Embed Size (px)
Citation preview
A RISK BALANCE ANALYSIS OF DIOXTN AND FURAN RELATED
SHELLFISH CLOSURES FOR ABOlRIGFNAL COASTAL
COMMUNITIES IN BRITISH COLUMBIA
Ctare L.S. Wiseman
B.E.S., University of Waterloo, 1992
Research Project Submitted in Partial FuifilIrnent of
the Requirements for the Degree of
Master of Natural Resources Management
in the
School of Resource and Environmen'd Management
Report No. 1 99
O Clare L.S. Wiseman 1997
Simon Fraser University
March 1997
Al1 rights reserved. This work may not be reproduced in whole or in part, by photocopy or other means, without permission of the author.
Acquisitions and Acquisitions et Bibliograp hic Services services bibliographiques
395 Wellington Street 395. rue Weilington Ottawa ON K I A ON4 Ottawa ON K I A ON4 Canada Canada
The author has granted a non- exclusive licence allowing the National Library of Canada to reproduce, loan, distriiute or sell copies of this thesis in microform, paper or electronic formats.
L'auteur a accordé une licence non exclusive permettant à la Bibliothèque nationale du Canada de reproduire, prêter, distri'buer ou vendre des copies de cette thèse sous la forme de microfiche/nlm, de reproduction sur papier ou sur format électronique.
The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts £kom it Ni la thèse ni des extraits substantiels may be printed or othemise de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation.
Abstract
Although the science of risk assessment/risk management has substantially improved in
recent years, there remains a tendency for regdators to focus primarily on the direct risks
of concern. The indirect or countervaihg risks that may be created by risk management
decisions are ofien overlooked. Govemment attempts to manage the human health risks
of consuming dioxin- and furan-contaminated shellfish in coastal areas of British
Columbia seem to continue this tradition. Beginning in 1988, many shellfish fisheries in
coastal areas of British Columbia were closed andior under consumption advisories due
to elevated levels of chlorinated dibenzo-p-dioxins and dibenzofurans in the edible tissues
of various crustacea and mollusca. A nwnber of these areas involved First Nations'
fisheries. Risk management activities intended to protect shellfish consumers could be
expected to dismpt aboriginal harvesting and consumption patterns; patterns which have
become widely recognized as being nutntionally beneficial. Only the direct health risks
(i.e. cancer) of consuming dioxin- and furan-contaminated shellfish were, however,
considered by the Govemment in the formulation of risk management options. It is
argued that a focus on the direct nsks alone does not provide an adequate basis for risk
management decisions which would best protect aboriginal peoples fiom chemical health
risks. Management actions such as fishery closures may serve to create an even greater
countervailing risk if the dietary substitution of sheIIfish with higher-fat, store-bought
foods is encouraged.
This study attempts to describe and compare the potential heaith impacts of aiternative
risk management options for First Nations peoples in the management of dioxin and furan
contamination in CO& areas of British Columbia. Kitimat, GoId River and Powell
River are the areas of focus. The excess cancer risks of consuming contaminated
shellfish for these three sites are estimated. To partially quanti@ the countervailing risks
of risk management decisions for comparison, a scenario was developed in which First
Nations peoples would substihte shellfish with store-bought foods in their diets in the
event of a fishery closure or advisory. ïncreases in mortality due to coronary heart
disease, associated with an increase in dietary saturated fats, were estimated. The health
nsks of dietary changes among aboriginal peoples appear to be greater than those related
to eating dioxin- and furan-contaminated shellfish. A nurnber of uncertainties and issues,
however, inject a large degree of complexity into the evaluation of alternative chernical
risk management options. It is recommended that aboriginal peoples be involved in
decisions regarding fishery risk management activities in the future.
Acknowledpents
1 would like to thank my senior supervisor, Dr. Frank Gobas fiom the School of Resource
and Environmental Management of Simon Fraser University, for his guidance, support and
advice. 1 am also indebted to my supervisor, Dr. Pamela Wright, fiom the School of
Resource and Environmental Management at Simon Fraser University, for her help and
support in this research project.
1 would also like to express my gratitude to the Kitamaat Village Council of the Haisla
Nation, for providing valuable information for this research. A speciai thanks must be
given to Morris Amos, Manager of the Haisla Fisheries Commission, who supported this
project and acted as a liaison between myself and the Kitamaat Village Council. 1 would
also like to thank Parnela Winquist, a Registered Diet Nutntionist, whose help and support
was invaluable. Other individuals whom I would like to thank include Wayne Knapp,
Senior Biological Technologist, Water Quality Unit, Habitat and Enhancement Branch,
Department of Fisheries and Oceans and Dr. Neville Thornpson, Nutrition Research
Division, Health Canada (retired). The perspectives presented and the conclusions made in
this paper do not reflect the opinions or beliefs of the Kitamaat Village Council nor those
of the above-mentioned individuals uniess otherwise stated.
Finally, 1 would Iike to express my gratitude ?O Patricia McCuny and Harald Bathelt for
their support, encouragement and valuable advice.
Table of Contents
Approval Page
Absiract
Acknowledgmenw
Tables, Maps and Figures
1. Introduction
1.1 Purpose and Objectives
2. Methods
2.1 Estimating the Excess Cancer Risk of SheIlfish Consumption
2.2 Characterizhg the Health Impacts of Fishery Risk Management Actions
3.1 Aboriginal Shellfish Consumption
3.2 The Excess Cancer Risks of ShelIfish Consumption
3 -3 Estimated Increases in Coronary Heart Disease Mortality Due to a Dietary Change
4. Discussion
4.1 Evaluating the Excess Cancer Risks of Shellfish Consumption
4.2 Comparing Calculated Cancer Eüsks with Increases in Coronary Heart Disease Mortdity for First Nations Peoples: Estimates, Uncertainties and Considerations
5. Conclusions, Recornmendations and Thoughts for the Future
Appendix A: Scientific Terms for Shelifîsh Species Discussed
Appendix B: Calculated TEQ 's (mghg wet weight) According to Species/Tissues for the Examined Areas for 1989 - 1995 for which Data was Avnilable
Appendix C: Background to the Assessment of the Excess Cancer Risks of Consuming Shellfih
Appendix D: Merhod Used to Derive Parameter Estimates for the Multistage Mode1
Appendix E: Distributions Shapes for Some Inputs into the Calculation of the Excess Cancer Risks of Consuming Shellfish
Appendix F: Distriburion Shapes for Selected Inputs into the Calculation of lncremes in Excess CHD MortaZity Due to the Subsrirution of Shellfsh with Chicken, Beef and Pork
Appendïx G: Excess Lifetime Cancer Risks According to Area and Species/Tissues for 1989 - 1995 for which Tissue Residue Data wus AvailabZe
References Cited
vii
Tables, lMaps and Figures
Tables
Table 1 : Results of the Histopathological Re-Evaiuation of Hepatic Lesions in Female Sprague-Dawley Rats in the Kociba et ai. (1978) B ioassay
Table 2: Percent Reductions in Amencan CHD Mortality Rates Resulting fiom an Average 7% Reduction in Daily Energy Consmed as Saturated Fat According to Age and Gender
Table 3: Number of Reported Deaths Due to Ischaernic Heart Disease for 1987-1 993 and Cnide Annual Death Rates per 10 000 Aboriginal Population According to Sex
Table 4: Estimated Daily Aboriginal Shellfish Consurnption Rates
Table 5: Excess Lifetime Cancer Risk Estirnates According to Area and Shellfish Species/Tissues for the First Two Years of DFO Management
TabIe 6: Excess Lifetime Cancer Risks of Consurning a Mixed Species/Tissue Diet for Each Site for the First Two Years of DFO Management
Table 7: Estimated Excess Nurnber of Cancers per 10 000 Individuals Over a 70 Year Period According to 1989 Shellfish Tissue Residue Levels
Table 8: Percent Change in Daily Energy Derived fiom Saturated Fat with Shellfish Substitution According to Gender
Table 9: Estimated Increases in Excess CHD Mortality per 10 000 Individuais Over a 70 Year Penod According to Gender Due to Dietary Substitution
Table 10: A Comparison of Health Canada's Species-Specific Risk Management Recommendations and DFO's Decisions in 1989 for the Three Study Areas
Table 11: Total 0-3 Fatty Acid and EPA Contents of Some Shellfish Species (gI100 g wet weight)
Table 12: Calculated Cnide and Adjusted CHD Mortality Risk Ratios for the Amount of Fish Consumed
Table 13: Summary Table of Factors Which May or May not Favor the Use of Risk Management Actions to Restrîct Shellfish Consumption Among Aboriginal Peoples 62
Table 14: Calculated TEQs (mgkg wet weight) According to SpeciesfTissues for the Examuied Areas for 1989- 1995 for which Data was Available
Table 15: Excess Lifetirne Cancer Risks According to Area and Species/Tissues for 1989-1995 for which Tissue Residue Data was Available
Maps
Map 1 : British Columbia Dioxin- and Furan-Contaminated Coastal Sites (1 989- 1995)
Map 2: Kitirnat Areas of Contamination and Associated Risk Management Actions (1989-1995)
Map 3 : Gold River Areas of Contamination and Associated Risk Management Actions (1 989-1 995)
Map 4: Powell River Areas of Contamination and Associated Risk Management Actions (1989-1995)
Figures
Figure 1 : General Conceptuai Frarnework to Study Analysis
Figure 2: Overview of the Method Used to Estirnate the Excess Cancer Rkks of Consurning Shellfish
Figure 3: A Cornparison of Saturated Fat Contents of Some Shellfish Species with that of Several Common Store-bought Protein Alternatives
Figure 4: Overview of the Method Used to Estirnate Increases in CHD Mortality Due to Shellfish Substitution
Figure 5: 1989 Upper Bound Excess Cancers for a Mixed Shellfish Diet for the Three Areas vs. That for Some Common Foods
Figure 6: A Cornparison of the Estimated Upper Bound Excess Cancer Deaths of Consuming a Mixed Diet of Shellfish Using Keenan et al.'s (1991) Cancer Potency Factor b e r 10 000170 years) and Excess CHD Mortality Due to Shellfish Substitution @er 10 000170 years) 50
Figure 7: Shape of Distribution of Tissue Residue Toxic Equivalents in Kitimat Crab Hepatopancreas (mgkg), 1995 74
Figure 8: Shape of Distribution of Tissue Residue Toxic Equivalents for Gold River Crab Muscle (mgkg), 1990 74
Figure 9: Shape of Distribution of Tissue Residue Toxic Equivalents in Powell River Oyster (mgkg), 1995 75
Figure 10: Shape of Distribution of Human Body Weight (kg) 75
Figure 1 1 : Shape of Distribution of Crab Muscle Consumption Rate (glday) 76
Figure 12: Shape of Distribution of Crab Hepatopancreas Consumption 76 Rate (glday)
Figure 13: Shape of Distribution of Percent Change in Energy Consumed as Saturated Fat Among Men Due to Crab Substitution
Figure 14: Shape of Distribution of Percent Change in Energy Consumed as Saturated Fat Among Women Due to Crab, Clam and Prawn~Shrimp Substitution
1. Introduction
Risk management decision-making among regdatory agencies has often been fiawed.
Although the science of human heaith risk assessmenthisk management has substantiaily
improved, there d l 1 remains a tendency to focus prirnarily on immediate or direct risks.
The broader implications of policy and regdatory measures in the management of nsk,
notably the indirect or countervailing risks that rnay result, have traditionally received
scant attention (Keeney and von Winterfeldt 1986; Zeckhauser and Viscusi t 990; Keeney
1994; Graham and Wiener 1995). In other words, there has often been a faiiure to fully
compare alternative management options and their potential consequences before decisions
are made.
This narrow approach to risk assessrnent/risk management is the product of a number of
different factors. For instance, many risks rnay be difficult or impossible to quanti@ and
hence are simply ignored (Lave 198 1). Environmental laws and regulations, which
overwhetmingly focus on the amelioration of direct risks, have aiso served to discourage
the andysis of indirect risks (Keeney and von Winterfeldt 1986; Lave and Malès 1989).
Additionally, countervailing risks can be overlooked as a result of the hgrnentation in
decision-making beîween governrnent departments and agencies (Graham and Wiener
1995). Whatever the reasons may be, the outcome is often the same; that is, unsuitable risk
management policies are sometimes implemented. The direct risk rnay be substituted by
another, or a new risk created, that rnay pose an even greater hazard than the one initially
targeted (see Whipple 1985; Keeney and von Witerfeldt 1986; Ames et al. 1987; Ames
and Gold 199 1 ; Putman and Graham 1993; Graham and Wiener 1995).
As part of a national sampling program in 1987, some shellfishl sarnples taken from areas
close to pulp and paper mills were found to contain elevated levels of dioxins and furaus
(Department of Fisheries and Oceans 1988; British Columbia Ministry of Environment,
Lands and ParksiEnvironment Canada 1993). Further sampling results led the Depvtment
of Fisheries and Oceans @FO) to close areas in Howe Sound and Prince Rupert to crab,
prawn and shrimp harvesting in 1988 (DFO 1988). Additionai shellfish fishery closures
occurred at other locations in 1989 (Le. Kitimat Arm, Gold River, Crofion, Nanaimo,
Powell River, Campbell River and Cowichan Bay) @FO 1989b).~ In addition, advisories
conceming the consumption of certain fish and shellfish organ meats were issued (Le.
bottomfish liver and crab hepatopancreas). A number of existing closures were expanded
in the early 1990's (DFO 1990, 199 1, 1 993).3 Burrard Inlet and Victoria Harbor were also
closed at this time. See Map 1 for an ovewiew of the above areas.
1 The tenn shellfish is used here to refer both to crustacea (e.g. crab) and mollusca (e.g. clam).
2 Where shellfish fishery closures have occurred and consumption wamings issued, govemment documents have typically not specified the specific species of concem. Rather, a crab consumption advisory, for example, would generally refer to al1 crab species in a specified area. In certain instances, particular species have been the actual focus of risk management. Crab sampling and management efforts, for instance. have concentrated on Dungeness Crab in most areas. A list of scientific tenns for species discussed in this text c m be found in Appendix A.
3 Based on the DFO Criteria for the Reducrion or Eliniination of Dioxin-Mediated Marine Fishev Closrrres and Consumprion Advisories @FO 1994), many fisheries have since been re-opened and a number of advisories iifted since Febmary 1995 @FO 1995a, 1995b, 1996a).
Map 1 : British CoIurnbia Dioxin- and Furan-Contaminated Coastd Sites (1 989-1 995)
7 1 - ', \ -1 1 ----,
t - L i
Adapted h m DFO (1989a. 1989b. 1990. 1991. 1993,1995a, 1995bl
Many of these fishery closures and consumption advisories involved First Nations'
fisheries. Fish, especially species of saimon, have traditiondly been the most important of
country foods among coastal peoples. Shellfish resources have, however, fomed a
vaiuable part of the fish-based diet for rnany First Nation peopIes (Drucker 195 1; Ellis and
Swan 198 1) . DFO's risk management activities could thus be expected to have
interrupted traditionai harvesting and consumption patterns; patterns which have becorne
widely recognized as nutntionally beneficial (e-g. Kuhnlein et ai. 1982; Doolan et al. 1990;
Kuhnlein 1992; Health Canada 1994). Country foods, for instance, tend to have a higher
nutritionai quaiity than equivalent market foods. For example, regular ground beef
contains about 18 gram of fat per 90 gram serving (Williams 1995), while the body and
leg tissue of Dungeness crab (Cancer magister) contains about 1 gram (King et al. 1990).
Market foods have progressively displaced traditional foods fiom the diets of First Nations
peoples. Greater consumption of high-carbohydrate? low-nutrient, cheap foods has been
especially dominant where poverty limits buying-power (KuhnIein 1993). in conjunrtion
with changed lifestyles, such dietary changes have been identified as a major factor in the
alteration of disease patterns among aboriginal peoples and in the deterioration of their
nutritionai health (Wirsing 1985; Young 1988; Kuhniein 1993). Specificaily, chronic
diseases characteristic of 'western civilization' such as diabetes, obesity and cardiovascular
disease have rapidly displaced infectious diseases as the primary causes of morbidity and
mortality. Certain diseases such as diabetes have become a serious health concern in some
cornmunities, with rates that often exceed those in the general popdation (Mao et al. f 986;
Evers et ai. 1987; Young et al. 1989; Young 1990; Heffernan 1995).
The dietary importance of marine resources for coastal First Nations peopies in British
Columbia warrants consideration in efforts to assess and manage risk for targeted fishery
species. For instance, the potential that risks for coronary hem disease (CHD) may be
enhanced for those who substitute shellfish with higher-fat, store-bought foods in the event
of a fishery closure is necessarily a concern. In the f o d a t i o n of risk management
actions for dioxin- and furan-contaminated areas though, oniy the direct cancer risks of
consuming shellfish were considered (Dalpé, C., Chernical Heaith Hazard Assessrnent
Division, Bureau of Chernicai SaTety, Food Directorate, Health Canada, pers. cornrn.
1996). The p~tential cancer risks may have indeed necessitated fishery closures in some
instances, especially for First Nation peoples who tend tu eat greater quantities of fish
resources. The fact remains, however, that in the absence of a full consideration of al1
risks, both direct and indirect, it cannot be determined whether the chosen management
actions were optimal. The countemaiIing risks associated with alternative foods such as
beef and the health benefits of consuming traditional foods may outweigh the health risks
posed through the intake of shellfish.
1.1 Purpose and Objectives
This study is a retrospective anaiysis of the risk management actions undertaken by the
Government in coastal areas of British Columbia to protect shellfish consumers from
dioxin- and hnan-related health risks! The purpose is to describe and compare the heaith
risks of consuming shellfish with that of the chosen risk management strategies for coastaf
Fust Nation peoples. This first entail a quantification of the excess cancer risks of
consuming dioxin- and furan-conbmuiated crustacean and molluscan species which have
been targeted by DFO for management. Potential countervailing risks which may be
created by fishery management actions will be partially quantified for comparison. This
will involve the development of a scenario whereby individuals would replace shellfish in
their diets with common store-bought protein alternatives in the event of a fishery closure
or health advisory. The potential resultant increases in mortaiity due to CHD will then be
caiculated to provide a comparative estimate of the risks associated with store-bought
foods. Literature regarding the issues related to such a risk vs. risk comparison and a store-
bought vs. country food diet will also be examined. The intent of this analysis is neither to
recommend a preferred diet nor specific risk rnanagement actions. The goal is rather to
elucidate a decision-making frarnework for the formulation of risk rnanagement activities
that will aid in the protection of aboriginal peoples fiom excess risk in the future. Figure i
displays the generalized conceptual frarnework that will be used for the anaiysis and the
presentation format of this paper. Although health risks will be the focus of attention, it
should be noted that health is often integraily connected to culturai and economic weI1-
being5
4 As of Aprii 1996,46% of the total areas which was previously closed to the harvesting of shellfish has been re-opened OF0 1996b).
5 This has become a widely-accepted concept of health since it was developed by the World Health Organization (WHO) in 1946. They defined heairh as "a state of complete physical, mental and social well being, and not merely the absence of disease or infmity (WHO 1978: 21."
Figure 1: General Conceptual Framework to Study Analysis
Excess Cancer Risks of Shellfish Consurnption
Characterize Countervailing Risks:
CHD Mortality Due to Shellfish Substitution
Qualitative Analysis of Risks and Benefits of Country and Store-bought Foods
Compare Direct and Countervailing Risks:
Major Considerations: magnitude of cancer risks and increases in CHD mortality uncertainties in estimates
other factors to consider include: non-cancer health effectç of dioxin exposure qualitative health benefits and risks of country and store- bought foods
Risk Management Decision-making: Considerations/Recommendations
2. Methods
2.1 Estimating the Excess Cancer Risk of SheWsh Consnmption
Three of the identified dioxin- and furan-contaminated areas were chosen for the cancer
risk assessrnent of consurning sheliiïsh, i.e. Kitimat A m , Gold River and Powell River.
These sites were chosen for several reasons. They represent various degrees of dioxin- and
furan-contamination (Table 14 in Appendix B provides an overview of dioxin and furan
tissue residue levels that have been calculated for the years 1989-1995). As such, the range
of concomitant management actions undertaken by DFO to protect subsistence and
recreational fishermen6 are well-represented by these areas. Kitimat involved
comparatively lower levels of contamination, where consumption advisones for crab
hepatopancreas were issued and clam fishing was closed. Gold River and Powell River
were areas of medium to high contamination and involved total fishery closures for crab
muscIe, prawns and oysters. Advisories for the consumption of crab hepatopancreas were
also issued for these areas. Maps 2,3 and 4 provide an overview of the three sites. The
sites were aiso chosen because of the presence of First Nation peoples in the area.
6 Management activities to protect subsistence and recreationa1 fishermen are sometimes different from those concerning the commercial harvesting of species. White consumption advisories may have been issued for the former, the latter may have involved closure of the area. The rationaie for this is th2t subsistence and recreational fishermen can make their own decisions regardhg risk exposure once informed about potential hazards. The market consumer, in contrast, is not likely to know about the origins of the food products and the associated risks (Knapp, W. Senior Biological Technologist, Water Quality Unit, Habitat and Enhancement Branch, DFO, pers. comm. 1996).
Adaptecl fiom DFO (l98ga. 1989b. 1990,1991, 1993. 1995a. 19931
Map 3: Gold River Areas of Contamination and Associated Risk Management Actions (1989-1995)
Map 4: Powell River Areas of Contamination and Associated Risk Management Actions (1 989-1 995)
Connimption MWt i
Cnb Firhing Clonire
\ Texada Island
I Adapted from DFO (1989a. 1989b. 1990. 1991.1993, 1?95a, 1995b)
An approach sirnilar to that used by the U.S. Environmental Protection Agency @PA) was
chosen for the e=~olation of dioxin cancer risk.' The EPA approach is significantly
different fiom that wed by Health Canada, whose assessments form the basis of DFO's
risk management decisions. Differences between Health Canada and the EPA in their
assessrnent of rkk arise fiom dissimilar theoretical assurnptions made regarding the
carcinogenic mechanisms of dioxins and furans. The contrasting methodologies yields
divergent human health risk estimates of dioxin exposure, the EPA's approach being the
more conservative of the two. Appendix C details the two approaches used by the EPA
and Heaith Canada and the rationde as to why the more conservative approach was used
for this analysis.
A two-stage multistage mode1 was fitted to the results of a histopathologicai re-evaiuation
of hepatic Iesions in female Sprague-Dawley rats exposed to 2,3,7,8-tetrachlorodibenzo-p-
dioxin (TCDD) in the Kociba et al. (1978) bioassay (Keenen et al. 1991)~ The mode1 is as
fo~lows,
where P is the proportional tumor response at dose d, aa, represents the spontaneous rate of
occurrence, and rr,dl and a d depict the response at dose d.
7 See Covello and Merkhofer (1993) for a review of other rnethods to calculate hurnan health risk.
The Kociba et al. (1978) bioassay results were re-evaluated by an independent panel of pathologists in the U.S. (Pathology Workig Group (PWG)) in 1990 according to a new classification scherne for proliferative rat Iiver Iesions established by the U.S. National Toxicology Program (Keenan et al. 1991). Considerably fewer cancerou turnors were classified by the PWG than that previously reported.
Reported results for the total combined incidence of hepatocellular carcinomas and
adenornas were used (see Tabte 1). Background and chemicaily induced tumor incidence
were assumed to occur in an additive fashion.
Table 1 : Results of the Histopathologicai Re-Evaiuation of Hepatic Lesions in Female Sprague-Dawley Rats in the Kociba et al. (1978) Bioassay
O - 0.00 1 0.0 1 o. 1
Hepatocellular Carcinomas 0/86 O150 0150 4/45
Hepatocellular Adenornas Z86 1 /50 9/50 14/45
Total Incidence Z86 1 /50 9/50 18/45
(fiorn Keenan et al. 199 1)
The Solver function in ExceI (Microsoff Corp.), a built-in optimizing macro-function in
this program, was used to derive a best fit solution for the multistage model. The resultant
equation is as follows,
As shown, the parameter a? became zero during the fitting process. A one-hit model,
hence, results, which is essentidly a reduced form of the multistage model (CovelIo and
Merkhofer 1993). The parameter a,,, which represents spontaneous background tumor
incidence, was dropped fiom the equation. a, was then adopted as a cancer potencyfâctor9
9 The cancer potency factor derived here is not to be confused by those used by the U.S. EPA. This agency calculates a cancer potency factor as the upper-bound estimate of the carcinogenic potency of a chernical using a linearized form of the muItistage mode1 (Le. the upper 95 percent confidence lirnit) (US. EPA 1989). The cancer potency factor derived here represents a 'best estimate' of the slope of the dose-response function.
for dioxin to extrapolate estimates of risk in the low dose range.'' Appendix D describes
the multistage model in greater detail and how it was fitted to the rat bioassay data to
derive parameter estimates.
The caiculation of risk sirnply involves the multiplication of the derived cancer potency
factor (Le. 4747) with exposure dose. Figure 2 provides an overview of the method used to
estimate the excess cancer risks of shellfish consumption.
Figure 2: OveMew of the Method Used to Estimate the Excess Cancer Risks of Consuming Shellfish
Calculate Inputs1 Statistical Distribution Anaiysis
Toxic Equivalents Aboriginal Shellfish Consumption Rates
Monte Car10 Simulation
Fitted Multistage Model: Risk = Cancer Potency Factor x Erposure Dose
Distributions of Risk
10 Using a linearized fom of the multistage model, Keenan et al. (1991) derived a higher cancer potency factor (CPF) of 9700 from the sarne rat tumor incidence data used here. This difference is expected because the linearized multistage model (LMS) typically produces factors which are 2 to 3 tirnes larger than those estimated uing the standard model as done here (Covello and Merkhofer 1993).
The following equation was used for the estimation of the exposüre dose for First Nations
peoples located in the study areas,
ED = exposure dose (mg/kg/day)
C = tissue residue concentration in the edible part of species (mgkg)
CR = daily consumption rate of species (kg/day)
BW = human body weight (kg).
It was assumed that the exposure dose and effective or delivered dose are the same. Data
on body weight was denved fiom an anthropometric s w e y conducted by National Health
and Welfare in the 1970's (Department of National Health and Welfare 1980). Values
reported for Indian adults in this s w e y were used to calculate a mean body weight o f 70.5
kg and a standard deviation of 14.9 kg.
First Nation shellfish consumption rates were estimated h m the results of a diet survey of
mernbers of the Haisla Nation (Kitamaat Village Council 1994).' ' The survey entailed IWO
different question periods, summer and winter, involving a total of 1 1 1 persons (the Haisla
population is approximately 1200). Most individuais participated in both survey penods
(Le. 107 and 86 persons were involved in the winter and summer surveys, respectively).
I I The Haisla Nation is located on ihe eastern side of Kitimat Am, dose to the town of Kitimat, about 72@ km no& of Vancouver.
Average consumption rates for crab muscle, crab hepatopancreas,'2 clams and
shrimp/prawns were derived for both periods to yietd an annual daily average.I3 Reported
rates for oyster could not be used to estirnate the cancer risks of eating oyster in Gold
River. Due to the absence of oysters in the Kitimat area, oyster consumption rates reported
by survey participants were not considered to be reflective of aboriginal intakes in the other
coastai areas where this species is abundant. For ihis reason, rates of clam consurnption
were used to estimate the cancer nsks of eating GoId River oysters.
For those persons who participated in only one of the two surveys, it was assumed that
reported consumption rates for the given season would remain constant throughout the
year. This may have resulted in lower- or higher-than-normal calculated averages for
certain country foods for these persons. This arises out of the fact that some species are
eaten in varying amounts over the year depending on the season. For instance, more crab
muscle was eaten by survey respondents in the surnmer than in winter. It was assurned that
reported consumption rates would be representative of both actual Haisla consumption
patterns and those of other First Nations peoples located in coastal areas." Average
consumption rates were cdculated for those who eat the targeted shellfish species, as
-- - - -- -
'' Individuals were asked to indicate their consumption arnounts of crab orguns in the survey. This was assumed here to be hepatopancreas.
13 Consumption rates were not reported for specific species.
I4 It should be noted that it is difficult to establish actual food htakes through the use of dietary surveys (Thompson, Dr. N., Nutrition Research Division, Health Canada (retireci), pers. comm. 1996). For instance, it can be difficult for s w e y participants to report exact values of food consumption over a longer time period. Also, reported values may be indicative of the relative importance of a particular food in relation to others, as opposed to actual consumption arnounts. For example, favorite foods may be over-reported.
opposed to the whole survey population. As such, risk estimates would not apply to each
individuai in a population, but only to that segment which eats the specified
speciedtissues.
Reported shellfish consumption rates may be lower than is normaily the case. One
traditionally important harvesting area for the Haisla, notably Kitimat Arm, has been
irnpacted by pollution problems since the early 1970's. Reduced resource harvesting rnay
have occurred as a result. Furthe. the Haisla Diet Survey (Kitamaat Village Council 1994)
was conducted when the clam fishery closure aqd crab hepatopancreas advisory were in
effect. Reported clam and crab hepatopancreas consumption rates may hence not be
reflective of typical eating patterns under 'normal' conditions. Caution must, therefore, be
exercised in the interpretation of the results.
Dioxin- and han-tissue residue levels for shellfish species were obtained fiom DFO.
Residue levels were reported for the 17 dioxin and furan congeners of greatest concern."
International Toxicity Equivalency Factors (TEFS)'~ were used to estimate a toxic
equivalency quotient (TEQ)" for each reported sarnple in a given area. Where non-
15 The most toxic congeners are those that have chorine substitutions in the 2,3,7 and 8 positions (Safe 1989, 1990; Boddington et. al 1990). Other congeners are substantially less toxic in cornparison and are, hence, not usually considered.
16 Based on established structure-activity relationships (SARs), TEFs have been assigned to the rnost active dioxin and furan congeners (Safe 1989. 1990; Boddington et. al 1990). TCDD, the most toxic congener, has a TEF of 1. The others have TEFs that express their toxicity relative to TCDD.
17 TEQ is the total of the relative toxicity of the rnost toxic dioxin and furan congenen relative to TCDD.
detectable values were reported for congeners, a value of haif the detection limit was used
(see Travis and Land (1990) for a review of how to deai with non-detectable values). In
some instances, tissue residues were not reported for specific 2,3,7,8-substituted congeners,
but as congener groups. For example, 2,3,7,8-pentachiorodibenzofuran (PCDF) and
1,2,3,7,8-pentachlorodibe11~0furan (PCDF) were sometimes reported as one value (i.e.
2,3,7,8-substituted PCDF). As these two 2,3,7,8-PCDFs have different TEQ values, it was
necessary to use an average value in this case. Average toxic equivalents and their
variance for reported sarnples were then estimated for DFO-managed sites. Where the
numbcr of individuals in a particular composite sample were reported, a weighted average
was calculated.
The excess lifetime cancer risks of consuming contaminated shellfish were caiculated
probabilistically for each study area. This involved the development of a model in Excel
(Microsoji Corp.). Lognormal distributions were chosen to represent model inputs (i.e.
TEQs, body weight and consumption rates); the most comrnonly accepted distribution to
describe such parameters (Morgan and Henrion 1990; Adams et al. 1994; Hattis and
Burmaster 1994). Appendix E displays the shapes of the derived statistical distributions
for selected model inputs. Uncertainty was then propagated through the model using the
Latin Hypercube Sampling (LHS) option in the program Crystal Bal1 (Decisionsering
Corp.). LHS was used because it stabilizes the taiIs of the output distributions more
quickly than does regular Monte CarIo Simulation (Bmaster and Anderson 1994). A
number of test runs were first conducted to detennine the number of iterations that would
be necessary to ensure stability in the central moments such as the mean and in the tails of
the output distributions. Simulation nuis were then executed using 10 000 iterations.
Initial 'seed' values were generated by the pro- in a random fashion.
2.2 Characterizhg the Health Impacts of Fishery Risk Management Actions
The characterization of the health benefits and risks of foods is a very difficult task.
Methods for the estimation of such parameters are vimially non-existent (Institute of Food
Technologists 1988). Many risks and benefits are also essentially impossible to quanti@ .
To deal with this problem, a combination of two methods were needed to detennine the
acceptability of fishery risk management options through the cornparison of risks and
benefits. The first involved a weight-of-evidence approach, the resuits of which will be
presented in the discussion section. This entailed a review of the literature regarding such
issues as the bene& and risks of consumhg shellfish and higher-fat, store-bought foods.
In the second approach, possible health effects of fishery management actions such as
closures for First Nations peoples were modeled. Increases in coronary heart disease
(CHD) rnortality rates among coastal aboriginal peoples due to possible dietary changes in
response to fishery closures and advisories were the chosen health effect for this purpose.
A scenario was developed in which shellfish-eaters wodd eliminate shellfish fiom their
diets and eat equivalent arnounts of common store-bought protein alternatives (i.e. chicken,
beef and pork). In the case of a consumption advisory, it was assumed that individuals
wouid not eat the targeted species that were under advisory out of fear. It was also
assumed that sheufish from other non-contaminated areas could not be obtained. The
assumption of dietary substitution was based, in part, on the observation that contaminants
have been an important factor as to why many aboriginal peoples have reduced their
consumption of country foods over tirne (Kuhnlein 199 1,1993,1995). One study has also
estimated that aboriginal peoples tend to fish close to their local communities (Le. an
average distance of 26.3 km is traveled for fishing) (J2.A.G.L.E Project 1996). It would,
hence, not be unreasonable to assume that at least some individuals wodd reduce their
consumption of fishery foods if their comrnunities are impacted by contaminants.
With dietary substitution, it was postulated that dietary saturated fat and cholesterol intakes
would increase because store-bought items often contain greater arnounts of fats than
country foods. Figure 3 clearly displays the elevated saturated fat contents of some store-
bought protein alternatives in cornparison to that for some shellfish species. Scientific
terms for the shellfish species referred to in the figure can be found in Appendix A. Due to
the relation between dietary fat and senun cholesterol levels (Brown and Smith 1995;
Feldman 1994), edanced CHD risks were recognized as a possible effect. As Wald-am et
al. (1995: 86) state, for instance, "Abandoning a traditional diet for one which is likely to
be high in fats, particularly saturated fatty acids, cm be expected to have a detrimental
impact on the risk of heart disease."
Figure 3: A Cornparison of Saturated Fat Contents of Sorne Shellfish Species with that of Several Common Store-bought Protein Aiternatives
Gound bxf, broiled*
Suloin steak, h a e d *
Pork chop. hoiicd*
Chicken brcast, fric@
Pacific Oystcr. r a d *
ManiIa clam. aeamed8*
Dungracss crab. cooked**
Pink shrimp. cooked8*
0,OO 2.00 4.00 6.00 8,OO 10.00 12.00
Saturated Fat Content (g)
(*frorn Williams 1995; **from King et al. 1990)
The extrapolation of increases in CHD mortality due to the dietary substitution of shellfish
with store-bought protein alternatives was conducted in a nurnber of steps. Figure 4
provides an overview of the method used. The percentage of the total daily energy (Le.
caloric intake) consurned as saturated fat was first calculated for each adult who
participated in the Haisla survey using the following equation,
DSF = DFI x 9 / DEI x 100
where,
DSF = proportion of total energy derived fiom saturated fat on a daily bais (%)
DFI = daily saturated fat intake (g)
9 = the amount of energy contained in one gram of fat (kcal/g)
DEI = daily energy intake (kcal)
Calculate Inputs/ Statistical Distribution Analysis
Cnide Annual Aboriginal CHD Death Rates
( C m )
Figure 4: Overview of the Method Used to Estunate Increases in CHD Mortality Due to Shellfish Substitution
- Change in % Energy
Consumed as Saturated Fat with the Substitution of SheIlfish with Chicken,
Beef & Pork (dSF)
Estimated Proportional Changes in American CHD
Death Rates Due to a 7% Reduction in Energy
Consumed as Saturated Fat (ACNDD)
Monte CarIo Simulation
Annual Excas CHD Mortality =
(ACHD D x ASF/O. O 7) x CHDDR
Distributions of Excess Increases in CE-D Mortality
Average percent saturated fat intakes were calculated separately for males and femaies.
Crab was then elUninated from the diet of each individual and replaced with equivaient
amounts of chicken, beef and pork. For instance, it was assumed that if an individual eats
24 g of crab muscle per day, this would be replaced with the same amount of chicken, beef
and pork (Le. 8 g of chicken, 8 g of beef, 8 g of pork). The consumption of possible other
protein aitematives to contaminated shellfish were not considered for this analysis. The
percentage change in d d y energy derived Eom saturated fat was estimated for each
individuai as a result of this dietary change. An overail average was then derived
separately for males and fernales. The same process was also done for crab, clam and
prawdshrimp substitution, a situation which wodd represent a 'worst case scenario.'
The extrapolation of potential increases in mortality as a h c t i o n of percent changes in
saturated fat were based on the work of Browner et al. (1991). Based on the equations
developed by Keys et ai. (1965, 1974) and Hegstedt et al. (1965), Browner and his
colleagues assumed that changes in s e m cholesterol concentrations are a linear function
of the change in the percent of total energy consumed as saturated fat- Browner et al.
(1 99 1) estimated that s e m cholesterol concentrations would increase by 0.08 mmoVl
(3 mg/dl) with each one percent increase in daily energy consumed as saturated fat. They
assumed a reduction of 20 mg/day of dietary cholesterol per percent reduction of saturated
fat. Browner et al. (1 991) then modeled the proportional reductions in CHD mortality rates
among the US. population that would result if individuals would reduce the arnount of
their present percent total daily energy derived fiom saturated fats by no more than 7% on
18 average. Displayed in Table 2, their results were based on curent data on fat intakes
among Amencans, CHD mortality rates and availabie logistic regression coefficients
18 Browner et al. (199 1 ) had assurned that Americans would reduce their totaf fat intakes to 30% of the percent total energy or caIories consumed in their modeling scenario. The average percent daily energy consumed as fat by Amencans was 37% at the time of their study* This would represent an overaii average of a 7% reduction in saturated fats for the age-sex-race categories they studied as it is only the saturiited fat component of the diet that is related to semm cholesteroi IeveIs.
which relate the degree of coronary health risk to s e m cholesterol concentrations as a
function of saturated fat intakes.
Table 2: Percent Reductions in American CHD Mortality Rates Resulting from an Average 7% Reduction in Daily Energy Consumed as Saturated Fat According to Age and Geoder
A S (Years) Males (%) FemaIes (%)
25 16 10
3 5 30 I I
45 15 I O
55 11 9
265 5 6
( fiom Browner et al. 1991)
The above estirnates fiom Browner et ai. (1 99 1) are based on a linear relationship between
serurn cholesterol levels and changes in the percent intake of d d y energy consumed as
saturated fat. Although their modehg scenario entailed estimating reductions in CHD
mortaiity rates, the linear function used allows for the extrapolation of their scenario to the
one developed for abonginal peopies here (i.e. increases in CHD deaths as a fiinction of
increases in senun cholesterol leveis due to a dietary change involving greater fat intakes).
A number of assumptions had to be made for this purpose. First, it was assumed that the
relationships between energy fiom saturated fat, semm cholesterol levels and mortality
rates which were modeled by Browner et al. (1 99 1) would aiso be applicable to the study
population here. For instance, it was assumed that the established distributions of serum
cholesterol concentrations among Americans, as a function of dietary fat intake, would be
the sarne for First Nations peoples. Second, established CHD mortality risk levels and
serum cholesterol concentrations for American populations were also assumed to be
similar to that for aboriginal peoples. Third, like Browner et al. (1 99 l), changes in
saturated fat intake were assurned to be accompanied by proportionai changes in dietary
cho1esterol. Fourth, it was assumed that serum cholesterol levels were the only mediating
factor through which saturated fat affects CHD mortaiity.
Estimated changes in First Nation mortality rates were based on the reported nurnber of
CHD deaths (listed as Ischaemic Heart Disease, ICD9 Code 420414,4292) for British
Columbia Status Indian maies and females fiom 1987-1993 (Health Canada 1995).19 It
was assumed that rates would be simiIar for aboriginal peoples who do not have statu.
Crude death rates were calculated according to given annual population estimates for this
period and are presented in Table 3. As deaths were not reported for age groups, male and
female populations had to be analyzed as a whole.
Table 3: Number of Reported Deaths Due to Ischaemic Heart Disease From 1987-1 993 and Cnide Annud Death Rates per 10 000 AboriginaI Population According to Sex
Number of Deaths, Annual Cnide Death Rate per
1987-1993 1 O 000 Aboriginal Population
Male 3 05 10.4
Female 15 1 4.9
(Health Canada 1995)
19 It would have been preferable to use reported rates for specific coastal areas as CHD mortality is likely to be geographically variable. There is only one other source which reports rates on a regional basis (according to goverrunent detüied health regions) (ive. Burd 1994). Rates, however, are onIy reported for the year 1992 and are hence not very reliable. Further, rates for males and females are presented together, precluding an analysis of gender-related differences in CHD mortality.
Similar to the excess cancer risk assessrnent of shelifïsh consumption, Crystal Bal1
(Decîsioneering Corp.) was used to perform a probabilistic analysis of potential increases
in CHD mortality. The following equation was used to mode1 increases in CHI3 mortality
as a result of a dietary change fiom sheIlfish to a mix of beef, pork and chicken,
ECHDD = (ACHDD x ASF / 0.07) x CHDDR
where,
ECHDD = annual excess number of aboriginal CHD deaths due to a dietary change
ACHDD = proportional change in CHD deaths among the US. population per 7% change in daity
energy consurned as saturated Fat (from Browner et al. (1991) (see Table 2))
ASF = proportional change in the amount of daily enerm consumed as saturated fat among
aboriginal peoptes due to a dictary change
CHDDR = annual cmde aboriginal CHD death rate (see Table 3)
The LHS option was used again in place of standard Monte Carlo simulation. Lognormal
distributions were chosen to describe changes in the proportion of total energy consumed
as saturated fat for the sample population. Appendix F displays the shapes of two of these
derived lognormal distributions for example (Le. for men due to the replacement of crab
with chicken, beef and pork and for wornen due to clam, cIam, prawn and shnrnp
substitution). Estimated proportional changes in CHD rnortality rates from Browner et d.
(1991) were defined by a triangular distribution. Triangular distributions have been
recornmended in instances where the actual distribution is difficult to establish (Finley et
al. 2994). Due to a variety of reasons, the British Columbia Status Indian population has a
young age structure, with few individuals that reach the ages of 65 and over (Health
Canada 1995). CHD deaths are, thus, likely to occur among comparatively younger
individuals than is the case in the general population. To account for this, the Likeliesi
parameter for the triangular distribution was defined as being an average of the Browner et
al. (1 99 1 ) estimates for those between the ages of 25 and 64 (see Table 2).
3.1 Aboriginal Shellfish Consumption
Average daily shellfish consumption rates caicuiated fiom the Haisla Diet Survey
(Kitamaat Village Council 1994) are presented in Table 4. The lower 2.5 and Iower 97.5
percentiies of the derived consumption distributions are also displayed. Rates have been
estimated assuming lognormal distributions. Values represent rates for adult shellfish
eaters only. The nurnber of survey participants who reported eating some amount of
shellfrsh/tissue are aiso shown.
Table 4: Estimated Daily Aboriginal Shellfish Consumption Rates
Specieflissues Number of Survey Average Consumption Lower 2.5% Lower 97.5%
Respondents (@day (gfda~ ) b ' d a ~ 1
Crab 69/86 (80%) 17.0 1 .O 79.0
Crab Organs 7/86 (8%) 1.4 O. 1 6.0
PrawnsIShrirnp 18/86 (2 1%) 6.3 0.5 28.0
Clams 36/86 (429'0) 15.4 1 .O 77.0
(calculated frorn the Haisla Diet Survey (Kitamaat Village Council 1994))
Crab appears to be the most popular food of the exarnined shellfish species. It is eaten in
the greatest quantities (1 7 g/personfday) by the majority (80%) of survey respondents.
Variability in the consumption of this food is greatest. The central 95th percentile of the
crab consumption distribution lies between 1 .O glday and 79.0 glday. Clams also appear to
be an important food, eaten in comparatively ample arnounts (1 5 g/person/day on average)
by 42% of the aduit survey population. Variability is also large, with 95% of individuals
28
eating between 1 g/day and 72 glday. Prawns and shrimp are the third most popdar of the
examined shelltish foods, with a consumption average of 6.3 g/day. DifTerences in shrirnp
and prawn consumption rates between individuals are comparatively smdl (the lower 2.5
percentile and the lower 97.5 percentile of the consurnption distribution is 0.5 g/day and 28
g/day, respectively). Crab organs (assumed to be crab hepatopancreas here) are eaten by
the smailest proportion of survey participants (only 8%) in the smallest quantities (1.4
g/day 1.
3.2 The Excess Cancer Risks of SheW~sh Consumption
The calculated excess lifetime cancer risks for the three sites for the first two years of DFO
management action are shown in Table 5. As with the risk analysis conducted by Hedih
Canada, excess risks have been calculated according to the consumption of specific
species/tissues. Management actions undertaken by DFO are aiso presented. It shouId be
noted that the risks of eating clams fiom Kitirnat could only be caicuIated for 1989 and
1992 because these were the only years for which tissue residue data were available.
Results for those years between 1989-1995 are presented in Appendix G and include the
minimums and maximums of the nsk distributions. The risk estimates over the time period
observed in Appendix G show a clear downward trend in risks, reflecting decreased
contamination in these areas?' are en dix B shows the calculated species-specific TEQs
Dioxin and furan concentrations in effluents from pulp rnills have been declining in recent years (DFO 1994). This has been largely due to the new regulations established in 1992 under the Canadian Environmental Protection Act, which require the elirnination of measurable quantities o f 2,3,7,8- TCDD and 2,3,7,8- TCDF from effluents.
Table 5 : Excess Lifetirne Cancer Risk Estimates According to Area and Shelifïsh Species/Tissues for the First Two Years of DFO Management
Area Speciesfîissues Year ' Management Mean Risk Upper 95%
Action
Kitimat
Gold River
Powell River
Crab Hepatopancreas
Ciam '
Crab Hepatopancreas
Crab Muscle
Prawns
Crab Hepatopancreas
Crab Hepatopancreas
Crab Muscle
Oyster
Advisory
Advisory
Closure
Closure
CIosure
Closure
Closure
Closure
Closure
Closure
Closure
Closure
Advisory
Advisory
Closure
Closure
Closure
Closure
' Year refers to the year of the completion of Health Canada's risk assessrnent and concomitant management decisions by DFO. Actual sampling periods often took place one year pnor to management decisions. ' Risk estirnates for clam could only be calculated for i 989 and 1992 because of the lack of tissue residue data for other years. 3 The area for which consurnption advisories were issued lay outside the zone of the total crab fishing closure (see Map 4).
for the managed sites for the sarne years. Both mean lifetime cancer rkks and the upper
95th percentiles of the risk distributions are presented. The latter cm be assumed to
represent a 'worst case scenario' and is s h o w because of its importance in the formulation
of management actions for protection of the 'maximalIy exposed individual' (e.g. U.S.
EPA 1989).
Caiculated mean lifetime cancer nsks for the consumption of individual species for the first
two years of management range fiom a low of about 3 in 10,000,000 (for clam
consumption in Kitimat in 1992) to a maximum of approximately 1 in 10,000 (for Gold
River crab hepatopancreas in 1990 and Powell River oyster in 1989). Upper bound risks
(95th percentile) reach a maximum of almost 4 in 10,000 for crab hepatopancreas and
oyster sampled in Gold River and Powell River, respectively. The estimated species-
specific risks appear to be greatest in Gold River and Powell River. The risks associated
with consuming clams and crab hepatopancreas in Kitimat are comparatively the lowest.
The denved distributions of cancer rÏsk for the consumption of shellfish speciesltissues
span about three to four orders of magnitude (i.e. minimum to maximum cancer nsk) (see
Appendix G). This range is common, reflecting largeiy variability between individuais in
their consumption of species and tissues residue levels. Dioxins and furans tend to
concentrate in the hepatopancreas in crab, as opposed to the muscle. This is not reflected
in the estimated nsks due to the fact that much larger quantities of muscle are eaten than
hepatopancreas (see Table 4).
The calculation of species-specific health risks c m be valuable for it allows for the
identification of individuai species ancilor tissues which have the greatest associated tisks
for consumers. The harvesting and consumption of species can then be managed
accordingly. Considering that individuais are likely to consume a varïety of shellfish,
however, the estimation of risks for a mixed species diet is cruciai in the choice of
appmpriate management decisions." The cancer risks for each site for the fim two yean
of DFO management were detennined. This assumed that individuals would consume a
mixed diet of the identified contaminated species/tissues at calculated consumption rates
fiom the Haisla Diet Survey (Kitamaat Village Council 1994) for each area (e.g.
individuais in Kitirnat would eat a mixed diet of contarninated hepatopancreas and clams).
The results are presented in Table 6 . Both mean cancer risks and the upper 95th
percentiles of the distributions are shown. For Kitimat, risks associated with a mixed
diet were calculated for 1992 because of the unavailability of 1990 data on tissue residues
for clams.
Table 6: Excess Lifetime Cancer Risks of Consuming a Mixed Shellfish Species/Tissue Diet for Each Site for the First Two Years of DFO Management
Area Year Mean Risk Upper 95%
Kitimat 1989 4.70 x 1 O*' 1.19 x 10"
1992 1.68 x 10" 5.29 x 10"
Gold River 1989 9.91 x IO-' 2.58 loJ 1990 1.71 x 104 5.11 10"
Powell River 1989 1.39 x 10" 4.16 x 104
1990 3-92 x IO-:' 1.22 x IO-'
2 1 A mixed diet was not considered in HeaIth Canada's assessment of risk.
According to the caicuiated 1989 excess cancer risks, populations in Powell River were
exposed to the greatest risks in consuming a mixed diet. In 1990 though, the risks
increased for a Gold River mixed diet and were greatest for this year. Gold River risks are
higher for 1990 than they are for 1989 because of increased tissue residues in crab muscle
and hepatopancreas. This could be due to actual increases in contaminants levels. It may
also be a result of a p a t e r sample size collected by DFO in 1990 over 1989, which more
accurately reflects tnie tissue residue Levels. The estimated excess lifetime cancer nsks for
the other two areas decreased within the time period observed. In the upper ranges of the
risk distributions, calculated risks are relatively high for both Gold River and Powell River
(highs of 4 in 1 O 000 and 5 in 10 000 for Powell River (1 989) and Gold River [ 1 WO),
respectively). Excess cancer risks appeared comparatively the lowest for Kitimat (about 1
in 10 000 in 1989), reflecting Lower contaminant levels.
The above nsk estimates presented are expressed as an individual lifetime risk (averaged
over a 70 year period). The cornparison of excess cancer nsks and increases in CHD
mortality due to a dietary change necessitates the conversion of these results into
population nsks. This can be done by multiplying the lifetime cancer risk estimates with
the number of people at risk. The nurnber of individuals expected to develop cancer fiom
shellfish consurnption over a Iifetime can be calculated assuming that risks remain the
same over tirne (Le. tissue residue levels remain stable). Exact adult population estimates
for the exarnined areas were not available, requiring that nsks be calculated according to a
general population number. Table 7 presents estimates for the excess number of cancer
cases expected per 10 000 individuals at risk over a 70 year time span according to 1989
tissue residue levels." Cancer risk estimates for a rnixed shellfish diet have been used.
Table 7: Estimated Excess Number of Cancers per 10 000 Individuais Over a 70 Year Period According to 1989 Shelllish Tissue Residue Levels
Area Y ear Mean Excess Cancer Upper 95% of Excess Cancer Casedl0 000 Cases/ 1 O 000
Kitimat 1989 0.42 1.19
Gold River 1989 0.99 2.58
PoweII River 1989 1.39 4.16
Estimates are shown according to the specific areas. Readers are reminded that estimates
are only vaiid for those who eat shellfish and not the generd population. Less than 1
person per 10 000 over a 70 year period is predicted to develop cancer from consuming a
mixed diet of Kitimat shellfish according to the mean. For Gold River and Powell River
diets, about 1 individual per 10 000 may develop cancer over 70 years (mean estimates).
According to the upper 95 percentiles, about 1,3 and 4 persons per 10 000 rnay develop
cancer due to the consumption of shellfish fiom Kitimat, Gold River and Powell River,
respectively .
3.3 Estimated Increases in Coronaty Heart Disease Mortality Due a Dietary Change
Changes in the percent energy consurned as saturated fat with the displacement of shellfish
with equd amounts of beef, chicken and pork are presented in Table 8. Mean saturated fat
- --
Each of the three areas involve Iess than 10 000 aboriginal persons . nie expected number of cancer cases cdculated per actual population would hence be lower than that presented in Table 7.
changes are s h o w together with the lower 2.5 and 97.5 percentiles of the derived
distributions. Values have been calculated assuming lognormal distributions. Results for
both males and females are presented.
Table 8: Percent Change in Daily Energy Derived f?om Saturated Fat with Shellfish Substitution According to Gender
M a h Fernales Average (%) Lower Lower Average (Yo) Lower Lower
2.5% 97.5% 2.5% 97.5% Crab Substitution 0.42 0.04 1-70 0.48 0.02 2.4
Crab, Clam and PradShrimp 0.7 1 0.06 3.10 0.65 0.03 3.4 Substitution
(calculated from the Haisla Diet Swvey (Kitarnaat VilIage Council 1994)
With the substitution of crab with chicken, beef and pork, the daily energy derived fiom
saturated fat would increase by 0.42% and 0.48% for males and females, respectively.
Energy fiorn saturated fats would increase by 0.65% for females and 0.7 1% for males in
the event that crab, clam and prawn would be displaced fiom the diet.
Although changes in the amount of energy consumed as saturated fat with dietary
substitution appear small, they wodd have an impact on CHD mortality rates. The
modeling results are presented in Table 9. Calculated mean CHD deaths per 10 000
aboriginal population over a 70 year period are s h o w together with the upper 95th
percentiles of their respective distributions. The results represent only the extra nurnber of
deaths due to dietary change, not the expected total. Rates for males and females, as well
as for both, are presented for the hypothetical scenario of crab substitution and crab, clam
and pradsbrimp substitution.
Table 9: Estimated increases in Excess CHD Mortaiity per 10 000 Individuais Over a 70 Year Period According to Gender Due to Dietary Substitution
Species Mean CHD Upper 95% Mean CHD Upper 95% Mean CHD Upper 95%
Substituted DeathsIlO 000 Deathsi 1 O 000 DeathdlO 000
Crab 5.9 18.5 2 2 7.4 4.0 12.8
Crab, Clams Prawnd 9.9 32.0 3.8 9.7 6.3 20.6
Possible increases in mortaiity are greater for males than for females. With crab
substitution, means of 6 and 2 CHD deaths per 10 000 populations over 70 years are
possible for males and females, respectively (mean estimates). In the event that crab, clam
and prawnlshnmp are displaced from the diet, about 10 deaths among males and 3 deaths
among femaies per 10 000 populations are possible (mean estimates). The higher death
rate predicted for males is a function of the greater estimated proportional changes in CHD
mortality rates for this sex as calculated by Browner et al. (1991) (see Table 2). This
reflects the fact that men are considerably more often affected by CHD than women.
According to the upper bound estimates, anywhere from about 13 to 21 deaths per 10 000
population for both sexes in the event of crab only and crab, clam and prawn/shrimp
substitution are possible.
4. Discussion
4.1 Evaluating the Excess Cancer Risks of Shellfish Consumption
Several observations were made in the examination of the excess cancer risks of
consiuning shelifïsh for the study areas. To begin with, consistency between potentid risks
levels and the chosen management actions undertaken by DFO appears to be lacking. In
other words, the risk management decisions do not appear to have been a direct fünction of
quantified health risks. For instance, the cstimated risks of consuming Kitimat crab
hepatopancreas (advisory area) in 1989 were not substantially different fiom that for
species/tissues in other areas where closures occurred (i.e. a mean risk of 1.28 x 1 O-' for
Kitirnat hepatopancreas vs. 1.55 x lC5 for Gold River prawns). The 1989 risks for Powell
River hepatopancreas in the closure area were less than those estimated for hepatopancreas
fiom the advisory area in 1990 (mean risks of 1 -62 x 1 0" and 3 .O6 x 1 O", respectively).
This seeming inconsistency is likely a consequence of both Health Canada's risk
assessrnent and DFO's management jurisdiction over fisheries.
As discussed in Appendix C, Health Canada uses a safety factor approach to assess dioxin
risk. Although this approach provides a simple way of establishing the existence of a risk,
the degree or level of risk involved c m not be quantified. Only qualitative statements can
be made regarding calculated risks such as 'high7 or 'low.' This precludes the
establishment of a consistent, risk management decision-making fiamework which is
readily standardized to definitive, probabilistic risk levels. As such, inconsistency between
risk management strategies and estimated risks is to be expected.
Another factor which may contribute to inconsistency between chosen management
activities and estimated risks is the institutional separation between risk assessrnent and
rïsk management. Health Canada on1 y recommends management activities. DFO
considers them and, based on their own criteria and standards, may develop risk
management activities that ovemde these recommendations @FO 1994). For instance,
one of the most important criteria used by DFO in considering a fishery re-opening is that
tissue residues show a steady downward decline below the TDI over a two year period. It
appears that the criteria and standards that have been adopted by DFO have generally lead
to a more conservative approach in the management of risks by this department. In
vimially ail instances where closures occurred in 1989. for example, only advisories were
recommended by Health Canada. Table 10 shows where this did and did not occur.
The type of management action undertaken by DFO will Vary depending on several
considerations (DFO 1994). Where dioxin and firran levels are high according to Mealth
Canada, and the species of concem is often eaten whole (e.g shrimp), a cornplete
harvesting prohibition is likely. This would apply to commercial, recreational and native
harvesting. A complete closure would also be taken where contaminated species are
popular food items or are consurned in large quantities @FO 1994).
Table 10: A Cornparison of Health Canada's Species-Specific Risk Management Recommendations and DFO's Decisions in 1989 for the Three Study Areas
Site Specieflissue Heath Canada's Recornmendations DFO Management
Decisions
Kitimat Hepatopancreas Advisory (30 g/week)* Advisory (30 g/week)
Clam Advisory (1 50 g/week) Closwe
GoId River Hepatopancreas Advisory (10 g/week)
Crab Muscle Advisory (105 g/week)
Prawn Advisory (120 g/week)
Powe Il River Hepatopancreas Advisory ( 180 g/week)
Crab Muscle Advisory (1 80 g/week)
Oyster Advisory (3 5 ghveek)
Closwe
C losure
Closure
CIosure
C losure
C losure
(fiorn DFO 1989b; Health and Welfare Canada 1989) *recornrnended mauimurn consumption amounts are shown in brackets
Where dioxins and furans tend to accumulate in a particular tissue which is not usually
eaten (e.g. hepatopancreas), commercial harvesting may be prohibited but recreational and
aboriginal harvesting allowed with consumption restrictions (i.e. consumption advisory).
Management actions chosen based on harvesting type (Le. commercial, recreational,
aboriginal) in the latter case are based on the rationale that commercial consumers require
added protection fiom potential health risks (Knapp, W. Senior Biological Technologist,
Water Quality Unit, Habitat and Enhancement Branch, DFO, pers. comm. 1996). Such
consumers may not know about the origins of the product consumed and its associated
risks. Recreational and aboriginal harvesters, on the other hand, are assumed to be
informed through the advisory. These harvesters could then adopt the recommended
precautionary measures to avoid excessive risk.
The f o d a t i o n of management actions according to whether harvesters are commercial,
recreationai or subsistence fishermen is potentiaily problematic. The use of advisories, as
opposed to a closure, for subsistence and recreation harvesting assumes that individuals are
informed about the consurnption recommendations (Reinert et al. 1991). It also assumes
that the advisory is fblly understood and that the harvester is aware of the potential
consequences of following or disregarding it. Additionally, the possibility exists that
compounds such as dioxins and furans may migrate from the hepatopancreas to cornrnoniy
eaten parts (muscle) when cooked in the traditionai manner (boiled whole with the crab
intact) (Cooper et ai. 1991). If this is the case, then advisories for the consumption of only
hepatopancreas may not be protective.
According to some standards regarding risk acceptability, management activities
undertaken in some of the examined areas would be considered questionable. A number of
proposais for de minimus riskY ievels have been made over the years. The U.S.
Environmental Protection Agency, for instance, has suggested de minimus lifetime risk
Levels of 104 to 1 O" and 1 o6 to IO-' for smail and large populations, respectively (Travis et
ai. 1987). Othen have suggested a general range of 104 to 104 (Kocher and Hoffinan
199 1). Though some of the caiculated dioxin risks rnay slightly exceed these
recomrnended levels, such as the 1989 upper bound risks for Powell River oyster and Gold
River hepatopancreas (i.e. 3.76 x 104 and 3.95 x 104, respectively), many could be
considered de minimus risks (see Tables 5 and 6).
23 De minimus risk is tiiat which is considered too negligible to be of concern.
The estimated cancer risks are aiso comparable to some cornmonplace risks; comparisons
of which are often suggested as a usehl tool to place targeted risks irito perspective (Bro et
ai. 1987; Wilson and Crouch 1987; Reinert et al. 1991). For instance. Affatoxins,
especially afiatoxin BI, are potent carcinogens produced by a mold (AspergiIiusf7avus) that
commonly grows on peanuts and corn (Rodricks 1992). Products that are made ftom these
foods inevitably have associated cancer risks. At maximum aflatoxin Iimits set by the U.S.
Federal Department of Agriculture, eating 4 tbsp. of peanut butter per day has been
estimated to have a lifetime cancer risk of about 6 x 104 (Crouch and Wilson 1983, quoted
in Bro et ai. 1987). Food products such as milk and eggs can also contain aflatoxins
because corn and peanuts often form the basis of animai feeds. For mik, consumption of
480 ml (1 pint) on a daily basis is associated with a lifetime cancer risk of 1.4 x lo4
(Crouch and Wilson 1983, quoted in Bro et al. 1987). Charbroiling steaks aIso poses a
carcinogenic nsk because of the polycyclic aromatic hydrocarbons (PAHs) that are
produced by this method of cooking. Eating 227 grams (8 ounces) of charbroiled steak per
week c m have a Iifetime cancer risk of approximately 3 x 1 0 - ~ (Crouch and Wilson 1983,
quoted in Bro et al. 1987). Figure 5 compares these risks with the estimated 1989 upper
bound lifetime cancer risks of consuming a rnixed shellfish diet from Kitimat, Gold River
and Powell River.
Figure 5: 1989 Upper Bound Excess Cancer Risks for a Mixed Shellfish Diet for the Three Areas vs. That for Some Common Foods
Kit k a t Siellfish
PowII River SheUfish
Gold River Shellfish
227 g Charbroled SteaWWeek*
4 Tbsp. Peanut But t cr/Day+
#
(* fiom Crouch and Wilson 1983, quoted in Bro et ai. 1987)
The excess calculated risks for both a single-species and a mixed species diet for the
examined areas are generaily comparable to those estimated for cornrnon foods. Many of
the estimated cancer risks also meet recornrnended de minimus levels. As such, it could be
argued that the management decisions to close fisheries and issue consumption wamings
were not warranted in some instances. The exact question of what risk levels may be
acceptable, however, in comparing the excess dioxin cancer risks with suggested de
minimus levels and generalized relative risk comparisons is difficult to answer. Risk
acceptability is inherently subjective and can Vary dramatically according to the specific
characteristics of a risk situation (Fischoff et al. 198 1 ; Slovic 1987; Leiss and Chociolko
1994). Even high levels of risk, for instance, may be accepted if there are associated
benefits that are perceived as worthwhile. An examination of risks and benefits at the site-
specific level is needed to help illuminate appropriate risk management options and
provides a better basis for decision-making.
4.2 Comparing Calculated Cancer Risks with Increases in Coronary Heart Disease Mortality for FVst Nations Peoples: Estimates, Uncertainties and Considerations
The estimated number of possible deaths due to the consumption of contaminated shellfish
in the study areas wodd appear to be Iess than that due to the assumed dietary change.
According to 1989 mean estirnates of cancer risk for a Kitimat mixed diet, less than one
individual per 10 000 over 70 years is predicted to develop cancer (see Table 7). About 1
person per 10 000 over 70 years rnay develop cancer f iom eating Gold River and Powell
River mixed shellfish diets (mean estimates of risk for 1989). As risks decrease over the
time period observed (see Appendix G), the actual Iifetime cancer risks would be less than
that calcdated for the exarnined years.
Dietary substitution of shellfish with comrnon store-bought protein alternatives has been
calcuiated to potentidy result in anywhere fiom 4 to 2 1 deaths per 10 000 individuals over
a 70 year petïod (both sexes) (see Table 9). This is dependent on whether only crab or
more species are displaceci fiom the diet and if the upper 95th percentile is considered.
The potential number of deaths due to dietary substitution may be 4 to 8 times as many as
that which may occur in the three examined areas on average fiom consurning shellfish
(1989 tissue residue leveIs).
Differences between cancer and CHD in terms of the resultant Potential Years of Life Lost
(PYLL) for the exarnined populations are also important to consider in comparing the
results. Between the years of 1987 and 1993, cancers were estirnated to cause an average
of 16.7 PYLL in those under the age of 65 years (Kealth Canada 1995)." C m , on the
other hand, resulted in an average loss of 14.7 years. The number of PYLL is hence
potentially greater for the consumption of contarninated shellfish than that due to a dietary
change at the individuai level. This, however, is offset by the greater popuIation risks
associated with a dietary change. Assuming that the number estirnated to develop cancer
fiom consuming shellfish experience death, a total of about 16 to 44 PYLL per 10 000 are
expected over a 70 year period (according to the mean and upper 95th percentile of deaths
due to a mixed diet of shellfish for the three areas on average). For CHD deaîhs as a result
of diet substitution, 59 to 303 PYLL per 10 000 persons over 70 years are possible.
In light of the above, it may appear that risk management activities which curb shellfish
consumption because of dioxin-risk may serve to indirectly create an even greater health
risk for First Nations peoples. An assessment of the appropriateness of risk management
decisions, however, necessitates a more thorough analysis of the issues at hand than such a
simple comparison of results. There are a number of factors which inject a large degree of
complexity and uncertainty into the evaluation of risk management options. This includes
the limitations of this study. These factors can be grouped into five categories:
1. other negative health effects of both a high fat diet and dioxin exposure,
'' Al1 cancer types were considered in this estimation.
2. sensitive sub-populations that rnay require greater protection fiom dioxin exposure,
3. uncertainties in the estimates for increases in CHD mortality due to a dietary change
and the excess cancer risks of consuming shellfish,
4. health benefits of shellfish consumption, and
5. socio-cultural and economic benefits of country food harvesting and consumption.
Increased fat intakes due to a greater consumption of higher-fat, store-bought foods rnay
have other heaith effects apart from CHD that have not been accounted for in this analysis.
Some evidence suggests that high fat intakes rnay play an important role in prostrate,
breast, colon and rectal cancers. For instance, colon cancer rnay be induced by the
increased production of bile acids in the small intestine that is associated with a high fat
diet ( W m a n et aI. 1995). These biIe acids can be converted to metabolites such as
3-rnethylcholathrene in the large intestine or colon which are believed to be carcinogenic.
A strong correlation also appears to exist between high national rates of these types of
cancers and diets that are high in fat and meat products (DoIl and Peto 198 1). This is
strengthened by the observation that individuals who emigrate to the U.S. fiom other
countries, where diets are low in fat and these cancers are comparatively rare, will develop
similar rates of these cancers as Americans (Cairns 1975; Doll and Peto 198 1). This
phenomenon has been attributed to the adoption of a high-fat Arnerîcan diet.2s As such,
management strategies such as fishery closures rnay indirectly enhance the risk of breast,
2.5 It should be noted though that recent evidence suggests that caloric intake and body weight rnay play an equally great or even larger role in the developrnent of breast cancer, and rnaybe colon cancer, than fat intake alone (Waxman et al. 1995).
prostrate and colorectal cancers if they serve to promote the consumption of higher-fat,
store-bought foods.
Other potential health effects associated with dioxin and furan exposure have dso not been
considered in this assessment. These compounds may have a number of negative human
health eEects, apart fiom cancer, that may be more insidious and affect greater numbers of
individuals. For instance, TCDD has been found to be teratogenic in some species. At an
effect level of 1 pg/kg/day, clef? paiate and rnalformed kidneys are common teratogenic
effects in rnice (Mattison et al. 1983; U.S. EPA 1988). In rats, TCDD appears to be more
fetotoxic than teratogenic, causing kidney malformation. intestinal hemorrhage and edema
at doses greater than 0.01 pgkglday (Murray et al. 1979). Further, TCDD has also been
found to affect fertility and offspnng survivai. In a three-generation study on rats,
decreases in fertility, litter size, neonatal suMval and growth and gestation survivai were
observed in those groups fed 0.1 pg/kg/day and 0.0 1 pg/kg/day (Mvlurray et al. 1 979).
Additionally, TCDD has been demonstrated to be immunotoxic in some species. It appears
that this substance suppresses cell- and antibody-mediated immunity (Dean and Lauer
1983; Luebke et al. 1994). TCDD has also been shown to have adverse effects on the
thymus and cause hypersensitivity to antigens in non-human mamrnals (Dean and Lauer
1983). Possible reproductive, teratogenic and immunotoxic effects of TCDD and other
dioxin and h a n congeners substituted in the 2,3,7 and 8 positions have not yet been
established in humans. Human sensitivity to these substances rnay be sirnilar to that
demonstrated in animals Poddington et al. 1990). No methods have been developed yet to
adequately assess such possible health effects of exposure to dioxins and furans. This
shouid not preclude their considerauon though in the development of risk management
options to protect First Nations peoples from excess risk.
Further, the cancer risk of dioxin and furan exposure was not assessed for children and
infants. Due to their Iower body weight, they may be especially susceptible to the tissue
residue levels that have been found in shellfish. For infants, breast-feeding is a cause of
concern. Studies indicate that breast milk contains high levels of dioxin and furans,
resulting in probable intakes for infants that would likely exceed the established
permissible intake of IO pg TEQkgIday established by Health Canada (Gilman and
Newhook 1 9 9 1 ) ~ ~ ~ Shellfish consumption in the examined areas rnay hence lead to
excessive levels of dioxins and furans in the breast mik of aboriginal women.
There are also a number of uncertainties associated with the results of this study that
should be considered in the evalüation of risk management alternatives. It could be argued
that the estimated increases in CHD mortality may have been overestimated. Specifically,
fishery closures and consurnption advisories do not necessarily mean that individuals will
automaticaiIy replace shellfish with store-bought foods. For instance, greater amounts of
other 'safe' shellfish and fish may be eaten to compensate. Shellfish fiom other non-
26 It is believed though that the benefits of breast feeding would outweigh the potential risks of these cornpounds found in breast milk (WHO 1988, referred Lo in Boddington et al. 1990; Gilman and Newhook 199 1).
contaminated areas may aiso be obtained. Further, as one interviewee noted (anonymous,
pers. cornm. 1996)~' some people will even continue to fish in areas under a closure.
It would appear though that many First Nations peoples have reduced their consurnption of
shellfish fiom certain areas due to perceived polIution problems. Contaminants have been
identified by Kuhnlein (1 99 1, 1993, 1995) as one factor which has contributed to decreased
consumption of traditional foods in the Canadian North. Not only are individuals turning
away fiom identified contaminated species, but also from other country foods. Possible
fears that if one species is contaminated then others could be too might serve as one
rationale for this behavior. Such perceptions may be indicative of flawed government risk
communication strategies. If this is the case, the need for more effective communication is
highiighted. Further, unlike non-aborigulai fisherman, aboriginal peoples tend to harvest
in areas close to their cornmunities. For instance, in Ontario it was calculated that
aboriginal peoples travel an average distance of only 26.3 km to fish (E.A.G.L.E Project
1996). This contrasts with non-aboriginal fishemen, who travel an average distance of
1 19 km. The assumption that at least some First Nation peoples will reduce their overall
consurnption of country foods if they Live in an area that is impacted by pollution is hence
not an unreasonable one.
The excess cancer risks of consuming contaminated sheIlfish may also have been
overestimated because of some conservative assumptions that were made. First, the
27 This interviewee wished to remain anonymous for persona1 reasons.
relationship between dose and response was assumed to be lincar in the low-dose range.
The evidence suggests though that TCDD and its structural analogs elicit toxic responses
through their interaction with the aryl hydrocarbon (Ah) receptor (Safe 1989, 1990; Lucier
et al. 1993; Portier et ai. 1993). As receptor-mediated effects are believed to involve a
threshold level, below which no toxic effects can occur, a safety factor approach is often
suggested as best.
Second, it was aiso assumed that individuals would consume contarninated shellfish at
caicuiated tissue residue levels over a 70 year period. Dioxin and furan tissue residue
levels are rapidly declining though as a result of the new regulations for puip mil1 effluents
under the Canadian Envirotmental Protection Act (DFO 1996b). As such, actual Iifetime
risks should be less than that cdcdated here. Fwther, the effects of shellfish preparation
and cooking methods on the Ioss of dioxins and furans were not accounted for. Zabik and
Zabik (1995), for instance, fond that TCDD losses due to a variety of cooking and
processing methods of 5 species of Great Lakes fish varied anywhere fiom between about
23% (salt boihg) to a virtual 100% (smoking). On the other hand, cooking crab using the
traditionai method of boiling it whole, with the body cavity lefi intact, may actuaIly
increase the cancer risk (Cooper et al. 1991). The question of whether dioxins and furans
can migrate fiom the hepatopancreas to the muscle has yet to be answered.
It could be argued that the derived cancer potency factor of 4747 in this study wouId not
produce conservative cancer nsk estimates. Keenan et al. (1991) estimated a cancer
potency factor of 9700 using the same re-evduated data of the Kociba et al. (1978)
bioassay. This represents a cancer potency of about double that predicted here for TCDD
and its structurai anaiogs. In using the cancer potency factor of Keenan et ai. (1 99 l), the
estimated cancer risks for the three sites wouid be twice as large as those determined in this
study. Even taking this into consideration, the excess number of deaths estimated for CHD
due to a dietary change arnong coastal peoples wouid still be greater. Figure 6 compares
the estimated CHD death rate to that expected for shellfish conmmption if the excess
cancer risks were calculated using the Keenan et al. (1 991) cancer potency factor.
Figure 6: A Cornparison of the Estimated Upper Bound Excess Cancer Deaths of Consuming a Mixed Diet of Shellfish Using Keenan et al.'s (1991) Cancer Potency Factor (per 10 000 peopie/70 years) and Excess CHD Mortality Due to Shellfish Substitution (per 10 000 people/7O years)
Estimated Upper Bound Excess Nurnber of Deaths According to
Keenan et al. (1991) (per 10 000 lndividuals Over a 70 Year Period)
There are also a number of other uncertainties associated with the excess cancer risk
estimates whicii shouid be noted. To begin with, cancer risk assessment is, itself, an
uncertain endeavor. The choice of a mathematical model, for instance, to represent a dose-
response relationship is problematic. Commonly used models such as the mdtistage and
probit will often fit the observed data equally well but can produce very different results
upon extrapolation to the low-dose range (Portier and Hoel 1983; Covello and Merkhofer
1993). As a resuit, the assessor must rely on personal judgment and the bidogical basis for
choosing a model to estimate cancer risk.
Other uncertainties associated with cancer risk assessment involve the use of toxicity tests
conducted on animals to extrapolate human effects. For instance, basic genetic and
physiological differences between animals and hurnans may result in different dose-
response relationships (e.g. differences in target organ physiology and functioning, lifespan
and body size) (Covello and Merkhofer 1993). Further, tests are typically conducted under
simplistic, artificial laboratory conditions which may preempt their suitability for
application to 'real-world' conditions. For instance, substances are typicdly tested on a
chemical-by-chernical b a i s (Covello and Merkhofer 1993). In reaiiv, however, hurnans
may be exposed to a variety of chemical agents concurrently or sequentially, which rnay
interact additively, synergisticaily or antagonistically. One recent study conducted by the
Institute of Chemistry and Biology at the University of Oldenburg, Germany, has called the
use of individual chemical human health guidelines into question (Bartsch 1996). Ushg
human ceils, the Institute tested different combinations of individual chernicals at
concentrations at and below established guideline levels. The resdts revealed clear genetic
toxicity when substances were applied in combination, even at concentrations of one-third
of guideline levels. This was especially the case when pesticides were applied together
with various lipophilic substances. Smoking, in combination with exposure to a variety of
common environmental poilutants, is also suspected to enhance effects synergistically
(DoII and Peto 1983).
Several additional sources of uncertainty in both the CHD mortdity and cancer risk
estimates relate specifically to the data sources used here. To begin with, the
representativeness of estimated consumption rates for aboriginal peoples fiom the HaisIa
Diet Survey (Kitarnaat Village Council 1994) is uncertain. individuais were questioned
about their dietary patterns during the time when the clam fishery dosure and crab
hepatopancreas consumption advisones were in effect for Kitimat Atm. This may hztve
served to curb traditional eating patterns for these speciesltissues among survey
respondents. The determination of traditional eating patterns is M e r complicated by the
fact that Kitimat Arm has been impacted by pollution problems since the early IWO'S.
Estimates of the cancer risk of consuming shellfish and increases in CHD mortality due to
a dietary change must therefore be interpreted with caution.
IdealIy, it would have been best to compare the results of the HaisIa Diet Survey Wtamaat
Village Council 1994) with that of other diet studies of coastal aboriginal consumption to
determine the representativeness of estimated consumption patterns. Published data fiom
other studies are not available. Consumption patterns for specific shellfish species andlot
tissues for other populations are also limited. Some rates were reported by Rupp et al.
(1981) for dehed U.S. regions but were not presented for individual sheILfish species (i.e.
al1 shellfish were considered as one category). According to their study, those at the 90th
percentile of the distribution for the entire U.S. population ate on average about 40 g
shellfish/day. This would appear to be comparable to the estimates caiculated here if the
daily intake of al1 shellfish would be considered a s a whole.
Additionally, Haisla shellfish consumption patterns may not be fully representative of
those for other coastal aboriginal populations. Populations in other areas may have
different shellfish eating patterns due to, for instance, the geographicai unavailability of
certain shellfish species. Further, consumption patterns have been known to Vary to some
degree depending on the acceptance and beliefs held about e a h g shellfish. h o n g the
Kwakiutal, for example, clams were generaily considered the food of poorer individuais
(British Columbia Provincial Archives 1966). As such, estimates of the cancer risk of
consuming Gold River and Powell River shellfish and increases in CHD mortality because
of a change in diet may not be fully accurate.
The number of shellfish samples which were collected and analyzed by DFO were aIso less
than optimal during certain time periods. For instance, only one species sample was taken
fiom each site in 1989:' VarîabiIity in dioxin/furan tissue residues could not be examined
for this year as a remit. Greater uncertainty is hence associated with the 1989 cancer risk
estimates. Tissue residue data for clams from Kitimat were only available for 1989 and
1 992. The number of clam samples taken were also not very desirable, involving one
sample for each year fiom only one area in Kitirnat Arm (i.e. Alcan Beach). This lack of
appropriate sampling for clams, however, may be primady due to the fact that clam
fishing was closed anyway because of Paralytic Shellfish Poisoning. This would have
decreased the need to exhaustively collect and analyze samples.
The analysis of hcreases in CHD mortality due to a possible dietary change was based on
the resdts of the Browner et al. (1991) study. They had used a reforrnulation of the
regression equations fiom Keys et al. (1965, 1974) and Hegstedt et al. (1965), which
related changes in dietary fat intake with changes in s e m cholesterol levels. If this
relationship is not accurately represented by these equations, then the results here could be
biased. The use of these equations, however, seems to be well-accepted (e.g. Oster and
Thompson 1996). Further, Browner et ai. (1991) used several U.S. data sources on dietary
fat intûkes, s e m cholesterol levels and CHD mortality rates to derive their resutts.
Possible differences in the etiology of CHD between First Nation peoples and non-
aboriginal Amencan populations may preclude the application of the Browner et al. (1 99 1)
results to the analysis here. For instance, the Framingham Heart Study (Anderson et al.
'' It is iikely these were composite samples, including more than one individual per analyzed sample. This information was, however, not available for 1989. Although composite sampling is cheaper, it precludes the analysis of variability in tissue residue levels between individuals.
1987; Kannel 1987, 1988) was used to relate s e m cholesterol levels and CHD incidence
for women and older men. This study involved largely white, rniddle-class individuals
living in a Boston suburb. The application of these results to different populations may be
inappropriate. It has been suggested that the relationship between dietary fat consumption
and s e m cholesterol levels may not be as strong for some First Nations peoples as for
those of non-aboriginal origin. One study of Tsimshian peoples on Vancouver Island
revealed that individuals had low levels of arachidonic acid (AA)~' (Young 1994). Levels
of this 0-6 fatty acid remained low even after the exclusion of traditional foods fiom the
diet. This observation has led to the suggestion that Tsimshian peoples nay have a
lowered enzymatic activity or deficiency which is genetically determined (Young 1994). If
me, these peoples should have an inherited reduced risk of CHD. Increases in CHD
mortdity due to the diet substitution of shellfish with store-bought foods rnay be
overestimated. The Frarningharn Heart Study, as well as the other information sources
used by Browner et al. (1991) (e.g. the Multiple Risk Factor Intervention Trial), is widely
accepted though as being one of the best data sources available (e.g. Brown and Smith
1995; Oster and Thompson 1996).
The primary orientation of this study has been an assessrnent and cornparison of risk vs.
risk. There are a number of health benefits associated with shellfish consumption that
should be noted in evaluating alternative risk management decisions for fisheries. For
29 AA is produced in the body h m the parent polyunsaturated fatty acid, linoleic acid (Budowski 1988). AA, in turn, is converted by platelets to the prostanoid thromboxane A, (TXA,), a strong platelet aggregator and vasoconstrictor (Le. pro-thrombotic).
many years, it was recommended that hypercholesterolemic patients reslrict their
consumption of shellfish because of their presumed high cholesterol content. Et has now
been established, however, that about two-thirds of the sterols in most moliuscan shellfish
are non-cholesterol sterols that have potentidly important health benefits (Corner and Lin
1982; King et al. 1990; Ackman 1995). These sterols appear to inhibit the intestinal
absorption of cholesterol in animals and humans. They may have a hypocholesterolemic
effect as a result and, thereby, reduce the risk of heart disease (i.e. CHD). Fuaher, shellfish
contain 0-3 polyunsaturated fatty acids (PUFAs) (King et al. 1990; Ackman 1995). The
intake of these fatty acids, especially eicosapentaenoic acid (EPA), appear to have
hypocholesterolemic and significant hypotriglyceridemic effects in bath normal and
hyperIipidemic subjects (Budowski 1988; Leaf 1994). The rarity of cardiovascular disease
arnong the Inuit has been attributed to their marine-based diet, which is rich in these fatty
acids (Dyerberg 1989). Possible anti-thrombotic properties of o-3 PUFAs rnay also reduce
the risk of stroke. Further, they may be beneficial in the prevention of certain tumors such
as those of the breast and colon (Budowski 1988; Borek 1994). Such potentid health
benefits may be perceived to outweigh the possible dioxin-risks of eating shellfish.
It should be noted that the amounts of 0-3 fatty acids found in shellfish may not be high
enough to exert an effect on CHD risk factors. Table 11 displays the total 0-3 PUFA and
EPA contents of some shellfish species.
Table 1 1 : Total a-3 Fatty Acid and EPA Contents of Some Shellfish Species (g/100 g wet weight)
Pacific Oyster Blue Musse1 Manila Clam Dungeness Crab Pink Shrïmp
Total a-3 0.72 1 .O3 0.74 0.39 0.36
EPA 0.35 0.47 0.19 0.27 0.20
(fiorn King et aI. 1990)
Human intervention trials indicate that intakes of 2-3 glday of EPA are needed to have an
anti-thrornbotic effect (Budowski 1988). A study conducted by Kromhout et al. (1 985)
does suggest though that even srnall amounts of a - 3 fatty acids can reduce the rîsk of
0. In 1960, they coilected fish consumption information on 872 rniddle-aged men, free
of symptomatic CHD, from the t o m of Zutaphen, Netherlands. Subjects were divided into
five categories according to the arnount of fish consumed. In the following 20 years,
Kromhout et al. (1985) monitored those who had died fiom CHD. From their
observations, they caiculated crude and adjusted CHD mortality risk ratios3031 for each
consumption category. Table 12 displays their results. In ail categories, an inverse
relationship between fish consumption and CHD mortaiity was observed. They estimated
that about two-thirds of the fish consurned were lean fish, while one-third were fatty. The
highest fish-eating group of 145 g/day was estirnated to consume about 0.4 g EPNday
Hence, even srnaIl amounts of EPA over a longer time period may significantly reduce the
Risk ratio refers to the risk of CHD mortality, relative to that for those who do not eat any fish.
3 1 Risk ratios were adjusted to account for such health and lifestyle factors as age, cigarette smoking, subscapular skinfold thickness, physical activity, daiIy energy intake, dietary cholesterol and occupation.
risk of CHD. In light of this, the maintenance of a traditionai diet hi& Ui sheilfish is
potentially beneficiai.
Table 12: Calculated Cnide and Adjusted CHD Mortdity Risk Ratios for the Amount of Fish Consumed
Fish Consumption Rate Cmde Risk Ratio Adjusted Risk Ratio W ~ Y
O 1 .O0 1.00
1-14 0.60 0.64
15-29 0.57 0.56
304 0.46 0.36
245 0.42 0.39
(fiorn Kromhout et al. 1985)
The potentiai implications of risk management decisions for the health of First Nations
peoples has been the focus of this study; health being concephialized in the narrowest of
terrns (i.e. absence of disease or affliction). It has been emphasized that the physical health
of First Nations peoples is closely intertwined with their social and cultural well-being (e.g.
Kuhnlein 1993; E.A.G.L.E Project 1996). This, in turn, is strongly connected to their
relationship with the environment. As Beaton States (1 994, quoted in Elliott and Foster
1995: 11, "Good health for the Aboriginal peoples relies on an interconnechg system of
land and spirit, body and mind ... a living relationship of culture (land-language-law) and
health (minci-body-place)...". Although the socio-cultural benefits of shellfish harvesting
are not easily measured in quantifiable tems, their consideration is important. Some
benefits to be considered are briefly outlined in the following.
Country food harvesting in generai involves certain traditionai values, practices and
customs which are culturally signifïcant. In one study of aboriginal fishing in the Fraser
River Basin (&met 1973)' for instance, a hi& proportion of survey respondents thought it
was important to share the fish catch, especially with the old or sick. Fishing was also
found to be socially beneficiai for it was often a familial activity. It also provided an
opportunity to interact with other members of the community. Harvesting further helps to
maintain traditions and culturai knowledge such as fishing techniques. The physical
activity associated with harvesting also has associated health benefits. As stated by one
member of an aboriginal community (in Heffernan 1995: 276), "...I used to be an
outdoorsman ... 1 was always out gathering food and sickness was something that was
a!most unknown when you were out in the air al1 the the".
There are also economic benefits related to harvesting; that is, it helps to enhance
economic self-reliance. By supplementing the diet with resources available fiom the locai
environment, the costs of market foods can be off-set meaith Canada 1994). One program
designed to encourage the consumption of iraditional foods among the Nuxaik in the
1980's revealed that food expenditures decreased by 40% when country foods
supplernented the diet (Kuhnlein 1987). This can be especialIy advantageous for poorer
families who cannot &ord to buy nutritious, high quality market foods. Additionally,
country foods can provide a potentiai source of income and employrnent. In light of the
above, risk management decisions such as fishery closures can be expected to disrupt
cutturaliy and econornically significant country food harvesting and consumption patterns.
5. Conclusions, Recommendations and Thoughts for the Future
The primary purpose of this andysis was to describe and compare the potentiai health
impacts of alternative risk management option.. for First Nations peoples in the
management of dioxiri and furan contamination of coastai areas of British Columbia This
was based on the prernise that appropriate risk management options intended to protect
aboriginai peoples cannot be chosen without fully analyzing a nsk situation; that is, to
compare the target or direct risks with the potential implications of risk management
alternatives. The excess cancer risks posed to aboriginai peoples through consuming
dioxin- and furan-contaminated shellfish fiom selected coastal areas of British Columbia
were estimated in this study. The results were compared to potentiai increases CHD
mortality that codd cesult if fishery management actions encouraged the dietary
substitution of shellfish with higher-fat, store-bought alternatives. In the scenario
deveioped, it was assumed that individuals wodd no longer eat shellhsh in the event of a
fishery closure or consuniption advisory.
The estimated excess cancer risks for the study areas reveaied that the nsk management
activities undertaken by DFO may not have been necessary in some instances. With some
possible exceptions, many of the calcuiated cancer risks were comparabIe to suggested de
minimus levels and examined commonplace risks. Additiondly, the results indicate that
risk management actions such as fishery closures may even create an even greater heaith
risk for First Nations peoples if they serve to encourage greater consumption of market
foods. Substitution of sheIlfish with equivalent amounts of chicken, pork and beef has
been estimated here to potentidly result in 4 to 8 times as many deaths in the three study
areas on average than the number of that which rnay result fiom shellfish consumption (Le.
1989 cancer risks).
A number of factors inject a large degree of complexity and uncertainty into the analysis,
which dernand a more thorough examination of the issues at hand than a simple
cornparison of these results. Table 13 summarizes the discussed factors which rnay or rnay
not favor fishery risk management options to curb shellfish consumption. As shown, there
are severai factors that were discussed which rnay lead to the use of fishery closures and
advisories as the preferred management options. The possible non-cancer effects of
dioxins and the existence of potentidly sensitive sub-populations such as children rnay
warrant the use of such measures as consumption advisories.
The irnpIications of the uncertainty reiated to the use of risk assessrnent as a basis for
decision-making is Iess certain. Individuais typically tend to want to avoid potentialiy
serious consequences that have large associated uncertainties (Reckhow 1994). Activities
to manage the cancer risks of eating shellfish rnay hence be favored. On the other hand,
the benefits related to eating shellfish rnay be considered by some to be greater than the
potential cancer risks. For instance, shellfish consumption may help reduce the risks of
heart disease because of the non-cholesterol sterols many shellfish contain (Corner and Lin
1982; King et al. 1990; Ackrnan 1995).
Table 13: Summary Table of Factors Which May or May Not Favor the Use of Risk Management Actions to Restrict Shellnsh Consumption h n g Aboriginal Peoples
Factors for Consideration Risk No Risk UncIear Comrnents Management Management
Cancer risks are considered X unacceptable -----x-- -------__1--1-..
Cancer risks may be Comparable to suggested de considered acceptable minimus levels and some
- ---- commonplace risks -- Number of deaths predicted X for shellfish consumption rnay be lower than possible CHD deaths due to a dietary change
----.I__-...--------
Overestimation of cancer risks X Many of the cancer risks meet (e.g. Iow-dose Iinearity, some standards of acceptability decrease of dioxin and fiiran tissue residues over t h e ) -. -*---------------*--------.--**-*..-.-*--**-..-.--
0-n- X If actua1 CKD risks may be deaths Iower than those for cancer, (e.g. substitution for shellfish fishery closures and advisories with higher-fat, store-bought may be considered necessaq; foods asswned) but many cancer risks may
already be acceptable - ~ _ _ . _ ~ ~ _ _ . l - - - - - - - ~ - - - - - ~ - - - - . . . . . - ~ - . . - - C
If shellfish substituted with X high-fat foods, risks of breast, coIorecta1 and prostrate cancer rnay be enhanced ~...*-~1.~.-.*-~.--*-----*--------------------*--*---.---.--...~..--..-.*......~.-.~**~.....~***~-..-.-~-~-
Other dioxin-related health X effects possible (e.g. irnmunotoxic, negative reproductive effects ) .-.----~*.--*-.-.~----------.----~-----.*---.---.--..-----...*.-.*.----.--------.--- Sub-populations maybe be at X Certain sub-groups such as excessive risk chiidren may require special
management actions .-.-.-**.---.-.~.--*--.-*----.-*..- ~--------------------------------~~---.--.~.~~.-.-**.*-.-**...---..--*..-*-*.~--.-.--*~...*-~-.--~..-~..~.-.~~~-.*..~*~~~..-
Uncertainty of risk assessment X Nature of uncertainty, and the and data sources used* perceptions thereof, is
influential ------..-.*--- ~-*.---*.--.----**~--.-.-...*.*--.--~..-...-*---.----..-.-..--.-.-.*-.-..-***---.-.---
Uncertainty in CHD estimates X Nature of uncertainty, and the
(e.g. reduced risk of heart
benefits of harvesting *How uncertainty is dealt with can Vary depending upon its source, potential consequences and breadth and how this influences individual perceptions. Individuals, however, tend to avoid serious consequences that have large associated uncertainties (Reckhow 1994). As death is the potential outcome here, activities intended to thwart these risks would be likely.
In considering the various uncertainties and issues raised overail, it appears that the weight
of evidence suggests that the fishery management activities undertaken codd create more
h m than good. If greater consumption of higher-fat, market foods is indirectiy
encouraged through a fishery closure, the CHD risks of such foods may exceed that of
cancer in eating shellfish. Also, the risks of cancers such as those of the breast and
prostrate may be enhanced. There are also potentiai health benefits of eating shellfish such
as the effects of 0 - 3 PUFAs (Conner and Lin 1982; King et al. 1990; Ackman 1995).
Further, fishery closures and advisories negatively disrupt traditionai harvesting and
consurnption patterns that are culturally, spirituaily and economicaily beneficial.
The intent of this anaiysis was neither to suggest the exact management activities that
should be undertaken nor to make specific recornrnendations regarding diet. The choice of
management options, as indicated, involves subjective decisions regarding risk tradeoffs
and acceptable risk. Subjectivity is expected to be especially great when there are different
degrees of uncertainty related to different risks that are to be compared (Putnain and
Graham 1993). In the end, it is those who are exposed to risks, and who must potentidly
make major lifestyle changes in response to them, who should be involved in the decision-
making process as to what risks may and or may not be acceptable. As such, it is
recommended that aboriginal peoples be involved in the formulation of future fishery risk
management activities. Due to the importance of fishery resources for aboriginal coastal
peoples, they should aiso be included in the identification of research prionties and the
design and irnplementation of pollutant monitoring programs. With their involvement, risk
management decisions that unnecessarily or unfavorably impact the harvesting and
consumption of country foods rnay be avoided in the future. Treaty negotiations could
provide a forum to reach an agreement as to how and to what extent First Nations peoples
could constructiveiy work with the govenunent in the assessment and management of
contaminants.
This study has highlighted the potentid problems that may aise if only the direct risks of
concern are the focus of risk assessment and risk management. Without examining the
possible implications of aiternative risk management options, countervailing risks may
arise which could pose an even p a t e r risk tbm the one initiaily targeted. Risk vs. risk
approaches do have a number of associated problems. Many risks such as the non-cancer
effects of chernical exposure may be difficdt or impossible to quanti@ (Lave 198 1). This,
in turn, makes it problematic to make risk cornparisons and decisions. In contrast, it would
not be reaiistic to expect that al1 aspects of a particular risk situation can be quantified.
Further, the absence of numbers attached to certain risks does not necessarily mean that
their anaiysis cannot be informative. It may help to identify key issues that need to be
addressed and uncertainties that require further research and examination Gave 198 1 ;
Keeney and von Winterfeldt 1986). It could also be argued that some aspects of a risk
situation should not be quantified because it could result in the loss of critical qualitative
information such as the socid valuation of country food harvesting (Silbergeld 1993).
Risk vs. nsk approaches c m also be more time-consuming and costly. They may help to
identify poor risk management options, however, and thereby lead to more responsible
decision-making and effective nsk management choices (Lave 198 1; Keeney and von
Wmterfeldt 1986; Graham and Weiner 1995). This wodd serve to reduce the costs of nsk
management decisions in the long m. Even in using a risk vs. risk approach, however,
unforeseen nsks will inevitably occur in some instances. Not d l risks can be identified. It
is clear though that a more thorough analysis uf a risk situation and management options
shouid help to reduce the number of potential countervailing risks. Serious or large
magnitude risks should dso be thwarted. It should also be recognized that an attempt to
identifi and examine al1 potential countervailing risks wodd neither be desirable nor
possible. The question of where to stop modeling is a dificult one which requires
thorough consideration. As a mie, the costs of anaiyzing indirect nsks should not exceed
the potential benefits that may accrue in terms of overall nsk reduction (Graham and
Weiner 1995). In sum, the benefits of a risk vs. risk approach outweigh its related
disadvantages. Regulators should attempt to incorporate such an approach as part of a
decision-making framework for the assessrnent and management of risks.
Appendix A
Scientific Terms for Shellfish Species Discussed
Clam, butter
native littieneck
manila
Crab, dungeness
Mussel, blue
Oyster, pacXc
Shrimp, pink
Saidornus gzganteus
Pro tothaca staminea
Venerupis japonica
Cancer magister
Myti f us eduZis
Crasostrea gigas
Mixed species, e.g. P andulus boreaZiF,
Pandalis jordani
Appendix B
Table 14: Calculated TEQs (mgkg wet weight) According to Speciesfïissues for the Examined Areas for 1989-1995 for which Data was Available ' Area Speciesïïissue Year Average TEQ Lower 2.5% Lower 97.5%
Kitimat Crab Hepatopancreas 1989 1.33 x 104 N.A. N.A. 1990 7.97 x 10" 6.93 x 10" 9.13 x 10-~ 1992 1 . 4 loT5 3.96 x [06 3.76 x IO-' 1995 7.43 x 10" 3.37 [04 1.45 x IO-'
Clam 1989 2.72 x 1 O-' N.A. N. A. 1992 3.16 x IO-' N.A. N.A.
Gold River Crab Hepatopancreas 1989 1990 199 I 1993 1995
Crab Muscle 1989 1990 1993 1995 1989 1990 1991 1993 1995
Prawns
N.A. 1.67 x IO-' 8.49 x 10" 3.87 x 10'' 1.25 x l o 5
N.A. 2.63 x IO" 1-14 x lo4 3-89 x IO-7
N.A. 1.02 x IO"
N.A. 2 . 1 4 ~ lo4 5-30 x l ~ - ~
N.A. 3.68 x 10" 7.67 x loJ 1.05 x 10-~ 3.93 loJ
N.A. 7.52 x 10'' 5.38 x IO-' 4.85 x IO-^
N.A. 3.97 IO-'
N.A. 1.52 x 10" 1.42 x 106
Powell River Crab Hepatopancreas 1989 1.70 x IO" N.A. N.A. (closed area)
1990 1.13 x IO-' 3.35 x 10" 2.88 x IO-' 1993 1.00 x IO-' N.A. N.A. 1995 7.85 x 10" 1 . 9 6 ~ IO" 4.47 x IO-'
Crab Hepatopancreas 1990 3.31 x IO-' 1.32 x 10" 6.9 1 x 1 0" (advisory m a ) '
1991 2.72 x IO-' 7.02 x 10-' 1.54 x IO-' 1993 4.51 .u lg5 1.61 x 105 1.00 x loJ 1995 1.19 x 1tY5 N.A. N.A.
Crab Muscle 1989 2.20 IO-' N.A. N.A. 1990 7.93 x 104 4.79 x 1 0 - ~ 3-76 x IO-' 1993 4.06 x lO6 6.62 x IO-^ 1.33 x IO-' 1995 1.58 x 10" 2.48 x IO-^ 5.31 x 10"
Oyster 1989 1.04 x IO-' N.A. N.A. 1990 1.78 x 1 . 1 8 ~ 10" 8.35 x IO-' 1991 7.46 x 10" N.A. N.A. 1993 7.20 x 10" 4.3 1 IO-' 3.14 x l ~ - ~ 1995 7.06 x IO-' 1.59 x IO-^ 2.03 x 104
'Calculated from DFO 19896, 1990, 1991, 1992, 1993, 1995a. 'N.A. refers to those years for which an estimate of variance could not be calculated because only one composite sarnple was taken for the respective areas. 3 The area for which consumption advisories were issued Iay outside the zone of the total crab fishing closure (see Map 4).
Appendix C
Background to the Assessment of the Excess Cancer Risks of Consuming Shellnsh
The approach taken in this analysis to m e s s the cancer risks of eating dioxin and furan
contaminated sheMsh for aboriginal peoples in coastai areas of British Columbia is similar
to that taken by the U.S. Enviromentai Protection Agency (EPA). This approach is
fundarnentally different from that used by Hedth Canada, whose risk assessments form the
basis of DFO's decisions regarding fishery risk management strategies. Differences
between the two countnes in their assessment of dioxin risk are related to dissirnilm
theoreticai assumptions made regarding the carcinogenic mechanisms of 2,3,7,8-
tetrachiorodibenzo-pdioxin (TCDD) and its structural analogs.
A landmark study on dioxin toxicity, conducted by Kociba et al. (1978), provided the basis
for the assessment of the cancer risk of long-term dioxin exposure in both couniries. In
this bioassay, lhree groups of Sprague-Dawley rats, each containing 50 animals of each
sex, were fed 100 000 pg TCDDkgIday, 10 000 pg TCDDkgIday and 1 000 pg
TCDD/kg/day, respectively. Those fed the highest dose exhibited a significantly elevated
rate of excess tumors in cornparison to the control group, while those fed 10 000 pg
TCDD/kg/day displayed a slightly increased rate. The group fed 1 000 pg TCDDkgIday
showed no statistically significant elevated rate of excess tumors.
Based on these results, Health Canada concluded that TCDD is a tumor promoter which
has a threshold, below which there is a no-ef5ects level. A safety factor of 100 was applied
to the identified no-observable-effects level of 1 000 pg TCDD/kg/day to derive a tolerable
daily intake for humans (TDI) of no more than 10 pg TEQ/kg/day (Feeley and Grant 1993).
To determine the existence of dioxin-risk, the daily dose for an exposed population is
examined to see if this TDI is exceeded. For shellfish, assumed consumption rates are used
in the estimation of exposure dose (e-g. 40 dday crab muscle, 20 g/day hepatopancreas).
A maximum pennissible level of 20 ppt TEQ for fish has been established using the safety
factor approach (Dalpé, Chernical Health Hazard Assessrnent Division, Bureau of
Chernical Safety, Food Directorate, Health Canada, pers. comm. 1996).
The EPA, on the other hand, uses a more conservative approach to the assessment of
dioxin risk. In their analysis, the EPA concluded that the Kociba et ai. (1978) bioassay was
too insensitive to detect an effect at the lowest dose rate of 1 000 pg TCDD/kg/day
(Covello and Merkhofer 1993). The agency applied a linearized form of the multistage
mode1 (LMS) to the da% assuming that a linear relationship exists between dose and
response through zero dose. Using the 95% upper confidence limit on the linear term, they
derived a cancer potency factor of 156 000 for the assessment of dioxin risk.32J3 From
" To estimate cancer risk, the EPA sirnply multiplies this cancer potency factor, designated as q,*, by the estimated exposure dose (e.g. see U.S. EPA 1989).
33 The EPA is currently in the process of re-evaluating their denved cancer potency factor of 156 000 (Finkel 1988; Lucier et al. 1993).
this, the EPA estimated that a chronic exposure of 6 fg TCDDkglday in humans would
cause an increased risk of one in one million (1 04 (Keenan et al. 1991; Lucier et al. 1993).
The use of a Linear model to estimate dioxin-risk has been cnticized for producing overly-
conservative estirnates and as not being representative of the mechanisms through which
these substances exert their toxic effects. The evidence suggests that TCDD and its
structural analogs elicit toxic responses through their interaction with the Ah receptor (Safe
1989, 1990; Lucier et ai. 1993; Portier et al. 1993). As receptor-mediated effects rnay
involve a threshold below which no toxic effects c m occur, a threshold model or a safety
factor approach is often suggested as best (e.g. Health Canada (Feeley and Grant 1993)).
The safety factor approach used by Health Canada does provide a simple way of
d e t e m g the existence of a risk. Like the EPA, a linear model (Le. the multistage
model) was chosen here for the assessrnent of dioxin nsk, however, for a number of
different reasons." First, the çafety factor approach precludes a probabilistic quantification
of the level of nsks involved. In other words, only qualitative statements about rkk levels
can be made (e.g. 'high' or 'low,' 'safe' or 'unsafe'). This makes it difficult to establish
appropriate risk management decisions, or a decision fmmework thereof, which are readily
standardized according to definitive, probabilistic risk levels. Second, there is vimially no
scientific basis for the choice of a particular safety factor to account for uncertainty in the
use of animal data to extrapolate effects in humans (Rodricks 1992). There is also no way
34 The CPF derived in the analysis here using the multistage model must nor, however, be confuseci with that estimated by the EPA. The EPA's CPA is calculated as the upper confidence limit of the fitted LMS. The CPF derived here represents a 'best estimate' of the fitted standard multistage model and wiIl result in less conservative estimates of dioxin risk.
of knowuig how close the threshoId lies to the true threshold in any given population
because such factors are not capable of scientific validation. Third, the estimation of a
tolerable daily intake gives the unredistic impression that there is a clear dividing Iine
between what is 'safe' and 'unsafe.' Due to the heterogeneous nature of populations,
however, it can be expected that individuals will exhibit different thresholds (Weinstein
1983; Covello and Merkhofer 1993). This makes it difficuit to identify a threshold level
that will apply to the majority of individuals in a given population. Fourth, a mode1 has yet
to be developed which adequately represents the receptor-mediated effects of dioxins and
furans. Fifth, a threshold may not exist for some established biological effects of TCDD
exposure (Le. for the induction of CYPlAl and CYPlA2 and the loss of plasma membrane
epidermal growth factor in the rat liver) (Portier et al. 1993).
Appendix D
Method Used to Derive Parameter Estimates for the Multistage Mode1
The mdtistage model assumes that a neophm occurs through a series of mutational
stages, with the carcinogen linearly af5ecting at least one transition between stages (Portier
and Hoel 1983; Krewski, Gaylor and Szyszkowicz 1991). In using this model, the assessor
bas the flexibility to determine the number of stages required for a tumor to become
mdignant. No more than two-stages are generally used nor needed (Portier and Hoe1
1983). A two-stage multisbge model was tIius applied for the analysis, as folIows,
- ( a,, + a,dl + azdz) P(d) = 1 - e
where P is the proportionai turnor response at dose d, a. represents the spontaneous rate of
occurrence, and aldl and a-# depict the response at dose d.
To use Solver, it was first necessary to denve preliminary estimates for the mode1
parameters. Initiai parameter estimates were cdculated based on the premise that when d
is small,
P(d) z a,d
where P is the proportional turnor response at dose d and al represents the steepness of the
slope in the low-dose range (Krewski, Gaylor, Szyszkowicz 1991). Through this simple
assumption, an initial estimate for the pararneter al can be calculated. A first estimate for
the parameter ai is then easily decived. Using the lemt squares method, the model was
fitted with the initial parameter estimates. The Solver function was used to derive an
optimal fit.
Appendix E: Distribution Shapes for Some Inputs into the Calculation of the Excess Cancer RUks of Consuming ~ h e l l f i s h ~ ~
Figure 7: Shape of Distribution of Tissue Residue Toxic Equivaients in Kitirnat Crab
Tissue Residue Level (mgkg)
Figure 8: Shape of Distribution of Tissue Residue Toxic Equivalents for Gold River Crab Muscle (mgkg), 1990
Tissue Residue Level (mglkg)
35 Al1 distributions have been denved assuming a lognormal distribution.
Figure 9: Shape of Distribution of Tissue Residue Toxic Equivalents in Powell River Oyster (mgkg), 1995
Tissue Residue Level (mgkg)
Figure 10: Shape of Distribution of Human Body Weight (kg)
Body Weight (kg)
Figure 11 : Shape of Distribution of Crab Muscle Consumption Rate (glday)
Consumption Rate (g/day)
Figure 12: Shape of Distribution of Crab Hepatopancreas Consumption Rate (g/day)
Consumption Rate (glday)
Appendix F: Distribution Shapes for Selected Inputs into the Calculation of Increases in Excess CHD Mortality Due to the Substitution of SheLifîsh with Chicken, Beef and
~ o r k ~ ~
Figure 13: Shape of Distribution of Percent Change in Energy Consumed as Satutated Fat Among Men Due to Crab Substitution
Energy Consumed as Samrated Fat (%)
Figure 14: Shape of Distribution of Percent Change in Energy Consumed as Sahirated Fat Among Wornen Due to Crab, Clam and PrawnlShrimp Substitution
Probability
Energy Consumed as Saturated Fat (%)
36 The distributions have been derived assuming a lognomal disuibution.
Appendix G
Table 15: Excess Lifetime Cancer Risks According to Area and Speciesrïissues for 1989- 1995 for which Tissue Residue Data was Available
Excess Lifetime Risk Area Species Year Mean Upper 95% Minimum Maximum
Kitirnat Crab Hepatopancreas 1989 1.28x10-~ 4 .19~10" l .OIx10~~ 3 . 2 3 ~ 1 0 ~ 1990 7 . 6 2 ~ 10" 2.51 x IO" 5.81 x 104 1.91 x 1 0 ~ 1992 1.34 x 10" 4.76 x 10" 4.90 x 10'~ 4.85 x IO-^ 1995 7.08 x IO-? 2.42 x IO" 5.44 x IO-^ 27.5 x IO"
Clam ' 1989 2.92 x lo5 9.68 x IO-^ 2.38 x IO-? 1 .O3 x IO-^ 1992 3.39x10-? 1 .12~10" 7 . 7 6 ~ 1 0 ' ~ 1 . 5 4 ~ 1 0 ' ~
Gold River Crab Hepatopancreas 1989 3.82 x IO-' 1.26 x loJ 1990 1 . 0 5 ~ 1 0 ~ 3.95x10J 1991 2 . 8 4 ~ 1 0 ' ~ 1 . 0 0 ~ 1 0 ~ 1993 2.77~10" 1 . 0 2 ~ 1 0 ~ 1995 1.01 x IO-^ 3.67 x IO-'
Crab Muscle 1989 4.54 x 10A5 1.49 x 104 1990 5.57 x IO-^ 1.83 x IO-' 1993 1.47 x 10" 5.45 x IO-' 1995 1.19 x IO-' 4.44 x IO-'
Prawns 1989 1.55 x IO-' 4.98 x IO" 1990 9.31 x IO" 3-15 x 10" 199 1 7.99 x IO" 2.56 x 1 O" 1993 2.85 x 10" 9.92 x 10" 1995 3.93x10-~ 1.31~10"
Powell River Cmb Hepatopancreas 1989 1.62 x IO" 5.36 x IO" 9.30 x IO-' 3.43 x IO" (closed m a )
1990 1.10 x IO-' 3.91 x IO*' 2 . 0 2 ~ 10" 5-53 x IO-' 1993 9.55~10" 3 .16~10" 5.47~10" 2.02x10-' 1995 7.66~10" 3.04x10-' 2 . 1 6 ~ 1 0 ' ~ 1 . 5 5 ~ 1 0 ~ ~
Crab Hepatopancreas 1990 3.06 x 1 0 ~ 1 .O4 x IO-' 1.82 x 10" 1.2 1 x IO^ (advisory a m )
199 1 2.49 x IO" 9.33 x 10" 1.44 x 10" 4.47 x IO" 1993 4.42~10" 1 . 5 3 ~ 1 0 - ~ 1.67~10" 1 . 9 2 ~ 1 0 ~ 1995 1.14 x 104 3.75 x 10" 6.51 x IO-^ 2.40 x 10"
Crab Muscle 1989 2.62 x 8.76 x IO-' 1.82 x 1 O-' 1.6 1 x 1990 9.35 x IO" 3.61 x IO-^ 5.40 x los 7.62 x IO-' 1993 4.87~10" 1.83~10-' 1.10~10" 5 . 5 4 ~ 1 0 ~ 1995 1.87~10" 7 .00~10" 5.81x10-~ 1.12x10-' 1989 1.11 x loJ 3.76 x 104 9.73 x IO-? 3.26 x 10" 1990 1 . 8 8 ~ 1 0 ~ ~ 7.36~10" 1.54~10" 1 . 5 1 ~ 1 0 ~ ~ 1991 7.97 x IO" 2.69 x IO-' 6.98 x IO-' 2.33 x loJ 1993 7.40 x IO" 2.75 x 105 9.64 x IO" 9.0 1 x IO-' 1995 7.38x10-? 2.71~10" 2.62~10" 3 . 8 6 ~ 1 0 ~ '
' Risk estimates for clam could onIy be calculated for 1989 and 1992 because of the lack of tissue residue data for other years. 2 The area for which consumption advisories were issued lay outside the zone of the total crab fishing closure (see Map 4).
Oyster
References Cited
Ackman, RG. (1995), "Composition and Nutritive Value of Fish and Shellfish Lipids," In A. Ruiter (ed.) Fish and Fishery Products: Composition, Nutritive Properties and Stability, CAB International, Wallingford: 117-155.
Adams, M.R., C.A. Hanna, J.A. Mayernik and W.M Mendez, Jr. (1994), "Probabilistic Health Risk Assessment for Exposures to Estuary Sediments and Biota Contarninated with Polychiorinated Biphenyls, Polychiorinated Terphenyls and Other Toxic Substances," Risk Analysis 14(4): 577-594.
Ames, B. N., R. Magaw and L. S. Gold (1987), "Ranking Possible Carcinogenic Hazards," Science 236: 271 -280.
Ames, B.N. and L.S. Gold (1991), "Cancer Prevention Strategies Greatiy Exaggerate Risks," Chernical and Engineering News Jan. 7 : 28-32.
Anderson, KM., W.P. Casteiii and D. Levy (1987), Tholesterol and Mortality: 30 Years Follow-Up fiom the Framingham Study," Journal of the American Medical Association 257: 21 76-21 80.
Bartsch, M. (1 W6), LcUmweltgifte als "Cocktail" Hochbrisant: Mediziner Fordem Niedrigere Grenzwertelstudie Über Wechselwirkungen," FranyUrter Rundschau, November 9,262:24.
Bennet, M. (19731, Indian Fishing and its Cultural Importance in the Fraser River System, Department of the Environment and the Union of British Columbia Indian Chiefs, Victoria.
Boddington, M.J., A.P. Gilman, R.C. Newhook, R.C. Brame, D.J. Hay and V. Shantora (1 990), Priori@ Substances List Assessrnent Report No. 1: Polychlorinated Dibenzodioxins and PoIychlorinated Dibenzofirans, Canadian Environmental Protection Act, Minister of Supply and Services Canada, Ottawa
Borek, C. (1994), " 0 3 Fatty Acids as Anticarcinogens: CeIlular and Molecular Studies," In C.Galli, A.P. Sirnopoulos, E.Tremoli (eds.) Effects of Fatty Acids and Lipids in Health and Discase, World Review of Nutrition and Dietetics 76: 67-69.
British Columbia Ministry of Environment, Lands and Parks/Environment Canada (1 993), State ofthe Environment Report for British Columbicr, Ministry of Environment. Lands and Parks, Public Affairs Branch, Victoria.
British Columbia Provincial Archives (19661, Our Native Peoples: Kwakiutl (Vol. 7), Department of Education, Victoria.
Bro, KM., W.C. Sonzogni, M.E. Hanson (1987), "Relative Cancer Risks of Chemical Contaminants in the Great Lakes," Environmental Management 1 l(4): 495-505.
Brown, W.V. and D.A. Smith (1995), "Nutrition and Heart Disease," In V. Herbert and G.J. Subak-Sharpe (Eds.) Total Nutrition, St. Martin's Press, New York: 437-477.
Browner, W.S., J. Westenhouse and J.A. Tice (1991), "What if Americans Ate Less Fat?: A Quantitative Estimate of the Effect on Mortality," Journal of the American Medical Association 265(24): 3285-329 1 .
Budowski, P (1988), "o3-Fatty Acids in Health and Disease," World Review of Nutrition and Dietetics 57: 2 14-274.
Burd, M. (1994), Regional Analysis ofBritish Columbia S Status Indian Population: Birth-Related and Mortaliw Stutisrics- Interim Report, Division of Vitd Statistics, Ministry of Health and Ministry Responsible for Seniors, Victoria.
Burmaster, D.E. and P.D. Anderson (1994), "Principles of Good Practice for the Use of Monte Car10 Techniques in Human Health and Ecological Risk Assessments," Risk Analysis 14(4): 477-48 1.
Cairns, J. (19751, "The Cancer Problem," Scientifc American 233(5): 64-78.
Cornor, W.E. and D.S. Lin (1982), "The Effect of Shellfish in the Diet Upon the Plasma Lipid Levels in Humans," Metabolism 3 l(10): 1046- 105 1.
Cooper, C.B., M.E. Doyle and K. Kipp (1991), "Risks of Consumption of Contaminated Seafood: The Quincy Bay Case Study," Enviroizmental Health Perspectives 90: 133- 140.
Covel10,V. T. and M. W. Merkhofer (1993), Risk Assessment Methods: Approachesfor Assessing Health and Environmental Risks, Plenun Press, New York.
Crouch, E.A.C. and R. Wilson (1 982), RisWBenefit Analysis, Ballinger Publishing Co., Cambridge, MA.
Dean, J. H. and L. D. Lauer (1983), "Immunological Effects Following Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dio>iin: A Review," In William W. Lowrance (ed), Public Health Risks of the Dioxins (proceedings of a symposium held on October 19- 20 at the Rockefeller University, New York), William Kaufmann, Los Altos: 275-294.
Departrnent of Fisheries and Oceans (1988), Closure of Fisheries Areus (Nov. 30 News Release), Vancouver.
Department of Fisheries and Oceans (1 989a), "Extended Crab, Prawn and Shrimp Fishery Closures: Howe Sound and Prince Rupert," (Backgrounder to the June 14 Govemment of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1989b), "Shellfish Closures and Consumption Advisories: Coastal B.C. Sites," (Backgrounder to the Nov. 23 Govemment of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1990), "Shellfish Fishery Closures and Consumption Advisories, B-C,." (Backgrounder to the Nov. 29 Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1 99 l), "Shellfish Fishery Closures and Consumption Advisories, B.C.," (Backgrounder to the Aug. 9 Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1992), "Shellfish Fishery Closures and Consumption Advisories, B.C.," (Backgrounder to the May Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1993), "Shellfish Fishery Closures and Consumption Advisories, B.C.," (Backgrounder to the Aug. 27 Governrnent of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1 994), Criteria for the Reducfion or Elimination of Dioxin-Mediated Marine Fishery Closures and Consumption rldvisories on the British Columbia Coast, Water Quality Unit, Habitat Management Sector, Pacific Region, Departrnent of Fisheries and Oceans, Vancouver.
Departrnent of Fisheries and Oceans (1 995a), "Dioxin, Furan and PAH Sunrey Data," (Backgrounder to the Feb. 10 Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1 995b), "Dioxin and Furan Survey Data," (Backgrounder to the Aug. 14 Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1996a), "Dioxin and Furan Survey Data," (Backgrounder to the April 18 Government of Canada News Release), Vancouver.
Department of Fisheries and Oceans (1996b) "DioxidFuran Reductions and Coastal Fisheries Re-Openings," (Backgrounder to the April18 Government of Canada News Release), Vancouver.
Department of National Health and Welfare (1 980) Anihropometry Report: Height, Weight and Body DimenFiom, Nutrition Canada, Department of National Health and Welfare, Ottawa.
Doll, R and R Peto (198 1), "Avoidable Risks of Cancer in the U.S.," Journal of the National Cancer Imtitute 66(6): 1 193- 1265.
Doolan, N., D. Appavoo and H.V. Kuhnlein (1 WO), "Benefit-Risk Considerations of Traditional Food Use by the Sahtu (Hare) Dene/Metis of Fort Good Hope, N.W.T.," Circt~mpolur Heuith 90: 747-75 1.
Dmcker, P. (195 1), Indians ofthe Northwest Coast, The Naturd History Press, New York.
Dyerberg, J. (1 989), "Coronary Heart Disease in Greenland Inuit: A Paradox, Implications for Western Diet Patterns," Arctic Medical Research 48 : 47-54.
E.A.G.L.E Project (Effects on Abonginais Frorn the Great Lakes Environment) (1996), Annual Report 1991-1995, An Assembly of First Nations-Health Canada Partnership.
Elliott, S.I. and L.T. Foster (1995), "Mind-Body-Place: A Geography o f Aboriginal Health in British Columbia," In P.H. Stephenson, S.J. Elliott, L.T. Foster and J . Harris (eds.), A Persistent Spirit: Towardr Understanding Aboriginal Health in British Columbia, Canadian Western Geographical Series (Vol. 3 1), University o f Victoria, Victoria: 95- 127.
Ellis, D.W. and L. Swan ( 1 98 l), Teachings of the Tides: Uses of Murine Invertebrates by the Manhousut People, Theytus Books Ltd., Nanaimo, B.C..
Evers, S., E. McCracken, 1. Antone, G. Deagle (1987), "The Prevalence o f Diabetes in Indians and Caucasians Living in Southwestern Ontario," Canudian Jozirnnl of Public Health 78: 240-243.
Feeley, M.M. and D.L. Grant (1 993), "Approach to Risk Assessment of PCDDs and PCDFs in Canada," Journal of Regdatory Toxicology and Pharmacology 18: 428- 43 7.
Feldman, E.B. (1994), "Nutrition and Diet in the Management of Hyperlipidemia and Atherosclerosis," In M.E. Shils, J.A. Olsen and M. Shike (eds.) Modern Nuirition in Healrh and Disease (8th Ed.), Lea & Febiger, Philadelphia: 1298- 13 16.
Finley, B, D. Proctor, P. Scott, N. Harrington, D. Paustenbach and P. Pnce (1994), "Recomrnended Distributions for Exposure Factors Frequently Used in Health Risk Assessment," Risk Analysis 14(4): 533-553.
Fischoff, B., S. Lichtenstein, P. Slovic, S.L. Derby and RL. Keeney (1981), Acceptable Risk, Cambridge University Press, Cambridge.
Gilman, A- and R Newhook (1991), "An Updated Assessment of the Exposure of Canadians to Dioxins and Furans," Chemosphere 23(11/12): 1661-1667.
Govemment of Canada (1989a), Shellfsh Closures Announced for Howe Sound and Prince Rupert (June 14 News Release), Vancouver.
Govemment of Canada (1 989b), Fishing CIosures and Consumption Restrictions Isstred for Eighr B.C. Sites P o v . 23 News Release), Vancouver,
Governent of Canada (1990), Aàvisory to Limit Consumption of Some Fish, Shellfsh and Waterfowl in British Columbia and Waterfowl in the Yukon (Nov. 29 News Release), Vancouver.
Government of Canada (1991), Advisory to Limit Consztmption of Fish and Shelljkhfiorn the Viciniîy of British Columbia Pulp Mills (Aug. 9 News Release), Vancouver.
Govemment of Canada (1993), Dioxin Levels in Shelpsh Dropping But Contamination CZosures, Consumption Advisories Continue (Aug. 27 News Release), Vancouver.
Govemment of Canada (1995a), Reduced Dioxin Levels Lead to Fisheries Reopenings (Feb. 10 News Release), Vancouver.
Government of Canada (1 995 b), Reduced Dioxin Levels Lead fo Further Crab Fishery Reopenings (Aug. 14 News Release), Vancouver.
Graham, J.D. and J.B. Wiener (1995), "Confronthg Risk Tradeoffs," In J.D. Graham and J.B. Wiener (eds.), Risk Versus Risk: Tradeofs in Profecting Health and the Emironmenf, Harvard University Press, Cambridge: 1-28 1.
Hattis, D. and D. E. Bumaster (1 994), "Assessment of Variability and Uncertainty Distributions for Practical Risk Analyses," Risk Analysis 14(5): 7 13-730.
Health and Welfare Canada ( l989), Health Hazard Assessment of Dioxin and Furan Levels in Fish and Shellfishfiorn Eleven Sites on the Coast of British Columbia, Health Protection Branch, Heaith and Welfare Canada, Ottawa.
Health Canada (1 994), Native Food and Nutrition: An illustrated Reference Munual, Medical Services Branch, Health Canada, Ottawa.
He& Canada (1 993, Anulysis of Stutus Indians in British Columbia: A Vital Statistical Overview (Vol. 3: 1987-1993), Medical Services Branch, Heaith Canada, Ottawa.
Heffernan, M. C. (19951, "Diabetes and Aboriginal Peoples: The Haida Gwaii Diabetes Project in a Global Perspective," In P.H. Stephenson, S.J. Elliott, L.T. Foster and J. Harris (eds.), A Persistent Spirit: TowardY Understanding Aboriginal Health in British Columbia, Canadian Western Geographical Series (Vol. 3 l), University of Victoria, Victoria: 26 1-296.
Hegstedt, D.M., R.B. McGandy, M.L.Myers and F.J. Stare (1965): "Quantitative Effects of Dietary Fat on S e m Cholesterol in Man," American Journal of Clinical Nutrition 17: 28 1-295.
Institute of Food Technologists (1988), "The Risk/Benefit Concept as Applied to Food," Food Technology 42(3): 1 19-126.
Kannel, W.B. (1983, "Metabolic Risk Factors for Coronary Heart Disease in Women: Perspective fiom the Frarningham Study," American Heart Journal 1 14: 41 3-4 19.
Kannel, W.B. (1988), "Cholesterol and Risk of Coronary Heart Disease and Mortality in Men," Clinical Chemise 34 (suppl. B): B53-B59.
Keenan, R.E., D.J. Paustenbach, R.J. Weming and A.H. Parsons (1 99 1 ), "Pathology Reevaluation of the Kociba et al. (1978) Bioassay of 2,3,7,8-TCDD: Implications for Risk Assessment," Journal of Toxicology and Environmental Health 34: 379-296.
Keeney, R.L. (1994), "Sounding Board: Decisions About Life-Threatening Risks," New England Journal of Medicine 331(3): 193-196.
Keeney, R.L. and D. von Winterfeldt (1986), "Why Indirect Health Risks of Regulations Should Be Exarnined," Inteq5aces î 6(6): 1 3-27.
Keys, A., J. Anderson and F. Grande (1965), "Serum Cholesterol in Response to Changes in the Diet, II: The Effect of Cholesterol in the Diet," Metabolism 14: 759-765.
Keys, A, F. Grande and L. Watson (1974), "Bias and Misrepresentation Revisited: Perspective in Saturated Fat," Arnerican Jozirnal of Clinical Nutrition 34: 188-2 12.
King, 1, M.T. Childs, C. Dorsett, J.G. Ostrander and E.R. Monsen (1990). "Shellfish: Proximate Composition, Minerais, Fatty Acids, and Sterols," Journal of the American Dietetic Association 90(5): 677-685.
Kitamaat Village Council, Haisla First Nation (1994), Haisla Diet Study- Interim Report, unpublished.
Kociba, RJ., D.G. Keyes; J.E. Beyer, R.M. Carreon, C.E. Wade, D.A. Dittenber, R.P. Kalnins, L.E. Frauson, C.N. Park, S.D. Baniard, R.A. Hummel and C.G. Humiston (1978), "Results of a Two-Year Chronic Toxicity and Oncogenicity Study of 2,3,7,8- Tetrachiorodibenzo-p-Dioxin in Rats," Toxicology and Applied Pharmacology 46: 279-3 03.
Kocker, D.C. and F.O. Hofhan (1991), "Regulating Environmental Carcinogens: Where Do We Draw the Line?," Environmental Science and Technology X(l2): 1986- 1989.
Krewski, D., D. Gaylor and M. Szyszkowicz (1991), "A Model-Free Approach to Low- Dose Extrapolation," Environmental Health Perspectives 90: 279-285.
Kromhout, D., E.B. Bosschieter and C.L. Coulander (1985), "The Inverse Relation Between Fish Consumption and 20-Year Mortality fiom Coronary Heart Disea~e ,~ New England Journal of Medicine 3 lZ(19): 1205-1209.
Kuhnlein, H.V. (1987), Final Report: Nuxalk Food and Nuirition Program, McGill University, Montreal.
Kuhnlein, H.V. (1 99 1 ), Dietary Evalua~ion of Food, Nutrients, and Contaminants in Forr Good Hope and Colville Lake, Northwest Territories, Final Report to the NHRDP.
Kuhnlein, H.V. (1992), "Change in the Use of Traditional Foods by the Nuxalk Native People of British Columbia" Ecology of Food Nutrition 27(3/4): 259-288.
Kuhnlein, H.V. (1993), "Global Nutrition and the Holistic Environment of Indigenous Peoples," In The Path to Healing: Report of the National Round Table on Aboriginal Health and Social Issues, Minister o f Supply and Services Canada, Ottawa: 25 1-262.
Kuhnlein, H.V. (1995), "Benefits and Risks of Traditional Food for lndigenous Peoples: Focus on Dietary Intakes of Arctic Men," Canadian Journal of Physiology and Pharmacology 73 : 765-77 1.
Kuhnlein, H., A.C. Chan., J.N. Thornpson and S. Nakai (1982), "Ooligan Grease: A Nutritious Fat Used by Native People of Coastal British Columbiq" Journal of EthnobioZogy 2(2): 154-1 6 1.
Lave, L.B. (198 1), The Strategy of Social Regulation: Decision Frameworks for Policy, The Brookings Institution, Washington, D.C.
Lave, L.B. and E.H Malès (1989), "At Risk: the Framework for Regulating Toxic Substances," Environmental Science and Technology 23(4): 386-391.
Leaf, A. (1994), "Some Effects of o3 Fatty Acids on Coronary Heart Disease," In C.Galli, A.P. Simopoulos, E.Tremoli (eds.) Effects of Fatty Acids and Lipids in Heaith and Disease. World Review of Nutrition and Dietetics 76: 1-8.
Leiss, W. and C. Chociolko (1 994), Risk and Responsibility, McGi11-Queen's University Press, Montreal.
Lucier, G.W., C.J. Portier and M.A. Gd10 (1993), "Receptor Mechanisms and Dose- Response Models for the Effects of Dioxins," Environmental Health Perspectives lOl(1): 36-43.
Luebke, R.W., C.B. Copeland, J.J. Diliberto, P.I. Akubue, D.L. Andrews, M.M. Riddle, W.C. Wdliams and L.S. Bhbaum (1 994), "Assessrnent of Host Resistance to Trichinella spiralis in Mice Following Preinfection Exposure to 2,3,7,8-TCDD," Toxicology and Applied Pharmacology 125: 7- 1 6.
Mao, Y. H. Momson, R. Semeciw, D. Wigle (1986), "Mortality on Canadian Indian Reserves 1977-1982," Canadian Journal of Public Healrh 77: 263-268.
Mattison, D.R., M.S. Nightingale and E.K. Silbergeld (1983), "Reproductive EEects of Tetrachlorodibenzo-p-Dioxin," In Wi!liam W. Lowrance (ed.) Public Hedth Rish of the Dioxins (proceedings of a symposium held on October 19-20 at the RockefeIIer University, New York), William Kaufmann, Los Altos: 21 7-243,
Morgan, M.G. and M. Henrion (1990), Uncertainty: A Guide to Dealing w i h Uncertainty in Quantitative Risk and Policy Analysis, Cambridge Universiiy Press, New York.
Murray, F.J., F.A. Smith, K.D. Nitschke, C.G. Hurniston, R.J. Kociba and B.A. Schwetz (1979), "Three-Generation Reproduction Study of Rats Given 2,3,7,8- Tetrachlorodibenzo-p-Dioxin (TCDD) in the Diet," Toxicology and Applied Pharmacology 50: 241 -252.
Oster, G and D. Thompson (1996), "Estimated Effects of Reducing Dietary Saturated Fat Intake on the Incidence and Costs of Coronary Heart Disease in the United States," Journal of the American Dietetic Association 96(2): 127- 13 1.
Portier. C and D. Hoel (1983), "Low-Dose-Rate Extrapolation Using the Multistage Model," Biomerrics 39: 897-906.
Portier, C., A. Tritscher, M. Kohn, C. Sewall, G. Clark, L. Edler, D. Hoel and G. Lucier (L993), "Ligand/Receptor Bindiig for 2,3,7,8-TCDD: implications for Risk Assessrnent," Fundamental and Applied Toxicology 20: 48-56.
Putnam, S.W. and J.D. Graham (L993), "Chemicals Versus Microbids in Drinking Water: A Decision Sciences Perspective," Journal of the American Water Works Association 85: 57-6 1.
Reckhow, K.H. (1994), "Importance of ScientSc Unceaainty in Decision Making," Environmentu1 -Management 18(S): 16 1- 166.
Reinert, R.E., B.A. Knuth, M.A. Kamrin and Q.J. Stober (1991), "Risk Assessment, Risk Management, and Fish Consumption Advisones in the United States," Fisheries 16(6): 5- 12.
Rodricks, J. V. (1992), Calcul~ted Rish: Understanding the Toxiciw and Human Health Risks of Chemicals in Our Environment, Cambridge University Press, Cambridge.
Rupp, E.M, F.L. Miller and C.F. Baes, iIl(l98 l), "Some Results of Recent Surveys of Fish and ShelIfish Consurnption by Age and Region of US. Residents," Health Physics 39: 165-175.
Safe, S. (1989), "Risk Assessment of PCDDs and PCDFs Based on In Vitro and In Vivo Bioassays," Chemosphere 19(1-6): 609-6 13.
Safe, S. (1 990), "Polychlorinated Biphenyls (PCBs), Dibenzo-p-Dioxins (PCDDs), Dibenzofurans (PCDFs), and Related Compounds: Environmentd and Mechanistic Considerations Which Support the Development of Toxic Equivalency Factors (TEFs)," Critical Reviews in Toxicology 2 l(1): 5 1-88.
Silbergeld, E.K. (1993), "Revising the Risk Assessrnent Paradigrn: Limits on the Quantitative Ranking of Environmental Problems," In C.R. Cothern (ed.) Comparative Environmenfa1 Risk Assessment, Lewis Publishers, Boca Raton: 73-85.
Slovic, P. (1987), "Perception of Risk," Science 236: 280-285.
Travis, C.C., S.A. Richter, A.A.C. Crouch, R. Wilson and E.D. Klema (1 987), "Cancer Risk Management: A Review of 132 Federal Regdatory Decisions," Environmental Science and Technology 2 l(5): 4 15-420.
Travis, C.C. and M.L. Land (1990), "Estimating the Mean of Data Sets with NondetectabIe Values," Environmental Science and Technology 24(7): 96 1-962.
U.S. EPA (1 988), "2,3,7,8-Tetrachlorodibem-p-Dioxin," Reviews of Environmentd Contamination and Toxicology 1 07: 147- 1 63.
U.S. EPA (1 989), Assessing Human Health Rishfiom Chemically Contaminated Fish and ShellJsh: A Gridance Manual, US. EPA, Washington, D.C..
Waldram, J.B., D.A. Herring and T.K. Young (1995), Aboriginal Health in Canada, University of Toronto Press, Toronto.
Waxman, S., L-Gross, C.Shreiber and V-Herbert (1995), "Nutrition and Cancer," In V. Herbert and G.J. Subak-Sharpe (eds.) Total Nutrition, St. Martin's Press, New York: 479-495.
Weinstein, B.I. (1983), "Dioxins as Carcinogenic Promoters," In William W. Lowrance (ed.) Public Health Risks of the Dioxins (proceedings of a symposium held on October 19-20 at the Rockefeller University, New York), William Kaufhann, Los Altos: 255- 160.
Whipple, C. ( 1 985), "Red stributing Risk," Regulation May/June: 3 7-44.
Williams, S.R. (1995), Basic Nutrition and Diet Therapy (10th ed.), Mosby, St. Louis.
Wilson, R. and E.A.C. Crouch (1987), "Risk Assessrnent and Comparisons: An Introduction," Science 236: 267- 270.
Wïrsing, R.L. (1985), "The Health of Traditionai Societies and the Effects of Accuituration," Current Anthropology 26(3): 303-3 15.
World Health Organization (1978), Primnry Health Care: Report of the Internarional Conference on Primav Health Care, USSR, September 6-12, 1978, World Health Organization, Geneva.
Young, T.K. (1988), "Chronic Diseases Among Canadian Indians: Towards an Epidemiology of Culture Change," Arcfic Medical Research 47(1): 434-441.
Young, T.K. (1990) Cardiovasctilar Disease and Risk Factors Among North American Indians, Winnipeg: University of Manitoba.
Young, T.K. (1 994), The Henlth ofNative Americans: Toward a Biocultural Epidemiology, Oxford University Press, New York.
Young, T.K., J.M. Kaufert, J.K Mckenzie, A. Hawkins and J. O'Neil(1989), "Excessive Burden of End-State Rend Disease Among Canadian Indians: A National Survey," American Journal of Public Health, 79(6), 756-758.
Zabik, M.E. and M.J. Zabik (1 995), "Tetracholordibenzo-p-dioxin Residue Reduction by Cooking/Processing of Fish Fillets Harvested fiom the Great Lakes," Bulletin of Environmental Contamination and Toxicology 55,264-269.
Zeckhauser, R.J. and W.K. Viscusi (1990), "Risk Within Reason," Science 248 (4), 559-564.
l tS 1 TARGET (QA-3)
APPLIED 1 IMAGE. lnc 1653 East Main Street - -. , Rochester. NY 14609 USA -- -- - , Phone: 71 61482-0300 -- -- - - Fa: 71 6/288-5989
1993. Appïii Image. l x . All Righls Reserved
