released to the environment." No citations were provided regarding this statement. Cook et al. (1997) determined, that by 1940, lake trout exposures to 2,3,7,8-tetrachloro-dibenzo-p-dioxin (2,3,7,8-TCDD) and related chemicals in Lake Ontario probably contributed to the decline and virtual extinction of the indigenous lake trout population through complete reproductive failure. Among salmonid fish species that have been evaluated, lake trout was discovered to be the most sensitive to 2,3,7,8-TCDD-induced early life-stage mortality (Cook et al.1997). Further, the LaMP states "There is no indication that current levels of contaminants in the open waters are degrading fish populations." Again, no citations were provided. Lake trout eggs in Lake Ontario have been shown to have a 9-fold greater exposure to 2,3,7,8-TCDD than in Lake Michigan (Cook et al. 1997). While the current level of exposure is less than the 2,3,7,8-TCDD no observable effects level for early life-stage mortality from blue-sac syndrome; 2,3,7,8-TCDD and related compounds [at concentrations below those that produce mortality] may affect immune, reproductive, and nervous systems to cause functional alterations that seriously compromise fish survival (Cook et al.1997).
The LaMP states "Studies of bald eagles nesting on other Great Lakes shorelines suggest that levels of PCBs, dioxins, and DDT in the Lake Ontario food web may cause lowered reproductive success, increased eaglet deformities, and early adult mortality . . .", but references to a recovering bald eagle population may be misleading. Recovery in the Lake Ontario Basin is related to a large-scale bald eagle reintroduction program [hacking]. Since this population is not associated with the Lake Ontario food web, this progress does not reflect a recovery of contaminant levels in open lake waters. A 1996 survey showed that no pair of eagles had yet reestablished a territory on the shorelines of Lake Ontario (Grasman et al. 1998).
Historical decreases in contaminant levels in regard to fish and wildlife are documented. For example, the LaMP states "PCB levels in herring gull eggs decreased by an order of magnitude from the mid-1970s to the late 1980s." The LaMP further states "The low reproductive success rate of herring gulls in the 1960s and 1970s shifted to a full recovery, with no signs of contaminants, by the early 1980s." However, given the lack of systematic investigation of recent wildlife health effects, it is difficult to assess the present scope of colonial waterbird impairments. The LaMP should consider more carefully the current status of impairments of colonial waterbirds. In herring gulls, the "lowest observable effects level" (LOEL) for embryotoxic effects of PCBs has been reported to be 5.0 mg/kg wet weight (Ludwig et al. 1993) with Lake Ontario herring gull eggs uniformly above this concentration. While embryonic mortality has not precluded the expansion of the Lake Ontario herring gull populations, the findings suggest impairment of an important reproductive process. Grasman et al. (1996) examined three week old herring gulls at Hamilton Harbour in1992 and found that they exhibited suppressed T-cell-mediated immunity, similar to herring gulls and Caspian terns at other Great Lakes sites with high PCB contamination. Young gulls at Scotch Bonnet Island also have suppressed T-cell-mediated immunity and smaller thymus glands, both of which indicate toxicological effects on the immune system. Although currently much improved, the concentration of retinyl palmitate stored in livers of adult herring gulls from Hamilton Harbour and Scotch Bonnet Island remains severely depleted (Fox et al.1998).
In cormorants, the LOEL for embryotoxic effects of PCBs has been reported to be 3.5 mg/kg wt weight (Tillitt et al. 1992, Yamashita et al.1993, Ludwig et al. 1993). This concentration was associated with twice the embryonic mortality observed at reference sites. Lake Ontario cormorant eggs generally contain PCBs at concentrations above this LOEL (3.1-11.1 mg/kg for Snake Island, Little Galloo Island, and Hamilton Harbour; only one record below the LOEL). PCB concentrations of 5.5 mg/kg were associated with 28% embryonic mortality at Pigeon Island, Lake Ontario (Ludwig et al.1993). Cormorant egg mortality at reference sites is below 10%.
The fish and wildlife sections of the LaMP would have benefitted from closer consultation with Great Lakes fish and wildlife toxicologists. This consultation would have improved the literature citations, provided access to recent but unpublished data, given stronger documentation regarding impairment conclusions, and better explained important data gaps.
Has an evaluation of available information on concentration, sources, and pathways of Critical Pollutants including all information on loadings of Critical Pollutants from all sources, and an estimation of total loadings of the Critical Pollutants by modelling or other methods been completed?
Based on the information presented in the LaMP and information examined during the Commission's review activities, the Critical Pollutant selection (PCBs, DDT its metabolites, mirex, dioxin, mercury, and dieldrin) appears reasonable. But, references to dioxin are inconsistent. [For purposes of this review, we use the term "dioxin" to refer to all polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans.] The text utilizes various forms of reference (to dioxin) that render will render the discussion confusing to readers. Inconsistencies include the following:
In addition to a consistent definition, we suggest that quantitative loads and concentrations of dioxin-like compounds be reported as 2,3,7,8-TCDD TEQs, computed using defined toxicity equivalency factors. This would provide a better approximation of the toxicity for compounds with the ability to bind to the aryl hydrocarbon receptor.
Page 61 of the LaMP section on sources and loadings of Critical Pollutants states "Atmospheric deposition appears to be the largest known source of dioxins/furans, contributing approximately 5 grams per year." No citation is provided to document this statement. Two data sources are detailed for atmospheric loadings of Critical Pollutants in Table 3-3 on page 51 and the table estimates that 5 grams of "dioxins" are derived from atmospheric loadings. Cohen et al. (1995) estimated dioxin deposition to Lake Ontario at 6.4 grams TEQ/year with a range of 2-18 grams TEQ/year. Pearson et al. (1997) in research partially funded by U.S. Environmental Protection Agency, Great Lakes National Program Office state "We conclude that Lake Ontario must be receiving a significant portion of its current total PCDD/F [dioxin] input from non-atmospheric sources . . . non-atmospheric inputs would account for 70% of its current inputs." The LaMP's conclusion in regard to the atmospheric deposition of dioxin appears reasonable. Other research suggests that non-atmospheric inputs are also sizable and may exceed atmospheric deposition. Accordingly, a question is raised concerning the LaMP's conclusion that atmospheric deposition is the major source of dioxin. The LaMP states "data . . . indicate that there are several sources of both dioxins and furans in the Niagara River and that the River is a source of these pollutants to Lake Ontario." Further, the LaMP states "Dioxins and furans have been detected in a number of Lake Ontario tributaries using qualitative water and biological sampling methods." Dioxin has been detected [in qualitative monitoring programs or in effluent of facilities discharging to a tributary] in regard to 13 of the 23 major tributaries to Lake Ontario. No information was available for 9 other tributaries and 2,3,7,8-TCDD is labeled as not detected in the Niagara River. No estimates of loadings from these tributaries were presented in the LaMP. The LaMP document does not estimate [as required by Annex 2] the total loading of dioxin to Lake Ontario.
Nor does, the LaMP estimate the total loading for mercury [as required by Annex 2]. The LaMP states "Loading estimates for mercury could not be completed in time for this report since it was identified as a critical pollutant late in the Stage 1 development process . . ." Loading information for mercury could be incorporated in a future document along with information that is required to adequately define the threat to human health or aquatic life that is posed by Critical Pollutants.
The LaMP states "dieldrin concentrations in the lake have declined from .35 to .17 parts per billion . . ." Whereas a recent progress report for the Niagara River Toxics Management Plan (Niagara River Secretariat 1998) reports the dieldrin levels in waters of Lake Ontario as .17 parts per trillion (rather than parts per billion). Tables 3-3, 3-4, and 3-5 present information on the loading of dieldrin to Lake Ontario, but the loading numbers from various types of sources must be added to determine the total loading to the lake.
Estimates of loadings from some sources are provided for PCBs, total DDT, and mirex, but loadings from all sources are not estimated. Table 3-6, identifies a preliminary estimate of Critical Pollutants entering Lake Ontario via direct discharges in Canada, shows that no information is available from the majority of potential dischargers. A table note states "A more complete review of these dischargers will be performed as part of future LaMP activities." Further, no information was available regarding loadings of some compounds from several of the major tributaries to Lake Ontario. Existence of these data gaps precludes the estimate of total loading for these compounds, but there is no indication of plans to address this problem.
Have steps been taken to develop the information necessary to determine the schedule of load reductions of Critical Pollutants?
While significant data gaps related to loadings of Critical Pollutants exist, the efforts of the Lake Ontario Toxics Management Plan (LOTMP) and the Niagara River Toxics Management Plan (NRTMP) provide a substantial contribution toward the reduction of loadings of Critical Pollutants. For example, the NRTMP previously targeted the Critical Pollutants dioxin, mercury, mirex, and PCBs for 50 per cent reduction in loadings to the Niagara River. While the NRTMP has not provided a significant advantage to development and implementation of a load reduction schedule, it has proved to represent a step toward virtual elimination of these compounds. Actions taken under the LOTMP and the NRTMP will not only assist in development of the Stage 2 LaMP, but serve as an important step toward the virtual elimination of certain Critical Pollutants.
Has an ecosystem approach been taken to the restoration and protection of beneficial uses?
In setting out the General Principles, the Parties said that LaMPs, should embody a systematic and comprehensive ecosystem approach to restoring and protecting beneficial uses in open lake waters. This approach should include, among other things: an inventory of sources for Critical Pollutants in environmental media, an assessment of exposure pathways, an identification of highly exposed species and an assessment of impacts on these exposed human, fish and wildlife populations.
Appendix C of the LaMP states "The LaMP will provide a comprehensive ecosystem approach to restore beneficial uses by reducing levels of critical pollutants that cause lakewide problems." While maintaining a focus on impacts to waters of the open lake, an opportunity exists to better approximate a systematic and comprehensive ecosystem approach. One aspect of this approach is a more thorough definition of the threat posed by Critical Pollutants to human health or aquatic life. The inclusion of atmospheric loadings of Critical Pollutants (in Tables 3-3 and 3-4) also contributes to a more complete understanding of the pollutant delivery pathways and implementation of an ecosystem approach to the restoration and protection of the beneficial uses for the open waters of Lake Ontario. Confirmation of quantities of Critical Pollutants present in lake sediment and landfills would also assist in achieving a systematic and comprehensive ecosystem approach.
Was the public consulted adequately?
Annex 2 states "The Parties, in cooperation with State and Provincial Governments, shall ensure that the public is consulted in all actions undertaken pursuant to this Annex. The LaMP states "The Four Parties are committed to an active public involvement program." The goals for public involvement are:
The LaMP details plans to build a "Lakewide Advisory Network." Consultation with the diverse population of the Lake Ontario Basin represents a considerable challenge. The proposed actions are ambitious but should serve to facilitate consultation with many interested citizens and organizations. For example, considerable information is available to the public on the two web-sites noted in the LaMP. An opportunity exists to utilize these web-sites and other more direct means of consultation to better inform susceptible populations of potential human health risks in regard to the consumption of environmentally contaminated fish. Certain of these populations may prove to be particularly challenging with respect to public consultation and may therefore require alternative communication strategies.
The Lake Ontario Stage 1 LaMP provides considerable information toward documentation of the environmental problem as defined by Annex 2 of the GLWQA. The LOTMP and the NRTMP have provided a substantial advantage toward LaMP implementation activities. However, shortcomings exist particularly in the area of defining the threat to human health and estimation of total loadings of Critical Pollutants. The failure to include relevant human health studies in particular work involving the Oswego [Lake Ontario] cohort is an oversight that precludes, until corrected, a solid foundation for future LaMP activities. Acknowledgment and documentation of critical [at risk] human sub-populations can provide encouragement for necessary LaMP activities. This shortcoming can be readily addressed, but it requires immediate attention and action. In regard to loadings of Critical Pollutants, no estimation of mercury loads was developed and data gaps remain in regard to several other Critical Pollutants. Addressing these data gaps will help build the rationale that is necessary to achieve reductions in loadings of Critical Pollutants and will allow utilization of the expertise and momentum that has already been gained through the LOTMP and the NRTMP.
|Lake Michigan fisheaters cohort||PCB levels in breast milk and maternal serum correlates with consumption of contaminated fish.||Humphrey 1983|
|Native Americans (Mohawk) in New York State||Mean serum PCB levels in men was 5.4 parts ppb (max. 31.7 ppb), versus 5-7.7 ppb in the general population (Jensen 1989). Serum PCB levels were positively related to the number of fish meals consumed per year and increasing age.||Fitzgerald et al. 1996|
|Elderly cohort of Lake Michigan sport anglers||PCBs, DDE, and mercury levels were significantly higher in high fisheaters. High fisheaters presented disproportionately higher body burden levels of PCBs and DDE than low fisheaters in each age group, i.e., 50-59, 60-69.||Schantz et al. 1996|
|Pregnant women who consumed Lake Ontario fish||Women in the high-fish-consumption group ate an average of 2.3 salmon or trout meals per month for an average of 16 years.||Lonky et al. 1996|
|Pregnant African-American women who consumed Lake Michigan fish||Women were exposed to PTSs via fish consumption during most of their reproductive years. Seventy-five percent were less than 26 years of age and consumed lake fish for more than 15 years.||Waller et al. 1996|
|Reproductive age (18-34) Lake Michigan sport anglers||Approximately 50% ate 1 to 12 sport-caught meals in the past year, and 20% consumed 13 to 24 meals. Fish consumption was greater in males than females, with some males consuming 49 or more fish meals per year.||Courval et al. 1996|
|Charter boat captains, their spouses, and Great Lakes anglers||Serum levels of dioxin, furans, and coplanar PCBs vary by gender, and fish species predict coplanar PCBs and furan body burden levels but not dioxin levels.||Falk et al. 1997|
|Asian origin sport anglers on the St. Lawrence River||Bangledeshi fisheaters consumed an average 46.8 sport fish meals and Vietnamese fisheaters ate 40.7 meals, considerably less than the average 57 sport fish meals eaten annually by native Quebecers.||Shatenstein et al. 1997|
|3,751 individuals from five Canadian Great Lakes Areas of Concern (AOC)||Individuals are consuming species for which local guidelines do not exist, preparing fish in different ways, and eating fish more frequently than recommended in current guidelines.||Cole et al. 1997|
|Canadian fishermen from the St. Lawrence River basin||Mercury intake exceeded acceptable the daily dose for the most contaminated fish species. The estimated intake of PCBs was 10 to 100 times lower than the daily acceptable dose.||Gauvin et al. 1997|
Adapted from Johnson et al. 1998.
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Buck G.M., Mendola P., Vena, J.E., Sever, L.E., Sweeney, A.M., Kostyniak P., Greizerstein, H. and Olson, J. 1997b. Prospective pregnancy study, New York State Angler Cohort (work in progress). p. 35, Abstracts, Health Conference Great Lakes/St. Lawrence, Montreal, Quebec, May 12-15, 1997.
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Cohen, M., Commoner, B., Eisl, H., Bartlett, P., Dickar, A., Hill, C., Quigley, J. and Rosenthal, J. 1995. Quantitative estimation of the entry of dioxins, furans and hexachlorobenzene into the Great Lakes from airborne sources. Published by the Center for the Biology of Natural Systems, Queens College, Flushing, NY.
Cole, D.C., Dawson, J., Sheeshka, J., Keating, L.J., Owens, S. and Kraft, D. 1997. Quantitative results of an assessment of fish and wildlife consumption in Ontario Areas of Concern - 1995-1996 data. p. 9, Abstracts, Health Conference Great Lakes/St. Lawrence, Montreal, Quebec, May 12-15, 1997.
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Daly, H.B., Steward, P.W., Lunkenheimer, L. and Sargent, D. 1998. Maternal Consumption of Lake Ontario Salmon in Rats Produces Behavioral Changes in the Offspring. Toxicology and Industrial Health 14(1/2):25-39.
Falk, C., Hanrahan, L., Anderson, H.A., Patterson, Jr. D., and the Great Lakes Consortium. 1997. Body burdens levels of dioxin, furans, and PCBs among frequent consumers of Great Lakes sport fish. Health Conference '97 Great Lakes and St. Lawrence. Montreal, Quebec, Canada.
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Fox, G.A., Trudeau, S., Won, H. and Grasman, K.A. 1998. Monitoring the elimination of persistent toxic substances from the Great Lakes: Chemical and physiological evidence from adult herring gulls. Environ. Monit. Assess. 53:147-160.
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Waller, D.P., Presperin, C., Drum, M.L., Negrusz, A., Larsen, A.K., van der Ven, H. and Hibbard, J. 1996. Great Lakes fish as a source of maternal and fetal exposure to chlorinated hydrocarbons. Toxicology and Industrial Health 12:335-345.
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